Download Clinical Cases Discussion 3: Motor Systems - Dr

Clinical Cases Discussion 3: Pathophysiologic Correlations - Motor System:
Neuropathy, Radiculopathy, Myelopathy, Cortical Motor Deficit
William Broaddus, M.D. Ph.D.
READING ASSIGNMENT:
Clinical Case Report 1 - Herniated lumbar disc
Clinical Case Report 2 - Peripheral polyneuropathy
Clinical Case Report 3 - Syringomyelia
Clinical Case Report 4- Tabes dorsalis
Clinical Case Report 5 - Brown-Séquard syndrome
Clinical Case Report 10 - Amyotrophic lateral sclerosis (motor neuron disease)
OBJECTIVES
1. To use the anatomic and functional features of the motor nervous system to explain the
clinical findings from neuropathology involving these components.
2. To deduce the motor nervous system components involved by a neuropathologic process
from the findings in a clinical case.
3. To understand and differentiate upper motor neuron (UMN) and lower motor neuron
(LMN) signs of motor system pathology.
MOTOR FEATURES:
Case 1. Herniated lumbar disc
A. Weakness of segmentally innervated muscles (plantar flexion, dorsiflexion, extensor
hallucis) - LMN sign - due to compression of motor fibers from ventral root in L5 and/or
in S1
B. Decreased ankle reflex - LMN sign - due to compression of L5 and/or S1 root
Case 2. Peripheral polyneuropathy
A. Absent ankle reflexes - LMN sign - due to involvement of afferent and efferent fibers in
reflex arc
B. Weakness and wasting of muscles of lower extremities - LMN sign - due to involvement
of motor fibers with decreased power and muscle atrophy
C. Stepping gait - effect of combined weakness and loss of sensation
Case 3. Syringomyelia
A. Atrophy of hand muscles - LMN sign - due to encroachment on anterior horns
B. Ptosis, miosis (Horner's syndrome) - due to involvement of descending sympathetic tract
to intermediolateral cell column
C. Lower extremity hyperreflexia (UMN sign) - involvement of corticospinal tracts, disinhibition of spinal reflex arc
Case 4. Tabes dorsalis
A. Pupils constrict (accommodate) on near vision, but lack light reflex (Argyll-Robertson
pupil) - due to pretectal area lesion from neurosyphilis
Case 5. Brown-Séquard syndrome
A. Ipsilateral lower extremity weakness - due to interference with corticospinal tract
B. Hyperreflexia, clonus - UMN signs - due to interference with corticospinal tract (UMN
fibers), dis-inhibition of spinal reflex arc
C. Babinski sign - UMN sign - interference with flexor response and disinhibition of
withdrawal (extensor) plantar response
Case 10. Amyotrophic lateral sclerosis (motor neuron disease)
A. Weakness of upper and/or lower extremities
B. Atrophy and muscle fasciculations - LMN signs - due to involvement of anterior horn
cells
C. Hyperreflexia - UMN sign - due to involvement of corticospinal fibers/neurons
D. Babinski sign - UMN sign - interference with flexor response and disinhibition of
withdrawal (extensor) plantar response
E. Hoffmann's sign - UMN sign - "Babinski" sign of upper extremity
F. Presence of UMN and LMN signs is a key feature
Clinical Cases Discussion 3 (cont’d): Pathophysiologic Correlations - Motor
System: Cranial Nerves, Brain Stem, Cerebellar Function
William Broaddus M.D. Ph.D.
READING ASSIGNMENT:
Clinical Case Report 6 - Lateral medullary (Wallenberg's) syndrome
Clinical Case Report 7 - Vestibular Schwannoma (Cerebellopontine angle mass)
Clinical Case Report 8 - Basal midbrain (Weber's) syndrome
Clinical Case Report 9 - Medial medullary syndrome
Clinical Case Report 12 - Cerebellar tumor
Clinical Case Report 16 - Middle cerebral artery infarction - posterior frontal branch
OBJECTIVES
1. To use the anatomic and functional features of the motor nervous system to explain the
clinical findings from neuropathology involving these components.
2. To deduce the motor nervous system components involved by a neuropathologic process
from the findings in a clinical case.
MOTOR FEATURES:
Case 6 - Lateral medullary (Wallenberg's) syndrome
A. Cerebellar signs - ataxia, ipsilateral (left) dysmetria - involvement of olivocerebellar and
spinocerebellar fibers
B. Nystagmus - due to cerebellar effects and involvement of vestibular nuclei
C. Ipsilateral (left) ptosis, miosis (Horner's syndrome) - due to involvement of descending
sympathetic tract to intermediolateral cell column
D. Slurred speech (dysarthria), difficulty swallowing (dysphagia) - involvement of ipsilateral
nucleus ambiguus
Case 7 - Vestibular Schwannoma (Cerebellopontine angle mass)
A. Facial weakness (right) - peripheral type - compression of facial nerve (VII) fibers in CP
angle and internal auditory meatus
B. Ataxia, ipsilateral (right) dysmetria - cerebellar, cerebellar peduncle compression
C. Diplopia on right gaze - weak lateral deviation OD (right eye) - compression of VIth
nerve
D. Slurred speech (dysarthria), uvula deviated to left - compression of vagus nerve (X)
Case 8 - Basal midbrain (Weber's) syndrome
A. Ipsilateral (left) IIIrd nerve paresis - ptosis; downward outward deviation (unopposed
IVth and VIth); pupillary dilation - due to impairment of all components of C.N. III:
innervation of levator palpebrae; innervation of superior, inferior and medial rectus
muscles; innervation (parasympathetic) of pupillary constrictors
B. Contralateral hemiparesis with Hoffman's and Babinski signs and hyperreflexia involvement of corticospinal tract in cerebral peduncle
Case 9 - Medial medullary syndrome
A. Contralateral (right) hemiparesis with Hoffman's and Babinski and hyperreflexia involvement of (left) corticospinal tract in pyramid of ventral medulla
B. Left C.N. XII paresis - atrophy of left side of tongue, protrusion to left - involvement of
exiting fibers of XIIth nerve
Case 12 - Cerebellar tumor
A. Ataxia, tendency to fall to side of lesion (left) - impairment of cerebellar function
B. Dysmetria (past-pointing, intension tremor) ipsilateral to lesion (left) - as above
C. Nystagmus, more on gaze to side of lesion - as above
Case 16 - Middle cerebral artery infarction - posterior frontal branch
A. Paresis of contralateral (right) side with hyperreflexia and Babinski (UMN sign) infarction of motor cortex
B. Initial hemiplegia improves to weakness of (right) arm, lower face, right tongue - initial
loss of all (left) hemisphere function resolves to permanent loss of function in lateral
precentral gyrus
C. Expressive aphasia (motor speech deficit) - infarction of Broca's area
Case 17 - Middle cerebral artery stroke/Wernicke's aphasia
A. Mild contralateral (right) side paresis with hyperreflexia and Babinski sign (UMN sign)involvement of left motor cortex
B. Receptive aphasia (deficit in language comprehension)- infarction of Wernicke's area