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Descending Motor Pathways: NSB 2016 A. L. Gard, PHD

1) Upper motor neurons originate primarily in the primary motor cortex and project through the corticospinal tract or corticobulbar tract to control lower motor neurons. 2) The corticospinal tract descends through the internal capsule and cerebral peduncles before terminating on lower motor neurons or interneurons in the spinal cord. 3) Damage to upper motor neurons can cause signs like hyperreflexia, spasticity, and extensor plantar responses due to disinhibition of lower motor neurons.

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35 views

Descending Motor Pathways: NSB 2016 A. L. Gard, PHD

1) Upper motor neurons originate primarily in the primary motor cortex and project through the corticospinal tract or corticobulbar tract to control lower motor neurons. 2) The corticospinal tract descends through the internal capsule and cerebral peduncles before terminating on lower motor neurons or interneurons in the spinal cord. 3) Damage to upper motor neurons can cause signs like hyperreflexia, spasticity, and extensor plantar responses due to disinhibition of lower motor neurons.

Uploaded by

IM
Copyright
© © All Rights Reserved
Available Formats
Download as PPTX, PDF, TXT or read online on Scribd
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Descending Motor Pathways

NSB 2016
A. L. Gard, PhD

Cortical UMNs originate primarily in layer V of


primary motor cortex (Brodman area 4)
layers

Largest UMNs = pyramidal cells of Betz

Primary motor cortex


Area 4

Corticospinal
UMN control

Corticobulbar
UMN control

Corticospinal tracts
Only ~50% cortical UMNs originate in
1 motor cx (Shh!!!)
Remainder from PMA/SMA, and
sensory areas 1, 2, 3, 5 and 7!!
Pyramidal (Betz) cells project directly
onto LMNs for digit movements; smaller
UMNs project onto segmental
interneurons
85% fibers in pyramids decussate
lateral corticospinal tract (LCST)
uncrossed fibers ventral corticospinal
tract (VCST)
LCST lesions disrupt fine digit movements

Ventral
corticospinal tr

Corticospinal axons descend through the posterior limb


of the internal capsule; corticobulbars through the genu

somatotopy

somatotopic organization

UMN organization in cerebral peduncles

middle third

Corticobulbar neurons: Cortical UMNs to


brainstem motor nuclei
Two origins: cortical eye fields and 1 motor cx
Indirect or direct innervation of CN motor nuclei
indirect

direct

Cortical
Eye fields

CN 3,4,6**

Motor strip
face area

RF*
brainstem tegmentum

RF* = reticular formation

CN 5,7,11,12

Primary motor cortex


Area 4

Cord locations of the lateral & ventral corticospinal tracts


Lateral corticospinal tract projects to distal extremity muscles
Ventral corticospinal tract projects to axial muscles

UMNs are excitatory and glutamatergic


Only a few synapse directly on LMNs
e.g pyramidal cells of Betz
GLU

Ach

LMN

segmental gray
matter

Most corticospinals signal LMNs indirectly


through polysynaptic control via intervening
segmental interneurons
Segmental interneuron banks tonically inhibit
LMNs and unintended movement breakthrough

contraction

2
LMN

Most corticospinals signal LMNs indirectly


through intervening segmental interneurons

Excitation of UMN disinhibits LMN

contraction

2
LMN

UMN damage does not interrupt reflex arcs


Final common pathway still intact, but disinhibited
Test LMN-muscle reaction to assess upstream UMN
dysfunction

Disorders can produce LMN signs that


obscure detection of upstream UMN damage

LMN activity controlled by balance of excitatory


and inhibitory synaptic inputs
(+)
(-)
(+)

(-)
LMN
(-)

(+)

(+)

(-)

(+) = glutamatergic UMNs


(-) = GABAergic or
glycinergic interneurons

sk. muscle

LMNs prevented from spontaneous firing by tonically active inhibitory


local interneurons under descending control by various UMNs
LMNs become overactive when tonic inhibition is reduced by UMN lesions
or toxins affecting interneurons, e.g. tetanus toxin

UMN Signs
Caused by lesion anywhere along corticospinal tr.
above the level
of deficit
What you look for on examination:
DTRs - hyperreflexia
Superficial reflexes - Hoffmanns sign; Babinski sign
(extensor
plantar response; normal in neonates)
Hypertonia
Atrophy - mild (<30%) disuse
Weakness, loss of dexterity, pronator drift

Posturing in unilateral UMN lesions (supratentorial)


Lesion to motor cortex and underlying WM
contralateral inf. facial hemiparesis (usually not hypertonic)
contralateral spastic monoparesis
Lesion to internal capsule
contralateral spastic hemiparesis/hemiplegia
- LE extension and circumduction (brainstem UMN spared)
- UE flexion at elbow and wrist
Spastic gait

DTR rating
0
+1
+2
+3
+4
+5

arreflexia
absent
hyporreflexia
trace
normal
brisk
clonus
hyperreflexia
(if used, tetanus)

Clonus
alternating contractions and relaxations of muscle seen in an
extreme
form of hyperreflexia associated with UMN lesions
equivalent to partial tetanus
muscles not given time to relax
evoked by reflex testing, usually the ankle jerk

Hyperreflexia and clonus

Clonus

Relationship between AP frequency in LMN, muscle and


muscle-generated force

AP frequency
outpaces Ach
clearance time from NMJ

twitch

clonus

tetanus

Extensor plantar response caused by corticospinal tr.


damage anywhere along its course

UMN Signs
Hoffmanns sign

Upper motor neurons originate in two places


command, coordinate and modulate LMNs and associated
local circuits to organize and execute movements
motor cortex
corticospinal tr.
corticobulbar tr.

initiate complex fractionated voluntary


movements of extremities and face

corticoreticular fibers

brainstem
rubrospinal tr.
tectospinal tr.
reticulospinal tr.
vestibulospinal tracts

balance and postural maintenance that is


largely reflexive, below level of consciousness
voluntary movements of proximal limbs

Reticulospinal pathway
Originates in brainstem RF
Targeted by upstream corticoreticular
fibers
Descends bilaterally to LMN pools
destined for axial and proximal
musculature, and local circuit neurons
within in cord gray matter

CNs, e.g. 8

Reticulospinals respond to special


sensory and somatosensory input with
a postural change e.g. start reflex

Reticulosp. tr

Also synapse on gamma-motor neurons


RF is a general structure - includes nonmotor neurons, e.g. descending
raphespinal tr.

Reticulospinal tracts control axial


and proximal musculature
Pontine

Pontine RF medially directed


reticulospinals
Supply medial LMN groups throughout cord
Control axial adjustments

Medullary
Medullary RF lateral reticulospinals
Control proximal limb adjustments

TECTOSPINAL TRACT

Path
- superior colliculus
- contralateral
- targets medial LMNs, cervical
- coordinates reflex neck and
eye movement

Path
- contralateral
- to flexor LMNs
- upper extremity

Vestibulospinal tracts
Medial

Medial vestibular nucleus


Bilateral projections
Target cervical cord LMN pools
coordinates head position and
neck movements, especially extension

Lateral - clinically most important


Lat. vestibulosp. nucleus
Ipsilateral projections only
Target ispilateral LMN pools to antigravity
muscles in proximal limbs
keeps us upright
Unilateral lesion fall to same side
No Romberg sign

Vestibulosp. tract activity regulated by


sensory apparatus of the inner ear via CN8
and cerebellum (unconscious control)

Severe UMN lesions can


produce posturing signs
Associated with impending or ongoing
central herniation and the descending
pressure cone, or direct brainstem
lesions affecting UMN pathways,
e.g. pontine stroke in basis pontis
Can also be produced by a higher
capsular infarct affecting one side
Reflect loss of UMN subsets depending
on the lesion level
Can be unilateral or bilateral

Lesion above brainstem, centralized to thalamus, IC

Lesioned: corticospinals
corticoreticulars
corticobulbars
UMNs below lesion spared
and disinhibited:
rubrospinals (red nucleus)
vestibulosp. (vestibular n.)
reticulosp. (RF)

Decorticate
rigidity

UE flexed, pronated; LE extension with plantar flexion, legs inward,


extended neck

Unilateral capsular infarction can produce


contralateral spastic hemiparesis
UE flexion
LE extension
Produces a spastic gait with circumduction of the
affected LE

+
_

+
+

Red nucleus

Rubrospinal neuron

Corticospinal neuron

Rubrospinal neuron

Corticospinal neuron

Corticospinal lesion facilitates rubrospinal activity


X
+
_

+
+

Descending lesion includes corticospinals + rubros

Lesioned: corticospinals
corticoreticulars
corticobulbars
rubrospinals
Spared and disinhibited:
vestibulosp. (vestibular n.)
reticulospinals (RF)

Profound extensor tone in neck and all extremities

Decerebrate
rigidity

Cord lesion at this


level:
Ipsilateral
UMN Sx below
lesion level
Ipsilateral LMN
signs at lesion
Level
No motor impairment
above lesion

UMN axons and


LMNs are affected by
cord compression
a
om
gi
in
en
m

LE UMN signs
precede UE signs
as meningioma
compresses cord
May see UE signs
first with expanding
central lesion

Superficial reflexes
Other signs of hyperreflexia, but not DTRs
Graded as absent or present
Motor responses to scraping of skin
For plantar response
Polysynaptic-signal must reach cord, ascend to brain, and
descend via UMNs
Although abolished by severe LMN or afferent damage,
superficial reflexes typically test the brain-cord pathway
Abdominal
Above umbilicus
Below umbilicus

cord segment
or nerve roots
T8-T10
T10-T12

Cremasteric
L1-L2
Bulbocavernosus
S2-S4
Anal wink
S2-S4
Plantar

Distal LE UMNs

Tetanus toxin
tetanospasmin (150 kDa protease) hematogenously distributed from
infection site to NMJ
binds ganglioside (receptor) on LMN - subsequently endocytosed
transported retrogradely by axonal transport (via dynein system) along
LMNs into cord and brainstem

LMN
TT

ganglioside
T

T
TT T

CNS

intra-axonal toxin NOT


accessible to antibodies!!
too late for immunization

ganglioside

Tetanospasmin moves transynaptically, upstream from


LMN into axon terminals of CNS inhibitory neurons
(+)
(+)

XT
(-)

(+)

(-) = GABAergic or
glycinergic

(-)

T
T
T

(+) = glutamatergic

LMN T
T

(-)

sk. muscle

blocks release of GABA and glycine by inhibitory neurons


synapsing on LMNs
disinhibits LMNs due to unopposed excitatory inputs
hyperreflexia, muscle spasm, tetanus

Renshaw cells
site of tetanus toxin action

normally allow LMN to self-limit activity


glycinergic ventral horn interneurons
excited by LMN collaterals
suppress LMN activity

++

Specific peripheral synaptic vesicle proteins are


vulnerable to the effect of tetanus toxin

Recall that vesicles released from the cytoskeleton by


synapsin phosphorylation become anchored to the
presynaptic membrane

synapsin-P

Actin

synapsin

Ca+2-CAMK*

Ca+2-CAMK

Ca+2
Glu
Asp
GABA
Gly

Tetanospasmin proteolyzes synaptobrevin to prevent


vesicle docking and NT exocytosis

Sequential effects of tetanus poisoning


Toxin first reaches CNS through the shortest LMNs
- explains early masseter rigidity and facial effects due to LMN
disinhibition
- axial musculature affected before appendicular
Normal sensory stimuli trigger motor neuron hyperactivity
somatic sensory stimulation produces exaggerated reflex
special sensory stimulation, e.g. auditory
- all attributed to loss of normal inhibitory neuronal dampening of
LMN activity
Death ensues from respiratory failure

Clinical signs of tetanus

face and neck spasticity and rigidity


trismus - tonic contraction of muscles of mastication
elevated jaw-jerk reflex
(+) spatula test - touching posterior pharynx
produces brisk reflexive contraction of masseters
(negative result: attempted expulsion - gag reflex)

spasticity - back, abdomen, face


hyperreflexia - elevated DTRs
bilateral hypertonicity
extreme sustained muscular spasms

opisthotonus

trismus
risus sardonicus

By the end of this lesson students will be able to:


Map the somatotopic organization of the corticospinal tract
Discuss the descending control of LMNs from the standpoint of tonic
inhibition of function
List and discuss the principal upper motor neuron lesion signs
Describe the non-pyramidal UMN pathways and their principle functions
on muscle groups
Explain the principle of facilitation in relationship to decorticate and
decerebrate rigity
Contrast the lesions associated with decorticate and decerebrate rigidity
Explain the unilateral posturing of spastic gait resulting from capsular infarct
Explain the finding of clonus
Explain the superficial reflexes assessed for UE and LE function and
abnormal findings
Explain the anatomic basis for the anal wink and bulbocavernosus reflexes
and abnormal findings
Explain the mechanism of tetanus transport to its site of action in the CNS
and its disinhibitory effect on LMNs

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