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i

Cerebrovascular
Disease
ii

What Do I Do Now?

S E R I E S C O -​E D I TO RS-​I N-​C HIE F

Lawrence C. Newman, MD
Director of the Headache Institute
Department of Neurology
St. Luke’s-​Roosevelt Hospital Center
New York, New York

Morris Levin, MD
Co-​director of the Dartmouth Headache Center
Director of the Dartmouth Neurology Residency Training Program
Section of Neurology
Dartmouth Hitchcock Medical Center
Lebanon, New Hampshire

OT H E R VO L U M E S IN T HE SE RIE S

Headache and Facial Pain


Peripheral Nerve and Muscle Disease
Pediatric Neurology
Stroke
Epilepsy
Neuro-​ophthalmology
Neuroimmunology
Pain
Neuroinfections
Emergency Neurology
Cerebrovascular Disease
Movement Disorders
Neurogenetics
Neurotology
iii

Cerebrovascular
Disease

SECOND EDITION

Ji Y. Chong, MD
Assistant Professor of Neurology
Weill Cornell Medical College
Chief of Neurology and Director of the Stroke Center
New York-​Presbyterian Lower Manhattan Hospital
New York, New York

Michael P. Lerario, MD
Assistant Professor of Clinical Neurology
Weill Cornell Medical College
Attending Physician
New York-​Presbyterian Queens Hospital
Flushing, New York

1
iv

1
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Published in the United States of America by Oxford University Press
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First Edition published in 2013
Second Edition published in 2017
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You must not circulate this work in any other form
and you must impose this same condition on any acquirer.
Library of Congress Cataloging-​in-​Publication Data
Names: Chong, Ji Y., author. | Lerario, Michael P., author.
Title: Cerebrovascular disease / Ji Y. Chong, Michael P. Lerario.
Description: Second edition. | Oxford ; New York : Oxford University Press,
[2017] | Series: What do I do now? | Includes bibliographical references
and index. | Description based on print version record and CIP data
provided by publisher; resource not viewed.
Identifiers: LCCN 2016018874 (print) | LCCN 2016017898 (ebook) |
ISBN 9780190495558 (e-book) | ISBN 9780190495565 (e-book) |
ISBN 9780190495572 ( online) | ISBN 9780190495541 (alk. paper)
Subjects: | MESH: Stroke—diagnosis | Stroke—therapy | Cerebrovascular
Disorders—diagnosis | Cerebrovascular Disorders—therapy | Case Reports
Classification: LCC RC388.5 (print) | LCC RC388.5 (ebook) | NLM WL 356 |
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v

Preface

Nearly 800,000 people have a stroke each year in the United States. On average,
this means someone has a stroke every 40 seconds. Stroke is the leading cause of
disability in the United States and the fifth leading cause of death. These num-
bers add up to a huge public health problem that needs to be dealt with from all
directions: prevention of first and recurrent strokes, diagnosis and acute treat-
ment of stroke, and improving the recovery from stroke.
Neurologists, and specifically vascular neurologists, are the specialists who pri-
marily treat patients with cerebrovascular disease. However, the sheer number of
patients with stroke, as well as the multiple risk factors for stroke, guarantees that
physicians of all disciplines will see a stroke patient.
Although several unusual cases are presented, most of this book deals with
common, practical questions clinicians will encounter. Case presentations high-
light evidence-​based practice. There are clinical trial data to support many rec-
ommendations, but there are also areas in cerebrovascular disease treatment that
are still uncertain. Usual practice in the absence of strong data is noted as such.
Cerebrovascular disease is an exciting and evolving field. Since the previous
edition, there have been major advancements in acute stroke care through the
use of endovascular techniques. Multiple recent clinical trials have demonstrated
intra-​arterial thrombectomy to be superior to intravenous tissue plasminogen
activator alone for some patients with acute intracranial occlusions. As a result,
large-​scale changes in the systems and coordination of care need to be imple-
mented in order to provide this treatment option to as many eligible patients as
possible. Many other novel acute therapies, preventative strategies, and rehabili-
tation techniques are being investigated, and there is much promise for contin-
ued advances in the coming years.
vi
vii

Contents

1 Treatment of Acute Right-​Sided Weakness 1

2 Large Vessel Occlusion 7


3 Masquerade 13

4 Improving Symptoms 15

5 Progressive Quadriplegia 19

6 Malignant Edema 25

7 To Treat or Not to Treat (Blood Pressure) 29

8 Unidentified Bright Objects 33

9 Detected Bruit 39

10 Small Vessel Disease 43

11 Obstructed Flow 49

12 Aphasia and Atherosclerosis 53

13 A New Arrhythmia 57

14 Arch Disease 63

15 Hole in My Heart 67

16 Investigating the Occult 71

17 A Horner’s Syndrome Following Trauma 75

18 Young Adult with Headache and Blurred Vision 81

19 Cancer and Coagulopathy 85

20 Fevers in a Patient with Valve Replacement 91

21 Seeing Jellyfish 95

22 Driving Is a Headache 99

23 Puff of Smoke 103

24 Thunderclap Headache 109

25 Hypertension and Confusion 113


26 A Protean Presentation 119

27 Can I Go Home Now? 125


viii

28 Cardiac Arrest 129

29 A Sickle Pickle 133

30 Numbness While on Anticoagulation 139

31 Hemorrhage in a Patient with Dementia 143

32 An Unusual Hemorrhage 147

33 Recurrent Headaches 151

34 Progressive Gait Dysfunction 155

35 Worst Headache of Her Life 159

36 An Incidental Finding 165

37 Forget About It 171

38 Seizures, Sadness, and Spasticity 177

Index 183

viii Contents
1

1 Treatment of Acute
Right-​Sided Weakness

A 58-​year-​old woman with hypertension and diabetes


presents to the emergency room with right hemiparesis.
She had worked her usual night shift and went home and
fell asleep at 3:30 a.m. She awoke at 5:30 a.m. and noticed
right-​sided weakness. She called emergency medical
services and arrived at the emergency room at 6:20 a.m.
She has a blood pressure of 153/​92. She has normal
speech and is without any evidence of aphasia. She has
a right facial droop. She has prominent weakness of the
right arm and leg. Her head computed tomography (CT)
scan shows no evidence of hemorrhage or infarct
(Fig. 1.1). Her international normalized ratio (INR) and
platelet count are normal. It is now 7 a.m.

What do you do now?

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FIGURE 1.1 Noncontrast head CT showing basal ganglia calcifications but otherwise normal findings.

INTRAVENOUS TISSUE PLASMINOGEN ACTIVATOR (IV TPA)


FOR ACUTE ISCHEMIC STROKE: INDICATIONS, BENEFITS,
AND COMPLICATIONS

This woman is having an acute ischemic stroke. Her symptoms are suggestive of
ischemia to the left hemisphere, but there is no language involvement so a large
artery occlusion is less likely. A pure motor syndrome involving the face, arm,
and leg indicates a small deep infarct. She was last known normal at 3:30 a.m.,
and we are faced with a decision regarding acute treatment at 7:00 a.m., which is
3.5 hours from onset (onset time is defined as “witnessed onset” or “last known
well” in patients with unwitnessed onset—​for instance, during sleep).
The benefits of IV tPA have been well established in patients with ischemic
stroke treated within 3 hours of symptom onset. The National Institute of
Neurological Disorders and Stroke (NINDS) trial of IV tPA administered within
3 hours of acute ischemic stroke showed that there is a significant improvement

2 WHAT DO I DO NOW? Cerebrovascular Disease


3

in outcome compared with placebo. In the NINDS trial, 35% of patients who
received placebo recovered to complete independence at 3 months compared
to 50% with IV tPA. The inclusion and exclusion criteria for this trial form
the basis for the inclusion and exclusion criteria for clinical use of tPA (Box
1.1). Careful patient selection for IV thrombolysis will maximize the benefit
and minimize the hemorrhagic risk of treatment. IV tPA remains the mainstay
of treatment for acute ischemic stroke, despite recent advances in endovascular
therapy for strokes due to large vessel occlusions.
Unfortunately, the rates of tPA use are very low, and one of the major rea-
sons is delay in presentation to the emergency room. Therefore, there has been
increased interest in trying to extend the time window for treatment. A pooled
analysis of thrombolysis clinical trial data suggested benefit of IV tPA out to
4.5 hours. This led to the European Cooperative Acute Stroke Study (ECASS)

BOX 1.1 Inclusion/​Exclusion Criteria for IV tPA Within 3 Hours of Stroke Onset

Inclusion

Age >18 years


Clinical diagnosis of ischemic stroke with measurable deficit
Treatment can be initiated within 3 hours

Exclusion

Hemorrhage on head CT
Hypodensity greater than one-​third of a cerebral hemisphere on head CT
History of ICH
Subarachnoid hemorrhage
Intracranial neoplasm, arteriovenous malformation, or aneurysm
Minor or rapidly improving symptoms
Seizure at onset with postictal residual impairments
Stroke or head trauma within 3 months
Major surgery within 14 days
Recent intracranial or intraspinal surgery
Acute myocardial infarction within 3 months
Gastrointestinal or genitourinary bleeding within 21 days
Arterial puncture at noncompressible site within 7 days
Heparin within 48 hours and increased partial thromboplastin time
Current use of novel oral anticoagulant within 48 hours or if activated
partial thromboplastin time or INR remains elevated
INR >1.7 or prothrombin time >15
Platelets <100,000
Aggressive treatment to lower blood pressure <185/​110
Glucose <50 or >400

1. Treatment of Acute Right-Sided Weakness 3


4

3 trial. In this study, patients in the 3-​to 4.5-​hour window were randomized to
IV tPA 0.9 mg/​kg (standard dose) versus placebo. There were additional exclu-
sion criteria beyond those from the NINDS trial: age greater than 80 years, any
anticoagulant use (even with INR <1.7), National Institutes of Health Stroke
Scale (NIHSS) >25, and history of both prior stroke and diabetes. In the ECASS
3 trial, 45% recovered with placebo and 52% with tPA in the extended window,
thus showing a benefit even out to 4.5 hours. Nevertheless, it is well known
that the net clinical benefit of IV tPA is optimized the earlier the treatment is
initiated.
The major concern with IV tPA is brain hemorrhage risk. In the NINDS trial,
6.8% of the patients treated with IV tPA suffered symptomatic intracerebral
hemorrhage (ICH) compared to 0.6% of the patients treated with placebo, with
similar mortality between groups. In ECASS 3, the symptomatic ICH rate was
higher in the tPA group than in the placebo arm but was comparable to rates

FIGURE 1.2 MRI diffusion-​weighted imaging of the brain showing small scattered infarcts in the left
hemisphere.

4 WHAT DO I DO NOW? Cerebrovascular Disease


5

in patients treated within 3 hours. Overall, tPA appears beneficial and with-
out significant additional risk of ICH out to 4.5 hours. Although not US Food
and Drug Administration (FDA)-​approved in the extended time window, the
American Heart Association and other societies have recommended TPA use out
to 4.5 hours from stroke onset in select patients.
Post tPA, blood pressure (BP) must be monitored and treated carefully, with
a goal BP <180/​105. Antihypertensive medications with short duration of action
and that are easily titratable are preferred, such as labetalol and nicardipine. For
24 hours following IV thrombolysis, patients cannot receive any antiplatelet or
anticoagulant medications and invasive procedures must be avoided.
In this patient, IV tPA was given at 7:20 a.m. (3 hours and 50 minutes after
last known well) because she met ECASS 3 criteria for the extended window (i.e.,
age <80 years, NIHSS <25, no history of diabetes and prior stroke, and no use of
anticoagulation). The next day, she had only a slight right arm drift. Her follow-​
up imaging showed no evidence of hemorrhage and small infarcts on magnetic
resonance imaging (MRI) (Fig. 1.2). She was discharged home after 2 days in
the hospital.

KEY POINTS TO REMEMBER

• IV tPA is the mainstay of acute ischemic stroke treatment and is FDA-​


approved within 3 hours of symptom onset.
• Patients benefit when treated early, but the window for treatment
may be extended to 4.5 hours in select patients.
• Inclusion and exclusion criteria need to be reviewed carefully to
minimize hemorrhage risk and maximize the clinical benefit of tPA.
• Blood pressure monitoring and control is important before and after
thrombolysis.

Further Reading
Demaerschalk BM, Kleindorfer DO, Adeoye OM, et al. Scientific rationale for the inclusion
and exclusion criteria for intravenous alteplase in acute ischemic stroke: A statement
for healthcare professionals from the American Heart Association/​American Stroke
Association. Stroke 2016;47(2):581–​641.
Emberson J, Lees KR, Lyden P, et al. Effect of treatment delay, age, and stroke severity
on the effects of intravenous thrombolysis with alteplase for acute ischaemic
stroke: A meta-​analysis of individual patient data from randomised trials. Lancet
2014;384(9958):1929–​1935.

1. Treatment of Acute Right-Sided Weakness 5


6

Hacke W, Kaste M, Bluhmki E, et al. Thrombolysis with alteplase 3 to 4.5 hours after acute
ischemic stroke. N Engl J Med 2008;359:1317–​1329.
Jauch EC, Saver JL, Adams HP Jr, et al. Guidelines for the early management of patients
with acute ischemic stroke: A guideline for healthcare professionals from the
American Heart Association/​American Stroke Association. Stroke 2013;44(3):870–​947.
The National Institute of Neurological Disorders and Stroke rt-​PA Stroke Study
Group. Tissue plasminogen activator for acute ischemic. N Engl J Med
1995;333(24):1581–​1587.

6 WHAT DO I DO NOW? Cerebrovascular Disease


7

2 Large Vessel Occlusion

An 80-​year-​old woman with hypertension and atrial


fibrillation was admitted to the hospital following a left
ankle fracture. Her warfarin was held prior to surgical
treatment with internal fixation. Three days after her
surgery, she develops acute-​onset left-​sided weakness
and numbness. She also has a right gaze preference and
left-​sided visual field cut on examination. Her NIHSS is
20, suggesting a high likelihood of a proximal arterial
occlusion. Her INR is subtherapeutic since anticoagulation
had been held. Her head CT shows only an old right basal
ganglia infarct. Her “last seen normal” was 4.5 hours prior
during her last vital sign check.

What do you do now?

7
8

ENDOVASCULAR TREATMENT FOR ACUTE ISCHEMIC STROKE

This case illustrates some of the limitations of intravenous thrombolysis in acute


ischemic stroke. This patient is suspected to be having a severe stroke but is
unable to receive IV tPA because she meets two exclusionary criteria: She has
had recent major surgery and is outside of the 4.5-​hour treatment window.
Regardless, this patient likely has a proximal artery occluded given the severity
of her symptoms (i.e., her NIHSS score is >10) and the presence of cortical
signs (e.g., neglect, aphasia, visual field cut, and gaze preference). In strokes
due to proximal arterial occlusions, IV tPA only recanalizes the affected vessel
less than one-​third of the time. Therefore, this patient should be considered
for an alternative acute treatment, such as mechanical clot retrieval, because
she is still within a 6-​hour treatment window. Mechanical thrombectomy has
been shown to have higher rates of recanalization than IV tPA alone and can
be used in situations in which tPA may be contraindicated (e.g., recent surgery,
coagulation abnormalities, and history of intracranial hemorrhage) because clot
extraction does not expose the patient to the systemic effects of pharmacological
thrombolysis.
If this patient is not currently at a hospital with capability for neurovascular
intervention, she should be immediately transferred to a stroke center that could
more thoroughly evaluate whether she meets selection criteria for clot extraction
(Box 2.1). At such a center, this patient should be taken emergently for CT angi-
ography in order to confirm that she indeed has a demonstrable proximal artery
occlusion (e.g., an occluded internal carotid artery or proximal middle cerebral
artery). Two previous studies published in 2013 (SYNTHESIS Expansion and
IMS III), which did not evaluate for a proximal arterial occlusion prior to ran-
domization, found no benefit of intra-​arterial therapy. In addition, these two
trials, along with one other called MR RESCUE, mainly used older generation
devices and intra-​arterial tPA. Such older methods of treatment have lower rates
of recanalization compared to more modern stent retreivers that are used today.

BOX 2.1 Suggested Emergency Diagnostic Evaluation for Patients


with Large Vessel Occlusion

1. Noncontrast head CT
2. Administer IV tPA if eligible (within 4.5 hours of symptom onset)
3. CT angiography of the head and neck
4. Perform intra-​arterial therapy if eligible (within 6 hours for anterior
circulation; within 12 hours for posterior circulation)

8 WHAT DO I DO NOW? Cerebrovascular Disease


9

This and other methadologic issues are the main reasons why these three trials
had neutral results.
Two stent retriever devices are currently on the market—​Trevo and Solitaire.
Both have been used in recent trials demonstrating the benefit of mechanical clot
retrieval in acute stroke patients with proximal occlusions. The first and largest of
these studies to be published was MR CLEAN. MR CLEAN enrolled 500 acute
stroke patients in the Netherlands to compare intra-​arterial therapy using a stent
retriever with the standard of care, including IV tPA. The authors found that
patients receiving treatment with a stent retriever had a 59% chance of arterial
recanalization and a 13.5% absolute increase in being functionally independent
at 90 days. In response to the publication of Multicenter Randomized Clinical
Trial of Endovascular Treatment for Acute Ischemic Stroke in the Netherlands
(MR CLEAN), four other enrolling endovascular treatment trials underwent
interim analyses and also demonstrated benefit of intervention. These trials
included the Endovascular Treatment for Small Core and Anterior Circulation
Proximal Occlusion with Emphasis on Minimizing CT to Recenalization Times
(ESCAPE), Extending the Time for Thrombolysis in Emergency Neurological
Deficits—​ Intra-​
Arterial (EXTEND-​ IA), Solitaire with the Intention for
Thrombectomy as Primary Endovascular Treatment for Acute Ischemic Stroke
(SWIFT PRIME), and Randomized Trial of Revascularization with Solitaire
FR Device Versus Best Medical Therapy (REVASCAT), all published in 2015
(Table 2.1). A meta-​analysis of all these trials showed that patients undergoing
thrombectomy had a significantly higher rate of angiographic revascularization
and improved functional outcomes while having no increase in symptomatic
intracranial hemorrhage or mortality. The benefit of endovascular intervention
is quite profound: The number needed to treat to obtain one more patient with
functional independence ranged from 3 to 4 in these trials. However, the net
clinical benefit of treatment diminishes with time, so intra-​arterial therapy needs
to be initiated as soon as safely possible. In the MR CLEAN trial, for every hour
of treatment delay, its absolute benefit was reduced by 6%.
It is important to note that in all the stent retriever trials, the majority of
patients undergoing endovascular treatment also were treated with IV tPA.
Therefore, patients who are eligible candidates for intravenous thrombolysis
should still receive IV tPA within previously defined time windows, as a bridging
therapy, while the clinician considers if the patients should be selected for intra-​
arterial therapy. This is a Class I, Level A recommendation in the most recent
guidelines from the American Heart Association.
Our patient was not a candidate for IV tPA; however, she was taken for an
emergent CT angiogram, which confirmed an occlusion of the right internal

2. Large Vessel Occlusion 9


10
TABLE 2.1 Comparison of 2015 Randomized Endovascular Trials
Trial N Age, Mean NIHSS, IV tPA LKN to Successful 90-​Day Functional ICH Mortality
(Years)a Meana (%) Punctureb Recanalization Independence (%) (%)
(%)c (%)d

IAT MED IAT MED IAT MED

MR CLEAN 500 66 17 90 260 59 33 19 7.7 6.4 21 22


ESCAPE 315 71 16 76 200 72 53 29 3.6 2.7 10 19
EXTEND-​IA 70 69 17 100 210 86 71 40 0 6 9 20
SWIFT PRIME 196 65 17 98 224 88 60 36 0 3 9 12
REVASCAT 206 66 17 73 269 66 44 28 1.9 1.9 18 16
a
For IAT arm only. No significant differences reported between control and intervention arms.
b
Time from last known normal to groin puncture (initiation of procedure) in minutes.
c
Patients who achieved thrombolysis in cerebral infarction (TICI) 2B/​3 (complete or near-​complete) revascularization.
d
Patients who scored 0–​2 on the modified Rankin scale at 90 days.
IAT, intra-​arterial therapy; ICH, intracerebral hemorrhage; MED, control arm.
11

A B

FIGURE 2.1 Cerebral angiogram showing an occluded internal carotid artery terminus (A), followed by complete
reperfusion after successful clot removal using a stent retriever (B).

carotid artery terminus. Given that the noncontrast head CT did not show obvi-
ous signs of a sizable, completed acute infarct, she was taken for clot extraction
with a stent retriever. The interventionalist was able to successfully remove the
thrombus and restore full cerebral perfusion (Figure 2.1). The patient immedi-
ately improved to her baseline function following the procedure, and the MRI of
the brain 1 day later showed only a small completed infarct in the basal ganglia
(Figure 2.2).

FIGURE 2.2 MRI brain 1 day post-​procedure showing only a small acute right basal ganglia infarct.

2. Large Vessel Occlusion 11


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KEY POINTS TO REMEMBER

• Patients eligible for intravenous thrombolysis should receive IV tPA,


even if they will later undergo mechanical thrombectomy. However,
if ineligible for intravenous thrombolysis, certain patients may still
meet selection criteria for intra-​arterial treatment.
• A CT angiogram should be used to confirm a proximal arterial
occlusion prior to intervention.
• Intra-​arterial clot extraction using stent retriever devices has been
shown to improve arterial recanalization and functional outcomes
in stroke patients with large vessel occlusions. Such procedures
should be performed within 6 hours of symptom onset. The sooner
treatment is initiated, the better the outcomes.
• If a patient is suffering an ischemic stroke due to a suspected
proximal artery occlusion (based on the NIHSS score and the
presence of cortical signs), he or she should be transferred to a
stroke center capable of performing intra-​arterial therapy, if not
already at one.

Further Reading
Badhiwala JH, Nassiri F, Alhazzani W. Endovascular thrombectomy for acute ischemic
stroke: A meta-​analysis. JAMA 2015;314(17):1832–​1843.
Berkhemer OA, Fransen PS, Beumer D, et al. A randomized trial of intraarterial treatment
for acute ischemic stroke. N Engl J Med 2015;373(1):11–​20.
Fransen PS, Berkhemer OA, Lingsma HF, et al. Time to reperfusion and treatment effect for
acute ischemic stroke: A randomized clinical trial. JAMA Neurol 2016;73(2):190–​196.
Powers WJ, Derdeyn CP, Biller J, et al. 2015 American Heart Association/​American Stroke
Association focused update of the 2013 guidelines for the early management of
patients with acute ischemic stroke regarding endovascular treatment. Stroke
2015;46:3024–​3039.

12 WHAT DO I DO NOW? Cerebrovascular Disease


13

3 Masquerade

A 41-​year-​old woman with hypertension and migraines


presented with acute left arm weakness and numbness
and headache. She had migraines for 5 years with
holocephalic headaches but no aura. Three years prior to
presentation, she was hospitalized at another hospital for
left-​sided sensory loss and dysarthria in the setting of a
migraine. She was told she had a stroke. She returned to
normal after that event. The day of this presentation, she
noticed acute left arm weakness and numbness without
involvement of the face or leg. On examination, her blood
pressure was initially 190/​105 and spontaneously dropped
to 151/​98. She was very uncomfortable from severe
headache. She had a flaccid plegic left arm with anesthesia
of the left arm. She was within the window for IV tPA and
had no contraindications for thrombolysis.

What do you do now?

13
14

STROKE MIMIC AND ACUTE TREATMENT

Migraine may be a stroke mimic and, in rare cases, can cause ischemic stroke.
In the acute setting, there is little time to complete a full evaluation and wait for
resolution of symptoms if tPA is being considered. Therefore, risks and benefits
need to be carefully reviewed and discussed with the patient. Hemorrhage rates
from tPA increase with higher NIHSS scores since patients with larger strokes
are more likely to bleed with tPA. Conversely, patients with stroke mimics are
unlikely to have spontaneous ICH because there is no brain infarct.
In one series of 512 patients treated with IV tPA, 14% were thought to have
a stroke mimic. The most common diagnoses for these patients were seizure,
migraine, and conversion disorder. None had hemorrhagic complications with
tPA. Other cohorts of stroke mimic patients also showed low risk of symptom-
atic ICH following thrombolysis, with the risk estimated to be 1%.
This patient had a history of migraine, and she developed a focal motor deficit
in the setting of a migraine attack. On the one hand, her young age and history
of migraine make complicated migraine a possibility. However, she had reported
a prior history of stroke. She also had hypertension. These factors would increase
the risk of recurrent stroke. Furthermore, she had never had motor deficit with
migraine before. Therefore, waiting to see if symptoms improve to make a diag-
nosis of migraine would remove the possibility of treatment if this were indeed
stroke. Hospital protocols that employ MRI in the evaluation of acute stroke
may help to distinguish stroke mimics from true stroke more accurately than
clinical examination and history.
The benefits outweighed the risks of treatment for this patient, and she was
given IV tPA. Her symptoms persisted for 3 days, then resolved. Her MRI was
subsequently normal and showed no evidence of recent stroke.
This patient was given the diagnosis of complicated migraine and treated with
migraine prophylaxis after a complete workup.

KEY POINTS TO REMEMBER

• Patients with stroke mimics likely have a low risk for ICH.
• The benefits outweigh the risks of treatment because the diagnosis
of a stroke mimic typically occurs after the tPA window closes.

Further Reading
Chernyshev OY, Martin-​Schild S, Albright KC, et al. Safety of tPA in stroke mimics and
neuroimaging-​negative cerebral ischemia. Neurology 2010;74:1340–​1345.
Zinkstok SM, Engelter ST, Gensicke H, et al. Safety of thrombolysis in stroke
mimics: Results from a multicenter cohort study. Stroke 2013;44(4):1080–​1084.

14 WHAT DO I DO NOW? Cerebrovascular Disease


15

4 Improving Symptoms

A 57-​year-​old man with hypertension and high cholesterol


presented to the emergency room (ER) with acute right
arm weakness and right face numbness. He had no
language or speech involvement. While in the ER, his
symptoms improved, but he was still left with distal hand
weakness and clumsiness. He had no pronator drift and
only slight widening of the right palpebral fissure. His
brain CT was normal.

What do you do now?

15
16

MINOR STROKE SYMPTOMS AND ACUTE TREATMENT

More than 30% of patients presenting to medical attention with acute ischemic
stroke are found on evaluation to have suffered only minor or rapidly improv-
ing deficits. However, minor or rapidly improving stroke symptoms remain a
major reason (in one-​third of cases) why clinicians exclude patients from receiv-
ing intravenous thrombolysis who would otherwise meet criteria for treatment
with IV tPA. In the National Institute of Neurological Disorders and Stroke
(NINDS) trial, patients were excluded from the study with the following minor
symptoms: pure sensory syndrome, isolated dysarthria, isolated facial weakness,
and isolated monoparesis with only minor weakness. Minor stroke has been
more standardly defined by an NIHSS score of less than 6 in recent trials.
Because these patients were either excluded or underrepresented in the
initial landmark trials, one of the contraindications for tPA has historically
been mild or rapidly improving symptoms. However, emerging data have
demonstrated the relative safety of intravenous thrombolysis in minor stroke
patients and a natural history that is not always benign if these patients are
left untreated. One study of 29,200 stroke patients who were not treated with
IV tPA solely because of rapid improvement or minor symptoms found that
28.3% of these patients were discharged to a facility and 28.5% were depen-
dent for ambulation. Furthermore, the same authors also reported that patients
who had more than a 4-​point improvement on the NIHSS were more likely
to have subsequent worsening. This is consistent with clinical observation
that rapid improvement is often a more ominous sign than static symptoms.
Rapid improvement implies a dynamic state and is often followed by wors-
ening. If worsening occurs outside the IV tPA window, the patient has lost
his or her opportunity for treatment. In addition, hemorrhage risk follow-
ing thrombolysis has been shown to increase with increasing stroke severity.
For example, in the NINDS trial, rates of intracerebral hemorrhage following
treatment with IV tPA ranged from 2% (if NIHSS was <6) to 17% (if NIHSS
was >20). A total of 5910 minor stroke patients were recently analyzed for rates
of adverse events in the Get with the Guidelines–​Stroke Registry. This study
demonstrated a low risk of hemorrhage (1.8%) and mortality (1.3%) following
thrombolysis of minor stroke. Although no randomized trials have rigorously
evaluated the use of IV tPA in patients with minor stroke syndromes, it appears
that the usage of thrombolytics in these patients should be safe from a hemor-
rhage standpoint. For this reason, the US Food and Drug Administration has
recently removed rapidly improving or minor stroke symptoms as a contrain-
dication for thrombolysis.

16 WHAT DO I DO NOW? Cerebrovascular Disease


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minulle tällä kertaa sananvuoron muiden edellä, varsinkin kun minä
olen iloissani sinun valitsemisestasi. Olen sitä mieltä, että juuri sinä
kykenet edustamaan meitä kaikkia, joiden elämä ja toimeentulo
useinkin riippuu tuulista ja pilvistä, kevätsateista ja kesähalloista.
Nuorukaisvuosistasi saakka olemme joka päivä omin silmin
seuranneet sinun askeleitasi ja olemme löytäneet kolme tähteä sinun
elämäsi taivaalla suuntaa vilkuttamassa. Ne tähdet ovat puhtaus,
totuus ja rakkaus. Kerran ne peittyivät pilveen, sinä eksyit
nousemaan vuorelle, maailma, kaikkine iloineen ja nautintoineen,
kultineen ja rikkauksineen, kumarteli jalkojesi juuressa. Mutta pilvi
meni ohi, tähdet tulivat jälleen näkyviin ja sinä otit entisen suunnan.
Silloin minun vanha sydämmeni riemuitsi yhtä rajusti, kuin se oli
surrut tähtien ollessa piilossa. Harha-askeleesi jälkeen astuit sinä
elämän kouluun ja siinä koulussa on sinusta kasvanut todellinen
kansan mies. Sinä tunnet, kuten mekin tunnemme, jotka elämme
sinun ympärilläsi, sinä ymmärrät, kuten mekin ymmärrämme, sinä
elät samoista iloista ja suruista, joista mekin elämme. Kaitselmus
lähetti sinulle kärsimyksiä ja koettelemuksia ja ne kirkastivat sieluusi
uuden valon, ijankaikkisen elämän toivon. Haudan tällä puolen ja
haudan tuolla puolen, elämässä ja kuolemassa kuulut sinä meidän
joukkoomme. Sinussa näemme oman paremman itsemme
hioutuneena ja kirkastuneena. Kun sinut nyt lähetämme valtiopäiville
puhumaan meidän puolestamme, olemme vakuutettuja, että vanhat
tähtesi, puhtaus, totuus ja rakkaus yhä vilkuttavat sinulle suuntaa,
ettei suosio, valta, maine, eikä mikään voima horjauta askeleitasi
oikeaan eikä vasempaan. Siitä on meillä takeina entinen
harrasmielinen ja lämminsydämminen koulupoika, elämän
kärsimyksissä karaistu torppari ja nykyinen kansan mies, joka,
samalla kun loihtii maankamaroista kullan, alati silmäilee
ijankaikkisuuden taivaan rantaa kohti.
Selkä kyyryssä ja kädet roikkuen velttoina sivuilla puhui ukko
puhettaan tuttavallisin vaikka särkynein äänin. Hänen hiuksensa
olivat entistä harmentuneemmat ja raihnainen vartalo näytti jo
tutisemisen eleitä.
JALON ELÄMÄN SYNTYSANAT.

Satoi rankasti ja herkeämättä, satoi vallan vimmatusti. Oli alottanut


jo edellisenä iltana. Raikkaan syksypäivän piiloutuessa hämärän
helmoihin näytti taivas tuoreutumisen oireita ja idätti ensin
tihkusateen, joka pitkän ja pimeän yön vaiheissa voimistui
semmoiseksi roimasateeksi, jota ainoastaan syksy osaa antaa.
Suuret pisarat laukkasivat hurjaa vauhtia maahan, synnyttäen
unettavan ja korvaa väsyttävän rapinan, joka ei tuntikausiin
väsähtänyt eikä vaihtanut säveltä.

Jonni istui ikkunan ääressä, silmäillen kirkonkylän maisemia ja


rakennuksia, joiden ympäri sateen synnyttämät harmajat huurut
kääriytyivät. Hänen mieleensä muistui aamu, jolloin hän vapisevin
sydämmin, herpoutuneena ja ärtyneenä kahden yön valvonnasta,
ajoi kotia kohti kyytimiehen rattailla. Silloinkin satoi vimmatusti.
Tarkan haukunta, äidin ja siskojen hämmästyneet katseet, kun hän
työntyi ovesta tupaan, tuima kohtaus isän edessä, kaikki hyristykset,
masennukset ja mielen hyrskyt elpyivät nyt muistiin yhtä nuotteina,
kuten olisivat eilen tapahtuneet.

Liisin astuessa tupaan heräsi Jonni muistelmistaan.


— Joko on kuolema käynyt?

— Jo kävi.

Liisi antoi Jonnille kirjelipun, johon Jullu oli kirjoittanut: ukko veti
nyt juuri viimeisen henkäyksensä. Elä unhota saapua huomenna
kunnallislautakunnan kokoukseen, siinä käsitellään m.m. parin
orvoksi joutuneen pojan kansakoulussa käyttämistä.

Kirkonkellojen ruvetessa soimaan tuli Lauri isän polvien väliin ja


alkoi udella:

— Miksi kelloja soitetaan? Onko pyhä?

— Ei ole pyhä, vaan vanha Taivonen on kuollut.

Poika oli kotvan vaiti, mutta jatkoi sitte:

— Isä, kuoletko sinäkin?

— Kuolen.

— Miksi sinä kuolet?

Jonni jäi vastauksen velkaa.

Oletko sinä nähnyt kuolemaa?

— Olen.

— Onko äitikin nähnyt?

— On.

— Onko sillä rikkinäiset sukat?


— Äiti tietää, mene kysymään äidiltä.

Pojan kysymys verestytti kuoleman muiston. Tuli silmiin kehto,


pienet, ruusuttomat kasvot, tuonen armottomat rynnäköt ja heikon
vartalon suoristuminen. Mutta niiden muistojen takaa heloitti Eliinan
tähti. Ja tähti oli ristin muotoinen ja se heloitti lähellä ja lämpöisesti.
Ja sillä oli pikku Eliinan silmät, vaaleat suortuvat, otsa, suu, nenä.

Jonni katsahti tähteen, samoin tähti katsoi häneen.

Ja tähti näki kookkaan vartalon, kumaraisen niskan, jaloilmeiset


kasvot ja kauniin, kaarevan otsan. Sairauden jälkeen oli otsaan
ilmaantunut jotakin samanmoista kuin tähden omakin valo oli eikä
kukaan voinut sanoa, mitä se oli ja mistä se oli, mutta sen
vaikutuksen tunsivat kaikki. Siitä säteili joku voima, joka tyynnytti
rauhattoman rinnan, lohdutti riitaisen ja vihaisen mielen, lämmitti
kylmän ja välinpitämättömän sydämmen, siitä säteili voima, joka
tunkeutui ihmisen sisimpään.

Ja sen valon rinnalla, jota ei kukaan tiennyt, mitä se oli ja mistä se


oli, pulppuili lämpöisen sydämmen kaikki voittava ja kaikki sulattava
säde, pulppuili matalasointuisessa ja pehmeässä äänessä, silmän
katseessa, huulen hymyssä, pulppuili kookkaassa vartalossa ja
kumaraisessa niskassakin.

Sen säteen tenhon kaikki tunsivat, voimatta kuitenkaan sen


pohjavoimia keksiä, voimatta sanoiksi lausua jalon elämän
syntysanoja.

Mutta tähti ne sanat keksi.


Ne olivat kuin tulikirjaimilla kirjoitetut miehen koko olentoon.
Korkea ja kaareva otsa, matalasointuinen ääni, kasvojen hymy, kaikki
julistivat jalon elämän syntysanoja, jotka olivat koulupojasta
kasvattaneet kansan miehen, seudun kunnian ja maineen.

Niitä sanoja oli vain kolme, kolme maisessa elämässä tärkeätä


sanaa, usein kuultuja, harvoin ymmärrettyjä, mutta vielä harvemmin
toteutettuja.

Ne kolme sanaa olivat:

minä rakastan ihmisiä.


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