Spinal Neurosurgery
ii

NEUROSURGERY BY EXAMPLE
Key Cases and Fundamental Principles
Series edited by: Nathan R. Selden, MD, PhD, FACS, FAAP

Volume 1: Peripheral Nerve Surgery, Wilson and Yang

Volume 2: Surgical Neuro-​Oncology, Lonser and Elder
Volume 3: Spinal Neurosurgery, Harrop and Maulucci
 

Spinal Neurosurgery

Edited by

James S. Harrop, MD, FACS

Professor, Departments of Neurological and Orthopedic Surgery
Director, Division of Spine and Peripheral Nerve Surgery
Neurosurgery Director of Delaware Valley SCI Center
Thomas Jefferson University
Philadelphia, Pennsylvania

and

Christopher M. Maulucci, MD, FACS

Associate Professor of Neurological Surgery
Director of Spine Surgery
Tulane University
New Orleans, Louisiana

1
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1
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Library of Congress Cataloging-​in-​Publication Data

Names: Harrop, James S., editor. | Maulucci, Christopher M., editor.
Title: Spinal neurosurgery /​edited by James S. Harrop, Christopher M. Maulucci.
Description: New York, NY : Oxford Unversity Press, [2019] | Includes bibliographical references.
Identifiers: LCCN 2018029143 | ISBN 9780190887773 (pbk.)
Subjects: | MESH: Spine—​surgery | Spinal Diseases—​surgery | Spinal
Injuries—​surgery | Neurosurgical Procedures—​methods
Classification: LCC RD533 | NLM WE 727 | DDC 617.4/​71059—​dc23
LC record available at https://​lccn.loc.gov/​2018029143

This material is not intended to be, and should not be considered, a substitute for medical or other professional
advice. Treatment for the conditions described in this material is highly dependent on the individual
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Contents

Series Editor’s Preface  vii

Contributors  ix

1. Odontoid Fracture Type II  1

Daniel Tarazona and Alexander R.Vaccaro
2. Cervical Fracture Dislocation  11
Jason Liounakos, G. Damian Brusko, and Michael Y. Wang
3. Occipitocervical Dislocation  21
Alexander B. Dru and Daniel J. Hoh
4. Central Cord Injury  31
Bizhan Aarabi, Charles A. Sansur, David M. Ibrahimi, Mathew Kole, and Harry Mushlin
5. Atlantoaxial Instability  41
Jonathan M. Parish and Domagoj Coric
6. Basilar Invagination and Cranial Settling  49
Benjamin D. Elder and Jean-​Paul Wolinsky
7. Cervical Myelopathy: Lordosis  63
Randall J. Hlubek and Nicholas Theodore
8. Cervical Myelopathy: Kyphosis  71
Mario Ganau, So Kato, and Michael G. Fehlings
9. Ossification of the Posterior Longitudinal Ligament: Cervical  81
Todd D.Vogel, Hansen Deng, and Praveen V. Mummaneni
10. Cervical Radiculopathy Due to Central Disc: ACDF/​Arthroplasty  93
Mazda K.Turel and Vincent C.Traynelis
11. Cervical Radiculopathy: Lateral Disc Foramintomy  101
Michael Karsy, Ilyas Eli, and Andrew Dailey
12. Thoracic Disc Herniation  109
Derrick Umansky and James Kalyvas
13. Thoracolumbar Burst Fractures  123
Omaditya Khanna, Geoffrey P. Stricsek, and James S. Harrop
14. Thoracic Cord Compression: Extradural Tumor  133
Tej D. Azad, Anand Veeravagu, John K. Ratliff, and Atman Desai

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Contents

15. Spinal Cord Tumor: Intramedullary  141

Rajiv R. Iyer and George I. Jallo
16. Spinal Cord Tumor: Intradural Extramedullary  149
Michael A. Galgano, Jared Fridley, and Ziya Gokaslan
17. Radiation-​Sensitive Spine Tumor  159
Adam M. Robin and Ilya Laufer
18. Cauda Equina Syndrome  175
Emily P. Sieg, Justin R. Davanzo, and John P. Kelleher
19. Lumbar Stenosis  183
Miner N. Ross and Khoi D. Than
20. L4–​L5 Degenerative Spondylolisthesis  191
Rani Nasser, Scott Zuckerberg, and Joseph Cheng
21. Isthmic Spondylolisthesis  199
Evan Lewis and Charles A. Sansur
22. Lumbar Degenerative Scoliosis  207
Michael LaBagnara, Durga R. Sure, Christopher I. Shaffrey, and Justin S. Smith
23. Flat Back Deformity  215
Yusef I. Mosley and James S. Harrop
24. Diskitis  225
Jacob R. Joseph, Brandon W. Smith, and Mark E. Oppenlander
25. Epidural Abscess  235
Hector G. Mejia Morales and Manish K. Singh
26. Nonsurgical Spinal Diseases  243
Lahiru Ranasinghe and Aimee M. Aysenne

Index  253

vi
 

Series Editor’s Preface

I am delighted to introduce this volume of Neurosurgery by Example:  Key Cases and

Fundamental Principles. Neurosurgical training and practice are based on managing a
wide range of complex clinical cases with expert knowledge, sound judgment, and
skilled technical execution. Our goal in this series is to present exemplary cases in the
manner they are actually encountered in the neurosurgical clinic, hospital emergency
department, and operating room.
In this volume, Dr. Jim Harrop, Dr. Christopher Maulucci, and their contributors
share their extensive wisdom and experience with all major areas of spinal neurosur-
gery. Each chapter contains a classic presentation of an important clinical entity, guiding
readers through assessment and planning, decision-​making, surgical procedure, after
care, and complication management. “Pivot points” illuminate the changes required to
manage patients in alternate or atypical situations.
Each chapter also presents lists of pearls for the accurate diagnosis, successful treat-
ment, and effective complication management of each clinical problem. These three
focus areas will be especially helpful to neurosurgeons preparing to sit for the American
Board of Neurological Surgery oral examination, which bases scoring on these three
topics.
Finally, each chapter contains focused reviews of medical evidence and expected
outcomes, helpful for counseling patients and setting accurate expectations. Rather than
exhaustive reference lists, the authors provide lists of high-​priority additional reading
recommended to deepen understanding.
The resulting volume should provide you with a dynamic tour through the prac-
tice of spinal neurosurgery, guided by some of the leading experts in North America.
Additional volumes cover each subspecialty area of neurosurgery using the same case-​
based approach and board review features.
Nathan R. Selden, MD, PhD
Campagna Professor and Chair
Department of Neurological Surgery
Oregon Health and Science University
Portland, Oregon

vii
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Contributors

Bizhan Aarabi, MD, FRCSC, FACS Domagoj Coric, MD

Professor, Neurosurgery Chief, Department of Neurosurgery
Director of Neurotrauma, R. Adams Carolinas Medical Center
Cowley Shock Trauma Center Carolina Neurosurgery and Spine
Department of Neurosurgery Associates
University of Maryland School of Charlotte, North Carolina
Medicine
Baltimore, Maryland Andrew Dailey, MD
Professor
Aimee M. Aysenne, MD, MPH Department of Neurosurgery
Director of Neurocritical Care University of Utah
Department of Clinical Neurosciences Salt Lake City, Utah
Tulane University, School of Medicine
New Orleans, Louisiana Justin R. Davanzo, MD
Department of Neurological Surgery
Tej D. Azad, BA Penn State Health Milton S. Hershey
Medical Student Medical Center
Department of Neurosurgery Pennsylvania, Pennsylvania
Stanford University School of Medicine
Stanford, California Hansen Deng, BS
Medical Student
G. Damian Brusko, BS Department of Neurological Surgery
Department of Neurological Surgery University of California, San Francisco
The Miami Project to Cure Paralysis San Francisco, California
University of Miami Miller School of
Medicine Atman Desai, MD
Miami, Florida Assistant Professor
Department of Neurosurgery
Joseph Cheng, MD, MS Stanford University School of Medicine
Professor of Neurosurgery Stanford, California
Frank H. Mayfield Chair
Department of Neurological Surgery Alexander B. Dru, MD
University of Cincinnati Health University of Florida
Cincinnati, Ohio Department of Neurosurgery
Gainesville, Florida

ix
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Contributors

Benjamin D. Elder, MD, PhD James S. Harrop, MD, FACS

Assistant Professor of Neurosurgery, Professor, Departments of Neurological
Orthopedic Surgery, and Biomedical and Orthopedic Surgery
Engineering Director, Division of Spine and Peripheral
Mayo Clinic School of Medicine Nerve Surgery
Rochester, Minnesota Neurosurgery Director of Delaware Valley
SCI Center
Ilyas Eli, MD Thomas Jefferson University
Resident Philadelphia, Pennsylvania
Department of Neurosurgery
University of Utah Randall J. Hlubek, MD
Salt Lake City, Utah Department of Neurosurgery
Barrow Neurological Institute
Michael G. Fehlings, MD, PhD, St. Joseph’s Hospital and Medical Center
FRCSC, FACS Phoenix, Arizona
Vice Chair Research
Professor of Neurosurgery Daniel J. Hoh, MD
McLaughlin Scholar in Molecular Medicine Associate Professor
Co-​Chair Spinal Program Dunspaugh-​Dalton Endowed Professorship
University of Toronto Department of Neurological Surgery
Gerry and Tootsie Halbert Chair in University of Florida
Neural Repair and Regeneration Gainesville, Florida
Head, Spinal Program
Toronto Western Hospital David M. Ibrahimi, MD
Toronto, Ontario, Canada Assistant Professor
Department of Neurosurgery
Jared Fridley, MD University of Maryland School of
Assistant Professor of Neurosurgery Medicine
Brown University Baltimore, Maryland
Department of Neurosurgery
Providence, Rhode Island Rajiv R. Iyer, MD
Department of Neurosurgery
Michael A. Galgano, MD The Johns Hopkins University School
Clinical Instructor of Neurosurgery of Medicine
Brown University Baltimore, Maryland
Department of Neurosurgery
Providence, Rhode Island George I. Jallo, MD
Professor of Neurosurgery, Pediatrics
Mario Ganau, MD, PhD, FACS and Oncology
Spine Fellow Director, Institute for Brain Protection
Toronto Western Hospital Sciences
Toronto, Ontario, Canada Johns Hopkins All Children’s Hospital
St. Petersburg, Florida
Ziya Gokaslan, MD
Professor and Chair Jacob R. Joseph, MD
Brown University Department of Neurosurgery
Department of Neurosurgery University of Michigan
Providence, Rhode Island Ann Arbor, Michigan

x
 

Contributors

James Kalyvas, MD Evan Lewis, MD

Neurosurgeon Neurosurgeon
Ochsner Clinic Foundation Baptist Medical Group–​Neurosurgery
New Orleans, Louisiana Pensacola, Florida

Michael Karsy, MD, PhD Jason Liounakos, MD

Resident Resident
Department of Neurosurgery Department of Neurological Surgery
University of Utah Univeristy of Miami Miller School of
Salt Lake City, Utah Medicine
Miami, Florida
So Kato, MD
Spine Fellow Christopher M. Maulucci,
Toronto Western Hospital MD, FACS
Toronto, Ontario, Canada Associate Professor of Neurological
Surgery
John P. Kelleher, MD Assistant Residency Program Director
Department of Neurological Surgery School of Medicine
Penn State Health Milton S. Hershey Tulane University
Medical Center New Orleans, Louisiana
Pennsylvania, Pennsylvania
Hector G. Mejia Morales
Omaditya Khanna, MD Medical student
Resident Tulane University School of Medicine
Thomas Jefferson University Hospital New Orleans, Louisiana
Philadelphia, Pennsylvania
Yusef I. Mosley, MD
Mathew Kole, MD Department of Neurosurgery
Resident in Training Thomas Jefferson University
Department of Neurosurgery Philadelphia, Pennsylvania
University of Maryland School of
Medicine Praveen V. Mummaneni, MD
Baltimore, Maryland Joan O’Reilly Endowed Professor
Vice Chairman
Michael LaBagnara, MD University of California, San Francisco
Assistant Professor of Neurological Neurosurgery
Surgery San Francisco, California
University of Tennessee
Semmes-​Murphey  Clinic Harry Mushlin, MD
Memphis, Tennessee Resident in Training
Department of Neurosurgery
Ilya Laufer, MD University of Maryland School of
Department of Neurosurgery Medicine
Memorial Sloan Kettering Cancer Center Baltimore, Maryland
New York, New York

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Contributors

Rani Nasser, MD Christopher I. Shaffrey, MD

Clinical Instructor of Neurosurgery John A. Jane Professor of Neurological
University of Cincinnati Health Surgery
Cincinnati, Ohio Division Head Spinal Surgery
Professor of Orthopaedic Surgery
Mark E. Oppenlander, MD University of Virginia Medical Center
Assistant Professor Charlottesville, Virginia
Department of Neurosurgery
University of Michigan Emily P. Sieg, MD
Ann Arbor, Michigan Department of Neurological Surgery
Penn State Health Milton S. Hershey
Jonathan M. Parish, MD Medical Center
Resident Physician Pennsylvania, Pennsylvania
Carolinas Medical Center
Charlotte, North Carolina Manish K. Singh, MD
Assistant Professor of Neurological
Lahiru Ranasinghe, BS Surgery
Medical Student Director of Spine Surgery Program
Department of Clinical Neuroscience Tulane University School of Medicine
Tulane University School of Medicine New Orleans, Louisiana
New Orleans, Louisiana
Brandon W. Smith, MD, MS
John K. Ratliff, MD Department of Neurosurgery
Professor University of Michigan
Department of Neurosurgery Ann Arbor, Michigan
Stanford University School of Medicine
Stanford, California Justin S. Smith, MD, PhD
Harrison Distinguished Professor
Adam M. Robin, MD Neurological Surgery
Department of Neurosurgery University of V
  irginia Medical Center
Memorial Sloan Kettering Cancer Center Charlottesville,Virginia
New York, New York
Geoffrey P. Stricsek, MD
Miner N. Ross, MD, MPH Resident
Resident Physician Thomas Jefferson University
Department of Neurological Surgery Philadelphia, Pennsylvania
Oregon Health and Science University
Portland, Oregon Durga R. Sure, MD
Department of Neurosurgery
Charles A. Sansur, MD University of Virginia
Associate Professor Charlottesville, Virginia
Department of Neurosurgery
University of Maryland School of Daniel Tarazona,  MD
Medicine Department of Orthopedics
Baltimore, Maryland Rothman Institute
Philadelphia, Pennsylvania

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Contributors

Khoi D. Than, MD Anand Veeravagu,  MD

Assistant Professor Assistant Professor
Neurological Surgery Department of Neurosurgery
Oregon Health and Science University Stanford University School of Medicine
Portland, Oregon Stanford, California

Nicholas Theodore,  MD Todd D. Vogel, MD

Department of Neurosurgery Minimally Invasive and Complex
Barrow Neurological Institute Spine Fellow
St. Joseph’s Hospital and Medical Center Department of Neurological Surgery
Phoenix, Arizona University of California, San Francisco
San Francisco, California
Vincent C. Traynelis, MD
Professor Michael Y. Wang,  MD
Department of Neurosurgery Chief of Neurosurgery
Rush University Medical Centre University of Miami Hospital
Chicago, Illinois Professor
Departments of Neurological Surgery
Mazda K. Turel, MBBS and Rehabilitation Medicine
Clinical Fellow in Cerebrovascular and University of Miami School of Medicine
Bypass Surgery Miami, Florida
Department of Neurosurgery
Rush University Medical Centre Jean-​Paul Wolinsky,  MD
Chicago, Illinois Department of Neurosurgery and
Oncology
Derrick Umansky, MD Clinical Director of the Johns Hopkins
Resident Spine Program
Department of Neurosurgery Johns Hopkins University
Tulane University School of Medicine Baltimore, Maryland
New Orleans, Louisiana
Scott Zuckerberg, MD, MPH
Alexander R. Vaccaro, MD, Co-Director
PhD, MBA Research of the Vanderbilt Sports
Department of Orthopedic Surgery Concussion Center Research Group
Rothman Institute (President) Department of Neurological Surgery
Philadelphia, Pennsylvania Vanderbilt University Medical Center
Nashville, Tennessee

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Odontoid Fracture Type II

Daniel Tarazona and Alexander R. Vaccaro

Case Presentation

A 79-​year-​old woman presents to the emergency department after falling at a nursing

1
home. She denies loss of consciousness. She arrived in a cervical collar placed prior to
transfer with a chief complaint of neck pain. She denies any paresthesias or weakness.
She is hemodynamically stable and is awake, alert, and oriented. Upon physical examina-
tion there is midline cervical spine tenderness without step-​offs or deformities. A neu-
rological exam revealed 5/​5 motor strength throughout, no sensory deficits, 1+ DTR
throughout, and a normal rectal examination.

Questions

1. What is the likely diagnosis?

2. What is the most appropriate imaging modality?
3. How are odontoid fractures classified?

Assessment and Planning

Based on the history and physical exam, the surgeon suspects a cervical spine frac-
ture. The differential diagnosis includes injuries to the upper cervical, subaxial cervical,
and upper thoracic spine. Due to the initial concern for a cervical spine injury, spine
precautions are maintained and a dedicated computed tomographic (CT) scan of the
cervical, thoracic, and lumbar spine is obtained revealing a type II odontoid fracture.

Oral Boards Review: Diagnostic Pearls

1. The Anderson and D’Alonzo classification for odontoid fractures lends prog-
nostic information for risk of nonunion and assists with treatment planning.
2. CT scan is the preferred imaging modality with high inter-​and intrarater
agreement. It also assists with diagnosis of concomitant spinal injuries.20
3. CT or magnetic resonate (MR) angiography should be considered if vertebral
artery injury is clinically suspected.

Initial radiographic evaluation of the cervical spine includes anteroposterior (AP),

lateral, and open-​mouth odontoid views and CT of the cervical spine. Magnetic

1
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Spinal Neurosurgery

Anderson and D’Alonzo

Type I

Type II

Type III

Figure 1.1  Anderson and D’Alonzo.

resonance imaging (MRI) is warranted with neurologic injury or concern for concom-
itant ligamentous injury. If posterior instrumentation is anticipated, then a CT angio-
gram may be obtained to evaluate for potential vascular anomalies that would preclude
safe C2 pars, C2 pedicle, C1–​C2 transarticular, or C1 lateral mass screw placement.
Odontoid fractures can be classified into three types as described by Anderson and
D’Alonzo (Figure 1.1).3 Type I odontoid fractures represent an avulsion fracture of the tip
of the odontoid through the alar ligament. Type II is the most common C2 fracture pat-
tern and is defined by a fracture line at the base of the odontoid. Type II fractures have the
greatest risk of nonunion due to the disruption of the tenuous blood supply.Type III fractures
occur through the vertebral body and extend into the superior articular facets. Greater vas-
cularity in the C2 body results in a low nonunion rate with cervical orthosis for this frac-
ture type. Grauer and colleagues proposed subclassifying type II fractures to guide treatment
decisions (Figure 1.2).Type IIA are transverse fractures, type IIB are angled anterosuperior to
posteroinferior, and type IIC are either angled from anteroinferior to posterosuperior or are
comminuted fractures.23 This fracture classification is useful when considering an odontoid
screw as patients with a IIC are not appropriate for odontoid screw fixation.
In the present case, CT of the spine demonstrates a displaced type II odontoid frac-
ture with type IIC obliquity (Image 1)  and a C3 right transverse process fracture.
There is no apparent cord compression. A CT angiogram does not reveal any vascular
insult or anomalies (Figure 1.3).

2
 

Grauer

Type II
Subclass A
(Nondisplaced)

Type II
Subclass B
(Displaced transverse
or ant superior to
post inferior)

Type II
Subclass C
(Comminuted or
ant inferior to post
superior)

Figure 1.2  Grauer classification.

Figure 1.3  Sagittal view of cervical spine showing type IIC odontoid fracture.
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Spinal Neurosurgery

Questions

1. What are risk factors for nonunion?

2. How should management be approached in a patient of advanced age?
3. How do these clinical and radiological findings influence surgical planning?

Decision-​Making

No uniform treatment algorithm has been established for odontoid fractures. Instead,
each case should be tailored with special considerations for comorbidities, concomitant
injuries, prior functional status, neurological status, and fracture morphology. Treatment
options are also based on the risk of nonunion, favoring surgical intervention for patients
with a higher risk of nonunion. Known risk factors for nonunion include age 50 years
or greater, comminution, greater than 5 mm of posterior displacement, fracture gap of
more than 1 mm, more than 4 days between injury and treatment, and greater than 10
degrees of angulation. Furthermore, there is extensive literature demonstrating a de-
crease in mortality with operative fixation and an improvement in health-​related quality
of life outcomes in type II fractures in the geriatric population.18,19,24
Adults with a type II fracture without nonunion risk factors can be managed in a
hard collar or a halo vest to prevent subsequent displacement. Most commonly, adults
with risk factors for nonunion or geriatric patients who may safely undergo anesthesia
are treated with a posterior C1–​C2 fusion. In the properly selected patient, an odontoid
screw may be beneficial, but this has been demonstrated to lead to a high risk of dysphagia
in the elderly as well as screw pull-​out in the setting of osteopenia/​osteoporosis.16,26
The management of type II odontoid fractures in the elderly has changed in the past
decade. Historically, acceptable outcomes with asymptomatic stable fibrous nonunions
in the elderly have been reported.4 More recent literature supports operative manage-
ment for patients 65 years or older, reporting improved functional outcomes and union
rates, no difference in complications, and a trend toward improved mortality.19 However,
an increased risk of complications can be seen in surgically treated patients 80 years or
older.24 Rigid external immobilization (halo vest) is contraindicated in the elderly due
to high morbidity and mortality rates.5 They generally have lower overall functional
reserve and decreased pulmonary function, so prolonged immobilization could have
morbid implications. Consequently, more surgeons are advocates for early surgical inter-
vention, and there is a growing body of evidence to support this as well.18–​20,22,24
There are multiple surgical treatments for odontoid fractures with the most com-
monly used being segmental fixation consisting of C1 lateral mass with either C2 ped-
icle or pars screws. Other options included an anterior odontoid osteosynthesis and
C1–​C2 transarticular screw fixation. While posterior instrumentation demonstrated
greater rates of osseous union, anterior odontoid osteosynthesis avoids fusion of the
C1–​C2 articulation, which is responsible for 50% of cervical rotation. Each option has
unique advantages and disadvantages which should be balanced with the fracture pat-
tern, body habitus, and patient expectations.
In this case, due to the displacement and instability of the odontoid fracture, as
well as the potential serious complications of immobilization, the surgeon opted

4
 

Odontoid Fracture Type II

for surgical fixation. The surgeon elected for C1–​C2 posterior instrumented fusion.
Anterior screw osteosynthesis is often not indicated because of the patient’s age and
potential for fixation failure due to poor screw purchase with osteoporosis, as well as
the fact that lag screw fixation would result in translation and displacement with a type
IIC fracture. Body habitus is also an important consideration as this patient’s obesity
makes anterior odontoid osteosynthesis technically challenging to place a screw due
to the trajectory.

Surgical Procedure

As previously mentioned, there are multiple surgical options for type II odontoid
fracture but here the focus will be on segmental C1–​C2 instrumentation and fusion
(C1 lateral mass technique, Figure 1.4).

Positioning and Preparation

The patient should undergo intubation with in-​line cervical immobilization to prevent
excessive neck hyperextension. This may be done with a GlideScope or as a fiber-​optic
intubation.The Mayfield clamp is applied after intubation. Neuromonitoring is routinely
utilized, and preintubation and prepositioning somatosensory and transcranial motor
evoked potentials (SSEPs and tcMEPs) are recorded. The patient is then positioned
prone with the neck in a slightly flexed position followed by repeat SSEPs and tcMEPs.
The cervical spine is prepped and draped in sterile fashion. If iliac crest bone graft
harvesting is required, then the posterior iliac crest should also be prepped and draped.

Approach

A midline longitudinal incision is utilized. Intraoperative radiographs should be taken to

confirm spinal levels. Particular care should be taken to stay in the midline and follow
the midline raphe for an avascular approach. Subperiosteal dissection of the posterior
elements of C2 and inferior arch of C1 is performed. Avoid sharp dissection lateral to
the C1 lateral masses and cephalad to the C1 ring to reduce risk of injuring the verte-
bral artery. As dissection extends from the base of the C1 arch to the C1 lateral masses,
significant bleeding from the venous plexus in this region may be encountered.

A B

Figure 1.4  (A) C1 lateral mass technique. (B) Retraction of C2 nerve root and

exposure of lateral mass.

5
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Spinal Neurosurgery

Procedure

Fluoroscopy is initially used to confirm adequate position of C1 relative to C2. Next,

the starting point of the C2 pars screw is determined. A pilot hole is made approxi-
mately 2–​3 mm proximal to the C2–​C3 facet joint and slightly laterally (2–​3 mm) to
the palpated medial border of the C2 isthmus. The drill is angled cephalad and slightly
medial along the path of the C2 isthmus and advanced to the predetermined unicortical
depth. Next, a probe is used to confirm the absence of bony breach, the tract is tapped,
and the screw is placed.
Following placement of C2 pars screw, fluoroscopy is then used to help identify the
starting point and trajectory of the C1 lateral mass screw. Prior to screw placement, the
C2 nerve root must be gently retracted inferiorly, exposing the bony anatomy (Figure
1.5). The entry point is identified 5 mm lateral to the medial aspect of the lateral mass
and just caudal to the C1 posterior arch. A drill can be used to cannulate the lateral
mass, aimed approximately 10 degrees medial with fluoroscopy guiding a cephalad par-
allel trajectory to the midpoint of the C1 anterior arch. Depth gauge measurements
can then confirm the screw length and size prior to its insertion into the lateral mass.
This is repeated for the contralateral C1 lateral mass. Screw positions are checked under
lateral fluoroscopy and rods are placed. The C2 lateral masses and inferior arch of C1
is decorticated and a structural graft is placed in the C1–​C2 interspace. Final x-​rays are
then taken to confirm hardware positioning.

Oral Boards: Management Pearls

1. Evaluation of vertebral artery anatomy with preoperative imaging,

minimizing sharp dissection around the cephalad edge of the atlas, and using
a superomedial trajectory of C1 lateral mass screw trajectory will reduce the
risk of injury to the vertebral artery.
2. Suboptimal lateral fluoroscopic imaging for C1–​C2 instrumentation can re-
sult in improper screw placement and neurologic or vascular injury.
3. C1–​C2 polyaxial screw and rod fixation does not require direct odontoid
anatomic reduction, and intraoperative reduction by manipulation can be
achieved using direct manipulation of the C1 posterior arch.

Pivot Points

1. If an aberrant vertebral artery is present, then an alternative operative tech-

nique, such as a C2 laminar screw, should be considered. C1–​C2 transarticular
screw and C2 pedicle screw placement should be avoided with aberrant
anatomy.
2. Although the lateral mass screw placement may initially appear to be without
complication, if the screw tip is in close proximity to the vertebral artery,
normal pulsatile flow may result in delayed damage to the vessel. Any concern
for excessive screw length should prompt screw removal, with a shorter screw
subsequently inserted.

6
 

Odontoid Fracture Type II

A B

Figure 1.5  (A,B) Anteroposterior and lateral view of cervical spine with posterior
C1–​C2 fusion.

Aftercare

It is recommended that patients undergoing fixation of type II odontoid type fractures

be placed in a cervical orthosis and admitted for close monitoring of potential postoper-
ative complications. In geriatric patients, a soft collar is used, but in high-​energy injuries
a hard collar is used. The patient can be mobilized immediately after surgery.
Follow-​up imaging should be obtained at 2 weeks and 6–​8 weeks to ensure there is
no early hardware failure (Figure 1.5). Also, functional radiographs in flexion and exten-
sion can be obtained to evaluate stability 3–​6 months after surgery. Once initial healing
and maintenance of stability is established, the patient may be weaned from the cervical
orthosis.

Complications and Management

The different complications of surgery are largely dependent on the approach and tech-
nique used.These complications can be further categorized into intraoperative and post-
operative complications.

Intraoperative Complications

Neurovascular injuries are the most concerning intraoperative complications. With a

posterior approach, one of the feared complications is injury to the vertebral artery with
screw malposition. An anomalous vertebral artery further increases the risk of injury,
especially with C1–​C2 transarticular or C2 pedicle screw placement. Preoperative im-
aging should be closely evaluated for aberrant vessels. Careful intraoperative technique,
avoiding C2 pedicle screws with aberrant vertebral artery anatomy, and directing the C1
lateral mass screw superomedially is essential to avoid vertebral artery damage.13 Damage
to a single vertebral artery may be asymptomatic with intact contralateral supply, but
bilateral injury can be catastrophic.
With an anterior approach, careful retraction and dissection should be used to
avoid injury to the internal carotid and esophagus. Other potential rare complications

7
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Spinal Neurosurgery

include neurologic injury from past-​point drilling or excessive depth of the anterior
odontoid screw.

Postoperative Complications

Following a posterior cervical approach, occipital neuralgia is a common complaint.

To minimize the risk, the C2 nerve root should be gently retracted downward and
protected with a Penfield dissector during lateral mass screw placement. Additionally,
partially threaded screws are used at C1. Wound complications are also more common
with a posterior approach.17 Sterile technique, antibiotics, and proper wound irrigation
help reduce the risk of infection. Surgical site infections with any concern for deep ex-
tension should be addressed with surgical debridement.
Following an anterior approach, dysphagia can be common and may necessitate the
use of a feeding tube.27 This approach can be further complicated by aspiration pneu-
monia, which should be promptly treated with antibiotics.11,27 Hoarseness or vocal cord
paralysis may ensue from neurapraxia or ischemic injury to the superior laryngeal and
recurrent laryngeal nerves, respectively. Patients should also be closely monitored for
signs of respiratory distress as this may be a sign of a retropharyngeal hematoma, which
should be emergently surgically evacuated.
Failure of instrumentation and pseudarthrosis can complicate the postoperative re-
covery. Routine follow-​up radiographs are scrutinized for evidence of union. CT scans
can be utilized if the surgeon is concerned for nonunion.

Oral Boards Review: Complications Pearls

1. If there is an inadvertent injury to the vertebral artery, bleeding should be

immediately controlled with primary vascular repair, temporary insertion
of screw into the drilled hole, or by occlusion with a hemostatic agent or
bone wax. If hemorrhage control is not possible and ligation is planned,
intraoperative angiography should be performed.28 Contralateral screw place-
ment should not be attempted to avoid bilateral injury.
2. C2 neuralgia can be a result of C1 lateral mass screw placement or excessive
traction during exposure of lateral mass.
3. Bicortical fixation of lateral mass screw could place the internal carotid artery
at risk for injury.10
4. The congenital arcuate foramen can be confused with the C1 lamina and
must be identified to avoid vertebral artery injury

Evidence and Outcomes

The optimal surgical technique for type II odontoid fractures remains a matter of debate,
with both anterior odontoid screw fixation and posterior cervical atlantoaxial fusion
being acceptable choices.16,24 However, a posterior approach is especially indicated in
geriatric patients and when anterior approaches are contraindicated in cases such as type
IIC odontoid fracture, associated C1–​C2 injury, nonreducible fractures, nonunion, large
body habitus with a barrel chest, severe kyphosis, and severe osteoporosis.16 Posterior

8
 

Odontoid Fracture Type II

C1–​C2 fusions may also be used for salvage of an anterior fixation failure. Overall, pos-
terior atlantoaxial fixation has been associated with a high rate of fusion, approaching
100%, with a low complication rate thus making it a very effective treatment option for
type II odontoid fractures.12 When appropriately indicated, anterior screw fixation can
provide similar clinical results.24
Another previous area of uncertainty was the optimal management of elderly
patients; however, there has been a significant amount of research in the past decade
demonstrating the superiority of surgery. Vaccaro et al. conducted a multicenter, pro-
spective cohort study comparing operative and nonoperative treatments for patients
65 years of age or older. The study revealed better outcomes, lower nonunion rates, no
difference in complication rates, and a nonsignificant trend toward lower mortality.19
Schroeder et al. performed a systematic review that found a decrease in both short-​and
long-​term mortality in patients treated surgically. However, there is likely an upper age
to surgery.24 Schoenfeld et al. conducted a retrospective study, and, although patients be-
tween 65 and 74 years old who underwent surgery had lower mortality rates, there was
no difference when patients approached 85 years of age.22

References and Further Readings

1. Boos N, Aebi M, eds. Spinal Disorders:  Fundamentals of Diagnosis and Treatment. Berlin:
Springer-​Verlag;  2008.
2. Keller S, Bieck K, Karul M, et  al. Lateralized odontoid in plain film radiography:  Sign of
fractures?—​A comparison study with MDCT. RöFo—​Fortschritte Auf Dem Geb Röntgenstrahlen
Bildgeb Verfahr. 2015;187(09):801–​807. doi:10.1055/​s-​0035-​1553237.
3. Anderson LD, D’Alonzo RT. Fractures of the odontoid process of the axis. J Bone Joint Surg
Am. 1974;56(8):1663–​1674.
4. Pal D, Sell P, Grevitt M.Type II odontoid fractures in the elderly: An evidence-​based narrative
review of management. Eur Spine J. 2011;20(2):195–​204. doi:10.1007/​s00586-​010-​1507-​6.
5. Majercik S, Tashjian RZ, Biffl WL, Harrington DT, Cioffi WG. Halo vest immobilization in
the elderly: A death sentence? J Trauma. 2005;59(2), 350–​358.
6. Goel A. Treatment of odontoid fractures. Neurol India. 2015;63(1):7. doi:10.4103/​
0028-​3886.152657.
7. Robinson Y, Robinson A-​L, Olerud C. Systematic review on surgical and nonsurgical treat-
ment of type II odontoid fractures in the elderly. BioMed Res Int. 2014;2014. doi:10.1155/​
2014/​231948.
8. Posterior C1–​ C2 Fusion, ClinicalKey. https://​www-​clinicalkey-​com.ezproxy.rowan.edu/​
#!/​content/​book/​3-​s2.0-​B9781437715200000279. Accessed May 1, 2016.
9. Bodon G, Patonay L, Baksa G, Olerud C. Applied anatomy of a minimally invasive muscle-​
splitting approach to posterior C1–​C2 fusion:  An anatomical feasibility study. Surg Radiol
Anat SRA. 2014;36(10):1063–​1069. doi:10.1007/​s00276-​014-​1274-​x.
10. Seal C, Zarro C, Gelb D, Ludwig S. C1 lateral mass anatomy: Proper placement of lateral mass
screws. J Spinal Disord Tech. 2009;22(7):516–​523. doi:10.1097/​BSD.0b013e31818aa719.
11. Dailey AT, Hart D, Finn MA, Schmidt MH, Apfelbaum RI. Anterior fixation of odontoid
fractures in an elderly population: Clinical article. J Neurosurg. 2010;12(1):1–​8.
12. Harms J, Melcher RP. Posterior C1–​C2 fusion with polyaxial screw and rod fixation. Spine.
2001;26(22):2467–​2471.

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Spinal Neurosurgery

13. Gautschi OP, Payer M, Corniola MV, Smoll NR, Schaller K, Tessitore E. Clinically relevant
complications related to posterior atlanto-​axial fixation in atlanto-​axial instability and their
management. Clin Neurol Neurosurg. 2014;123:131–​135. doi:10.1016/​j.clineuro.2014.05.020.
14.
Spine Surgery Basics, Springer. http://​link.springer.com.ezproxy.rowan.edu/​book/​
10.1007%2F978-​3-​642-​34126-​7. Accessed May 1, 2016.
15. Wang L, Liu C, Zhao Q-​H, Tian J-​W. Outcomes of surgery for unstable odontoid fractures
combined with instability of adjacent segments. J Orthop Surg. 2014;9:64. doi:10.1186/​
s13018-​014-​0064-​9.
16. Joaquim A, Patel A. Surgical treatment of type II odontoid fractures: Anterior odontoid screw
fixation or posterior cervical instrumentation fusion. Am Assoc Neurosurg. 2015:38(4):E11.
17. Harel R, Stylianou P, Knoller N. Cervical spine surgery:  Approach-​related complications.
World Neurosurg. 2016;94:1–​5.
18. Chapman J, Smith JS, Kopjar B, et  al. The AOSpine North America Geriatric Odontoid
Fracture Mortality Study:  A retrospective review of mortality outcomes for opera-
tive versus nonoperative treatment of 322 patients with long-​ term follow-​ up. Spine.
2013;38(13):1098–​1104.
19. Vaccaro AR, Kepler CK, Kopjar B, et al. Functional and quality-​of-​life outcomes in geriatric
patients with type-​II dens fracture. J Bone Joint Surg. 2013;95(8):729–​735.
20. Barker L, Anderson J, Chesnut R, Nesbit G, Tjauw T, Hart R. Reliability and reproducibility
of dens fracture classification with use of plain radiography and reformatted computer-​aided
tomography. J Bone Joint Surg (Am). 2006;88(1):106–​112.
21. Koivikko MP, Kiuru MJ, Koskinen SK, Myllynen P, Santavarita S, Kivisaari L. Factors associ-
ated with non-​union in conservatively treated type II fractures of the odontoid process. J Bone
Joint Surg (Br). 2004;86-​B:1146–​1151.
22. Schoenfeld AJ, Bono CM, Reichmann WM, et al. Type II odontoid fractures of the cervical
spine:  Do treatment type and medical comorbidities affect mortality in elderly patients?
Spine. 2011;36(11):879–​885.
23. Grauer JN, Shafi B, Hilibrand AS, et al. Proposal of a modified, treatment-​oriented classifica-
tion of odontoid fractures. Spine J. 2005;5(2):123–​129.
24. Schroeder GD, Kepler CK, Kurd M, et al. A systematic review of the treatment of geriatric
type II odontoid fractures. Neurosurgery 2015;77:S6–​S14.
25. Smith HE, Kerr SM, Maltenfort M, et al. Early complications of surgical versus conserva-
tive treatment of isolated type II odontoid fractures in octogenarians: A retrospective cohort
study. J Spinal Disord Tech. 2008;21(8):535–​539.
26. Andersson S, Rodrigues M, Olerud C. Odontoid fractures: High complication rate associated
with anterior screw fixation in the elderly. Eur Spine J. 2000;9(1):56–​59.
27. Vasudevan K, Grossberg JA, Spader HS, Torabi R, Oyelese AA. Age increases the risk of im-
mediate postoperative dysphagia and pneumonia after odontoid screw fixation. Clin Neurol
Neurosurg. 2014;126:185–​189.
28. Peng CW, Chou BT, Bendo JA, Spivak JM. Vertebral artery injury in cervical spine sur-
gery:  Anatomical considerations, management, and preventive measures. Spine J.
2009;9(1):70–​76.

10
 

Cervical Fracture Dislocation

Jason Liounakos, G. Damian Brusko, and Michael Y. Wang

Case Presentation

A 30-​year-​old man was transferred to a local level 1 trauma center by emergency med-
2
ical services (EMS) 3 hours after diving into a shallow pond head first. He presents with
a Glasgow Coma Scale (GCS) score of 15, without loss of consciousness, and states that
immediately after the dive he was unable to move his arms or legs. He also complains of
an intermittent burning sensation in his arms and neck pain. He is rigidly immobilized
on a backboard with strict spine precautions. His blood pressure is 90/​60 mm Hg with
a heart rate of 55 bpm. Detailed physical examination is significant for 5/​5 strength in
deltoids, 4+/​5 in biceps, and 0/​5 distally. He has absent rectal tone. Biceps reflexes are
2+ bilaterally. Brachioradialis, triceps, patellar, and achilles reflexes are absent bilaterally.
Hoffman sign is negative, and no clonus or plantar response is equivocal. Sensation to
pin prick and light touch is preserved throughout, including the perianal region.

Questions

1. What is the most likely diagnosis?

2. At what level is the suspected injury?
3. What is the international standardized classification system used for spinal
cord injury?
4. What imaging examinations are most appropriate to accurately diagnosis the
injury?
5. Describe common fracture patterns associated with cervical facet dislocations.

Assessment and Planning

Given the acute onset of symptoms in an otherwise healthy patient sustained after an
obvious traumatic injury, the on-​call neurosurgeon suspects a traumatic spinal cord in-
jury. Spinal cord injuries in the cervical spine are frequently associated with cervical
fracture dislocation. An initial complete trauma evaluation is necessary to rule out other
injuries, particularly in the setting of neurogenic shock where hypotension may be
related to hemorrhagic shock rather than to a loss of sympathetic tone secondary to
the spinal cord injury. Until the injury has been identified and stabilized, strict spine
precautions are necessary, particularly in the setting of an incomplete spinal cord injury
(as in this case). Instability due to a fracture predisposes the patient to further injury

11
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Spinal Neurosurgery

and risks worsening neurological status so the utmost care must be taken in patient
positioning and transfers.
Assuming a spinal cord injury is present, a complete neurological exam will often
accurately reveal the level of injury. In this patient with grossly intact deltoid and biceps
strength and nothing below, the level of injury is likely C5. Given the presence of in-
tact sensation, this injury is classified as incomplete American Spinal Injury Association
(ASIA) B. The complete guide to the ASIA neurologic exam and ASIA Impairment
Scale is provided in the References and Further Reading section. The neurologic level
is defined as the most caudal level with normal function. Importantly, to accurately di-
agnose a complete (ASIA A) injury, the function of the most caudal spinal segments
(S4–​S5) must be evaluated and found to be absent.
Per the 2013 update to the Guidelines for the Management of Acute Cervical Spine
and Spinal Cord Injury provided by the Congress of Neurological Surgeons (CNS),
computed axial tomography (CT) is the recommended initial imaging study for symp-
tomatic trauma patients. CT will quickly and accurately uncover the level of bony injury,
if present, and guide further workup and treatment.
Magnetic resonance imaging (MRI) is extremely useful after the patient has been
initially stabilized to assist in determining the extent of neurologic injury, the presence
of active compression of the spinal cord, and, perhaps somewhat more controversially,
the safety of closed reduction in the presence of facet dislocation. Disrupted or herniated
discs occur in one-​third to one-​half of patients with cervical facet dislocations. It has
been argued that prereduction MRI is important to identify a traumatic disc hernia-
tion that has the potential to exacerbate spinal cord compression if closed reduction
is performed. In the worst-​case scenario, this could potentially lead to an incomplete
injury becoming complete. It is further argued that, in the presence of such a disc
herniation, treatment should proceed with anterior cervical discectomy, followed by
open reduction and internal fixation. Interestingly, however, only a few reports of such
complications exist, and numerous studies have failed to demonstrate an association
between a traumatic herniated disc and postreduction neurologic deterioration in the
awake patient. Even so, the practice at many institutions, including our own, typically
involves urgent MRI in the awake patient with an incomplete spinal cord injury and
cervical fracture dislocation.
In our case, CT demonstrated a grade 2 anterolisthesis of C5 on C6 (Figure 2.1A)
with complete dislocation (“jumped” or “locked” facet) of the right facet joint (Figure
2.1B) and subluxation (“perched” facet) of the left facet joint (Figure 2.1C), associated
with a flexion teardrop-​type fracture of C6. An MRI was subsequently obtained (Figure
2.2) that did not demonstrate an obvious disc herniation. Clearly evident injury to the
spinal cord and posterior ligamentous complex was indicated by the presence of high
T2 signal in both.
Cervical facet dislocations are caused by hyperflexion and posterior distraction with
or without a rotational component. Rotational injury is often a major component of
unilateral facet dislocations. They are commonly seen after high-​energy trauma such as
motor vehicle and diving accidents. When the inferior articulating process of the rostral
vertebra dislocates anteriorly to the superior articulating process of the caudal vertebra,
the condition is commonly referred to as “jumped” or “locked” facets. When the infe-
rior articulating process sits superior to the superior articulating process, the facets are

12
 

Cervical Fracture Dislocation

Figure 2.1  Computed tomography (CT) scan demonstrating cervical fracture

dislocation at the C5–​C6 level. A grade 2 anterolisthesis of C5 on C6 exists (A). The
right facet is fully dislocated (jumped) with the inferior articulating process of the
C5 vertebra dislocated anteriorly to the superior articulating process of C6 (B). By
comparison, the left facet is perched (C).

referred to as being “perched.” Unilateral facet dislocation often results in a grade 1

anterolisthesis. Isolated unilateral facet dislocation may present with monoradiculopathy
secondary to nerve root compression at the level of the neural foramen. Bilateral facet
dislocations often result in a more significant degree of anterolisthesis (often greater than
50%) with a high incidence associated spinal cord injury.
In addition to facet dislocation, hyperflexion, distraction, rotational, and axial loading
forces may result in fractures that include simple compression fractures, fractures of
the facet joint including the superior or inferior articulating processes and the pars
interarticularis, and flexion teardrop fractures. In this case, a nonclassical but teardrop-​
type fracture of C6 is present. Flexion tear drop fractures are highly unstable as they
involve both the anterior and posterior columns, demonstrating severe ligamentous dis-
ruption of the facet joint, ligamentum flavum, and posterior longitudinal ligament.They
often result in damage to the anterior spinal cord, as in this patient presenting with
motor, but not sensory, deficits. Fractures of the anteroinferior corner of the affected
vertebral body are classically seen, and retrolisthesis of the rostral vertebral body over the

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Spinal Neurosurgery

Figure 2.2 T2-​weighted magnetic resonance image (MRI) depicting significant spinal

canal comprise as a result of the cervical fracture dislocation at C5–​C6 with increased
T2 signal present in the spinal cord but without evidence of a grossly herniated disc at
that level.

caudal one may be present. These fractures require surgical fixation as the primary form
of treatment as they are highly unstable.

Oral Boards Review: Diagnostic Pearls

1. The physical examination is the most important component in the initial

evaluation of cervical spine trauma.
a. A complete neurologic evaluation and ASIA grade is important in deter-
mining prognosis.
b. A palpable step-​off may be felt, likely indicating a severe dislocation injury.
2. Depending on the mechanism of injury, there may be other bodily injuries
associated with cervical spine trauma, and a full trauma evaluation is indicated.
Even in the setting of spinal cord injury, hemodynamic instability should raise
concern for other sites of hemorrhage, rather than simply being attributed to
neurogenic shock.
3. The 2013 update to the Guidelines for the Management of Acute Cervical
Spine and Spinal Cord Injury recommend CT scan as the best first imaging
study to be performed in the setting of cervical spine trauma. If not available,
plain radiographs are recommended.
4. Cervical dislocations occur as a result of flexion and rotational (in the case of
unilateral facet dislocation) forces. Fractures with the same mechanism may
be associated, and these include simple compression fractures, fractures of the
facet complex, and flexion teardrop fractures.

14
 

Cervical Fracture Dislocation

5. Much controversy surrounds whether prereduction MRI should be

performed in a patient with a cervical fracture dislocation injury. According
to the most recent guidelines, MRI should be performed prior to closed re-
duction in a patient who cannot reliably be examined during the procedure,
or, if the procedure fails, prior to anterior or posterior open surgical reduction
and fixation. It has been reported that disc herniation may be found on MRI
anywhere between one-​third to one-​half of the time; however, their clinical
significance remains largely uncertain.

Questions

1. After a diagnosis is made, what is the next best step in management, and
when should this be performed?
2. What different techniques may be used to reduce facet dislocations?
3. How does a patient’s mental status influence the decision to proceed with
closed reduction?

Decision-​Making

Cervical facet dislocations are unstable injuries, and their initial management should
focus on reduction followed by internal fixation or external immobilization. Reduction
should be performed expeditiously, particularly in the setting of ongoing spinal cord
compression and/​or incomplete spinal cord injury as reduction potentially may lead
to improvement in neurologic status and ongoing compression may lead to worsening
neurologic injury. Closed reduction may be performed via craniocervical traction or via
cervical manipulation under anesthesia. Alternatively, open surgical reduction may also
be performed. Treatment algorithms vary widely between institutions, and no concrete
evidence supports one over the other; however, it appears that craniocervical traction
in an awake patient is likely more safe than cervical manipulation under anesthesia as a
method of closed reduction.
Numerous studies have been conducted on the efficacy of closed reduction for uni-
lateral and bilateral facet dislocation injuries, showing an 80–​90% success rate with closed
reduction and an approximately 1% risk of permanent neurological complications. Closed
reduction via craniocervical traction may be performed with Gardner-​Wells tongs and
sequential application of weight while closely monitoring the patient’s neurologic exam
and using fluoroscopy to confirm reduction. The CNS’s guidelines for the acute man-
agement of cervical spine and spinal cord injuries suggests that closed reduction not be
performed in a sedated or obtunded patient as they are unable to be adequately assessed
for any neurologic deterioration as a result of the procedure. Rather, an MRI should be
performed first to rule out any complicating injuries that could preclude closed reduc-
tion. If closed reduction fails, MRI is recommended prior to attempting open surgical
reduction and fixation for the purposes of planning the approach and assessing the need
for anterior decompression and discectomy prior to reduction and fixation.

15
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Spinal Neurosurgery

Questions

1. What options are available for internal fixation and external immobilization?
2. How do the results of halo orthosis immobilization compare to surgical
fixation?
3. What are the major complications associated with ACDF?
4. How should the occurrence of a new neurologic complaint or deficit
encountered during the process of closed cervical reduction be managed?

Surgical Procedure

Cervical fracture dislocation injuries are highly unstable, and internal fixation or ex-
ternal immobilization is necessary to prevent recurrent injury and possible neurologic
compromise. After closed reduction, external immobilization via a halo orthosis is an
option. Alternatively, open or closed reduction may be followed by internal surgical fix-
ation. Protocols vary from center to center.
Halo immobilization is a fairly morbid and quality-​of-​life affecting treatment and, for
this reason, has fallen out of favor at our institution. While external immobilization can
be used to treat these injuries, it does not seem to be as effective or reliable at producing
successful results compared to surgical fixation. A  2002 study directly comparing the
halo orthosis and anterior arthrodesis in the treatment of flexion teardrop fractures
favored surgery, finding a 20% failure rate in the halo group as well as significantly
worsened cervical kyphosis on follow-​up. No significant postoperative complications
occurred in the surgical group.
Internal fixation may be performed anteriorly, posteriorly, or circumferentially.
According to the 2013 CNS guidelines, all such procedures are effective, and the deci-
sion on how to proceed must be made on a case-​by-​case basis. Anterior surgery has the
benefit of supine surgery, a straightforward dissection, the ability to remove a herniated
disc prior to open reduction, and a relatively benign complication profile. A downside
is that open reduction may be somewhat more difficult than a posterior approach. The
posterior approach allows for easier access to the facet joints to facilitate reduction.
This is followed by lateral mass screw and rod placement. Posterior cervical fusion has a
somewhat higher morbidity than anterior cervical discectomy and fusion (ACDF), and a
theoretical risk neurologic injury exists when turning the patient prone. Circumferential
fusion may be necessary for extremely unstable injuries, although surgical morbidity
particularly due to position and time of surgery are significantly higher.
At our institution, we prefer a management strategy of urgent MRI to evaluate for
any compressive anterior pathology, followed by open reduction and ACDF. The patient
is placed in a Mayfield head holder, and, after the discectomy is performed, the dislocated
facet joints are reduced manually via slight flexion and distraction. If necessary, further
distraction may be accomplished by using a Cobb elevator placed in the disc space.

16
 

Cervical Fracture Dislocation

Oral Boards Review: Management Pearls

1. Cervical fracture dislocation injuries are highly unstable. Even if closed reduc-
tion is performed successfully, either internal fixation or external immobili-
zation is necessary as there may be a high rate of recurrence and subsequent
neurologic injury.
2. Anterior or posterior approaches to internal fixation are both effective, and
the approach should be decided on a case-​by-​case basis, taking into account
the need for neurologic decompression.

Pivot Points

1. If, during closed reduction, the patient begins to experience new neurologic
symptoms, the last weight placed should be removed and the patient
reassessed by physical exam and fluoroscopy. More than likely, the procedure
will need to be aborted. At that point, it is recommended to proceed with
MRI and open reduction and fixation.
2. Based on the literature, prereduction MRI showing a cervical herniated disc
in conjunction with facet dislocation does not necessarily mandate discec-
tomy prior to reduction; however, this is the bias at our institution.

Aftercare

Postoperative care for cervical fusion following traumatic fracture dislocation is fairly
straightforward and entails wearing a rigid cervical collar for 8 weeks per our institution’s
protocol, followed by plain radiographs versus CT scan (depending on the extent of in-
jury) to assess for bony healing. However, because of the significant morbidity and phys-
iologic derangements associated with spinal cord injury, an intensive care unit (ICU)
level of care is necessary.
Spinal shock is commonly associated with acute spinal cord injury. Spinal shock is
characterized by a temporary loss in motor, sensory, and autonomic function below the
neurologic level that gradually returns in four phases. Areflexia in phase 1 lasts about
2 days (as seen in our case). In phase 2, some initial reflexes return during days 2–​4 post-​
injury, with early hyperreflexia appearing during phase 3 and lasting approximately a
month. Finally, phase 4 may last up to a year following the injury and is characterized
by hyperreflexia and spasticity. Spinal shock should not be confused with neurogenic
shock, which involves hypotension and bradycardia resulting from damage to the auto-
nomic fibers within the spinal cord, although these complications may occur together
(as in our patient).
In the ICU, blood pressure augmentation should be utilized to maintain a mean
arterial pressure (MAP) greater than 80 mm Hg for approximately 1 week. This serves
to maintain adequate systemic perfusion in the face of neurogenic shock, as well as to
provide maximal safe perfusion to the spinal cord in the hopes of facilitating potential
neurologic recovery. Anticholinergic medications such as atropine may be used in the

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Spinal Neurosurgery

setting of symptomatic bradycardia. Higher level cervical injuries result in disruption

of the phrenic nerve and may lead to inadequate ventilation. These patients may re-
quire mechanical ventilation if PaO2 is less than 70 mm Hg or PaCO2 is greater than
45 mm Hg. Foley catheterization will be necessary until the patient is systemically stable,
and neurogenic bladder causes a significant problem. Autonomic dysreflexia is another
common problem facing spinal cord injury patients. Frequent patient repositioning,
range of motion exercises (to combat spasticity), and early management of pressure
ulcers is necessary. Finally, kinetic therapy via a rotorest bed may also be beneficial as a
cardiovascular and respiratory prophylactic measure.

Complications and Management

Complications of rigid external fixation with a halo orthosis commonly include pin
loosening, pin site infection, and discomfort. Other rarer complications include skull
fracture and injury to the supratrochlear and/​or supraorbital nerves. Because of the
fairly high incidence of morbidity associated with the halo vest, our center has largely
abandoned its use.
ACDF is generally a low-​morbidity procedure; however, significant complications
may occur. Postoperative dysphagia is the most common complication. Efforts at
minimizing the degree of and time under retraction may reduce its incidence, but the
etiology is likely multifactorial. While largely transient, a short course of steroids may be
beneficial in severe cases.
Recurrent laryngeal nerve palsy and vocal cord paresis may result from division or
traction injuries to the nerve during exposure and/​or retraction. Careful dissection,
minimizing time under retraction, deflation of the endotracheal tube cuff after the self-​
retaining retractors are placed, and, as argued by some studies, a left-​sided approach may
minimize its occurrence. In general, symptomatic injuries are transient, however otolar-
yngology referral may be indicated.
Postoperative wound hematoma is a potentially catastrophic complication of the
anterior approach. A large retrospective review by Fountas et al. found a 5.6% chance
of this complication with 24 of 57 affected patients requiring emergent surgical evacu-
ation. If respiratory compromise is suspected, emergent evacuation of the hematoma is
indicated.
Durotomy and cerebrospinal fluid (CSF) leak may occur in a very small percentage
of patients, and this should be treated with the prompt placement of a lumbar drain and
careful attention to a watertight wound closure. In the majority of cases, several days
of CSF diversion and head of bed elevation will resolve the leak. Durotomy is more
common in posterior cervical cases where laminectomies are performed, but because of
the wider exposure, these tears should be attempted to be closed primarily. Placement of
a dural substitute or sealant may also be beneficial.
Other rare but catastrophic complications of ACDF include vertebral artery injury
and esophageal or pharyngeal perforation. This likely occurs in less than 1% of cases.
For esophageal injuries, prompt intraoperative identification and primary repair by a
general surgeon is paramount as unidentified injuries may lead to mediastinitis and over-
whelming infection. Care should be taken during lateral dissection and when performing
foraminotomies to avoid vertebral artery injury. At our center, any vertebral artery injury

18
 

Cervical Fracture Dislocation

is treated with packing and emergent angiogram to assess the injury and potentially
sacrifice the artery. Similarly, the vertebral arteries are at risk when instrumenting the
cervical spine posteriorly. The screw should not be removed if an injury is suspected.
The wound should be packed and, at our institution, prompt referral to the endovascular
suite should be initiated.
In regards to the patient with an unstable cervical fracture and spinal cord in-
jury, simple maneuvers such as patient transfers and positioning could have serious
consequences. Strict spine precautions are necessary at all times to prevent the produc-
tion or worsening of a neurologic injury.

Oral Boards Review: Complications Pearls

1. Minimizing time under retraction and deflation of the endotracheal tube

once the self-​retaining retractors are placed may minimize the risk of postop-
erative dysphonia.
2. Postoperative dysphagia is more common in three-​level procedures compared
to one-​or two-​level procedures.
3. CSF leak encountered during ACDF should be treated with several days of
lumbar drainage and is successful in most cases.

Evidence and Outcomes

Level 1 evidence suggests that both anterior and posterior approach surgeries are ef-
fective at treating cervical fracture dislocation injuries. One prospective randomized
controlled trial found that, compared to posterior fixation, ACDF was associated with
less postoperative pain, higher rate of fusion, better alignment, and fewer postoperative
wound infections. Numerous cohort studies have found similar results. Closed reduction
of cervical dislocations is associated with high success rates and a low rate of neurologic
complications, ranging from 1% to 4%.

References and Further Reading

Anissipour AK, Agel J, Baron M, Magnusson E, et  al. Traumatic cervical unilateral and bilat-
eral facet dislocations treated with anterior cervical discectomy and fusion has a low failure
rate. Global Spine J. 2017;7(2):110–​115. doi: 10.1177/​2192568217694002. Epub Apr 6, 2017.
https://​www.ncbi.nlm.nih.gov/​pubmed/​28507879
Belirgen M, Dlouhy BJ, Grossbach AJ, et al. Surgical options in the treatment of subaxial cer-
vical fractures: A retrospective cohort study. Clin Neurol Neurosurg. 2013;115(8):1420–​1428.
doi:  10.1016/​j.clineuro.2013.01.018. Epub Mar 5, 2013. https://​www.ncbi.nlm.nih.gov/​
pubmed/​23481897
Casha S, Christie S. A systematic review of intensive cardiopulmonary management after spinal
cord injury. J Neurotrauma. 2011;28(8):1479–​1495. doi: 10.1089/​neu.2009.1156. Epub Apr 8,
2010. https://​www.ncbi.nlm.nih.gov/​pubmed/​20030558
Ditunno JF, Little JW,Tessler A, et al. Spinal shock revisited: A four-​phase model. Spinal Cord. 2004
Jul;42(7):383–​395. https://​www.ncbi.nlm.nih.gov/​pubmed/​15037862

19
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Spinal Neurosurgery

Fisher CG, Dvorak MF, Leith J, et al. Comparison of outcomes for unstable lower cervical flexion
teardrop fractures managed with halo thoracic vest versus anterior corpectomy and plating.
Spine (Phila Pa 1976). 2002;27(2):160–​166. https://​www.ncbi.nlm.nih.gov/​pubmed/​
11805662
Fountas KN, Kapsalaki EZ, Nikolakakos LG, et al. Anterior cervical discectomy and fusion asso-
ciated complications. Spine (Phila Pa 1976). 2007;32(21):2310–​2317. https://​www.ncbi.nlm.
nih.gov/​pubmed/​17906571
Kirshblum SC, Burns SP, Biering-​Sorensen F, et  al. International standards for neurological
classification of spinal cord injury (revised 2011). J Spinal Cord Med. 2011;34(6):535–​546.
doi:  10.1179/​204577211X13207446293695. https://​www.ncbi.nlm.nih.gov/​pmc/​articles/​
PMC3232636/​
Kwon BK, Fisher CG, Boyd MC, et  al. A prospective randomized controlled trial of anterior
compared with posterior stabilization for unilateral facet injuries of the cervical spine.
J Neurosurg Spine. 2007;7(1):1–​12. https://​www.ncbi.nlm.nih.gov/​pubmed/​17633481
Lee JY, Nassr A, Eck JC, et al. Controversies in the treatment of cervical spine dislocations. Spine
J. 2009 May;9(5):418–​423. doi: 10.1016/​j.spinee.2009.01.005. Epub Feb 23, 2009. https://​
www.ncbi.nlm.nih.gov/​pubmed/​19233734
Song KJ, Lee KB. Anterior versus combined anterior and posterior fixation/​fusion in the treat-
ment of distraction-​flexion injury in the lower cervical spine. J Clin Neurosci. 2008;15(1):
36–​42. https://​www.ncbi.nlm.nih.gov/​pubmed/​18061456
Walters BC, Hadley MN, Hurlbert RJ, et  al. Guidelines for the management of acute cer-
vical spine and spinal cord injuries:  2013 update. Neurosurgery. 2013;60 Suppl 1:82–​91.
doi:  10.1227/​01.neu.0000430319.32247.7f. https://​www.ncbi.nlm.nih.gov/​pubmed/​
23839357

20
 

Occipitocervical Dislocation

Alexander B. Dru and Daniel J. Hoh

Case Presentation

A 28-​year-​old woman presents to the emergency department after being struck by

3
a car at high speed while changing a tire on the side of a road. The patient arrives
intubated for airway protection and with a cervical collar in place. She has multiple
deep lacerations to the head and neck, an open left humerus fracture, and a distended
abdomen. She has no significant past medical or surgical history.
Upon arrival, the patient’s vital signs are blood pressure 130/​71, pulse 79, respiratory
rate 14 (mechanically ventilated), and temperature 37.1°C. Neurologic examination (off
sedation) is remarkable for a Glasgow Coma Scale (GCS) of 7T (does not open eyes,
intubated, localizes right greater than left upper extremity to noxious stimuli). Cranial
nerve examination is consistent with pupils of 2 mm, equal and reactive to light, intact
corneal reflexes, and present cough and gag reflexes. On motor examination, the patient
weakly withdraws all four extremities, right greater than left.

Questions

1. What radiologic studies are indicated as part of the initial neurosurgical eval-
uation (imaging modality and anatomic area to image)?
2. What is the most appropriate management of the cervical collar?
3. In the setting of a potential spinal cord injury (SCI), what is the importance
of cardiopulmonary vital signs?

Assessment and Planning

Given a history of high-​energy mechanism of injury to the head and neck, the ini-
tial neurosurgical survey includes evaluation for acute intracranial pathology and spinal
column injury resulting in instability and/​or spinal cord or nerve compression. The pa-
tient should be assessed for both possibilities with an emergent head computed tomog-
raphy (CT) and full spine CT. Since the patient has depressed mental status, the patient
should be maintained in a cervical collar until cervical spine CT and further clinical
assessment is made. If the patient is suspected of having a potential cervical SCI, heart
rate and blood pressure should be closely monitored for neurogenic shock. Upper cer-
vical SCI can result in impaired respiratory motor function. A secure airway should be
confirmed at time of the initial survey.

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Spinal Neurosurgery

Occipitocervical dislocation (or atlanto-​occipital dislocation, AOD) is a highly un-

stable injury to the cranio-​cervical junction (Figure 3.1). Historically, AOD was only re-
ported in autopsy findings likely due to a high rate of mortality related to severe cervical
spine instability and concomitant upper cervical SCI. Currently, AOD is estimated to
cause up to 35% of fatalities in motor vehicle collisions and 10% of fatal cervical spine
injuries. Better management by first responders, established advanced trauma life support
protocols, and modern imaging modalities have contributed to improved survival rate
after traumatic AOD.
AOD is typically a result of high-​ energy deceleration forces. Distraction with
hyperextension-​flexion, often with a rotational component, are necessary to cause forces
significant to disrupt the robust ligamentous attachments at the occipital-​cervical junc-
tion. Mortality is likely related to dislocation at the craniocervical junction causing
upper cervical spinal cord compression and acute respiratory dysfunction and/​or hemo-
dynamic instability secondary to neurogenic shock. Immediate immobilization in the
field (e.g., cervical collar) followed by prompt diagnosis and external stabilization (e.g.,

A B

C D

Figure 3.1  Radiograph (A), computed tomography (CT) sagittal (B), coronal (C), and three-​dimensional
reconstruction (D) of demonstrating atlanto-​occipital dislocation (AOD).

22
 

Occipitocervical Dislocation

halo vest) may prevent or mitigate neurologic injury, with some patients presenting as
neurologically intact or with an incomplete SCI.
SCI can be a result of dislocation leading to compression, contusion, laceration, or
ischemia of the spinal cord. SCI at the cranio-​cervical junction can present with a va-
riety of complete or incomplete motor and sensory deficits. Bell cruciate paralysis is an
incomplete syndrome unique to the cranio-​cervical junction characterized by weak-
ness of the upper extremities with little to no involvement of lower extremity muscle
groups. The pattern of injury is secondary to midline damage to the upper pyramidal
decussation. The somatotopy of the decussation is such that the injured upper extremity
motor fibers cross more superomedially, whereas the spared lower extremity fibers are
inferolateral in the medulla.
Other associated neural and vascular injuries are often observed in the setting of
AOD. Individual cranial nerves are susceptible to injury following AOD, specifically
lower cranial nerves IX, X, XI, and XII as they traverse the jugular or hypoglossal fo-
ramen. Most commonly, cranial nerves IX, X, and XI are affected due to tethering
and traction within the jugular foramen. The hypoglossal nerve (CN XII) may be at
high risk if there is a concomitant fracture of the occipital condyle extending into the
hypoglossal canal.
Carotid and vertebral artery injuries may occur due to stretching or laceration, with
either intimal tears, dissection, or thrombosis. Pontomedullary subarachnoid blood may
be an indication of AOD with posterior circulation injury.Vertebral artery injury can re-
sult in posterior inferior cerebellar artery distribution ischemia with a lateral medullary
syndrome characterized by cerebellar dysmetria; ipsilateral cranial nerve V, IX, X, and XI
deficits; an ipsilateral Horner syndrome; and contralateral loss of pain and temperature
sensation.

Oral Boards Review: Diagnostic Pearls

1. Prompt multiplanar CT imaging is crucial to the timely and accurate diag-

nosis of AOD.
a. Displacement of the occipital condyle from C1 lateral mass by more than
2 mm (adults) or more than 4 mm (children) indicates potential AOD.
2. One should have a high index of suspicion for AOD if:
a. High cervical SCI is present without evidence of cervical fracture and/​or
dislocation in the subaxial spine.
b. Bell cruciate paralysis is present with only upper extremity paralysis.
c. Isolated lower cranial nerve dysfunction (e.g., IX, X, XI, XII) is present.
d. Subarachnoid blood is present at the pontomedullary junction.
e. Significant soft-​tissue swelling (e.g., retropharyngeal) is present at the
upper cervical spine.

Questions

1. Describe the utility of x-​ray, CT, and magnetic resonance imaging (MRI) in
the diagnosis and management of AOD.

23
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Spinal Neurosurgery

2. Describe image-​based diagnostic criteria for AOD.

3. What are two classification systems for AOD?

Decision-​Making

The diagnosis of AOD is made based on imaging studies. Historically,AOD was identified
using two-​dimensional lateral plain x-​ray characterizing the radiographic relationship
between structures of the skull base and upper cervical vertebrae. With the advent of
modern CT imaging technology, the current gold standard for diagnosing AOD is with
multiplanar thin-​slice CT. A basic knowledge of lateral x-​ray criteria for AOD, however,
may be helpful in understanding the pathophysiology of AOD and for supplementary
diagnostic evaluation in questionable cases.
The Harris method or “rule of twelves” calculates the basion-​axial interval (BAI)
and basion-​dental interval (BDI) (Figure 3.2A). BAI is the distance between the vertical
extension of the posterior cortex of C2 and the posterior-​most tip of the basion. BDI is
the distance from the tip of the dens to the basion. In normal adults, both BAI and BDI
should be less than 12 mm.
The Powers ratio is the ratio of two distances (Figure 3.2B). The numerator is the
distance between the tip of the basion to the ventral midpoint of the posterior arch of
C1. The denominator is the distance from the tip of the opisthion to the dorsal mid-
point of the anterior arch of C1. A ratio greater than 1 suggests anterior dislocation of
the head relative to the spine.
Multiplanar CT imaging provides the highest sensitivity and specificity for diagnosing
AOD. The condyle-​C1 interval (CCI) is measured by selecting four equidistant points

A B C

Figure 3.2  (A) The Harris method. In the radiograph, the basion-​dental interval (BDI; white) and basion-​axial
interval (BAI; yellow) are both greater than 12 mm. (B) The Powers ratio. The numerator is the distance between the
tip of the basion to the ventral midpoint of the posterior arch of C1. The denominator is the distance from the tip of
the opisthion and the dorsal midpoint of the anterior arch of C1. A ratio of greater than 1 suggests atlanto-​occipital
dislocation (AOD). (C) The condyle–​C1 interval (CCI). Four equidistant points along the articulating surface of the
occiput–​C1 joint on sagittal CT are measured. AOD is suspected if the average of the four measurements is greater
than 2 mm in adults or greater than 4 mm in children.

24
 

Occipitocervical Dislocation

along the articulating surface of the occiput–​C1 joint on sagittal or coronal CT (Figure
3.2C). AOD is suspected if the average of the four measurements is greater than 2 mm
in adults or greater than 4 mm in children.
Additional imaging modalities may be useful in further characterizing the extent of
injury after AOD. MRI is generally not required for routine diagnosis, but it provides
superior visualization of neurologic and soft tissue structures. Particularly in the setting
of neurologic deficit, MRI may elucidate the underlying etiology, whether spinal cord
compression, contusion, ischemia, or epidural hematoma. MRI may also identify liga-
mentous disruption at the occipital-​cervical articulation, as well as elsewhere in the cer-
vical spine (e.g., transverse ligament). CT angiography may identify associated vascular
injuries with potential risk of thromboembolic stroke.
There are two major classification systems for AOD. The Traynelis Classification
System characterizes the direction of head dislocation relative to the spine (Figure 3.3).
Type 1 is ventral head dislocation, type 2 is vertical displacement, and type 3 is dorsal dis-
location relative to the cervical spine.The Bellbarba system is based on imaging findings
in neutral position as well as with controlled test traction. It is designed to assess spinal
stability and facilitate management decision-​making. Type 1 AOD is considered stable.
It is characterized by both BAI and BDI within 2 mm of normal and less than 2 mm
displacement with traction. Type 2 AOD is unstable. It is characterized by both BAI
and BDI within 2 mm of normal, but significant displacement with test traction. Type
3 AOD is also unstable and demonstrates BAI and BDI values of greater than 2 mm of
normal in neutral position.

Questions

1. What is the immediate management of AOD?

2. What is the risk of cervical traction in AOD?
3. What are the goals of surgical treatment?
4. What is potential loss of range of motion after surgical treatment?

Surgical Procedure

AOD is an acute, highly unstable injury with potential risk of permanent upper cer-
vical SCI. Once the diagnosis is made, the patient should be placed in immediate ex-
ternal immobilization with strict cervical spine precautions. Patients presenting with
acute trauma are usually already in a cervical collar. Halo vest immobilization generally
provides better stabilization of the cranio-​cervical junction than a rigid cervical collar
alone, and securing the patient in a halo vest should be considered.
Ultimately, AOD is a result of disruption of the ligamentous attachments between
the occiput and the upper cervical spine. Therefore, external bracing alone is unlikely to
provide long-​term healing and stability. Reduction of AOD and internal fixation and fu-
sion across the occipital-​cervical junction is generally recommended for definitive treat-
ment. In the setting of polytrauma with cardiopulmonary compromise, it is appropriate
to maintain the patient in halo external immobilization with strict cervical precautions
until the patient is stable enough to be safely taken to the operating room.

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Spinal Neurosurgery

Figure 3.3 The Traynelis classification system. Type 1 (top) is ventral head dislocation.

Type 2 (middle) is vertical displacement. Type 3 (bottom) is dorsal dislocation relative to
the cervical spine.

The role of closed reduction with traction for AOD is controversial. Due to instability
at the occipital-​atlantal articulation with potential for further vertical head displacement
and neurovascular injury, one should generally avoid traction. There is a reported 10%
risk of neurologic deterioration with the use of traction in the setting of AOD.
The goals of surgical treatment are to immediately stabilize the cranio-​cervical junc-
tion with internal fixation, decompress the spinal cord by reduction and/​or removal
of any compressive lesions, and provide long-​term maintenance of correction with ar-
throdesis.Various posterior surgical techniques for stabilization have been described with
current approaches generally involving screw fixation of the occiput and upper cer-
vical spine connected by occipital plate-​rod constructs (Figure 3.4). Determining how
many cervical levels are necessary for fixation depends on individual patient anatomy,
bone integrity, and the presence of other concomitant cervical injuries. The cranio-​
cervical junction can be a challenging region in which to achieve successful arthrodesis.
Various autologous (e.g., iliac crest, rib harvest), allogeneic, and synthetic graft options
supplemented by graft wiring techniques may be used to optimize fusion rate.

26
 

Occipitocervical Dislocation

Figure 3.4  Occipital–​C4 fusion for internal stabilization of atlanto-​occipital

dislocation (AOD).

Surgical treatment for AOD often involves stabilization across the occiput–​C2, thereby
eliminating motion across both the occipital-​atlantal and atlantal-​axial articulations. As
a result, patients can expect loss of 50% of head flexion/​extension and 50% of right–​left
rotation. Adult patients with subaxial cervical spondylosis and baseline restricted range
of motion may experience even greater overall functional impairment. This permanent
loss of range of motion should constitute an important part of the preoperative discus-
sion with patients and caregivers to appropriately align expectations after surgery.

Oral Boards Review: Management Pearls

1. AOD is a highly unstable injury and patients should be immediately placed in

a rigid external orthosis. A halo vest generally provides better immobilization
at the occipital-​cervical junction than a rigid cervical collar.
2. Definitive treatment for AOD generally involves reduction with surgical
decompression (if needed) and stabilization across the occipital–​cervical
junction.
a. Current surgical stabilization techniques include screw fixation of the
occiput and the cervical spine with a connecting occipital plate-​rod
construct.
b. Determining adequate points of fixation in the cervical spine depends on
the patient’s individual anatomy and bone integrity.

27
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Spinal Neurosurgery

3. Perioperative intensive care management may be necessary to treat cardiopul-

monary issues related to neurogenic shock and upper cervical SCI leading to
diaphragm paralysis.
a. Neurogenic shock is best treated with dopamine and phenylephrine. The
presence of bradycardia and hypotension that fail to respond to intrave-
nous fluids suggest neurogenic rather than hypovolemic shock.

Aftercare

Early postoperative care after surgical treatment for AOD is generally determined by the
extent of neurologic deficits and other associated injuries. Patients with cardiopulmo-
nary compromise from cervical SCI should be managed in an intensive care unit until
hemodynamic and respiratory issues are stabilized. Hypotension and bradycardia in the
setting of acute cervical SCI should alert for potential neurogenic shock. Management
consists of intravenous sympathomimetic agents and fluid resuscitation. Patients with
upper cervical SCI with diaphragmatic paralysis and who fail ventilator weaning should
be expeditiously transitioned from an endotracheal tube to a tracheostomy. Aggressive
pulmonary toilet and respiratory rehabilitation should be implemented to reduce risk of
pneumonia. Additional SCI management should be directed toward preventing venous
thromboembolic, urinary tract, and pressure ulcer complications.
Patients with adequate surgical reduction and internal fixation generally do not re-
quire supplementary external bracing. Continued postoperative use of a rigid cervical
collar or halo vest may lead to skin breakdown or halo pin site complications and can
impede rehabilitation. Patients with poor bone mineral density or with high risk of
instrumentation failure, however, may benefit from additional postoperative external
orthosis, and may be considered in select individuals. Serial routine follow-​up should
be performed at regular intervals up to generally 12 months postoperative to assess for
neurologic function and for eventual successful fusion. Maintenance of correction, stable
instrumentation, and the presence of bridging bone across the occipital-​cervical junc-
tion indicate bony healing.

Complications and Management

Surgical complications after occipital-​cervical fusion include those that may be encountered
after any posterior spine fusion including surgical site infection, blood loss, cerebrospinal
fluid leak, pseudarthrosis, and instrumentation failure. New postoperative neurologic
deficits after surgery are uncommon. Given the relatively favorable spinal canal-​to-​spinal
cord ratio at the craniocervical junction, direct injury to the spinal cord during surgery
is rare. Placing patients prone with AOD, however, can potentially cause new neurologic
deficits given the highly unstable injury and risk of further dislocation during positioning.
Positioning patients in a halo vest with pre-​and postpositioning electrophysiologic spinal
cord monitoring and intraoperative fluoroscopy are measures that may reduce this risk.
The course of the vertebral artery as it traverses the cranio-​cervical junction can
be variable, and preoperative assessment of its anatomy is recommended prior to screw
placement, specifically at C1 and C2. Bilateral vertebral artery injuries are generally fatal,

28
 

Occipitocervical Dislocation

and therefore, careful evaluation for any vertebral artery anomalies (e.g., unilateral dom-
inant, torturous) or associated traumatic occlusion (e.g., dissection) should be made. In
situations of an incompetent unilateral vertebral artery, careful consideration should be
made to avoid screw placement that may put the contralateral artery at risk.
The occipital-​cervical junction is a region that can be challenging to achieve successful
arthrodesis. Instrumentation failure with screw loosening or rod fracture on routine post-
operative x-​ray indicate likely pseudarthrosis. Late postoperative new onset or worsening
pain may be an early sign of failed fusion. Further investigation of suspected pseudarthrosis
includes fine-​cut CT imaging to assess for the presence or absence of bridging bone across
the occipital–​cervical junction. Asymptomatic pseudarthrosis with intact instrumentation
may be treated conservatively. Instrumentation failure, progressive deformity, worsening pain,
or new neurologic deficits in the setting of failed fusion may be indications for revision
surgery.

Oral Boards Review: Complication Pearls

1. AOD is a highly unstable injury and therefore maintaining strict immobiliza-

tion is critical.
a. Neurologic deterioration may occur with any excessive motion, and
therefore cervical traction should generally be avoided.
b. Special care should be made in positioning patients prone for surgery, with
pre-​and postpositioning fluoroscopy and electrophysiologic spinal cord
monitoring.
2. The vertebral artery may be at risk during surgical fixation at the occipital-​
cervical junction due to preexisting anatomic anomalies or secondary to trau-
matic injury.
a. Careful preoperative assessment of both vertebral arteries should be made
to avoid potential risk of bilateral vertebral artery compromise.
3. The occipital–​cervical junction is susceptible to pseudarthrosis, which may
present with late-​onset pain, neurologic worsening, progressive deformity, or
instrumentation failure.
a. Evaluation includes multiplanar thin-​cut CT imaging to assess for
bridging bone.
b. Symptomatic pseudarthrosis should be treated with revision fusion.

Evidence and Outcomes

AOD is relatively uncommon compared to other traumatic cervical spine injuries,

which may in part be secondary to a high mortality risk immediately at the time of
injury. Existing literature, therefore, regarding treatment, prognosis, and outcomes
is limited. Modern advances in care by first responders, emergency trauma serv-
ices, diagnostic imaging, and spine surgery have likely contributed to better survival.
Long-​term outcome after AOD is most likely related to neurologic function at time
of initial presentation, including both SCI and any potential concomitant traumatic
brain injury. Complete upper cervical SCI portends a worse prognosis than incom-
plete and lower cervical injuries. Recent literature suggests that early decompression

29
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Spinal Neurosurgery

and stabilization of cervical spine injuries may enhance potential for neurologic re-
covery. Additionally, better medical management with aggressive rehabilitation and
chronic preventative care for SCI-​related complications have improved overall life
expectancy post-​SCI.

References and Further Reading

Fisher CG, Sun JC, Dvorak M. Recognition and management of atlanto-​ occipital disloca-
tion: Improving survival from an often fatal condition. Can J Surg. 2001;44(6):412–​420.
Horn EM, Feiz-​erfan I, Lekovic GP, Dickman CA, Sonntag VK, Theodore N. Survivors of
occipitoatlantal dislocation injuries:  Imaging and clinical correlates. J Neurosurg Spine.
2007;6(2):113–​120.
Kleweno CP, Zampini JM,White AP, Kasper EM, Mcguire KJ. Survival after concurrent traumatic
dislocation of the atlanto-​occipital and atlanto-​axial joints: A case report and review of the
literature. Spine. 2008;33(18):E659–​E662.
Pang D, Nemzek WR, Zovickian J. Atlanto-​occipital dislocation—​part  1:  Normal occipital
condyle-​C1 interval in 89 children. Neurosurgery. 2007;61(3):514–​521.
Pang D, Nemzek WR, Zovickian J. Atlanto-​occipital dislocation—​part  2:  The clinical use of
(occipital) condyle-​C1 interval, comparison with other diagnostic methods, and the mani-
festation, management, and outcome of atlanto-​occipital dislocation in children. Neurosurgery.
2007;61(5):995–​1015.

30
 

Central Cord Injury

Bizhan Aarabi, Charles A. Sansur, David M. Ibrahimi,

Mathew Kole, and Harry Mushlin

Case Presentation
4
A 45-​year-​old police officer sustained a cervical spine “whiplash” injury during a high-​
speed car chase and was momentarily unconscious. Immediately following the motor
vehicle collision (MVC), he was unable to move any of his extremities and EMTs were
there within 30 minutes of the accident. He gradually regained function in his legs,
but his arms were burning, tingling, and powerless. His Glasgow Coma Scale score was
14, his pulse rate 55 bpm, and blood pressure 90/​60 mm Hg. He was complaining of
neck pain and severe burning and tingling of his hands and forearms. His cervical spine
was tender, his chest clear, and abdomen soft. He was given a liter of normal saline and
transferred to the trauma center within 56 minutes. Upon presentation, he was con-
scious and alert; he was complaining of severe hypersensitivity of his hands and weak
arms. His respiratory rate was 12, pulse rate 60 bpm, blood pressure 100/​75 mm Hg,
and O2 saturation 99% on room air. Primary and secondary surveys did not reveal addi-
tional findings. Following resuscitation, neurosurgery was called to evaluate the patient.
Neurological examination showed normal speech and cranial nerves. His American
Spinal Injury Association (ASIA) motor score (AMS) was 56 and ASIA Impairment
Scale (AIS) grade D (see Table 4.1).
His hands and forearms were extremely sensitive to sensory examination and touch.
Deep tendon reflexes were absent in the upper extremities but slightly hyperactive in
the lower extremities. Digital rectal examination indicated good sensation and volition.

Questions

1. What is the likely neurological diagnosis?

2. What imaging modalities best aid in management?
3. What anatomical regions of the vertebral column would you study in im-
aging studies?
4. What is the most appropriate timing for imaging studies and treatment?

Assessment and Planning

The composite picture described here is a typical presentation of what is called acute
traumatic central cord syndrome (ATCCS). ATCCS is the most frequently encountered

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Spinal Neurosurgery

Table 4.1
ASIA motor score of the presented case
C5 C6 C7 C8 T1 L2 L3 L4 L5 S1
Right 4 2 2 1 1 5 5 5 5 5
Left 4 3 3 2 2 5 5 5 5 5

clinical picture of a mild to moderate (AIS grade C or D) incomplete blunt traumatic

spinal cord injury (SCI). Dr. R. C. Schneider was the first to describe ATCCS: in his
21 patients, upper extremities were much weaker than the lower extremities, there
were varying degrees of sensory loss, and the patients had difficulty with sphincter con-
trol.1–​3 Close to half of patients with ATCCS have no radiographically obvious fracture
dislocations and instead suffer from congenital or degenerative spinal stenosis (Figure
4.1). Ten of 21 patients in Dr. Schneider’s series had radiographically proven fracture
dislocations, and 11 had degenerative spinal stenosis.
In another clinical series of 42 patients with ATCCS due to congenital stenosis or
disc/​osteophyte complex, 33 (~80%) were AIS grade D at admission.4 These elderly
patients sustained their cervical spine hyperextension injury mostly following a mechan-
ical fall during which the spinal cord was presumably pinched between an acutely bulged
intervertebral disc and the buckled ligamentum flavum. While the most frequent seg-
mental injury was at C3–​C4, the compressive contusive lesion may be in more than two
separate skeletal segments. Approximately 35% of patients with degenerative ATCCS
exhibit magnetic resonance imaging (MRI) or computed tomography (CT) evidence

Figure 4.1  Admission imaging studies of the case presented above. Plates A and C
indicate right and left lateral computed tomography (CT) views of facet joints and
plate B the midsagittal view of the vertebral bodies. There is no evidence of fracture
dislocation, and morphology is essentially normal. Plates D, E, and F indicate T2-​
weighted sagittal magnetic resonance imaging (MRI) showing prevertebral soft tissue
swelling (long arrow), spinal cord compression with signal change at C3-​C4 (short arrow),
and spinal stenosis at three skeletal segments (C3–​C6).

32
 

Central Cord Injury

of extension injury (Extension Distraction Stage 1 of Allen et al.)5 to one or more of

the intervertebral discs.4 Under such circumstances, there may be an avulsion fracture of
the antero-​inferior edge of the rostral vertebral body at the disc level, and T2-​weighted
MRI may indicate signal change at the disc level (mostly at the C6–​C7 disc level).
Skeletal stenosis may range from 1 to 5 segments; however, T2-​weighted MRI usually
indicates signal change at one short segment of spinal cord, mostly at the C3–​C4 level
(Figure 4.1). There may be nonspecific signal change in the prevertebral or supraspinal
soft tissues (Figure 4.1). The intramedullary lesion signal change typically is short and
within one skeletal segment (Plate E). Postmortem studies indicate that translation of
kinetic energy into cytoskeletal damage is dispersed within the posterolateral funiculus
of the spinal cord, disrupting neural transmission in the lateral corticospinal tract.6 Minor
necrosis of the central gray has been reported; however, in a typical ATCCS exhibiting
AIS grades C or D functional loss, there is no intraparenchymal bleeding, as originally
suggested by Dr. Schneider.1,2,6,7

Oral Board Review: Diagnostic Pearls

1. Almost 50% of ATCCS patients are those with fracture dislocations.

2. In ATCCS due to hyperextension injuries, morphology is almost always well-​
maintained with no evidence of structural instability.
3. ATCCS due to hyperextension injuries is usually a mild to moderate (AIS
grades C and D) SCI.
4. Intramedullary hemorrhage in hyperextension ATCCS is almost always
absent.
5. ATCCS primarily involves upper extremities with variable degrees of sensory
loss and sphincter dysfunction.

Questions

1. How do clinical and radiological findings influence surgical planning?

2. What is the most appropriate timing for intervention in this patient?
3. What is the best surgical technique to fully decompress the spinal cord under
compression?

The neurosurgeon confronted with an elderly patient with positive past medical his-
tory of comorbidities and hyperextension ATCCS due to multisegmental spinal stenosis
bases treatment decisions on certain critical considerations:  (1) the cervical spine in
this patient is stable, therefore, there is no urgency for speedy cervical spine anatomical
realignment, spinal cord decompression, and internal fixation; (2) the SCI in ATCCS
is usually mild to moderate and incomplete; (3) regardless of management, surgical or
nonsurgical, significant recovery of neurological deficit over time is almost guaranteed;
(4) surgical intervention is usually complex, tedious, meticulous, and may take several
hours; and (5) although there is low-​level evidence that decompression within 24 hours
may help recovery of function, this issue remains controversial and is usually applied only
to the most severe SCI.4,8,9

33
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Spinal Neurosurgery

Decision-​Making

Oral Board Review: Decision-​Making Pearls

1. The spinal cord is usually under compression at one or several skeletal

segments.
2. The surgeon has to plan a timely and extensive surgery, taking into consider-
ation a meticulous, multisegmental, complex anterior or posterior approach
with or without internal fixation.
3. Though the surgery does not have to be urgent or emergent, the literature is
quite varied and inconclusive concerning surgical timing.

Surgical Procedure

Before surgery, one needs to review the imaging studies and look for the following:

1 . Is the patient’s cervical spine kyphotic, straight, or lordotic?

2. How many stenotic skeletal segments are to be dealt with?
3. Where is the site of most stenosis on MRI with signal change?
4. Should the surgical technique be anterior, posterior, or circumferential?
5. Is laminectomy needed?
6. What is the relationship of signal change on MRI and the length of the stenotic canal?

Anterior Cervical Discectomy and Fusion

This surgical technique is suitable when the pressure on the spinal cord is primarily an-
terior. ACDF is especially indicated in patients who need corrective surgery for sagittal
imbalance and the probability of worsening kyphotic deformity is high with laminec-
tomy. Figures 4.2 and 4.3, respectively, belong to the case under discussion and a 60-​
year-​old man with ATCCS and an AMS of 94 following an automobile accident. The
first patient has well-​maintained sagittal balance, but the second patient suffers an early
kyphotic deformity, and the compression on the cord at C4–​C5 and C5–​C6 dictated an
anterior approach. In order to reverse early kyphosis, posterior osteophytes needed to
be resected generously, followed by insertion of lordotic implants. In both cases, decom-
pression was enough with no need for laminectomy.

Laminoplasty

Laminoplasty is appropriate in patients who do not have prominent soft disc herniation
and only suffer from hard disc osteophyte complex across several motion segments with
preserved cervical lordosis.10 In the presence of multiple-​segment spinal stenosis and
kyphotic deformity, anterior approach or posterior laminectomy and posterior spinal fu-
sion may take precedence (Figure 4.4). Laminoplasty is contraindicated in the presence
of fracture dislocations.

34
 

Figure 4.2  Management of the case presented. The patient had three-​level anterior
cervical discectomy and fusion (ACDF) with resection of osteophytes and satisfactory
decompression of the segmental damage to the cord and spinal stenosis. The patient
did not need laminectomy and fusion.

Figure 4.3  A 60-​year-​old man with acute traumatic central cord syndrome (ATCCS)
following an automobile accident who was managed by two-​level anterior cervical
discectomy and fusion (ACDF) to relieve pressure from the spinal cord. ACDF was
particularly indicated since the patient had kyphotic deformity and significant pressure
ventrally The surgery resulted in relief of spinal cord compression and kyphotic
deformity with no need for laminectomy.
36

Spinal Neurosurgery

Figure 4.4  A 43-​year-​old man with acute traumatic central cord syndrome (ATCCS)
and managed by laminoplasty, which relieved spinal cord compression while
maintaining a modest degree of axial spine movements, with maintenance of the
patient’s posterior tension band.

Laminectomy

Laminectomy with or without posterior spinal fusion should be considered for

multisegmental spinal stenosis with well-​maintained sagittal alignment.We prefer trough
laminectomy in patients with severe stenosis and rigid spines. In this technique, a high-​
speed drill is used to remove the outer table of each skeletal segment to the inner table;
this is followed by a 2  mm Kerrison Punch to remove the inner table and then lift
up the lamina following resection of the ligamentum flavum. At times there are ad-
hesion strands between the dura and the inner table that need to be sectioned with
microscissors (Figures 4.5 and 4.6).

Oral Board Review: Surgical Technique Pearls

1. For extensive ACDFs, look for the superior laryngeal nerve at C3–​C4 and
inferior thyroid artery and recurrent laryngeal nerve at the level of C6–​C7
skeletal segments.
2. It is vital to resect osteophytes at the level of posterior annulus and then pro-
ceed with resection of the posterior longitudinal ligament and complete
foraminotomy.
3. Your implants need to be lordotic in order to reverse kyphotic deformity.
4. In patients with straight or kyphotic cervical spine, avoid laminectomy
without fusion.

36
 

Central Cord Injury

Figure 4.5  A 33-​year-​old man who sustained acute traumatic central cord syndrome
(ATCCS) following a motor vehicle accident. His ASIA motor score was 54, and 24
hours following admission he underwent laminectomy for spinal cord decompression.

Aftercare

1. Venous thromboembolism prophylaxis 72 hours after admission is instituted whether

management is non-operative or surgical intervention.
2. Develop a rehabilitation plan as soon as possible.
3. Perform tracheostomy for high cervical AIS grade C or worse patients.

Figure 4.6  Schematic view of trough laminectomy. Two troughs are produced on

each side of the lamina followed by removal of the inner tables using a Kerrison
rongeur. Incision of the ligamentum flavum will release the lamina, which is removed
without aggressive surgery using a Leksell rongeur or the thick footplate of a rongeur
over a spinal cord parenchyma tightly compressed by spinal stenosis.

37
38

Spinal Neurosurgery

Preoperative Five years postop

Figure 4.7 Ten years following successful decompression of the spinal cord, the

patient was working in a car dealership suffering from lack of dexterity of his hands
(50%), burning and numbness of his hands, and urinary frequency. He was on baclofen
for severe spasms and gabapentin for numbness and tingling of his hands.

4 . Discuss a long-​term disability financial coverage plan.

5. Administer medications such as gabapentin or pregabalin for dysesthetic hand and
forearm pain.
6. Schedule long-​term MRI studies to present evidence for central cord syrinx. These
patients may have an AMS of 100, but their lives are miserable owing to lack of dex-
terity and presence of dysesthetic pain and paresthesia (Figure 4.7).

Pivot Pearls

1. If a patient presents with ATCCS while being on warfarin or antiplatelet

agents, it is recommended to wait until the patient has an appropriate coagu-
lation profile and only then proceed with surgical intervention.

Complication Pearls

1. Management of major venous thromboembolism takes precedence over sur-

gical decompression of the spinal cord.
2. Significant swallowing difficulty should be managed by gastrostomy without
too much delay in the nutritional requirements of the patient.
3. AIS grade C patients with ATCCS due to high cervical cord SCI may need
short-​term tracheostomy in order to prevent complications such as pneu-
monia or atelectasis.

References and Further Reading

1. Schneider RC. A syndrome in acute cervical spine injuries for which early operation is indi-
cated. J Neurosurg. 1951;8:360–​367.

38
 

Central Cord Injury

2. Schneider RC, Cherry G, Pantek H. The syndrome of acute central cervical spinal cord in-
jury. J Neurosurg. 1954;13:546–​577.
3. Schneider RC, Thompson JC, Bebin J. The syndrome of acute central cervical spinal cord
injury. J Neurol, Neurosurg Psychiatry. 1958;21:216–​227.
4. Aarabi B, Alexander M, Mirvis SE, et al. Predictors of outcome in acute traumatic central
cord syndrome due to spinal stenosis. J Neurosurgery Spine. 2011;14:122–​130.
5. Allen BL, Jr., Ferguson RL, Lehmann TR, O’Brien RP. A mechanistic classification of closed,
indirect fractures and dislocations of the lower cervical spine. Spine. 1982;7:1–​27.
6. Quencer RM, Bunge RP, Egnor M, et  al. Acute traumatic central cord syndrome:  MRI-​
pathological correlations. Neuroradiology. 1992;34:85–​94.
7. Martin D, Schoenen J, Lenelle J, Reznik M, Moonen G. MRI-​pathological correlations in
acute traumatic central cord syndrome: Case report. Neuroradiology. 1992;34:262–​266.
8. Lenehan B, Fisher CG,Vaccaro A, Fehlings M, Aarabi B, Dvorak MF. The urgency of surgical
decompression in acute central cord injuries with spondylosis and without instability. Spine.
2010;35 (21 Suppl):S180–​S186.
9. Dvorak MF, Fisher CG, Hoekema J, et al. Factors predicting motor recovery and functional
outcome after traumatic central cord syndrome:  A long-​term follow-​up. Spine. 2006;30
(20):2303–​2311.
10. Hirabayashi K, Bohlman HH. Multilevel cervical spondylosis. Laminoplasty versus anterior
decompression. Spine. Aug 1 1995;20(15):1732–​1734.

39
40
 

Atlantoaxial Instability

Jonathan M. Parish and Domagoj Coric

Case Presentation

An 80-​year-​old man presents with a complaint of neck and bilateral shoulder pain as
5
well as bilateral hand pain and numbness. Patient states the pain has been progressive for
2 months and has been unrelieved by antiinflammatory medication, oral steroids, muscle
relaxants, and physical therapy. The patient has a history of rheumatoid arthritis and
chronic obstructive pulmonary disease (COPD) with chronic steroid use but no other
significant past medical history. The patient describes tingling in his hands, right greater
than the left, as well as bilateral hand weakness, noting difficulty with opening jars and
buttoning his shirt. The patient also complains of tingling and weakness in his legs and
has been using a walker to assist with ambulation over the preceding 6 weeks. The pa-
tient denies any difficulties with bowel or bladder control.
On examination, patient is alert and appropriate. Motor exam shows 4/​5 strength
in his left upper extremity and 4/​5 in his right upper extremity. He has proximal right
lower extremity strength of 4/​5 and right distal lower extremity strength 4/​5. He has
4/​5 left lower extremity strength. Sensory exam is intact to light touch and pinprick
although the patient complains of paresthesias in his hands and feet. The patient has 2+
equal and symmetric biceps, triceps, patellar, and Achilles deep tendon reflexes. The pa-
tient has positive Hoffman sign bilaterally but no clonus or Babinski. Gait is stable with
a walker.

Questions

1. What is the likely diagnosis?

2. What is the appropriate imaging modality and anatomical areas to image?

Assessment and Planning

Given the history and physical examination, the clinical picture raises the suspicion for
the diagnosis of cervical myelopathy. Cervical spine computed tomography (CT) (Figure
5.1) reveals multiple levels of spondylosis with a soft tissue pannus at C1–​C2 causing
severe narrowing of the cervical canal. Cervical magnetic resonance imaging (MRI)
(Figure 5.2) reveals severe stenosis with compression of the cervical cord at C1 and signal
change at C1–​C2 and multilevel spondylosis without significant cord compression at
C5–​T1.The patient is diagnosed with C1–​C2 stenosis with spinal cord compression and
myelopathy and is consented for C1–​C2 posterior decompression and fusion.

41
42

Figure 5.1  Sagittal computed tomography (CT) scan of the cervical spine with
evidence of rheumatoid pannus causing upper cervical stenosis.

Figure 5.2  Sagittal T2-​weighted magnetic resonance imaging (MRI) of the cervical

spine with evidence of severe canal stenosis and associated T2 signal abnormality
at  C1–​C2.
 

Atlantoaxial Instability

A number of different imaging modalities can be used to confirm atlantoaxial insta-

bility. Plain film radiographs of the cervical spine can be used to assess the atlantodental
interval (ADI). The ADI is measured from anterior margin of the dens to the nearest
point on the arch of C1. An ADI of greater than 5  mm or greater than 8  mm in
rheumatoid arthritis suggests instability and need for C1–​C2 fixation. The posterior
atlantodental interval (PADI) is measured from the posterior dens to the anterior as-
pect of the posterior ring of C1 and defines the neural canal width. A PADI of less than
14 mm suggests needs for decompression and stabilization of the C1–​C2 joint.
Cervical CT is necessary to assess the atlantoaxial bony anatomy as well as to assess
the foramen transversarium at C1 and C2. In particular, CT scan should be used to es-
timate screw length and medial/​lateral and cranial/​caudal screw trajectory. Preoperative
assessment of the vertebral artery anatomy with cervical CT is imperative for safe C1–​
C2 screw placement.
When there is concern for atlantoaxial instability but no clear evidence of pathology
on CT or plain films, it is necessary to assess the integrity of the transverse atlantal liga-
ment (TAL). Most commonly, cervical MRI is used to evaluate for any incompetence of
the TAL. MRI can also evaluate the extent of cervical cord compression or cord injury
that has occurred due to atlantoaxial instability. Flexion-​extension cervical x-​rays can
also be used to evaluate for subluxation and TAL injury. Instability of C1–​C2 typically
requires surgical intervention for stabilization.

Oral Boards Review: Diagnostic Pearls

1. History and physical exam must evaluate for radicular and myelopathic signs/​
symptoms.
2. Imaging required:
a. CT scan with coronal and sagittal reconstruction.
b. CT angiography (CTA) may be obtained to assess for vertebral artery
anomalies.
c. Flexion/​extension x-​rays or MRI to assess TAL integrity.
3. Radiographic measurements.
4. ADI greater than 5 mm or greater than 8 mm in rheumatoid arthritis suggests
instability.

Questions

1. What radiological findings influence surgical planning?

2. What is the most appropriate timing for intervention in this patient?

Decision-​Making

When atlantoaxial instability is identified, surgery should be considered, especially if the

patient is symptomatic. Signs of atlantoaxial instability are extremely variable, ranging
from neck pain to nerve root injury to cervical myelopathy. Trauma and infections are

43
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Spinal Neurosurgery

indications for acute intervention, whereas congenital or chronic instability may be

followed with serial imaging and examinations until the patient becomes symptomatic
or stenosis becomes critical. Surgical techniques are numerous, but the overall goal is to
decompress neural structures, restore normal or close to normal alignment, and stabilize
the atlantoaxial joint.

Questions

1. What are the possible complications from screw placement?

2. If there is concern for intraoperative vertebral injury, how should the proce-
dure be altered?

Surgical Procedure

Surgical fixation options for C1–​C2 stabilization include anterior and multiple poste-
rior techniques. Anterior approach is rarely used but is preferred in cases where patients
cannot tolerate prone positioning due to cardiac or pulmonary issues or the posterior
bony elements are unsuitable for adequate screw placement. Regardless of surgical ap-
proach, care must be taken by the anesthesiologist with cervical precautions during in-
tubation, which is often accomplished by nasal fiber-​optic intubation. Traction may be
used to achieve reduction prior to fixation.
Anterior approaches include transoral, retropharyngeal, or lateral. It is not un-
common for anterior compressive pathology to necessitate anterior decompression,
but anterior C1–​C2 screw/​plate fixation remains rare due to infection and soft tissue
healing concerns.
For posterior approaches, the patient is positioned prone in military position with
the chin tucked and the head in a Mayfield skull clamp. C1–​C2 transarticular screw fix-
ation (Magerl’s technique) has a high rate of fusion, ranging from 90% to 99%.Vertebral
artery injury is a major risk with transarticular screws. K-​wires are placed under fluor-
oscopic guidance starting 1–​2 mm cephalad to the midpoint of the C2–​C3 facet joint
and proceeding down the C2 pars interarticularis, across the C1–​C2 joint space and into
the lateral mass of C1. This procedure may be accomplished via a standard open tech-
nique exposing C1 to C6–​C7 or a less invasive technique utilizing an open exposure of
C1–​C2 with bilateral paracentral percutaneous stab incisions at the C6–​C7 level.
C1 lateral mass and C2 pars screw/​rod fixation, originally described by Goel and
Laheri and modified by Harms and Melcher, provides a safer alternative to transarticular
screw fixation by avoiding the vertebral artery anatomy. With exposure of the C1 lat-
eral mass, care should be taken to control bleeding from the C1–​C2 venous plexus
during lateral dissection. The vertebral artery in the sulcus arteriosus on top of C1 does
not need to be completely exposed for placement of the C1 lateral mass screw. The
C2 nerve root should be mobilized inferiorly or can be sacrificed if necessary. There
are multiple options for C2 screw placement including pars, pedicle, and translaminar
screws. For the C2 pars screws, care should be made to measure the distance to the fo-
ramen transversarium on preoperative CT. It is important to verify a sufficient width for
C2 pars screw placement so as to not breach medial into the neural canal or lateral into

44
 

Atlantoaxial Instability

the foramen transversarium. The C2 pars screw is angled at a steep trajectory mirroring
the C2 pars, generally 20–​30 degrees superior as well as 5–​10 degrees medially. For a
C2 pedicle screw placement, the entry point is slightly superior and medial to the pars
screw and medially angled approximately 15–​30 degrees. The C2 superior trajectory is
less steep than for the pars screw, typically 5–​10 degrees. C2 translaminar screws can be
used as a salvage technique for failed C2 pars screws. Screws are placed at the junction
of the lamina and spinous process with a trajectory matching the slope of the lamina.
Care should be taken to place the screws at appropriate craniocaudal locations so as to
not have the translaminar screws intersect.
Laminar wiring techniques were initially described as a primary treatment for C1–​
C2 fixation but contemporarily are utilized as an adjunct to screw fixation. Posterior
cervical wiring of C1 and C2 was first described by Gallie in 1939. The Gallie tech-
nique consists of a graft placed over the C2 spinous process and the posterior arch of C1,
which is held in place with steel wire placed under the C1 lamina and looped around
the C2 spinous process. Later, Brooks and Jenkins described bilateral graft placement
between the C1–​C2 lamina, secured in place by bilateral C1 and C2 sublaminar wires.
In the early 1990s, Sonntag modified the Gallie technique with a single sublaminar wire
at the C1 and C2 spinous process, wiring to secure a strut-​graft wedged between the
posterior arches of C1 and C2.
In the presented case, a hybrid technique was utilized with a right C1–​C2 transarticular
screw placement and C1 lateral mass and C2 pars screw/​rod construct on the left. A stab
incision was made at approximately the C7 level on the right and a K–​wire was placed
under fluoroscopic guidance followed by drilling, tapping, and placement of a C1–​C2
transarticular screw under lateral fluoroscopic guidance. Care is taken to maintain con-
trol of the K-​wire during all portions of the procedure. The C1 posterior ring and the
superior portion of the C2 lamina were then resected to complete the spinal cord de-
compression. Following decompression, a C1 lateral mass and C2 pars screw was placed
on the right (Figure 5.3). Rods were secured from C1 to C2, and local autograft mixed
with morselized allograft was placed posterior and posterolaterally over the decorticated
posterior elements of C1–​C2 (Figure 5.4).

Figure 5.3  Intraoperative lateral and anteroposterior (AP) cervical x-​rays after right
C1–​C2 transarticular and left C1 lateral mass–​C2 pars screw-​rod placement.

45
46

Spinal Neurosurgery

Figure 5.4  Postoperative lateral and anteroposterior (AP) cervical x-​rays.

Oral Boards Review: Management Pearls

1. Appropriate alignment with initial patient positioning is key for transarticular

screw placement and appropriate reduction if necessary.
2. Preoperative CT should be reviewed carefully for a high-​r iding vertebral ar-
tery or other anomalous vertebral artery pathway prior to deciding type of
C2 screw placement.

Pivot Points

1. If patient has subaxial stenosis in addition to C1–​C2 instability, the C1–​C2

construct, regardless of type of posterior technique, can be extended with
lateral mass screws and posterior decompression to involve subaxial stenotic
levels.
2. Transarticular screw placement requires reduction of C1–​C2 prior to screw
placement. If reduction cannot be achieved, lateral mass and C2 pars/​pedicle
screw fixation should be used.
3. Translaminar screws may be used as salvage technique if C2 pars/​pedicle
screws are unable to be placed.
4. If occipito-​cervical instability is noted intraoperatively, the stabilization/​fusion
can be extended up to the occiput.

Aftercare

Postoperative x-​rays may be obtained to confirm screw placement. Patient should be

evaluated postoperatively for signs of radicular pain related to screw placement. If the
C2 nerve root is sacrificed, patients should be informed of expected occipital numb-
ness or paresthesias. A postoperative CTA should be obtained if there is any concern

46
 

Atlantoaxial Instability

for vertebral injury. Depending on surgeon preference, a cervical collar may be used
postoperatively.
Patient can be mobilized as early as the night of surgery. A Foley catheter should
be removed by postoperative day 1 unless there are underlying bladder concerns.
Postoperative cervical x-​rays should be obtained at follow-​up appointments over the
next year to confirm bony fusion.

Complications and Management

If there is a likely vertebral artery injury noted after drilling/​ tapping the initial
transarticular screw, that screw can still be placed to tamponade the bleeding or redirected
to a more optimal trajectory. But no attempt should be made to place the contralateral
screw due to concerns of potentially catastrophic bilateral vertebral artery injury leading
to brainstem stroke. Mean arterial pressure should be elevated to maintain posterior
circulation and prevent possible neurological insult. A  postoperative CTA should be
obtained to evaluate for thrombosis or dissection or even arteriovenous fistula.

Oral Boards Review: Complications Pearls

1. If there is concern for vertebral artery injury, the contralateral transarticular

screw should not be placed, and a lateral mass or pars/​pedicle screw should
be placed instead. A postoperative CTA should be obtained to evaluate for
thrombosis or dissection.
2. The surgeon should be aware of the C1–​C2 venous plexus and be prepared
with cautery/​hemostatic agents to decrease bleeding in this area.

Evidence and Outcomes

Numerous posterior fixation techniques have evolved to address C1–​C2 instability. The
Gallie fusion provides good initial fixation in flexion and extension but poor stabiliza-
tion with rotation and a relatively high nonunion rate approaching 25%. Similarly, the
Brooks/​Jenkins fusion provides reasonable biomechanical stability in flexion and ex-
tension and has been reported to achieve fusion in the 90% range with the addition of
halo immobilization. Of course, halo fixation can be a source of significant morbidity
itself. Sonntag and colleagues reported a 97% fusion rate in 36 patients treated with their
modification of the Gallie interspinous process technique.
The advent of screw fixation techniques brought more rigid biomechanical stability
and concomitantly higher fusion rates. Magerl’s C1–​C2 transarticular technique pro-
vided increased rotational stability with fusion rates approaching 100%. Stillerman and
Wilson reported on 22 patients utilizing a modification of this transarticular technique
without additional bone-​wire fusion and reported a 95% fusion rate. Similar clinical
results were also achieved by C1 lateral mass fixation and C2 pars fixation, as described
by Goel and Laheri, as well as by Harms and Melcher. This technique provides superior
biomechanical stability in rotation as well as flexion and extension but with significantly
decreased risk of vertebral artery injury. This C1 lateral mass and C2 pars screw/​rod
technique has enjoyed widespread adoption.

47
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Spinal Neurosurgery

References and Further Reading

Brooks AL, Jenkins EB. Atlantoaxial arthrodesis by the wedge compression method. J Bone Joint
Surg Am. 1978;60A:279–​284. http://​www.ncbi.nlm.nih.gov.ahecproxy.ncahec.net/​pubmed/​
348703
Coric D, Branch CL, Wilson JA, Robinson J. Arteriovenous fistula as a complication of C1–​
C2 transarticular screw fixation:  Case report and a review of the literature. J Neurosurg.
1996;85:340–​343. http://​www.ncbi.nlm.nih.gov/​pubmed/​8755766
Coyne TJ, Fehlings MG, Wallace MC, Bernstein M, Tutor CH. C1-​C2 posterior cervical fu-
sion:  Long term evaluation of results and efficacy. Neurosurgery. 1995;37:688–​693. http://​
www.ncbi.nlm.nih.gov/​pubmed/​8559297
Dickman CA, Sonntag VK, Papadopoulos SM, Hadley MN. The inter-​spinous method of pos-
terior atlantoaxial arthrodesis. J Neurosurg. 1991 Feb;74:190–​198. http://​www.ncbi.nlm.nih.
gov.ahecproxy.ncahec.net/​pubmed/​1988587
Gallie WE. Fractures and dislocations of cervical spine. Am Surg. 1939;46:495–​499.
Goel A, Desai K, Mazumdar D. Atlantoaxial fixation using plate and screw method:  A report
of 160 treated patients. Neurosurgery. 2002;51:1351–​1356. http://​www.ncbi.nlm.nih.gov/​
pubmed/​12445339
Goel A, Laheri V. Plate and screw fixation for atlanto-​axial subluxation. Acta Neurochir (Wien).
1994;129(1–​2):47–​53. http://​www.ncbi.nlm.nih.gov.ahecproxy.ncahec.net/​pubmed/​7998495
Harms J, Melcher RP. Posterior C1-​C2 fusion with polyaxial screw and rod fixation. Spine.
2001;26(22):2467–​2471. http://​www.ncbi.nlm.nih.gov.ahecproxy.ncahec.net/​pubmed/​
11707712
Magerl F, Seemann PS. Stable posterior fusion of the atlas and axis by transarticular screw fixation.
In Kehr P, Weidner A (eds.), Cervical Spine (vol. 1). New York: Springer;1987:322–​327.
Rahimi SY, Stevens EA,Yeh DJ, Flannery AM, Choudhri HF, Lee MR. Treatment of atlantoaxial
instability in pediatric patients. Neurosurg Focus. 2003 Dec 15;15(6):ECP1. http://​www.ncbi.
nlm.nih.gov/​pubmed/​15305843
Stillerman CB, Wilson JA. Atlanto-​axial stabilization with posterior transarticular screw fixa-
tion: Technical description and report of 22 cases. J Neurosurg. 1993 Jun;32:948–​954. http://​
www.ncbi.nlm.nih.gov/​pubmed/​8327097

48
 

Basilar Invagination and Cranial Settling

Benjamin D. Elder and Jean-​Paul Wolinsky

Case Presentation

A 65-​year-​old woman with a history of rheumatoid arthritis presented with neck pain,
6
frequent falls, and difficulty with fine motor movements of the hands. On neurological
exam, she had full strength but had 3+ reflexes in the upper and lower extremities and
positive Babinski and Hoffman signs. A magnetic resonance image (MRI) of the cervical
spine demonstrated a pannus formation at C1–​C2 with mild ventral cord compression
and T2 signal change. Additionally, lateral flexion-​extension radiographs demonstrated
8 mm of translation of C1 with respect to C2. She was recommended to undergo a
C1–​C2 decompression and C1–​C2 arthrodesis, but declined the operation. She ne-
glected to follow-​up but presented 2 years later with increased weakness, particularly in
her upper extremities. Additionally, she had been treated for multiple episodes of aspi-
ration pneumonia. On neurological exam, she had 3/​5 strength in her bilateral upper
extremities, and 4–/​5 strength in the bilateral lower extremities. She had 3+ reflexes in
the bilateral upper extremities, and 4+ reflexes with clonus in the Achilles reflex bilat-
erally. A computed tomography (CT) image demonstrated new upward translation of
the odontoid with extension of the tip of the odontoid 14 mm above the McGregor
line (Figure 6.1).

Questions

1. What is the likely diagnosis?

2. How are basilar impression, basilar invagination, cranial settling, and platybasia
defined and distinguished?
3. What imaging modalities should be utilized to assess these patients?
4. The presence of what other occipitocervical (OC) pathologies should be
assessed?
5. What other disorders are frequently associated with OC pathologies?

Assessment and Planning

The neurosurgeon suspects a diagnosis of basilar impression with cranial settling due to
progression of the patient’s C1–​C2 instability from rheumatoid arthritis.
Basilar impression, basilar invagination, cranial settling, and platybasia are often used
synonymously, but they represent discreet terminology.1 Basilar impression represents

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Spinal Neurosurgery

Figure 6.1  (A) Sagittal computed tomography (CT), (B) axial CT of the posterior

fossa, and (C) axial CT at the level of the foramen magnum demonstrating
basilar invagination with significant upward translation of the odontoid into the
posterior fossa.
(Adapted with permission from Wolinsky et al., Endoscopic image-​guided odontoidectomy for
decompression of basilar invagination via a standard anterior cervical approach, J Neurosurg Spine
2007;6:184–​191.)

the broader category of OC junction pathologies. Basilar invagination results from mi-
gration of the entire spine into the skull base as the skull base remodels or invaginates
(Figure 6.2), usually from congenital hypoplasia or dysplasia of various osseous structures
at the OC junction or achondroplasia. Common pathologies leading to basilar invag-
ination include osteogenesis imperfecta (most commonly type III), disorders of bone
metabolism such as Paget disease, rickets, and hyperparathyroidism. In osteogenesis im-
perfecta, the load-​bearing capacity of the skull base is exceeded with microfractures in
the region of the foramen magnum, leading to gradual deformity and softening of the
skull base. OC junction tumors, trauma, and infection can lead to basilar invagination,
but usually result in cranial settling. Cranial settling is a form of basilar impression due
to C1–​C2 instability (commonly in the setting of rheumatoid arthritis), defined as up-
ward migration (or rotation) of the C2 complex into the cranial vault. Atlanto-​occipital
assimilation can develop into cranial settling, with ligamentous laxity at the C1–​C2 level
that develops over time. This laxity may result from stress on the C1–​C2 complex from
assimilation of the condyles and C1. The lack of flexion-​extension at the craniocervical
junction leads to stress at C1–​C2 that ultimately results in the cranial settling. Platybasia
is simply deformation and flattening of the skull base that can be found alone or in com-
bination with other OC pathology.
Patients with basilar invagination frequently have concurrent Chiari type
I malformations, with rates of 54% reported in a series of 190 patients.2 In this series,

50
 

Basilar Invagination and Cranial Settling

Figure 6.2  Sagittal computed tomography (CT) scan of a patient with osteogenesis

imperfecta demonstrating basilar invagination with upward migration of the C1–​C2
complex into the cranial vault.
(Reproduced with permission from Johns Hopkins University, 2016. All rights reserved. Benjamin
Elder and Jean-​Paul Wolinsky.)

most patients presented between the second and fourth decades of life, with earlier and
more acute presentation in patients without a concurrent Chiari type I malformation.
Many patients reported neck pain, and common physical exam findings in both groups
included myelopathy with weakness and paresthesias, gait abnormalities, bowel and/​
or bladder dysfunction, short necks, webbed necks, and lower hairlines. Additionally,
patients may present with lower cranial nerve dysfunction depending on the extent of
brainstem compression.
Basilar invagination was historically identified on open-​mouth anteroposterior (AP)
plain film radiographs in which the C1–​C2 facet complex was incompletely visualized.
More detailed assessment can be made by determining the relationship of the odon-
toid tip with the Chamberlain line and McGregor line. Basilar invagination is typ-
ically diagnosed with extension of the tip of the odontoid at least 5  mm above the
Chamberlain line or more than 7  mm above the McGregor line. Cranial settling is
identified with protrusion of the tip of the odontoid more than 4.5  mm above the
McGregor line in the setting of rheumatoid arthritis.
Currently, CT images with sagittal, coronal, and three-​dimensional reconstructions
are ideal for characterizing and defining OC junction abnormalities, particularly as
these patients often have complex osseous anatomy with potentially Klippel-​Feil and/​
or cranial assimilation of C1. Additionally, MRI is critical for assessment of neurologic
structures and spinal cord and/​or brainstem compression, as well as soft tissue and lig-
amentous structures. Flexion-​extension radiographs can be used to assess for instability,
though caution should be exercised in the setting of often severe spinal cord and brain-
stem compression. Finally, vascular imaging such as CT angiography or even four-​vessel
cerebral angiography is useful to define the vertebral artery anatomy, which may have an
aberrant course in the setting of craniocervical pathology.

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Spinal Neurosurgery

Oral Boards Review: Diagnostic Pearls

1. Radiographic imaging with CT scans or lateral radiographs is used to differ-

entiate basilar invagination and cranial settling.
a. Basilar invagination: Upward migration of the entire spine into the skull
base as the skull base remodels or invaginates.
b. Cranial settling: Upward migration (or rotation) of the C2 complex into
the cranial vault in the setting of C1–​C2 instability.
2. Each patient should undergo a detailed history and physical exam. Important
historical information includes the length of the symptoms, progression of
symptoms, and acuity of any changes change in neurological status, as well
as presence of any medical comorbidities that may be associated. Important
physical exam assessments include visual inspection, assessment of cervical
range of motion, and performance of a detailed neurological exam including
cranial nerve assessment.
3. Performance of CT imaging of the craniocervical junction is imperative for
adequately assessing the potentially complex osseous anatomy.
4. Performance of MRI of the craniocervical junction is required to adequately
determine the extent of compression of neurological structures, as well as as-
sess the soft tissue and ligamentous structures.
5. Vascular imaging, typically with CT angiography, is important to adequately
identify the vertebral artery anatomy, which may often have an aberrant
course in these patients.

Questions

1. What is the most appropriate timing for operative intervention?

2. How do the clinical and radiographic findings influence surgical options?
3. How should cervical traction be used to determine the optimal surgical
strategy?
4. What is the importance of oral hygiene prior to surgical intervention?
5. What is the significance of preoperative nutritional status and pulmonary
function?

Decision-​Making

If untreated, basilar invagination and cranial settling may lead to significant neurolog-
ical deterioration and even death. Although no specific criteria for surgical interven-
tion exist, most patients present with some degree of neurological compromise and
will require surgical intervention with decompression and stabilization in order to
prevent further neurological decline. However, a small subset of patients who present
without neurological deficits and with minimal extension of the odontoid into the
foramen magnum and no spinal cord or brainstem compression could be followed
closely clinically.

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Basilar Invagination and Cranial Settling

Before surgical intervention, many patients with basilar impression undergo a trial
of cervical traction to determine the amount of reduction of the odontoid that may
be achieved. However, significant caution should be exercised in patients with signifi-
cant compression to prevent further neurological injury. In general, low weights (5–​10
pounds) should be used with close neurological monitoring and the angulation of the
traction modified to reduce neurological compression, often with the head elevated
approximate 15 degrees above the horizontal plane. If the odontoid is completely re-
ducible, the patient may be a candidate for posterior decompression and fusion alone.3
However, if the odontoid cannot be reduced, the patient often requires anterior decom-
pression in conjunction with posterior stabilization (and often posterior decompression
as well).
There is a spectrum of severity of patients with cranial settling. Initially, there is
C1–​C2 instability, followed by C1–​C2 instability with pannus formation. If left un-
treated, C2 starts to migrate upward and pseudostabilization occurs, with regression of
the pannus. This is followed by complete cranial settling. All of these patients require
posterior stabilization, but the degree of stabilization is determined by where the pa-
tient lies in the spectrum of severity. For C1–​C2 instability with or without a pannus,
the patient can be treated with only C1–​C2 instrumented fusion. For early migration
of C2 with pseudostabilization, the patient can be treated with reduction and C1–​C2
fusion, or OC fusion if the C1 lateral masses are destroyed. Finally, full cranial settling, if
irreducible, requires ventral decompression and OC fusion.
As anterior surgical approaches often involve a transoral approach, preoperative as-
sessment of dental hygiene is critical to minimize bacterial contamination of the sur-
gical field. Dental caries and gingivitis require treatment prior to surgery as these may
result in hematogenous spread or surgical site infection with a risk of meningitis if a
durotomy is encountered. Furthermore, loose dentition should be guarded or prophy-
lactically extracted preoperatively.
Also, patients often have lower cranial nerve dysfunction, particularly of the glos-
sopharyngeal, vagus, and hypoglossal nerves. If there is significant dysfunction of these
cranial nerves, preoperative tracheostomy placement should be considered. Additionally,
patients may have concurrent swallowing dysfunction with resultant poor nutritional
status. In these patients, preoperative placement of a percutaneous gastrostomy should
be considered to optimize nutritional status preoperatively for improved wound healing.
Finally, some patients, both children and adults, may have inadequate mouth opening
to establish a sufficient surgical corridor, necessitating use of alternative approaches.

Questions

1. What regions of the craniocervical junction can be approached with the dif-
ferent ventral approaches?
2. What is the significance of the presence of a pannus in terms of the surgical
procedure?

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Spinal Neurosurgery

Surgical Procedure
Transoral-​Transpharyngeal Approach

Posterior decompression alone is generally inadequate to treat patients in the absence of

a reducible basilar invagination and may actually lead to rapid neurological deterioration
without concomitant anterior decompression.4,5
The classical surgical approach for treatment of pathology at the ventral craniocervical
junction is the transoral-​transpharyngeal approach. This approach provides access to the
anterior foramen magnum and from the lower clivus down to possibly as low as the
C3 vertebral body, with lateral exposure approximately 14–​20  mm bilaterally off the
midline. Injury to the Eustachian tube, hypoglossal nerve, vidian nerve, carotid arteries,
and/​or vertebral artery are likely if additional lateral exposure is attempted. The carotid
arteries are at higher risk than the vertebral arteries as they usually run approximately
1 cm off midline at C1 and can be right at midline in some patients.
While awake, the patient is positioned supine with the head in extension on a horse-
shoe or, alternatively, in a halo crown attached to the Mayfield brace. Intraoperative
neurological monitoring is performed with motor evoked potentials and somatosen-
sory evoked potentials, as well as free running electromyography for lower cranial nerve
monitoring. Intubation is performed with a prophylactic tracheostomy or with awake
fiber-​optic endotracheal intubation, with the endotracheal tube retracted outside of the
surgical field as much as possible. Packing is placed in the throat to prevent flow of blood
into the stomach. Oral chlorhexidine gluconate solution is used to prepare the oral
cavity, and preoperative intravenous antibiotics are administered.The patient is draped in
the usual sterile fashion, with the oral and nasal cavities exposed.The tongue is retracted

Figure 6.3  Intraoperative photograph demonstrating the transoral approach to the

craniocervical junction. Self-​retaining retractors keep the mouth open and retract the
tongue away from the operative field. Note the red rubber catheter used to retract the
soft palate. The initial pharyngeal incision has been made in preparation for exposure
of the C1 ring.
(Reproduced with permission from Hsu et al., Transoral approaches to the cervical spine,
Neurosurgery, 2010;66:A119–​A125.)

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Basilar Invagination and Cranial Settling

with a self-​retaining retractor (Figure 6.3), which should be released every 30 minutes
to prevent lingual venous congestion.
Following injection of 1% lidocaine with 1/​100,000 epinephrine in the posterior
pharyngeal mucosa, the mucosa is incised in the midline, from the lower clivus to the
superior aspect of the C3 vertebral body, with fluoroscopy or stereotactic navigational
guidance. A  myomucosal flap containing the pharyngeal mucosa, constrictor muscles,
longus colli, and longus capitis muscles is then elevated off the anterior longitudinal
ligament (ALL) and retracted with self-​retaining retractors, and the ventral osseous
structures are then exposed with insulated electrocautery.The osseous structures causing
ventral compression can then be decompressed in piecemeal fashion using a diamond
burr (Figure 6.4). The two layers (pharyngeal muscles and pharyngeal mucosa) should
be closed separately in a watertight fashion to minimize the risk of wound dehiscence.
When a soft tissue pannus is present around the odontoid, care should be taken
during the decompression as the posterior longitudinal ligament and tectorial mem-
brane may be thinned and potentially adherent or even fused to the ventral dura,
with a greater potential for intraoperative durotomy. Since the pannus may resolve
following posterior stabilization, aggressive ventral decompression may not always be
required.
Although some surgeons may delay posterior stabilization procedures in order to
allow for recovery from the anterior decompression, the craniocervical junction is highly
unstable following ventral decompression, even in a halo vest. Therefore, we advocate
that the patient be immediately stabilized posteriorly following the ventral decompres-
sion. If it is not possible to complete the two-​staged operation in a single day, the patient
can be secured in a halo vest and maintained intubated and sedated on flat bedrest until
posterior stabilization the following day.
If there is a concomitant Chiari type I malformation, or posterior spinal cord and/​
or brainstem compression remains following ventral decompression, posterior decom-
pression is performed as well. The classical approach to posterior stabilization involved
a construct with structural rib or iliac crest autograft wired from the occiput to the
cervical spine. However, this approach required prolonged immobilization in a halo
vest to provide stabilization at the OC junction. Currently, posterior OC rod-​screw
constructs are most often used, which provide rigid fixation at the craniocervical junc-
tion. Depending on the extent of ventral resection and instability, constructs typically
span from the occiput to C2 or C3, but may be extended to C6 or even across the
cervicothoracic junction if necessary. An occipital plate is placed, with pedicle, pars, or
translaminar screws at C2, and lateral mass screws in the subaxial spine if necessary. C1
screws are rarely placed as it is difficult to bend a rod to fit a plate as well as the C1 lat-
eral mass screws.

Extended Transoral Approaches

The detailed surgical techniques for the extended transoral approaches have been
described in detail previously.6 If the surgical corridor is inadequate, additional superior
and lateral exposure of the lower clivus can be obtained by dividing the soft palate in the
midline and deviating the uvula. The soft palate is incised in the midline at the junction
with the hard palate and extended down and extended off midline around the uvula.
If the soft palate is divided for additional exposure, it should be closed in three layers
(nasal mucosa, muscularis, oral mucosa) in a watertight fashion. A maxillary ostomy can

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Spinal Neurosurgery

Figure 6.4  Intraoperative photographs showing exposure of the C1 ring (A) and

subsequent resection using a diamond burr (B). (C) Intraoperative photograph
showing resection of the anterior C1 ring and odontoid, revealing the transverse
ligaments.
(Reproduced with permission from Hsu et al., Transoral approaches to the cervical spine,
Neurosurgery, 2010;66:A119–​A125.)

be added to the transoral-​transpharyngeal approach to provide further exposure of the

midline cranial base and middle clivus. A transmandibular circumglossal or transglossal
approach can be used to provide exposure from the level of the sella all the way down
the cervical spine.

Endoscopic Approaches

With additional advances in endoscopic surgery, endonasal or sublabial endoscopic

approaches can be used for access to the clivus and even a complete odontoidectomy.7
Also, a transcervical endoscopic approach for odontoidectomy has recently been
described.8 This approach uses the standard Smith-​Robinson anterior cervical approach
with a transodontoid screw trajectory (Figure 6.5). This allows for exposure from the
inferior clivus down to C7 and may allow for ventral decompression in cases which

56
 

Basilar Invagination and Cranial Settling

Figure 6.5  Artist’s rendition showing the tubular retractor placed against the anterior
cervical spine acting as a working channel for instruments and endoscope. The inset
shows the orientation of the patient in the operating room. a = artery.
(Adapted with permission from Wolinsky et al., Endoscopic image-​guided odontoidectomy for
decompression of basilar invagination via a standard anterior cervical approach, J Neurosurg Spine,
2007; 6:184–​191.)

would otherwise require a maxillary osteotomy (Figure 6.6). Figure 6.7 demonstrates
the surgical corridors from these alternative approaches.

Oral Boards Review: Management Pearls

1. Patients with a completely reducible basilar invagination may be treated with

posterior decompression and stabilization alone.
2. However, posterior decompression alone is generally inadequate to treat
patients without a completely reducible basilar invagination and may actually
lead to rapid neurological deterioration.
3. The transoral-​transpharyngeal is the classical gold standard approach for ven-
tral decompression of the craniocervical junction. It provides access from the
lower clivus down to as low as the C3 vertebral body, with lateral exposure
approximately 14–​20 mm bilaterally off the midline.
4. Posterior stabilization is typically performed with OC screw-​rod constructs,
generally with an occipital plate and construct spanning from the occiput
down to C2 or C3, but potentially down to C6 or across the cervicothoracic
junction if necessary.

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Spinal Neurosurgery

Figure 6.6  (A) Sagittal computed tomography (CT), (B) axial CT of the posterior

fossa, and (C) axial CT at the level of the foramen magnum following transcervical
endoscopic decompression demonstrating adequate ventral decompression in
conjunction with posterior decompression and stabilization.
(Adapted with permission from Wolinsky et al., Endoscopic image-​guided odontoidectomy for
decompression of basilar invagination via a standard anterior cervical approach, J Neurosurg Spine,
2007;6:184–​191.)

Pivot Points

1. If the basilar invagination is completely reducible with axial cervical traction,

a posterior-​only approach (with decompression and stabilization) may be
utilized.
2. If the basilar invagination is not completely reducible with cervical traction,
then ventral decompression is required with posterior stabilization performed
immediately afterward.
3. Additional posterior decompression may be required following ventral de-
compression if spinal cord and/​or brainstem compression remains, as in the
presence of a concomitant Chiari type I malformation.

Aftercare

If a tracheostomy was not performed preoperatively, the patient should remain intubated
for 48–​96 hours or until airway and oral edema are adequately reduced. In the ab-
sence of a percutaneous gastrostomy, typically placed in patients with poor preoperative
nutritional status, a nasogastric tube is placed to allow for adequate enteral nutrition
postoperatively. Finally, an external orthosis such as a halo vest or Minerva brace is often

58
 

Basilar Invagination and Cranial Settling

Figure 6.7  Illustration demonstrating the relevant normal anatomy and operative

angles for the (A) sublabial, (B) transoral, and (C) transcervical approaches to the
skull base.
(Reproduced with permission from Johns Hopkins University, 2009. All rights reserved, Ian Suk.
Previously published in Bettegowda et al., Sublabial approach for the treatment of symptomatic
basilar impression in a patient with Klippel-​Feil syndrome, Neurosurgery, 2011;69(Suppl 1):77–​82.)

placed for 4–​6 months to provide increased stabilization of the OC junction while fu-
sion is occurring.

Complications and Management

Durotomy with cerebrospinal fluid (CSF) leak can be a devastating complication with
increased risk of meningitis and wound dehiscence with potential fistula formation. If
a CSF leak occurs, primary closure should be attempted, with additional placement of
fibrin glue and fascial graft or dural substitute. Additionally, a lumbar subarachnoid drain

59
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Spinal Neurosurgery

should be placed with drainage of 5–​10 cc/​hr of CSF for 3–​5 days to minimize the risk
of continued CSF leakage.
The vertebral artery can be injured during lateral exposure beyond 15–​20  mm
from the midline or in the presence of aberrant vertebral artery anatomy. The carotid
arteries are at higher risk than the vertebral arteries as they usually run approximately
1  cm off midline at C1 and can be right at midline in some patients. Therefore, it
is critical that preoperative vascular imaging is reviewed to better understand the
vascular anatomy. If there is a vertebral artery injury, direct repair is typically impos-
sible, whereas repair of a carotid artery injury may be attempted. The main goal is to
use hemostatic agents to control bleeding, and a formal catheter angiogram should
be performed as soon as possible to assess for vessel injury and perform potential
endovascular vessel sacrifice.
If the soft palate is divided for additional exposure, velopalatine incompetence may
occur due to fibrosis of the soft palate or pharynx, with dysphagia, nasal speech, and liquid
regurgitation. Pharyngeal retraining and use of a dental obturator can be considered for
symptomatic improvement.
Additional complications include both superficial and deep surgical site infections,
which may require debridement of the wound. Deep infections are typically treated
with prolonged courses of intravenous antibiotics, although the surgical hardware can
often be left in place. Finally, as with any spinal fusion procedure, there is a risk of
pseudarthrosis, which may require surgical revision and a more extensive posterior
construct.

Oral Boards Review: Complications Pearls

1. An intraoperative CSF leak can be a devastating complication that should be

managed aggressively, with ideally primary closure, placement of fibrin glue
and a dural graft, and strong consideration for several days of CSF diversion
with a lumbar subarachnoid drain.
2. Vertebral artery injury may occur with excessive lateral exposure or with ab-
errant vertebral artery anatomy. The carotid arteries are at higher risk than the
vertebral arteries as they usually run approximately 1 cm off midline at C1
and can be right at midline in some patients. Preoperative vascular imaging
should also be reviewed before surgery. An attempt at hemostasis should be
made and catheter angiogram with potential vessel embolization performed
as soon as clinically feasible.

Evidence and Outcomes

Randomized controlled trials to determine the optimal treatment approaches for

these patients are lacking due to the relative rarity of this constellation of pathologies
and the variation in diseases that may result in basilar invagination or cranial settling.
However, several large retrospective cohort studies are available. These studies have gen-
erally demonstrated that ventral decompression with posterior stabilization and some-
times additional posterior decompression is the optimal treatment approach, but the

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Basilar Invagination and Cranial Settling

posterior-​only approaches can be considered in patients with completely reducible bas-

ilar invagination. As the majority of patients present with neurological deficits including
myelopathy and often lower cranial nerve deficits, the treatment goal is to prevent fur-
ther neurological deterioration and stabilize the craniocervical junction.

References and Further Reading

1. Smith JS, Shaffrey CI, Abel MF, Menezes AH. Basilar invagination. Neurosurgery.
66:39–​47,  2010.
2. Goel A, Bhatjiwale M, Desai K. Basilar invagination: a study based on 190 surgically treated
patients. J Neurosurg. 88:962–​968, 1998.
3. Hsu W, Zaidi HA, Suk I, Gokaslan ZL, Wolinsky JP. A new technique for intraoperative re-
duction of occipitocervical instability. Neurosurgery. 66:319–​323; discussion 323–​314, 2010.
4. Menezes AH. Surgical approaches:  Postoperative care and complications “transoral-​
transpalatopharyngeal approach to the craniocervical junction.” Childs Nerv Syst.
24:1187–​1193,  2008.
5. Menezes AH,VanGilder JC.Transoral-​transpharyngeal approach to the anterior craniocervical
junction. Ten-​year experience with 72 patients. J Neurosurg. 69:895–​903, 1988.
6. Hsu W, Wolinsky JP, Gokaslan ZL, Sciubba DM. Transoral approaches to the cervical spine.
Neurosurgery. 66:119–​125, 2010.
7. Kassam AB, Snyderman C, Gardner P, Carrau R, Spiro R.The expanded endonasal approach: A
fully endoscopic transnasal approach and resection of the odontoid process: Technical case
report. Neurosurgery. 57:E213; discussion E213, 2005.
8. Wolinsky JP, Sciubba DM, Suk I, Gokaslan ZL. Endoscopic image-​guided odontoidectomy
for decompression of basilar invagination via a standard anterior cervical approach. Technical
note. J Neurosurg Spine. 6:184–​191, 2007.

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Cervical Myelopathy

Lordosis

Randall J. Hlubek and Nicholas Theodore

7
Case Presentation

A 65-​year-​old man presents with a chief complaint of numbness in his hands that has
been present for more than a year. He reports that he is unable to open jars or lift heavy
objects as he used to. He enjoys working with his hands, but he finds it more difficult
to complete tasks because of his lack of dexterity. His wife is concerned about his bal-
ance and states that he has been falling more frequently. On further questioning, he
denies any neck pain or radiating arm pain but does note some neck stiffness. A detailed
neurological examination reveals bilateral grip weakness, diffuse hyperreflexia, bilateral
Hoffman sign, bilateral positive Babinski reflex, positive Romberg sign, and negative
Tinel sign. Motor strength assessment is 4+/​5 bilateral deltoids, 4+/​5 bilateral biceps, 4/​
5 bilateral triceps, 4−/​5 bilateral grips, and 5/​5 strength in all lower extremity muscle
groups.

Questions

1. What is the likely diagnosis?

2. What is the most appropriate imaging modality?

Assessment and Planning

The differential diagnosis is broad, and it includes cervical spondylotic myelopathy, carpal
tunnel syndrome, subacute combined degeneration, transverse myelitis, and spinal cord
tumor. The clinical history and physical examination results for this patient indicate that
the most likely diagnosis is cervical spondylotic myelopathy. Cervical spondylotic my-
elopathy is compression of the cervical spinal cord secondary to degenerative changes.
Symptoms, which include gait disturbance, upper extremity paresthesia, weakness, and
loss of dexterity, tend to progress gradually. A rapid onset of symptoms would be unusual
for spondylotic myelopathy and would likely be secondary to transverse myelitis, mul-
tiple sclerosis, or cervical abscess.
Electromyography and nerve conduction studies cannot confirm the diagnosis of
cervical myelopathy. However, they are useful for excluding disorders such as carpal
tunnel syndrome and diabetic neuropathy that present with similar features.

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Spinal Neurosurgery

Figure 7.1  Sagittal T-​2 weighted magnetic resonance imaging of the cervical spine
demonstrates circumferential stenosis at the levels of the C3–​C4, C4–​C5, and C5–​C6
disc spaces.
(Reproduced with permission from Barrow Neurological Institute, Phoenix, Arizona.)

The diagnosis of cervical spondylotic myelopathy cannot be made without im-

aging. Magnetic resonance imaging (MRI) is the most useful imaging modality in that
it provides clear resolution of the neural elements.
T2-​weighted MRI allows for careful inspection of the spinal cord and can reveal
hyperintensity that may represent myelomalacia secondary to chronic compression.
However, if the hyperintensity is disproportionate to the degree of compression,
then pathology such as primary spinal cord tumors and transverse myelitis should
be carefully considered in the differential diagnosis and further workup may be
warranted.
Computed tomography (CT) myelography may be useful in patients for whom MRI
is contraindicated. Although CT myelograms do not visualize the spinal cord very well,
they provide excellent visualization of the bony anatomy. Thus, they facilitate analysis of
the extent of cervical canal stenosis.
Flexion and/​or extension cervical radiographs should be obtained for any patient
who reports neck pain. Dynamic imaging should be used to evaluate for cervical insta-
bility and to aid in surgical planning.
In the present case, MRI of the cervical spine revealed circumferential stenosis at the
levels of the C3–​C4, C4–​C5, and C5–​C6 disc spaces with preserved cervical lordosis
(Figure 7.1).

Questions

1. How do this patient’s clinical picture and MRI findings influence surgical
planning?
2. What are the surgical options for this patient?

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Cervical Myelopathy: Lordosis

Oral Boards Review: Diagnostic Pearls

1. A thorough physical examination is crucial to the diagnosis of cervical

spondylotic myelopathy. Myelopathic signs include Hoffmann reflex, posi-
tive Babinski reflex, and Romberg sign. There may be both upper and lower
motor neuron signs, depending on the level of the lesion (i.e., hyporeflexia in
the upper extremities and hyperreflexia in the lower extremities).
2. Careful history-​taking is important because the timing of symptoms may lead
to the consideration of another diagnosis. Acute onset of symptoms is atypical
and may be secondary to transverse myelitis, cervical epidural abscess, or mul-
tiple sclerosis.
3. Cervical spondylosis is a common disease in the elderly. If physical exami-
nation findings are out of proportion to the severity of cervical spondylosis,
then additional pathology may be present. Additional workup should be
performed, including electromyograms and/​or nerve conduction studies to
evaluate for demyelinating disorders. MRI with and without contrast may be
helpful in evaluating for intraparenchymal tumors, especially when there is
severe T2 hyperintensity in the spinal cord.

Decision-​Making

Surgery should be performed in patients with cervical spondylotic myelopathy to pre-

serve the function of the spinal cord. The goals of surgery are to decompress the neural
elements and to preserve or restore cervical sagittal alignment. Both anterior (cervical
discectomy and fusion, cervical arthroplasty, and cervical corpectomy) and posterior
(cervical laminectomy, cervical laminoplasty, and cervical laminectomy with fusion) sur-
gical approaches have been developed to achieve these goals effectively. Cervical align-
ment may be the most important factor to consider when determining which approach
is most appropriate.
In patients with cervical lordosis, maintaining lordotic alignment is crucial to suc-
cessful treatment. Maintaining lordotic alignment may be achieved with either an ante-
rior or a posterior approach.
An anterior approach may be favored when there are only one or two levels of ste-
nosis at the disc space or when there is significant compression anteriorly with minimal
posterior compression. Cervical stenosis involving more than two levels requires much
more extensive anterior decompression and may demand a corpectomy if there is com-
pression posterior to the vertebral body rather than at the level of the disc space. This
approach is more technically demanding for diffuse pathology but may be necessary if
the alignment is kyphotic.
Factors that may favor a posterior approach include a congenitally narrow canal,
compression greater than two levels, ossification of the posterior longitudinal ligament,
circumferential compression, and multiple medical comorbidities. The theoretical ben-
efit of posterior decompression is to remove the lamina and the ligamentum flavum,
thus allowing the spinal cord to shift posteriorly away from any anterior compressive
elements.Although laminectomy alone is effective in decompressing the neural elements,

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Spinal Neurosurgery

its main drawback is the potential for development of cervical kyphosis or instability,
which occurs in 13–​41%, and 18% of patients, respectively.1,2
In patients with cervical myelopathy and lordotic sagittal alignment, the preference
of the senior author is to perform a cervical laminectomy and fusion when there is mul-
tilevel circumferential compression.

Questions

1. What steps should be performed when there is a significant decrease in so-

matosensory evoked potentials (SSEPs) during the operation?
2. If the patient were to develop unilateral deltoid and biceps weakness on post-
operative day 1, what would be the most likely diagnosis?

Surgical Procedure

During intubation of patients with cervical instability or severe cervical stenosis,

hyperextension of the neck should be avoided because of the potential for spinal
cord injury. Either awake fiber-​optic intubation or video-​assisted intubation with
the GlideScope (Verathon, Inc.) video laryngoscope should be considered to limit
hyperextension.
Neurophysiological monitoring is performed by monitoring intraoperative changes
in SSEPs and motor evoked potentials (MEPs). Baseline recordings are obtained before
positioning the patient, and intraoperative monitoring is done continuously throughout
the case.
The patient is positioned prone, with all pressure points padded, on either a Jackson
table with the face resting in a foam head support or on a flat table with the chest
supported on a gel chest roll and the head rigidly fixed in a Mayfield clamp.The arms of
the patient should be well padded and tucked close to the sides. Before initiation of sur-
gery, it is imperative to assess the cervical alignment with fluoroscopy to ensure that it is
optimal. Analysis of postpositioning SSEPs and MEPs ensures that spinal cord compres-
sion has not been exacerbated. If there is a significant decrease in SSEPs or MEPs after
positioning, then common sources for alarm should be interrogated, including hypoten-
sion, hypothermia, anesthetic agents, verification of electrode integrity, arm positioning,
and cervical alignment. MEPs are especially sensitive to inhalational agents, and their use
should be limited to ensure that the monitoring is reliable.
When the patient is adequately positioned and draped in a sterile fashion, a midline
incision is performed and dissection is carried down through the avascular median raphe
between the paraspinal musculature. If the dissection strays laterally, extensive bleeding
may be encountered from the musculature and venous plexus. At the bony elements, the
muscles are dissected off the spinous process and lamina in a subperiosteal fashion. The
lateral masses are then carefully exposed to prevent violation of the facet joints above
and below the operative segments. When the level has been confirmed with anatomical
landmarks and fluoroscopy, the facet joints should be curetted to remove cartilaginous
material and to prepare the joints for fusion. Doing so also allows the surgeon to place an

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Cervical Myelopathy: Lordosis

instrument (e.g., a Penfield 4 dissector) into the facet joint to determine the facet angle
and assist with screw trajectory.
Lateral mass screws may be placed at C3–​C6 for fixation. The lateral mass of C7 is
relatively thin and may not be amenable to a lateral mass screw, so pedicle screws may be
required if fixation is necessary at this level. For fixation above the C3 level, the senior
author prefers to use C2 pars screws and C1 lateral mass screws, but a discussion of these
screws is beyond the scope of this chapter.
A pilot hole is then created through the cortex of the lateral mass (2 mm medial to
center) with a high-​speed drill. A manual twist drill is angled approximately 30 degrees
laterally and then angled cephalad parallel to the slope of the facet to maximize screw
length and to avoid the nerve root and vertebral artery.3 The lateral mass is drilled
to a depth of either 12 or 14 mm, and a ball-​tipped probe is used to interrogate for
any breach of the lateral mass. Before placement of the hardware, the laminectomy is
initiated with a high-​speed drill at the junction of the lamina and the lateral mass. Care is
taken to keep the drill perpendicular to the cortical surface and to copiously irrigate to
prevent thermal injury to the nerves. After the bilateral troughs have been drilled down
to the epidural space, the lamina is removed en bloc by placing towel clamps on the cra-
nial and caudal-​most spinous processes. While lifting upward with the clamps, we use a
curette to strip adhesions and ligamentum flavum from beneath the lamina. Any residual
compressive ligamentum flavum or lamina may be removed with Kerrison rongeurs.
After completion of the decompression, the lateral mass screws (typically 3.5 mm
in diameter and 12 or 14 mm in length) are inserted. A lordotically curved rod is then
seated in the screw heads and locking caps are provisionally tightened. Fluoroscopy is
used to confirm proper alignment and screw placement. The locking caps are then fi-
nally tightened with an antitorque screwdriver. The lateral masses are then decorticated
with a high-​speed drill, and autologous bone from the laminectomy and allograft is
placed over the cancellous surface. After adequate hemostasis is achieved, the incision is
closed in a standard multilayer fashion.

Oral Boards Review: Management Pearls

1. If posterior decompression is to be performed, then fixation and fusion must

be strongly considered to prevent development of postlaminectomy kyphosis
and instability.
2. Checking cervical alignment with lateral fluoroscopy after positioning is crit-
ical to ensure proper alignment.
3. Mean arterial pressures should be maintained at 80 mm Hg or higher to en-
sure adequate perfusion to the spinal cord during the entire operation.

Pivot Points

1. If the patient presents with a medical history and physical examination

findings consistent with cervical myelopathy, then the next step is to order
MRI of the cervical spine to assess for spinal cord compression.

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Spinal Neurosurgery

2. If the sagittal alignment is kyphotic, then an anterior approach would be fa-

vored both to decompress the spinal cord and to restore alignment. A pos-
terior approach may not be effective because the kyphosis would prevent
the posterior shift of the spinal cord, and the neural elements would remain
draped over the anterior disc osteophyte complexes.
3. If the sagittal alignment is lordotic, then either an anterior approach or a pos-
terior approach may be effective, and the surgery should be customized to
each patient.

Aftercare

Postoperative pain may be severe secondary to the extensive muscle dissection. Thus,
patients are typically placed on intravenous muscle relaxants and on intravenous patient-​
controlled analgesia. When the pain has been adequately controlled, a transition to oral
pain medication should be attempted.
Rigid cervical collars provide additional immobilization and may be especially useful
in patients with poor bone quality. Patients are typically advised to wear a cervical collar
for about 6–​12 weeks. Its use is discontinued when follow-​up radiographs reveal no ev-
idence of hardware failure.
Physical and occupational therapists evaluate the patient during the hospitalization.
Their input assists with early mobilization and discharge recommendations.
Radiographic follow-​up consists of anteroposterior and/​or lateral cervical radiographs
at 6 weeks, 6 months, and 1 year after surgery. Additional diagnostic imaging is obtained
if new symptoms develop.

Complications and Management

Vertebral artery injury is a rare but potentially devastating complication of cervical lam-
inectomy that can result in hemorrhage, stroke, and death. The vertebral artery is most
vulnerable to injury during screw placement. Preoperative imaging should be studied
meticulously to determine the course of the arteries and to evaluate for any aberrant
anatomy. If injury to the artery occurs during screw placement, then the screw should
be inserted for hemostasis and the contralateral instrumentation should be aborted if it
has not been completed.
Cerebrospinal fluid leak may occur during decompression of the spinal cord, and any
dural violation may be repaired primarily with sutures. If the durotomy is not amenable
to repair with sutures, then a piece of muscle may be placed over the defect and attached
using fibrin sealant.
The incidence of postoperative C5 palsy after a cervical laminectomy with fusion is
about 11%.4 The etiology of C5 palsy is poorly understood, and proposed mechanisms
in posterior cervical surgery include tethering of the nerve root secondary to poste-
rior shift of the spinal cord and foraminal stenosis. C5 palsy is manifested by pain in the
shoulder, sensory loss in the C5 distribution, and paresis of the deltoid and/​or biceps
brachii. These symptoms may occur immediately after surgery or may be delayed. There
is no established treatment for C5 palsy; however, most patients tend to recover sponta-
neously, with a mean time to recovery of 5.4 months.5

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Cervical Myelopathy: Lordosis

Oral Boards Review: Complications Pearls

1. Careful preoperative assessment of the vertebral arteries for aberrant anatomy

will reduce the risk of iatrogenic injury during screw placement.
2. Postoperative C5 palsy may occur either immediately after surgery or may be
delayed.

Evidence and Outcomes

There is no Level 1 evidence regarding which approach (anterior vs. posterior) is more
effective for treatment of multilevel cervical spondylotic myelopathy. A systematic re-
view of retrospective studies demonstrated no clear advantage for anterior and posterior
cervical approaches in terms of safety and effectiveness.6 The determination of which
approach to use should be customized to each patient.

References and Further Reading

1. Li Z, Xue Y, He D, et  al. Extensive laminectomy for multilevel cervical stenosis with
ligamentum flavum hypertrophy:  More than 10  years follow-​ up. Eur Spine J. Aug
2015;24(8):1605–​1612.
2. Kato Y, Iwasaki M, Fuji T, Yonenobu K, Ochi T. Long-​term follow-​up results of laminec-
tomy for cervical myelopathy caused by ossification of the posterior longitudinal ligament. J
Neurosurg. Aug 1998;89(2):217–​223.
3. Kim HS, Suk KS, Moon SH, et  al. Safety evaluation of freehand lateral mass screw fixa-
tion in the subaxial cervical spine: Evaluation of 1256 screws. Spine (Phila Pa 1976). Jan 1
2015;40(1):2–​5.
4. Nakashima H, Imagama S,Yukawa Y, et al. Multivariate analysis of C-​5 palsy incidence after
cervical posterior fusion with instrumentation. J Neurosurg Spine. Aug 2012;17(2):103–​110.
5. Dai L, Ni B,Yuan W, Jia L. Radiculopathy after laminectomy for cervical compression mye-
lopathy. J Bone Joint Surg Br. Sep 1998;80(5):846–​849.
6. Lawrence BD, Jacobs WB, Norvell DC, Hermsmeyer JT, Chapman JR, Brodke DS. Anterior
versus posterior approach for treatment of cervical spondylotic myelopathy: A systematic re-
view. Spine (Phila Pa 1976). Oct 15 2013;38(22 Suppl 1):S173–​S182.

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Cervical Myelopathy

Kyphosis

Mario Ganau, So Kato, and Michael G. Fehlings

8
Case Presentation

A 72-​year-​old woman presents with rapid decline of neurological function evolving over
three decades after an uneventful multilevel posterior cervical laminectomy performed
for an intradural benign neoplasm (left C4 schwannoma). The patient had quit smoking
when she was diagnosed with diabetes mellitus type 2, and she also suffers from poorly
pharmacologically controlled high blood pressure.
She has been wheelchair bound for the past few weeks and describes several months
of urinary urgency, multiple mechanical falls due to gaze disturbances, and progressive
weakness, scoring at best 3/​5 on the Medical Research Council (MRC) muscle scale,
in the upper and lower limbs. Recently, her inability to grip/​hold objects in both hands
has made her unable to eat independently and safely ambulate despite the aid of a walker.
The physical examination reveals a short neck with reduced range of motion in both
lateral rotation and flexion-​extension, bilateral loss of muscle tone in legs, brisk patellar
reflexes, and ankle clonus.
Given her incomplete tetraplegia American Spinal Injury Association (ASIA) C, the
patient is admitted for further investigations.

Questions

1. Which are the most common causes of cervical kyphosis?

2. What further radiological and neurophysiological investigations can be
helpful?
3. Which functional scales are used for degenerative cervical myelopathy
(DCM), and what do they tell us about prognosis?

Assessment and Planning

The computer tomography (CT) and magnetic resonance imaging (MRI) (Figure 8.1)
results disclose a severe multilevel cervical kyphotic deformity, likely related to the pre-
vious multilevel posterior cervical laminectomy. Other causes of kyphotic deformity
include ankylosing spondylitis, Pott disease, and previous cervical trauma. Dropped head
syndrome is in the differential diagnosis, and this has many causes such as Parkinson di-
sease, scleroderma, neuromuscular diseases, inflammatory polymyositis (i.e., due to Zika
virus), and secondary myopathies due to metabolic or endocrine dysfunction.

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Spinal Neurosurgery

Figure 8.1  Preoperative bone window computed tomography (CT; left) and T2-​
weighted magnetic resonance imaging (MRI; right) scans of the cervical spine with
sagittal views showing multiple degenerative changes causing severe kyphosis (C2–​C7
Cobb angle: −46 degrees) and spinal stenosis.

A careful study of the radiological investigations demonstrates a C2 to C7 Cobb

angle of −46 degrees with a sagittal vertical axis (SVA, the distance between the plumb
line from the C2 centroid and that from the posterosuperior corner of C7) of 46 mm.
The modified Japanese Orthopedic Association (mJOA) score is 7, which confirms se-
vere nontraumatic DCM and therefore a poor prognosis.

Oral Boards Review: Diagnostic Pearls

1. Clinical assessment:
a. In kyphotic patients, stretching of the posterior paravertebral muscles as a
tension band frequently causes axial pain, which can be the primary phys-
ical complaint of these patients.
b. Being unable to lift the skull upright, patients with kyphotic deformities
compensate with a typical upward gaze.
c. Dysphagia can also be a common symptom, usually caused by collapse of
pharyngeal space and inefficient coordination of swallowing muscles.
2. Radiological assessment:
a. Radiometric measures of cervical alignment provide information on spinal
balance and should always be carried out on long, standing cassette x-​rays.
As a general rule, cervical kyphosis is defined by a C2–​C7 Cobb of less
than −10 degrees and/​or an SVA greater than 40 mm.
b. Although at more advanced stages of DCM, conventional T1-​and T2-​
weighted 1.5 Tesla MR images are sensitive enough to confirm the

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Cervical Myelopathy: Kyphosis

presence of myelopathy, discrepancies between the actual clinical status and

imaging findings can be found in early stages of this condition.
c. Myelopathic changes can appear even without T2 signal
alterations: decreased fractional anisotropy (FA) values and increased ap-
parent diffusion coefficient (ADC) values found in stenotic segments can
reflect the spinal cord condition and its reversibility. Diffusion tensor im-
aging (DTI) and microstructural MRI may be promising modalities to
predict functional recovery after surgery.
3. Functional assessment:
a. The recovery rate for the mJOA score can be calculated using Hirabayashi’s
method; of note, mJOA well defines moderate and severe DCM but is rela-
tively insensitive in predicting outcomes for mild DCM patients.
b. Other general scales, such as Short Form 36 (SF36), as well as those specific
for cervical spine pathologies, like the Neck Disability Index (NDI), have
a role in the functional assessment of patients with DCM and kyphotic
deformity. Their findings, however, should always be weighed in light of
the minimally clinical important difference and substantial clinical benefit
achievable after cervical spine fusion.

The clinical findings were confirmed by electromyogram (EMG) and nerve conduction
studies, which revealed an acute on chronic myelopathy with signs of bilateral denerva-
tion of the median and ulnar nerves.
A careful study of the flexion/​extension films (Figure 8.2) and CT reconstructions
revealed the persistence of some cervical spine motion and excluded fusion of the facets
joints. Additional measurements performed on the long cassette x-​rays, such as the tho-
racic slope (TS; the angle made by the T1 upper endplate and a horizontal line) and its
mismatch with the C2–​C7 Cobb angle, as well as on T2-​weighted MRI, such as the
modified K line, were considered in evaluating the global spinal balance and the most
suitable management options.

Figure 8.2  Preoperative static and dynamic lateral x-​rays of the cervical spine, with
neutral (left), flexion (center), and extension (right) views ruling out fusion of the facet
joints and showing some preserved motion of the cervical segments.

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Spinal Neurosurgery

Questions

1. How do clinical and radiological findings influence the management?

2. What is the optimal time of intervention in DCM? What are the goals of
surgery?
3. Which kind of surgical approach would be more effective in this kyphotic
deformity, and why?

Decision-​Making

Since the patient was showing myelopathic signs and symptoms associated with features
related to her kyphotic deformity, such as the alteration in visual horizon, both patho-
logical aspects required appropriate surgical management.
The goals of surgery in patients with DCM are to timely decompress the spinal cord
and prevent progression of the demyelination processes responsible for the progressive
neurologic deterioration seen at later stages. The optimal timing of intervention is still
an area of ongoing debate; however, experimental studies have shown that delays in de-
compression could increase the extent of ischemia-​reperfusion injury and astrogliosis,
resulting in poorer neurological recovery. Realignment may be particularly important
when spinal cord compression is associated with kyphosis as the distance between the
anterior compressive factors and the spinal cord can be increased by restoring lordotic
alignment.
Whenever a cervical deformity is evident on preoperative scans, spinal osteotomies
must be considered in the surgical plan as an adjuvant to standard decompression
techniques. Osteotomies represent powerful techniques that enable deformity correc-
tion of the cervical spine, and they range from relatively limited facet joint releases to
complete vertebrectomy. These complex procedures have evolved through generations
of surgeons, with the most recent classification being composed of seven anatomical
grades of resection (anterior, posterior, and combination of the two) representing pro-
gressive degrees of potential destabilization.
Overall, the greatest advantages of anterior (A)  approaches are the possibility to
address any anterior pathology, such as discs and bony spurs, allowing for a sufficient
distraction that can unbuckle the ligamentum flavum and indirectly treat spinal cord
compression. Key to the anterior correction is a wide anterior release including the
uncovertebral joints and a hybrid construct making use of multiple osteotomies and
inserting longer than normal (bicortical) screws. This method is generally sufficient for
stabilization; however, if two or more corpectomies are done, a posterior instrumented
fusion is usually advisable.
Posterior (P) approaches, including laminectomies and laminoplasties, are technically
easier and therefore more suitable for older and osteoporotic patients; they can address
various posterior sources of compression directly, such as the ligamentum flavum, or in-
directly, such as ossification of the posterior longitudinal ligament (OPLL).
Combined approaches (A + P, P + A, A + P + A and P + A + P) offer a way to per-
form multilevel decompression and osteotomies to address complex rigid deformities;

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Cervical Myelopathy: Kyphosis

however, they are burdened by longer operation time, larger intraoperative blood loss,
and delayed recovery that is associated with increased hospital costs.

Questions

1. What are the most important anesthesiological considerations in terms of pre-

medication, intubation, and intraoperative monitoring?
2. What are the foreseeable surgical and medical complications?
3. What strategies can enhance the chances of fusion?

Surgical Procedure

Following fiberscopic intubation and induction of general anesthesia, the patient was
positioned supine and Gardner-​Wells tongs were applied for perioperative traction.
She underwent C3–​C4, C4–​C5, C5–​C6, and C6–​C7 anterior cervical discectomies,
supplemented with C5 corpectomy for reduction of kyphotic deformity.
The intraoperative realignment was obtained through traction performed under
fluoroscopic imaging with continuous intraoperative multimodality electrophysiologic
recordings (monitoring the motor and somatosensory evoked potentials as well as the
segmental EMG activity).
The anterior cervical reconstruction was performed through anterior cervical bone
grafting with multilevel fibular strut and allografts combined with a local morselized
vertebral body autograft followed by the insertion of a four-​level anterior cervical tita-
nium plate fixation (C3 to C7).
A postoperative anterior and posterior x-​ray (Figure 8.3) confirmed the satisfactory
cervical alignment obtained.

Figure 8.3  Postoperative static x-​rays of the cervical spine, with lateral (left) and
anteroposterior (right) views showing that satisfactory sagittal and coronal alignment
was achieved.

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Spinal Neurosurgery

Oral Boards Review: Management Pearls

1. Setting for surgery:

a. Correct positioning to maximize lordosis is fundamental to obtain a satis-
factory intraoperative spine alignment; use Gardner-​Wells tongs for trac-
tion if needed.
b. Consider steroids and tranexamic acid at induction.
c. Use intraoperative somatosensory and motor evoked potential monitoring.
d. Make careful use of intraoperative imaging or radiographic guidance.
e. Avoid hypotension: during surgery maintain mean arterial pressure at
greater than 85 mm Hg.
2. Surgical nuances:
a. Magnification counts: use surgical loupes or microscope throughout the
intervention.
b. Place the Caspar distraction pins in a divergent fashion to guarantee a sat-
isfactory working channel.
c. Use diamond burr on the OPLL segment to avoid injuring spinal cord.
d. Expect possible dural breach and anticipate its repair.
e. Collect bone dust and use it along with morselized vertebral body to en-
hance fusion.
f. Always obtain a final radiological check before closure to ensure adequate
reconstruction of the cervical lordosis and rule out malpositioning of the
instrumentation.
g. Carefully check the hemostasis; plan to keep a surgical drain for 48 hours
and ensure a good multilayer closure.

Pivot Points

1. The following strategies may be considered to achieve correction of kyphotic

deformity and management of DCM:
a. Anterior standalone approach: To obtain a good alignment, multiple anterior
cervical discectomies with partial uncovertebral joint resection, also known
as grade 1 osteotomy, require mobility (nonfusion) of the facet joints. They
are usually performed in association with grade 3 or 4 osteotomies, which
include partial or complete corpectomy with complete uncovertebral
joint resection to transverse foramen. Overall, anterior osteotomies allow
for substantial release and correction of deformity but also facilitate the
decompression of the spinal canal and foramina, leading to successful man-
agement of DCM. The risk of subsidence can be reduced by adding au-
tograft bone or bone morphogenic proteins (BMP) to the body and disc
substitutes (cages or bone grafts). The screw–​plate interface can be used to
facilitate reduction maneuvers, and adequate bending of the plate further
helps to obtain a satisfactory postoperative cervical lordosis.

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Cervical Myelopathy: Kyphosis

b. Posterior standalone approach: Alternatively, a posterior standalone approach

may be used, providing decompression of the spinal cord and room for de-
formity correction. Grade 2 osteotomy involves laminectomy with resection
of both superior and inferior facets. A more complex deformity correc-
tion at the cervicothoracic junction can be obtained through grades 5 and 6
osteotomies: namely, complete posterior element resection with osteoclastic
fracture and open or closing wedge creation. Posterior approaches require fix-
ation with lateral mass screws or with pedicle screws; in this option, properly
bent rods can effectively recreate the cervical lordosis. Furthermore, to in-
crease the stability of the construct, attention should be focused toward both
intraarticular and extraarticular fusion. To this extent, cartilage removal from
the facet surface can be obtained by facet joint cauterization or decortication
with a high-​speed drill; tightly pack them with bone dust or BMP after this
process.
c. Combined anterior and posterior approach: Patients with severe and rigid cervical
kyphosis may require both anterior and posterior approaches or osteotomies.
The anterior plating can be supplemented with lateral mass screws in the
subaxial spine and pedicle screws beyond the junctional level (T1, T2, or
lower, depending on the characteristics of the scapular cingulus and the need
for additional point of fixation).

Aftercare

Following surgical intervention, patients do not need to wear a collar for any reason
other than subjective comfort. Concerns regarding swelling of the respiratory tract due
to long operative time or conditions like ankylosing spondylitis require admission to the
intensive care unit for additional postoperative monitoring before extubation. Patients
undergoing anterior approaches may demonstrate minimal dysphonia or dysphagia in
the early postoperative period; however, these side effects are self-​limiting and usually
improve within 48–​72 hours.
Early postoperative mobilization should be encouraged to avoid complications re-
lated to vein thromboembolism.The wound should be kept dry until removal of sutures.
A postoperative radiological study is always advisable; it may serve as a baseline for future
comparisons during follow-​up.
In the case presented here, the C2–​C7 Cobb angle showed a tenfold reduction: from
−46 degrees to −4 degrees after surgical correction (Figure 8.4). The patient had a re-
markable postoperative improvement; she regained normal power in upper and lower
extremities, being able to ambulate independently with a stick. She is now in the fourth
year of her follow-​up, and the latest mJOA score is 13.

Complications and Management

In case of dural tears, a lumbar drain (LD) should always be considered, with its height
being adjusted to allow for drainage of 10–​15 mL of cerebrospinal fluid (CSF) hourly for
5 postoperative days to ensure dural and wound healing without tension.

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Spinal Neurosurgery

Figure 8.4  Postoperative bone window computed tomography (CT; left) and

T2-​weighted magnetic resonance imaging (MRI; right) scans of the cervical spine,
with sagittal views confirming good correction of cervical kyphosis (C2–​C7 Cobb
angle: –4 degrees) and decompression of the spinal cord.

Devascularization and secondary atrophy of paravertebral muscles can become a

source of delayed complication, including infections and wound dehiscence, which
may become dramatic whenever associated with the exposure of the hardware and its
contamination.

Oral Boards Review: Complications Pearls

1. Complications related to surgery:

a. Intraoperative:
• Any anterior approach can be complicated by injury to the structures
pertaining to the carotid triangle (carotid artery, jugular vein, vagus
nerve) or prevertebral region (esophagus, trachea, recurrent laryngeal
nerve).
• Discectomy and corpectomy can lead to injury of the vertebral artery
(V2 segment) or spinal cord, with edema and anterior or central cord
syndrome.
• The management of dural tears depends on the location of the
breach and the type of surgical exposure; as a general rule, if the sur-
geon has a direct visualization of the CSF leak, an attempt to close it
through microsuture should be pursued. However, this may be tech-
nically challenging, especially in cases of ventrally or laterally located

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Cervical Myelopathy: Kyphosis

dural tears. Dural sutures in these areas increase the risk of making the
tear even larger; in those instances, it is therefore better to simply use
dura substitutes and fibrin glue. A Valsalva maneuver should be finally
carried out to confirm the good quality of the dural closure.
b. Perioperative:
• Spinal epidural hematoma or pseudomeningocele
• Graft dislodgment
c. Postoperative:
• Screws/​plate subsidence or pullout
• Delayed adjacent disc disease
2. Complications related to general anesthesia:
a. Blood pressure should be maintained within the normal range, avoiding
hypotension and the related risk of spinal cord infarction, as well as hyper-
tension and related risk of bleeding in the surgical site.
b. Lingering effect of paralytics or anesthetics should be monitored.
3. Complications related to medical conditions:
a. Comorbidities such as osteoporosis, ankylosing spondylitis, rheumatoid ar-
thritis, and diabetes mellitus are known to increase the risk of instrumenta-
tion failure.
b. Active and passive smoking affect osteoinduction and increase the risk of
nonfusion.
c. The rate of nonfusion is similar in nonsmoking and in patients with a pre-
vious history of smoking.
d. Pharmacological and mechanical prophylaxis should be considered to re-
duce the risk of deep vein thrombosis and pulmonary embolism.

Evidence and Outcomes

Patients with cervical kyphotic deformity tend to have worse preoperative NDI scores
and significantly lower physical component scores on SF-​36 than do patients with DCM
alone. Despite the significant attention paid by several authors to the correction of ky-
photic deformity, a recent subanalysis of two prospective international multicenter AO
Spine studies failed to demonstrate significant differences in postoperative outcomes
regardless of achievement of deformity correction. These findings suggest that an ag-
gressive realignment in this cohort might not always be necessary, especially when the
symptoms directly related to the kyphosis are not the primary complaint.
A prospective randomized Patient-​Centered Outcome Research Institute (PCORI)
sponsored trial (www.ClinicalTrials.gov identifier: NCT02076113) is currently under
way to evaluate cervical and global sagittal imbalance as a predictor of outcome fol-
lowing surgery for CSM.

References and Further Reading

Ames CP, Blondel B, Scheer JK, et al. Cervical radiographical alignment: Comprehensive assess-
ment techniques and potential importance in cervical myelopathy. Spine (Phila Pa 1976).

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2013 Oct 15;38(22 Suppl 1):S149–​S160. doi:  10.1097/​BRS.0b013e3182a7f449. Review.

https://​www.ncbi.nlm.nih.gov/​pubmed/​24113358
Ames CP, Smith JS, Scheer JK, et al.; International Spine Study Group. A standardized nomen-
clature for cervical spine soft-​tissue release and osteotomy for deformity correction: clinical
article. J Neurosurg Spine. 2013 Sep;19(3):269–​278. doi: 10.3171/​2013.5.SPINE121067. Epub
Jul 5, 2013. https://​www.ncbi.nlm.nih.gov/​pubmed/​23829287
Hirabayashi K, Miyakawa J, Satomi K, Maruyama T, Wakano K. Operative results and postopera-
tive progression of ossification among patients with ossification of cervical posterior longi-
tudinal ligament. Spine (Phila Pa 1976). 1981 Jul-​Aug;6(4):354–​364. https://​www.ncbi.nlm.
nih.gov/​pubmed/​6792717
Kato S, Nouri A, Wu D, Nori S, Tetreault L, Fehlings MG. Impact of cervical spine deformity on
pre-​operative disease severity and post-​operative outcomes following fusion surgery for de-
generative cervical myelopathy: Sub-​analysis of AOSpine North America and international
studies. Spine (Phila Pa 1976). 2017 Jun 27. doi: 10.1097/​BRS.0000000000002307. [Epub
ahead of print] https://​www.ncbi.nlm.nih.gov/​pubmed/​28658043
Liu S, Lafage R, Smith JS, et al. Impact of dynamic alignment, motion, and center of rotation
on myelopathy grade and regional disability in cervical spondylotic myelopathy. J Neurosurg
Spine. 2015 Dec;23(6):690–​700. doi: 10.3171/​2015.2.SPINE14414. https://​www.ncbi.nlm.
nih.gov/​pubmed/​26315953
Martin AR, De Leener B, Cohen-​Adad J, et al. Clinically feasible microstructural MRI to quan-
tify cervical spinal cord tissue injury using DTI, MT, and T2*-​weighted imaging: Assessment
of normative data and reliability. AJNR Am J Neuroradiol. 2017 Jun;38(6):1257–​ 1265.
doi:  10.3174/​ ajnr.A5163. Epub Apr 20, 2017. https://​www.ncbi.nlm.nih.gov/​pubmed/​
28428213
Martin AR, Reddy R, Fehlings MG. Dropped head syndrome: Diagnosis and management. Evid
Based Spine Care J. 2011 May;2(2):41–​47. doi: 10.1055/​s-​0030-​1267104. https://​www.ncbi.
nlm.nih.gov/​pubmed/​23637681
Roguski M, Benzel EC, Curran JN, et  al. Postoperative cervical sagittal imbalance negatively
affects outcomes after surgery for cervical spondylotic myelopathy. Spine (Phila Pa 1976).
2014 Dec 1;39(25):2070–​2077. doi: 10.1097/​BRS.0000000000000641. https://​www.ncbi.
nlm.nih.gov/​pubmed/​25419682
Taniyama T, Hirai T,Yoshii T, et al. Modified K-​line in magnetic resonance imaging predicts clinical
outcome in patients with nonlordotic alignment after laminoplasty for cervical spondylotic
myelopathy. Spine (Phila Pa 1976). 2014 Oct 1;39(21):E1261–​ E1268. doi:  10.1097/​
BRS.0000000000000531. https://​www.ncbi.nlm.nih.gov/​pubmed/​25077905
Tetreault L, Kopjar B, Nouri A, et  al. The modified Japanese Orthopaedic Association
scale:  Establishing criteria for mild, moderate and severe impairment in patients with de-
generative cervical myelopathy. Eur Spine J. 2017 Jan;26(1):78–​84. doi: 10.1007/​s00586-​016-​
4660-​8. Epub Jun 24, 2016. https://​www.ncbi.nlm.nih.gov/​pubmed/​27342612
Tetreault L, Wilson JR, Kotter MR, et al. Predicting the minimum clinically important differ-
ence in patients undergoing surgery for the treatment of degenerative cervical myelopathy.
Neurosurg Focus. 2016 Jun;40(6):E14. doi: 10.3171/​2016.3.FOCUS1665. https://​www.ncbi.
nlm.nih.gov/​pubmed/​27246484

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Ossification of the Posterior Longitudinal

Ligament

Cervical

Todd D. Vogel, Hansen Deng, and Praveen V. Mummaneni

9
Case Presentation

A right-​handed 61-​year-​old woman presents with a 2-​week history of progressive right

leg weakness and left leg decreased sensation to pain and temperature exacerbated at
presentation with a fall. She is now nonambulatory. She has numbness and tingling into
her hands. She has noticed difficulty with her hands in doing fine motor tasks. She takes
medications for hypertension and hyperlipidemia. She has a long-​standing history of
right leg sciatica that has been treated conservatively. On exam, her cranial nerves are in-
tact. Her bilateral upper extremities are full strength except for some mild grip strength
and hand intrinsic weakness. She is unable to lift her right leg off the bed. Her left leg
is full strength. She has a T3 sensory level on the left to pin prick and temperature. She
is hyperreflexive throughout including bilateral Hoffman, clonus, and Babinski sign. She
has normal rectal tone (Figures 9.1–​9.3).

Questions

1. What is the likely diagnosis?

2. What is the most appropriate imaging modality? What anatomical areas
should be imaged?

Assessment and Planning

In this clinical case, consideration needs to be given to the possibility of cervical mye-
lopathy aggravated by mild trauma. The differential diagnoses for etiologies of cervical
myelopathy include degenerative cervical spondylosis, congenital stenosis, tumor, spinal
epidural abscess, and ossification of the posterior longitudinal ligament (OPLL). OPLL
is seen in 25% of patients presenting with cervical myelopathy in the United States.1 It
is more common in males (2:1) than females. OPLL typically presents in the fifth and
sixth decades of life. There is a higher prevalence in the Asian population. It is located
in the cervical spine in 70% of cases, and the remaining 30% is split between the upper
thoracic and upper lumbar spine.2

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Figure 9.1  Midline sagittal computed tomography (CT) scan from case presentation
demonstrating extensive ossification of the posterior longitudinal ligament (OPLL) in
the cervical and upper thoracic spine. This CT demonstrates the “continuous” type of
ossification.

Figure 9.2  Axial computed tomography (CT) from case presentation at the

cervicothoracic junction demonstrating a double-​layer sign. Note the hypodense
layer between vertebral body and the intraspinal calcified mass representing intradural
ossification of the posterior longitudinal ligament (OPLL).
 

Ossification of the Posterior Longitudinal Ligament: Cervical

Figure 9.3  Midline sagittal magnetic resonance imaging (MRI) from case presentation
demonstrates hypodensity behind the vertebral bodies and across the disk spaces suggesting
ossification of the posterior longitudinal ligament (OPLL). Note that the sagittal MRI at the
cervicothoracic junction underrepresents the severe stenosis as demonstrated in Figure 9.2.

Oral Boards Review: Diagnostic Pearls

1. Careful history-​taking is important in the diagnosis of early myelopathy.

Early symptoms may include a history of difficulty with buttoning but-
tons, a history of falls, imbalance ascending or descending stairs (i.e., need
to use a handrail), numbness and tingling in the fingers, and difficulty with
micturition.
2. Physical exam findings may include both radicular and myelopathic features.
Gait assessment should be included in the physical exam.
3. Imaging studies include dynamic cervical x-​rays, cervical magnetic resonance
imaging (MRI), and cervical computed tomography (CT). The diagnosis of
OPLL is most accurately made on cervical CT.

Clinical presentation is typically that of a progressive cervical radiculopathy and my-

elopathy over months to years, whereas 10% of patients will present with an immediate
deterioration following minor trauma.3 Initial imaging studies for myelopathy include
dynamic x-​rays and a cervical spine MRI. Normal cervical canal width on x-​rays is
17 mm in the anterior-​posterior dimension.There is stenosis of the cervical canal when
this measures less than 10mm.4 OPLL may appear hypointense on T2-​weighted MRI
studies. MRI may also demonstrate spinal cord edema, myelomalacia, and gliosis with
hyperintense signal on T2-​weighted imaging, thus demonstrating spinal cord impinge-
ment.5 However, MRI does a poor job differentiating ossification and may underes-
timate the amount of canal stenosis, thus CT is the preferred imaging modality for

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Spinal Neurosurgery

Figure 9.4  Sagittal computed tomography (CT) with representative segmental

variant ossification of the posterior longitudinal ligament (OPLL). This type of OPLL
is located behind the vertebral bodies. Additional types include the continuous, as
demonstrated in Figure 9.1; mixed type; and other. The mixed type is a combination of
the segmental and continuous variants of OPLL.

OPLL (Figure 9.3). Non-​contrast CT imaging with reconstructed sagittal images best
demonstrate the location and extent of OPLL (Figures 9.4 and 9.5). Dural penetration
can be assumed when there is a double-​layer sign characterized by a hyperdense line
of OPLL behind the vertebra followed by a hypodense mass representing the dura and
finally an intradural hyperdense mass.6 The single-​layer sign is seen with a large central
mass of OPLL with extensions laterally along the dura on axial imaging. Patients with
a single-​or double-​layer sign have a high correlation with absent dura and subsequent
cerebrospinal fluid (CSF) fistulas if operated anteriorly.7

Questions

1. How do clinical and radiographic findings influence surgical planning?

2. What is the appropriate timing for surgical intervention?
3. How should surgery be approached if there is dural penetration on imaging?

Decision-​Making

Decisions regarding the type of treatment are based on clinical and radiological findings.
Two major myelopathy scales are used worldwide and may be helpful in determining the
timing of surgery.The Nurick myelopathy scale covers six grades of neurological classifica-
tion based upon gait dysfunction (Box 9.1).8 The modified Japanese Orthopedic Association

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Ossification of the Posterior Longitudinal Ligament: Cervical

Figure 9.5  Axial computed tomography (CT) demonstrate the single-​layer sign for
dural penetration. This type is characterized by a single mass of ossification of the
posterior longitudinal ligament (OPLL) between the vertebral body and the dura.
Note that as the calcification expands laterally along the dura, it forms a “C” shape
within the canal that can help with identification.

scale has four domains covering upper extremity motor dysfunction, lower extremity motor
dysfunction, sensory deficits, and sphincter dysfunction (Box 9.2).9 In patients with mild
radiculopathy, oral nonsteroidal antiinflammatory drugs (NSAIDs), conservative physical
therapy, and bracing can be provided along with regular follow-​up for signs of growth.
Patients with progressive symptoms or mild to moderate myelopathy may be offered sur-
gery. Comorbidities in elderly patients need to be weighed with the surgical risks. Surgical
decompression is advised for patients with severe cervical myelopathy. For patients younger
than 65 years with marked radiographic evidence of canal compromise and minimal clinical

Box 9.1  Nurick’s Classification System for Myelopathy Based on Degree

of Difficulty in Walking

Grade 0: Signs or symptoms of root involvement but without evidence of spinal

cord disease
Grade 1: Signs of spinal cord disease but no difficulty in walking
Grade 2: Slight difficulty in walking that does not prevent full-​time employment
Grade 3: Difficulty in walking that prevented full-​time employment or the
ability to do all housework, but which was not so severe as to require
someone else’s help to walk
Grade 4: Able to walk only with someone else’s help or with the aid of a frame
Grade 5: Chairbound or bedridden

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Spinal Neurosurgery

Box 9.2  Modified Japanese Orthopedic Association Scale

This scale has four domains measuring upper and lower motor dysfunction, sen-
sory dysfunction, and bladder dysfunction.

I. Motor dysfunction score of the upper extremities

• Inability to move hands (0 points)
• Inability to eat with a spoon but able to move hands (1 point)
• Inability to button a shirt but able to eat with a spoon (2 points)
• Able to button shirt with great difficulty (3 points)
• Able to button shirt with slight difficulty (4 points)
• No dysfunction (5 points)
II. Motor dysfunction score of the lower extremities
• Complete loss of motor and sensory function (0 points)
• Sensory preservation without ability to move legs (1 point)
• Able to move legs but unable to walk (2 points)
• Able to walk on flat floor with a walking aid (3 points)
• Able to walk up and/​or down stairs with hand rail (4 points)
• Moderate to significant lack of stability but able to walk up and/​or
down stairs without hand rail (5 points)
• Mild lack of stability but can walk unaided with smooth reciproca-
tion (6 points)
• No dysfunction (7 points)
III. Sensation dysfunction score
• Complete loss of hand sensation (0 points)
• Severe sensory loss or pain (1 points)
• Mild sensory loss (2 points)
• No sensory loss (3 points)
IV. Sphincter dysfunction score
• Inability to micturate voluntarily (0 points)
• Marked difficulty with micturition (1 point)
• Mild to moderate difficulty with micturition (2 points)
• Normal micturition (3 points)

symptoms, a prophylactic operative decompression is recommended in an attempt to avoid

rapid neurological decline following minor trauma.3
Much controversy surrounds whether anterior or posterior surgical approaches are
superior for managing cervical OPLL. Anterior approach techniques include the ante-
rior cervical diskectomy with fusion (ACDF) and anterior cervical corpectomy with
fusion (ACCF). Anterior approaches offer direct decompression of the spinal cord with
removal of the OPLL mass. Anterior approaches should be avoided when dural calcifi-
cation is suspected as a ventral CSF leak may occur in such patients. Posterior approach
techniques indirectly decompress the spinal cord. These include laminectomy alone,
laminoplasty, and laminectomy and fusion.The number of segments to be decompressed
should be considered. Anterior techniques work well for one to three segments, but are

86
 

Ossification of the Posterior Longitudinal Ligament: Cervical

limited beyond three segments without adding significant soft tissue morbidity. Posterior
techniques are favored in longer segment decompressions. Baseline dysphagia or a prior
history of an anterior neck surgery for lymph node dissection or thyroid cancer may
offer a relative contraindication to an anterior approach. Relative contraindications to
the posterior approach include a cervical kyphotic deformity. Finally, elderly patients
older than 65 years may do better postoperatively from a posterior approach as they have
less dysphagia postoperatively and can maintain a better nutritional status.

Questions

1. What are the particular intraoperative advantages and risks associated with
each procedure?
2. What is the degree of OPLL progression and postoperative changes in cer-
vical motion associated with each approach?

Surgical Procedure
Anesthesia and Neuromonitoring

An awake, fiber-​optic intubation is preferred in patients with significant OPLL and

myelopathic findings on exam. For patients undergoing anterior surgery, we may opt
for a nasotracheal intubation over an orotracheal intubation. The nasotracheal route does
not inferiorly extend the jaw, allowing for a slightly larger operative field in patients
with more rostral OPLL. Additionally, this avoids hyperextension or hyperflexion of the
cervical spine. We routinely use intraoperative multimodality neuromonitoring (IONM)
during cervical surgeries. We believe IONM may assist the surgeon in taking corrective
measures to reduce or prevent permanent neurological deficits.10 This includes free-​run
electromyography (EMG), motor evoked potentials (MEPs), and somatosensory evoked
potentials (SSEPs). Ideal anesthesia for neuromonitoring utilizes no paralytics during the
procedure and uses total intravenous anesthetic (TIVA) with a combination of ketamine,
propofol, and short-​acting narcotics (remifentanil or fentanyl) while avoiding the use of
inhalation agents.11 Communication to the anesthesia team prior to surgery about an-
esthetic needs is of utmost importance when using IONM to prevent delays. Finally, we
routinely obtain supine MEP and SSEP baselines prior to flipping a patient prone for final
positioning. New MEP and SSEP results are compared to our baseline and adjustments
made as needed to avoid spinal cord injury or nerve root injury during positioning.

Oral Boards Review: Management Pearls

1. Anterior or posterior decompression of the cervical spine is acceptable. The

number of levels to be treated, patient age, history of dysphagia or prior ante-
rior neck surgery, and degree of cervical lordosis may affect which approach is
best suited for the patient.
2. Avoid anterior surgery if there is suspicion of dural calcification.
3. Mildly symptomatic patients younger than 65 years with a high degree of
canal compromise may be candidates for prophylactic decompression.

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Spinal Neurosurgery

Anterior Approach

The anterior approach is used in cases in which there is only one to two levels of com-
pression and the ventral dura does not appear to be involved on the CT with the absence
of the single-​or double-​layer sign. Depending on the extent of OPLL at a single level or
at two adjacent levels, we favor an ACCF over a two-​level ACDF. Anterior approaches
greater than three segments are generally avoided secondary to high pseudarthrosis rates
in the authors’ experience.While this approach in general provides a more direct decom-
pression of the OPLL and reduction myelopathy scores, there is a significantly higher
risk of durotomy with CSF fistula.12 Fessler et al. and Iwasaki et al. have demonstrated
significant improvement in Nurick or Japanese Orthopedic Association scores when
utilizing ACCF with direct ventral resection of the OPLL mass as compared to indi-
rect decompression with a posterior approach.13,14 Fixation should be performed with
a system that allows for subsidence of the bone–​graft interface to avoid pseudarthrosis.
Using either variable-​angle screws or a dynamic plate has demonstrated decreased rates
of pseudarthrosis as compared to fixed plating systems.15–​17

Posterior Approach

The posterior approach is favored in cases in which long segment (>3 levels) de-
compression is needed, for elderly patients (>65 years), and for patients with a his-
tory of dysphagia or a prior anterior neck approach. Posterior approaches may not
adequately decompress the spinal canal if greater than 60% is occupied by the OPLL
mass.18,19 Simple laminectomy is avoided as there is a concern for cervical kyphosis
over time and worsening of neurological status 5–​10  years from the time of sur-
gery.20 This may be remedied by performing a laminectomy and fusion at the time of
surgery. This is indicated if there is documented instability, loss of lordosis, or partial
swan-​neck deformity. Advantages of a laminectomy and fusion include decompres-
sion of bilateral foramina as well. We prefer the Magerl screw trajectory for lateral
mass screws,21 pars screws over pedicle screws at the C2 level to avoid vertebral ar-
tery injury, and we avoid stopping our fusion at C7 above the cervicothoracic junc-
tion (Figure 9.6). Disadvantages include cost, increased blood loss, and removing
motion from the cervical spine. An alternative is laminoplasty, which offers indirect
dorsal decompression without the need for a traditional fusion.22–​24 An advantage of
laminoplasty is that there is some preserved range of motion in cervical laminoplasty
patients.25 About half the range of motion is lost following laminoplasty. One disad-
vantage of laminoplasty is that only unilateral foraminotomies can typically be safely
performed on the open side of the construct, thus making it less than ideal for a pa-
tient with bilateral symptoms. Additionally, laminoplasty may not adequately decom-
press a patient with congenital stenosis.15 Additionally, there has not been significant
improvement of visual analog scale neck scores for patients using laminoplasty.26
This posterior approach reduces the risks of cervical CSF fistulas, carotid/​vertebral
vascular injuries, and esophageal compromise that may be encountered through the
anterior surgery.

88
 

Ossification of the Posterior Longitudinal Ligament: Cervical

Figure 9.6  Postoperative images from case presentation. This patient was operated
for a C4 to T10 laminectomy and fusion over two different stages. She had extensive
disease in both her cervical and thoracic canals.

Pivot Points

1. A change of MEP/​SSEP while positioning a patient prone should prompt

further positioning changes, traction, or returning a patient back to the su-
pine position. If a patient is unable to be positioned prone without IONM
changes, an anterior decompression may need to be considered first.
2. Patients with greater than three levels of involvement should be considered
for a posterior decompression.
3. Patients with greater than 60% canal compromise should be considered for an
anterior decompression.

Aftercare

Patients presenting with an acute decline in neurological status following minor

trauma are typically observed in the intensive care unit (ICU) with a goal mean
arterial pressure (MAP) of greater than 85  mm Hg preoperatively and immedi-
ately postoperatively. Electively operated patients are typically admitted to the floor
postoperatively. Physical and occupational therapy services are consulted for dis-
charge assessment and to begin therapy on patients. Speech therapy is consulted if
there is concern for dysphagia postoperatively. Antibiotics are given perioperatively
for up to 24 hours. Surgical drains are left in place until less than 50 mL output per
12-​hour  shift.

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Spinal Neurosurgery

Complications and Management

If a CSF leak occurs, a primary repair will be attempted intraoperatively. A lumbar suba-
rachnoid drain may be placed in the postoperative period for 3–​7 days. The head of bed
is elevated at 30 degrees in the postoperative period. Surgical drains are taken off suction,
placed to gravity, and left in place until adequate wound healing has been achieved to
prevent CSF leaking through the incision.
Neurological deterioration following the procedure will prompt imaging with CT
and MRI to look for reversible causes of spinal cord compression including hematoma,
graft migration, or misplaced instrumentation. If no immediately nonreversible cause of
neurological compromise is found, we may consult our neurology colleagues to look
for additional causes of neurological deterioration. This differential would include cord
infarct, demyelination, and neurological decline from detethering the cord. Additionally,
we will admit these patients to the ICU and maintain their MAP at greater than 85 mm
Hg for a few days postoperatively. We do not give steroids to these patients.
Postoperative C5 palsy occurs in 5–​20% of cases.27,28 There does not appear to be a
significant difference between ACCF and posterior laminoplasty approaches.29 While
this complication may be distinguished from C5 nerve root injury or impingement
by its painless nature, the weakness of the deltoid and/​or biceps postoperatively can be
quite distressing for the patient. Imaging is generally obtained to check for graft migra-
tion or malpositioned instrumentation that could be corrected. The vast majority of C5
palsies will improve with time and therapy, although the time course is difficult to pre-
dict. Counseling the patient about this complication and expected recovery is best done
during the preoperative period.

Oral Boards Review: Complications Pearls

1. C5 palsy occurs in 5–​20% of cases. Imaging may be obtained to rule out graft
migration or malpositioned instrumentation.
2. Attempts to repair CSF leaks should be made intraoperatively. Early CSF di-
version with a lumbar subarachnoid drain may be considered for concerns of
persistent CSF fistula.

Evidence and Outcomes

Prospectively controlled studies for conservative management as compared to surgical

treatment do not exist to date. Multiple studies have looked at anterior compared poste-
rior decompression and demonstrated statistically significant neurological improvement
with an anterior approach.13,14 However, the Fessler et al. study is limited by the fact
that they compared an anterior approach to a laminectomy alone, a technique that has
fallen out of favor. Iwasaki et al. demonstrated a better neurological outcome for anterior
approaches in patients who had an OPLL mass occupying greater than 60% of the canal.
However, their study is tempered by the fact that they had graft migration in 15% and
reoperation in 26% of cases.

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Ossification of the Posterior Longitudinal Ligament: Cervical

References and Further Reading

1. Epstein NE. Ossification of the posterior longitudinal ligament in evolution in 12 patients.

Spine (Phila Pa 1976). 1994;19(6):673–​601.
2. Kim TJ, Bae KW, Uhm WS, Kim TH, Joo KB, Jun JB. Prevalence of ossification of the poste-
rior longitudinal ligament of the cervical spine. Joint Bone Spine. 2008;75(4):471–​474.
3. Katoh S, Ikata T, Hirai N, Okada Y, Nakauchi K. Influence of minor trauma to the neck on
the neurological outcome in patients with ossification of the posterior longitudinal ligament
(OPLL) of the cervical spine. Paraplegia. 1995;33(6):330–​333.
4. Miyasaka H. Consideration on pathophysiology of OPLL. Clin. Orthop. Relat. Res.
1975;10:1091–​1096.
5. Mummaneni PV, Kaiser MG, Matz PG, et al. Preoperative patient selection with magnetic
resonance imaging, computed tomography, and electroencephalography: does the test predict
outcome after cervical surgery? J. Neurosurg. Spine. 2009;11(2):119–​129.
6. Epstein NE. Identification of ossification of the posterior longitudinal ligament extending
through the dura on preoperative computed tomographic examinations of the cervical spine.
Spine (Phila Pa 1976). 2001;26(2):182–​186.
7. Min JH, Jang JS, Lee SH. Significance of the double-​layer and single-​layer signs in the os-
sification of the posterior longitudinal ligament of the cervical spine. J. Neurosurg. Spine.
2007;6(4):309–​312.
8. Nurick S. The pathogenesis of the spinal cord disorder associated with cervical spondylosis.
Brain. 1972;95(1):87–​100.
9. Benzel EC, Lancon J, Kesterson L, Hadden T. Cervical laminectomy and dentate ligament
section for cervical spondylotic myelopathy. J. Spinal Disord. 1991;4(3):286–​295.
10. Clark AJ, Ziewacz JE, Safaee M, et al. Intraoperative neuromonitoring with MEPs and pre-
diction of postoperative neurological deficits in patients undergoing surgery for cervical and
cervicothoracic myelopathy. Neurosurg. Focus. 2013;35(1):E7.
11. Ziewacz JE, Berven SH, Mummaneni VP, et al.The design, development, and implementation
of a checklist for intraoperative neuromonitoring changes. Neurosurg. Focus. 2012;33(5):E11.
12. Epstein NE, Hollingsworth R. Anterior cervical micro-​dural repair of cerebrospinal fluid fis-
tula after surgery for ossification of the posterior longitudinal ligament. Technical note. Surg.
Neurol. 1999;52(5):511–​514.
13. Fessler RG, Steck JC, Giovanini MA. Anterior cervical corpectomy for cervical spondylotic
myelopathy. Neurosurgery. 1998;43(2):257–​265; discussion 265–​257.
14. Iwasaki M, Okuda S, Miyauchi A, et al. Surgical strategy for cervical myelopathy due to ossi-
fication of the posterior longitudinal ligament: Part 2: Advantages of anterior decompression
and fusion over laminoplasty. Spine (Phila Pa 1976). 2007;32(6):654–​660.
15. Epstein NE. The management of one-​level anterior cervical corpectomy with fusion using
Atlantis hybrid plates: preliminary experience. J. Spinal Disord. 2000;13(4):324–​328.
16. Epstein NE. Evaluation and treatment of clinical instability associated with pseudoarthrosis
after anterior cervical surgery for ossification of the posterior longitudinal ligament. Surg.
Neurol. 1998;49(3):246–​252.
17. Mummaneni PV, Haid RW, Rodts GE, Jr. Combined ventral and dorsal surgery for myelop-
athy and myeloradiculopathy. Neurosurgery. 2007;60(1 Supp1 1):S82–​S89.

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18. Iwasaki M, Okuda S, Miyauchi A, et al. Surgical strategy for cervical myelopathy due to os-
sification of the posterior longitudinal ligament:  Part  1:  Clinical results and limitations of
laminoplasty. Spine (Phila Pa 1976). 2007;32(6):647–​653.
19. IshidaY, Ohmori K, Suzuki K, Inoue H.Analysis of dural configuration for evaluation of poste-
rior decompression in cervical myelopathy. Neurosurgery. 1999;44(1):91–​95; discussion  95–​96.
20. Kato Y, Iwasaki M, Fuji T, Yonenobu K, Ochi T. Long-​term follow-​up results of laminec-
tomy for cervical myelopathy caused by ossification of the posterior longitudinal ligament. J.
Neurosurg. 1998;89(2):217–​223.
21. Jeanneret B, Magerl F, Ward EH, Ward JC. Posterior stabilization of the cervical spine with
hook plates. Spine (Phila Pa 1976). 1991;16(3 Suppl):S56–​S63.
22. Morimoto T, Matsuyama T, Hirabayashi H, Sakaki T, Yabuno T. Expansive laminoplasty for
multilevel cervical OPLL. J. Spinal Disord. 1997;10(4):296–​298.
23. Sodeyama T, Goto S, Mochizuki M, Takahashi J, Moriya H. Effect of decompression en-
largement laminoplasty for posterior shifting of the spinal cord. Spine (Phila Pa 1976).
1999;24(15):1527–​1531; discussion 1531–​1522.
24. Deutsch H, Mummaneni PV, Rodts GE, Haid RW. Posterior cervical laminoplasty using a
new plating system: Technical note. J Spinal Disord Tech. 2004;17(4):317–​320.
25. Fujimori T, Le H, Ziewacz JE, Chou D, Mummaneni PV. Is there a difference in range of mo-
tion, neck pain, and outcomes in patients with ossification of posterior longitudinal ligament
versus those with cervical spondylosis, treated with plated laminoplasty? Neurosurg. Focus.
2013;35(1):E9.
26. Meyer SA, Wu JC, Mummaneni PV. Laminoplasty outcomes: Is there a difference between
patients with degenerative stenosis and those with ossification of the posterior longitudinal
ligament? Neurosurg. Focus. 2011;30(3):E9.
27. Sakaura H, Hosono N, Mukai Y, Ishii T, Yoshikawa H. C5 palsy after decompres-

sion surgery for cervical myelopathy:  Review of the literature. Spine (Phila Pa 1976).
2003;28(21):2447–​2451.
28. Chen Y, Chen D, Wang X, Guo Y, He Z. C5 palsy after laminectomy and posterior cer-
vical fixation for ossification of posterior longitudinal ligament. J Spinal Disord Tech.
2007;20(7):533–​535.
29. Gandhoke G, Wu JC, Rowland NC, Meyer SA, Gupta C, Mummaneni PV. Anterior

corpectomy versus posterior laminoplasty: Is the risk of postoperative C-​5 palsy different?
Neurosurg. Focus. 2011;31(4):E12.

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Cervical Radiculopathy Due to Central Disc

ACDF/​Arthroplasty

Mazda K. Turel and Vincent C. Traynelis

10
Case Presentation

A 37-​year-​old women presented with neck pain radiating to her right arm and right
middle finger for 6 months. Physical therapy increased the pain. On examination she
had a positive right Spurling maneuver, 4/​5 strength in her right triceps, and hypesthesia
in the right C7 dermatome.

Questions

1. What is the most likely clinical and radiological diagnosis?

2. What are the differential diagnoses in a case like this?
3. What are the various imaging modalities you would use confirm your diag-
nosis and plan your management?
4. Describe the radiological findings seen in Figure 10.1.

Assessment and Planning

This woman has a right C7 radiculopathy that has failed to respond to a course of
nonoperative therapy. Disc herniation usually occurs in patients with mild to moderate
degenerative changes.
The initial evaluation includes a careful history, which is important for distinguishing
between vascular, infectious, neoplastic, and traumatic etiologies of the symptoms.
Magnetic resonance imaging (MRI) allows direct visualization of neural structures
and provides the greatest soft tissue detail. Because herniated discs can be found in about
20% of asymptomatic individual between the ages of 20 and 40, MRI findings must
be strictly correlated with the clinical presentation, which remains the cornerstone of
decision-​making. The MRI in this patient shows a very large right C6–​C7 lateral disc
extrusion with extension into the neural foramen. There is indentation of the cord and
narrowing of the foramen (Figure 10.1,A–​C).
Plain and dynamic radiographs evaluate alignment, stability, bony anatomy, and degen-
erative disc disease. Cervical alignment parameters are important. In this patient, the neutral
lateral cervical radiograph shows a C2–​C7 sagittal vertical angle (SVA) of 18.1 mm, C2–​C7
lordosis is 15.5 degrees, C1–​C7 lordosis is 57.6 degrees, and the T1 slope is 39.2 degrees.
On flexion and extension views, there is no significant instability (Figure 10.1,D–​F).

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Figure 10.1 T2-​weighted axial (A, B) and sagittal (C) magnetic resonance images

(MRI) of the cervical spine showing a large right C6–​C7 lateral disc extrusion with
extension into the neural foramen. There is indentation of the cord and narrowing of
the foramen. On flexion and extension and neutral lateral radiographs of the cervical
spine there is no significant instability. (D–​F) The computed tomography (CT)
scan in this case was done to rule out any associated fractures due to her previous
trauma and to ascertain of there was evidence of posterior osteophytes or facetal
hypertrophy  (G–​I).
 

Cervical Radiculopathy Due to Central Disc

Computed tomography (CT) provides optimal visualization of bony detail and has a
high sensitivity in terms of detecting bony foraminal stenosis.The addition of myelography
to CT provides an excellent adjunctive study to further delineate specific anatomy, such
as the lateral recess, or to reconcile against an MRI study in which the etiology of clinical
symptoms is not demonstrated. The CT scan in this case was done to rule out any asso-
ciated fractures due to her previous trauma and to assess facet arthrosis (Figure 10.1,G–​I).

Oral Boards Review: Diagnostic Pearls

Neutral and lateral flexion and extension radiographs should be obtained to assess
alignment, motion, and stability.
An MRI scan or CT myelogram is needed to determine whether there is
impingement of any neural structures. The axial MRI or CT scan should be
carefully reviewed for the vertebral artery position, and any anomalies should be
carefully noted.

Decision-​Making

Since this patient has failed nonoperative therapy, surgery is a reasonable option. The
goal of surgical decompression is symptom relief. She could be treated with an anterior
cervical discectomy and fusion (ACDF) or cervical disc replacement (CDR).
An anterior approach allows for direct decompression which will alleviate the
symptoms, and the reconstruction can be with either a fusion or a total disc replace-
ment. Arthrodesis can enlarge the neural foramina, maintain or restore proper alignment,
and provide solid stabilization. It can be effective in the presence of facet arthropathy.
Factors to consider when selecting suitable candidates for arthroplasty include the de-
gree of segmental pathology,stability,and overall segmental motion.CDR is contraindicated
in the setting of significant segmental or global deformity. Similarly, patients without pre-
existing motion or spinal instability should not be treated with a CDR.
Currently, in the United States, CDR is approved by the Food and Drug
Administration (FDA) for intractable neck pain with radiculopathy or myelopathy at a
single level or two levels between C3 and C7 in a patient who has failed a minimum of
6 weeks of conservative treatment.

Surgical Procedure

The timing of surgical intervention for symptomatic disc disease depends on the clinical
situation. Emergent surgical intervention is indicated for patients with severe or rapidly pro-
gressive motor radiculopathy, myelopathy, or bowel or bladder dysfunction. Patients without
evidence of spinal instability who present with pain, sensory disturbances, and mild or fixed
motor deficits or those exhibiting neurological improvement should not be considered for
emergent surgical decompression. Instead, these patients should be treated with nonoperative
modalities. If they fail to improve, then elective surgical intervention should be considered.
ACDF has been a successful surgical strategy for more than 60 years. The patient is
positioned supine with the head resting on a doughnut and with an axillary roll below
the shoulder. The ventral approach to the cervical spine is performed sharply through a

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plane between the sternocleidomastoid muscle and the carotid sheath laterally and the
strap muscles and tracheoesophageal viscera medially. The omohyoid muscle crossing at
C5–​C6 may be tagged, divided, and reapproximated at the time of closure. Caudal ex-
posure at C6–​C7, C7–​T1 is facilitated by dividing the inferior thyroid artery, while at
C2–​C3 or C3–​C4 it is important to carefully fully isolate the superior thyroid artery
prior to dividing it to minimize the potential of injuring the superior laryngeal nerve.
The disc space is identified using intraoperative fluoroscopy, and the medial attachments
of the longus colli muscle are released with cautery. The exposure is maintained with a
retractor system.The disc annulus is incised, and disc removal is done using a combination
of curettes and pituitary forceps until the posterior longitudinal ligament is seen.The disc
space may be distracted to improve visualization. The endplates are prepared for grafting,
and then the operating microscope is brought into the field to complete the rest of the
discectomy, expose the dura from one uncovertebral joint to the other to achieve an ad-
equate lateral decompression, and visualize the origin of the nerve roots. The posterior
osteophytes and posterior portion of the uncinate are removed. The reconstruction can
be performed with allograft, autograft, or a cage. An anterior plate decreases subsidence,
increases the fusion rate, and often eliminates the need for a rigid orthosis. The wound is
thoroughly irrigated, hemostasis is achieved, and the closure is done in layers.
The procedure for an arthroplasty remains the same up until completion of the disc-
ectomy, when a CDR is placed instead of the graft and plate with the aim to preserve
motion. The CDR should be implanted with strict adherence to the recommendations
of the manufacturer, which will vary depending on the implant selected. Figure 10.2
demonstrates an intraoperative radiograph of this patient who underwent a CDR.
The dorsal approach is discussed in detail in the next chapter.

Figure 10.2  Lateral cervical intraoperative radiograph of the patient after cervical disc
replacement.

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Cervical Radiculopathy Due to Central Disc

Oral Boards Review: Surgical Technique Pearls

1. The head and neck are stabilized and held in a neutral position or slightly ex-
tended for all procedures. The vertebral endplates at the operative level should
be maintained in as close to a neutral position as possible.
2. On the left side, the recurrent laryngeal nerve loops under the arch of the
aorta and is protected in the left tracheoesophageal groove; hence, we prefer
the left-​sided approach. On the right side, however, it travels around the sub-
clavian artery, passing dorsomedially to the side of the trachea and esophagus.
The nerve is vulnerable as it passes from the subclavian artery to the right
tracheoesophageal groove.
3. The vertebral artery is usually 5 mm lateral to the uncovertebral joint and is
not covered by bone between two transverse foramina. There can be signif-
icant variations in its position, though, and it should be examined preopera-
tively on every MRI scan prior to the procedure.
4. The plate should not be near the adjacent disc space because this has been
shown to accelerate disc degeneration. The utmost care should be taken to
ensure the adjunct disc space is not violated by a screw as this will hasten de-
generation at the adjacent level.

Pivot Points

1. The main objectives of treatment of cervical radiculopathy are to relieve pain,

improve neurologic function, and prevent recurrences.
2. The indications for cervical arthroplasty are not synonymous with those for
cervical fusion, and this technique should not be assumed to be appropriate
for all patients who may benefit from an ACDF.
3. ACDF has the advantage of improving cervical lordosis and is the most ap-
propriate option in patients with severe spondylosis, facet joint degeneration,
and loss of motion at the pathological level, all of which are contraindications
for arthroplasty.
4. Patients receiving a CDR should have normal cervical alignment and mo-
bility. If one wishes to replicate the results from the prospective disc studies,
then one should adhere to the entry criteria.

Aftercare

Patients are observed overnight in the hospital with a continuous pulse oximeter to
watch for airway compromise from postoperative hematoma/​seroma. Diet and activity
are allowed as tolerated. Drains, if placed, are typically removed on postoperative day 1.
We do not prescribe any restriction of activity with the exception of carrying heavy
loads on the head.
Patients are seen in the clinic at 6 weeks and at progressively regular intervals up to
12 months.

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Complications and Management

Complications of anterior cervical spine surgery at a single level are extremely infre-
quent. Dysphagia is the most common complication and varies in incidence from 5%
to 50%. However, less than 1% is permanent. Neurological deterioration can result from
direct injury to the cord and is also very unlikely. Injury to the cervical sympathetic
chain leads to Horner syndrome but is very rare. Injury to the esophagus and the carotid
and vertebral arteries has been reported, and the incidence of these complications is less
than 1%. Airway compromise is the most dreaded complication and can occur due to
a postoperative hematoma, soft tissue swelling, or implant/​graft dislodgement. Prompt
intubation before the development of stridor and reexploration can be life-​saving. Dural
tear and cerebrospinal fluid leak occur exceedingly rarely and are treated with Gelfoam,
tissue glue, and, in selected cases, a lumbar subarachnoid drain.
Some patients may experience posterior interscapular pain, which can be severe but
should resolve with time. Delayed complications include nonunion (pseudoarthrosis)
and adjacent segment disease, both of which require revision surgery in symptomatic
patients. Implant migration or subsidence, though rare, remains a potential complica-
tion following CDR. Postcervical kyphosis is another complication following CDR.
Heterotopic ossification, defined as formation of bone outside the skeletal system has
been reported following arthroplasty with variable incidence among different studies.

Oral Boards Review: Complications Pearls

1. Intermittent release of the retractor and deflating the cuff of the endotracheal
tube may reduce the incidence of recurrent laryngeal nerve injury.
2. An adequate fascial dissection minimizes retraction and reduces postoperative
soft tissue swelling and airway compromise.
3. Meticulous hemostasis of every layer of soft tissue within the neck before
wound closure will ensure that the patient does not develop a postoperative
hematoma.
4. The incidence of heterotopic ossification in patients treated with a CDR may
be decreased by copious irrigation intraoperatively, limited muscle retraction,
and nonsteroidal antiinflammatory drugs (NSAIDs) during the perioperative
period.

Evidence and Outcomes

Postoperative neurological outcome is related to the type, duration, acuteness, and se-
verity of the preoperative deficit. Data from prospective observational studies indicate
that 2 years after surgery for cervical radiculopathy caused by soft cervical disc herni-
ation (without myelopathy), 85% of patients have substantial pain relief from radicular
symptoms. Radicular symptoms are more likely to improve with surgical decompression
compared with myelopathy; however, several small reports note significant improvement
in myelopathic patients if surgery is performed early. Overall quality of life as assessed by
the Short-​Form 36 inventory and Oswestry Disability Index (ODI) also show significant
improvement. Patients with deficits from acute disc herniations have a more favorable
surgical outcome compared with those with deficits from spondylotic disease. Patients

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Cervical Radiculopathy Due to Central Disc

who present with severe or long-​standing symptoms and signs have a poorer functional
outcome than those with only a short clinical history and minor neurological deficits.
In an analysis of outpatient versus overnight-​admitted patients, a total of 7,288
ACDF cases were identified (outpatient = 1,168, inpatient = 6,120). Unadjusted rates
of major morbidity (0.94% vs. 4.5%) and return to the operating room (OR) within
30 days (0.3% vs. 2.0%) were significantly lower in outpatient versus inpatient ACDF.
After propensity matching, 1,442 cases (outpatient  =  792, inpatient  =  650) based on
baseline 32 covariates, rates of major morbidity (1.4% vs. 3.1%, p = 0.03), and return to
the OR (0.34% vs. 1.4%, p = 0.04) remained significantly lower after outpatient ACDF.
Multivariate logistic regression demonstrated that ACDF performed in the outpatient
setting had 58% lower odds of having a major morbidity and 80% lower odds of return
to the OR within 30 days. It should be recognized that those treated as an outpatient represent
an extremely select group in which one would expect minimal complications.
In a recently concluded meta-​analysis comparing more than 1,000 patients each for
ACDF versus CDR, the latter had a higher rate of overall success and better NDI scores
with lower rates of secondary surgery and adverse events.The reoperation rate at 10 years
following arthroplasty was around 10%, while it was 30% following ACDF. Fusion rates
are greater than 95% for a single-​level ACDF and 85% for two levels. Although preven-
tion of adjacent segment disease has been a compelling rationale for CDR, there is no
conclusive supporting clinical evidence for this hypothesis at this point.

Reference and Further Reading

Burkus JK, Traynelis VC, Haid RW Jr, Mummaneni PV. Clinical and radiographic analysis of an
artificial cervical disc: 7-​year follow-​up from the Prestige prospective randomized controlled
clinical trial:  Clinical article. J Neurosurg Spine. 2014 Oct;21(4):516–​ 528. doi:  10.3171/​
2014.6.SPINE13996. Epub Jul 18, 2014.
Engquist M, Löfgren H, Öberg B, et al. Factors affecting the outcome of surgical versus nonsurgical
treatment of cervical radiculopathy: A randomized, controlled study. Spine (Phila Pa 1976).
2015 Oct 15;40(20):1553–​1563. doi: 10.1097/​BRS.0000000000001064.
Gornet MF, Burkus JK, Shaffrey ME, Argires PJ, Nian H, Harrell FE Jr. Cervical disc arthroplasty
with PRESTIGE LP disc versus anterior cervical discectomy and fusion:  A prospective,
multicenter investigational device exemption study. J Neurosurg Spine. 2015 Jul 31:1–​16.
[Epub ahead of print].
Loumeau TP, Darden BV, Kesman TJ, Odum SM,Van Doren BA, Laxer EB, Murrey DB. A RCT
comparing 7-​year clinical outcomes of one level symptomatic cervical disc disease (SCDD)
following ProDisc-​C total disc arthroplasty (TDA) versus anterior cervical discectomy and
fusion (ACDF). Eur Spine J. 2016 Jul;25(7):2263–​2270. doi:  10.1007/​s00586-​016-​4431-​6.
Epub Feb 11, 2016.
McGirt MJ, Godil SS, Asher AL, Parker SL, Devin CJ. Quality analysis of anterior cervical discec-
tomy and fusion in the outpatient versus inpatient setting: Analysis of 7288 patients from the
NSQIP database. Neurosurg Focus. 2015 Dec;39(6):E9. doi: 10.3171/​2015.9.FOCUS15335.

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Cervical Radiculopathy

Lateral Disc Foramintomy

Michael Karsy, Ilyas Eli, and Andrew Dailey

11
Case Presentation

A 53-​year-​old woman presents to clinic with the chief complaint of right shoulder
pain of 3 months’ duration. She describes a sharp pain emanating from the right lateral
aspect of her neck into her trapezius and then down across the deltoid. She describes
the intensity of the pain as a 6/​10 in her right shoulder. The pain worsens as the day
progresses. Her symptoms are most notably worse in her right shoulder, and, as a result,
she has become less active. She unsuccessfully tried treating the pain with nonsteroidal
antiinflammatory drugs (NSAIDs) and physical therapy. She subsequently underwent a
right C5 selective nerve root block; however, she reports having no pain relief with the
injection and no resolution of her symptoms. She otherwise denies any clumsiness or
weakness in her right upper extremity.
A neurological examination reveals a motor strength of 5/​5 in the deltoid, biceps,
triceps, wrist extension, wrist flexion, dorsal interosseous, flexor digitorum profundus,
and abductor pollicis brevis. On sensory examination, there is diffuse decreased sensa-
tion throughout the patient’s right upper extremity that is not in a dermatomal pattern.
The reflex examination reveals 2+ biceps bilaterally with a 1+ triceps reflex seen on the
right. She has no evidence of Hoffman sign or gait abnormality. Magnetic resonance
imaging (MRI) of the cervical spine without contrast demonstrates diffuse cervical disc
degeneration from C3 to C7 (Figure 11.1). The most notable finding is a severe neural
foraminal stenosis at the C4–​C5 level eccentric to the right side.

Questions

1. What is the differential diagnosis of this patient?

2. What is the initial conservative management of this patient, and when should
this patient be referred for surgical treatment?
3. What imaging should be completed to evaluate this patient?

Assessment and Planning

On the basis of the patient’s presentation, physical examination, and imaging findings,
the diagnosis is cervical radiculopathy. Cervical radiculopathy results from direct com-
pression and inflammation of a cervical nerve root, often because of disc herniation or

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Figure 11.1  (A) Axial T2-​weighted magnetic resonance imaging (MRI) without

gadolinium demonstrates foraminal stenosis on the right C5 nerve root. An oblique
cut (line) is shown in B. (B) Oblique T2-​weighted MRI without gadolinium
demonstrates disc herniation causing compression of the exiting C5 nerve root.
(C) Sagittal cervical spine x-​ray shows normal cervical lordosis with multilevel loss of
disc height most pronounced at C4–​C5.

osteophyte formation. Patients with cervical radiculopathy present with complaints of

sharp, numbing, shooting, or lancinating pain attributable in a dermatomal distribution.
Physical examination is notable for a depressed reflex arc in the affected nerve root.
Additionally, the Spurling test, which involves head turn toward the symptomatic side
and placement of downward axial pressure, can reproduce the radicular pain. Conversely,
axial traction reduces the pain. Subtle changes in sensation and strength are not un-
common; however, a detailed neurological examination should be performed to rule
out myelopathy.
An initial workup to confirm the diagnosis includes obtaining cervical lateral x-​rays
to evaluate the cervical spine curvature and identify degenerative changes such as oste-
ophyte formation or disc collapse (Figure 11.1). Flexion and extension radiographs are
also helpful in evaluating cervical spine stability prior to selecting patients for cervical
foraminotomy versus arthroplasty or arthrodesis. Computed tomography (CT) imaging
allows for visualization of the cervical bony anatomy, which is helpful in determining
the etiology of the cervical root compression. Oblique reconstructions will depict
foraminal narrowing. MRI is currently the standard imaging modality used for clear vis-
ualization of soft tissue, enabling the identification of disc herniation and impingement
of nerve roots. In some situations, a CT myelogram may be helpful for patients with
contraindications to an MRI to assess cervical stenosis and disc bulges.The direction and
degree of disc herniation, course of the vertebral arteries, and trajectory to the sympto-
matic level should be assessed on preoperative imaging.

Oral Boards Review: Diagnostic Pearls

1. Management of patients with cervical radiculopathy requires a complete as-

sessment, including history and physical examination. Findings that suggest
cervical radiculopathy include pain radiating down the arm along a particular
dermatomal distribution. The presence of upper motor neuron signs, such as

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Cervical Radiculopathy: Lateral Disc Foramintomy

hyperreflexia and the Hoffman sign, which could suggest the presence of my-
elopathy, should be ruled out.
2. MRI should be utilized to look for disc herniation or osteophytes as causes
for nerve root compression. The course of the vertebral artery should be
assessed as well as the presence of anatomic variants.
3. Cervical radiculopathy is initially managed conservatively with physical
therapy, medication, and spinal injection. Most patients obtain adequate pain
relief with nonsurgical management. Only after these measures fail to provide
the patient with pain relief is surgery then indicated.
4. Laminoforaminotomy is contraindicated in patients with myelopathy and cer-
vical spine instability.

Nonoperative management is recommended for most patients who have cervical

radiculopathy. Conservative measures include physical therapy, activity modification, use
of NSAIDs, and spinal injections. Most patients notice improvement and pain relief with
conservative treatment; however, patients who continue to suffer despite such measures
should consider surgery. Surgical intervention is thus reserved for patients who continue
to have severe pain despite 6 weeks of conservative management.

Questions

1. What features of imaging modalities should be evaluated in the management

of this disease?
2. What are the indications for surgery?
3. What are the contraindications to surgery?
4. What anatomical features limit use of this surgical approach?

Decision-​Making

Indications for cervical foraminotomy include radiographic documentation, with either

CT or MRI, of foraminal stenosis caused by either an osteophyte or disc herniation and
symptoms that correlate to the affected nerve root. Contraindications to performing
cervical foraminotomy include the presence of kyphosis or cervical spine instability,
symptoms of cervical myelopathy, and signs of spinal cord compression on imaging
modalities. Among the advantages of a cervical foraminotomy are that the disc space is
not destabilized, cervical fusion is avoided, and direct decompression of the foramen is
achieved.
Anterior and posterior approaches have been explored in the treatment of lateral
disc herniation. Anterior discectomy was described by Robinson and Smith in 1955 and
Cloward in 1958; it involves direct access to the ventral cervical root where compression
was most often noted. Anterior microforaminotomy was described by Jho to avoid re-
moval of the lateral disc and preserve the functional integrity of the spine.1,2 Candidates

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for anterior or posterior cervical foraminotomy approaches have clear unilateral cervical
radiculopathy and foraminal stenosis caused by either an osteophyte or a disc herniation
with symptoms that correlate to the affected nerve root; minimal neck pain; no prior
cervical spine surgery; and no significant cervical kyphosis, stenosis, or instability. These
two approaches minimize complete disc removal. This is an advantage because disc re-
moval necessitates arthrodesis, which can be associated with complications including
longer operative times and greater blood loss, adjacent segment disease, and hardware
failure, as well as pseudarthrosis.

Complications Management

1. What anatomical features favor an anterior versus posterior approach for cervical
foraminotomy?
2. What are the critical structures in this approach? How can an injury to those structures
be managed intraoperatively and postoperatively?

Surgical Procedure
Anterior Approach

After the patient is positioned supine, an incision is localized to the uncovertebral junc-
tion of the symptomatic level, medial to the border of the sternocleidomastoid and per-
pendicular to the disc space (Figure 11.2A). A standard anterior cervical dissection to the
level of the longus colli is performed. A knife is used to remove a rectangular area of the
longus colli muscle at the area of the uncovertebral joint, with bipolar electrocautery used
for hemostasis. The sympathetic trunk runs along the longus colli above the transverse
foramen and lateral to the uncovertebral joint. A long, thin, malleable retractor is placed
between the uncinate process and the vertebral artery to protect the transforaminal seg-
ment of the artery. The uncinate process is partially removed by creating a hole 5 mm
in diameter in the medial wall of the neural foramen with a 2 mm drill bit followed by
curettes and Kerrison rongeurs. Ruptured and migrated disc fragments commonly lie in
the axillary region of the nerve root and can be identified on MRI. Opening the poste-
rior longitudinal ligament can be useful in identifying fragments.

Posterior Approach

The patient is placed prone in the reverse Trendelenburg position with 30 degrees of tilt
to reduce cervical venous pressure or in a sitting position (Figure 11.2B).The advantages
of the sitting position can include use of gravity to remove blood from the surgical field,
but this position increases the risk of air embolism and is a less familiar approach to most
surgeons. The neck should be maintained in a slightly flexed position, and a Mayfield
skull clamp can reduce intraoperative movement. An incision is localized over the lam-
inar interspace in the midline. A standard posterior cervical dissection is performed with
the goal to localize to the lamina–​facet interface of the superior and inferior cervical
level where the exiting nerve root is found. Drilling is centered at the lamina–​facet junc-
tion to expose the lateral border of the thecal sac, the exiting nerve root, and the disc

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Cervical Radiculopathy: Lateral Disc Foramintomy

Figure 11.2  Anterior and posterior approaches for cervical foraminotomy. (A) Artist’s

illustration showing an anterior foraminotomy approach, outlining the location of
a herniated disc fragment (dotted circle). The lateral retractor is placed to protect the
exiting nerve root and vertebral artery. The longus colli has been split to allow access
to the disc. (B) Artist’s illustration showing a posterior foraminotomy approach. The
lamina–​facet junction has been drilled to give access to the exiting nerve root. A nerve
hook is shown retracting the exiting nerve root.

space. Localization of the depth and lateral extent of neural structures from the incision
can be ensured by identifying the lateral border of the facet. The medial third of the
facet and lateral third of the superior and inferior lamina are thinned using a high-​speed
drill. Curettes and the Kerrison rongeur are used to remove the remaining bone. The
ligamentum flavum is identified medially and incised to allow access to the nerve root
and disc space. Disc material superior or inferior to the exiting nerve root is removed
depending on the extent of disc herniation. A cruciate incision into the posterior longi-
tudinal ligament and annulus is made to decompress disc extrusion. Use of endoscopic
assistance to improve illumination of the working area has also been well described for
these approaches.

Oral Boards Review: Management Pearls

1. Anterior or posterior approaches can be planned based on preoperative im-

aging. Attention should be paid to the exiting nerve root and vertebral artery
with both approaches. The extent and direction of disc herniation causing
foraminal stenosis should be identified. The artery will be lateral to the

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uncovertebral joint in a soft tissue plane not visualized during surgery. The
most common entry for the vertebral artery is at the C6 cervical level.
2. The open and endoscopic approaches have shown equivalent efficacy.

Pivot Points

1. If the patient has preoperative neck pain, spine instability, stenosis or compres-
sion, or myelopathy, a larger anterior discectomy and fusion procedure may be
needed. Arthroplasty may also be an option.
2. Anterior and posterior foraminotomy approaches can be used equivalently
and based on individual patient characteristics

Aftercare

A cervical orthosis is not required postoperatively, and patients who have undergone an
anterior approach can usually be discharged same day. Posterior approaches may involve
more pain than anterior approaches, and most patients require 1 day in the hospital prior
to discharge.

Complications and Management

Complications during anterior or posterior approaches can include bleeding from in-
jury to the vertebral artery or perivertebral venous plexus. The vertebral artery runs
lateral to the uncinate process within the transverse foramen and most often enters the
foramen at the C6 level. After injury, packing of the wound with hemostatic agents
should be attempted to assess whether the injury is controllable. Primary repair of the
vertebral artery is difficult given the narrow corridor but has been described. Immediate
postoperative angiography is recommended to evaluate the degree and type of injury as
well as whether there is adequate flow to the posterior circulation. Endovascular consul-
tation can be helpful in further management.
As with standard anterior cervical approaches, neck hematoma may be a signifi-
cant comorbidity warranting urgent reexploration. Hematomas are most likely to occur
within the first few hours postoperatively. Minimizing agitation and coughing during
extubation can reduce postoperative hematoma risk but requires close communication
with the anesthesia team.
Air embolism is possible during cases performed with the patient in a sitting position.
The most sensitive monitoring for air embolism is a precordial ultrasound monitor, but
a decrease in end tidal CO2 is another common sign. Placement of a central line before
the case can be a strategy to draw air bubbles if they occur. Immediate treatments in-
clude flooding the field with irrigation, lowering the head of bed below the heart, and
positioning the patient in the left lateral position to trap air in the right heart.
Lack of pain resolution postoperatively is possible; it is related to inadequate nerve
root decompression or additional cervical spondylotic disease, which may require
a wider decompression and fusion procedure. Injury to the thecal sac or nerve roots
can occur during overzealous dissection. Other complications during dissection can

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Cervical Radiculopathy: Lateral Disc Foramintomy

include Horner syndrome from injury of the sympathetic chain. Attention to minimize
longus colli dissection lateral to the uncinate process can aid in reducing injury risk.
Cerebrospinal fluid leak is a possibility in both anterior and posterior approaches but
can usually be managed conservatively, with a combination of primary closure, Gelfoam
and/​or fibrin-​thrombin surgical glue along with instructing the patient to keep his or
her head elevated.
With anterior approaches, the patient’s airway and any swallowing dysfunction (e.g.,
dysphagia) should be evaluated postoperatively. Postoperative dysphagia can be managed
conservatively in most cases. Postoperative C5 myeloradiculopathy can be a rare compli-
cation related to mobilization of the thecal sac and traction on the C5 nerve root.While
more common in anterior cervical discectomies, C5 radiculopathy can be distressing to
patients and can usually be managed conservatively with observation or a short course
of steroids.

Oral Boards Review: Complications Pearls

1. Vertebral artery injury can occur with anterior or posterior approaches.

2. Postoperative dysphagia or C5 distribution myeloradiculopathy are rare
complications and can be usually managed conservatively.

Evidence and Outcomes

Overall success rates and complication rates with anterior or posterior cervical
foraminotomy and disc decompression are good in properly selected patients.1,3–​6
A  meta-​analysis of 20 studies showed very good clinical outcomes with both open
foraminotomy (92.7% [95% confidence interval (CI):  88.9, 95.3]) and minimally in-
vasive (94.9% [95% CI:  90.5, 97.4]) approaches.4 One limitation of this analysis was
that long-​term follow-​up and standardized quality-​of-​life metrics varied depending
on study. A  more recent analysis of 26 studies comparing open foraminotomy and
microendoscopic foraminotomy showed that microsurgical approaches showed lower
blood loss (by 100.1 mL), shorter operating times (by 24.9 minutes), and shorter hospital
stays (by 3.0 days) compared with open approaches.7 The pooled clinical success rate was
89.7% (95% confidence interval [CI]: 87.7, 91.6) for open approaches and 92.5% (95%
CI: 89.9, 95.5) for microsurgical approaches. Overall complication rates were not sig-
nificantly different between microsurgery and open approaches; complications included
dural tears (1.07 vs. 0.27%), infections (0.4 vs. 0.54%), root injury (0.8 vs. 1.48%), and
revision surgery (2.32 vs. 3.35%). Improvement in visual analog scale for arm pain was
75% (95% CI: 66.0, 84.0) for open approaches and 87.1% (95% CI: 76.7, 97.5) for mi-
crosurgical approaches, which were not significantly different. Similarly, improvement
in neurological function was not significantly different between groups, at 55.3% (95%
CI: 18.6, 91.9) in open surgery and 64.9% (95% CI: 34.6, 95.2) in microsurgery.
Risk of future need for surgical intervention has ranged from 1% to 24.3% at the
index level or adjacent level depending on study type and follow-​up.6,8–​10 One study of
151 patients who underwent posterior cervical foraminotomy showed a reoperation
rate of 9.9% (6.6% same level, 3.3% other level) over a mean time of 2.4 years8; however,

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reoperation rates increased to 18.3% and 24.3% at follow-​up greater than 2 and 10 years,
respectively. Most patients (80%) who underwent reoperation had an anterior cervical
discectomy and fusion. Preoperative neck pain was a significant predictor of revision sur-
gery. Another study using propensity-​matched scoring of anterior cervical discectomy
with fusion and posterior cervical foraminotomy showed reoperation rates of 4.8% and
6.4% within 2 years of index surgery, which were not significantly different.9 Another
study suggested that patients older than 60 years at time of initial surgery and presence
of preoperative cervical lordosis less than 10 degrees predicted later surgical correction.6
One limitation of comparing patients who underwent fusion and those who had de-
compression alone is the lack of randomized data supporting clinical decision-​making,
making it possible for bias to select patients for one procedure or another despite pos-
sible clinical equipoise.

References and Further Reading

1. Jho HD. Microsurgical anterior cervical foraminotomy for radiculopathy: A new approach to
cervical disc herniation. J Neurosurg. 1996;84(2):155–​160.
2. Epstein NE. A review of laminoforaminotomy for the management of lateral and foraminal
cervical disc herniations or spurs. Surg Neurol. 2002;57(4):226–​233; discussion 233–​224.
3. Johnson JP, Filler AG, McBride DQ, Batzdorf U. Anterior cervical foraminotomy for unilat-
eral radicular disease. Spine (Phila Pa 1976). 2000;25(8):905–​909.
4. McAnany SJ, Kim JS, Overley SC, Baird EO, Anderson PA, Qureshi SA. A meta-​
analysis of cervical foraminotomy:  Open versus minimally-​invasive techniques. Spine J.
2015;15(5):849–​856.
5. Burke TG, Caputy A. Microendoscopic posterior cervical foraminotomy: A cadaveric model
and clinical application for cervical radiculopathy. J Neurosurg. 2000;93(1 Suppl):126–​129.
6. Jagannathan J, Sherman JH, Szabo T, Shaffrey CI, Jane JA. The posterior cervical
foraminotomy in the treatment of cervical disc/​osteophyte disease: A single-​surgeon ex-
perience with a minimum of 5  years’ clinical and radiographic follow-​up. J Neurosurg
Spine. 2009;10(4):347–​356.
7. Song Z, Zhang Z, Hao J, et al. Microsurgery or open cervical foraminotomy for cervical
radiculopathy? A systematic review. Int Orthop. 2016.
8. Bydon M, Mathios D, Macki M, et al. Long-​term patient outcomes after posterior cervical
foraminotomy: An analysis of 151 cases. J Neurosurg Spine. 2014;21(5):727–​731.
9. Lubelski D, Healy AT, Silverstein MP, et al. Reoperation rates after anterior cervical disc-
ectomy and fusion versus posterior cervical foraminotomy: A propensity-​matched analysis.
Spine J. 2015;15(6):1277–​1283.
10. Wang TY, Lubelski D, Abdullah KG, Steinmetz MP, Benzel EC, Mroz TE. Rates of ante-
rior cervical discectomy and fusion after initial posterior cervical foraminotomy. Spine J.
2015;15(5):971–​976.

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Thoracic Disc Herniation

Derrick Umansky and James Kalyvas

Case Presentation

A 52-​year-​old Caucasian man presents with chronic mid back pain and bilateral lower
12
extremity weakness. The patient notes the weakness began more than a year ago and
has been progressive. He drags the left leg when walking and complains of stumbling
with loss of balance. The patient also complains of shooting pain down the left leg. He
denies any urinary incontinence or retention. He has no bowel dysfunction. On phys-
ical exam, the patient is unable to stand without assistance. He has a spastic gait, clonus
of the left foot, weakness of all left lower extremity muscles, and decreased sensation to
all modalities in his bilateral lower extremities.There is no obvious sensory level and the
remainder of the physical exam was normal.

Questions

1. What is the likely clinical diagnosis?

2. Where does the pathology localize anatomically?
3. What are the most appropriate imaging modalities for further evaluation?

Differential Diagnosis

The symptoms and physical signs here suggest myelopathy and more strongly fit with
thoracic cord pathology than cervical cord pathology given the lack of upper extremity
involvement. With suspicion of thoracic myelopathy, a broad differential diagnosis
should be considered to guide the selection of the most appropriate diagnostic studies.
The differential diagnosis can be divided into compressive and non-compressive tho-
racic pathologies.

Differential Diagnosis with Diagnostic Pearls

Compressive Pathologies

1. Degenerative:
a. Spondylosis is common as patients age, but is more typically seen in the
more mobile cervical and lumbar regions. Nevertheless, it occurs in
the thoracic spine, too, and often presents with axial mid-​back pain,

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pseudoclaudication, and unsteadiness of gait (Brown et al., 1992). The

exam can range from grossly normal to hyperreflexia, presence of patho-
logical reflexes, paraplegia, and loss of proprioception. The loss of sphincter
function and pain/​temperature sensation tends to occur later in the disease
course. Magnetic resonance imaging (MRI) with T2-​weighted sequences
is usually sufficient to make the diagnosis (Blumenkopf, 1988).
b. Disc herniations of the thoracic spine comprise less than 1% of all
herniated discs and less than 4% of all herniated disc operations (Chen
et al., 2012). Herniated thoracic discs (HTD) affect men more often than
women, typically between the ages of 40 and 50 years. They occur more
frequently in the lower thoracic spine (T8 and below) than the more
rigid upper thoracic spine. Symptoms can be nonspecific, including pain,
sensory changes, and weakness of the lower extremities, but, in approxi-
mately 15–​20% of cases, more specific symptoms like bowel and bladder
dysfunction may occur (Brown et al., 1992). In most cases, physical exam
plays a critical role in narrowing the diagnosis. Myelopathic signs involve
proximal muscle weakness, mild paraparesis of the lower extremities, a
wide-​based gait, positive Babinski, abnormal abdominal reflexes, and
spasticity. To differentiate lower cervical from upper thoracic pathology,
hyperreflexia of lower extremities with a negative Hoffman sign is in-
dicative of thoracic involvement. Radiculopathic pain is in a band-​like
distribution radiating anteriorly and inferiorly in associated dermatomes
and can occasionally be reproduced with weight-​bearing, lateral bending,
or palpation. In general, evaluation of sensory dermatomes is much more
reliable than myotomes in thoracic pathology.
MRI T2-​weighted sequences or a computed tomography (CT)
myelogram are the best diagnostic imaging modalities for assessment of
neurologic compression (Williams & Cherryman, 1988), and CT is best for
assessment of disc calcification (Awwad et al., 1991). In some cases dynamic
x-​rays and long scoliosis films can be useful for assessment of concomitant
spinal instability or deformity.
c. Arachnoid cysts are typically asymptomatic though rarely can be a cause of
myelopathy (Santiago et al., 2004). Cysts typically occur in the thoracic
spine and can be congenital or acquired. The best imaging modality is
an MRI, but CT myelogram is also useful to distinguish arachnoid cysts
from ventral cord herniations. Cysts demonstrate cerebrospinal fluid (CSF)
signal (sometimes increased intensity on T2-​weighted sequences given less
pulsation) with no enhancement or restricted diffusion.
2. Traumatic:
This includes herniated discs, fractures, and ligamentous injury. The history
should provide the nature of the injury and guide imaging studies.
3. Infectious:
a. Epidural abscesses most commonly present in the thoracic spine, and they
can present with thoracic radiculopathy or myelopathy (Fessler, 2006).
Onset may be rapid or slowly progressive. Suspicion should be raised
when there is severe local spine tenderness, systemic signs of infection,

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Thoracic Disc Herniation

immunocompromised state, or recent invasive spinal or dental procedures.

Fever, back pain, and tenderness to percussion is the classic triad but rarely
do patients present with all three.
MRI T1-​weighted sequences with and without gadolinium are best to
evaluate the abscess, and T2-​weighted sequences are best for assessment of
neurologic compression. Lab studies should include complete blood count
(CBC) with differential, c-​reactive protein (CRP), erythrocyte sedimenta-
tion rate (ESR), and procalcitonin.
4. Neoplastic:
a. Extradural and intradural masses: Most neoplastic spinal cord pathologies
present initially with pain only (85%) that may be radicular (20%) or
generalized, though myelopathy or radiculopathy can be seen later in the
disease course (Vialle, 2014). The pain is typically worse at night, progres-
sive, and unrelated to position. On exam, it can often be reproduced on
palpation of the involved segments. Myelopathic signs are usually absent
early in the disease, but 35% of benign and 55% of malignant tumors even-
tually progress to some degree of myelopathy.
Diagnostic workup of the spinal pathology should include MRI
with and without contrast (CT myelogram if patient is unable to un-
dergo MRI) as well as CT without contrast if there is bone involvement.
Additional workup will not be discussed in this chapter.
5. Vascular:
a. Arteriovenous malformations (AVMs) and arteriovenous fistulas (AVFs) are
lesions that shunt arterial blood directly to venous vasculature without
resistance from capillary flow, and they typically occur in the midthoracic
spine (Deshaies & Eddleman, 2011). Symptoms can be gradual with pro-
gressive myelopathy or acute due to subarachnoid or intramedullary
hemorrhage. Up to 15% of patients present with Foix-​Alajouanine syn-
drome, which is a rapid decline in neurological function due to venous
hypertension, thrombosis, and ultimately spinal cord infarction. Spinal
subarachnoid hemorrhage (coup de poignard of Michon) may also occur
leading to sudden-​onset back pain, rapid neurological decline, and
meningismus. MRI without contrast is the modality of choice to localize
the lesion and reveals signal voids on T1 and T2 sequences. Angiography
is the gold standard of diagnosis and treatment planning.

Noncompressive Pathologies

1. Demyelinating:
a. Multiple sclerosis (MS) is a demyelinating disease of the central nervous
system that occurs most commonly in the corticospinal tracts and pos-
terior columns (Sartor, 2002). Presentations can be confused with tho-
racic myelopathy due to commonality of spastic paraparesis, bladder
disturbances, sensorimotor weakness, and gait ataxia. MRI with and
without contrast is the imaging modality of choice and will show high

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signal on T2-​weighted sequences, +/​−enhancement on T1-​weighted

images—​usually in the absence of cord compression.
b. Transverse myelitis is an acute/​subacute motor, sensory, and autonomic
spinal cord dysfunction caused by interruption of pathways in the trans-
verse plane of the spinal cord. Demographic distribution is bimodal
with peaks at 10–​19 years and 30–​39 years of age. Most causes are au-
toimmune, and patients often have a history of recent infection or
vaccination (60%).
Diagnostic criteria are specific and require bilateral (though not
symmetric) sensorimotor and autonomic dysfunction with a clearly
delineated sensory level deficit. MRI with gadolinium typically shows
poorly delineated altered intensity in the cord with variable enhancement.
Lumbar puncture demonstrates pleocytosis.
2. Vascular:
a. Spinal arterial thrombosis patients present with acute onset of symptoms.
Spinal artery syndromes include anterior spinal artery syndrome, posterior
spinal artery syndrome, and Brown Séquard syndrome.
MRI without contrast is the imaging modality to confirm the diagnosis
and reveals altered T2 signal intensity in the area of the corresponding ar-
tery. Diffusion-​weighted imaging can be used but is limited by CSF flow
artifact.
3. Metabolic:
a. Vitamin B12 deficiency can lead to subacute combined degeneration of the
spinal cord with symptoms and signs including loss of proprioception and
vibration, hyperreflexia, ataxic gait, weakness, and positive Romberg sign
(Botelho, 2017). CBC typically demonstrates anemia and elevated mean
corpuscular volume (MCV). MRI can show symmetrically increased T2
signal in the posterolateral columns.

In this case, our suspicion is highest for degenerative thoracic myelopathy, and there-
fore MRI without contrast or CT myelogram (if MRI is contraindicated) is most appro-
priate (Ghostine et al., 2011). As seen in Figure 12.1, MRI reveals a large central HTD
compressing the cord. With this information, a CT without contrast is then appropriate
to determine the presence and degree of disc calcification, which would influence man-
agement. We see in Figure 12.2 that the pathology is a giant central calcified disc. The
term “giant” is applied when the disc occupies at least 40% of the spinal canal, and
these are approached much differently than smaller noncalcified discs, which will be
discussed later.

Questions

1. For this case presentation, is surgical or nonsurgical management most

appropriate?
2. If surgery is pursued, what is the most appropriate approach?
3. How does thoracic disc size and location and degree of calcification influence
the surgical approach?

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Thoracic Disc Herniation

A B

Figure 12.1 T2 sequence of MRI of thoracic spine without contrast. Sagittal (A) and

Axial (B) slices demonstrating HTD at T8-​9 level with severe spinal canal stenosis

Decision-​Making

Consensus in the literature supports surgery for severely symptomatic or disabling

HTDs only, with all others requiring observation or nonsurgical intervention (Dietze
et al., 1993). Specifically, patients with localized/​axial pain, radiculopathy alone, and even
mild and stable myelopathy should be treated with close observation, physical therapy, or
localized spinal injections/​nerve blocks for pain.
For those patients requiring surgery, a variety of approaches are used depending
on symptomatology, spinal level, disc size, disc location relative to the canal and to
the neural elements, presence of calcification, and overall health status of the patient.
Of note, single-​level laminectomy alone is not an appropriate treatment for HTDs as
the literature has shown that this treatment can cause spinal cord kinking and devas-
tating neurologic consequences, including paralysis (Chen, 2000). Appropriate surgical
options can be divided based on the approach angle and working corridor to the spine
and include dorsolateral/​lateral, ventrolateral, and ventral approaches.

A B

Figure 12.2  CT thoracic spine. Sagittal (A) and axial (B) slices demonstrating large

calcified thoracic disc at T8-​9 level.

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Spinal Neurosurgery

Dorsolateral/​lateral approaches include transpedicular, transfacet pedicle-​ sparing,

costotransversectomy, extracavitary, and parascapular approaches (Aizawa et al., 2007).
The transpedicular approach is most appropriate for lateral soft discs but can also be
used for other soft discs, small lateral calcified discs, and for patients with medical risk
factors (Chen et al., 2012). This approach involves exposure of the facet, drilling of the
caudal pedicle until flush with the body, and usually an ipsilateral hemilaminectomy to
expose the lateral dura. Gentle medial retraction of the thecal sac is usually required to
expose the disc space and the herniated disc. Soft extruded fragments can be mobilized
away from the ventral thecal sac with microinstruments and removed with pituitary
rongeurs. An annulotomy may also be required if the disc is not sequestered. Small
calcified discs may require drilling to achieve adequate decompression of the thecal sac.
Shorter operating time and hospital stay, less blood loss, and earlier return to activity
are advantages of the transpedicular approach when compared to the more invasive
approaches to be discussed later. Given the lack of visualization of the ventral dura and
risks associated with thoracic cord manipulation, the transpedicular approach is limited
for giant discs and central discs, particularly those with intradural extension of the HTD
or those with dense calcifications. Endoscopic technique can help with visualization,
though use of the endoscope can have a steep learning curve. Another disadvantage of
the transpedicular approach is localized back pain, which occurs commonly.
A transfacet pedicle-​sparing approach compares favorably to the transpedicular ap-
proach in terms of back pain (Chen et al., 2012). The positioning and exposure for the
transfacet pedicle-​sparing approach is similar to the transpedicular approach. Instead of
marking the pedicle, the facet is localized using fluoroscopy in relationship to the disc
space. A partial facetectomy is then performed with preservation of the lateral facet. The
rostral nerve root may be seen in the upper thoracic spine, although it is not typically
exposed or seen below the upper thoracic levels. After completion of the bony drilling
and cauterization of the epidural fat, the annulus should be evident. Microdiscectomy is
then performed in the usual fashion.The main disadvantage is that the working corridor is
smaller with less bone removal.This smaller corridor may not be an issue for certain favor-
able disc herniations, but the key is adequate exposure to the disc herniation with minimal
spinal cord manipulation. If this cannot be achieved, then more bone removal is necessary.
The costotransversectomy is a more lateral approach that provides greater access to
the ventral spine at the expense of more invasiveness and surgical morbidity (Stillerman
et al., 1991). The patient is typically placed in the prone position similar to the two
aforementioned approaches. Skin incisions vary and include midline, paramedian, and
semilunar. Depending on the skin incision used, the fascial flap will then be retracted
medially or laterally to expose the posterior spinal elements and the appropriate rib
and rib head. Fluoroscopy is used to confirm the appropriate rib that articulates with
the disc space of interest, realizing that the correct rib level corresponds to the caudal
vertebral body (e.g., T10 rib head articulates at the T9–​T10 disc space). A  laminec-
tomy is performed in the usual fashion. The transverse process is resected with rongeurs.
Approximately 8  cm of rib are partially drilled down. The intercostal nerve is then
identified and traced into the neuroforamen. The caudal pedicle is then resected. The
exiting nerve root is then ligated and divided near its exit from the neuroforamen. The
lateral disc space is entered and disc material is removed, leaving the dorsal aspect of disc
and posterior longitudinal ligament (PLL) intact. Partial corpectomies are drilled above

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Thoracic Disc Herniation

and below the disc space including both endplates and subjacent bone. This maneuver
creates a defect into which the disc can be delivered, away from the spinal cord.The ven-
tral dura can be palpated with a probe or inspected with an endoscope or dental mirrors
to ensure adequate decompression. The main advantages of this approach are greater
visualization and access to the ventral canal compared to more dorsal procedures and less
rib resection compared to more lateral approaches, with possible decreased perioperative
pain. Disadvantages include less visualization when compared to more lateral and ven-
tral approaches, which becomes a problem in the case of discs that are adherent to or
transgress the dura.These cases may be better approached with a ventrolateral technique.
The lateral extracavitary approach is very similar to the costotransversectomy, except
that the entire rib head is removed, allowing for a more lateral approach to the ventral
spinal elements and canal (Maiman et al., 1984). A midline, paramedian, or hockey-​stick
incision can be used, and the surgery proceeds as described for the costotransversectomy.
The rib head is disarticulated at the superior and inferior costal facets, which preserves
anatomic planes and exposes the lateral disc space and the lateral wall of the rostral and
caudal endplates and subjacent bodies. Care should be taken not to violate the parietal
pleura during this maneuver. Partial corpectomies can then be performed as needed to
deliver the disc into the corpectomy defect, away from the cord. Advantages of this ap-
proach over the other dorsal and dorsolateral approaches is that greater visualization of
the ventral dura and disc space lead to less need for spinal cord manipulation and its at-
tendant hazards. On the other hand, it is the most invasive of the dorsolateral approaches
and therefore comes with greater morbidity and pain. It is less invasive than most ventral
approaches though, and it avoids their known pulmonary complications. The primary
disadvantage compared to ventral approaches is relatively less ventral cord visualiza-
tion and relatively more cord manipulation. This is primarily an issue concerning giant
calcified discs, which can be approached by lateral extracavitary or ventral techniques. If
the calcified disc is fused to or transgresses the dura, which is common in this disc type,
adequate decompression from dorsolateral approaches is a significant challenge.
A variation of the lateral extracavitary approach in the upper thoracic spine is called
the lateral parascapular extrapleural approach (Fessler et al., 1991). This approach mobilizes the
rhomboid and trapezius muscles laterally toward the medial border of the scapula. The
caudal fibers of the trapezius are cut and the scapula is rotated laterally to increase exposure.
The remainder of the procedure is carried out similarly to the lateral extracavitary approach.
Advantages of this approach are similar to the lateral extracavitary approach and also include
avoidance of damage to mediastinal structures associated with a ventral approach and avoid-
ance of recurrent laryngeal nerve injury. Disadvantages include shoulder-​and scapular-​
related problems,T1 nerve injury, Horner syndrome, and intercostal neuralgia.
Ventrolateral approaches include transthoracic thoracotomy, transthoracic thoracoscopy, and
retropleural thoracotomy approaches (Stillerman et al., 1998; Vollmer & Simmons, 2000).
The transthoracic thoracotomy is a transpleural approach that provides an excel-
lent anterolateral view of the thoracic spine, particularly of the anterior and middle
columns (Chen et al., 2012). It is used primarily for giant calcified disc herniations,
and it requires special considerations and preoperative planning not typical of pos-
terior spinal approaches. First, it requires intubation with a double-​lumen endotra-
cheal tube for lung deflation and manipulation. Next, patient positioning is in lateral
decubitus, with the up-​side arm resting in an airplane arm rest. During positioning,

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Spinal Neurosurgery

the surgeon must consider that his working station will be at the patient’s abdominal
side working toward the spine and ensure that there is adequate space. In addition,
localization in the thoracic spine from ventral approaches is a particular challenge.
Careful study of the patient’s spine and rib anatomy on preoperative imaging is es-
sential. Preoperative marking of the index level with intrapedicular gold beads or
other radiopaque markers can be quite helpful. A side-​on approach is usually selected
ipsilateral to the side of the disc herniation. For central discs in the upper thoracic
spine, a right-​side approach is typically used to avoid the heart and major vessels that
can be obstructive on the left side. In the mid and lower thoracic spine, a left-​side
approach is used to avoid damage to the vena cava, which is challenging to repair.
A  cardiothoracic approach surgeon for the thoracotomy is recommended but not
required. The rib overlying the disc space is identified, and an incision is made along
the rib from the lateral edge of the paraspinal muscles to the sternocostal margin. The
muscles are incised off the rib, and the level is confirmed once again with fluoroscopy.
The periosteum is dissected from the rib using a Doyen elevator. The proximal and
distal portions of the rib are cut and the edges are waxed. Careful attention should be
paid to any defects in the endothoracic fascia or pleura, which will need to be closed
primarily. Adjacent ribs can be removed as needed for exposure. Next, a rib retractor
is placed, and the parietal pleura is incised in-​line with the rib. The lung is covered
with a moist laparotomy pad, collapsed, and retracted ventromedially. The parietal
pleura overlying the vertebral bodies is then incised and stripped from the vertebral
surface with a Cobb elevator. The sympathetic chain running over the midportion of
the bodies should be preserved, and injury to the segmental vessels should be avoided,
though they may be ligated or clipped if needed. The radiate ligament is incised and
the rib head is drilled to expose the working window. It is of supreme importance
that normal dura is identified above and below the disc herniation in order to define
the extent of the disc herniation and to limit cord manipulation. At a minimum, this
requires drilling down the ipsilateral caudal pedicle to access the ventrolateral canal,
and it may require drilling of the rostral pedicle as well. Partial corpectomies above
and below the disc space are drilled down at the posterior wall, and the remaining
thinned posterior wall is back fractured into this defect with curettes, thus exposing
the ventral canal. The disc herniation can then be dissected away from the thecal sac
with minimal manipulation. Transdural transgression or dural adhesion may require
excision of dura and dural repair. Packing the dural defect with dural substitute and
fibrin glue and backstopping with a sewn pleural patch are usually adequate to pre-
vent dreaded CSF–​pleural fistulae. Typically, spinal stabilization or reconstruction at
the site of the corpectomy is not required as less than 50% of the body is usually
taken. The defects can be packed with the resected rib head removed earlier. To close,
the lung is expanded, a chest tube placed, and the parietal pleura closed. The main
advantage of this approach is the visualization of the ventral dura for resection of
densely calcified or intradural giant HTDs. Disadvantages of this approach are mainly
related to postoperative pain, pulmonary complications, need for a chest tube, the
lack of surgeon familiarity with the anatomy from this view, and the usual need for
an approach surgeon.

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Thoracic Disc Herniation

Transthoracic thoracoscopy is another approach to the ventral canal with the

same approach angle as the transthoracic thoracotomy (Ghostine et al., 2011).
Though also transpleural, work is done through three to four small endoscopic ports,
which minimizes the exposure, pain, and morbidity. It is ideally suited for small disc
herniations, and it is not appropriate for giant calcified discs. Aside from less invasive-
ness, its other advantage compared to the thoracotomy is that an approach surgeon is
not needed. Unfortunately, the main disadvantage of this method is the steep learning
curve and need for costly specialized equipment.
For the retropleural thoracotomy approach, the patient is positioned similar to the
transthoracic thoracotomy approach. The incision is centered more posteriorly than the
transthoracic approach and the proximal 4 cm of rib connected to the vertebral body
is left in place. Once the endothoracic fascia is incised, the parietal pleura is bluntly dis-
sected ventrally. The rib head is removed, and the remainder of the surgery proceeds
similarly to the transthoracic approach. Advantages of this procedure include a shorter
working distance to the spine as the approach is more posterior and lateral to that of
the standard thoracotomy and does not traverse the entire chest cavity, avoidance of
complications associated with entering the pleural space, less soft tissue dissection, easier
mobilization of the diaphragm, and less need for intercostal nerve ligation. The main
disadvantage is that the view of the ventral thecal sac is more tangential compared to the
thoracotomy and the muscle dissection and retraction needed for exposure.
Ventral approaches include transsternal and manubrial window (Chen et al., 2012).
The ventral approaches are typically reserved for HTDs from T2–​T4 that cannot be
approached from one of the lateral or dorsal approaches. High thoracic disc herniations are
rare, and ventral approaches to the spine are associated with significant risks. Fortunately,
most of these discs can be accessed using one of the aforementioned approaches. When
needed, these approaches typically require an approach surgeon.
Minimally invasive approaches include transpedicular, extracavitary, and transthoracic
approaches. These procedures involve tubular retractor systems and endoscope (Sheikh
et al., 2007). The main limitation of these procedures is the additional equipment and
steep learning curve.

Surgical Procedure

For the patient described in this case presentation, an open dorsolateral extracavitary ap-
proach was selected to address the giant central calcified disc herniation at T8–​T9. More
specifically, a T8–​T9 costotransversectomy, T8–​T9 partial corpectomies, and T7–​T10
laminectomies were performed.The patient underwent general endotracheal anaesthesia
and Foley catheter placement and was positioned prone on an open Jackson table. MEPs,
SSEPs, and electromyography (EMG) were used during the procedure, and the mean
arterial blood pressure was sustained at 85 mm Hg. A midline incision spanning T7 to
T10 was marked using the C-​arm. A standard subperiosteal takedown of the paraspinal
muscles was performed exposing the T7 to T10 laminae. The rib head attachments were
exposed bilaterally for anatomical orientation.
Pedicle screws were then placed at T7 and T10 in the standard fashion using a high-​
speed drill, a pedicle finder, a ball-​tipped probe, a tap, and finally the screws measuring

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5.5 × 45 mm at T7 and T10 bilaterally.Anteroposterior (AP) and lateral fluoroscopic shots
of the fusion were obtained demonstrating correct positioning of the instrumentation.
Laminectomies were performed from T7–​T10 bilaterally. This was extended laterally
to the left, exposing the T8 and T9 pedicles.The left T8 nerve root was identified, ligated
with 4-​0 Nurolon, injected with 1 cc of lidocaine and then sharply transected. The li-
gature was then used for gentle retraction and rotation of the thecal sac. The T8 and T9
rib heads were then exposed laterally and transected with Leksell rongeurs, exposing
the thoracic pleura at this level. The T8 pedicle was then partially removed by drilling
it with a matchstick burr, and the T9 pedicle was removed in its entirety. At this point,
the microscope was brought into the field for microdissection. Gentle retraction was
then applied to the thoracic cord, and its lateral ventral aspect was exposed. The bone
window was further expanded by drilling the T8 and T9 vertebral bodies and removing
the intervertebral disc at T8–​T9. This was a partial corpectomy yielding one-​third re-
moval of each vertebral body and creating an anterior bone window into which the os-
teophyte could be collapsed. The osteophyte was then carefully dissected away from the
dura using microsurgical technique and gradually pushed inferiorly and laterally with
curettes. The mass showed dense calcification and ossification and was densely adherent
to the dura. At this point in the case, there was significant improvement in bilateral lower
extremity SSEPs on neuromonitoring. The remainder of the dissection was carried out,
and the calcified disc was removed in its entirety.
Posterolateral instrumentation was then completed with placement of pedicle screws
on the right at T8 and T9 followed by contouring and placement of titanium rods, screw
caps, and crosslink (Figure 12.3). Thorough irrigation, decortication, laying down bone
substitute and graft, and drain placement were then performed. Multilayer wound clo-
sure was completed, and the patient was transferred to PACU.

A B

Figure 12.3  Sagittal (A) and axial (B) images of post-​operative CT of thoracic

spine status post T7-​T10 posterior instrumentation and T8-​9 costotransversectomy.
Pedicle screws were placed from T7-​10 on the right. No screws were placed at T8 or
T9 on the left where the costotransversectomy was performed. The calcified HTD
has been removed in its entirety and troughs (partial corpectomies) were performed
at the caudal posterior edge of T8 and rostral posterior edge of T9 to assist in ventral
depression of the HTD away from the dura.

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Thoracic Disc Herniation

The most important decision regarding this case is which technique is best to ac-
cess a giant central calcified disc. As mentioned earlier, giant central calcified discs are
best approached by lateral extracavitary approaches, as done here, or by thoracotomy/​
retropleural thoracotomy. There are pros and cons to each, and, with equipoise, the de-
cision should be based on surgeon comfort and experience.

Oral Boards Review: Management Pearls

1. There are multiple reasonable approaches to address thoracic disc herniations,

and the selection is driven largely by the morphology and location of the disc
with respect to the canal and the neural elements.
2. The overarching surgical principle in all cases is to perform the least invasive
procedure that allows adequate visualization and, most importantly, requires
the least degree of spinal cord manipulation.

Aftercare

Postoperative care for surgery on an HTD depends on the technique used, patient’s
comorbidities, intraoperative complications, and blood loss. Typically, patients
can be monitored on a floor or step-​down unit. The exception for this are those
with intraoperative complications such as those with significant decreases in the
neuromonitoring parameters, those patients with significant blood loss, patients with a
chest tube, and, last, those with significant cardiac or pulmonary comorbidities.

Complications and Management

Benzel compared a review of 13 contemporary series of HTD surgeries with Stillerman

et  al.’s series and found the following (Chen et al., 2012; McCormick et al., 2000).
Stillerman et al. (1998) reported a major complication rate of 3.6% while the review
noted a rate of 6.1%. No deaths were reported in the review group. Minor complications
were found to be 11% by Stillerman et al. and 8.7% in the review group, with a total
complication rate of 14.6% and 14.8%, respectively.There were no significant difference
when comparing the series and the review group. As reported by Stillerman et al., the
most common complications were superficial wound infection and pneumonia. Loss of
spinal integrity and new transient and new permanent weakness each occurred at a rate
of less than 2%.

Evidence and Outcomes

Based on a study by Stillerman et al. (1998), the authors created a management algo-
rithm for HTD that divides patients into three groups based on symptoms: localized/​
axial pain, radiculopathy, and myelopathy.Treatment arms exist for each group, which are
further divided based on medical risks, location of the HTD, and degree of calcification.
This can be seen in Figure 12.4. Advances in the management of HTD are continually
being made with less invasive approaches and with the emergence of computer navi-
gation and robotic technology that are allowing improved visualization and navigation.

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Spinal Neurosurgery

Localized/T-L Myelopathy Radiculopathy

spinal pain

Improving Static Progressive deterioration

No functional impairment Severe myelopathy

Pain tolerable and pain
Conservative Conservative
treatment treatment

Intractable symptoms

Consider surgery

High medical risk Low medical risk

Densely calcified All except densely Centrolateral disc Lateral disc

centrolateral disc calcified centrolateral disc

Static Progressive Densely

myelopathy deterioration Soft Mildly calcified calcified

Conservative
treatment

Refractory
symptoms

• Dorsolateral
• Lateral
• Thorascopic (thoracotomy) • Dorsolateral (anterolateral) • Lateral
• Retropleural • Dorsolateral (thoracoscopy?) • Anterior • Ventrolateral • Dorsolateral

Figure 12.4  Management algorithm for treating symptomatic HTD’s. Printed with permission from Stillerman CB.

References

Aizawa T, Sato T, Sasaki H, et al.: Results of surgical treatment for thoracic myelopathy: minimum

2-​year follow-​up study in 132 patients. J Neurosurg Spine. 7:13–​20 2007.
Awwad EE, Martin DS, Smith KR, et  al.:  Asymptomatic versus symptomatic herniated tho-
racic discs:  their frequency and characteristics as detected by computed tomography after
myelography. Neurosurgery. 28:180–​186 1991.
Blumenkopf B: Thoracic intervertebral disc herniations: Diagnostic value of magnetic resonance
imaging. Neurosurgery. 23:36–​40 1988.
Botelho R, De Oliveira M, Kuntz C: “Chapter 280: Differential Diagnosis of Spinal Disease.”
Neurological Surgery, edited by Youmans and Winn, 7th ed., Elsevier/Sauders, 2017,
pp. 2322–2336.

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Thoracic Disc Herniation

Brown CW, Deffer PA, Akmakjian J, et al.: The natural history of thoracic disc herniation. Spine
(Phila Pa 1976). 17:S97–​S102 1992.
Chen TC:  Surgical outcome for thoracic disc surgery in the postlaminectomy era. Neurosurg
Focus. 9 (4):e12 2000.
Chen,Thomas C, et al. “Chapter 77: Thoracic Discectomy.” Spine Surgery: Techniques, Complication
Avoidance, and Management, edited by Edward C. Benzel and Todd B. Francis, 3rd ed.,
Elsevier/​Saunders, 2012, pp. 741–​756.
Deshaies E, Eddleman C: “Chapter 20: Spinal Arteriovenous Malformations.” Handbook of
Neuroendovascular Surgery, edited by A Boulos, 1st ed.,Thieme, 2011. doi:10.1055/b-002-85450.
Dietze DD, Fessler RG: Thoracic disc herniations. Neurosurg Clin N Am. 4:75–​90 1993.
Fessler R: “Chapter 61: Thoracic Epidural Abscess.” Atlas of Neurosurgical Techniques, edited by
L Sekhar, 1st ed., Thieme, 2006. doi:10.1055/b-006-149694.
Fessler RG, Dietze DD, MacMillan M, et al.: Lateral parascapular extrapleural approach to the
upper thoracic spine. J Neurosurg. 75:349–​355 1991.
Ghostine, Samer, et  al. “Chapter  283:  Treatment of Thoracic Disk Herniation.” Youmans
Neurological Surgery, edited by Julian R. Youmans and H. Richard Winn, 6th ed., vol. 3,
Elsevier/​Saunders,  2011.
Maiman DJ, Larson SJ, Luck E, El-​Ghatit A: Lateral extracavitary approach to the spine for
thoracic disc herniation: report of 23 cases. Neurosurgery. 14:178–​182 1984.
McCormick WE, Will SF, Benzel EC:  Surgery for thoracic disc disease. Complication avoid-
ance: overview and management. Neurosurg Focus. 9(4):13 2000.
Santiago P, Fine AD, Shafron D, et al.: Benign extradural lesions of the dorsal spine. Winn RH
Youmans Neurological Surgery. 5th ed., 2004. Saunders Philadelphia 4491–​4506.
Sartor K, ed. “Demyelinating and Degenerative Diseases of the Spinal Cord.” Diagnostic and
Interventional Neuroradiology, 1st ed., Thieme, 2002. doi:10.1055/b-002-52047.
Sheikh H, Samartizis D, Perez-​Cruet MJ: Techniques for the operative management of thoracic
disc herniation:  minimally invasive thoracic microdiscectomy. Orthop Clin North Am.38
(3):351–​361  2007.
Stillerman CB, Chen TC, Couldwell WT, et  al.:  Surgical experience in the operative
management of 82 symptomatic herniated thoracic discs and review of the literature.
J Neurosurg. 88:623–​633 1998.
Stillerman CB,Weiss MH: Management of thoracic disc disease. Clin Neurosurg. 38:325–​352  1991.
Vialle, L, ed. “Evaluation and Decision Making.” AOSpine Masters Series,Volume 2: Primary Spinal
Tumors, 1st ed., Thieme, 2014. doi:10.1055/b-002-98011.
Vollmer DG, Simmons NE:  Transthoracic approaches to thoracic disc herniations. Neurosurg
Focus. 9 (4):E8 2000.
Williams MP, Cherryman GR:  Thoracic disk herniation:  MR imaging. Radiology.
167:874–​875  1988.

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Thoracolumbar Burst Fractures

Omaditya Khanna, Geoffrey P. Stricsek, and James S. Harrop

Case Presentation

A 32-​year-​old man presents to the emergency room after sustaining a fall from four
13
stories while attempting to escape a building during a fire.The patient reports he landed
on his feet and then fell backward onto his buttocks. He states that he hit his head, but
denies any loss of consciousness. Emergency medical services (EMS) immobilizes the
patient using a rigid cervical collar and backboard in the field prior to transport to the
emergency room.

Questions

1. What is involved in the initial evaluation of patients presenting with acute

trauma?
2. What imaging studies are indicated?
3. What are the various classification systems of thoracolumbar burst fractures?

Assessment and Planning

The initial evaluation of the trauma patient is conducted using the advanced trauma life
support (ATLS) ABCDE framework (Airway, Breathing, Circulation, Deficit, Exposure).
This provides a standardized pathway for identifying injuries and establishing treatment
priorities to guide resuscitation efforts. All suspected spinal trauma patients should remain
in a rigid cervical collar until a thorough neurological evaluation and appropriate imaging
can be performed, even in the absence of any overt reported focal neurologic deficits.
The primary survey for the patient identifies the following:  despite having facial
abrasions and a gross deformity of his nose, his airway and breathing are intact, evidenced
by fluent, nonlabored conversation and unremarkable chest auscultation. His cardiovas-
cular system is also stable with a blood pressure of 112/​82 mm Hg and heart rate of
88 bpm. On neurological exam, the patient is found to have full strength in his bilat-
eral upper and lower extremities; he notes ankle pain while assessing dorsiflexion and
plantar-​flexion, but there is no weakness. He describes numbness and tingling spreading
into the right leg, but sensation to light touch is intact and symmetric between all
extremities. Biceps, Achilles, and patellar reflexes are all 1+ and symmetric; there is no
clonus or Hoffman sign; he has a negative Babinski bilaterally. There is tenderness to
palpation over his low thoracic and upper lumbar spine. His rectal examination reveals
normal tone, sensation, and volitional push.

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Spinal Neurosurgery

Following completion of the primary survey, the patient had imaging obtained in-
cluding a computed tomography (CT) scan of the brain and cervical, thoracic, and lumbar
spine, given that he hit his head during the fall and also had severe back pain. CT imaging
of the thoracic and lumbar spine was significant for a T12 spinous process fracture and a
sagittally oriented fracture through the L1 vertebral body with fracture of the L1 lamina,
as well as a burst fracture of the L2 vertebral body with retropulsion of fragments into the
spinal canal and an L2 laminar fracture. Magnetic resonance imaging (MRI) was obtained
after CT evidence of lumbar fracture. MRI demonstrated compression of the thecal sac
and the conus medullaris at L1–​L2 secondary to the bony retropulsion; there was asso-
ciated epidural blood surrounding the thecal sac. MRI also showed a signal abnormality
at T12–​L1 extending from the intradural to the extradural space, which could represent
dural laceration (Figure 13.1). CT scans of the brain and cervical spine were unremarkable.

Figure 13.1  Sagittal (A) and axial (B) computed tomography (CT) scans demonstrate

a burst fracture of the L2 vertebral body with retropulsion of bony fragments into
the spinal canal. T2-​weighted magnetic resonance image (MRI) (C) demonstrates
compression of the thecal sac and the conus medullaris at L1–​L2 and disruption of the
posterior ligamentous complex secondary to the bony retropulsion, associated with
epidural blood surrounding the thecal sac. The patient underwent posterior pedicle
screw fusion from T11 through L4 (C) on hospital day 1.

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Thoracolumbar Burst Fractures

Fractures in the thoracic and lumbar spine are more common than in the cervical
spine. The majority of thoracolumbar spine fractures occur in the transition zone be-
tween the lower thoracic and upper lumbar spine (between T11 and L2), accounting for
approximately 20% of all spine fractures. This region is particularly susceptible to injury
owing to the fact that it is a junction between the fixed, kyphotic thoracic spine and the
more mobile lordotic lumbar spine, causing a concentration of stress forces upon the
ventral thoracolumbar vertebral column. The majority of thoracolumbar fractures are
caused by high-​energy mechanisms, which could result in concomitant injuries to other
nearby organ and soft tissues.
Ten to twenty percent of all thoracolumbar spine fractures are burst fractures. Burst
fractures are typically a result of an axial-​loading mechanism, such as from jumping or
a fall from height. Axial load injuries can also result in both thoracolumbar and calca-
neal fractures. On imaging, burst fractures are characterized by fracture of the vertebral
body with retropulsion of fractured vertebral body fragments into the spinal canal. The
displacement of bony fragments into the vertebral canal can cause significant neurologic
compromise. As such, it is imperative to promptly recognize these injuries in order to
guide further management.
There are several systems in place to evaluate thoracolumbar fracture:  the Denis
three-​column concept, the Arbeitsgemeinschaft für Osteosynthesefragen (AO) Spine
thoracolumbar classification, and the Thoracolumbar Injury Classification and Severity
(TLICS) Scale. Denis, in 1984, proposed a three-​column classification scheme to de-
scribe the thoracolumbar spine. The first column extends from the anterior longitu-
dinal ligament (ALL) to the midpoint of the vertebral body; the second column is from
the midpoint of the vertebral body to the posterior longitudinal ligament (PLL); and
the third column spreads from the PLL through the posterior elements, including the
pedicles and facet joints. The AO Spine thoracolumbar classification system, proposed
in 2013, would assign the patient an A4 fracture of the L1 and L2 vertebral bodies,
since both levels have disruption of the superior and inferior endplates, as well as the
posterior wall of the vertebral body. Additionally, edema in the L1–​L2 interspinous lig-
ament and the T12 spinous process fracture suggests disruption of the posterior tension
band, which would further classify this injury as B2 with an N0 modifier given that
he was neurologically intact. In 2005, the Spine Trauma Study Group proposed a novel
grading criteria for evaluation of thoracolumbar fractures: the Thoracolumbar Injury
Classification and Severity Score (TLICS). Injuries are defined according to insult
morphology (compression: 1 point; burst: 2 points; translational/​rotational: 3 points;
distraction: 4 points), patient’s neurologic status (intact: 0 points; nerve root injury: 2
points; cord or conus medullaris incomplete injury: 2 points; cord or conus medullaris
complete injury: 3 points; cauda equina syndrome: 3 points), and integrity of the pos-
terior ligamentous complex (intact: 0 points; injury suspected/​indeterminate: 2 points;
injured: 3 points). Under the TLICS classification scheme, a summation of point values
from the categories of 3 or less can be treated with nonoperative management, scores
of 4 may be treated either operatively or nonoperatively, and a cumulative score of 5
or above usually warrants surgical decompression and stabilization. This patient has a
TLICS score of 5 (2 points for burst morphology and 3 points for posterior ligamen-
tous complex injury).

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Oral Boards Review: Diagnostic Pearls

1. The initial imaging evaluation of patients with suspected spine fractures

can include anteroposterior (AP) and lateral x-​rays. Plain films are useful in
assessing for loss of vertebral body height, pedicle fractures, and malalignment
of the spine.
2. CT imaging provides a more comprehensive evaluation of bony anatomy by
providing coronal, sagittal, and axial plane reformatted images. In the presence
of a known vertebral body fracture, the entire spinal axis should be imaged
due to the high prevalence (5–​20%) of noncontiguous fractures.
3. MRI aids in the physician’s ability to visualize the spinous ligaments, sur-
rounding soft tissues, intervertebral discs, and the underlying neural elements.
MRI is especially important for evaluation of thoracolumbar pathology be-
cause of the variable level of the conus medullaris.
4. The AOSpine Thoracolumbar Classification System:
Type A (Compression injuries)
A0: Minor, nonstructural fractures
A1: Wedge compression
A2: Split fracture
A3: Incomplete burst
A4: Complete burst
5. TLICSS:
a. Morphology:
i. Compression (1 point)
ii. Burst (2 points)
iii. Translational/​rotational (3 points)
iv. Distraction (4 points)
b. Neurological status:
i. Intact (0 points)
ii. Nerve root or cord/​conus (complete) (2 points)
iii. Cord/​conus (incomplete) or cauda equina (3 points)
c. Posterior ligamentous complex:
i. Intact (0 points)
ii. Suspected injury/​indeterminate (2 points)
iii. Injured (3 points)
6. The summation of the preceding categories helps guide management:
a. Less than 4: Usually treated nonoperatively
b. Equal to 4: May be treated operatively or nonoperatively
c. More than 4: Usually considered for operative management

Decision-​Making

Management of thoracolumbar burst fractures is based on neurological and structural

considerations. Unless there are severe medical comorbidities precluding surgery, any pa-
tient with a neurological deficit in the presence of a burst fracture should be considered

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Thoracolumbar Burst Fractures

to undergo surgery for decompression of neurological elements. For patients without

neurological deficit, mechanical stability of the spine should be evaluated to deter-
mine the need for surgical intervention. According to both the Denis’s classification
and TLICS criteria, the patient’s injuries should be treated surgically if unstable. While
some surgeons advocate intervention when burst fractures cause greater than 50% cen-
tral canal narrowing, neurological recovery from burst fractures is not predicted by the
amount of canal narrowing, and this should not be used as an indication for surgery in
isolation.
Surgical approaches for the treatment of thoracolumbar burst fractures include an-
terior, posterior, and lateral. For each approach, further options are available, including
direct versus indirect compression, open versus percutaneous instrumentation, and
short-​versus long-​segment constructs. A  review of prospectively collected data from
733 patients receiving care at German and Austrian hospitals suggests that the combined
anterior-​posterior approach is the most commonly used at the thoracolumbar junction
(47.3%), followed closely by a posterior alone (47%), and, infrequently, a stand-​alone
anterior approach (5.7%).
The choice of whether to pursue an anterior versus posterior approach depends
on many factors, including the site of the pathology, degree of mechanical instability
and kyphosis, the presence of other concomitant injuries incurred, and, last, surgeon
preference. An anterior approach allows the surgeon to both effectively decompress
the neural elements via removal retropulsed bone fragments and simultaneously re-
construct anterior and middle column support in patients with significant kyphotic
deformity. However, adequate exposure of impacted vertebral bodies can be a chal-
lenge, particularly in the posttrauma setting and requires an experienced surgeon. In
addition, in the acute setting, there can be a tremendous amount of bleeding from
anterior epidural veins. From a posterior approach, decompression of the spinal cord
is achieved by laminectomy or by the unilateral removal of the pedicle and facet joints,
which allows reduction of fracture fragments. Dorsal decompression via laminectomy
(without reduction or stabilization) alone has been shown to be an ineffective treat-
ment strategy.
Regardless of whether decompression is achieved via an anterior or posterior
approach, segmental instrumentation is recommended for treatment of mechanical
instability. The load-​sharing classification developed by McCormack can be used
to help decide the number of levels requiring instrumentation and fusion. In the
thoracolumbar junction, fractures tend to be more kyphogenic, which increases the
corrective bending strain placed upon each pedicle screw. When looking at load-​
sharing, three characteristics are assessed, each on a three-​point scale: vertebral body
comminution, fragment apposition, and the amount of kyphotic deformity correc-
tion. Fractures with load-​sharing classification (LSC) scores of 6 or less have been
successfully treated via short-​segment instrumented fusion at two levels above and
two levels below. LSC scores of 7 or more suggest poor load transfer through the
vertebral body and often necessitates anterior instrumentation for restoration of
alignment.
In neurologically intact patients who do not have overt mechanical instability,
nonoperative treatment is a viable management option. Tezer et  al. suggested that
nonoperative treatment is appropriate when the PLL complex is intact, evidenced by

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Spinal Neurosurgery

anterior vertebral body height of greater than 50% of the posterior height and kyphotic
angulation of less than 30 degrees.

Questions

1. What are the treatment options for patients with thoracolumbar burst
fractures?
2. What are the surgical indications for thoracolumbar burst fractures?
3. What are the various factors to take into consideration when determining
whether to pursue an anterior versus posterior versus combined/​staged
anterior-​posterior surgical approach (see Table 13.1)?

Surgical Procedure

This patient underwent a posterior thoracolumbar decompression and fusion for

the treatment of his L1 and L2 burst fractures. Following induction of general an-
esthesia, a prepositioning baseline neurophysiological recording was obtained; the
patient had monitorable signals, as was expected given his intact neurological exam.
Iliac crest and chest pressure points were padded, and he was positioned prone on
an open Jackson frame with his hips extended. Postpositioning neurophysiolog-
ical monitoring confirmed there was no change in signals following the flip from
supine to prone. Exposure with subperiosteal dissection was performed to expose
from T11 to L4; the patient had a LSC score of 6 and it was decided to go two levels
up and two levels down from his index levels. Pedicle screws were placed at T11,
T12, L1, L3, and L4; the pedicles at L2 were not cannulated due to the extensive
nature of the fracture. Laminectomies were performed at L1 and L2. A rod and caps
were placed into the left-​sided instrumentation, and then the right L2 pedicle was
removed so that fracture fragments from the L2 vertebral body could be tamped
forward out of the spinal canal. The right-​sided rod was placed and secured with
caps; AP and lateral x-​rays were obtained to confirm hardware trajectories and
alignment; a surgical drain was placed, and the incision was subsequently closed.

Aftercare

A postoperative neurological evaluation should be performed shortly after the patient

returns to the recovery room. If the patient develops a delayed postoperative neurolog-
ical deficit, CT or MRI is indicated to evaluate for epidural or subdural hematomas,
nerve entrapment, or failure of instrumentation. Intermittent pneumatic compression

Table 13.1.
Indications for surgical intervention in patients presenting with thoracolumbar
burst fractures
1. Anterior vertebral body height <50% of posterior height
2. Kyphotic angulation >20 degrees
3. Incomplete/​progressive neurologic injury
4. Spinal canal narrowing >50% (*relative indication)
5. Multiple noncontiguous spinal fractures

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Thoracolumbar Burst Fractures

devices should be continued in the immediate postoperative period, prophylactic

anticoagulation should be started on postoperative day 1, and perioperative antibiosis is
administered for 24 hours. Adequate pain control is also a point of emphasis in order to
facilitate early mobilization and disposition planning.
In both patients who have been managed conservatively or treated surgically, serial
evaluation with AP and lateral flexion-​extension x-​rays for 4–​12 months is indicated to
assess for any progressive kyphosis or other deformity. In patients who develop progres-
sive neurologic deficits or who develop mechanical instability, surgical intervention may
be necessary.

Complications and Management

Possible complications in the thoracolumbar burst patient are similar to those in the
elective patient population. Postoperative neurological deficit should be thoroughly
investigated for reversible causes, which includes CT imaging to evaluate instrumenta-
tion placement and spinal alignment as well as MRI to assess spinal canal integrity and
epidural hematoma formation. The surgeon should be prepared for the need to repair a
traumatic dural laceration in the thoracolumbar burst patient including possible lumbar
drain placement. Suspicion for cerebrospinal fluid leak may also guide preoperative deci-
sion making: if there is high clinical concern in the setting of a thoracic or high lumbar
burst fracture, it may be advantageous to avoid a lateral approach given the need for chest
tube placement.
Medical complications can also disrupt the recovery in patients with thoraco-
lumbar burst fractures. Deep venous thrombosis (DVT) is also a concern in this
population given their decreased mobility secondary to pain, neurological deficit, or
bed rest for dural healing. Vigilant prophylaxis is the best defense against DVT, but,
in the patient where is arises, inferior vena cava filter should be considered to reduce
the risk of pulmonary embolism if therapeutic anticoagulation is not a manage-
ment option. Prolonged intubation and reduced ambulation also increase the risk of
pneumonia; patients should have regular chest physiotherapy, and clinicians should
have a low threshold for chest radiography if symptoms develop.

Oral Boards Review: Complications Pearls

1. Patients who are treated via conservative measures (brace, pain control, phys-
ical therapy) should be followed every few months in order to assess for any
developing kyphosis or other deformity.
2. In patients who present neurologically intact and are treated via conservative
measures, the rate of neurological worsening lies between 0% and 20%.
3. In patients who develop progressive neurologic deficits, mechanical instability,
or worsening intractable back pain, prompt surgical intervention is necessary.

Evidence and Outcomes

The development of novel instrumentation techniques has improved the efficacy of

surgical treatment of thoracolumbar burst fractures. However, there is no universal

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Spinal Neurosurgery

agreement in regards to the timing of surgery, extent of stabilization, or the preferred

surgical approach that should be employed for the correction of deformity or decom-
pression of neural elements.
In a study by Mumford et al. evaluating the efficacy of nonoperative management
of thoracolumbar burst fractures, 41 neurologically intact patients treated conservatively
were followed for more than 2 years. The study found that 49% of patients reported
excellent outcomes relative to pain and function at 2-​year follow-​up. Only one patient
developed neurologic deterioration that prompted surgical intervention. Several other
studies have corroborated the role of nonoperative treatment in neurologically intact
patients.
The TLICS score was proposed to aid surgeons in the decision-​making process
for treating thoracolumbar burst fractures. Since its development, several studies have
evaluated the TLICS’s reliability and validity in assessing and guiding treatment of thora-
columbar injuries. A study of 71 cases of thoracolumbar fractures graded independently
by five separate spine surgeons found a 97% rate of agreement on the management.
Other studies have validated the intraobserver reliability in grading of thoracolumbar
fractures, which suggests it is a grading scale that can be readily taught and utilized to
guide treatment.
However, there have been scant prospective randomized studies that have investigated
outcomes in surgically versus nonsurgically treated patients who present neurologically
intact. In a study by Wood et al., 47 neurologically intact patients with thoracolumbar
burst fractures were randomized into surgical versus nonsurgical treatment; operative
treatment provided no major long-​term advantage compared with nonoperative treat-
ment and was associated with a higher risk of complications.
Several studies have corroborated the use of short-​segment posterior fixation for
the treatment of thoracolumbar burst fractures. Parker et  al. showed that fractures
with LSC scores of 6 or less can be treated via instrumented fusion with four screws
at the level above and below, allowing sufficient mechanical stability in the interim
while the bony fracture heals. In a study by Pellise et al., 86 patients with a mean
LSC score of 6.3 who were treated with a six-​screw construct (one level above, one
below, and one at the level of the fracture) were followed for more than 2  years
postoperatively. The study revealed that short-​segment posterior fixation, including
instrumentation insertion at the level of the fracture, was a viable treatment option
that adequately restored alignment; none of the patients required repeat surgical in-
tervention for postoperative complications. In a study by Park et al. in 2016, there
was no difference in the long-​term outcomes in 45 patients with LSC scores of 7
or 8 treated with posterior short-​segment fixation at two versus three levels, thereby
possibly obviating the need for anterior reconstruction.

References and Further Reading

Denis F. The three column spine and its significance in the classification of acute thoracolumbar
spinal injuries. Spine. 1983;8(8):817–​831.
Kaneda K, Abumi K, Jujiya M. Burst fractures with neurologic deficits of the thoracolumbar-​
lumbar spine. Results of anterior decompression and stabilization with anterior instrumen-
tation. Spine. 1984;9:788–​795.

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Knight RQ, Stornelli DP, Chan DP, Devanny JR, Jackson KV. Comparison of operative versus
nonoperative treatment of lumbar burst fractures. Clin Orthop. 1993;293:112–​121.
Muller U, Berlemann U, Sledge J et al. Treatment of thoracolumbar burst fractures without neu-
rological deficits by indirect reduction and posterior instrumentation: Bisegmental stabiliza-
tion with monosegmental fusion. Eur Spine J. 1999;8:284–​289.
Parker J, Lane JR, Karaikovic EE, Gaines RW. Successful short-​segment instrumentation
and fusion for thoracolumbar spine fractures. A  consecutive 4 1⁄2  years series. Spine.
2000;25:1157–​1169.
Patel AA, Dailey A, Brodke DS, et al. Spine trauma study group. Thoracolumbar spine trauma
classification:  The thoracolumbar injury classification and severity score system and case
examples. J Neurosurg Spine. 2009;10(3):201–​206.
Reinhold M, Knop C, Beisse R, et al. Operative treatment of 733 patients with acute thoraco-
lumbar spinal injuries: Comprehensive results from the second, prospective, internet-​based
multicenter study of the Spine Study Group of the German Association of Trauma Surgery.
Eur Spine J. 2010;19:1657–​1676.
Verlaan et  al. Surgical treatment of traumatic fractures of the thoracic and lumbar spine:
A systematic review of the literature on techniques, complications and outcome. Spine.
2004;29(7).
Wood K, Buttermann G, Mehbod A, et al. Operative compared with nonoperative treatment of a
thoracolumbar burst fracture without neurological deficit. A prospective, randomized study.
J Bone Joint Surg Am. 2003;85A(5):773–​781.

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Thoracic Cord Compression

Extradural Tumor

Tej D. Azad, Anand Veeravagu, John K. Ratliff, and Atman Desai

14
Case Presentation

A 69-​ year-​
old man presents to an outside facility with concerns of an enlarging
pigmented lesion on the bottom of his right foot. Punch biopsy reveals melanoma in
situ, which is excised. Three years later, the patient develops new-​onset upper back pain
and is referred to neurosurgery.
The pain is reported as worst in the morning and relieved when in the supine po-
sition. The patient reports 7/​10 pain that localizes to the right shoulder blade, does not
radiate, and worsens with upper arm movement. The patient denies any urinary incon-
tinence, numbness, tingling, or weakness of the lower extremities. The patient has not
fallen but endorses unsteady gait. No upper or lower extremity deficits in strength were
elicited. Pin prick and light touch are normal in all extremities. Reflexes are 2+ and
symmetric bilaterally. No clonus is elicited, and a negative Hoffman sign is observed.

Questions

1. What is the most likely diagnosis?

2. What imaging modalities should be utilized?
3. What is the most likely etiology of the patient’s pain?

Assessment and Planning

The differential diagnosis for this presentation, shoulder pain with possible radiculopathy
and mild myelopathy, includes musculoskeletal pathologies such as muscle spasm, rotator
cuff injury, disc herniation, and spinal stenosis. Lesions such as metastases, primary spinal
neoplasms, and vascular malformations need to be considered as well. Primary malignant
spinal tumors include chondrosarcoma, chordoma, osteosarcoma, and Ewing’s sarcoma,
while primary benign spinal neoplasms include osteoid osteoma, osteoblastoma, aneu-
rysmal bone cyst, hemangioma, meningioma, schwannoma, and neurofibroma. Treatment
is surgical, except for Ewing’s sarcoma, which is often chemosensitive. However, 90% of
extradural spinal tumors are metastatic, and primary tumors necessitate a unique set of
management considerations; therefore, this discussion will focus on metastatic neoplasms.
Given the patient’s oncologic history, the neurosurgeon maintains a high degree of
suspicion for metastatic melanoma. Spinal metastases occur in 1 out of 5 cancer patients
and 5–​10% of patients with cancer develop spinal cord compression.1 Breast, prostate, and

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lung cancer are the most common primary tumors that are metastatic to the spine.2 Pain
is the most common presentation of symptomatic spinal metastasis, reported in 83–​95% of
patients,3 followed by motor dysfunction, sensory complaints, and urinary incontinence.4
Spinal instability pain in the thoracic spine can be elicited with extension. Upon extension,
the patient will likely report constant pain while unstable kyphosis is straightened.

Oral Boards Review: Diagnostic Pearls

1. A detailed history and neurological examination are essential to under-

standing the clinical presentation of a patient with a spinal metastasis.
2. Neurological symptoms such as weakness, numbness, paraesthesias, imbalance,
and urinary incontinence are suggestive of symptomatic spinal cord compres-
sion, as are objective motor and sensory deficits and abnormal reflexes and
gait on clinical examination.
3. Pain worsened with movement and improved with recumbency is suggestive
of a mechanical pain generator. This may be in the form of a compromised
intervertebral disc, facet complex, or progressive spinal deformity induced by
a pathological lesion.
4. A known history of a radiation-​sensitive tumor such as myeloma or small cell
lung carcinoma may obviate the need for surgery.
5. Imaging should ideally include magnetic resonance imaging (MRI) predom-
inantly for evaluation of the tumor and its relationship to the spinal cord and
nerve roots. Computed tomography (CT) scan may give additional informa-
tion including evaluation of bony lysis and involvement of anterior and pos-
terior bony elements. Bony lysis, junctional location, vertebral body loss of
height, and kyphotic deformity are all suggestive of spinal instability.

MRI is the gold standard diagnostic imaging modality for assessment of a thoracic epi-
dural tumor with spinal cord compression.5 The primary advantage of MRI, compared
to other imaging modalities, is that MRI is noninvasive and provides precise spatial and
contrast resolution, imperative for surgical planning. Moreover, MRI demonstrates sig-
nificant utility in elucidating soft tissue structures, tumor margins, and neural elements.
First, sagittal images of the entire spinal axis should be obtained to identify areas of met-
astatic involvement. Kyphotic pathology involving regions of transition, specifically the
cervicothoracic and thoracolumbar segments, may function as a lever arm and therefore
may induce more significant global sagittal malalignment. More focused studies, in-
cluding alternative views, can then be obtained for further evaluation. Sagittal T2-​and
T1-​weighted images, with and without intravenous contrast, are obtained. Axial images,
both T2-​and T1-​weighted, can then be obtained to extend the preliminary assessment
and provide details about adjacent structures and landmarks.
A useful adjunct to MRI, CT details bony anatomy and extent of bony tumor in-
volvement.This modality can be valuable distinguishing between cord compression sec-
ondary to tumor extension into the spinal canal and bony canal compromise.When used
in combination with myelography, CT elucidates the bony anatomy and may provide
significant insight into spinal reconstruction planning. A combination of MRI for tumor

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Figure 14.1  Preoperative sagittal T1 and postoperative T2 magnetic resonance images

(A) reveal T3 spinal cord compression.

and soft tissue evaluation and CT for defining the osseous anatomy is the most effective
method of assessing patients with extradural tumor and thoracic cord compression.
In the present case, MRI demonstrated a destructive lesion of the T3 vertebral body
and right pedicle, causing significant deformity and spinal compression, with no facet
involvement (Figure 14.1).

Questions

1. How do these clinical and radiological findings influence surgical planning?

2. What is the most appropriate timing for intervention in this patient?
3. How does the likely diagnosis and pathology of metastatic melanoma influ-
ence surgical planning?

Decision-​Making

The objectives of treatment in a patient with extradural thoracic tumor include re-
covery or preservation of neurologic function, pain relief, local oncologic control, main-
tenance of mechanical stability, and quality of life.6 Mainstay therapeutic options include
corticosteroids, radiation therapy, and surgery. Corticosteroids may prevent short-​term
neurological deterioration, mediate edema, and provide analgesia; however, this line of
treatment is not definitive.
A valuable decision-​making tool in approaching such a patient is the neurologic,
oncologic, mechanical, and systemic (NOMS) paradigm. Consideration of the ex-
tent of epidural extension (neurologic) in conjunction with tumor sensitivity to

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Table 14.1.
Epidural spinal cord compression scale.7
Grade Definition
0 Bone-​only disease
1a Epidural impingement, without deformation of the thecal sac
1b Deformation of the thecal sac, without spinal cord abutment
1c Deformation of the thecal sac with spinal cord abutment, but without
cord compression
2 Spinal cord compression, but with CSF visible around the cord
3 Spinal cord compression, no CSF visible around the cord.

radiation (oncologic) enables determination of a patient-​specific treatment algo-

rithm. Stability of the spine (mechanical) and overall disease burden and health status
considerations (systemic) further help determine the need and the feasibility of sur-
gical intervention.1
The chief neurologic considerations are the degree of spinal canal compro-
mise, evaluated through imaging and clinical assessment of myelopathy and/​ or
radiculopathy. A  six-​point grading system, based on axial T2-​weighted images, has
been proposed and validated to delineate the degree of epidural spinal cord compres-
sion (Table 14.1).7
Patients with manifestations of thoracic mechanical instability, irrespective of
neurologic or oncologic evaluation, may require surgical stabilization because mechan-
ical pain does not typically improve with steroids, bracing, and/​or radiation.2 An 18-​point
Spinal Instability Neoplastic Score (SINS) has been developed and validated to guide as-
sessment of neoplastic instability.The SINS covers six domains: location, pain, alignment,
osteolysis, vertebral body collapse, and posterior elements involvement.8 Importantly, the
patient’s overall health and comorbidities must be accounted for in treatment decisions.
If surgical management is pursued, the approach should be tailored to the specific
characteristics of the patient’s lesion with the goal of achieving circumferential spinal
cord decompression. Traditionally, posterior decompressive laminectomy was the sole
surgical treatment offered for neoplastic spinal cord compression. While laminectomy
can be used for disease isolated to the posterior elements, transthoracic, transpedicular
lateral extracavitary and retroperitoneal approaches provide more direct access to the
anterior thoracic and thoracolumbar regions.

Questions

1. What approaches can be taken to stabilize the spinal column in cases of in-
stability (getting at, e.g., pedicle screws, rods and hooks, anterior struts and
plates)?
2. What surgical approaches may be taken for ventral spinal cord decompression
and spinal column reconstruction?
3. For anterior and anterolateral approaches to the spine, which factors influence
laterality of approach?

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Thoracic Cord Compression: Extradural Tumor

An additional decision-​making point arises if the lesion is highly vascular. Renal cell car-
cinoma, thyroid carcinoma, melanoma, and hepatocellular carcinoma are lesions which
may warrant preoperative embolization to mediate intraoperative blood loss.

Surgical Procedure

Resection of a thoracic extradural tumor is performed under general anesthesia. In

this patient, a lateral extracavitary approach was employed to allow access to the an-
terior elements. Sensory and motor evoked potentials may be helpful to mediate risk
of new-​onset postoperative neurologic deficits and ensure neurologic integrity during
positioning and resection.
Patients are placed prone on the operating room table and an x-​ray is taken to lo-
calize the appropriate skin incision. A  midline linear skin incision is made and taken
down through the subcutaneous tissue. Electrocautery is used to perform subperiosteal
dissection of the spinous processes, laminae, and transverse processes of T1 through T5.
An x-​ray is taken to confirm the correct levels.
The pedicles of T1, T2, T4, and T5 are bilaterally cannulated. This is done using a
high-​speed drill, followed by a gearshift pedicle finder, a tap, and a ball-​tip probe. Pedicle
screws are then placed at these levels bilaterally. Next, a laminectomy is performed one
level above and one level below the compression. This is done using a combination of
high-​speed drill and Kerrison rongeurs.
Next, subperiosteal dissection of the T3 transverse process and the third rib on the
right is performed, and the transverse process is removed with a combination of the
high-​speed drill and rongeurs. A curette is used to develop a surgical plane between the
rib and the surrounding pleura, and the rib head is removed. At this time, a combination
of rongeurs is used to remove the pedicle—​in the present case, the pedicle was grossly
infiltrated with tumor and epidural spinal cord compression was evident.
After removal of the tumor-​infiltrated pedicle, corpectomy is pursued. The tumor is
dissected from the dura using a Penfield dissector and resected using a combination of
suction and rongeurs. Curettes are used to perform a discectomy at T2–​T3 and T3–​T4;
the inferior endplate of T2 and the endplate of T4 are identified and decorticated. To
complete the corpectomy and perform a decompression, transpedicular decompression
is performed. This is done using a high-​speed drill to remove part of the transverse pro-
cess and pituitary rongeurs to remove any tumor that has infiltrated the pedicles. The
contralateral pedicle may also require removal if the cord is not adequately decompressed
or if more tumor needs to be removed to decrease oncologic burden. If infiltration is
identified, the pedicle is drilled down in its entirety and the corpectomy is completed.
In the present case, more than 80% of the vertebral body was removed.
An appropriately sized expandable cage is placed after packing it with cadaveric bone
chips and demineralized bone matrix (DBM). The cage is cautiously expanded until
a secure fit is achieved. X-​ray is taken to confirm proper instrumentation placement.
Next, rods are placed in the tulip heads of the screws bilaterally. In the current case, we
applied a compressive force from T2 to T4 to assist in correction of the kyphotic de-
formity. After compression, locking caps are placed and x-​ray is again taken to confirm
the cage has not subsided or migrated, appropriate thoracic kyphosis is maintained,
and all instrumentation has maintained integrity during final tightening. The wound is

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Spinal Neurosurgery

Figure 14.2  Postresection sagittal (A) and axial (B) T2 magnetic resonance images.

Lateral x-​ray (C) depicts T3 cage.

irrigated and bony surfaces are decorticated using the high-​speed drill. Cadaveric bone
chips mixed with DBM are placed in the facet joints. In the present case, arthrodesis was
performed from T1 through T5. Drains are placed in the epidural space and tunneled
through separate skin incisions.The wound is closed in multiple anatomic layers, the skin
is closed with staples, and sterile dressings are applied (Figure 14.2).

Oral Boards Review: Management Pearls

1. In a patient with mild or no neurological or mechanical compromise and a

radiosensitive tumor, nonsurgical management only with radiation therapy
and/​or chemotherapy can be considered. Radiation (either fractionated or
stereotactic radiosurgery) may be also used as an adjuvant treatment after sur-
gery for many tumors.
2. In cases of ventral spinal cord compression or deformity with instability, di-
rect ventral decompression and anterior column stabilization in addition to
posterior fixation will often provide optimal decompression and stabilization.
Retraction of the dura from a posterior approach carries a high risk of neu-
rological injury and must be avoided.
3. In all cases of possible surgery, extent of disease and patient life expectancy
should be considered.

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Thoracic Cord Compression: Extradural Tumor

Aftercare

If a cerebrospinal fluid (CSF) leak is detected or a durotomy identified, primary closure

is ideal treatment. If repair of the CSF leak is watertight, patients are typically encouraged
to ambulate approximately 36–​48 hours after surgery. During this time, thigh-​length
graduated compression stockings and/​or intermittent pneumatic compression or foot
impulse devices should be utilized to prevent formation of venous thromboemboli
(VTE). Anticoagulant prophylaxis may also be considered. Bowel and bladder func-
tion should also be monitored postoperatively to ensure return of function and prevent
delayed diagnosis of spinal cord injury. As pain improves, ambulation is encouraged.
Pain management is often achieved through a multimodal approach involving physical
therapy and pharmaceuticals.

Pivot Points

1. If a patient presents with acute neurological compromise from epidural spinal

tumor that is not known to be radiation sensitive, then urgent surgical de-
compression is warranted.
2. For a patient presenting with mechanical pain, deformity, and radiographic
characteristics of spinal instability from tumor, surgical stabilization should be
strongly considered.
3. In patients with radiosensitive disease, widely disseminated disease, or poor life
expectancy, then nonsurgical management may be most appropriate.

Complications and Management

Reported complication rates following surgical management of extradural spine tumors

causing spinal cord compression range widely. In a recent prospective trial, 29.6% of
patients experienced an adverse event within 30 days.9 Complications following resec-
tion and stabilization can be classified as surgical, instrumentation-​related, or medical.
Commonly reported complications include wound infection, CSF leakage, and hema-
toma formation. Rarer adverse events include VTE, instrumentation complications, and
new-​onset neurologic deficits. Reported risk factors for complications include morbid
obesity, posterior approach, malnutrition, preoperative radiation, and steroid use.10

Oral Boards Review: Complications Pearls

1. Postoperative patients with metastatic cancer are at high risk for deep vein
thrombosis (DVT) and thromboembolism. Early mobilization and use of pro-
phylactic anticoagulation when considered safe from a surgical viewpoint
should be encouraged.
2. Neurological injury intraoperatively may be minimized by taking great care
to avoid any retraction of dura or excessive distraction of instrumentation.
The use of intraoperative neuromonitoring may assist in this.

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Spinal Neurosurgery

Evidence and Outcomes

Management of metastatic epidural spinal cord compression was assessed in a randomized

prospective clinical trial by Patchell et al.11 This trial compared direct decompressive surgical
tumor resection plus radiation therapy versus radiation alone. The study included patients
with displacement of the cord visible on imaging, compression restricted to a single area,
and an expected survival of at least 3 months. This study concluded that patients with sur-
gery and radiation retain the ability to ambulate longer and recover the ability to ambulate
more frequently than those treated with radiation therapy alone. Improvement in survival
was also noted for patients treated surgically. A more recent trial by Fehlings et al. enrolled
142 surgically managed patients with single metastatic epidural spinal cord compression
tumors, including 116 patients (81.7%) with thoracic lesions.9 The investigators found that
surgical intervention, adjunctive to chemotherapy and radiation, yields short-​and long-​term
improvements in pain, neurologic functional, and health-​related quality of life outcomes.

References and Further Reading

1. Laufer I, Rubin DG, Lis E, et al.The NOMS framework: approach to the treatment of spinal
metastatic tumors. Oncologist. 2013;18(6):744–​751.
2. Sciubba DM, Baaj AA, Gokaslan ZL. Spinal cord compression. In: Abeloff’s Clinical Oncology.
5 ed. Philadelphia, PA: Elsevier; 2014:715–​725.
3. Bach F, Larsen BH, Rohde K, et  al. Metastatic spinal cord compression. Occurrence,
symptoms, clinical presentations and prognosis in 398 patients with spinal cord compression.
Acta Neurochirurgica. 1990;107(1-​2):37–​43.
4. Helweg-​Larsen S, Sorensen PS. Symptoms and signs in metastatic spinal cord compres-
sion: A study of progression from first symptom until diagnosis in 153 patients. Eur J Cancer.
1994;30A(3):396–​398.
5. Loblaw DA, Perry J, Chambers A, Laperriere NJ. Systematic review of the diagnosis and
management of malignant extradural spinal cord compression:  The Cancer Care Ontario
Practice Guidelines Initiative’s Neuro-​ Oncology Disease Site Group. J Clin Oncol.
2005;23(9):2028–​2037.
6. Witham TF, Khavkin YA, Gallia GL, Wolinsky JP, Gokaslan ZL. Surgery insight:  Current
management of epidural spinal cord compression from metastatic spine disease. Nat Clin
Pract Neurol. 2006;2(2):87–​94; quiz 116.
7. Bilsky MH, Laufer I, Fourney DR, et al. Reliability analysis of the epidural spinal cord com-
pression scale. J Neurosurg Spine. 2010;13(3):324–​328.
8. Fisher CG, DiPaola CP, Ryken TC, et al. A novel classification system for spinal instability
in neoplastic disease:  An evidence-​based approach and expert consensus from the Spine
Oncology Study Group. Spine. 2010;35(22):E1221–​E1229.
9. Fehlings MG, Nater A, Tetreault L, et al. Survival and clinical outcomes in surgically treated
patients with metastatic epidural spinal cord compression:  Results of the prospective
Multicenter AOSpine Study. J Clin Oncol. 2016;34(3):268–​276.
10. Klimo P, Jr., Schmidt MH. Surgical management of spinal metastases. Oncologist.

2004;9(2):188–​196.
11. Patchell RA, Tibbs PA, Regine WF, et  al. Direct decompressive surgical resection in the
treatment of spinal cord compression caused by metastatic cancer: A randomised trial. Lancet.
2005;366(9486):643–​648.

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Spinal Cord Tumor

Intramedullary

Rajiv R. Iyer and George I. Jallo

15
Case Presentation

A 45-​year-​old woman presents to her primary care physician complaining of 1 month

of intermittent bilateral hand numbness in addition to occasional sharp, shooting pain
down her neck and spine when she flexes her neck. Bowel and bladder function is
normal. She reports no medical problems, no cancer history, and no history of prior
neck pain or arthritis. Due to suspicion for cervical spondylosis, magnetic resonance
imaging (MRI) is obtained, which demonstrates an expansile lesion within the spinal
cord at the level of C7–​T1 (Figure 15.1). She is referred to a neurosurgeon for evalua-
tion. Neurological examination reveals normal muscle bulk and tone but slight weakness
with handgrip bilaterally. Sensory examination is unremarkable. Patellar reflexes are 3+
and Babinski sign is positive bilaterally.

Questions

1. What is the most likely diagnosis?

2. What are the common imaging findings associated with intramedullary spinal
cord tumors (IMSCTs)?
3. What is a common classification system for spinal cord tumors?

Assessment and Planning

Based on the neurological examination and imaging findings, the neurosurgeon is

concerned about the presence of an IMSCT. Spinal cord tumors can be subdivided
into extradural, intradural-​extramedullary and intramedullary subtypes, the least
common being the intramedullary group. The most common types of IMSCTs
are ependymomas and astrocytomas, with ependymomas being more likely in
adults and astrocytomas more commonly found in the pediatric population. Other
lesions in the differential diagnosis for IMSCTs include hemangioblastomas, es-
pecially in cases of the inherited disorder von Hippel Lindau (vHL) disease, as
well as gangliogliomas, cavernous malformations, subependymomas, and several
other rare lesions. Clinical characteristics of patients with IMSCTs can range
widely, with the most common complaint being axial back or neck pain. Other

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Spinal Neurosurgery

Figure 15.1  Cervicothoracic intramedullary spinal cord tumor (A–​F). T2-​weighted

(A,B) and post-​contrast T1-​weighted preoperative (C,D) magnetic resonance imaging
(MRI) demonstrating an expansile, T2-​hyperintense, rim-​enhancing lesion concerning
for an intramedullary spinal cord tumor (IMSCT). A gross total resection was achieved
through an osteoplastic laminoplasty (E,F).

features may include radicular pain, sensory disturbances, progressive motor def-
icit, and, in more severe cases, bowel or bladder dysfunction and myelopathy.
MRI is the diagnostic modality of choice in the diagnosis of IMSCTs. The ma-
jority of lesions appear as expansile lesions within the spinal cord and are often
hyperintense on T2-​weighted MR imaging. T1-​weighted post-​gadolinium im-
aging is variable and may demonstrate homogenous enhancement, especially in
the case of ependymomas, or patchy enhancement, more commonly seen with
spinal astrocytomas (Figure 15.2). Sharp, demarcated borders are more commonly
seen in cases of ependymomas. In some cases, adjacent spinal cord edema may be
obvious on T2-​weighted imaging, in addition to the presence of syringomyelia or
tumor-​a ssociated  cysts.

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Spinal Cord Tumor: Intramedullary

Figure 15.2  Spinal astrocytoma (A–​D). Magnetic resonance imaging (MRI)

demonstrates a T2-​hyperintense lesion (A) centered at the level of C4–​C5 with
irregular borders (B), concerning for an intramedullary astrocytoma. Postoperative
imaging (C,D) is also shown following resection.

Oral Boards Review: Diagnostic Pearls

1. MRI is crucial to the diagnosis and localization of IMSCTs.

a. IMSCTs typically appear as hyperintense intramedullary lesions on T2-​
weighted MRI. Enhancement post-​gadolinium administration varies—​for
ependymomas, homogenous enhancement is common, while astrocytomas
are more variable and may demonstrate a patchy enhancement pattern.
b. Well-​demarcated borders on MRI are more characteristic of
ependymomas, consistent with well-​defined dissection planes often dis-
covered in the operating room. For astrocytomas, their infiltrating nature
correlates with their poorly demarcated borders on MRI. A more eccen-
tric location is characteristic of astrocytomas, while ependymomas are
more centrally located.
c. The third most common IMSCTs in adults are hemangioblastomas.
Unique features on imaging include flow voids on T2-​weighted MRI, a
contrast-​enhancing nodule within the spinal cord, and a syrinx out of pro-
portion in size to the tumor bulk itself. Ancillary imaging with cerebral
angiography may be useful in identifying hypertrophic feeding vessels that
supply the tumor.

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Spinal Neurosurgery

2. The cervical and thoracic regions are the most common locations for
IMSCTs.
3. Risk factors for developing IMSCTs are not well known, but inherited
disorders including neurofibromatosis type 2 (NF2) predispose patients to de-
veloping spinal ependymomas, while vHL predisposes patients to the devel-
opment of hemangioblastomas of the spinal cord.

Questions

1. What are some risk factors for the development of IMSCTs?

2. What are some favorable imaging features for surgical intervention?
3. Is there a benefit to performing an osteoplastic laminoplasty versus
laminectomies for tumor resection?

Decision-​Making

Generally, ependymomas and astrocytomas of the spinal cord are low-​grade lesions that
are amenable to surgical resection. Rarely, they are of a higher grade, which is associated
with increased aggressiveness and invasion. Patients with high-​grade IMSCTs tend to
fare poorly regardless of surgical intervention. In such cases, radiation therapy may be
appropriate as an adjuvant treatment modality.
If a patient presents with symptoms that are attributable to an IMSCT, surgical inter-
vention is the mainstay of treatment. The goal of surgery is to obtain a diagnosis and to
perform a maximal safe resection without causing a permanent neurological deficit. For
ependymomas, gross total resection (GTR) is often achievable given the well-​defined
dissection planes that allow the surgeon to carefully spare normal surrounding neural
structures. On the other hand, astrocytomas of the spinal cord have irregular borders and
an infiltrating pattern and thus discerning tumor tissue from normal neural parenchymal
may be challenging. Intraoperative neurophysiological monitoring is critical in such
cases as its use can prevent permanent iatrogenic deficits.

Surgical Procedure

IMSCT resection is performed under general anesthesia using rigid skull fixation
and prone positioning. Intraoperative electrophysiological monitoring includes motor
evoked potentials (MEPs) and somatosensory evoked potentials (SSEPs). A  localizing
x-​ray may be useful in guiding incision placement. A midline skin incision is made and
electrocautery is used to expose the lamina at the level(s) of interest. Use of an ultrasonic
bone-​cutting device can be used to perform an osteoplastic laminoplasty, which can be
reaffixed following tumor resection and dural closure. Depending on surgeon preference,
standard laminectomies may also be performed. During this stage, care must be taken to
avoid facet joint entry or sacrifice so as to not destabilize the spinal column. There does
not appear to be any significant difference in spinal deformity outcomes after IMSCT
surgery regardless of the use of laminectomies compared to the osteoplastic laminoplasty.
However, there is a trend toward a decreased cerebrospinal fluid (CSF) leak rate with

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Spinal Cord Tumor: Intramedullary

the use of the osteoplastic laminoplasty. Once the laminae are removed, further tumor
localization can be achieved with intraoperative ultrasound. The use of the ultrasound
also allows one to determine whether there is sufficient bony exposure allowing for a
large enough intradural exposure above and below the lesion of interest. Other features
such as tumor-​cysts or syrinxes can be visualized during this step and aid in localization
when compared to preoperative imaging.
Once an adequate dural exposure is achieved, intraoperative epidural electrodes can
be placed for electrophysiological monitoring of the D-​wave. This measure represents
the number of functional units of the corticospinal tract above and below the lesion
and provides real-​time feedback to the surgeon about graded motor function during
tumor resection. While MEPs provide an all-​or-​none measure of motor function, D-​
wave monitoring can be used as a threshold at which a surgeon may pause or termi-
nate tumor resection in order to avoid an iatrogenic, permanent neurologic deficit.
Commonly, once the D-​wave threshold reaches 50%, tumor resection is halted as this
represents a threshold predicting permanent rather than transient postoperative neu-
rological dysfunction.
Once the dura is opened, obvious surface abnormalities may be present on the
spinal cord surface. A midline myelotomy is made, and, many times, SSEP function is
compromised due to dorsal column manipulation. Identifying midline may be chal-
lenging due to cord rotation or asymmetric enlargement, but the presence of dorsal
sulcal veins or identification of the midpoint between dorsal root entry zones can aid in
this step. The myelotomy should extend the rostro-​caudal extent of the tumor in order
to avoid harmful manipulation of normal structures. Once the tumor is encountered,
careful microscopic dissection can proceed, freeing the tumor from surrounding normal
neural tissue. Circumferential dissection is often utilized, especially when good dissec-
tion planes exist. Sometimes, tumor cysts or a syrinx will aid in the identification of
these planes. If significant retraction is required to circumnavigate the tumor, internal
debulking can be performed with a laser contact probe or an ultrasonic aspirator. The
goal of surgery is maximal resection without causing a permanent neurological deficit.
Especially in cases of infiltrating astrocytomas, subtotal resection may be necessary if a
decline in electrophysiological monitoring occurs. Meticulous hemostasis is performed
following tumor resection.
After the tumor is removed, the dura is closed in a watertight fashion with a
nonabsorbable suture such as a 5-​0 Prolene. In some cases, if the dura cannot be well
opposed, a dural substitute patch may be necessary. Fibrin sealants may help in avoiding
postoperative CSF leak. If a laminoplasty was performed, this is fixed in place with ti-
tanium miniplates. The fascia and superficial tissues are closed in a layered fashion in a
tight, interrupted manner in order to minimize the risk of postoperative CSF leak.

Oral Boards Review: Management Pearls

1. Surgical resection is the mainstay in the management of IMSCTs with the

goal of maximal safe resection. Dissection planes are usually clearer with
ependymoma resection compared to astrocytomas, which have irregular
borders due to their infiltrating nature.

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2. Surgical treatment often entails the use of an osteoplastic laminoplasty with

care taken to avoid joint space disruption. Additional use of electrophysiolog-
ical monitoring with MEPs, SSEPs, and D-​waves provides critical informa-
tion to the surgeon during tumor resection. A greater than 50% reduction in
epidural D-​wave monitoring is often a threshold used to pause or terminate
tumor resection as this can be the difference between a transient versus per-
manent postoperative neurological deficit.
3. Watertight dural closure, the use of fibrin sealants, and an osteoplastic
laminoplasty, as well as meticulous fascial and skin closure, all help to prevent
postoperative CSF leak.

Pivot Points
1. If during IMSCT resection, changes or loss of SSEPs occur, postoper-
ative sensory disturbances can be expected due to manipulation of the
dorsal columns. These may be transient or long-​term. If MEPs are un-
changed and D-​wave monitoring decreases by less than 50%, the patient’s
motor abilities are expected to be unchanged. If MEPs are lost and D-​wave
monitoring decreases by less than 50%, a transient motor deficit can be ex-
pected postoperatively. If bilateral MEP loss occurs in addition to greater than
50% loss of D-​wave monitoring, a prolonged motor deficit can be expected
postoperatively.
2. Postoperative functional status is highly dependent on preoperative functional
status, and maximal safe resection is performed in an attempt to preserve ex-
isting preoperative function. Functional status pre-​and postoperatively can
be measured with the McCormick grading scale, which takes into account
motor and sensory function, as well as the patient’s functional independence.

Aftercare

Following surgery for IMSCT resection, it is common practice to keep the patient
in a recumbent position initially to minimize the chance of a postoperative CSF leak.
Elevation can normally start 24 hours postoperatively, with special attention paid to the
wound to monitor for signs or symptoms of CSF leak. Generally, a postoperative MRI
is obtained that aids in determining the extent of surgical resection.
While some patients present with minimal symptomatology associated with their
IMSCT, others are discovered only after significant, progressive neurologic deficit has
occurred. In these situations, symptoms may be exacerbated initially by surgery, with
transient postoperative motor or sensory disturbances. The purpose of intraoperative
electrophysiological monitoring is to prevent permanent neurologic deficits. However,
transient changes may occur in the postoperative period, and patients should be counseled
regarding this possibility. Thus, physical therapy and rehabilitation play a significant role
in the recovery period following surgery.

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Serial monitoring with gadolinium-​enhanced MRI allows the surgeon to monitor

for tumor recurrence or progression following surgical resection of IMSCTs. For symp-
tomatic tumor recurrence, repeat surgical resection can be considered, but the risks and
benefits of re-​resection must be weighed against factors including preoperative func-
tional status, tumor location, and multiplicity and extent of disease, as well as medical
comorbidities. Generally, radiation therapy is reserved for cases of multifocal or aggres-
sive tumors that are not amenable.

Complications and Management

Postoperative CSF leak and pseudomeningocele are some of the potential complications
of IMSCT surgery. During initial surgery, several methods can be undertaken to avoid
these phenomena. For example, watertight dural closure and a multilayered soft tissue
closure with special attention to the muscular fascia is critical. The use of a laminoplasty
in addition to dural substitutes and fibrin sealants can also help to avoid this complica-
tion. If CSF leak occurs, the use of a lumbar drain and recumbent positioning can be
attempting to heal the source of the leak. If the leak persists, re-​exploration may be nec-
essary to avoid the risk of meningitis. Exploration can involve the use of a dural patch
or buttressing dural sutures, as well as a subfascial drain placed to straight drainage. If
further CSF accumulation occurs, a drain allows for diversionary fistula formation that
can be subsequently closed with a figure-​of-​eight suture after the wound has been given
sufficient time to heal.
Postlaminectomy kyphosis and spinal deformity can also occur, more frequently in
children and especially when there is violation of the facet joints during bony exposure
for intradural tumor resection. Large tumors spanning several segments may harbor a
higher risk for the development of deformity postoperatively. Typically, if spinal fixation
is required for a destabilized segment, it occurs after recovery has occurred from the in-
itial tumor resection.

Oral Boards Review: Complications Pearls

1. The use of osteoplastic laminoplasty compared to laminectomies for IMSCT

resection is not a definitive measure to prevent postoperative kyphosis and
spinal deformity.
2. Pseudomeningocele formation or CSF leak can be managed with lumbar
drainage and recumbency, but may require re-​exploration for attempted pri-
mary repair in order to avoid open communication between the intradural
space and the atmosphere, which can lead to meningitis.

Evidence and Outcomes

In the majority of reports, excellent outcomes have been reported for patients
undergoing surgical resection of low-​grade IMSCTs. While there is no concrete data
to suggest that extent of resection affects progression-​free survival or overall survival,
several groups maintain that maximal safe resection should be performed at the time of
first surgery. Previously, open biopsy followed by radiation was posed as an alternative

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to aggressive resection. However, excellent outcomes have been reported for patients
undergoing aggressive resection, regardless of age, and this should be attempted to avoid
the need for repeat surgery for tumor recurrence. The largest predictor of postoperative
function following IMSCT surgery is preoperative functional status. Generally, transient
motor deficits postoperatively can improve with physical therapy up to 6–​12 months
postoperatively.

References and Further Reading

Hanbali F, Fourney DR, Marmor E, et al. Spinal cord ependymoma: Radical surgical resection
and outcome. Neurosurgery. 2002;51:1162–​1172; discussion 1172–​1164.
Jallo GI, Danish S, Velasquez L, Epstein F. Intramedullary low-​g rade astrocytomas:  Long-​term
outcome following radical surgery. J Neurooncol. 2001;53:61–​66.
Jallo GI, Kothbauer KF, Epstein FJ. Intrinsic spinal cord tumor resection. Neurosurgery.
2001;49:1124–​1128/​
McGirt MJ, Garces-​Ambrossi GL, Parker SL, et al. Short-​term progressive spinal deformity fol-
lowing laminoplasty versus laminectomy for resection of intradural spinal tumors: analysis of
238 patients. Neurosurgery. 2010;66:1005–​1012.

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Spinal Cord Tumor

Intradural Extramedullary

Michael A. Galgano, Jared Fridley, and Ziya Gokaslan

16
Case Presentation

A 52-​ year-​
old woman presented to the emergency department with progressively
worsening mid-​back pain, bilateral leg weakness and numbness, urinary retention, and
balance dysfunction over the course of a few weeks. She had no significant past medical
or surgical history and denied any recent trauma, travel, or fever. Detailed neurological
examination revealed a well-​developed middle-​aged female with appropriate mentation
and cognitive function. She was found to have 4+/​5 motor strength in all major muscle
groups of the bilateral lower extremities, a mid-​upper chest sensory level, brisk patellar
and ankle reflexes, and bilateral clonus. Upper extremity sensorimotor exam was unre-
markable. Hoffman sign was negative in both hands, and upper extremity reflexes were
within normal limits. Basic laboratory studies were unremarkable.

Questions

1. To what part of the neuroaxis can the patient’s neurological signs and
symptoms be localized?
2. What are some differential diagnoses based on the patient’s history and
physical exam?
3. What would be the most appropriate imaging modality now?
4. What is the urgency of the diagnostic workup given the patient’s progressive
neurological decline?

Assessment and Planning

This patient has signs and symptoms consistent with thoracic myelopathy. Differential
diagnoses include thoracic disc herniation, spinal tumor, spinal epidural abscess, and
spinal arteriovenous malformation. Although thoracic disc herniations can certainly
cause thoracic myelopathy, their clinical course tends to be drawn out over a period of
many months. Spinal vascular malformations are incredibly rare entities that can cause
symptoms in a progressive fashion or acutely from an intradural hemorrhage. Spinal
vascular pathology should be kept in mind with any myelopathy that is unexplained by
radiographic imaging, as the findings on magnetic resonance imaging (MRI) may be
missed due to their subtleness. Patients harboring infectious etiologies generally have

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more systemic signs and symptoms, often coupled with abnormal inflammatory markers
and leukocytosis. The current patient was afebrile and did not have an elevated white
blood cell count; however, if there is a strong clinical suspicion for a spinal infection,
c-​reactive protein (CRP) and erythrocyte sedimentation rate (ESR) should both be or-
dered. Neoplastic processes leading to thoracic myelopathy have significant variability.
If a tumor is suspected, it cannot be determined whether the lesion is intradural or ex-
tradural based solely on history and physical examination. Imaging is needed for further
differentiation.
When dealing with progressively worsening myelopathy, it is important to obtain
the proper imaging in a timely fashion. An MRI with and without contrast of the tho-
racic spine is warranted on an urgent basis. If the thoracic spine MRI is suggestive of a
neoplasm or infection, the whole spine should be imaged to look for additional lesions
because this might affect patient treatment. If a spinal fusion is being considered to sup-
plement the decompression en route to the site pathology, a computed tomography
(CT) scan may be warranted to plan out instrumentation trajectories and for purposes
of measuring screw lengths.
An MRI of the cervical and thoracic spine with and without contrast was completed
revealing a dorsolateral, intradural, extramedullary mass at the level of T2 measuring 1.9 ×
0.7 × 0.9 cm.There is homogenous contrast enhancement with evidence of a “dural tail.”
The mass causes cord displacement and severe central canal stenosis. T2 hyperintensity
within the cord is consistent with edema versus myelomalacia (Figure 16.1). The most
common intradural extramedullary neoplasms of the thoracic spine are meningiomas and
peripheral nerve sheath tumors such as schwannomas and neurofibromas. Less common
lesions found in this compartment are metastases, paragangliomas, extramedullary
cavernomas, neuroenteric cysts, ependymomas, and arachnoid cysts.

Figure 16.1  Preoperative T1-​weighted magnetic resonance image (MRI) with

contrast revealing a dorsally located contrast enhancing mass at the level of T2–​T3,
causing mass effect on the underlying spinal cord

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Spinal Cord Tumor: Intradural Extramedullary

Based on history and physical examination as well as imaging findings, the most likely
diagnosis in this case is a thoracic spine meningioma. Meningiomas are histologically
benign tumors that arise from arachnoid cap cells. There are more aggressive subtypes,
although these are quite rare in the spine. There is a female preponderance, likely be-
cause of hormonal receptor types that are common in women.

Oral Boards Review: Diagnostic Pearls

Neurological presentation in the patient with an intradural extramedullary tumor:

1. Cervical: Cervical spine intradural extramedullary lesions often present with

features of cervical myelopathy, including gait/​balance disturbance and diffi-
culty with manual dexterity. If the tumor causes compression of a nerve root,
there may be a significant radiculopathic component causing pain or senso-
rimotor deficits in the affected nerve distribution. Neck pain is a common
symptom in these patients. Depending on the size of the lesion, these patients
may have brisk reflexes and positive Hoffman and Babinski signs, as well as
myo-​/​dermatomal weakness and numbness, respectively. Dorsal column tracts
in the cord may be affected, causing imbalance and discoordination.
2. Thoracic: Thoracic spine intradural extramedullary lesions often present with
myelopathic features. Back pain with recumbency is often a complaint of the
patient. Thoracic radiculopathy as a band-​like pain may be manifested. Gait
disturbance may be present, as well as varying degrees of lower extremity
weakness, depending on the level of the lesion and chronicity of symptoms.
A thoracic sensory level is often discovered on neurological assessment.
Clonus, brisk lower extremity reflexes, and positive Babinski sign are often
found as well. The thoracic corticospinal tracts are particularly vulnerable and
sensitive to mass effect from ventrally located lesions. Lesions situated more
dorsally may cause a sensory ataxia. Bowel and bladder involvement may be a
late finding.
3. Lumbar: Lumbar spine intradural extramedullary lesions may also present with
back pain brought on by recumbency. If a tumor is located at the level of the
conus medullaris, bowel and bladder symptoms may be present. However,
lesions distal to this will often cause nerve root symptoms, such as weakness
and numbness. The degree of weakness depends on the size of the mass and
amount of canal compromise. Nerve sheath tumors often cause isolated sen-
sory symptoms as these tumors usually arise from the dorsal root.

MRI with and without contrast is the imaging modality of choice for differentiating
intradural and extradural lesions because it can delineate in detail the relationship of the
tumor to its surroundings. Meningiomas are often iso-​or hypointense on T1 and iso-​or
hyperintense on T2. They typically display avid homogenous enhancement with con-
trast. An enhancing dural tail is also characteristic of meningiomas. CT scan may demon-
strate calcifications within the tumor. It is important to differentiate meningiomas from
peripheral nerve sheath tumors, such as schwannoma, as both are contrast-​enhancing

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and both can cause cord compression. Schwannomas are iso-​or hypointense on T1
and hyperintense on T2. Some schwannomas display markedly increased regions of T2
intensity, often indicating a cystic component (Figure 16.2). Areas of T2 hypointensity
can be representative of hemorrhage or collagen formation. Unlike meningiomas,
schwannomas arise from the nerve sheath and therefore a significant tumor component
can be seen in the neural foramen, often with dilation and thinning of the surrounding
bone. Dural tails are not associated with schwannomas, unlike meningiomas. The MRI
appearance of neurofibromas is similar to that of schwannomas, although neurofibromas
do not typically harbor cystic changes. Spinal radiographs and CT may reveal thinning
of the pedicles (Figure 16.2), increased interpedicular distance, scalloping of the poste-
rior vertebral bodies (especially with schwannomas and neurofibromas), and enlarged
neural foramina.

Questions
1. To maximize surgical resection of this lesion, what steps can be taken to en-
sure the dural attachment is excised along with the tumor?
2. What modifications to the surgical approach would need to be made if the
lesion was situated ventral to the spinal cord?
3. Why should a distinction be made between an intradural tumor with outward
extension through the nerve root sleeve into the neural foramen and an ex-
tradural tumor with inward extension into the neural foramen?

Figure 16.2  Axial computed tomography (CT) scan at the level of the conus,
showing an intradural partially calcified tumor causing thinning of the pedicles
bilaterally.

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Spinal Cord Tumor: Intradural Extramedullary

Decision-​Making

Most intradural extramedullary tumors are histologically benign. Small, asymptomatic

lesions in this compartment can often be watched radiographically over time. Many
intradural extramedullary lesions are discovered, however, because they have become
symptomatic. The patient in this case has had progressive worsening back pain, bilateral
lower extremity weakness, numbness, urinary dysfunction, and difficulty ambulating. In
addition to her lower extremity weakness, she is displaying signs and symptoms of sen-
sory ataxia. Although this is likely a histologically benign lesion, the mass effect on the
spinal cord is concerning. Progression of the tumor may cause further worsening of her
existing deficits, potentially leading to paraplegia. Intervention to decompress her spinal
cord and resect the mass would allow the best chance of neurological recovery. Barring
medical contraindications to surgery, observation is not a good option. Additionally, sur-
gical resection of the tumor is helpful in terms of tissue diagnosis. This may affect the
patient’s prognosis, dictate whether adjuvant therapy may be needed, and determine the
frequency of clinical and radiographic follow-​up.

Questions

1. Unlike their intracranial counterparts, spinal meningiomas do not penetrate

the pia. What two factors have been proposed to account for this?
2. Why is bony remodeling not seen in the spine with meningiomas, as opposed
to intracranial meningiomas?

Surgical Procedure

A posterior approach is commonly utilized for most intradural extramedullary tumors,

regardless of whether they are dorsal, lateral, or ventrally located. Large ventrolateral
meningiomas commonly push the spinal cord toward the contralateral side. This gives
the surgeon a reasonable working corridor without having to engage in additional re-
traction of the cord. If necessary, sacrifice of a noncritical thoracic nerve root or a di-
vision of a dentate ligament may be utilized to allow further safe manipulation of the
spinal cord. A ventral or ventral-​lateral intradural extramedullary thoracic tumor can al-
ternatively be accessed utilizing a costotransversectomy or lateral extracavitary approach.
Utilizing a more lateral approach minimizes the need for retraction of the cord. A typ-
ical approach to a dorsal meningioma entails a standard posterior spinal subperiosteal
dissection, followed by a laminectomy or laminoplasty at the levels of interest. The po-
tential for postlaminectomy kyphosis must be discussed with the patient prior to per-
forming surgical intervention. A preoperative loss of cervical lordosis, for example, can
potentially place the patient at risk for postoperative kyphosis. A laminoplasty can be
considered in such a situation to keep the dorsal supporting structures intact. In the tho-
racic spine, the risk of abnormal kyphosis after a laminectomy is less, likely in part to the
further stability rendered by the rib cage. Another potential advantage of laminoplasty
versus laminectomies is reduced epidural scarring, which can make surgery for tumor
recurrences more challenging.

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Spinal Neurosurgery

The surgical approach utilized for the presenting patient was a posterior T1–​T3
laminectomy. Neuromonitoring of free running electromyogram (EMG) and somato-
sensory and motor evoked potentials (SSEPs and MEPs) was utilized. An alteration in
neuromonitoring signals during the tumor resection may alert the surgeon that spinal
cord perfusion needs to be optimized. Neuromonitoring also allows the surgeon to
stimulate selected nerve rootlets during the tumor excision to preserve their function-
ality. The operative levels were localized with an anteroposterior (AP) x-​ray. The T1
through T3 pedicles should associate with their respective ribs at the same level. A mid-
line incision was made and subperiosteal dissection performed, followed by the laminec-
tomy. It is important to expose above and below the tumor to minimize risk of neural
element injury and allow total tumor resection with excision of any dural attachments.
Because the lesion was purely dorsal, there was no indication to perform a facetectomy
and remove more bone laterally. Once the laminectomy was completed, an ultrasound
was brought into the surgical field to confirm that the tumor is in fact beneath the
exposed dura. The operating microscope was then draped and brought into the field.
A split-​thickness durotomy was made using an 11-​blade scalpel. Care was taken to not
violate the tumor capsule. The superficial dural layer was dissected from the inner dural
layer. The superficial dural layer was then tacked up using appropriate-​sized sutures.
Once the lateral margins of the meningioma were identified, the inner layer of the dura
was opened sharply, followed by circumferential dissection around the capsule. Once
the capsule was freed from the underlying cord and any attached nerve rootlets, it was
removed en bloc with the inner dural attachment (Figure 16.3). If the tumor is too large
to safely be removed in one piece, it can be cored out utilizing an ultrasonic aspirator
and then folded in on itself prior to fully being excised. If an en bloc excision is not
achieved, then the dural edges once attached to the tumor capsule should be cauterized

Figure 16.3  Postoperative T1-​weighted magnetic resonance image (MRI) with

contrast revealing gross total resection of the previously enhancing mass at the level
of  T2–​T3.

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Spinal Cord Tumor: Intradural Extramedullary

with a bipolar device. Optimal hemostasis was achieved, followed by intradural irri-
gation. Dural sutures were then used to close the remaining superficial layer of dura.
Alternatively, a dural substitute graft can be sewn to the native dura. A Valsalva maneuver
was then done to ensure there is no cerebrospinal fluid (CSF) leak. Care was taken to
close the fascial layer tightly to minimize risk of a CSF leak.

Oral Boards Review: Diagnostic Pearls

1. Excision of intradural meningiomas can be achieved via an en bloc fashion by

utilizing a split-​thickness durotomy or by ultrasonic aspiration and piecemeal
removal.
2. Osseous involvement is exceptionally uncommon with spinal meningiomas.
This is likely due to the well-​defined epidural space in the spine.
3. Spinal meningiomas uncommonly penetrate the pia. One theory is that there
is an “intermediate leptomeningeal layer.” The other concept that has been
postulated to explain pial preservation is that spinal meningiomas often be-
come symptomatic sooner than their intracranial counterparts. Patients often
become symptomatic from spinal cord compression earlier than mass effect
on the brain. Therefore, surgical resection may be undertaken before pial pen-
etration occurs.
4. Neurofibromas commonly arise as a fusiform enlargement of the nerve,
making it necessary to sacrifice the root during excision of the tumor.
5. Schwannomas arise from the nerve root of origin, which is usually a non-
functional dorsal sensory root that can be sacrificed; there is always a corre-
sponding nerve root, which is typically a functional ventral motor root, that
needs to be dissected off the tumor.

Pivot Points

1. A traditional laminectomy or, alternatively, laminoplasty can be utilized to

gain access to the dura.
2. Paying close attention to the patient’s spinal alignment is important. A patient
with a kyphotic cervical spine prior to the intradural tumor excision may
require supplemental instrumentation and fusion to ensure she does not de-
velop further kyphosis after surgery.
a. More lateral approaches to the spine for intradural tumors with a foraminal
or very ventral component may require removal of the facet joints and po-
tentially proximal ribs for optimal access
3. Three options exist for dural opening and closure with a dorsal spinal
meningioma:
a. Traditional two-​layer dural opening with coagulation of tumor
attachments to the dura, followed by a primary dural closure
b. Traditional two-​layer dural opening with excision of both dura layers
overlying the tumor, followed by duraplasty

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c. Split-​thickness dural opening, followed by excision of the meningioma

with the inner dural layer, followed by a primary superficial dural layer
closure

Aftercare

Most surgeons keep patients flat for 24–​48 hours after performing an intradural tumor
resection. This is done to discourage a postoperative CSF leak or pseudomeningocele
from forming. A bladder catheter is left in place so the patient does not need to use a
bedpan repeatedly. After the first 24–​48 hours following surgery, it may be advisable
to have physical therapy work with the patient for mobilization. We generally give 24
hours of prophylactic antibiotics after the operation. Steroids are usually not indicted
unless there is concern for cord edema from manipulation during the surgery. Tylenol,
narcotics, and muscle relaxants are generally given for the first few days after surgery.
A postoperative MRI with and without contrast is obtained prior to discharge to ensure
the desired degree of resection has taken place. Depending on the pathological grade of
the tumor and degree of tumor resection, a repeat MRI is generally obtained within the
first 6 months of surgery to ensure there has been no recurrence.

Complications and Management

During an operation to resect an intradural extramedullary tumor, the adjacent neural

elements are at risk of injury. Both nerve sheath tumors and meningiomas have very
intimate anatomic relationships with surrounding nerve roots and the spinal cord,
depending on the level. It is important to have a reliable neuromonitoring technician on
hand during the case to stimulate surrounding nerve roots and ensure functional roots
are not sacrificed. Obtaining MEPs periodically throughout the case ensures that the
corticospinal tracts have not been compromised.
Although an attempted watertight dural closure is undertaken after excision of the
tumor, CSF can sometimes leak through the suture holes, leading to a pseudomeningocele.
Most pseudomeningoceles will resolve with time on their own. However, if symp-
tomatic, or if a CSF leak develops through the incision, placement of a lumbar drain
or re-​exploration of the dural closure should be performed. Antibiotics are generally
administered for a few days if CSF is noted to be draining through the skin after surgery.
Immaculate hemostasis prior to both dural and soft tissue/​skin closure is necessary to
prevent intradural and epidural clot formation. A good tumor resection can quickly be
complicated by a compressive hematoma within the first days of surgery. It is advisable
to ensure patients are kept off antiplatelet agents and therapeutic anticoagulation for up
to 2 weeks after surgery.
Postoperative infection is always a risk with any open surgery. Violation of the dura
puts the patient at increased risk of meningitis after surgery. One dose of preoperative
antibiotics is given within 1 hour of making incision, and 24 hours of postoperative
antibiotics are generally administered.
Urinary retention is a potential obstacle after the patient’s Foley catheter is removed.
The risk for this is higher with increased narcotic usage and in men with benign pros-
tatic hypertrophy.

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Spinal Cord Tumor: Intradural Extramedullary

Delayed cervical postlaminectomy kyphosis may be seen in a small percentage of

patients after the posterior tension band is removed along with the dorsal elements.This
may require supplemental instrumented fusion if the patient is symptomatic.

Oral Boards Review: Complication Pearls

1. Intraoperative neuromonitoring can be a valuable tool, especially when

excising tumors intimately involved with nerve roots.
2. Utilization of a postdural closure Valsalva maneuver may reveal sites of CSF
leak which can be addressed prior to soft tissue closure.
3. Use of hemostatic agents with gentle cottonoid tamponade in the epidural
space can keep a clear surgical field, diminishing the likelihood of blood
leaking into the intradural space.
4. Once the dural closure has been performed, pulse irrigation with
antibiotic-​impregnated saline can be utilized on the soft tissue prior to
closure.

Evidence and Outcomes

There is an abundance of literature documenting a variety of surgical techniques and

outcomes for resecting intradural extramedullary tumors. Due to their typical benign
histological nature, patients harboring such tumors generally have a good oncological
outcome following resection.

References and Further Reading

Dickman C, Fehlings M, Gokaslan Z. Intradural extramedullary spinal tumors. In Spinal Cord and
Spinal Column Tumors, Principles and Practice (­chapter 21). Stuttgart: Thieme; 2006.
Galgano M, Beutler T, Brooking A, Deshaies E. Spinal meningiomas: A review. J Spine. 2014;3(1).
doi: 10.4172/​2165-​7939.
Hirabayashi H, Takahashi J, Kato H, Ebara S, Takahashi H. Surgical resection without dural recon-
struction of a lumbar meningioma in an elderly woman. Eur Spine J. 2009 Jul; 18(Suppl 2):
232–​235.
Levy WJ, Latchaw J, Hahn JF, Sawhny B, Bay J, Dohn DF. Spinal neurofibromas:  A report of
66 cases and a comparison with meningiomas. Neurosurgery. 1986; 8:331.
Seppälä MT, Haltia MJ, Sankila RJ, Jääskeläinen JE, Heiskanen O. Long-​term outcome after re-
moval of spinal neurofibroma. J Neurosurg. 1995;82:572.

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Radiation-​Sensitive Spine Tumor

Adam M. Robin and Ilya Laufer

Case Presentation

A 71-​ year-​old right-​handed woman with a history of childhood asthma and hip
17
arthroplasty presented to her primary care physician complaining of progressive back
pain that radiated down her left leg. Her pain was initially attributed to deconditioning
and compensation from her hip replacement, and she was treated with steroids and pain
medication. After modest improvement initially she continued to worsen, developing
difficulty sitting and sleeping at night.
Referral was then made to the neurosurgeon. Cranial nerve evaluation is unremark-
able, as is segmental muscle group testing of the upper extremities. She prefers to stand
during her examination, but with effort is able to sit and participate with segmental
muscle group testing in her lower extremities. She has mild pain limitation in her left hip
flexors and extensors. Sensory examination for light touch and temperature sensation
is within normal limits. Normal patellar reflex responses are found bilaterally; she has
plantar flexor responses bilaterally without clonus. Although antalgic when rising from a
chair, once under way, her gait is normal. She is unable to tolerate a fully supine position
on the examining table and has significant leg pain and discomfort in an L3 dermatomal
distribution when seated. Her Karnofsky Performance Scale (KPS) is 60.

Questions

1. What is the likely diagnosis?

2. What is the next step in her evaluation?
3. What is the most likely anatomical region to be involved?
4. What is a reasonable differential diagnosis?

Assessment and Planning

Considering the history and physical exam findings, particularly the patient’s age, pro-
gressive back pain, and mechanical radiculopathy with axial loading, her findings are
highly suggestive of a progressive process involving the spine near the left L3 nerve
root.1,2 Other diagnostic considerations include osteoporotic compression fracture,
spondylosis, spondylolisthesis, degenerative or isthmic pars fracture, and synovial cyst.
A magnetic resonance imaging (MRI) scan is the next step in the evaluation of
this patient. The scan should be ordered with gadolinium and can be requested with
perfusion imaging if available when neoplastic disease is suspected. T1 sequences with

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Spinal Neurosurgery

gadolinium provide excellent anatomic detail of the spinal and neural anatomy and
demonstrate well the enhancement characteristics of a lesion if identified. Note is made
of the spinal sagittal alignment; involvement of anterior, middle, and posterior column
structures; vertebral body morphology; cortical integrity; marrow signal; and presence
of epidural disease within the central canal and neural foramen. Importantly, on the
gadolinium-​enhanced images the reader should be certain to evaluate lumbar nerve
roots for signs of leptomeningeal disease.
This patient’s MRI revealed a T2 hyperintense lesion arising from within the marrow
space of the L3 vertebral body and involving the bilateral pedicles. There is an associ-
ated pathologic compression-​burst fracture at this level with approximately 35% loss of
vertebral body height and retropulsion associated with loss of integrity of the posterior
vertebral body line/​cortical margin and roughly 50% canal compromise. There is no
associated kyphotic deformity. Additionally, there is a ventral epidural soft tissue com-
ponent suggestive of tumor extending along the cranio-​caudal axis from L3 to L5 and
into bilateral L3 foramen causing nerve root compression on the left more so than the
right (Figure 17.1).

Figure 17.1 T2 axial (A) magnetic resonance image (MRI) at the level of L3

demonstrating a vertebral compression burst fracture, increased intrapedicular distance,
and cortical compromise/​retropulsion of the posterior vertebral body into the
central canal causing stenosis and nerve root compression. Sagittal (B) T1 sequence
demonstrating the hypointense bone marrow and pathologic compression fracture at
L3. Panel C depicts the degree of hyperintense disease infiltration into the pedicle on
sagittal short T1 inversion recovery (STIR) imaging at L3. Sagittal T2 (D) sequence
demonstrating the L3 vertebral compression burst fracture and resultant degree of
canal stenosis.

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Radiation-Sensitive Spine Tumor

Questions

1. Do these radiographic features explain the patient’s findings?

2. Is the patient mechanically unstable?
3. What is the significance of left L3 pedicle involvement?
4. Are there any additional studies that would aid in the assessment of this
patient?
5. What is the differential diagnosis?

Oral Boards Review: Diagnostic Pearls

1. Patients with multiple so-​called red flags in association with complaints of

back pain should be evaluated with MRI. In a recent systematic review ad-
vanced age, prolonged use of corticosteroids, severe trauma, and a prior his-
tory of malignancy were all associated with a higher post-​test probability of
fracture or malignancy detection.3 In this case, the patient is advanced in age;
had relatively insidious, progressive onset of back pain in conjunction with
worsening radiculopathy on axial loading; and, on further questioning, was
found to have a component of “biological,” tumor-​related pain unresponsive
to standard conservative therapy. These are all factors that should prompt the
clinician to evaluate the patient with MRI.
2. Owing to improving longevity in patients with metastatic cancer, up to 40%
of patients will develop spinal metastases with epidural disease.2 It is often
possible to predict disease severity based on the patient’s presenting symptoms,
which often include pain and less often neurological deficit:
a. Biologic or “tumor-​related” pain is more prominent at night and in the
early morning, with resolution later in the day and is secondary to the di-
urnal variation in endogenous steroid secretion, which is diminished at
night. It is an early symptom of bony metastasis and is responsive to radia-
tion and steroid therapy.
b. Mechanical pain is less common and is related to movement. In the cer-
vical spine, mechanical pain worsens with rotation, flexion, and extension.
In the thoracic spine, where the facets are oriented in the coronal plane
and there is less mobility owing to the stability provided by the thorax,
pain may be worse when lying down or worsen in the process of changing
positions from lying down to sitting and vice versa. In the lumbar spine,
the facets are arranged in the sagittal plane and often there is adjacent ped-
icle involvement. This patient has a classic presentation of a mechanically
insufficient pedicle from invaded tumor within the pedicle itself and into
the neural foramen space, manifested as severe radicular pain elicited by
axial loading of the spine.1,2,4
3. Evaluation of spinal stability is an important consideration independent
from both the cancer and neurological assessments. Pathological fracture
from tumor and traumatic fracture represent different pathologies and thus
have distinct biomechanical implications. The Spinal Oncology Research

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Spinal Neurosurgery

Group developed and tested a scoring system, the Spinal Instability in

Neoplasia Score (SINS), to aid in determining the stability of the spine in
neoplastic disease. This system uses six domains: location, pain, bone lesion
character, radiographic spinal alignment, degree of vertebral body collapse,
and the degree of posterolateral involvement of the spinal elements (Figure
17.2).5,6

Figure 17.2  SINS system: Spinal Instability Neoplastic Score.

4. If a neoplastic process is suspected based on initial non-​contrast lumbar

MRI, then a gadolinium-​enhanced MRI of the complete spine should be

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Radiation-Sensitive Spine Tumor

obtained to rule out involvement of the spine at other locations. Additionally,

a computed tomography (CT) scan of the chest/​abdomen/​pelvis or positron
emission tomography-​CT (PET-​CT) can be obtained to assess systemic di-
sease burden.
5. If multiple myeloma is suspected, serum and urine electrophoresis for as-
sessment of a monoclonal hypergammaglobulinemia or urinary Bence-​
Jones protein can aid in diagnosis. IgG followed by IgA protein spikes are
most commonly seen on electrophoresis, evident in up to 80% of patients.
Hypercalcemia, hyperuricemia, and increased alkaline phosphatase can all be
diagnostic clues.7
6. Metastatic lesions, multiple myeloma, and other lymphoproliferative tumors
are the most common malignant tumors of the spine. The differential diag-
nosis of an enhancing soft tissue lesion arising from the bone marrow of a
vertebral body and involving the pedicles, epidural, and paraspinal spaces in-
clude metastasis, hematopoietic neoplasia, chondrosarcoma, chordoma, osteo-
sarcoma, and liposarcoma in order of decreasing frequency.8

Decision-​Making

In this case, a 71-​year-​old woman presents with an L3 pathologic burst fracture involving
her pedicles, there exists epidural extension of the mass, and resultant thecal sac and
nerve root compression manifests with mechanical back pain and radiculopathy. Further
workup reveals positive Bence-​Jones urinary protein and an IgG spike on protein elec-
trophoresis. CT of the chest, abdomen, and pelvis did not demonstrate additional di-
sease. There are many factors to consider in the treatment of this patient with a spinal
tumor. After initial radiographic diagnosis, a biopsy may be required in order to make a
diagnosis, especially if a primary spinal tumor is suspected. In this case, the protein elec-
trophoresis facilitated the diagnosis of multiple myeloma. A decision-​making framework
called NOMS (Neurologic, Oncologic, Mechanical and Systemic) facilitates and guides
therapeutic decisions for patients with spinal metastases. This decision-​making tool is
designed for use in a multidisciplinary fashion by surgeons in conjunction with med-
ical and neuro-​oncologists, interventionalists, pain physicians, and radiation oncologists
(Figure 17.3).9
The neurologic assessment consists of evaluating the patient for evidence of my-
elopathy or cauda equina syndrome and the extent of radiographic epidural spinal
cord compression (ESCC). The ESCC scale facilitates reporting of the degree of
spinal cord compression (Figure 17.4).4 In our case, the patient had radiculopathy
without signs of myelopathy or cauda equina syndrome. In general, the oncologic
assessment within the NOMS framework consists of determining the histology-​
specific expected degree of tumor response to conventionally fractionated external
beam radiation (cEBRT) and systemic therapy.9 In considering our patient’s onco-
logic status, she has laboratory and diagnostic testing suggestive of multiple myeloma,
a tumor which is amenable to treatment with conventional radiotherapy (Figure
17.5).9 Radiation therapy effectively treats biologic pain. The mechanical assessment

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Figure 17.3 The NOMS framework: Neurologic, Oncologic, Mechanical and Systemic.

 

Radiation-Sensitive Spine Tumor

3
1c 2
1b
0 1a

Schematic representation of the 6-point ESCC grading scale.

Grade 0 Bone-only disease
Grade 1a Epidural impingement, without deformation of thecal sac
Grade 1b Deformation of thecal sac, without spinal cord abutment
Grade 1c Deformation of thecal sac with spinal cord abutment, without cord compression
Grade 2 Spinal cord compression, with cerebral spinal fluid (CSF) visible around the cord
Grade 3 Spinal cord compression, no CSF visible around the cord

Figure 17.4  Epidural Spinal Cord Compression Grading Scale.

requires careful evaluation for the presence of movement-​associated pain and de-
termination of tumor-​associated mechanical instability is facilitated by the SINS
scoring system.5,6 Since radiotherapy and systemic therapy do not restore mechan-
ical stability of the spine, patients with mechanical instability require stabilization.
Assessment of mechanical instability as an independent factor in surgical decision-​
making even for radiosensitive tumors can be of great benefit to patients.1,2 SINS
scoring for assessment of spinal stability in this patient yields a potentially unstable
score of 12 (Location = 2 [mobile lumbar spine], Pain = 3 [mechanical], Lesion = 2
[lytic], radiographic spinal alignment  =  0 [minimal de novo deformity], vertebral
body collapse = 2 [involvement of the vertebral body with less than 50% height loss],
posterolateral involvement of spinal elements  =  3 [bilateral pedicle involvement]).
A significant number of patients will score in the SINS 7–​12 range, indeterminate
or potentially unstable, and that’s where additional information such as the character
and circumstances of the patient’s pain aid in the assessment of spinal stability and
suitability for surgical intervention. Patients who have no radiculopathy at rest, but
which is then invariably elicited on sitting or standing, or back pain that is most se-
vere when changing position from lying to sitting and from sitting to standing make
excellent candidates for surgical stabilization and are thought to have mechanical
pain. In the authors’ single-​center study of patients with mechanical pain, nearly
98% of patients had improvement in their mechanical pain with spinal fixation.2
Radiographically, these tumors often manifest as burst fractures with some degree of
posterior element involvement. The mechanical problem arises when a pedicle and/​
or facet complex is compromised by tumor infiltration rendering these structures
unable to maintain the patency of the neural foramen with axial load stress. Hence,

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Figure 17.5  Summary of expected radiation response by histology.

 

Radiation-Sensitive Spine Tumor

when patients load the facet when standing or sitting, there is foraminal collapse and
impingement of the exiting nerve root.2,4
To summarize, this patient has spinal instability and mechanical radiculopathy as a re-
sult of a myelomatous L3 pathologic burst fracture with high-​grade epidural extension.
Neurologically, she has back pain and radiculopathy without cauda equina syndrome
and high-​grade epidural disease. Oncologically, her treatment will consist largely of ra-
diation and systemic therapy. Independent of her oncologic treatment, on mechanical
assessment, she has a SINS of 12 with mechanical radiculopathy, indicating she would
benefit from surgical stabilization. Systemically, there are no major contraindications to
surgery or immediate concerns about the durability of her disease control.
There are multiple options for surgical stabilization including external orthosis alone,
or kyphoplasty or vertebroplasty alone or in addition to short-​or long-​segment open
or percutaneous posterior fixation with or without cement augmentation. Percutaneous
cement augmentation represents an excellent stabilization option for fractures confined
to the vertebral body.10 However, pathologic compression fractures that extend into the
posterior elements (pedicle and joint) require stabilization of the posterior elements
using posterior instrumentation.1 Surgical excision of the tumor is not required since
durable local control is expected after cEBRT and systemic therapy. Therefore, the pri-
mary goal of surgical intervention is restoration of mechanical stability. Surgery should
be designed to expedite systemic and radiation therapy. The patient in this case was
offered cement-​augmented, short-​segment percutaneous transpedicular fixation with
kyphoplasty for the symptomatic level at L3.

Questions

1. What are the treatment options for this patient’s L3 pathologic burst fracture?
2. What are some of the considerations that might inform your
decision-​making?
3. Is surgical fixation, kyphoplasty, or radiotherapy the superior treatment of this
disease?
4. If radiotherapy is used, should it be conventional fractionated radiotherapy or
stereotactic radiosurgery (SRS)?

Surgical Procedure

The patient is positioned prone on an open Jackson operating table or other table with a
radiolucent frame. Care is taken to pad all pressure points. Leads for intraoperative free-​
running electromyography (EMG), somatosensory evoked potentials, and transcranial
motor evoked potentials are placed. The patient is prepped and draped in the standard
fashion. Fluoroscopy or neuronavigation may be used to guide the Jamshidi needles
for the placement of the instrumentation and cement-​injection cannulas (Figure 17.6).
Kirschner wires are then passed through L2 and L4 pedicles, dilators are utilized se-
rially, and the cannulated pedicles are tapped. In general, 6.5  mm × 45  mm screws
are used throughout the midlumbar spine. Cannulated pedicle screws are placed over
the Kirschner wires and advanced to near the anterior vertebral body cortical margin.

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Figure 17.6  Intraoperative fluoroscopy for guidance of Jamshidi needle placement (A, anteroposterior [AP] view). Lateral fluoroscopic views
of Kirschner wires (B) and cement cannulas (C) as they are passed through L2 and L4 pedicles. Balloon kyphoplasty (C) followed by cement
injection (D) viewed via lateral fluoroscopy. Cannulated pedicle screws are placed over the Kirschner wires and advanced to near the anterior
vertebral body cortical margin. Cement injection, in order to improve the bony purchase in patients with osteoporotic vertebrae, may be carried
out prior to placement of the screws. The wires are removed and rods are placed percutaneously and secured to the pedicle screws using locking
set screws (E).
 

Radiation-Sensitive Spine Tumor

Cement injection, in order to improve the bony purchase in patients with osteoporotic
vertebrae, may be carried out prior to placement of the screws. Fenestrated screws that
permit cement injection after the screw is placed facilitate cement augmentation of the
screws and decrease the risk of cement extravasation. The wires are removed (Figure
17.6). Care is taken not to overdrive the screw and to maintain the polyaxial nature of
the tulip head. Cement augmentation of the vertebral body fracture may be carried out
using balloon kyphoplasty or vertebroplasty technique (Figure 17.6). A series of fluor-
oscopic images aids in early identification of any cement extravasation. Approximately
2.5–​3.5 mL of cement is used to fill the fracture cleft and restore vertebral body integrity
(Figure 17.6). Rods are placed percutaneously and secured to the pedicle screws using
locking set screws.
Meticulous hemostasis is obtained.The wounds are irrigated with antibiotic solution,
and vancomycin powder is used at level of the hardware. The fascia and subcutaneous
tissues are closed with 0 and 2-​0 absorbable suture in an interrupted fashion, and the
subcuticular layer closed with interrupted 3-​0 absorbable suture. The skin is closed with
4-​0 Monocryl suture in a subcuticular fashion. In patients requiring longer constructs, a
midline skin incision with multiple transfascial incisions may provide improved cosmesis
and healing.

Oral Boards Review: Surgical Management Pearls

1. Cement augmentation of the pedicle screws provides improved pull-​

out strength and decreased screw subsidence in patients with cancer and
osteoporosis.
2. Neurophysiological monitoring including free-​running EMG and nerve stim-
ulation can help to avoid suboptimally placed instrumentation.
3. Ensuring optimal cement viscosity and serial fluoroscopy during cement aug-
mentation of fenestrated transpedicular instrumentation and kyphoplasty can
help avoid extravasation of cement into the central canal or neural foramen as
well as embolization of cement material.

Aftercare

Postoperatively, patients undergo close neurologic observation. Steroids are con-

tinued in the perioperative period to reduce swelling and improve radicular pain.
Postoperative films are obtained as a baseline for future comparison (Figure 17.7).
Radiation oncology is involved early in the patient’s postoperative course so that
conventional radiotherapy can begin shortly after surgery, often within 1–​2 weeks.
In the case of more radioresistant histology, SRS can be given within 7–​10 days of
surgery. Most importantly, care is taken to minimize undue delay in the initiation
of systemic therapy. Surveillance MRI scans are obtained every 2 months following
surgery and treatment.

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Figure 17.7  Lateral (A) and anteroposterior (AP) (B) plain films and T2 axial (C) and
sagittal (D) magnetic resonance images (MRIs) through the index level approximately
3–​4 weeks after spinal instrumentation and conventional radiotherapy.
ESCC, epidural spinal cord compression; SRS, stereotactic radiosurgery; SINS, Spinal Instability
Neoplastic Score; NOMS, Neurologic, Oncologic, Mechanical, and Systemic scoring.

Complications and Management

Surgery for radiosensitive spinal tumors can be complicated by pseudarthrosis or

wound dehiscence, both sequelae of postoperative radiation therapy. Often, a solid bony
lion does not occur and the surgical construct should be strong enough to function
on its own and not necessarily rely upon bone formation. Wound complications can
be prevented by careful communication with the oncology team members regarding
timing of adjuvant treatments and involvement of wound care specialists.

Oral Board Reviews: Complications Pearls

1. Bony fusion at the site of the tumor stabilization is a rare event since radia-
tion therapy and systemic therapy severely impair arthrodesis. Therefore, spinal
constructs should be designed to provide stand-​alone stabilization. Utilization
of larger rod diameters (e.g., 6.5 mm) and cement reinforcement of the ped-
icle screws may improve the durability of spinal instrumentation in patients
with metastatic spinal tumors.
2. Additional consideration should be made to wound closure techniques
that minimize the risk of wound dehiscence or infection. In the setting

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Radiation-Sensitive Spine Tumor

of wound dehiscence or infection, early involvement of plastic surgeons is

recommended.
3. Progression of disease can be managed with salvage open surgery and de-
compression with or without intraoperative brachytherapy followed by re-​
irradiation when applicable.

Evidence and Outcomes

The NOMS framework takes advantage of the increasingly multidisciplinary nature of

the treatment of patients with neoplastic spine disease and allows for the incorpora-
tion of newer treatments and technologies as they become available, adapting as treat-
ment paradigms shift. It is important to note that surgery for the treatment of spinal
metastases is palliative. For solid cancers, 2-​year survival from the time of a cancer di-
agnosis for most patients is in the range of 10–​20%, although with immunologic and
targeted therapies this may be improving.9 In the case of lymphoproliferative neoplastic
disease like multiple myeloma, with current medical therapies including bone marrow
transplant 10-​year survival approximates 30%. The primary indication for spinal sur-
gery among patients with multiple myeloma is restoration of mechanical stability, which
results in pain control and improvement in quality of life. Surgery for maintenance or
improvement of neurological status and local disease control is rarely required in patients
with radiosensitive tumors such as multiple myeloma.9
From a neurologic and oncology perspective, patients with multiple myeloma, even
in the setting of spinal cord compression, respond readily to conventional fractionated
radiotherapy, both clinically and radiographically. However, in the setting of progres-
sive neurologic deterioration secondary to spinal cord compression, surgical decom-
pression may be beneficial for rapid decompression of the spinal cord and optimization
of neurologic function restoration. More often, patients with multiple myeloma are
operated on for mechanical instability, as was the case with our patient. With respect
to mechanically unstable patients with pathological vertebral compression fracture and
radiosensitive histology, cement-​augmented, short-​segment percutaneous fixation with
kyphoplasty has been shown to decrease the proportion of patients in severe pain from
86% to 0%, with as many 65% of patients reporting no pain referable to instability
postoperativly.1
For pathologic vertebral compression fractures of all histologies associated with de-
formity or debilitating pain refractory to opioid analgesics and corticosteroids, there is
class 1 data that demonstrate pain-​and back-​specific functional status is significantly
improved at 1 month in those who undergo balloon kyphoplasty when compared to
patients who are managed without intervention.10
In contrast, for patients with solid tumor metastases resulting in ESCC and/​or
neurologic deficit, Roy Patchell et al. published class I evidence for direct surgical de-
compression.11 Patients in this study who were randomized to receive 30 Gy conven-
tional radiotherapy in addition to direct surgical decompression fared better with respect
to recovery and maintenance of ambulation and preservation of bladder and bowel func-
tion, as well as subsequent decreased need for corticosteroids and narcotic medications

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Spinal Neurosurgery

than patients who received 30 Gy conventional radiotherapy alone.11 Importantly, 70%

of these patients had local recurrence at 1-​year postoperative evaluation. More recently,
advancements in radiation technology, instrumentation, and surgical technique have led
to the development of newer approaches for treatment of ESCC from metastatic disease,
with a trend toward less surgical morbidity, less invasive surgery, and a greater reliance on
radiosurgical therapy (SRS) for local disease control.With high enough single-​fraction or
hypofractionated SRS, ablative doses of radiation may be delivered to cancer histologies
previously thought of as radioresistant (Figure 17.5). SRS in the range of 18–​27 Gy pro-
vided in 1–​3 fractions have yielded radiographic progression-​free survival ranging from
at least 84% at 2 years to potentially as high as 96% at 3 years in retrospectively reviewed
large multi-​institutional series comprised of all solid tumor histologies.12,13 In another
analysis of patients with ESCC and instability manifesting in mechanical radiculopathy,
“separation” surgery followed by posterior instrumented fixation resulted in 98% of
patients reporting improvement in pain and a 41% improvement in performance status
as determined by Eastern Cooperative Oncology Group (ECOG) scoring.2 In so-​called
separation surgery, a posterolateral approach is utilized to obtain ventrolateral access to
nerve roots, the posterior longitudinal ligament, and, most importantly, ventral epidural
disease. Circumferential decompression and reconstitution of the thecal sac is achieved
such that high-​dose single-​fraction or hypofractionated radiosurgery can be given to
remaining disease. “Separation” surgery followed by SRS within our institution yielded
an 84% 1-​year progression-​free survival rate on evaluation of one of the earlier cohorts
in our experience.14 Recent cohorts have demonstrated even higher progression-​free
survival at 2 and 3 years and will be reported shortly (unpublished data).
The NOMS framework is broadly applicable to spinal neoplastic disease of
radiosensitive and radio-​resistant histology and is able to incorporate new technologies
and shifting disease management paradigms.

References and Further Reading

1. Moussazadeh N, Rubin DG, McLaughlin L, Lis E, Bilsky MH, Laufer I. Short-​segment percu-
taneous pedicle screw fixation with cement augmentation for tumor-​induced spinal instability.
Spine J Off J North Am Spine Soc. 2015;15(7):1609–​1617. doi:10.1016/​j.spinee.2015.03.037.
2. Moliterno J,Veselis CA, Hershey MA, Lis E, Laufer I, Bilsky MH. Improvement in pain after
lumbar surgery in cancer patients with mechanical radiculopathy. Spine J Off J North Am Spine
Soc. 2014;14(10):2434–​2439. doi:10.1016/​j.spinee.2014.03.006.
3. Downie A, Williams CM, Henschke N, et al. Red flags to screen for malignancy and fracture
in patients with low back pain: Systematic review. BMJ. 2013;347:f7095.
4. Bilsky M, Smith M. Surgical approach to epidural spinal cord compression. Hematol Oncol
Clin North Am. 2006;20(6):1307–​1317. doi:10.1016/​j.hoc.2006.09.009.
5. Fourney DR, Frangou EM, Ryken TC, et al. Spinal instability neoplastic score: An analysis
of reliability and validity from the spine oncology study group. J Clin Oncol Off J Am Soc Clin
Oncol. 2011;29(22):3072–​3077. doi:10.1200/​JCO.2010.34.3897.
6. Fisher CG, DiPaola CP, Ryken TC, et al.A novel classification system for spinal instability in ne-
oplastic disease: An evidence-​based approach and expert consensus from the Spine Oncology
Study Group. Spine. 2010;35(22):E1221–​E1229. doi:10.1097/​BRS.0b013e3181e16ae2.

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7. Bilsky MH, Azeem S. Multiple myeloma: Primary bone tumor with systemic manifestations.
Neurosurg Clin N Am. 2008;19(1):31–​40. doi:10.1016/​j.nec.2007.09.001.
8. Rodallec MH, Feydy A, Larousserie F, et al. Diagnostic imaging of solitary tumors of the
spine: What to do and say. RadioGraphics. 2008;28(4):1019–​1041. doi:10.1148/​rg.284075156.
9. Laufer I, Rubin DG, Lis E, et al.The NOMS framework: Approach to the treatment of spinal
metastatic tumors. Oncologist. 2013;18(6):744–​751. doi:10.1634/​theoncologist.2012-​0293.
10. Berenson J, Pflugmacher R, Jarzem P, et al. Balloon kyphoplasty versus non-​surgical frac-
ture management for treatment of painful vertebral body compression fractures in patients
with cancer: A multicentre, randomised controlled trial. Lancet Oncol. 2011;12(3):225–​235.
doi:10.1016/​S1470-​2045(11)70008-​0.
11. Patchell RA, Tibbs PA, Regine WF, et  al. Direct decompressive surgical resection in the
treatment of spinal cord compression caused by metastatic cancer: A randomised trial. Lancet.
2005;366(9486):643–​648. doi:10.1016/​S0140-​6736(05)66954-​1.
12. Guckenberger M, Mantel F, Gerszten PC, et al. Safety and efficacy of stereotactic body radi-
otherapy as primary treatment for vertebral metastases: A multi-​institutional analysis. Radiat
Oncol Lond Engl. 2014;9:226. doi:10.1186/​s13014-​014-​0226-​2.
13. Yamada Y, Lovelock DM,Yenice KM, et al. Multifractionated image-​guided and stereotactic
intensity-​modulated radiotherapy of paraspinal tumors:  A preliminary report. Int J Radiat
Oncol Biol Phys. 2005;62(1):53–​61. doi:10.1016/​j.ijrobp.2004.09.006.
14. Laufer I, Iorgulescu JB, Chapman T, et al. Local disease control for spinal metastases following
“separation surgery” and adjuvant hypofractionated or high-​dose single-​fraction stereo-
tactic radiosurgery: Outcome analysis in 186 patients. J Neurosurg Spine. 2013;18(3):207–​214.
doi:10.3171/​2012.11.SPINE12111.

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Cauda Equina Syndrome

Emily P. Sieg, Justin R. Davanzo, and John P. Kelleher

Case Presentation

A 34-​year-​old woman with no past medical history presents to the emergency depart-
18
ment with acute loss of motor function and significant radicular type pain in both lower
extremities. In addition, she was noted to have significant urinary retention and loss of
rectal tone with bowel incontinence. A detailed neurologic examination is performed
which reveals 5/​5 motor strength in the bilateral upper extremities; 2/​5 motor strength
in the bilateral iliopsoas, quadriceps, and hamstrings; and 0/​5 motor strength in the bi-
lateral tibialis anterior, gastrocnemius, and extensor hallucis longus. Sensory examination
reveals normal sensation in the bilateral upper extremities and decreased sensation to
light touch and pin prick throughout the bilateral lower extremities. Testing of reflexes
revealed 2+ reflexes in the bilateral upper extremities and absent patellar and ankle jerk
reflexes bilaterally. A urinary catheter is placed with return of 1,000 mL of clear, yellow
urine. A rectal exam reveals absence of rectal tone.

Questions

1. What is the most likely diagnosis?

2. What imaging modality should be used to confirm this diagnosis?
3. What anatomic location should be imaged based on this constellation of
symptoms?
4. What is the most appropriate timing of the diagnostic workup for this
patient?

Assessment and Planning

This constellation of symptoms is most consistent with cauda equina syndrome. The
cauda equina is a group of nerves in the lumbosacral spine that provide motor and sen-
sory function to most of the lower extremities, pelvic floor musculature, and sphincters.
Cauda equina syndrome (CES) arises secondary to compression of or injury to these
roots.The signs and symptoms of this disease include lower extremity motor and sensory
dysfunction, autonomic dysfunction (including loss of bowel and bladder control), and
pain. While these symptoms are most consistent with CES, other pathologies must be
on the differential diagnosis. Most importantly, compression of the cervical or thoracic
spinal cord must be considered. Other pathologies such as multiple sclerosis, neoplasms,
and vascular malformations should also be included in the differential.

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Spinal Neurosurgery

A multitude of pathologies can lead to CES, and distinguishing between these

pathologies is important as it may lead to dramatically different treatment strategies. It is
of paramount importance to determine if the etiology is compressive or noncompressive
in nature as this is the primary determinant with regards to the need for surgical man-
agement. Compressive etiologies are far more commonly the cause of CES, the most
common of which is a midline disc herniation. This can lead to either the acute or sub-
acute development of CES. Spinal stenosis can lead to a more chronic development of
CES. It is also important to note that, in the setting of significant spinal stenosis, even
a small disc herniation can lead to the acute development of CES. Other compres-
sive causes of CES include spinal fractures with retropulsion, hematomas, iatrogenic
(i.e., hardware failure), vascular lesions (i.e., arteriovenous malformations), and neo-
plastic lesions (i.e., schwannomas, ependymomas, metastases). Noncompressive causes of
CES include ischemic insults and inflammatory conditions. While these are much less
common, it is important to keep them in mind as their treatment is often nonsurgical
in nature.
When a patient presents with acute loss of motor and sensory function in the lower
extremities, the first step in diagnostic evaluation is often a computed tomography (CT)
scan of the lumbar spine.While this will rule out any bony cause of compression, it does
not have the resolution to show compression due to soft tissue, such as an intervertebral
disc. Thus, any patient with this constellation of symptoms should undergo magnetic
resonance imaging (MRI) of the lumbar spine. In a normal T2-​weighted axial image,
the cauda equina appears as a number of hypointense circular structures, which are the
nerve roots, within a large area of hyperintensity, the cerebrospinal fluid (CSF)-​filled
thecal sac. Typically, areas of hyperintensity can be seen between each of the nerve roots.
With compression significant enough to cause CES, there is usually a complete loss of
this hyperintense CSF, especially between the nerve roots. When working up a patient
with new onset of motor and sensory loss, it is important to consider imaging of the
brain and cervical and thoracic spine as well. This is of greater significance if the lumbar
spine MRI is unrevealing or if symptoms suggestive of cervical or thoracic myelopathy
are present on exam.
In the case at hand, MRI of the lumbar spine revealed an acute disc herniation at the
L4–​L5 level with complete obliteration of the CSF space (Figure 18.1).

Oral Board Review: Diagnostic Pearls

1. Timely acquisition of the MRI of the lumbar spine is important in the setting
of CES. Not only does this confirm the suspected diagnosis, but it also reveals
the level of the disease if needed for surgical planning.
2. In patients who cannot undergo MRI, a CT myelogram should be obtained
to confirm the diagnosis as well as the level of disease.
3. If the routine workup, including MRI of the rest of the neuroaxis, is negative,
other diagnostic considerations should include lumbar puncture for acquisi-
tion of CSF and vascular imaging to rule out arteriovenous malformation.

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Figure 18.1  (A) Sagittal T2-​weighted magnetic resonance image (MRI) of the

lumbosacral spine revealing a disc herniation at the L4–​L5 level causing significant
mass effect on the thecal sac. (B) Axial T2-​weighted MRI of the lumbosacral spine at
the L4–​L5 level showing an acute disc herniation with complete obliteration of the
cerebrospinal fluid space and severe nerve root compression.

Questions

1. How do the findings on MRI and clinical exam influence surgical planning?
2. Based on the case presentation, what is the most appropriate timing for sur-
gical intervention to optimize patient outcome?
3. In the setting of acute disc herniation, what consideration needs to be given
to stabilization techniques?

Decision-​Making

In the setting of acute loss of motor, sensory, or autonomic function and a disc hernia-
tion noted on lumbar spine MRI, emergent decompression via laminectomy should be
undertaken. Partial or incomplete CES, when patients have difficulty voiding or urinary
frequency and resultant urinary retention, is often a precursor to complete CES. Since
recovery is less certain once nerves have become extensively damaged, surgical inter-
vention early in partial CES is recommended. While most would recommend that this
decompression for both partial and complete CES be done as soon as possible, patients
should never wait more than 48 hours from their presentation to undergo decompres-
sion in acute CES. By delaying decompression, the risk of permanent damage to the
nerve roots is increased. This could lead to long-​term loss of motor, sensory, or auto-
nomic function.
The main surgical option in this case is lumbar laminectomy at the level of the disc
herniation to decompress the nerve roots. In addition, with an acute disc herniation, a
micro-​discectomy is typically performed. Consideration can be given to performing the
decompression via a minimally invasive technique in which the primary goal becomes

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removal of the herniated disc fragment to decompress the nerve roots. However, in an
emergent setting, most experts recommend performing this operation via a traditional
open technique.
Prior to surgery, the risk and benefit profile for this particular disease state and sur-
gical procedure should be discussed with the patient.The risks of this procedure include
bleeding, infection, damage to the nerve roots, CSF leak, and need for further surgical
intervention. When discussing the need for future surgical intervention, consideration
must be given to the need for spinal fusion. If the laminectomy performed at the time
of surgery needs to be particularly wide, including removal of parts of the facet joints
or pars interarticularis, over time, the patient may develop degeneration at this level
requiring spinal fusion. Most often, spinal fusion is not required at the time of initial
decompression for CES, especially when this is secondary to an acute disc herniation;
however, there are situations where this should be considered, especially in neoplastic
disease processes resulting in instability.

Questions

1. What intraoperative techniques should be used to localize the appropriate

level of operation?
2. If an acute disc herniation cannot be located, what steps should be taken to
ensure an adequate decompression has been performed?

Surgical Procedure

Once CES is diagnosed based on both clinical examination and imaging, emergency
surgical decompression within 48 hours is recommended. Several surgical options exist
depending on patient pathology, including laminectomy with or without discectomy.
The mainstay of treatment in patients presenting with CES due to lumbar stenosis or a
lumbar disc is posterior laminectomy and decompression in order to relieve the pres-
sure on the nerves. If CES is caused by a more complicated structural lesion, such as a
retropulsed bone fragment in the setting of trauma, chronic inflammation, tumor inva-
sion, or metabolic disease such as lipomatosis, the addition of concurrent instrumenta-
tion or an anterior staged procedure in the future should be considered.
Premorbid conditions as well as age should be considered when determining the
anesthetic plan. A lumbar laminectomy can be done either under general anesthesia or
using a spinal epidural if patient is high risk for anesthesia. A urinary catheter should be
placed preoperatively due to the high risk of urinary retention and bladder distention
in the setting of CES. Fluoroscopy should be available for localization of level, and the
need for neurophysiologic intraoperative monitoring should be considered. The patient
should be positioned prone on a Wilson or Jackson table. The Wilson frame allows for
flexion of the lumbar spine which opens the posterior elements, while the Jackson table
maintains more normal lumbar lordosis. All pressure points should be carefully padded
to prevent pressure sores and peripheral neuropathies. Pressure on the abdomen should
be checked preoperatively after final positioning as excessive abdominal compression
can make epidural bleeding more difficult to control due to venous congestion.

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A linear midline incision should be made after a spinal needle is used to obtain
x-​ray verification that the level is appropriate. Subperiosteal dissection then removes
the erector spinae muscles from the lamina. Care should be taken to remain in this
subperiosteal plane to minimize bleeding. Dissection is then carried out laterally to the
medial aspect of the facet joint complex and the bilateral pars are exposed. It is impor-
tant not to violate the facet joint capsule as this significantly increases the risk of insta-
bility. A Leksell rongeur is then used to remove the spinous processes, and a high-​speed
drill is used to thin out the lamina. A Kerrison rongeur can then be used to complete the
remainder of the boney laminectomy as well as removal of the ligamentum flavum. The
lateral recesses are then decompressed using a Woodson elevator and Kerrison rongeur.
In the setting of a disc herniation leading to CES, the thecal sac should then be
retracted medially using a nerve root retractor. An 11 blade is used to incise the posterior
longitudinal ligament and the disc annulus, and an upgoing curette in combination with
a pituitary rongeur is used to remove the disc material. The surgeon should always be
aware of where the anterior longitudinal ligament is in order to prevent accidental in-
jury to the retroperitoneal vessels. Once the disc has been removed, a nerve hook should
be used to feel under the posterior longitudinal ligament (PLL) and a Woodson elevator
should be passed over the dura to feel and for any residual fragments.
Hemostasis should be obtained using bipolar electrocautery and hemostatic agents.
Bone wax should be used to help obtain hemostasis at boney edges. Once immaculate
hemostasis has been achieved, the wound should be copiously irrigated. A  subfascial
drain may be used. It is more likely to be required if multiple levels are involved and can
help with wound healing and prevention of postoperative epidural hematoma. Attention
is then turned to closing. Tight fascial closure is important to minimize wound dehis-
cence and other postoperative wound complications. The fascia should be closed with
0 or 2-​0 absorbable sutures. The subcutaneous layer is closed with interrupted inverted
3-​0 absorbable sutures. The skin should then be closed in standard fashion.

Oral Boards Review: Management Pearls

1. If the patient has advanced degenerative disease, spondylolysis, or

spondylolisthesis on flexion-​extension, imaging should be obtain preopera-
tively to rule out spinal instability.
2. Adequate hemostasis should always be obtained using hemostatic agents to
prevent postoperative epidurals. If minor bleeding persists, a subfascial drain
should be considered.
3. When using the 11 blade to incise the disc, always go medial to lateral thus
incising away from the dura.

Pivot Points

1. Use caution to avoid decompression or dissection that is too lateral and leads
to destruction of the facet, pars interarticularis, or facet capsule thus poten-
tially causing instability requiring a spinal fusion.

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2. Due to severe compression of the thecal sac, these patients are at high risk for
dural tear. Drilling the lamina to a thin shelf before carefully using a combi-
nation of a curette and Kerrison punch can help minimize this.
3. The ligamentum flavum ends at the superior aspect of the lamina, leaving the
dura unprotected in this area and making the risk of durotomy higher at this
location. Additional care should be taken to ensure the dura is protected.

Aftercare

Postoperatively, a detailed neurologic examination of both upper and lower extremity

sensory and motor function should be done and documented as soon as possible. Many
surgeons require that these patients remain in a horizontal position for the first 24 hours,
to help prevent a CSF leak or pseudomeningocele if there was a known intraoperative
durotomy. While flat, the urinary catheter is typically left in place. Patients without a
CSF leak should be encouraged to ambulate as early as postoperative day 0. Early am-
bulation helps prevent atelectasis, pneumonia, deep venous thrombosis, and pulmonary
embolus.
Physical therapy and occupational therapy consults should be considered. Stool
softeners should be used to prevent postoperative ileus. Once the urinary catheter has
been removed, postvoid residuals should be followed and straight catheterization or
catheter replacement used as needed to prevent bladder distension.
Perioperative antibiotics are generally given and should not be continued beyond
24 hours in a routine case. Narcotic pain medications are often needed, as well as
muscle relaxants. Tylenol as well as nonsteroidal antiinflammatory medications should
be considered to decrease narcotic needs. Nonsteroidal antiinflammatory medications
should not be used if a fusion is done.
Although short-​term recovery of bladder function often lags behind reversal of lower
extremity motor deficits, the function may continue to improve up to 18–​24 months
after surgery. In the postoperative period, drug therapy combined with catheterization
can help with a slow recovery of bladder and bowel function.

Complications and Management

Potential complications range from structural damage intraoperatively to more general

postsurgical complications and can occur intraoperatively or in a delayed fashion. Direct
injury to nerve roots can lead to new or worsening neurologic deficits or neuropathic
pain. A dural tear can lead to an immediate or delayed CSF leak requiring either primary
repair or re-​exploration.
If a durotomy is seen at the time of surgery and a primary repair is done, a Valsalva
should be performed to assess for any continued leak. The need for postoperative flat
bed rest should be considered at the discretion of the surgeon depending on the in-
tegrity of the repair. Poor surgical positioning can lead to compressive neuropathies or
pressure sores.
Postoperative complications can be related directly to the procedure or to general
hospital complications. Wound infections, urinary tract infections, atelectasis, and pneu-
monia can all be the cause of postoperative fevers or leukocytosis. An epidural hematoma

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or CSF collection can lead to recompression requiring a surgical revision. Deep vein
thrombosis is a potential complication that can be minimized by early ambulation if
possible.
Delayed complications seen in clinic range from continued pain to spinal instability.
In the setting of radicular or neuropathic pain with no evidence of nerve compression
on MRI, the addition of gabapentin or pregabalin (Lyrica) should be considered. If
the patient presents with continued back pain, dynamic imaging should be obtained.
Instability may warrant instrumentation and fusion.

Oral Boards Review: Complications Pearls

1. In the case of a CSF leak, use of a lumbar drain to remove tension on the
wound should be considered.
2. If the patient develops new or worsening symptoms postoperatively, an im-
mediate scan should be obtained to rule out a compressive hematoma or CSF
collection.
3. If the patient complains of persistent or worsening back pain at postoperative
visits, dynamic imaging should be obtained to rule out instability requiring
instrumented fusion.

Evidence and Outcomes

CES is rare, and the evidence for the timing of surgical intervention is thus poor quality.
It depends almost exclusively on retrospective observational studies that show a low level
of evidence, grade III or IV. A logistic regression analysis of previously published studies
by Ahn et al. in 2000 of 322 CES patients concluded that although there was a signif-
icant advantage to treating patients before versus after 48 hours from symptom onset,
there was no difference in outcomes when comparing patients treated before 24 versus
at 24–​48 hours. Criticism of Ahn’s review includes the fact that both acute and nonacute
patients were included in the analysis.
In a 2014 meta-​analysis by Chau et al., the authors concluded that there is no strong
evidence to support 48 hours as a safe time point for surgical delay. They argued that
both early and delayed surgery may result in improved neurologic outcomes; however, it
is more likely that earlier surgical intervention is more beneficial, especially in the setting
of acute neurologic compromise. Operating on CES patients at the earliest opportunity
seems to be the most appropriate clinical practice.

References and Further Reading

Ahn UM, Ahn NU, Buchowski JM, Garrett ES, Sieber AN, Kostuik JP. Cauda equina syn-
drome secondary to lumbar disc herniation:  A meta-​analysis of surgical outcomes. Spine.
2000;25:1515–​1522.
Chau AM, Xu LL, Pelzer NR, Gragnaniello C. Timing of surgical intervention in cauda
equina syndrome: A systematic critical review. World Neurosurg. 2014 Mar–​Apr;81(3-​4):
640–​650. doi: 10.1016/​j.wneu.2013.11.007. Epub Nov 13, 2013. Review. PubMed PMID:
24240024.

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Fehlings MG, Zeidman SM, Rampersaud YR. Cauda equina syndrome. In:  Benzel EC, ed.
Spine Surgery. Techniques, Complications, Avoidance and Management. Philadelphia, PA: Elsevier
Churchill Livingstone; 2005.
Qureshi A, Sell P. Cauda equina syndrome treated by surgical decompression: The influence of
timing on surgical outcome. Eur Spine J. 2007;16(12):2143–​2151.

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Miner N. Ross and Khoi D. Than

Case Presentation

A 68-​year-​old man is referred to a neurosurgeon for a chief complaint of heaviness in his

19
legs. He noted the onset of this symptom, accompanied by a feeling of “tightness” in his
lower back, roughly 1 month ago. There was no inciting event or trauma. He feels a con-
stant, dull, aching heaviness that radiates from his lower back into both of his lateral thighs,
although the left leg is somewhat worse than the right. None of his symptoms extends
below his knees. This is exacerbated particularly by climbing stairs, as well as by standing
or walking for prolonged periods, and is alleviated by sitting or lying down. He feels
that his gait is stiff due to these symptoms and has also noted decreased endurance while
exercising on his stationary bicycle. These symptoms have been progressively worsening
and detracting from his quality of life. He denies any changes in his bowel or bladder habits.
This patient’s past medical history includes hypertension, hyperlipidemia, gout, and
obstructive sleep apnea, which are all under adequate control. He has osteoarthritis of
both knees, for which he has undergone bilateral arthroscopy; he has no other sur-
gical history relating to his back or legs. By the time of his presentation, he had already
attempted physical therapy, which provided minimal improvement, as well as acupunc-
ture, which relieved his back pain but not his lower extremity symptoms.
On neurological examination, he has full strength of all major muscle groups as well
as intact sensation throughout. The patellar and Achilles reflexes are diminished bilater-
ally; there is no Babinski sign or clonus present. Coordination is normal, as is regular gait;
however, he is observed to have difficulty with tandem gait.

Questions

1. What is the most likely diagnosis?

2. What imaging modality will be most helpful in making the diagnosis?
3. What anatomical areas must be imaged?
4. What is the appropriate timing of the diagnostic workup?

Assessment and Planning

This patient’s history is strongly suggestive of neurogenic claudication, a common pre-

sentation of symptomatic lumbar canal stenosis. As the lumbar and sacral nerve roots de-
scend through the stenotic canal, their blood supply is compromised, and this ischemia
is thought to give rise to pain, weakness, and sensory changes of the lower extremities.

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Classically, the symptoms of claudication are worsened by activity and relieved at rest,
but they are also sensitive to positional changes of the spine. In extension, as in walking
downhill or lying flat, the lumbar canal is narrowed further, whereas in flexion the canal
is opened and symptoms are relieved. For instance, many patients will report that they
need to lean on a shopping cart to complete a trip through the grocery store.
Subacute to chronic onset of symptoms is more typical of claudication than of cauda
equina or conus medullaris syndromes, which are surgical emergencies and invariably
accompanied by acute bowel and bladder incontinence and saddle anesthesia due to
compression of sacral nerve roots. Neurogenic claudication can be confused with vas-
cular claudication due to arterial insufficiency, but this is generally excluded prior to
referral to a neurosurgeon. A significant history of cardiovascular disease, diminished or
absent peripheral pulses, or an abnormal ankle-​brachial index (ABI) of blood pressures
should prompt reconsideration of a vascular diagnosis.
Claudication due to lumbar stenosis may occur in isolation, as in the case example, or
it may be accompanied by radicular symptoms. The pathologic processes (degeneration,
trauma, infection) that can cause stenosis of the lumbar canal can similarly affect the lat-
eral recesses or neural foramina.
Magnetic resonance imaging (MRI) is the mainstay imaging technique for evaluation of
the spine. It is excellent at visualizing the neural elements of the spinal cord and nerve roots,
as well as the intervertebral discs and soft tissues. Canal stenosis is often identified due to a
disc bulge or extrusion, chronic degenerative spondylosis, ligamentum flavum hypertrophy,
or spondylolisthesis. In patients who are unable to undergo MRI, computed tomography
(CT) myelography can be considered. Failure of the myelography dye to migrate cranially
(i.e., a myelographic block) indicates a level of severe stenosis. For patients with identified
spondylolisthesis, flexion-​extension plain films should be obtained to assess for pathologic
motion, the presence or absence of which will guide surgical planning.
In this patient, MRI of the lumbar spine demonstrated severe central as well as bi-
lateral foraminal stenoses at L2–​L3 and L3–​L4; at L4–​L5 and L5–​S1 he had bilateral
foraminal stenoses as well as grade I spondylolistheses of L4 on L5 and L5 on S1. See
Figure 19.1A, B for sagittal and axial MRI slices. Flexion-​extension films in this case did
not show any dynamic instability.

Oral Boards Review: Diagnostic Pearls

1. Lumbar stenosis does not usually cause focal neurological exam findings.
In the presence of focal pain, sensory changes, or weakness of the lower
extremities, attention should be given to the nerve roots or the peripheral
nerves as a source for the findings.
2. The symptoms of lumbar stenosis are subacute to chronic in onset. In patients
with sudden onset of weakness, numbness, or in those with bowel or bladder
dysfunction, more urgent diagnoses such as cauda equina syndrome or conus
medullaris syndrome should be ruled in or out expediently.
3. MRI is the first-​line imaging modality for evaluating neurological disorders
of the lumbar spine. CT and plain films can aid in evaluation and surgical pla-
nning in select cases.

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A B

Figure 19.1  (A) T2-​weighted sagittal magnetic resonance image (MRI)

demonstrating this patient’s canal stenosis, most notable at L2–​L3. (B) T2–​weighted
axial MRI through the L2-​L3 disc space. Note broad-​based stenosis extending into
the lateral recesses as well as poor visualization of cerebrospinal fluid around the
lumbosacral nerve roots.

Questions

1. How do these radiologic findings direct surgical planning?

2. What is the appropriate timing of intervention in this patient?

Decision-​Making

Lumbar canal stenosis is diagnosed by imaging, with MRI being the gold standard.
Neurogenic claudication is diagnosed by careful history-​taking, as described in the case
presentation, typically in conjunction with a benign neurological examination.The cor-
roboration of imaging findings with the patient’s described symptoms provides a sur-
gical indication. It is entirely possible to have imaging findings of lumbar stenosis in an
asymptomatic patient; likewise, patients may have many stenotic levels but only one that
is the cause of their symptoms. A careful attempt should be made to determine where,
and how much, to operate.
Patients with degenerative spondylosis will frequently have more than one com-
plaint. They may describe radicular symptoms in addition to those of neurogenic clau-
dication. With appropriate imaging findings for foraminal stenosis, these patients can be
offered a foraminotomy in addition to a laminectomy. A not-​infrequent finding of an
extruded disc fragment may occur and cause or contribute to the symptoms of lumbar
stenosis as well as lateral recess or foraminal stenosis. In these patients, a discectomy could
be performed as well. Axial back pain is common but unlikely to respond to any surgical
intervention; thus, in cases where this is the predominant complaint, surgery may be of
very limited benefit to the patient.
Lumbar stenosis is often managed conservatively, especially given that it tends to
develop in an older population where patients may have comorbidities that make
them poor surgical candidates. Conservative management may include nonsteroidal

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antiinflammatory medications, exercise, physical therapy/​rehabilitation, steroid injections,

massage, yoga, or acupuncture. As these techniques are of minimal risk to the patient, it
is reasonable to trial several of them before considering surgery. In most cases, primary
care providers do not make the referral to a spine surgeon until conservative manage-
ment has failed.

Questions

1. What represents an appropriate trial of conservative management?

2. How should surgery be approached in a patient with multiple complaints re-
lated to the lumbar spine?

Surgical Procedure

Surgical decompression of the stenotic lumbar canal is best accomplished by laminec-

tomy at the affected level or levels. This procedure can be performed in the traditional
open fashion or with the use of more modern minimally invasive techniques.
Prone positioning can be aided by the use of a Wilson frame, which can be opened
to induce kyphosis that will open the interlaminar spaces. Fluoroscopy is obligatory for
the proper localization of the level or levels to be operated on and can also be employed
at the conclusion of the decompression to verify that no radiographic stenosis remains.
The use of neuromonitoring is at the discretion of the surgeon, but in a case where no
hardware is being placed and the decompression is extradural, it is unlikely to influence
the outcome of the case.
For an open procedure, once the correct levels are located fluoroscopically, a midline
incision is made and a subperiosteal dissection is carried out using monopolar electrocau-
tery to expose the spinous process and lamina bilaterally at each level to be decompressed.
The interspinous ligaments above and below the level should be transected, and then a
Leksell rongeur can be used to remove the spinous process. The remainder of the bony
decompression can be accomplished with a high-​speed drill followed by the use of a
Kerrison rongeur for more careful bone removal. It is helpful to leave the ligamentum
flavum intact during this stage as it will protect the dura during the bone removal.
Ultimately, the ligamentum flavum should also be removed, as it often contributes to
canal stenosis even in the absence of bony compression. This can be accomplished with
a combination of blunt dissection with a nerve hook as well as taking small pieces with
a Kerrison rongeur. The adequacy of decompression can be verified by palpation with
a nerve hook rostrally and caudally as well as out into the lateral recesses and foramina.
Nerve hooks can be placed into the margins of the decompression and a fluoroscopic
x-​ray taken to verify the radiographic extent of the decompression. Alternatives to nerve
hooks include curettes and/​or Woodson elevators, depending on surgeon preference.
If a durotomy is incurred, it can be repaired primarily by suturing, with or without
a muscle graft, and a fibrin-​based sealant can be applied over the closure. Meticulous
hemostasis should be achieved prior to wound closure to prevent formation of a spinal
epidural hematoma. For wound protection and improved functional outcomes, the
paraspinal muscles should be reapproximated.

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Many variations on the basic technique of laminectomy exist. In open laminectomy,

some surgeons prefer to make partial laminectomies above and below the interlaminar
space, with the idea of preserving the spinous processes and their ligamentous attachments
(i.e., the posterior tension band). Hemilaminectomy (approaching from one side only)
can provide adequate decompression if care is taken to drill under the contralateral
lamina and remove all of the ligamentum flavum. Minimally invasive surgery through a
tubular retractor relies on this concept and can provide excellent results in one-​or two-​
level decompressions. Minimally invasive surgery offers the advantages to the patient of
smaller incisions and decreased muscle dissection, which reduces postoperative pain and
allows faster return to activity.

Oral Boards Review: Management Pearls

1. There are multiple surgical approaches to lumbar decompression; selecting the

correct approach for each patient depends on understanding the history, the
imaging, and patient-​specific factors as they contribute to surgical risk.
2. The ligamentum flavum can be a major contributor to canal stenosis, and de-
compression is not complete unless it is removed.

Pivot Points

1. A patient presenting with bowel or bladder incontinence with saddle anes-

thesia has cauda equina syndrome until proven otherwise, and this surgical
emergency should be ruled out before other evaluation is undertaken.
2. Patients with primarily axial back pain, without a significant history of neuro-
genic claudication, are unlikely to benefit from lumbar decompression even if
they have radiographic stenosis on MRI.
3. Fusion may be considered in patients who have significant spondylolisthesis
or pathologic motion where these are felt to be contributors to their clinical
picture.

Aftercare

Most postoperative patients are able to mobilize within hours of surgery. Consultation
with rehabilitation providers such as physical therapists may be helpful postoperatively,
depending on each patient’s prior level of functioning. Antibiotics do not need to be
continued beyond the intraoperative period. Pain can be managed with moderate-​
strength opioid medications in conjunction with acetaminophen, and muscle relaxers
can be added as needed.
A single overnight stay in the hospital following surgery provides a reasonable length
of time over which to observe patients for any complications. One-​or two-​level open
and minimally invasive cases can be discharged on the same day as surgery. Follow-​up
imaging is typically not necessary in uncomplicated cases. Indeed, postsurgical changes
make any spine MRI obtained within a short interval of surgery difficult to interpret.

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A follow-​up visit in the clinic setting for wound healing and pain management review
is appropriate within 2–​3 weeks.

Complications and Management

The most common intraoperative complication of lumbar decompression is an un-

intentional durotomy. However encountered or repaired in the operating room, most
surgeons will opt to keep the patient on flat bed-​rest for 24 hours during recovery.
The conventional wisdom holds that this decreases the pressure in the lumbar cis-
tern until the durotomy closes, thereby decreasing the risk of cerebrospinal fluid
(CSF) leak or pseudomeningocele formation. There is limited evidence for or against
this practice, but the challenges of managing CSF leaks encourage caution when a
durotomy is incurred. Some evidence does suggest that early mobilization in patients
treated minimally invasively is well tolerated, as the amount of dead space into which
CSF can leak is less.
The most serious postoperative complications of lumbar decompression will man-
ifest as a decline in the patient’s neurological exam. New or worsening weakness or
sensation loss in the lower extremities is concerning for a compressive lesion affecting
the lumbosacral nerve roots. Spinal epidural hematoma is the most feared of these; it can
even present as a new-​onset cauda equina syndrome. Suspicion of an epidural hematoma
necessitates emergent imaging and likely operative re-​exploration. A postsurgical abscess
or a symptomatic pseudomeningocele can also present in this manner, but more often
in a delayed fashion.
Pain, paresthesias, or weakness in a dermatomal distribution may represent a nerve
root that was injured in the course of surgery. These symptoms can be managed
expectantly. A short course of steroids may be of benefit for patients in significant
distress.
Lumbar surgical incisions are at increased risk for wound complications due to being
on a less visible part of the body, as well as being subject to the chafing of clothes and
pressure when sitting or lying down. Surgical washout and revision may be necessary in
cases of dehiscence or where a deep tissue infection is suspected. Superficial infections
often respond well to a course of oral antibiotics directed at common skin flora.

Oral Boards Review: Complications Pearls

1. A durotomy should be repaired and is often managed with 24 hours of strict

bed-​rest, but long-​term outcomes are equivalent in patients with and without
a durotomy.
2. Any decline in a postsurgical patient’s neurological examination should be
evaluated promptly as it will likely require operative management.

Evidence and Outcomes

Limited evidence is available comparing surgical intervention versus conservative

management in lumbar stenosis. Amassing enough data for a systematic review is

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Lumbar Stenosis

hindered by the lack of a well-​defined paradigm for conservative management as

this may include a wide variety of medications and techniques that are themselves of
varying effectiveness.
Recent comparisons of minimally invasive surgical techniques with those of tradi-
tional open laminectomy are proving favorable. Minimally invasive surgery is frequently
able to accomplish an equivalent decompression with less postoperative pain, a shorter
hospital stay, and a lower risk for complications. Conventional open surgery as well
as minimally invasive surgery should be complementary tools in the spine surgeon’s
armamentarium.

References and Further Reading

Machado GC, et  al. Surgical options for lumbar spinal stenosis. Cochrane Database Syst Rev.
2016;11:CD012421.
Naraim AS, et al. Minimally invasive techniques for lumbar decompressions and fusions. Curr Rev
Musculoskelet Med. 2017;10:559–​566.
Overdevest G, et al. Effectiveness of posterior decompression techniques compared with conven-
tional laminectomy for lumbar stenosis. Eur Spine J. 2015;24:2244–​2263.
Zaina F, et al. Surgical versus non-​surgical treatment for lumbar spinal stenosis. Cochrane Database
Syst Rev. 2016;1:CD010264.

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L4–​L5 Degenerative Spondylolisthesis

Rani Nasser, Scott Zuckerberg, and Joseph Cheng

Case Presentation

A 59-​year-​old woman with no significant past medical history presents with bilateral
20
radicular leg pain (right worse than left), as well as axial back pain. She describes the
radicular component of her pain as progressive over 9 months, and the axial back pain
as constant over 4 years. The radicular pain crosses below the knee to the medial foot.
Moreover, the shooting pain is greater than her axial back pain. She is only able to am-
bulate two blocks without her legs “giving out.” Leaning forward, such as leaning over
a shopping cart, gives her transient relief. She has not had any success with conservative
measures such as physical therapy or epidural steroid injections. On physical examina-
tion, she is full strength in all muscle groups, with good muscle bulk and intact reflexes.
However, she had decreased light touch in her right medial foot.

Questions

1. What is the most likely diagnosis?

2. What is the highest yield imaging modality?
3. What are the initial steps in management?

Assessment and Planning

Based on the clinical picture, the clinician may suspect foraminal narrowing.These findings
are substantiated by the foraminal stenosis, as well as the L4–​L5 spondylolisthesis noted
on computed tomography (CT) (Figure 20.1) and MRI (Figure 20.3). When assessing
a spondylolisthesis, the clinician should suspect an underlying pars interarticularis defect
(Figure 20.2). In addition, dynamic imaging may be beneficial to assess movement of the
spondylolisthesis (Figure 20.4). This may guide management toward fusion as oppose to
decompression alone.

Decision-​Making

The initial management of patients presenting with axial back pain with radicular
symptoms is largely conservative in the absence of neurological deficit.1 If the patient
has persistent or progressive symptoms despite conservative measures, surgical decom-
pression and/​or stabilization might be indicated.The Spine Patient Outcomes Research
Trial (SPORT) was a 13-​center randomized cohort study comparing surgical with

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Figure 20.1  Sagittal computed tomography (CT) scan: L4–​L5 grade 1 spondylolisthesis.

Figure 20.2  Sagittal computed tomography (CT) scan: Right pars interarticularis

visualized without defect (right). Left pars interarticularis visualized also without defect
or fracture (left).
 

Figure 20.3  Sagittal magnetic resonance imaging (MRI) (left to right) demonstrating foraminal stenosis without
significant central canal stenosis.

Figure 20.4  Flexion (left) and extension (right) lumbar x-​rays, not demonstrating any
pathological movement.
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Spinal Neurosurgery

nonoperative management of degenerative spondylolisthesis.2 This study demonstrated

that, after 4  years, patients treated surgically had substantially increased pain relief as
compared to patients managed nonoperatively.2
Patients with a symptomatic L4–​L5 degenerative spondylolisthesis who are refrac-
tory to conservative management have been shown to have a beneficial treatment effect
based on the SPORT trial (Treatment Effect = Change in Surgical Oswestry Disability
Index − Nonoperative Change in Oswestry Disability Index).3 The decision to offer a
laminectomy alone as oppose to a laminectomy and fusion must be carefully considered
by the clinician. The degree of spondylisthesis may influence the surgeon’s decision-​
making toward offering a fusion.4 This, in concert with the degree of facet arthropathy,
may also potentially destabilize a patient if he or she is treated with laminectomy alone.5
Ultimately, the decision to fuse/​decompress or decompress alone must be assessed on a
case-​by-​case  basis.

Surgical Procedure

If the surgeon opts to fuse and decompress a degenerative L4–​L5 spondylolisthesis,

multiple options are available. Based on the surgeon’s preference, the patient may be
stabilized using an open or minimally invasive transforaminal lumbar interbody fusion
(TLIF), posterior lumbar interbody fusion (PLIF), or even posterolateral fusion with
pedicle screw fixation.
If the patient is positioned on an open Jackson table, they will fall into alignment,
and often low-​grade spondylolisthesis maybe reduced by positioning alone.6 Special at-
tention should be given to the padding on the anterior superior iliac spine (ASIS) and
greater trochanter, so the patient is not rotated. Fusing a patient in a suboptimal position
could lead to patient discomfort and construct failure. After positioning, a confirmatory
x-​ray may help confirm proper alignment.
During the standard subperiosteal dissection, care must be taken not to disturb the
adjacent facets as this may accelerate their degeneration.
Once the pars interarticularis–​transverse process junction is exposed, a match stick
burr or awl maybe used to decorticate the pedicle screw starting point. Using a pedicle
finder (straight sharp), the pedicle maybe cannulated with little force perpendicular to
the plane of the superior articulating process. The surgeon may check the depth with
a ball probe at 20  mm, to ensure no medical breaches. Afterward, the surgeon may
medialize further and check again for breaches at 40 mm. Injecting a hemostatic matrix
into the cannulated hole often controls bleeding. The surgeon at this point may decide
to use pedicle markers with a confirmatory intraoperative CT spine or proceed to place
the instrumentation. When deciding on a pedicle thread, it is beneficial to allow space
for a rescue screw in the event of future revisions. Furthermore, depending on the de-
gree of spondylolisthesis, the surgeon may opt to use reduction screws to help reduce
the slip.
Interbody fusion may augment the construct as well as help restore lordosis while
reducing the slip (Figure 20.5).7 The decision on whether to place interbody via a
transforaminal technique may vary, but meticulous endplate preservation is a key factor
throughout all these techniques.8 In addition to restoring the natural disc height,
the interbody graft will also indirectly decompress the foramina. The choice in graft

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L4–L5 Degenerative Spondylolisthesis

Figure 20.5  Postoperative sagittal computed tomography (CT) scan demonstrating

L4–​L5 transforaminal lumbar interbody fusion (TLIF) with complete facetectomy and
reduction of spondylolisthesis.

footprint and shape may vary; however, the more anterior the graft is placed, the more
lordosis maybe achieved.9
The surgeon may decide to augment the interbody fusion with a posterolateral ar-
throdesis. Once the L4 and L5 transverse processes are exposed and decorticated, auto-
graft from the decompression or allograft maybe packed into the gutter.
The rods should be as short as possible to not disturb the adjacent levels. Often,
for a one-​level fusion, these rods are precut. When attempting to reduce an L4–​L5
spondylolisthesis, the L5 set screw should be placed bilaterally, anchoring the rod that
has been shaped into lordosis. Once that is preliminarily secured, the L4 screw may
be reduced to the rod using a tower reducer and then finally tightened. If neuro-
physiological monitoring is used, the technician should be notified before and after
reduction.

Aftercare

On postoperative day 1, the hematocrit and hemoglobin should be monitored as well

drain output (if used). If the patient is meeting her goals, the Foley maybe removed and
the patient should be allowed to ambulate with physical therapy. On postoperative day
2, intravenous narcotics should be weaned to oral medications, and the diet should be
advanced. If the patient is unable to ambulate because of persistent pain and discom-
fort, a chemical deep vein prophylaxis in addition to mechanical prophylaxis may be
considered.10 Postoperative imaging maybe obtained before discharge if intraoperative
imaging was not acquired.

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Spinal Neurosurgery

Complications and Management

Intraoperative complications such as a dural tear should be repaired primarily if possible.

If cerebrospinal fluid leak persists, a lumbar drain maybe considered.11 Postoperatively,
the patient should follow-​up for standard wound checks to ensure there is no dehiscence
or infection. If there is suspected drainage, an MRI may be helpful to rule out a deeper
collection. Moreover, the patient should follow up with plain film x-​rays at 4 weeks and
3 months to monitor the hardware (if instrumented).

Evidence and Outcomes

SPORT was a combined prospective randomized controlled and observational cohort

study which determined the treatment effect of surgical versus nonsurgical management
in patients with degenerative spondylolisthesis.2 The treatment effect (TE) was described
as the change in Oswestry Disability Index (surgery) minus Change in Oswestry
Disability Index (nonoperative).2 Across 13 centers, 395 patients were treated surgically
as opposed to 210 who were managed conservatively. After 4 years, all the patients with
degenerative spondylolisthesis in the surgical group had overall improvement in TE as
compared to the nonsurgical group.2

References and Further Reading

1. Matsudaira K, Hara N, Oka H, et al. Predictive factors for subjective improvement in lumbar
spinal stenosis patients with nonsurgical treatment: A 3-​year prospective cohort study. PloS
One. 2016;11:e0148584.
2. Weinstein JN, Lurie JD, Tosteson TD, et al. Surgical compared with nonoperative treatment
for lumbar degenerative spondylolisthesis. Four-​year results in the Spine Patient Outcomes
Research Trial (SPORT) randomized and observational cohorts. J Bone Joint Surg (Am Vol).
2009;91:1295–​1304.
3. Pearson AM, Lurie JD, Tosteson TD, Zhao W, Abdu WA, Weinstein JN. Who should undergo
surgery for degenerative spondylolisthesis? Treatment effect predictors in SPORT. Spine.
2013;38:1799–​1811.
4. Gandhoke GS, Kasliwal MK, Smith JS, et al. A multi-​center evaluation of clinical and radio-
graphic outcomes following high-​g rade spondylolisthesis reduction and fusion. J Spinal Dis
Techn. 2014.
5. Blumenthal C, Curran J, Benzel EC, et al. Radiographic predictors of delayed instability fol-
lowing decompression without fusion for degenerative grade I  lumbar spondylolisthesis. J
Neurosurg. Spine. 2013;18:340–​346.
6. Asiedu GB, Lowndes BR, Huddleston PM, Hallbeck S. “The Jackson Table is a pain in
the . . . ”: A qualitative study of providers’ perception toward a spinal surgery table. J Patient
Safety. 2016.
7. Glassman SD, Carreon LY, Ghogawala Z, McGirt MJ, Asher AL. Benefit of transforaminal
lumbar interbody fusion vs posterolateral spinal fusion in lumbar spine disorders: A propensity-​
matched analysis from the National Neurosurgical Quality and Outcomes Database Registry.
Neurosurgery. 2015.

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L4–L5 Degenerative Spondylolisthesis

8. Kuraishi S,Takahashi J, Mukaiyama K, et al. Comparison of clinical and radiological results of

posterolateral fusion and posterior lumbar interbody fusion in the treatment of L4 degener-
ative lumbar spondylolisthesis. Asian Spine J. 2016;10:143–​152.
9. Shau DN, Parker SL, Mendenhall SK, et al.Transforaminal lumbar interbody graft placement
using an articulating delivery arm facilitates increased segmental lordosis with superior ante-
rior and midline graft placement. J Spinal Dis Techn. 2015;28:140–​146.
10. Wang TY, Sakamoto JT, Nayar G, et  al. Independent predictors of 30-​day perioperative
deep vein thrombosis in 1346 consecutive patients after spine surgery. World Neurosurg.
2015;84:1605–​1612.
11. Kamenova M, Leu S, Mariani L, Schaeren S, Soleman J. Management of incidental

dural tear during lumbar spine surgery. To suture or not to suture? World Neurosurg.
2016;87:455–​462.

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Isthmic Spondylolisthesis

Evan Lewis and Charles A. Sansur

Case Presentation

The patient is a 57-​year-​old woman with a 3-​year history of low back pain and bilateral
21
leg pain. Over the past 5 months she has developed progressive weakness in her feet and
has an occasional trip due to her right foot being sporadically weak. Her past medical
history is negative other than hypothyroidism. She has normal body mass index (BMI)
and does not perform regular exercise. She works as a salesperson at a local large re-
tailer. She smokes a half-​pack of cigarettes per day. On examination she has 4+/​5 ankle
dorsiflexion weakness and extensor hallucis longus weakness bilaterally. She has a 1+
Achilles tendon reflexes bilaterally, and she has decreased sensation to light touch in the
dermatomes of L4 and L5.

Questions

1. What is the appropriate clinical workup, and what imaging modalities are
required?
2. What is the differential diagnosis for a person with this presentation?

It is appropriate to ask this patient if there are certain positions and/​or activities that
improve or worsen her symptoms. It is important to assess what therapy she has had thus
far. If the patient has not been prescribed physical therapy (PT) at this point, she should
get a referral for PT. If she has not already tried nonsteroidal antiinflammatory drugs
(NSAIDs), these should be recommended. She should be advised to stop smoking. She
should be advised to engage in daily walks and core strengthening exercises to improve
her overall spine support.
Imaging at this point should start with plain x-​rays of the lumbar spine in the
standing position with anteroposterior (AP) and lateral views, as well as dynamic studies
with flexion and extension views. Because the patient has a neurological deficit, one can
make the argument to request a non-​contrasted magnetic resonance imaging (MRI)
study in addition to assessing for nerve compression after x-​rays have been completed.
This patient had MRI (Figure 21.1) demonstrating severe bilateral facet arthropathy at
L4–​L5 with resultant lateral recess stenosis.
The primary differential diagnosis for a patient with this presentation should include
lumbar stenosis, lumbar spondylosis, lumbar spondylolisthesis, and lumbar disc hernia-
tion. Lower on the list of the differential diagnosis is a neoplastic process, infection, and
a vascular lesion such as arteriovenous fistula.

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Spinal Neurosurgery

Figure 21.1  Preoperative unenhanced T2-​weighted magnetic resonance image

(MRI). (A) Axial section thorough L4–​L5 disc space. (B) Midline sagittal image.

Assessment and Planning

It was determined that the patient has resolution of her leg pain when she lies on her side
and flexes forward. X-​rays demonstrate a grade 1 L4–​L5 spondylolisthesis with bilateral
L4 pars defects. The flexion and extension films reveal 7  mm of movement between
flexion and extension. The patient has near total resolution of sagittal malalignment
with extension. Appropriately exercise, smoking cessation, PT, and NSAIDs were
recommended. A follow-​up outpatient visit in 2–​3 months to was established to reassess
the patient’s neurological status and degree of benefit from the recommended treatment
strategy.

Questions

1. What type of isthmic spondylolisthesis does this patient have?

2. What additional nonsurgical treatment options does this patient have?
3. At what point should you recommend surgical treatment?

Oral Board Reviews: Diagnostic Pearls

Wiltse et  al. have created a classification system for isthmic spondylolisthesis
etiologies. This patient has a type A, or lytic, isthmic spondylolisthesis. Type B
isthmic spondylolisthesis is characterized by an elongated pars, and type C consists
of an acute pars fracture.
In the absence of severe neurologic findings, surgery should never be the initial
recommendation for intervention. Patients need to undergo conservative treat-
ment for at least 3  months prior to consideration of surgery. This patient was
instructed to quit smoking and to engage in activities to develop her core mus-
culature, including physical therapy. If, after the patient completes this course of

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Isthmic Spondylolisthesis

conservative treatment, she still continues to be debilitated by her symptoms, one

can start to offer more invasive treatment strategies. These options may consist of
epidural injections or facet rhizotomies. In the event that these treatments are not
desired by the patient, or in the event that they do not successfully control the
patient’s symptoms, surgical intervention is a reasonable treatment. At this point,
because surgery is being offered, most spine experts would advocate for the patient
to obtain additional x-​rays of the whole spine to assess global sagittal and coronal
alignment.

Decision-​Making

A variety of acceptable surgical options exist for this patient. These options include
decompression without fusion, decompression with instrumented fusion from a poste-
rior approach (with or without interbody grafting), decompression and fusion through
combined lateral interbody approach and posterior approach, decompression and fusion
using a combined anterior and posterior approach, and, finally, anterior or lateral stand-​
alone interbody fusion.
The benefits of decompression without fusion include maintenance of motion and
decreased risk of adjacent segment degeneration, while risks include inadequate relief of
back pain and worsening deformity.
The advantages of decompression with instrumented fusion from a posterior approach
(with or without interbody grafting) would be the opportunity to address the patient’s
back pain and radicular pain through a single approach. This approach also allows the sur-
geon to correct the spondylolisthesis, perform a wide decompression, and utilize the trans-
verse processes for a posterolateral fusion. The disadvantages of this approach are higher
blood loss (for an open case), limited ability to improve lumbar lordosis, and a decreased
surface area for interbody bone fusion when compared to anterior interbody surface area.
The advantages of fusion through a combined lateral interbody and posterior
instrumented fusion would be the ability to correct the deformity, obtain an indirect
decompression, and obviate the need for a posterior decompression. There would be a
greater surface area for interbody fusion and likely decreased blood loss. There still is an
opportunity to perform a posterior fusion. The disadvantages of this approach would be
potential injury to the lumbosacral plexus and risk of injury to the great vessels.
The advantages of fusion through an anterior approach with or without posterior in-
strumentation include the ability to correct the spondylolisthesis and obtain an indirect
decompression, as above. Also, as in the lateral approach, there would be a greater surface
area for interbody fusion and decreased blood loss. There still is an opportunity to per-
form a posterior fusion.The risks include potential injury to the lumbosacral plexus and
risk of injury to the great vessels. There also is a risk of hernia formation if inadequate
closure of the abdominal wall is performed.

Surgical Procedure

Several of the already mentioned approaches utilize similar posterior access to the
spine: decompression without fusion, decompression with fusion, or augmentation
of fusion with interbody. These procedures all begin in a similar fashion. First the

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patient is positioned in the prone position on a Jackson table with chest, hip, and
thigh pads. A fluoroscope is utilized to mark the appropriate levels. The surgical site is
then prepped and draped in the usual sterile fashion. Incision is made sharply using a
scalpel. Dissection is carried out with Bovie electrocautery. The fascia is divided over
the spinous processes, and subperiosteal dissection is continued down the lamina. The
dissection is stopped at the medial edge of the facet capsule and a L4 laminectomy
is completed for patients undergoing decompression alone. Dissection is carried out
over the joint capsule if the decision for fusion has been made. Care is taken to pre-
serve the facet capsule of the L3–​L4 joint, and the L4–​L5 joint capsule is removed.
Dissection is carried out over the transverse processes of L4 and L5. Attention is
turned to pedicle instrumentation at this point. Pedicle screws can be placed ei-
ther anatomically or radiographically. The entry point for the pedicle screw is at the
convergence of the mid-​point of the transverse process and the pars interarticularis.
Quite often, a mammillary process can be identified at this junction. A pilot hole is
created at this point, and, using a blunt Lenke pedicle finder, the pedicle is cannulated.
The tract is then palpated using a ball-​tip probe to assess for any breaches. Next,
the tract is tapped and the process of assessing for breaches is repeated. Finally, the
appropriate length and width pedicle screw is inserted. Once the instrumentation
is in place, decompression can be carried out. Due to the addition of instrumenta-
tion, a more complete decompression can be carried out that may include a total
facetectomy. Once the decompression has been completed, the rods can be secured.
Attention is turned to arthrodesis, which is completed by decorticating the trans-
verse processes bilaterally, and morselized autograft can be packed into the posterior
lateral gutters. If an interbody is desired, this can be placed by one of two methods
prior to placing the rods. Posterior lumbar interbody fusion (PLIF) does not require
access to the foramina. The thecal sac is retracted medially, exposing the disc space.
A box annulotomy is made in the disc space using a scalpel. Sequential paddle shavers
are used to perform a discectomy in a piecemeal fashion. Upon removal of the disc,
the endplates are thoroughly prepared. The PLIF cage is then malleted into position.
Often bilateral PLIF cages are inserted. The transforaminal lumbar interbody fusion
(TLIF) is carried out in a similar manner except some or all of the facet is removed,
giving access to the disc space through the foramina, and a single cage is placed in a
more oblique orientation (Figure 21.2). The operative incision is then closed. Care
is taken to reapproximate the muscle and fascia with interrupted absorbable sutures.
Next the dermis is closed using interrupted buried absorbable sutures and the skin
is then closed.
For an anterior approach, the patient is placed in the supine position on a Jackson
flat-​top table.The anterior approach often utilizes the assistance of a vascular surgeon for
the exposure. Commonly, a paramedian incision, lateral to the umbilicus, is made. When
the layers of the abdominal wall have been penetrated, the peritoneum is retracted medi-
ally exposing the aorta and iliac vessels at the bifurcation.The great vessels are mobilized
to grant exposure to the L4–​L5 disc space. A box annulotomy is created in the disc and
the disc is removed in piecemeal fashion using curettes and pituitary rongeurs. An appro-
priately sized interbody graft is placed to provide distraction and indirect decompression.

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Isthmic Spondylolisthesis

Figure 21.2  Postoperative x-​rays demonstrating pedicle screw fixation with Polyether

ether ketone (PEEK) interbody. (A) Anteroposterior (AP) view. (B) Lateral view.

An integrated interbody with screws or a plating system can be utilized to secure the
construct.

Oral Boards Review: Management Pearls

1. Preservation of the cephalad facet capsule reduces that likelihood of adjacent

segment disease.
2. During the approach, exposure of the cephalad transverse process (TP) is
often more difficult due to the anterior translation of the vertebral body. As
such, careful attention must be paid to avoid nerve injury of exiting nerve
during TP exposure.
3. It is important to perform a wide decompression of the exiting nerve roots
before attempting to reduce the spondylolisthesis.Very often, reduction
pedicle screws many facilitate reduction of the spondylolisthesis for higher
grade cases.

Pivot Points

1. If, upon total facetectomy, there is no ability to correct spondylolisthesis, then

discectomy and use of interbody grafting may facilitate correction.
2. If there is no motion or correction of slip with interbody grafting, then fusion
in situ is appropriate.
3. If during a planned decompression without fusion the patient is found to
have intraoperative instability, one should consider instrumented fusion.

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Spinal Neurosurgery

Aftercare

Postoperatively, the patient is recovered in the postanesthesia recovery room. Postoperative

antibiotics should be continued for no longer than 24 hours. Plain x-​rays either during
or after surgery are standard to assess hardware position. No further imaging studies are
required unless a change in neurological exam is detected. Patients should be encouraged
to ambulate as soon as possible. Efforts should be made to minimize bending, lifting, and
twisting activities for fusion patients. Pain management can be obtained with opioids
for the immediate postoperative period. NSAIDs should be avoided in fusion patients.
Patients should be followed-​up in clinic for a wound check in 14 days and then again
in several weeks. AP and lateral radiographs should be obtained for fusion patient to as-
sess the hardware construct. Patients with decompression only with lack of resolution of
pain or recurrent pain should undergo standing flexion/​extension radiographs to assess
for instability or progression of spondylolisthesis. Physical therapy is often important in
the aftercare to improve the patient’s core strength and ability to tolerate daily activities.

Complications and Management

Cerebrospinal fluid (CSF) leak is a potential complication of spinal surgery with

estimated incidence that varies widely throughout the literature. Durotomies are
more frequent in revision cases. Many different techniques and algorithms have been
described for management of CSF leaks. Primary closure of the durotomy with su-
ture is recommended when possible. If not feasible, tight muscle and facial closure is
recommended. Postoperative positioning for CSF leaks should be supine to reduce pres-
sure in the lumbar cistern. CSF diversion may be considered for complex dural tears.
Adjacent segment disease (ASD) is a problem associated with both instrumented and
noninstrumented fusion. It results in accelerated degeneration of the adjacent motion
segment. Different techniques, including dynamic fusion methods, have yet to demon-
strate any reduction in ASD. Attention to preserve the cephalad facet capsule is impor-
tant to reduce the chance of developing ASD.Treatment of ASD starts with nonoperative
management, such as injections, NSAIDs, and physical therapy. If conservative therapy
fails, extension of fusion to include the adjacent segment is considered.

Oral Boards Review: Complications Pearls

1. To properly close a durotomy, it is often necessary to allow more spinal fluid

to drain to further empty the thecal sac because this will help prevent the
nerves from drifting toward the durotomy.
2. Infection can often be addressed in the acute setting with a wound washout,
with preservation of the hardware.

Evidence and Outcomes

There is controversy regarding fusion techniques in the treatment of spondylolisthesis.

A 2016 study in The New England Journal of Medicine by Forsth et al. suggested that there
was no difference in patients who underwent decompression alone versus decompression

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Isthmic Spondylolisthesis

and fusion in the subset of patients with lumbar spondylolisthesis and claudication.
Another study presented in the same journal by Ghogawala et al. was a randomized trial
focusing on patients specifically with spondylolisthesis, and this study demonstrated sig-
nificantly better outcomes in the fusion group at 2 years.
There is some evidence to suggest that spondylolisthesis when treated with instru-
mentation and interbody arthrodesis has more favorable outcomes when compared to
patients who underwent posterolateral fusion alone.

References and Further Reading

Alentado V, et al. Independent predictors of clinically significant improvement after lumbar fusion
surgery. Spine J. 2016 Sept 21.
Forsth P, et al. A randomized, controlled trial of fusion surgery for lumbar spinal stenosis. N Engl
J Med. 2016 Apr 14:374(15): 1413–​1423.
Ghogawala Z, et al. Laminectomy plus fusion versus laminectomy alone for lumbar spondylolisthesis.
N Engl J Med. 2016 Apr 14:374(15): 1424–​1434.
Glassman SD, et  al. Benefit of transforaminal lumbar interbody fusion vs posterolateral
spinal fusion in lumbar spine disorders:  A propensity-​ matched analysis from the
National Neurosurgical Quality and Outcomes Database Registry. Neurosurgery. 2016
Sep:79(3):397–​405.

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Lumbar Degenerative Scoliosis

Michael LaBagnara, Durga R. Sure, Christopher I. Shaffrey,

and Justin S. Smith

Case Presentation
22
A 79-​year-​old man presents with low back and right buttock pain, which extends to
his right posterior thigh. The leg pain usually stops at the knee, but occasionally extends
to his posterior calf and the plantar surface of his foot. Symptoms started approximately
2 years ago without an inciting event and have been progressively worsening. He reports
that 40% of his overall pain is in his lower back, and 60% is in his right leg. Symptoms
are worse with prolonged standing and walking and are relieved by bending forward or
laying supine. Two years ago, he was able to walk several miles before having to stop and
rest. Now he states he can barely walk a quarter-​mile before the heaviness in his legs and
his back pain force him to rest. He is able to walk longer distances when using a shop-
ping cart at the store. Up until 2 years ago, he was an avid cyclist and would ride 18–​30
miles per week. His symptoms have made cycling impossible. He denies any history of
bowel or bladder incontinence and denies any altered sensation in his extremities. He
states that his right foot has felt weak for more than a year. He underwent 6 weeks of
ground-​based and aquatics-​based physical therapy 1 year ago without improvement and
has had two lumbar epidural steroid injections without relief.
His past medical history is significant for hypertension, gout, rheumatoid arthritis,
osteopenia, bicuspid aortic valve, atrial fibrillation, aortic aneurysm, coronary artery
disease, and hypothyroidism. His past surgical history includes coronary artery by-
pass graft, aortic repair, aortic valve replacement, left hip replacement, tonsillectomy,
adenoidectomy, cholecystectomy, right knee arthroscopy, and SA node ablation.
Detailed neurological examination reveals full strength in all extremities with the
exception of 4/​5 right ankle dorsiflexion, 4+/​5 plantar flexion, and 4/​5 right extensor
hallucis longus (EHL). Sensation to light touch and pin prick is preserved throughout.
Deep tendon reflexes are 2+ in his upper extremities and 1+ in bilateral lower extremities.
Toes are down-​going bilaterally. He has moderate difficulty moving from a seated po-
sition to standing, and his standing posture is preferentially bent forward. He is able to
stand more erect, but states this worsens his back pain. Tandem gait is steady, with mild
slapping of the right foot. He is able to elevate onto the toes and heel of his left foot, but
unable to do either on the right.There is no tenderness to palpation over his bony spine;
however, the lumbar spine is palpable eccentric to the right of midline.

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Spinal Neurosurgery

Questions

1. What is the most likely diagnosis?

2. What is the most appropriate imaging modality or modalities?

Assessment and Planning

This 79-​year-​old man has symptomatic lumbar spondylosis, lumbar spinal stenosis,
and degenerative lumbar scoliosis. His claudication symptoms are relieved by sitting or
bending forward, which is consistent with neurogenic claudication.This is in contrast to
vascular claudication, the symptoms of which would typically be relieved by rest alone.
His partial right foot drop suggests stenosis affecting the L5 nerve root, and his plantar
flexion weakness suggests stenosis affecting the S1 root. The palpable bony spine eccen-
tric to the midline suggests scoliosis of the lumbar spine.

Oral Boards Review: Diagnostic Pearls

1. Detailed history and physical exam are essential for reaching the correct diagnoses:
a. Lumbar spinal stenosis: The patient’s history of a progressive decline in
his ability to stand or walk, secondary to “heaviness” of his legs, suggests
narrowing of the central canal in the lumbar spine.
b. Spondylosis: Radiographic spondylosis is an expected finding in this
patient’s age group. The presence of radicular symptoms and their laterality
suggest asymmetric pathology.
c. Scoliosis: Palpation of the bony spine should be a routine part of every
neurologic examination. Deviation of the spine away from midline
suggests underlying scoliosis. Palpation of the spine may be difficult in
patients with larger body habitus.
2. Advanced imaging with either non-​contrast magnetic resonance imaging
(MRI) or computed tomography (CT) myelogram should be obtained to
evaluate the extent of disease and to formulate an interventional plan.
3. Standing long-​cassette radiographs (posteroanterior [PA] and lateral) should
be obtained to assess global spinal alignment. Limited imaging of the spine,
with either radiographs or advanced imaging modalities, may result in treat-
ment plans based on insufficient information and potentially result in less than
ideal outcomes.1 Even without the palpable deformity on this patient’s phys-
ical exam, surgeons should maintain a low threshold for obtaining standing
long-​cassette radiographs.1
4. Dual-​energy x-​ray absorptiometry (DEXA) bone densitometry should be
obtained in adult patients undergoing spinal deformity surgery, especially in
older patients and those previously diagnosed with osteopenia or osteopo-
rosis. The results may influence decision-​making with respect to implant se-
lection, timing of surgery, or both. In the setting of nonemergent surgery for
deformity correction, preoperative treatment with anabolic bone medications,
such as teriparatide, may be considered.

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Decision-​Making

Advanced imaging, including CT myelogram and/​or MRI, should be obtained in

patients with neurologic symptoms/​deficits and in cases in which treatment may in-
clude spinal implants. Comparing supine and standing imaging is also important when
assessing the spine for alignment and flexibility. The CT scout image may be sufficient
for the supine assessment in some cases. In this patient, MRI of the lumbar spine showed
multilevel central canal and foraminal stenosis most severe at L3–​L4, L4–​L5, and L5–​S1
(Figure 22.1A–​C). A  CT myelogram was also obtained and demonstrated severe ste-
nosis and provided detailed bony anatomy that can be helpful for surgical planning. For
patients with prior spinal instrumentation, CT myelogram is the preferred imaging mo-
dality since CT imaging is generally less susceptible to metallic artifact compared with
MRI. Standing full-​length PA and lateral radiographs are shown in Figure 22.2. These
demonstrate dextroscoliosis (curve to the right; in contrast to levoscoliosis, which is to
the left) of the lumbar spine with the apex at L2. Standard viewing orientation of the

A B

Figure 22.1 T2-​weighted magnetic resonance images. Left (A) and right

(B) paracentral sagittal sections demonstrate multilevel foraminal stenosis. Axial
(C) image at the level of L4–​L5 demonstrates severe canal stenosis.

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Spinal Neurosurgery

A B C

Figure 22.2  Posteroanterior (PA, A) and lateral (B and C) full-​length standing

radiographs at the time of presentation. PA imaging (A) illustrates measurement of the
global coronal alignment (−3.0 cm) and the coronal Cobb angle (47 degrees). Lateral
imaging (B and C) demonstrates measurement of the sagittal vertical axis (+8.4 cm),
T2–​T12 thoracic kyphosis (22 degrees), lumbar lordosis (37 degrees), pelvic incidence
(52 degrees), pelvic tilt (23 degrees), and sacral slope (29 degrees).

PA radiograph is to have the patient’s left side on the viewer’s left side (i.e., true left,
true right), and standard viewing orientation for the lateral long-​cassette radiograph is
to have the patient facing to the right. Several spino-​pelvic parameters should be rou-
tinely assessed. Based on the PA radiograph (Figure 22.2A), the global coronal align-
ment is −3.0 cm (offset of a vertical plumbline dropped from the center of C7 relative
to the central sacral vertical line, with shifts to the left and right represented as negative
and positive values, respectively) and the coronal Cobb angle is 47 degrees (angle be-
tween the most horizontally angled endplates at the cephalad and caudal aspects of the
curve). Based on the lateral radiograph (Figure 22.2B), the sagittal vertical axis (SVA) is
+8.4 cm (offset of a vertical plumbline dropped from the center of C7 relative to the
posterior-​superior corner of the sacrum, with shifts to the left and right represented
as negative and positive values, respectively), the thoracic kyphosis (TK) is 22 degrees
(often measured from T2–​T12 or T4–​T12), and the lumbar lordosis (LL) is 37 degrees
(measured from the superior endplate of L1 to the superior endplate of S1). In addition,
pelvic parameters should be measured (Figure 22.2C), including the pelvic incidence
(PI), which is 52 degrees (angle subtended by a perpendicular line from the center of
the sacral endplate and a line from the center of the sacral endplate to the center of the
femoral head); the pelvic tilt (PT), which is 23 degrees (angle subtended by a line from
the center of the sacral endplate to the center of the femoral head and a vertical refer-
ence line at the center of the femoral head); and the sacral slope (SS), which is 29 degrees
(slope of the sacral endplate). PI is a morphologic parameter that helps to determine

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the amount of LL an individual should have, while the PT is a measure of pelvic retro-
version, which is a compensatory measure for positive sagittal malalignment that, when
abnormally elevated, can be a source of pain and disability. The PI is the sum of the PT
and SS.
The threshold radiographic spinopelvic parameters for an Oswestry Disability Index
(ODI) score of more than 40 (severe disability) have been reported: PT of 22 degrees
or greater, SVA of 4.7 cm or greater, and PI–​LL mismatch of 11 degrees or more.2 It is
important to remember that these measures and thresholds do not, in and of themselves,
constitute an indication for surgery but are meant instead to aid in understanding the
complexities of spinal deformity in the context of patient symptoms. Notably, Lafage and
colleagues recently defined spinopelvic alignment thresholds based on patient age and
concluded that operative realignment targets should account for age and that younger
patients require more rigorous alignment objectives.3
DEXA scan of the right hip and left wrist demonstrated T scores of −1.7 and −1.5,
respectively, which reflect osteopenia. In scoliotic patients, DEXA scans of the spine have
been shown to be less accurate predictors of osteoporosis, while scans of the hip and
wrist have maintained reliability and are good alternatives in this patient population.4
This patient has progressively symptomatic lumbar spondylosis and stenosis, most
notably in the fractional portion of his scoliosis curvature (L4–​S1). Although the patient
demonstrates modest global coronal and sagittal malalignment, limited PI–​LL mismatch,
and slightly elevated pelvic retroversion (PT), these are not likely the primary sources of
this patient’s symptoms, especially if the patient’s advanced age is considered.3 After un-
successful nonoperative management, he is seeking operative treatment.The presence of
a moderate scoliosis, combined with a large component of mechanical lower back pain,
make a limited decompression a less attractive option. A short-​segment decompression
with segmental instrumentation and fusion from L3–​S1 may significantly improve his
claudication symptoms by addressing his stenosis. However, this would place the upper
instrumented vertebra near the apex of the coronal curvature. The risk of symptomatic
curve progression as a result of this intervention would be relatively high and, as a general
rule, is not recommended.This leaves the option of addressing both the stenosis and sco-
liosis at the same time.While this is a decidedly larger operation with increased operative
and medical risks, it offers the best chance for improving the patient’s symptomatology.

Questions

1. What additional testing should be performed prior to surgical intervention?

2. What expectations should be established prior to surgical intervention?

Surgical Procedure

After medical and cardiac clearance and an extensive discussion regarding the poten-
tial benefits, risks, and alternatives,5–​8 the patient underwent a T10–​iliac posterior seg-
mental instrumented fusion with Ponte osteotomies from L1–​S1 and transforaminal
interbody fusion at L4–​L5 and L5–​S1. There were no complications during the pro-
cedure. Intraoperative neuromonitoring, including motor evoked and somatosensory

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evoked potentials and free-​running electromyography (EMG), was used and did not
demonstrate any abnormalities. He was mobilized on postoperative day 1 with phys-
ical therapy, and was discharged to inpatient rehabilitation on postoperative day 6. His
leg pain had resolved by the time of his discharge. At the 6-​week postoperative visit,
he was able to walk with less back pain than preoperatively. Motor strength in dorsi-
flexion, EHL, and plantar flexion was improved to 4+. Full-​length standing PA and lat-
eral radiographs 36 months after surgery demonstrating improved alignment and spinal
balance are displayed in Figure 22.3. At last follow-​up, his leg pain and neurogenic
claudication remained resolved, his motor strength had returned to normal, and he only
noted occasional mild low back discomfort.

Oral Boards Review: Management Pearls

1. In the absence of significant or progressive neurological deficits, nonoperative

therapies should be attempted prior to surgical treatment for adult spinal
deformity.
2. Spinopelvic parameters should be assessed preoperatively and help guide
management decisions.
3. Full-​length standing films are essential for a proper assessment of alignment.

A B C

Figure 22.3  Posteroanterior (PA, A) and lateral (B and C) full-​length standing

radiographs at 36-​month postoperative follow-​up. Posterior segmental instrumentation
has been placed from T10 to the ilium, and interbody spacers have been placed at the
L4–​L5 and L5–​S1 levels. PA imaging (A) illustrates measurement of the global coronal
alignment (+1.1 cm) and the coronal Cobb angle (8 degrees). Lateral imaging (B and
C) demonstrates measurement of the sagittal vertical axis (+4.8 cm), T2–​T12 thoracic
kyphosis (29 degrees), lumbar lordosis (42 degrees), pelvic incidence (52 degrees),
pelvic tilt (21 degrees), and sacral slope (31 degrees).

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Pivot Points

1. In a patient with neurologic deficit, MRI and/​or CT with myelogram is

needed.
2. Age should be considered when determining goals for realignment.
3. Intraoperative neuromonitoring should be considered for surgical procedures
to treat spinal deformity.

Aftercare

After surgery, an immediate neurologic evaluation is made and plain radiographs are
obtained. If there is any decline in neurologic function, CT with or without myelogram
should be considered for assessment. Deep venous thrombosis (DVT) prophylaxis with
thromboembolic stockings and sequential compression devices are continued throughout
the postoperative period, and early aggressive respiratory management is administered.
Pharmacologic DVT prophylaxis (e.g., with heparin) should also be considered and is
typically employed by the authors as early as postoperative day 1. Pain control can be
challenging in the immediate postoperative period and use of patient-​controlled anes-
thesia and a pain team consult can both be beneficial. Physical therapy is begun early
in the recovery phase. When able, standing full-​length PA and lateral radiographs are
obtained to assess sagittal and coronal alignment. The authors use postoperative intrave-
nous antibiotics until all wound drains have been removed. Enteral nutrition is begun
as soon as possible postoperatively. If patients are unable to receive enteral nutrition,
hyperalimentation should be considered. Routine clinical and radiographic follow-​up,
including full-​length standing PA and lateral radiographs, are obtained at follow-​up
intervals (e.g., 6 weeks, 3 and 6 months, and 1 and 2 years).

Complications and Management

Complications can be divided into those that occur early and delayed.6,8,9 Early
complications include the development of neurologic deterioration and postoperative
wound infections. Deep wound infection rates vary between 1% and 8% and typically
require surgical washout and appropriate antibiotic treatment.6 Perioperative mortality is
fortunately rare and has been reported to be approximately 0.6%.6 Other complications
including cerebrospinal fluid leak, DVT, pulmonary embolism, pneumonia, urinary tract
infection, and cardiovascular sequelae can occur.6 Delayed complications, including
pseudarthrosis, instrumentation failure, and proximal junctional kyphosis/​failure, can
occur and may necessitate revision surgery.6,9

Evidence and Outcomes

Specific goals for adult spine deformity correction include global alignment res-
toration, decompression of neural elements, pain relief, and functional improve-
ment. To assess these outcomes, it is important to use patient-​centered instruments
that evaluate health-​related quality of life (HRQOL), such as the SF-​36, SRS-​22R,
and ODI.7,8,10,11 These outcome measures allow practitioners to properly evaluate a

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patient’s clinical progress. There is strong evidence linking worsening functional and
health status with increased positive SVA, increased PT, and decreased lumbar lordosis
(increased PI–​LL mismatch).2,12 Restoration of alignment has likewise been shown to
correlate with improved patient outcomes and decreased disability scores. Multiple
studies have demonstrated the potential for surgical treatment to improve HRQOL
in adults with lumbar scoliosis, and advances continue to be made in the management
of these patients.7,8,10,11

References and Further Reading

1. Maggio D,Ailon TT, Smith JS, et al.Assessment of impact of standing long-​cassette radiographs
on surgical planning for lumbar pathology:  An international survey of spine surgeons.
J Neurosurg Spine. Jul 31 2015:1–​8.
2. Schwab FJ, Blondel B, Bess S, et  al. Radiographical spinopelvic parameters and disability
in the setting of adult spinal deformity:  A prospective multicenter analysis. Spine. Jun 1
2013;38(13):E803–​E812.
3. Lafage R, Schwab F, Challier V, et al. Defining spino-​pelvic alignment thresholds: Should op-
erative goals in adult spinal deformity surgery account for age? Spine. Jan 2016;41(1):62–​68.
4. Pappou IP, Girardi FP, Sandhu HS, et al. Discordantly high spinal bone mineral density values
in patients with adult lumbar scoliosis. Spine. Jun 15 2006;31(14):1614–​1620.
5. Bess S, Line B, Fu KM, et  al. The health impact of symptomatic adult spinal deformity:
Comparison of deformity types to United States population norms and chronic diseases.
Spine. Feb 2016;41(3):224–​233.
6. Smith JS, Klineberg E, Lafage V, et  al. Prospective multicenter assessment of perioperative
and minimum 2-​year postoperative complication rates associated with adult spinal deformity
surgery. J Neurosurg Spine. Jul 2016;25(1):1–​14.
7. Smith JS, Lafage V, Shaffrey CI, et al. Outcomes of operative and nonoperative treatment for
adult spinal deformity:  A prospective, multicenter, propensity-​matched cohort assessment
with minimum 2-​year follow-​up. Neurosurgery. Jun 2016;78(6):851–​861.
8. Smith JS, Shaffrey CI, Glassman SD, et al. Risk-​benefit assessment of surgery for adult scoli-
osis: An analysis based on patient age. Spine. May 1 2011;36(10):817–​824.
9. Lapp MA, Bridwell KH, Lenke LG, et al. Long-​term complications in adult spinal deformity
patients having combined surgery a comparison of primary to revision patients. Spine. Apr
15 2001;26(8):973–​983.
10. Bridwell KH, Glassman S, Horton W, et  al. Does treatment (nonoperative and opera-
tive) improve the two-​year quality of life in patients with adult symptomatic lumbar
scoliosis:  A prospective multicenter evidence-​ based medicine study. Spine. Sep 15
2009;34(20):2171–​2178.
11. Smith JS, Shaffrey CI, Bess S, et  al. Recent and emerging advances in spinal deformity.
Neurosurgery. 2016 (invited submission).
12. Glassman SD, Bridwell K, Dimar JR, Horton W, Berven S, Schwab F. The impact of positive
sagittal balance in adult spinal deformity. Spine. Sep 15 2005;30(18):2024–​2029.

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Flat Back Deformity

Yusef I. Mosley and James S. Harrop

Case Presentation

A 68-​year-​old woman presents with a past medical history significant for rheumatoid
23
arthritis, osteoporosis, and lower back pain that radiates into her lower extremities for
more than 7 years. She underwent a lumbar decompression and fusion approximately
4 years prior to presentation. Approximately 2 weeks after her operative intervention,
she developed severe back, hip, and leg pain. Her back and leg pain are equal in severity
and both contribute to her diminished quality of life. She states that standing or walking
for long periods of time exacerbates her symptoms. She tried physical therapy after her
lumbar surgery; she had only mild improvement in her symptoms. She tried epidural
steroid injections (EDSI), which brought some relief. Unfortunately, the EDSI are no
longer effective in managing her symptoms. Currently, she states that she has weakness
in both lower extremities, with her right leg being weaker than her left. She has an
unsteady gait but requires no assistance with ambulation. She states that the pain has
affected the ability to perform activities of daily living, sleep, travel, exercise, and enjoy
her hobbies. Additionally, she complains of right arm numbness in the C6 distribution.
However, she does not endorse any clumsiness with fine motor movements in her hand
or bowel or bladder issues. She does not use any tobacco products.

Questions

1. What is the most likely diagnosis?

2. What imaging is necessary to complete the workup?
3. What are the important anatomical areas to obtain imaging? Why?
4. What are other nonoperative therapies that would improve the outcome of
an operation if it were needed?

Detailed neurological assessment was performed and positive for abnormal gait, pitched
forward posture while standing, and decreased range of motion in the cervical and
lumbar spines. She does not have any pathologic reflexes, Hoffman sign, Babinski sign,
or clonus in her lower extremities.

Assessment and Planning

The neurosurgeon suspects that the patient has a sagittal balance issue from her appear-
ance on physical exam and her clinical history. She also has complaints that could be

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Spinal Neurosurgery

indicative of a myelopathy caused by compression of the spinal cord below the cervical
spine. Cervical myelopathy is unlikely secondary to the absence of any upper extremity
signs or symptoms in the history and physical exam.
The patient should have magnetic resonance imaging (MRI) of the thoracic
and lumbar spine to rule out any severe stenosis that could be contributing to her
symptoms. Severe stenosis in the thoracic region could potentially explain the un-
steady gait, and severe stenosis in the lumbar spine could explain her posture. A pa-
tient will often obtain some relief of neural compression in the lumbar spine by
leaning forward to increase foraminal size. Additionally, this patient should have a
computed tomography (CT) scan of the lumbar and thoracic spine to better under-
stand the bony anatomy, rule out any potential hardware failure from the prior op-
erative intervention, rule out any pseudoarthrosis, and rule out any occult fractures
that may have occurred. Additionally, CT scans have been used to assess the bone
health by documenting Hounsfield units in patients with osteoporosis. Last, the
patient should have both lumbar x-​ray (anteroposterior [AP]/​lateral/​flexion/​exten-
sion) and complete standing scoliosis x-​rays. The lumbar x-​rays will allow the sur-
geon to assess the previous hardware, and the dynamic films (flexion/​extension) will
rule out any potential pseudoarthrosis or instability. The complete standing scoliosis
x-​rays are taken to assess the global alignment of the patient and to document any
pelvic incidence (PI) to lumbar lordosis (LL) mismatch and to evaluate her sagittal
vertical axis (SVA).
Another issue to assess in this patient are her history of rheumatoid arthritis and any
potential antiinflammatory medications that are being taken that would inhibit a bony
fusion. Also, the patient’s history of osteoporosis must be evaluated to see if she has been
taking any medications to help improve her overall bone quality. A recent dual-​energy
x-​ray absorptiometry (DEXA) scan would be useful to quantify the severity of her bone
disease.

Oral Boards Review: Diagnostic Pearls

1. Physical examination:
a. Complete neurological examination should be completed with atten-
tion paid to any myelopathic signs (Hoffman sign, clonus, hyperreflexia,
etc.). These are important to assess because if a patient has both cer-
vical and thoracolumbar pathology, the cervical may need to be
addressed first.
b. Careful assessment of the patient’s posture is needed. Patients with sagittal
balance issues will often stand with knees bent and hips slight flexed. This
posture is taken to compensate for the forward posture that the patient has
developed over time.
2. Imaging studies:
a. MRI can assess for any central or foraminal stenosis that would be
contributing to the patient’s signs and symptoms.

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b. CT scan assess for any hardware failure, pseudoarthrosis, or occult fractures.

Additionally, the Hounsfield units can be evaluated at a given vertebral
body to assess the bone quality.
c. Standing scoliosis x-​rays allow PI, LL, pelvic tilt (PT), and SVA to be meas-
ured. It is imperative to assess for any mismatch in the PI–​LL, which should
be within 10 degrees +/​−. Normal PT should be approximately less than15
degrees; if higher, the patient is likely retroverting his or her pelvis to com-
pensate for the positive sagittal balance. The SVA should be less than 5 cm
in front of the posterosuperior corner of the S1 vertebral body.
d. When evaluating a DEXA scan, it is important to assess the number and
which portion of the bone was used to assess the bone quality. When the
study concentrates on the spine, it can underestimate the severity of osteo-
porosis because of the osteophyte presence that increases the T-​score.Values
should be obtained from the hip. (See notes under CT scan for evaluation
of osteoporosis.)

The patient did not have any central stenosis in the thoracic and lumbar spine (Figure
23.1A,B). Her CT scan did not show any hardware failure, evidence of pseudoarthrosis,
or occult fractures (Figure 23.2). Her lumbar x-​rays showed previous instrumentation
from L3 to L5 without any evidence of pseudoarthrosis, hardware failure, or instability
(Figure 23.3A,B). The standing scoliosis x-​rays showed an SVA of +15.5 cm, PI of 60
degrees, LL of 20 degrees, and a PT of 28 degrees (Figure 23.4A,B).

A B

Figure 23.1  (A) T2 sagittal magnetic resonance image (MRI) of the thoracic spine
showing no central stenosis. (B) T2 sagittal MRI of the lumbar spine showing no
central stenosis.

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A B

Figure 23.2  (A) Sagittal computed tomography (CT) scan of the thoracic spine
without any occult fractures or bony abnormalities. (B) Sagittal CT scan of the
lumbar spine showing previous hardware without any instrumentation failures or
pseudoarthrosis.

A B

Figure 23.3  (A) Lateral lumbar spine standing x-​ray showing previous hardware.
(B) Anteroposterior (AP) lumbar spine standing x-​ray showing previous hardware.
 

Flat Back Deformity

A B

Figure 23.4  (A) Lateral standing scoliosis x-​ray. (B) Anteroposterior (AP) standing

scoliosis  x-​ray.

Questions

1. How do the clinical and radiographic findings influence the surgical

planning?
2. What is the appropriate timing of surgery?
3. What are the goals of the surgery, and how can they be accomplished?

Decision-​Making

This patient’s radiographic findings and clinical presentation suggest that she would ben-
efit from a procedure that corrects her global alignment and PI–​LL mismatch. However,
before discussing the appropriate operative approach, it is key to maximize this patient’s
overall bone health.There are studies showing that older patients undergoing spinal sur-
gery have a higher chance of having osteoporosis/​osteopenia compared to the rate of
occurrence in the population of the same age group.The first step in the treatment algo-
rithm should be a referral to an endocrinologist for medical management of the patient’s
osteoporosis. A few examples of preventative therapies include vitamin D and calcium
supplementation, parathyroid hormone, calcitonin, and estrogen replacement. There is
no consensus on the length of time during which a patient should be on osteoporosis
therapy prior to operative interventions. In fact, there have been publications that sug-
gest that delaying surgery for lumbar herniated disc in osteoporotic patient could lead
to less favorable outcomes 6 months after surgery.1 The patient in this presentation was
evaluated by an endocrinologist and treated with teriparatide (Forteo) prior to her op-
erative intervention.

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Spinal Neurosurgery

As stated, she has a significant PI–​LL mismatch, positive SVA, and increased PT.
The goals of surgery are to correct her deformity with an approach that minimizes
complications. She has about 40 degree mismatch between her PI and LL; additionally,
one has to consider her elevated PT. The increase in her PT is her body attempting to
correct the global alignment by retroverting her pelvis to bring her back into alignment.
Schwab et al. published an anatomical spinal osteotomy classification system that reviews
types of osteotomies and the amount of correction to be expected.2 This patient has a
prior fusion from L3 to L5 and a mismatch of greater than 40 degrees; thus, she will need
at least a Schwab grade 3 osteotomy (pedicle subtraction osteotomy [PSO]) to give her
the majority of the correction necessary.This grade 3 osteotomy gives at least 30 degrees
of correction. A  Schwab grade 4 osteotomy is an extended PSO with disc resection
and can give a correction up to 45 degrees. While the PSO is a powerful technique for
correction, it does come with an increase risk of hardware failure and pseudoarthrosis.
The usage of bone morphogenic protein (BMP) would be recommended to assist in
obtaining a solid fusion mass.
Deformity correction can be achieved via a multitude of approaches including
anterior/​posterior, lateral/​posterior, or posterior alone. An anterior approach via an-
terior lumbar interbody fusion (ALIF) combined with a posterior approach would
allow for a large interbody graft at L5–​S1, which typically gives more lordosis at
that level compared to a standard transforaminal lumbar interbody fusion (TLIF) at
that same level. However, Dorward et al. showed that a TLIF had a shorter overall
operative time in long constructs and had a better ability to correct any scoliosis or
fractional curves.3
Once the determination is made of how the lumbar deformity is to be corrected,
one must consider what will be the upper instrumented vertebrae (UIV) and distal an-
chor point for screws. This patient will likely need to have a distal instrumentation to
the pelvis. This technique is useful in longer constructs given its ability to protect the
sacral screw from failure and increase the chances of obtaining successful arthrodesis at
the lumbosacral junction. Regarding the UIV, one should take into account that this
patient has osteoporosis and this will increase the risk screw pullout and of proximal
junction kyphosis (PJK) or failure (PJF). Several techniques are used to reduce the risk
of PJK and PJF:

• Longer fusion constructs and avoiding constructs that start or end at the
cervicothoracic or thoracolumbar junction
• At least three fixation points above and below the apex of the deformity
• Hybrid constructs (pedicle screws, hooks, wires, percutaneous pedicle screws) to
possibly improve fixation strength
• Direction of the pedicle screw insertion affects pullout strength; purchase in
subchondral bone is recommend to maximize fixation
• Undertapping to increase the insertional torque and pullout strength of
pedicle screws
• “Hubbing” of pedicle screws adversely affects pullout strength and should be
avoided
• Use of cement augmentation at the UIV

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Flat Back Deformity

Questions

1. What are the perioperative complications associated with adult deformity

surgery?
2. What are some preventative measures to reduce the risk of complications?

Surgical Procedure

Spine deformity surgery is performed under general anesthesia with Foley catheter
placement, duplicate intravenous access, and arterial line placement. Neuromonitoring
(somatosensory evoked potentials [SSEP], motor evoked potentials [MEPs], and electro-
myography [EMG]) is utilized to ensure that all neural elements are safe during place-
ment of pedicle screws, osteotomies, and corrective maneuvers.
Patient is positioned in the prone position with appropriate padding of bony
prominences, such as the chest/​sternal region, hip/​anterior superior iliac spine (ASIS),
thighs, and knees. Typically, a Jackson OSI table is used. Patient should be positioned in
a manner that enhances lordosis in the lumbar spine.
Preparing for potential complications in surgery is key to a good outcome. Exposure
of spine from the posterior approach can lead to a significant amount of blood loss.
The use of tranexamic acid (TXA) is common to decrease blood loss and the need for
blood transfusion. Hui et al. showed in a meta-​analysis that TXA significantly reduces
intraoperative and postoperative blood loss and reduced cell salvage transfusion amount.
TXA is thrombogenic and can cause deep vein thrombosis or pulmonary embolism
(DVT/​PE); however, this seems to be a rare occurrence. Other methods of reducing
blood loss are usage of cell saver and high-​power coagulation devices.
After the appropriate spinal levels have been exposed (with great care taken not to
disrupt those facet joints that are not included in the construct), the removal of any prior
instrumentation should be performed. Next, new instrumentation can be inserted. At the
UIV, cement was injected into the vertebral body to reduce the risk of PJK/​PJF.5 Depending
on the experience of the surgeon, pedicle screw placement can occur via free-​hand tech-
nique, which does not utilized any imaging for placement, navigation, or fluoroscopy. It is
important to prevent any neurological injury with placement of pedicle screws; this can be
accomplished by checking MEPs after the cannulation of a pedicle and/​or placement of a
pedicle screw.Additionally, the pedicle screw can be directly stimulated after placement with
EMG. Another way to check for appropriate placement is to utilize an intraoperative CT
scan or fluoroscopy to assess for any screws that have not been placed adequately.
Pedicle subtraction osteotomies are no small feat to accomplish. These require me-
ticulous exposure of the pedicles located cranially and caudally to the pedicle that will
be resected. For example, if the goal is for L3 PSO, then the L2 and L4 pedicles should
be accessible and, at this point, should have a pedicle screw in place for the placement
a temporary rod. After bony exposure, the lamina should be removed and adequate ex-
posure should include the L2, L3, and L4 nerve roots. After the bone has been removed
and the nerve roots have been visualized, then one temporary rod should be placed
between the L2 and L4 pedicle screws. A wedge resection should then be performed bi-
laterally. After the appropriate amount has been removed, then the cap screws should be
loosened to allow reduction of the osteotomy and appropriate closure of the osteotomy.

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Spinal Neurosurgery

There should be bone-​to-​bone contact to ensure appropriate fusion. A rod should be

place connecting the UIV to the pelvic instrumentation. Appropriate decortication is
performed, and a combination of autograft, allograft, and other products (e.g., BMP)
should be placed on the bone to assist with fusion. It is important to place an additional
rod at the level of the PSO to reduce the chance of rod fracture.

Oral Board Reviews: Management Pearls

1. Prevention of further complication is the key after appropriate placement of

screws and placement of products both autograft and allograft for fusion.
a. During exposure, take care to leave the supraspinal and intraspinal
ligaments intact to prevent PJK/​PJF.
b. Utilize of some of the techniques just discussed to prevent PJK/​PJF.
2. Time that the patient has been in the prone position and amount of fluid that has
been given during surgery has been documented in contributing to a very rare
complication of spine surgery—​postoperative blindness.Thus, it is sometimes safer
to stage such large procedures to ensure adequate correction and patient safety.

Many surgeons perform additional steps to prevent PJK/​PJF.

Aftercare

Patients should be monitored in an intensive care or step-​down unit. There should be

invasive monitoring of blood pressure in case the patient requires increased mean arterial

A B

Figure 23.5  (A) Lateral postoperative scoliosis x-​ray. (B) Anteroposterior (AP)

postoperative scoliosis x-​ray.

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Flat Back Deformity

pressure (MAP) via pressors for appropriate spinal cord perfusion after the procedure.
Additionally, patients typically have a history of narcotic use and may require a consulta-
tion with an inpatient pain management service for adequate pain control.
There is no evidence that would suggest that patients have an improved outcome with
a thoracolumbosacral (TLSO) brace after operative intervention; however, prescribing
a TLSO brace postoperatively will allow the patient to maintain appropriate posture
during the healing process.
The patient will need physical therapy. Special attention should address hip
contractures that can developed over time, to help with an appropriate recovery process.
Appropriate follow-​up with imaging (Figure 23.5A,B) should be established to en-
sure that the patient does not develop any undiagnosed complications: PJK/​PJF, hard-
ware failure, or infection.

References and Further Reading

1. Lehman RA Jr, Kang DG, Wagner SC. Management of Osteoporosis in spine surgery. J Am
Acad Orthop Surg. 2015 Apr; 23(4): 253–​263. doi: 10.5435/​JAAOS-​D-​14-​00042.
2. Schwab F, Blondel B, Chay E, et al.The comprehensive anatomical spinal osteotomy classifica-
tion. Neurosurgery. 2014; 74(1): 112–​120.
3. Dorward IG, Lenke LG, Birdwell KH, et al. Transforaminal versus anterior lumbar interbody
fusion in long deformity constructs: A matched cohort analysis. Spine (Phila PA 1976). 2013
May 20; 38(12): E755–​E762. doi: 10.1097/​BRS.0b013e31828d6ca3.
4. Hui S, Xu D, Ren Z, Chen X, Sheng L, Zhuagn Q, Li S. Can tranexamic acid conserve blood
and save operative time in spinal surgery? A meta-​analysis. Spine J. 2017 Dec 122. Pii: S1529-​
9430(17)31192-​0. doi: 10.1016/​j.spinee.2017.11.017.
5. Ghobrial GM, Eichberg DG, Kolcun JPG, Madhavan K, Lebwohl NH, Green BA, Gjolaj
JP. Prophylactic vertebral cement augmentation at the uppermost instrumented vertebra and
rostral adjacent vertebra for the prevention of proximal junctional kyphosis and failure fol-
lowing long-​segment fusion for adult spinal deformity. Spine J. 2017 Oct; 17(10): 1499–​1505.
doi: 10.1016/​j.spinee.2017.05.015.

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Diskitis

Jacob R. Joseph, Brandon W. Smith, and Mark E. Oppenlander

Case Presentation

A 37-​year-​old woman with a history of intravenous heroin abuse presents to the emer-
24
gency department complaining of acute on chronic back pain. She states that the pain
began 3 months prior to presentation and was associated with nausea and chills. She
describes the pain as being constant and feeling like muscular spasms, with radiation
laterally across her back to both sides. She denies any pain radiating down her legs.
She denies numbness or tingling. The pain has been progressively worsening since the
onset and has only been responsive to heroin use. She denies any fevers but continues
to have intermittent chills. In regards to her drug use, she states that she is usually an
everyday user of heroin but has not had any for the past 3 days. She endorses symptoms
of sweating, diarrhea, nausea, and shaking. She denies a history of trauma, bowel or
bladder incontinence, urinary retention, or saddle anesthesia. On physical exam, she is
nontoxic and afebrile. Her detailed neurologic examination was unremarkable, with full
strength in all four extremities. Her sensation was intact without lateralization or sensory
level. Her reflexes were symmetric throughout, and no pathologic reflexes were present.
Palpation of her spine does not elicit significant pain, and no step-​offs are noted.

Questions

1. What is the likely diagnosis?

2. What laboratory studies would be appropriate to obtain?
3. What imaging studies would be appropriate to obtain?

Assessment and Planning

The history of this patient makes the neurosurgeon suspect the presence of osteomy-
elitis and diskitis. The differential includes degenerative disc disease, traumatic spinal
fracture, pathologic spinal fracture, bony tumor, leptomeningeal disease, sacroiliitis, pye-
lonephritis, and psoas abscess. However, the onset of back pain in a patient with a known
history of intravenous drug abuse should immediately cause concern for osteomyelitis
and diskitis.
Risk factors for the development of osteomyelitis/​diskitis include not only intra-
venous drug abuse, but also acquired immunodeficiency syndrome (AIDS) and other
immunocompromised states (such as transplant recipients or patients on chemotherapy).
Other risk factors include diabetes mellitus, renal failure, cirrhosis, and distant infections.

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Spinal Neurosurgery

Gram-​positive organisms are most common, with Staphylococcus aureus being the most
likely. Other common organisms include Staphylococcus epidermidis, Streptococcus viridans,
Streptococcus pneumoniae, and enterococcus. Gram-​negative organisms are less common
and are usually associated with gastrointestinal and genitourinary sources. Pseudomonas
species are a consideration in intravenous drug abusers as well.
Initial laboratory assessment should include a complete blood count (CBC) with
differential to assess for increased white blood cell count or left shift. A  neutrophilic
predominance suggests a typical bacterial infection, while a lymphocytic predominance
raises suspicion for a mycobacterial or fungal infection. In addition to a CBC, an eryth-
rocyte sedimentation rate (ESR) and c-​reactive protein (CRP) level should be obtained.
ESR and CRP are nonspecific markers of acute inflammation but are reasonably sensi-
tive for osteomyelitis/​diskitis. Even in cases where the diagnosis is obvious, measurement
of ESR and CRP are useful to obtain at presentation so that response to treatment can
be followed by serial measurements.
Magnetic resonance imaging (MRI) is the most clinically useful test to establish a
diagnosis of osteomyelitis/​diskitis. Imaging should be performed both with and without
intravenous gadolinium. The entire spine should be imaged as infections are commonly
multifocal. Typically, T1-​weighted precontrast images will reveal a hypointense signal in
the affected vertebral bodies, while T2-​weighted images show hyperintensity in the af-
fected vertebral bodies, disc space, and paravertebral soft tissues. The T2 hyperintensity
suggests edema in these structures. Postcontrast T1-​weighted images reveal enhance-
ment of the affected structures. If imaging reveals involvement of the bone, but not the
disc, consideration should be made for alternative diagnoses, such as osteonecrosis.
In certain patients such as those with incompatible implanted pacemakers or
defibrillators, obtaining MRI in a safe and timely fashion is difficult. In these patients, al-
ternative imaging modalities are necessary. Computed tomography (CT) can be helpful
to assess the amount of vertebral body destruction present, which can help determine
if instrumentation and fusion is indicated. In addition, the use of intravenous contrast
with CT can be helpful to identify enhancing abscesses, including those in the epidural
space and the psoas muscle. If there is concern for compression of the neural elements, a
CT myelogram can be performed with intrathecal contrast. Other imaging studies such
as radionuclide scans and positron emission tomography (PET) have been described to
evaluate for osteomyelitis/​diskitis, though they are rarely necessary.
Imaging of suspected osteomyelitis/​diskitis should also include evaluation for spinal
deformity. While MRI or CT could show a focal kyphosis around the affected levels,
they are performed in the lying position and could potentially miss a flexible deformity.
Standing scoliosis radiographs can be helpful in this circumstance.
In the present case, an MRI and CT were performed, demonstrating evidence of os-
teomyelitis/​diskitis at T10–​T11 (Figure 24.1).There was no evidence of epidural abscess
(Figure 24.2). Her ESR was 34 and CRP was 2.7.

Questions

1. What treatment is recommended for the patient at this time?

2. How would this patient’s pain be treated?
3. What would constitute treatment failure in this patient?

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Diskitis

A B

C D

Figure 24.1  Preoperative imaging in mid-​sagittal plane. (A) Sagittal computed

tomography (CT) non-​contrast showing vertebral body destruction and focal kyphosis
at T10–​T11. (B) Sagittal T2-​weighted magnetic resonance image (MRI) demonstrating
T2 hyperintensity in the vertebral bodies and disc at T10–​T11. (C) Sagittal T1-​
weighted non-​contrast MRI demonstrating T1 hypointensity of the vertebral bodies.
(D) Sagittal T1-​weighted gadolinium-​enhanced MRI showing diffuse contrast
enhancement in the disc and vertebral bodies at T10–​T11.

Oral Boards Review: Diagnostic Pearls

1. Risk factors for the development of spontaneous osteomyelitis/​diskitis in-

clude intravenous drug abuse, AIDS, immunosuppression, diabetes mellitus,
and renal failure.
2. Patients with risk factors who present with fever and back pain should be
evaluated for diskitis. Initial evaluation includes CBC, ESR, and CRP, along
with detailed neurologic examination.
3. MRI with and without contrast is the test of choice to evaluate for osteomy-
elitis/​diskitis.

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A B

Figure 24.2  Preoperative magnetic resonance image (MRI) in axial plane through

T10–​T11. (A) Axial T2-​weighted MRI showing no evidence of cord compression.
(B) Axial T1-​weighted non-​contrast MRI. (C) Axial T1-​weighted gadolinium-​
enhanced MRI showing no evidence of epidural abscess.

Decision-​Making

When there is high suspicion of spinal osteomyelitis/​diskitis, urgent evaluation and im-
aging is warranted. Initial examination should be focused on identification of any as-
sociated neurologic deficit. If there is evidence of neurologic deficit, emergent spinal
imaging should be performed.
In the absence of neurologic deficit, surgical treatment is usually not needed
emergently. However, the patient does require urgent medical treatment.The first step in
treatment should be acquisition of blood and urine Gram stain and cultures, along with
the previously mentioned lab testing. Direct cultures of the affected vertebral body or
disc space may also be needed if other cultures are negative; this is accomplished via per-
cutaneous needle biopsy under CT or fluoroscopic guidance. After cultures are drawn,
immediate treatment with broad-​spectrum antibiotics is warranted. Initial treatment
should be ensured to cover methicillin-​resistant Staphylococcus aureus (MRSA). Unless

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the patient is septic, or is likely to imminently become septic, then antibiotics can be
deferred until cultures are done.
Pain is a common presenting symptom and requires treatment. For acute pain, a
combination of narcotics and muscle relaxers can be helpful. Steroids are not advisable
due to the risk of worsening infection. Neuropathic pain medications such as gabapentin
or pregabalin can help with radicular pain. If the patient complains of mechanical pain
or pain with axial loading, consideration can be made for external bracing.
If there is evidence of neurologic deficit, then emergent spinal imaging is necessary
with MRI to identify a source of neural compression. If an epidural abscess is found,
emergent decompression of the neural elements is necessary to preserve neurologic func-
tion. Even in the absence of neurologic deficit, if there is evidence of epidural abscess, a
discussion should be had with the patient regarding risks and benefits of early operative
decompression. The location of infection may also contribute to decision-​making in
these cases. Infections near the spinal cord (cervical and thoracic spinal levels) are more
likely to result in rapid neurologic decline and thus may warrant earlier intervention.
There are several other considerations for operative intervention. If treatment with
intravenous antibiotics does not result in symptomatic improvement or improvement of
laboratory markers, then debridement of the disc space may be warranted. In addition,
the presence of focal, progressive spinal deformity can warrant correction. Recalcitrant
pain that does not respond to oral medications or bracing may also warrant fusion.
Finally, if bacteriologic diagnosis is unable to be obtained through other measures, a bi-
opsy may be needed.
In the present patient, CT-​guided biopsy revealed MRSA, and she was treated with
intravenous nafcillin. However, she continued to have severe mechanical and radicular
pain despite large doses of pain medications and bracing. Due to this, she was offered
surgical treatment.

Questions

1. What are the goals of surgery in this patient?

2. What approach should be used?

Surgical Procedure

The specifics of surgery for osteomyelitis/​diskitis depend on the levels involved, loca-
tion of infection, and degree of bone involvement. However, all procedures should be
performed under general anesthesia with neuromonitoring. In cervical or thoracic cases,
motor evoked potentials (MEPs) can be useful, while electromyography (EMG) and so-
matosensory evoked potentials (SSEPs) can be useful in all cases. Preoperative antibiotics
should be avoided if a bacteriologic diagnosis from a biopsy is required.
While the approaches are varied based on the level, the principles of surgery for
osteomyelitis/​diskitis are similar. The first goal should be decompression of the neural
elements. Also, a robust debridement of the disc space must be accomplished, with both
aerobic and anaerobic cultures. If necessary, in cases with severe bony involvement, de-
bridement of the vertebral bodies should also be completed. All cases with aggressive

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Spinal Neurosurgery

disc or bone debridement likely require fusion. Typically, anterior interbody fusion is
combined with posterior supplementation. Interbody fusion with metallic implants
or with bone autograft or structural allograft is likely safe. Titanium has bacteriostatic
properties and is safe to use for posterior instrumentation. If there is evidence of a focal
deformity, it should be corrected to restore anatomic alignment. Preoperative standing
scoliosis films can be useful to calculate spino-​pelvic parameters. In all surgeries for in-
fection, durotomy should be carefully avoided in these cases as there is a risk of inducing
meningitis. Finally, a detailed and robust multilayered wound closure is necessary to pre-
vent wound breakdown.
In the cervical spine, most cases are best treated with an anterior approach. This ap-
proach allows for aggressive debridement of the disc space and evacuation of ventral
abscesses. A corpectomy can be considered when necessary. Posterior instrumentation
to supplement the anterior fusion can also be utilized when necessary. In patients with
an isolated dorsal epidural abscess, a purely posterior approach with laminectomy with
or without fusion can be considered.
In the thoracic and lumbar spine, a posterior approach is sufficient if there is not sig-
nificant deformity or bony destruction. If there is a focal deformity or extensive anterior
compression, specialized ventral approaches are necessary. In the thoracic spine, these may
include a transpedicular approach, costotransversectomy, lateral extracavitary approach,
lateral retropleural approach, or thoracotomy. In the lumbar spine, this may involve an
anterior transperitoneal or retroperitoneal approach, lateral transpsoas approach, or a
transforaminal/​posterior approach to the disc. Again, extensive disc debridement should
be carried out. Posterior stabilization should be performed after aggressive diskectomy.
In the present patient, a T10–​T11 laminectomy with a left T11 transpedicular approach
for debridement of the T10–​11 disc space was completed. A T9–​T12 posterolateral fu-
sion was also completed (Figure 24.3). Bone allograft was used to perform an interbody
fusion.

A B

Figure 24.3  Postoperative x-​rays. Anteroposterior (AP) (A) and lateral (B) radiographs

showing T9–​T12 fusion.

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Diskitis

Oral Boards Review: Management Pearls

1. In the absence of neurological deficit, medical management is appropriate.

2. Failures of medical management are defined by the development of
neurologic deficit, progressive deformity, poor pain control, worsening labora-
tory markers, and persistent bacteremia.
3. Goals of surgery include bacteriological diagnosis, decompression of the
neural elements, aggressive debridement of the disc space, and correction of
deformity.

Pivot Points

1. If the patient presented with signs of sepsis, then aggressive fluid resuscitation
and antibiotic treatment prior to confirmation of microbiological diagnosis is
indicated.
2. If a large epidural abscess had been diagnosed preoperatively, then surgery
should have been performed on presentation.

Aftercare

Postoperatively, the patient should be admitted to the general care ward. Some patients may
warrant admission to the intensive care unit depending on blood loss during surgery or
sepsis as a result of the infectious process. Regular neurologic checks should be performed
to ensure stability of neurologic function. Postsurgical drains should be maintained in place
for an extended period of time to minimize fluid buildup.The patient should be mobilized
as soon as possible postoperatively with the assistance of physical and occupational therapy.
A brace may be provided at the discretion of the surgeon. Pain control should be obtained
with weaning of intravenous pain medications as soon as possible.
Broad-​spectrum intravenous antibiotics should be continued in the perioperative
period. A consultation with colleagues in infectious diseases should be obtained to help
narrow coverage when speciation and sensitivities are obtained. A thorough evaluation
to identify a source of the osteomyelitis/​diskitis is also critical. Specifically, an echocar-
diogram should be performed to rule out endocarditis. A dental evaluation should be
considered if there is suspicion for an intraoral source of infection.
An uncomplicated case of osteomyelitis/​diskitis usually requires at least 6 weeks of
intravenous antibiotics. Cases that are more complicated may require a longer course.
A peripherally inserted central catheter (PICC) should be placed for this purpose. Special
consideration should be made for patients who have a history of intravenous drug use. In
these patients, discharge to home with intravenous access may be unwise, and they may
require an inpatient stay for the entire course of antibiotics.
Standing scoliosis x-​rays (in a brace, if applicable) should be obtained postoperatively
if a fusion was performed. In addition, a repeat MRI near the end of the course of
antibiotics (6–​8 weeks after treatment initiation) can be helpful to follow disease pro-
gression. It should be noted that radiographic changes lag behind clinical changes. If
the patient is improving clinically and in laboratory parameters, then subtle worsening

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Spinal Neurosurgery

A B

Figure 24.4  An 8-​week follow-​up magnetic resonance image (MRI). Pre-​contrast

(A) and post-​contrast (B) sagittal T1-​weighted MRI showing improvement in contrast
enhancement.

of the MRI should be taken in context. In the present patient, follow-​up MRI showed
improvement of infection (Figure 24.4).

Complications and Management

Complications of surgery for osteomyelitis/​diskitis are similar to surgery for other

indications and are dependent on the spinal levels involved, approach, and extent of fu-
sion. These complications will be discussed in detail elsewhere.
A particular concern in surgery for primary spinal infections is wound infection and
breakdown.To counteract this, the initial wound closure should be performed with care,
ensuring an adequate fascial closure in the relevant areas. Wounds should be monitored
closely postoperatively. If there is evidence of wound breakdown or infection, then anti-
biotic coverage should be expanded to include skin flora. If the situation necessitates it,
a wound revision should be considered.
Patients should be closely monitored for the development of meningitis postoperatively,
particularly if the dura was violated. Early treatment with adequate dosing to ensure ce-
rebrospinal fluid (CSF) penetration can be helpful.
As with all spinal procedures, iatrogenic neurological injuries can occur, though they
are rare. Careful neurologic examinations should be performed routinely. If there is sus-
picion for neurologic worsening, repeat MRI should be performed to ensure that there
is no continued compression of the neural elements. If imaging is unremarkable, then
rehabilitation should be begun as soon as feasible.

Oral Boards Review: Complications Pearls

1. Careful neurologic assessments are critical postoperatively to identify recur-

rence of compression.
2. Meningitis and sepsis are possible postoperatively and should be treated as
early as possible when suspected.

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Diskitis

Evidence and Outcomes

While there are no randomized controlled trials of surgery for osteomyelitis/​diskitis, the
literature is strongly in favor of surgery when there is associated neurologic compromise,
progressive deformity, or recurrent bacteremia despite antimicrobial therapy without
other sources. In cases with epidural abscess, the literature is less clear. Many have argued
for early surgery and antibiotics, while others have argued for antibiotics alone. In cases
of spinal cord involvement (cervical or thoracic spine), it appears that there may be a
benefit to early surgery to preserve motor function, with a high rate of failure if medical
therapy alone is attempted.
There has been concern regarding the safety of instrumentation in the setting of
active infection. However, several studies have suggested that there is not a significant
added risk of perpetuating infection with decompression plus instrumentation when
compared to decompression alone. Overall reported rates of reoperation are less than
10% after surgery for infection.
While there have been numerous case reports and case series discussing various
approaches for osteomyelitis/​diskitis, there are no proven techniques which are superior
to others. In the cervical spine, most authors advocate for an anterior approach in cases
of diskitis in order to achieve a robust diskectomy. In other situations, there are a variety
of techniques that have been put forth with success, including open and minimally in-
vasive techniques.

References and Further Reading

Alton TB, Patel AR, Bransford RJ, Bellabarba C, Lee MJ, Chapman JR. Is there a difference
in neurologic outcome in medical versus early operative management of cervical epidural
abscesses? Spine J. 2015;15(1):10–​17.
Berbari EF, Kanj SS, Kowalski TJ, et al. 2015 Infectious Diseases Society of America (IDSA) clin-
ical practice guidelines for the diagnosis and treatment of native vertebral osteomyelitis in
adults. Clin Infect Dis. 2015;61(6):e26–​e46.
Bydon M, De la Garza-​Ramos R, Macki M, et al. Spinal instrumentation in patients with primary
spinal infections does not lead to greater recurrent infection rates: An analysis of 118 cases.
World Neurosurg. 2014;82(6):e807–​e814.
Duarte RM,Vaccaro AR. Spinal infection: State of the art and management algorithm. Eur Spine
J. 2013;22(12):2787–​2799.
Hadjipavlou AG, Mader JT, Necessary JT, Muffoletto AJ. Hematogenous pyogenic spinal infections
and their surgical management. Spine (Phila Pa 1976). 2000;25(13):1668–​1679.
Patel AR, Alton TB, Bransford RJ, Lee MJ, Bellabarba CB, Chapman JR. Spinal epidural
abscesses: Risk factors, medical versus surgical management, a retrospective review of 128
cases. Spine J. 2014;14(2):326–​330.
Urrutia J, Zamora T, Campos M. Cervical pyogenic spinal infections:  Are they more severe
diseases than infections in other vertebral locations? Eur Spine J. 2013;22(12):2815–​2820.

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Epidural Abscess

Hector G. Mejia Morales and Manish K. Singh

Case Presentation

A 61-​year-​old man was admitted to the hospital with a high-​grade fever of 103°F and
25
worsening confusion. Eight days prior to presentation, the patient began to complain
of leg pain in his right calf that radiated down to his foot. This was followed by pains
in his neck, then shoulder, and eventually progressed to generalized muscle spasms in
his back. He comes to the emergency department also with bilateral flank pain and
was diagnosed with a urinary tract infection. On physical examination, the patient was
assessed as having 4–/​5 generalized weakness in all four of his extremities. The patient,
though awake, showed significant confusion and no focal neurologic deficits.

Questions

1. What is the likely diagnosis?

2. What is the most appropriate imaging modality?
3. On what anatomical areas should the imaging studies be done?

Assessment and Planning

Despite low incidence rates, pyogenic infections of the spine are an important part of the
differential diagnosis when evaluating patients who present with symptoms involving
pain of the lower back, weakness of the extremities, radicular pain, and an accompanying
fever. Because there are several conditions that have similar signs and symptoms as those
seen in spine infections, it is important to apply effective use of imaging studies, labs, and
patient history in the workup. Other conditions that invariably present with some of the
nonspecific symptoms seen in spinal epidural abscesses (SEAs) can include pyelonephritis,
discitis, spinal trauma vertebral osteomyelitis, and spinal subarachnoid hemorrhages. In
the case of a true SEA there exists a tetrad of stages, as described by Heusner et al.These
stages can be characterized with an initial stage of spinal ache or pain that proceeds into
the second stage of nerve root pain; this is then followed by the third stage of weak-
ness in the voluntary muscles that ultimately culminates rather rapidly (within approxi-
mately 6 days) in the fourth stage of paralysis. Despite these four stages being distinctly
characterized in the literature, they most often exist on a continuum that lacks clearly
defined borders between the possible symptoms. Very rarely will patients present with
the described classical triad of fever, spine pain, and motor or sensory deficits. Patients
will in fact present with varying and unique scenarios that can involve both systemic and

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Spinal Neurosurgery

localized manifestations. Correctly diagnosing the condition can be further complicated

by the presence of nonspecific back or neck pains that are only sometimes accompanied
by systemic signs, especially when considering the fact that an overwhelmingly large
number of patients will present with symptoms of back pain at some point in their lives.
Some key points to remember when considering a diagnosis of SEA is that a majority
of patients with the condition will have focal tenderness (commonly in the lumbar
spine due to the existence of a larger epidural space) and an elevated erythrocyte sedi-
mentation rate (ESR), but less than half will have a fever or leukocytosis and only10%of
patients will have severe deficits such as paraplegia or incontinence.
Due to the sensitivity of the condition as well as the danger of rapid progression to
an irreversible stage, most SEAs are considered a neurosurgical emergency. Infections
of this nature can quickly lead to progressively worsening neurologic deficits brought
about by direct compression of the spine by the abscess or through vascular compro-
mise via venous thrombosis. Patients with cervical-​or thoracic-​level involvement have
been reported to have poorer neurological outcomes than those with more common
lumbar involvement. These types of outcomes and their uncertain variability make it
paramount that a delay in diagnosis and treatment be avoided. Efficiency in the diagnosis
of the condition can be improved by proper use of patient history, physical examination,
and imaging studies, as well as the ability to recognize the predisposing risk factors on
a patient-​to-​patient basis. Formation of the abscess will usually be due to direct inoc-
ulation secondary to some spinal trauma or surgical operation, through hematogenous
spread (accounting for about half of SEAs and frequently secondary to a bacterial en-
docarditis) or from an extension of an adjacent infection. Patients at the highest risk of
developing an abscess of this nature are those who are immunocompromised, but other
predisposing factors can include malignancies, bacteremia, intravenous drug use, and
the presence of foreign bodies. Imaging studies represent one of the most effective and
useful tools for confirmation of a suspected diagnosis and for initiating evaluation and
planning for surgical intervention. Radiography, while a less specific and sensitive test,
can give indications of overall mechanical stability of the spine and any compromise in
the alignment. Computed tomography (CT) will demonstrate the presence of spinal
infections at an earlier timepoint than plain radiography. CTs will not reflect soft tissue
involvement as readily as MRI but can help parse out any patterns of bony compromise.
MRI, however, boasts both a high sensitivity and specificity for spinal infections and
can provide a more accurate representation of the extent and involvement of the spinal
abscess as well as help elucidate the true extent of the spinal cord compression that may
be occurring. Therefore, the MRI remains the best tool for diagnosing SEAs through
imaging. Both T1-​and T2-​weighted images should be obtained of the suspected area
of the SEA, and diffusion-​weighted MRI should also be considered as scans showing a
pattern of restricted diffusion can also be suggestive of an epidural abscess. T2-​weighted
imaging also plays an important role in the determination of the composition of the
abscess. An image that shows a hypointense lesion with homogenous enhancement on
T2-​weighted imaging is indicative of a solid abscess, whereas a lesion appearing as a
hyperintense collection with a peripherally enhancing rim but lacking central enhance-
ment is characteristic of a fluid abscess. (On T1 this will be seen as a characteristically
hypointense center with a hyperintense rim.) These are distinctions that can affect the
surgical management of the abscess. It is also important to evaluate the entire spine when

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Epidural Abscess

imaging to determine the full extent of the infection and to rule out secondary abscesses
especially because thoracic or cervical level abscesses tend to produce rapid appearance
of neurologic deficits. Laboratory tests to determine the ESR and c-​reactive protein
(CRP) can also be used to partition those patients that are at higher risk.
In the case of our patient T1-​weighted, T2-​weighted, and short T1 inversion re-
covery (STIR) sagittal and axial MRI images were obtained of the thoracic and
lumbosacral spine. Additionally, contrast-​enhanced fat-​suppressed T1-​weighted sagittal
and axial images were obtained. On evaluation, images showed a peripheral contrast-​
enhancing homogenous fluid signal dorsal to the entirety of the thoracic spinal cord
which was compatible with an epidural abscess. Cervical imaging suggested that the
fluid collection extended superiorly to the level of C2. Similar results were found in the
lumbosacral images, which showed fluid collections at L1 and L3 as well as multilevel
facet arthropathy resulting in central spinal canal stenosis. Figure 25.1A–​C are repre-
sentative T1-​weighted post-​contrast images of the cervical, thoracic, and lumbar spines,
respectively.

Questions

1. What is the impact of these clinical and radiological findings in the surgical
planning?
2. What is the most appropriate timing for intervention in this patient?
3. How should surgery be approached in a patient with a fluid SEA versus a
fibrous one?

A B C

Figure 25.1  (A) T1-​weighted contrast-​enhanced sagittal cervical spine magnetic resonance image (MRI)
demonstrating dorsal epidural abscess from the level of C2 through C7. (B) T1-​weighted contrast-​enhanced
sagittal thoracic spine MRI demonstrating dorsal epidural abscess from the level of T1 through T12.
(C) T1-​weighted contrast-​enhanced sagittal lumbar spine MRI demonstrating dorsal epidural abscess from
the level of L3 through L4. There is a small ventral epidural abscess at L1.

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Spinal Neurosurgery

Decision-​Making

As mentioned previously, a series of stages spanning from spinal pain, to root pain, to
voluntary muscle weakness, to finally paralysis is the traditional progression diagnostic
of a SEA, but this is not often seen as distinctly in the hospital setting, and it requires
that action be taken before full progression to neurologic deficits occurs. Patients will
normally present to the doctor either in phase II (root pain) or phase III (voluntary
muscle weakness) of the condition’s progression, and these are considered neurosurgical
emergencies that must be immediately addressed. Though there has been some success
in medical management of SEAs under the correct circumstances, surgical intervention
remains the treatment of choice for management of many SEAs and should be imme-
diately considered in patients presenting with spinal instability or neurologic deficits.
Medical management coupled with surgical intervention has been often associated with
better outcomes, especially when antibiotic treatment has been tailored for the specific
organism obtained at the time of surgery. The initial antibiotic treatment should cover
gram-​positive, gram-​negative, and anaerobic organisms until a specific organism has
been isolated.
It is important to assess and take into account the extent and spread of the abscess
and to evaluate for any remote locations of secondary infection, as well as any spinal
compression that has occurred, and tailor the surgical approach to target these areas.
Surgical approaches can be targeted to the spinal level of the abscess and comprise the
full extent of spinal cord involvement (if present), Liquid abscesses can be addressed with
options for drainage and lavage (still dependent on spinal level and site of cord compres-
sion), whereas compressions caused by granulomatous abscesses may pose the challenge
of more case-​specific approaches depending on size and location. The patient in this
case presented with an MRI consistent with the formation of an epidural abscess along
the entirety of the thoracic spine and extending superiorly to C2 and inferiorly to the
level of L3. Due to the patient’s septic state as well as pain and muscle weakness of the
extremities, emergency surgery was immediately indicated.

Questions

1. How should levels of decompression be chosen?

2. Will laminectomies at the sites of maximal cord compression result in spinal
deformity (i.e.,-​at cervicothoracic or thoracolumbar junction)?

Surgical Procedure

Though the approach most frequently used is that of a posterior laminectomy at the
site of the abscess, abscesses that are causing ventral compression can be approached
either laterally or anteriorly and may require stabilization. The necessity of stabiliza-
tion and fusion in such cases poses an additional challenge because of the danger of
secondary infection of the instrumentation that may be used, but studies have shown
favorable results with the use of titanium mesh cages due to their reduced rates of
postoperative infections and their resistance to biofilm formation. Because of the ex-
tent of the epidural abscess throughout the spinal cord in our presenting patient, a

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Epidural Abscess

dorsal approach was decided upon with the patient positioned prone over a regular
table. Chest rolls may be used to help support the patient, and the head should be
placed in a Mayfield head adapter in a neutral position if posterior cervical access is
necessary. This position will afford access to the entirety of the spine. With the aid
of a C-​arm fluoroscope the desired levels must be localized. In a situation where the
abscess spans nearly the entire length of the spinal cord it is desirable to target and
mark a point of entry in each of the major anatomical regions of the spine, carefully
considering those areas with the maximum collection of the epidural abscess or the
major sites of spinal cord compression. The draping should allow for access down the
entire length of the spine along the dorsal approach.
The main goal for the procedure should be to address the issues of washing out the
epidural abscess and relieving the points of cord compression. Because this epidural ab-
scess extends throughout the spine, it is not advisable to perform a laminectomy of the
entire spine; it is instead better to opt for making multiple skin incisions at the levels
where there is the greatest cord compression from the epidural abscess and performing
multiple skipped laminectomies.This will afford access to the epidural space of the spinal
canal, which can then be washed out with the help of a catheter and an antibiotic ir-
rigation. Other options to be considered to avoid the use of multilevel laminectomies
included the creation of unilateral fenestrations at multiple levels or the use of suction
and irrigation catheters that are snaked superiorly and inferiorly through the spinal canal
from a mid-​level laminectomy access point.
Following the incision, a subperiosteal dissection should be carried out to expose the
lamina and the spinous processes of the targeted vertebrae. It is important to take care
to preserve the spinous processes, the interspinous and supraspinous ligaments, and the
facet joints at all levels in order to best preserve overall spine stability. After completion
of a laminectomy, introduction of an irrigation catheter can be performed superiorly or
inferiorly. Any purulent material should be thoroughly washed out with copious gentle
irrigation until clear irrigation fluid can be visualized coming out of the open end and
the epidural space has been cleared of purulent material. It is important to thoroughly
wash out the spinal canal in order to both avoid the recurrence of the abscess and to
make sure the spinal cord is properly decompressed. A similar procedure can be done at
the other points selected for the multiple skipped laminectomies.
Once the laminectomies and washout of the abscess have been performed, it is
important to perform antibiotic irrigation of the wound sites with broad-​spectrum
antibiotics with attention given to the paraspinous muscles at all incision sites. Surgical
drains should be left to maximize removal of all infected material.

Oral Boards Review: Management Pearls

1. Instrumentation or external orthosis should be utilized if spinal instability is

suspected either from the disease process or iatrogenic.
2. Routine repeat imaging is necessary to evaluate for recurrent disease or new
disease.
3. Involve other specialities to treat infection in nearby structures (lung,
pelvis, etc.).

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Spinal Neurosurgery

Pivot Points

1. Have a low threshold to reimage because recurrence of abscess is common.

2. There is no convincing evidence that instrumentation prevents resolution of
infection because it is a foreign body. If there is concern about spinal stability,
fusion should be pursued to prevent possible revision surgery.

Aftercare

Broad-​spectrum antibiotics should be administered, and the expertise of an infectious

disease specialist can be sought. Surveillance of infection in other body fluids, such as
blood and urine, should be monitored. A long-​term intravenous access catheter should
be placed once blood cultures are negative in patients for whom intravenous antibiotics
are indicated.
The patient should be mobilized as soon as possible, and adequate pain control
should be given. ESR and CRP values should be examined serially to ensure a down-
ward trend indicating resolution of the infection. Follow-​up imaging may be obtained in
2–​3 weeks to assess for possible recurrence of disease as well as to assess for development
of a spinal deformity.

Complications and Management

Complications of surgery for epidural abscess are similar to surgery for other indications
and depend on the spinal levels involved, approach, and number of levels treated.
A particular concern in surgery for primary spinal infections is wound infection and
breakdown.To counteract this, the initial wound closure should be performed with care,
ensuring an adequate fascial closure in the relevant areas. Wounds should be monitored
closely postoperatively. If there is evidence of wound breakdown or infection, then anti-
biotic coverage should be expanded to include skin flora. If the situation necessitates it,
a wound revision should be considered.
Patients should be closely monitored for the development of meningitis postoperatively,
particularly if a durotomy was incurred. This information should be communicated to
the infectious disease care team because this may alter the treatment regimen.
Any change in neurologic exam should prompt the acquisition of updated imaging.
Recurrences of abscess, new abscesses, or an epidural hematoma are all conditions that
would require surgical intervention.

References and Further Reading

Bond A, Manian FA. Spinal epidural abscess: A review with special emphasis on earlier diagnosis.
Biomed Res Int. 2016;2016:1614328.ypo.
Carragee EJ. The clinical use of magnetic resonance imaging in pyogenic vertebral osteomyelitis.
Spine. 1997;22(7):780–​785.
Colmenero JD, Jiménez-​mejías ME, Sánchez-​lora FJ, et al. Pyogenic, tuberculous, and brucellar
vertebral osteomyelitis: A descriptive and comparative study of 219 cases. Ann Rheum Dis.
1997;56(12):709–​715.

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Epidural Abscess

Cornett CA,Vincent SA, Crow J, Hewlett A. Bacterial spine infections in adults: Evaluation and
management. J Am Acad Orthop Surg. 2016;24(1):11–​18.
Dagirmanjian A, Schils J, Mchenry M, Modic MT. MR imaging of vertebral osteomyelitis
revisited. AJR Am J Roentgenol. 1996;167(6):1539–​1543.
Del curling O, Gower DJ, Mcwhorter JM. Changing concepts in spinal epidural abscess: a report
of 29 cases. Neurosurgery. 1990;27(2):185–​192.
Dietze DD, Fessler RG, Jacob RP. Primary reconstruction for spinal infections. J Neurosurg.
1997;86(6):981–​989.
Eastwood JD,Vollmer RT, Provenzale JM. Diffusion-​weighted imaging in a patient with vertebral
and epidural abscesses. AJNR. 2002;23:496–​498.
Gala FB, Aswani Y. Imaging in spinal posterior epidural space lesions: A pictorial essay. Indian J
Radiol Imaging. 2016;26(3):299–​315.
Grieve JP, Ashwood N, O’Neill KS, Moore AJ. A retrospective study of surgical and conservative
treatment for spinal extradural abscess. Eur Spine J. 2000;9(1):67–​71.
Hadjipavlou AG, Mader JT, Necessary JT, Muffoletto AJ. Hematogenous pyogenic spinal infections
and their surgical management. Spine. 2000;25(13):1668–​1679.
Heusner AP. Nontuberculous spinal epidural infections. N Engl J Med. 1948;239(23):845–​854.
Khanna RK, Malik GM, Rock JP, Rosenblum ML. Spinal epidural abscess: evaluation of factors
influencing outcome. Neurosurgery. 1996;39(5):958–​964.
Kuklo TR, Potter BK, Bell RS, Moquin RR, Rosner MK: Single-​stage treatment of pyogenic
spinal infection with titanium mesh cages. J Spinal Disord Tech. 2006;19(5):376–​382.
Mittal S, Khalid M, Sabir AB, Khalid S. Comparison of magnetic resonance imaging findings
between pathologically proven cases of atypical tubercular spine and tumour metastasis:
A retrospective study in 40 patients. Asian Spine J. 2016;10(4):734–​743.
Pfister HW,Von Rosen F,Yousry T. MRI detection of epidural spinal abscesses at noncontiguous
sites. J Neurol. 1996;243(4):315–​317.
Suppiah S, Meng Y, Fehlings MG, Massicotte EM, Yee A, Shamji MF. How best to manage the
spinal epidural abscess? A current systematic review. World Neurosurg. 2016;93:20–​28.
Tuchman A, Pham M, Hsieh PC. The indications and timing for operative management
of spinal epidural abscess:  Literature review and treatment algorithm. Neurosurg Focus.
2014;37(2):E8.
Youmans JR, Winn HR. Youmans Neurological Surgery. New York: Saunders; 2011.
Zimmerer SM, Conen A, Müller AA, et al. Spinal epidural abscess: Aetiology, predisponent factors
and clinical outcomes in a 4-​year prospective study. Eur Spine J. 2011;20(12):2228–​2234.

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Nonsurgical Spinal Diseases

Lahiru Ranasinghe and Aimee M. Aysenne

It is just as important to recognize diseases and disorders that affect the spinal cord
requiring surgical interventions as it to recognize medical etiologies of myelopathies and
26
know preferred treatments. Neurosurgeons are expected to have a strong understanding
of these disorders; they need to be able to recognize medical causes of myelopathies and
know when surgical interventions are not indicated.These conditions vary from trauma
and infections to autoimmune and degenerative conditions. This chapter will briefly
describe the clinical and imaging features of these etiologies as well as discuss treatment
options.

Trauma

Trauma to the spinal cord can be directly or indirectly caused by mechanical forces
and can be worsened with a subsequent inflammatory response leading to swelling and
vascular occlusion, which ultimately perpetuates secondary spinal cord damage. With
mechanisms varied from sport to falls to violence and motor vehicle accidents, trauma is
the most common cause of myelopathy, with nearly everyone at risk of possible injury.1
Typically, the diagnosis of trauma is known by history or other injuries. American Spinal
Injury Association (ASIA) and International Spinal Cord Society (ISCoS) scoring sys-
tems are effective and recommended tools for localizing and determining the severity
of the lesion. They have also been validated for prognostication.2–​4 Initial interventions
for patients with spinal cord trauma involve stabilization of the segment of spine likely
to be involved in the trauma. In the cervical spine, this includes immobilization collars
and in-​line mechanical stabilization with manual in-​line immobilization if intubation
is required.2,5,6 In the thoracic and lumbar spine, log roll precautions are used. These
techniques increase the likelihood of hospital-​acquired events that occur from im-
mobilization including deep venous thrombosis, pulmonary embolism, and aspiration
pneumonias and therefore should be discontinued as soon as the spine has safely been
excluded from injury. If an asymptomatic patient with suspected cervical spine trauma
is awake, neurologically intact, not intoxicated, and has no distracting injuries, the cer-
vical spinal cord can be accurately evaluated on clinical exam of range of motion and
point tenderness. If there is any question, a non-​contrasted computer tomography (CT)
is recommended to evaluate the bony structures.7,8 Depending on the severity and
mechanism of injury, protocolized vascular imaging of the cervical spine decreases the
incidence of stroke.9 Magnetic resonance imaging (MRI) adds the evaluation of liga-
mentous injury.10

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Spinal Neurosurgery

Nonsurgical treatment options have had a controversial history. While many

therapies have been shown to be effective in animal models, few have yielded success in
human populations. Currently, the only medical management recommended is to main-
tain a mean arterial blood pressure greater than 85 mm Hg for 7 days post-​injury.11,12
Corticosteroids, while thought to be effective at treating other causes of myelopathy,
have been shown to increase the likelihood of complications, including death, in the
setting of spinal cord trauma and corticosteroids have been removed as a recommen-
dation in the 2013 Guidelines for the management of acute cervical spine and spinal
cord injuries.2,13 Therapeutic hypothermia has had mixed outcomes as an effective treat-
ment option in spinal cord trauma, and more studies are needed to determine its role in
spinal cord trauma.2,14 GM-​1 gangliosides have not been shown to be effective treatment
options.2,15 In addition to the surgical management discussed in other chapters, rehabil-
itation is necessary for spinal cord recovery and for the patient to learn independence
following a new neurological injury.

Demyelinating Diseases: Transverse Myelitis, Multiple Sclerosis,

and Neuromyelitis Optica
Transverse Myelitis

Transverse myelitis is a broad catch-​all term for inflammation of the spinal cord. The
etiologies of transverse myelitis include autoimmune, demyelinating, infectious, or
postinfectious conditions. Infectious associations include bacteria such as Salmonella and
Campylobacter jejuni and viral agents including Zika and enteroviruses. Autoimmune
associations include lupus, sarcoidosis, systemic sclerosis, and Sjögren disease.16 Many
more associated conditions have been described. When a known etiology is found, the
diagnosis is more appropriately labeled with a more specific term. If transverse myelitis
occurs without other clinical features or imaging findings, it may be considered a clini-
cally isolated syndrome, previously thought to be a precursor to multiple sclerosis (MS),
with as many as 88% of these patients progressing to meet criteria of MS.17 With more
advanced immunologic evaluations and treatment options, this number has significantly
decreased.
Although numerous causes of transverse myelitis have been identified, many cases
are still thought to be idiopathic. The Centers for Disease Control is currently ac-
tively tracking cases since 2014 for a better understanding (https://​www.cdc.gov/​
acute-​flaccid-​myelitis/​index.html).18 Because transverse myelitis has a rapid onset, it is
common for patient to endorse an onset of symptoms over the course of a few hours to
days. MRI findings demonstrate swelling and hyperintense T2 lesions in the spinal cord.
Acute lesions may be contrast-​enhancing on T1-​weighted imaging and represent active
inflammation. Lesions may be focal and well-​demarcated or diffuse.19 Cerebrospinal
fluid (CSF) analysis often reveals an inflammatory process with leukocytosis but may
not in as many as 43% of inflammatory transverse myelitis, and other conditions can
also cause CSF leukocytosis.20 Treatment for transverse myelitis typically involves high-​
dose corticosteroids while some clinicians choose to add intravenous immunoglobulin
(IVIg) or plasma exchange. Because the etiologies of TM are so varied, so are the out-
come data.16,21

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Nonsurgical Spinal Diseases

Multiple Sclerosis

MS is a T-​cell–​mediated autoimmune condition causing demyelination of the cen-

tral nervous system. Typical onset of MS is between 20 and 50 years, and MS is more
common in women. The McDonald criteria, most recently updated in 2017, is the
agreed upon standard for distinguishing MS from clinically isolated syndrome.The diag-
nosis hinges on the separation of two or more lesions in time or space. MRI is the most
useful diagnostic tool, with CSF analysis helpful for demonstrating active inflammation
from inside the central nervous system. In the case of MS, oligoclonal bands are present,
and CSF is helpful to exclude other conditions that have specific antibody markers.22
There are four recognized patterns of progression for MS: relapsing-​remitting, pri-
mary progressive, secondary progressive, and relapsing-​progressive.These patterns display
a general progression of the disorder, but relapsing-​remitting, secondary progressive, and
relapsing-​progressive are marked by episodes of acute inflammatory attacks. This pro-
cess of demyelination and subsequent plaque formation ultimately leads to the devel-
opment of symptoms such as fatigue, difficulty walking, vision loss, urinary symptoms,
and dementia. It is important to note that an “attack” for patients suffering from MS
can be worsening old symptoms or the presentation of new symptoms.The severity and
number of symptoms can vary from patient to patient.22
Acute MS attacks are often treated with high-​dose steroids as they have been for
many years. The long-​term management of these patients has changed significantly in
recent history with eight new medications approved for use in MS since 2010 and two
more currently awaiting approval. The classes of these drugs include interferon, mono-
clonal antibodies, purine analogs, and sphingosine 1 phosphate receptor modulators.23,24
Due to the complexity and evolving therapies for MS, most patients should be treated
in specialized centers.

Neuromyelitis Optica and Neuromyelitis Optica Spectrum Disorder

Neuromyelitis optica (NMO) and neuromyelitis optica spectrum disorder (NMOSD)

are other autoimmune demyelinating disorders presenting with spinal cord myelitis
and optic neuritis. NMO is diagnosed with a longitudinal segment of the spinal cord
extending three or more contiguous segments and seropositivity for anti-​AQP4 IgG.19,25
These two diagnostic criteria are effective for distinguishing NMO from MS and trans-
verse myelitis Antibodies against aquaporin 4 (AQP4) water channels are found in the
serum of between 50% and 90% of patients. Of those with negative NMO antibodies,
antibodies to myelin oligodendrocyte glycoprotein (MOG-​IgG) have been found in
more than half with suspected NMODS.25–​27 These antibodies are also found in the
serum, and titers may help determine active state of disease. Over time, the spinal cord
will atrophy.28 NMO is most common in non-​Caucasian women and will typically pre-
sent with visual disturbances, spastic paresis, and loss of sensation. Bowel and bladder dys-
function as well as autonomic instability is also common with this condition. NMOSD
are associated with a poor prognosis, with treatment options focused on decreasing
inflammation. In the acute setting, steroids are again the mainstay, with some clinicians
using IVIg or plasma exchange.29 Recently, clinicians are beginning to use rituximab for
chronic treatment.30

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Spinal Neurosurgery

Vascular Myelopathies

Infarcts of the spinal cord are rare. They are described by location (cervical or thora-
columbar) and distribution of the spinal cord (anterior or posterior). Initially, patients
experience severe pain, but progression with neurological deficits occurs rapidly there-
after. The anterior spinal artery supplies the anterior two-​thirds of the spinal cord,
which include the spinothalamic and corticospinal tracts, and deficits include sensory
disturbances relating to temperature and pain sensation and weakness. The posterior
spinal artery supplies the posterior one-​third of the spinal cord, and this region includes
the fasciculus gracilis and cuneatus. An infarct in this part of the spinal cord impacts the
dorsal column–​medial lemniscus pathway resulting in a loss of proprioception and vi-
bratory sense. Evaluation for etiology and secondary prevention of strokes is required
for spontaneous infarcts. Additionally, spinal cord infarcts can occur with diseases of
the descending aorta, including aortic dissection because the artery of Adamkiewicz
supplies the thoracic cord via a direct branch from the aorta. This artery is also at risk
during cross-​clamp for cardiopulmonary bypass. Some advise using a lumbar drain to
allow for greater spinal cord perfusion pressure during and following surgery, but this is
controversial.31–​34
Surfer’s myelopathy is a particularly rare vascular disorder with theoretical pathogen-
esis due to rapid hyperextension of the spine in a novice surfer; this leads to compression
of the anterior spinal artery or embolization of fibrocartilaginous disc material from the
thoracic region.35 Diffusion-​weighted imaging of the spinal cord is diagnostic but infre-
quently used for spinal cord infarcts.36 Spinal arteriovenous malformations are also rare
causes of compressive myelopathies, which are covered in other chapters.

Infectious Myelopathies
Neurosyphilis

Syphilis is a sexually transmitted disease caused by the spirochete Treponema pallidum.

Tertiary syphilis is characterized by gummas, aortitis, and neurologic disorders. Tabes
dorsalis is a degeneration of the dorsal columns and dorsal roots below the lower tho-
racic region of the spinal cord resulting in positive Romberg sign, ataxia, paresthesias of
the lower extremity, and sudden, sharp shooting pains known as lightning pains. A diag-
nosis of syphilis can be made using dark-​field microscopy to evaluate for spirochetes, a
Venereal Disease Research Laboratory (VDRL) test, or fluorescent treponemal antibody
absorption (FTA-​ABS) which is more specific for syphilis. The primary therapy for all
stages of syphilis is penicillin G, with ceftriaxone being an alternative.37

HTLV-​1–​Associated Myelopathy/​Tropical Spastic Paraparesis

Human T-​lymphocyte virus 1 (HTLV-​1) is a retrovirus that preferentially infects CD4+

T cells and is more common in individuals infected with human immunodeficiency
virus (HIV). The virus can be transmitted via breast milk, sexual intercourse, or blood.
HTLV-​1 causes adult T-​cell leukemia and lymphoma, and can also cause tropical spastic
paresis (TSP). HTLV-​1 is most commonly found in Japan, the Caribbean, Latin America,
and Africa. Patients with TSP will classically present as 40-​to 50-​year-​olds who have
defective lower extremity control marked by spasticity and weakness, back pain, sensory

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Nonsurgical Spinal Diseases

deficits, and urinary dysfunction. CSF analysis reveals HTLV-​1 antibodies, and MRI will
show a hyperintense T2 lesion of the spinal cord.38,39 Unfortunately, treatment is mainly
based on symptoms, which includes steroids.40

West Nile and Polio Virus

Both West Nile virus and polio can affect the anterior horn cells of the spinal cord,
causing acute flaccid paralysis. Because the anterior horn is the synapse of the upper and
motor neuron, findings associated with both can be found clinically in these conditions.
Polio is caused by a human enterovirus of the Picornaviridae family and is transmitted via
saliva or fecal contact with infected persons. Most infected people are asymptomatic.41
Prevention is via vaccine. Polio eradication became a global priority of the World Health
Organization in 1988, and, by 2016, only three countries of the world still have the
wild-​type virus based on surveillance screening:  Nigeria, Pakistan, and Afghanistan.42
West Nile is an RNA arbovirus from the Flaviviridae family. Because it is a mosquito-​
borne illness, predilection is in the summer months and prevention centers on mosquito
control. Most human infections are asymptomatic but can affect nearly every part of the
nervous system, especially in an immunocompromised host. Immunoglobulin M to West
Nile virus may be found in the infected host and in the spinal fluid of those with central
nervous system manifestations. Long-​term postinfectious sequelae including persistent
denervation of affected muscle groups resulting in weakness.43,44

Metabolic Derangements: Combined Subacute Degeneration

(Vitamin B12 Deficiency) and Copper Deficiency Myelopathy
Combined Subacute Degeneration

Vitamin B12 deficiencies can present with neurological manifestations including ab-
normal sensation, spastic paresis, and gait and proprioception disturbances. Patients may
also show signs of dementia. These symptoms are manifested by demyelination of the
dorsal and lateral columns of the spinal cord resulting in a spongy appearance, gliosis,
and white matter edema. On T2-​weighted MRI, these morphological changes will be
presented as hyperintense T2 lesions within the affected region of the spinal cord. It is
important to note that folate, vitamin E, and copper deficiencies can present with sim-
ilar symptoms, and laboratory studies and assays are vital to diagnosis.45–​47 Additionally,
patients may demonstrate elevated homocysteine levels and megaloblastic anemia on
peripheral blood smear. Long-​ term treatment of subacute combined degeneration
depends on the cause of vitamin B12 deficiency, but supplementation with intramus-
cular injections of vitamin B12 is a common early intervention. Nitrous oxide expo-
sure inactivates vitamin B12, causing a functional deficiency and can result in a similar
manifestation.48

Copper Deficiency Myelopathy

Copper deficiency myelopathy (CDM) is clinically indistinguishable from subacute

combined degeneration. Patients most commonly affected by CDM are usually in
their fifth or sixth decade of life who have had prior upper GI procedures, zinc over-
load, or a malabsorption disorder, all of which lead to decreased absorption of dietary

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Spinal Neurosurgery

copper. Copper deficiency myelopathy can be treated with oral or parenteral copper
supplementation.49

Amyotrophic Lateral Sclerosis (Lou Gehrig’s Disease)

Amyotrophic lateral sclerosis (ALS) is a rapidly progressing neurodegenerative disorder

affecting the anterior horn cells of the spinal cord. Patients present with both upper and
lower neuron findings including muscle fasciculations, weakness, and spasticity. Bulbar
symptoms, including difficulties swallowing and speaking, often present first. Ultimately,
most patients die from respiratory dysfunction. Nerve conduction studies and elec-
tromyography (EMG) are gold standards for diagnosis. Treatment of ALS is primarily
symptomatic management. Riluzole has been approved by the US Food and Drug
Administration (FDA) for treatment of ALS but has marginal benefits.50,51

Friedrich Ataxia

Friedrich ataxia (FA) is an autosomal recessive disorder caused by a GAA trinucleotide

expansion of the frataxin gene on chromosome 9q13 resulting in disruption of oxidative
phosphorylation in the mitochondria. This disease typically presents by the age of 10
with gait ataxia, but over time, it progresses to loss of deep tendon reflexes, dysarthria,
loss of proprioception, kyphoscoliosis, and cardiomyopathy. Loss of myelinated neurons
in the dorsal root ganglion, dentate nucleus, dorsal columns, and sensory neurons are
all present in FA.52,53 MRI scans will typically reveal degeneration of the cervical spinal
cord and the superior cerebellar peduncles. Additionally, T2-​weighted scans will show
hypointensity in the dentate nucleus.54,55 Cardiac abnormalities can include concentric
hypertrophy, dilation, or mural thrombi, all of which can be demonstrated on echocar-
diography. Treatment is symptomatic management, addressing issues with coordination,
scoliosis, and cardiomyopathy.56

References and Further Reading

1. Spinal Cord Injury (SCI) 2016 facts and figures at a glance. J Spinal Cord Med. 2016
Jul;39(4):493–​494. doi:  10.1080/​ 10790268.2016.1210925. PubMed PMID:  27471859;
PubMed Central PMCID: PMC5102286.
2. Walters BC, Hadley MN, Hurlbert RJ, et al.; American Association of Neurological Surgeons;
Congress of Neurological Surgeons. Guidelines for the management of acute cervical spine
and spinal cord injuries: 2013 update. Neurosurgery. 2013 Aug;60 Suppl 1:82–​91. doi: 10.1227/​
01.neu.0000430319.32247.7f. PubMed PMID: 23839357.
3. Waters RL, Adkins R, Yakura J, Vigil D. Prediction of ambulatory performance based on
motor scores derived from standards of the American Spinal Injury Association. Arch Phys
Med Rehabil. 1994 Jul;75(7):756–​760. PubMed PMID: 8024420.
4. El Masry WS, Tsubo M, Katoh S, El Miligui YH, Khan A. Validation of the American
Spinal Injury Association (ASIA) motor score and the National Acute Spinal Cord Injury
Study (NASCIS) motor score. Spine (Phila Pa 1976). 1996 Mar 1;21(5):614–​619. PubMed
PMID: 8852318.
5. Gerling MC, Davis DP, Hamilton RS, Morris GF,Vilke GM, Garfin SR, Hayden SR. Effects
of cervical spine immobilization technique and laryngoscope blade selection on an unstable

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cervical spine in a cadaver model of intubation. Ann Emerg Med. 2000 Oct;36(4):293–​300.
PubMed PMID: 11020675.
6. Lennarson PJ, Smith DW, Sawin PD, Todd MM, Sato Y, Traynelis VC. Cervical spinal motion
during intubation: Efficacy of stabilization maneuvers in the setting of complete segmental
instability. J Neurosurg. 2001 Apr;94(2 Suppl):265–​270. PubMed PMID: 11302629.
7. Hoffman JR, Mower WR, Wolfson AB, Todd KH, Zucker MI. Validity of a set of clinical
criteria to rule out injury to the cervical spine in patients with blunt trauma. National
Emergency X-​Radiography Utilization Study Group. N Engl J Med. 2000 Jul 13;343(2):
94–​99. Erratum in: N Engl J Med 2001 Feb 8;344(6):464. PubMed PMID: 10891516.
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252
 

Index

acute traumatic central cord syndrome (ATCCS) antiplatelet agents, ATCCS and, 38
aftercare,  37–​38 AO (Arbeitsgemeinschaft für Osteosynthesefragen)
anterior cervical discectomy and fusion, 35 classification, 125, 126
ASIA motor score, 32 arachnoid cysts, 110
assessment and planning, 31–​32 arteriovenous fistulas (AVFs), 111
case presentation, 31 arteriovenous malformations (AVMs), 111
complications and management, 38 astrocytomas
decision-​making, 34, 38 assessment and planning, 141–​42
diagnosis, 33 diagnosis, 143
imaging studies showing ATCCS, 32 management, 145
surgical procedure, anterior cervical discectomy and surgical procedure, 145
fusion, 34 treatment, 144
surgical procedure, laminectomy, 36, 37 atelectasis, preventing, 38
surgical procedure, laminoplasty, 34, 36 atlantoaxial instability
surgical procedure, planning, 34 aftercare,  46–​47
surgical procedure, technique, 36 assessment and planning, 41–​43
two-​level anterior cervical discectomy and fusion, 35 case presentation, 41
adjacent segment disease (ASD), 204 complications and management, 47
adult degenerative scoliosis. See flat back deformity; lumbar CT scan showing rheumatoid pannus causing upper cervical
degenerative scoliosis stenosis, 42
air embolism, following cervical foraminotomy, 106 decision-​making,  43–​44
American Spinal Injury Association (ASIA), 12, 32, 243 diagnosis, 43
amyotrophic lateral sclerosis (ALS), 248 evidence and outcomes, 47
Anderson and D’Alonzo classification for fractures, 1, 2 intraoperative x-​rays showing C1 lateral mass–​C2 pars
anterior cervical corpectomy with fusion (ACCF), 86–​87, 88 screw-​rod placement, 45
anterior cervical discectomy with fusion (ACDF) management, 46
vs. CDR, 99 MRI showing severe canal stenosis and associated T2 signal
for cervical radiculopathy due to central disc, 93–​99 abnormality at 1–​11, 42
indications for, 34 postoperative lateral and anteroposterior cervical x-​rays, 46
for ossification of posterior longitudinal ligament, 86–​87, 88 surgical procedure, 44–​45
surgical procedure, ventral approach, 95–​97 See also basilar invagination and cranial settling
surgical technique, 36 atlantodental interval (ADI), measuring, 43
three-​level,  35 atlanto-​occipital dislocation (AOD)
two-​level,  35 aftercare, 28
anterior lumbar interbody fusion (ALIF), 220 assessment and planning, 21–​23
anticholinergic medications, for symptomatic Bellbarba classification system, 25
bradycardia,  17–​18 case presentation, 21

253
254

Index

atlanto-​occipital dislocation (AOD) (Cont.) burst fractures, L3 pathologic, 160, 163. See also thoracolumbar
complications and management, 28–​29 burst fractures
decision-​making,  24–​25 C5 palsy
diagnosis, 23 following cervical foraminotomy, 107
evidence and outcomes, 29–​30 following surgery for cervical myelopathy, 68
Harris method, 24 following surgery for ossification of posterior longitudinal
management,  27–​28 ligament, 90
occipital–​C4 fusion, 27 Campylobacter jejuni, 244
scans showing atlanto-​occipital dislocation, 22 cauda equina syndrome (CES)
surgical procedure, 25–​27 aftercare, 180
Traynelis Classification System, 25, 26 assessment and planning, 175–​76
atropine, for symptomatic bradycardia, 17–​18 case presentation, 175
autonomic dysreflexia, in cervical fracture dislocation, 17–​18 complications and management, 180–​81
axial back pain compressive vs. noncompressive etiologies, 176
management,  191–​94 decision-​making,  177–​78
treatment, 185, 187 diagnosis, 176
basilar impression, 49 differential diagnosis, 175
basilar invagination and cranial settling evidence and outcomes, 181
aftercare,  58–​59 management,  179–​80
assessment and planning, 49–​51 MRI at L4-​L5 level showing acute disc herniation, 177
case presentation, 49 surgical procedure, 178–​79
complications and management, 59–​60 central cord injury/​central cord syndrome. See acute traumatic
CT images showing adequate ventral decompression, 58 central cord syndrome
CT images showing basilar invagination with significant cerebrospinal fluid (CSF) leak
upward translation of the odontoid into the posterior in cervical fracture dislocation, 18
fossa, 50 decreasing risk of, 188
CT images showing basilar invagination with upward following cervical foraminotomy, 106–​7
migration of the C1-​C2 complex into the cranial following laminoplasty, 145, 146, 147
vault, 51 following surgery for basilar invagination, 59–​60
decision-​making,  52–​53 following surgery for intramedullary spinal cord tumors,
diagnosis, 52 146, 147
evidence and outcomes, 60–​61 following surgery for isthmic spondylolisthesis, 204
illustration of anterior cervical spine during surgery, 57 following surgery for ossification of posterior longitudinal
illustration showing relevant normal anatomy and operative ligament, 90
angles, 59 cervical arthroplasty
intraoperative photographs showing C1 ring, resection, and complications and management, 98
transverse ligaments, 56 contraindications for, 97
management,  57–​58 indications for, 97
surgical procedure, endoscopic approaches, 56–​57 reoperation rate following, 99
surgical procedure, extended transoral approaches, 55–​56 suitable candidates for, 95
surgical procedure, transoral-​transpharyngeal approach, 54–​55 surgical procedure, 96
basion-​axial interval (BAI), 24 See also cervical radiculopathy, central disc
basion-​dental interval (BDI), 24 cervical collar, in atlanto-​occipital dislocation, 21, 22–​23,
Bellbarba classification system, 25 25, 27, 28
bilateral hand pain and numbness, in atlantoaxial instability, 41 cervical disc replacement (CDR)
Brooks and Jenkins technique, 45, 47 vs. ACDF, 99

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Index

complications and management, 98 complications and management, 68–​69

contraindications for, 95 decision-​making,  65–​66
surgical procedure, ventral approach, 95–​97 diagnosis, 65
cervical foraminotomy. See cervical radiculopathy, central disc differential diagnosis, 63
cervical fracture dislocation evidence and outcomes, 69
aftercare, 17 management,  67–​68
assessment and planning, 11–​13 MRI showing 21–​41
case presentation, 11 surgical procedure, 66–​67
complications and management, 18–​19 cervical radiculopathy, central disc
CT demonstrating C5-​C6 cervical fracture dislocation, 13 aftercare, 97
decision-​making,  15 assessment and planning, 93–​95
diagnosis,  14–​15 case presentation, 93
evidence and outcomes, 19 complications and management, 98
jumped facets, 12–​13 decision-​making,  95
management, 17 diagnosis, 95
MRI depicting C5-​C6 spinal canal comprise, 14 evidence and outcomes, 98–​99
surgical procedure, 16 images showing lateral disc extrusion with extension to
See also odontoid fracture type II neural foramen, 94
cervical myelopathy postoperative image of disc replacement, 96
assessment and planning, 83–​84 surgical procedure, 95–​97
in atlantoaxial instability, 41 cervical radiculopathy, lateral disc foraminotomy
diagnosis, 83 aftercare, 106
differential diagnosis, 81 assessment and planning, 101–​2, 103
scales for, 84–​86 case presentation, 101
treatment,  84–​86 complications and management, 106–​7
cervical myelopathy, kyphosis contraindications to, 103
aftercare, 77 decision-​making,  103
assessment and planning, 71–​73 diagnosis,  102–​3
case presentation, 71 evidence and outcomes, 107
complications and management, 77–​79 illustration of anterior and posterior approaches for cervical
decision-​making,  74 foraminotomy, 105
diagnosis,  72–​73 images showing foraminal stenosis and disc herniation vs.
evidence and outcomes, 79 normal cervical lordosis, 102
images confirming good correction of cervical kyphosis, 78 management,  105–​6
images showing multiple degenerative changes causing severe surgical procedure, anterior approach, 104
kyphosis, 72 surgical procedure, posterior approach, 104–​5
management,  76–​77 cervical spine fracture. See cervical fracture dislocation
strategies to achieve correction of, 76–​77 Chiari type I malformations, in basilar invagination, 50–​51, 55
surgical procedure, 75 CNS (Congress of Neurological Surgeons), 12, 14
x-​rays of cervical spine ruling out fusion of facet joints, 73 combined subacute degeneration (vitamin B12 deficiency), 247
x-​rays of cervical spine showing satisfactory sagittal and compressive disc herniation pathologies
coronal alignment, 75 arachnoid cysts, 110
cervical myelopathy, lordosis degenerative, 109
aftercare, 68 disc herniation of thoracic spine, 110
assessment and planning, 63–​64 infectious (epidural abscesses), 110–​11
case presentation, 63 neoplastic, 111

255
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Index

traumatic, 110 preoperative MRI, 228

vascular (AVMs and AVFs), 111 surgical procedure, 229–​30
See also cauda equina syndrome dorsolateral/​lateral approaches to thoracic spine, 114–​15
condyle-​C1 interval (CCI), 24–​25 dropped head syndrome, causes, 71
congenital arcuate foramen, in odontoid fracture type II, 8 dysphagia
Congress of Neurological Surgeons (CNS), 12, 14 in cervical fracture dislocation, 18
copper deficiency myelopathy (CDM), 247–​48 following cervical foraminotomy, 107
costotransversectomy to thoracic spine, 114–​15 in odontoid fracture type II, 8
cranial settling, 49–​50, 52. See also basilar invagination and
cranial settling ECOG (Eastern Cooperative Oncology Group) scoring, 171–​72
cruciate paralysis, 23 elderly patients
CT myelogram is contraindications for rigid external immobilization, 4
indications for, 209–​11 posterior approach in odontoid fracture type II, 8–​9
degeneration, differential diagnosis, 63 superiority of surgery in odontoid fracture type II, 9
degenerative cervical myelopathy. See cervical myelopathy, enterococcus,  225–​26
kyphosis enteroviruses, 244, 247
degenerative spondylolisthesis. See spondylolisthesis, L4–​L5 ependymomas
degenerative assessment and planning, 141–​42
demyelinating disc herniation pathologies diagnosis, 143
multiple sclerosis, 111–​12 management, 145
transverse myelitis, 112 risk factors for, 144
demyelinating spinal diseases treatment, 144
multiple sclerosis, 245 epidural abscesses. See spinal epidural abscesses
neuromyelitis optica and neuromyelitis optica spectrum epidural spinal cord compression
disorder, 245 delineating degree of, 136
transverse myelitis, 244 management, 140
dens fracture. See odontoid fracture type II ESCC (Epidural Spinal Cord Compression) grading
DEXA (dual-​energy x-​ray absorptiometry) bone densitometry scale,  163–​67
evaluation of, 217 esophageal injuries, in cervical fracture dislocation, 18–​19
indications for, 208, 216 Ewing’s sarcoma, treatment, 133
dextroscoliosis,  209–​11 extradural spinal tumors
disc herniation of thoracic spine, 110 aftercare, 139
diskitis assessment and planning, 133
aftercare, 231 complications and management, 139
assessment and planning, 225–​26 decision-​making,  135–​37
case presentation, 225 diagnosis,  134–​35
complications and management, 232 differential diagnosis, 133
decision-​making,  228–​29 epidural spinal cord compression scale, 136
diagnosis, 227 evidence and outcomes, 140
differential diagnosis, 225 images depicting T3 cage, 138
evidence and outcomes, 233 images showing spinal cord compression, 135
followup MRI at 8 weeks, 232 management, 138
images showing vertebral body destruction and focal surgical procedure, 137
kyphosis, 227
management, 231 flat back deformity
postoperative x-​rays, 230 aftercare,  222–​23

256
 

Index

assessment and planning, 215–​16 as cause of cauda equina syndrome, 176

case presentation, 215 emergent decompression for, 177
CT scans showing previous hardware without images showing foraminal stenosis and disc herniation vs.
instrumentation failures, 218 normal cervical lordosis, 102
decision-​making,  219–​20 MRI at L4-​L5 level showing acute disc herniation, 177
diagnosis,  216–​17 risk and benefit profile of surgery for, 178
management, 222 surgical procedure, 179
MRIs showing no central stenosis, 217 thoracic disc herniation, 109–​19
surgical procedure, 221 herniated thoracic disc (HTD). See thoracic disc herniation
x-​rays showing postoperative scoliosis, 222 Hoffmann reflex, in cervical spondylotic myelopathy, 65
x-​rays showing previous hardware, 218 Horner syndrome, following cervical foraminotomy, 106–​7
x-​rays showing standing scoliosis, 219 HTLV-​1–​associated myelopathy,  246–​47
foraminotomy hyperextension spinal cord injury, ATCCS due to, 32–​33
contraindications to, 103
See also cervical radiculopathy, lateral disc foraminotomy infectious myelopathies
fracture dislocation. See cervical fracture dislocation HTLV-​1–​associated myelopathy/​tropical spastic
fracture reduction, in cervical fracture dislocation, 15–​17 paraparesis,  246–​47
Friedrich ataxia (FA), 248 neurosyphilis, 246
fusion West Nile virus and polio virus, 247
anterior cervical corpectomy with fusion, 86–​87, 88 See also spinal epidural abscesses
anterior cervical discectomy with fusion, 34, 35, 36, 86–​87, instrumented fusion
88,  93–​99 for isthmic spondylolisthesis, 205
anterior lumbar interbody fusion, 220 interbody fusion
C1-​C2 fusion for odontoid fracture type II, C1.P18 augmentations for, 195
CDR vs. anterior cervical discectomy and fusion, 99 benefits of, 194–​95
images of cervical spine with posterior C1-​C2 fusion, 7 for spondylolisthesis, 194
instrumented fusion for isthmic spondylolisthesis, 205 International Spinal Cord Society (ISCoS), 243
interbody fusion, 194–​95 intradural extramedullary spinal tumors. See spinal cord tumors,
occipital–​C4 fusion, 27 intradural extramedullary
posterior lumbar interbody fusion, 194–​95, 201–​2 intramedullary spinal cord tumor (IMSCT). See spinal cord
posterolateral fusion, 194–​95 tumors, intramedullary
transforaminal lumbar interbody fusion, 194–​95, 201–​2, 220 isthmic spondylolisthesis (IS)
aftercare, 204
Gallie technique, 45 assessment and planning, 200
Goel and Laheri technique, 44–​45, 47 case presentation, 199
Guidelines for the Management of Acute Cervical Spine and classification system, 200
Spinal Cord Injury, 12, 14 complications and management, 204
decision-​making,  201
halo orthosis, in cervical fracture dislocation, 18 diagnosis, 200
halo vest, in atlanto-​occipital dislocation, 22–​23, 25, 27, 28 differential diagnosis, 199
Harms and Melcher technique, 44–​45, 47 evidence and outcomes, 204–​5
Harm’s technique, 44–​45, 47 management, 203
Harris method, 24 MRI showing L4-​L5 disc space, 200
hemangioblastomas, diagnosis, 143 post-​operative x-​rays showing pedicle screw fixation with
hematomas, following cervical foraminotomy, 106 PEEK interbody, 203
herniated discs surgical procedure, 201–​2

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Japanese Orthopedic Association scale, 81, 86 decision-​making,  209–​11

jumped facets, 12–​13 diagnosis, 208
evidence and outcomes, 213–​14
kyphosis management,  212–​13
aftercare, 77 MRI showing foraminal and canal stenosis, 209
assessment and planning, 71–​73 radiographs at 36-​month postoperative follow-​up, 212
complications and management, 77–​79 radiographs at time of presentation, 210
decision-​making,  74 surgical procedure, 211–​12
diagnosis,  72–​73 lumbar lordosis (LL), documentation with standing scoliosis
evidence and outcomes, 79 x-​rays,  216
images confirming good correction of cervical kyphosis, 78 lumbar nerve compression. See cauda equina syndrome
images showing multiple degenerative changes causing severe lumbar stenosis
kyphosis, 72 aftercare, 187
management,  76–​77 assessment and planning, 183–​84
post laminectomy, 65–​66, 67, 147, 153, 157 case presentation, 183
reducing risk of PJK, 220, 222 complications and management, 188
selection of surgical approach in, 68 decision-​making,  185
strategies to achieve correction of, 76–​77 diagnosis, 184, 208
surgical procedure, 75 evidence and outcomes, 188–​89
x-​rays of cervical spine ruling out fusion of facet joints, 73 management, 187
x-​rays of cervical spine showing satisfactory sagittal and MRIs showing L2-​L3 stenosis, 185
coronal alignment, 75 surgical procedure, 186–​87
lupus, 244
laminectomy
kyphosis following, 147, 153, 157 Magerl’s C1–​C2 transarticular, 47
vs. laminoplasty, 144–​45, 147 meningiomas
for lumbar stenosis, 186 assessment and planning, 150–​51
surgical procedure, 187 complications and management, 156
traditional open vs. minimally invasive techniques, 186, 189 diagnosis, 151–​52, 155
laminoplasty surgical procedure, 153–​54, 155–​56
advantages of, 153 metabolic spinal derangements
avoiding CSF leak following, 145, 146, 147 combined subacute degeneration (vitamin B12
vs. laminectomy, 144–​45, 147 deficiency), 247
lateral disc foraminotomy. See cervical radiculopathy, lateral disc copper deficiency myelopathy, 247–​48
foraminotomy metastatic tumors
lateral extracavitary approach to thoracic spine, 115 deep vein thrombosis with, 139
lateral parascapular extrapleural approach to thoracic spine, 115 diagnosis, 134
levoscoliosis,  209–​11 management, 140
lightning pains, 246 thoracic cord compression due to, 133
lordosis. See cervical myelopathy, lordosis microdiscectomy, 103–​4, 107
Lou Gehrig’s Disease, 248 microsurgery, for intramedullary spinal cord tumors, 145
lumbar degenerative scoliosis minimally invasive approaches to thoracic spine, 117
aftercare, 213 minimally invasive surgery
assessment and planning, 208 aftercare,  187–​88
case presentation, 207 benefits of, 187
complications and management, 213 vs. traditional open laminectomies, 186, 189

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multiple myeloma aftercare, 7

diagnosis, 163 Anderson and D’Alonzo classification for fractures, 1, 2
indication for spinal surgery in, 171 assessment and planning, 1–​2
multiple sclerosis (MS), 111–​12, 244, 245 case presentation, 1
complications and management, 8
neck hematoma, following cervical foraminotomy, 106 complications and management, intraoperative, 7
neck pain, in atlantoaxial instability, 43–​44 complications and management, postoperative, 8
neoplastic disc herniation, 111 decision-​making,  3–​4
neurofibromas diagnosis, 1
assessment and planning, 150 evidence and outcomes, 8–​9
diagnosis, 151–​52, 155 Hamm’s technique and retraction of C2 nerve root, 5
neurogenic claudication images of cervical spine with posterior C1-​C2 fusion, 7
assessment and planning, 183–​84 management, 6
diagnosis, 185 risk factors for nonunion, 3
management, 187 sagittal view of cervical spine showing type II C odontoid
neurologic deficits fracture, 4
preventing, 238 sub classifications proposed by Grauer, 2, 3
in spinal epidural abscesses, 236 surgical procedure, 6
neuromonitoring surgical procedure, approach, 5
during surgery for intradural extramedullary spinal cord surgical procedure, positioning, and preparation, 5
tumors, 154–​55, 156, 157 odontoid screw fixation, 2
during surgery for intramedullary spinal cord tumors, 144–​46 ossification of posterior longitudinal ligament, cervical
neuromyelitis optica (NMO), 245 aftercare, 89
neuromyelitis optica spectrum disorder (NMOSD), 245 assessment and planning, 81–​83
neurosyphilis, 246 case presentation, 81
NOMS (neurologic, oncologic, mechanical, and systemic) complications and management, 90
framework, 135–​36, 163, 164, 171, 172 CT image showing continuous type of ossification., 82
noncompressive disc herniation pathologies CT image showing double-​layer sign, 82
demyelinating,  111–​12 CT image showing single-​layer sign for dural penetration, 85
metabolic (vitamin B12 deficiency), 112 CT image with representative segmental variant ossification
vascular (spinal arterial thrombosis), 112 of the posterior longitudinal ligament, 84
nonsurgical spinal diseases decision-​making,  84–​86
amyotrophic lateral sclerosis, 248 diagnosis, 83
demyelinating diseases, 244–​45 differential diagnosis, 81
Friedrich ataxia, 248 evidence and outcomes, 90
infectious myelopathies, 246–​47 management, 87
metabolic derangements, 247 Modified Japanese Orthopedic Association Scale, 86
trauma,  243–​44 MRI image showing ossification of the posterior longitudinal
vascular myelopathies, 246 ligament, 83
Nurick myelopathy scale, 84–​86 Nurick’s Classification System, 85
postoperative images of C4 to T10 laminectomy, 89
occipital neuralgia, in odontoid fracture type II, 8 surgical procedure, anesthesia and neuromonitoring, 87
occipitocervical dislocation. See atlanto-​occipital dislocation surgical procedure, anterior approach, 88
occipitocervical junction pathology. See basilar invagination and surgical procedure, pivot points, 89
cranial settling surgical procedure, posterior approach, 88
odontoid fracture type II osteogenesis imperfecta, basilar invagination and, 49–​50

259
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Index

osteomyelitis radiation therapy

antibiotic treatment, 231 determining response to, 163–​67
complications and management, 232 impairment of arthrodesis during, 170
diagnosis,  226–​27 role of surgery in, 167
evidence and outcomes, 233 radiation-​sensitive spine tumors
risk factors for, 225–​26 aftercare, 169
surgery for, 229–​30 assessment and planning, 159–​60
See also spinal epidural abscesses case presentation, 159
Oswestry Disability Index (ODI) score, 196, 211 complications and management, 170
decision-​making,  163–​67
pars interarticularis defect diagnosis,  161–​63
assessment and planning, 200 ECOG (Eastern Cooperative Oncology Group)
classification system for isthmic spondylolisthesis, 200 scoring,  171–​72
underlying spondylolisthesis, 191 ESCC (Epidural Spinal Cord Compression) grading
pedicle screw fixation, surgical procedure, 194–​95 scale,  163–​67
pedicle subtraction osteotomies, 221–​22 evidence and outcomes, 171–​72
PEEK (polyether ether ketone), 203 images showing L3-​level fractures, 160
pelvic incidence (PI) intraoperative fluoroscopy for guidance of Jamshidi needle
assessment of, 217 placement,  167–​69
documentation with standing scoliosis x-​rays, 216, 217 NOMS (Neurologic, Oncologic, Mechanical and Systemic)
PI–​LL (pelvic incidence and lumbar lordosis) mismatch framework, 163, 164, 171, 172
assessment of, 217 post-​treatment images, 170
treatment,  219–​20 SINS (Spinal Instability Neoplastic Score), 161–​62, 163–​67
platybasia,  49–​50 summary of expected radiation response by histology, 166
pneumonia surgical procedure, 167–​69
preventing, 38 radiculopathy
polio virus, 247 in ossification of posterior longitudinal ligament, 83–​84
positive Babinski reflex, in cervical spondylotic treatment,  84–​86
myelopathy, 65 retropleural thoracotomy approach to thoracic spine, 117
posterior atlantodental interval (PADI), measuring, 43 rule of twelves, 24
posterior longitudinal ligament, ossification of. See ossification
of posterior longitudinal ligament, cervical Salmonella sp., 244
posterior lumbar interbody fusion (PLIF), surgical procedure, sarcoidosis, 244
194–​95,  201–​2 schwannomas
posterolateral fusion, surgical procedure, 194–​95 assessment and planning, 150
postlaminectomy kyphosis diagnosis, 151–​52, 155
following surgery for intradural extramedullary spinal cord scoliosis. See flat back deformity; lumbar degenerative scoliosis
tumors, 153, 157 SINS (Spinal Instability Neoplastic Score), 136, 161–​62, 163–​67
following surgery for intramedullary spinal cord Sjögren disease, 244
tumors, 147 slipped vertebra. See isthmic spondylolisthesis
Powers ratio, 24 spinal arterial thrombosis, 112
prereduction MRIs, controversy over in cervical fracture spinal cord tumors, extradural
dislocation, 15 aftercare, 139
proximal junction failure (PJF), reducing risk of, 220, 222 assessment and planning, 133
proximal junction kyphosis (PJK), reducing risk of, 220, 222 case presentation, 133
Pseudomonas species, 225–​26 complications and management, 139

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decision-​making,  135–​37 diagnosis,  161–​63

diagnosis,  134–​35 ECOG (Eastern Cooperative Oncology Group)
differential diagnosis, 133 scoring,  171–​72
epidural spinal cord compression scale, 136 ESCC (Epidural Spinal Cord Compression) grading
evidence and outcomes, 140 scale,  163–​67
images depicting T3 cage, 138 evidence and outcomes, 171–​72
images showing spinal cord compression, 135 images showing L3-​level fractures, 160
management, 138 intraoperative fluoroscopy for guidance of Jamshidi needle
surgical procedure, 137 placement,  167–​69
spinal cord tumors, intradural extramedullary NOMS (Neurologic, Oncologic, Mechanical and Systemic)
aftercare, 156 framework, 163, 164, 171, 172
assessment and planning, 149–​51 post-​treatment images, 170
case presentation, 149 SINS (Spinal Instability Neoplastic Score), 161–​62, 163–​67
cervical spine presentation, 151 summary of expected radiation response by
complications and management, 156–​57 histology, 166
CT showing intradural partially calcified tumor, 152 surgical procedure, 167–​69
decision-​making,  153 spinal deformity
diagnosis, 151, 155 causes of, 71
differential diagnosis, 149–​50 See also cervical myelopathy, kyphosis
evidence and outcomes, 157 spinal epidural abscesses (SEA)
lumbar spine presentation, 151 aftercare, 240
MRI showing gross total resection of T2-​T3 mass, 154 assessment and planning, 235–​37
MRI showing T2-​T3 mass, 150 case presentation, 235
surgical procedure, 153–​54, 155–​56 complications and management, 240
thoracic spine presentation, 151 decision-​making,  238
spinal cord tumors, intramedullary differential diagnosis, 235–​36
aftercare,  146–​47 evidence and outcomes, 233
assessment and planning, 141–​42 images showing dorsal epidural abscesses, 237
case presentation, 141 infectious disc herniation, 110–​11
complications and management, 147 management,  239–​40
decision-​making,  144 risk factors for, 225–​26
diagnosis,  143–​44 risks and benefits of operative decompression, 229
differential diagnosis, 141–​42 surgical procedure, 238–​39
evidence and outcomes, 147–​48 surgical procedure and, 230, 231
images showing cervicothoracic intramedullary spinal cord tetrad of stages, 235–​36, 238
tumor, 142 spinal infections. See spinal epidural abscesses
images showing spinal astrocytoma, 143 spinal instability
management,  145–​46 due to multiple myeloma, 171
risk factors for, 144 SINS (Spinal Instability Neoplastic Score), 136,
surgical procedure, 144–​45 161–​62,  163–​67
spinal cord tumors, radiation-​sensitive treatment outcomes, 171–​72
aftercare, 169 spinal metastasis
assessment and planning, 159–​60 incidence of, 133–​34
case presentation, 159 symptoms,  133–​34
complications and management, 170 Spine Patient Outcomes Research Trial (SPORT), 191–​94, 196
decision-​making,  163–​67 Spine Trauma Study Group, 125

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Index

spondylolisthesis, isthmic thoracic cord compression, extradural tumor

aftercare, 204 aftercare, 139
assessment and planning, 200 assessment and planning, 133
case presentation, 199 case presentation, 133
classification system, 200 complications and management, 139
complications and management, 204 decision-​making,  135–​37
decision-​making,  201 diagnosis,  134–​35
diagnosis, 200 differential diagnosis, 133
differential diagnosis, 199 epidural spinal cord compression scale, 136
evidence and outcomes, 204–​5 evidence and outcomes, 140
management, 203 images depicting T3 cage, 138
MRI showing L4-​L5 disc space, 200 images showing spinal cord compression, 135
post-​operative x-​rays showing pedicle screw fixation with management, 138
PEEK interbody, 203 surgical procedure, 137
surgical procedure, 201–​2 thoracic disc herniation
spondylolisthesis, L4–​L5 degenerative aftercare, 119
assessment and planning, 191 case presentation, 109
case presentation, 191 complications and management, 114
complications and management, 196 compressive pathologies, 109–​11
CT showing L5-​L5 grade 1 spondylolisthesis, 192 decision-​making,  113–​17
CT showing right and left pars interarticularis, 192 differential diagnosis, 109–​12
CT showing TLIF with complete facetectomy and reduction dorsolateral/​lateral approaches,  114–​15
of spondylolisthesis, 195 evidence and outcomes, 114
decision-​making,  191–​95 management, 119
evidence and outcomes, 196 minimally invasive approaches, 117
MRI showing foraminal stenosis, 193 noncompressive pathologies, 111–​12
x-​rays (no pathological movement), 193 surgical procedure, 117–​19
spondylosis, 109–​10, 208 ventral approaches, 117
Spurling test, 101–​2 ventrolateral approaches, 115–​17
Staphylococcus aureus,  225–​26 thoracic giant disc, 112
Staphylococcus epidermidis,  225–​26 thoracic lateral disc, 114–​15
stenosis thoracic myelopathy
C3–​C4, C4–​C5, and C5–​C6 stenosis, 64–​64 diagnosis, 112
foraminal stenosis and C5 palsy, 68 differential diagnosis, 111–​12
intubation in severe cervical stenosis, 66 thoracolumbar burst fractures
selection of surgical approach, 65 aftercare, 129
See also lumbar stenosis assessment and planning, 123–​25
Streptococcus pneumoniae,  225–​26 case presentation, 123
Streptococcus viridans,  225–​26 complications and management, 129–​30
Surfer’s myelopathy, 246 decision-​making,  127–​28
syphilis, 246 diagnosis,  126–​27
systemic sclerosis, 244 evidence and outcomes, 130–​31
images showing burst fractue, compression, and disruption, 124
the transverse atlantal ligament (TAL), assessment of, 43 images showing burst fracture with mild bony
thoracic central disc, 114, 115 retropulsion, 126

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Index

indications for surgical intervention, 128 traumatic spinal conditions, 243. See also acute traumatic central
surgical procedure, 128–​29 cord syndrome–​44
TLICS (Thoracolumbar Injury Classification and Severity) Traynelis Classification System, 25, 26
score, 125, 126–​27, 130 Treponema pallidum, 246
tranexamic acid (TXA), benefits and drawbacks of, 221 tropical spastic paraparesis, 246–​47
transarticular screw type II odontoid fracture. See odontoid fracture type II
in atlantoaxial instability, 44, 45–​46, 47
complications and management, 47 vascular compromise, in spinal epidural abscesses, 236
intraoperative x-​rays showing C1 lateral mass–​C2 pairs vascular myelopathies, 246
screw-​rod placement, 45 venous thromboemboli (VTE), preventing, 139
transforaminal lumbar interbody fusion (TFIL) ventral approaches to thoracic spine, 117
for spondylolisthesis, 194 ventrolateral approaches to thoracic spine, 115–​17
surgical procedure, 194–​95 vertebral artery injury
transforaminal lumbar interbody fusion (TLIF) in cervical fracture dislocation, 18–​19
for flat back deformity, 220 following cervical foraminotomy, 107
surgical procedure, 201–​2 in odontoid fracture type II, 7, 8
transoral-​transpharyngeal approach, in basilar invagination and vitamin B12 deficiency, 112, 247
cranial settling, 54–​55, 57
transpedicular approach to thoracic spine, 114 warfarin, ATCCS and, 38
transthoracic thoracoscopy to thoracic spine, 117 West Nile virus, 247
transthoracic thoracotomy to thoracic spine, 115–​16 Wiltse classification system, 200
transverse myelitis, 112, 244
traumatic disc herniation, 110 Zika virus, 244

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