Neuroanatomy Ch 6 241-254
Corticospinal Tract and Other Pathways
Upper Motor Neuron vs Lower Motor Neuron Lesions
-Upper motor neurons project from cortex to lower motor neurons in anterior horn of cord
-Lower motor neurons project via peripheral nerves to skeletal muscle
-signs of LOWER motor neuron lesions include muscle weakness, atrophy, fasciculations,
decreased tone, and hyporeflexia
-Fasciculations are abnormal muscle twitches caused by spontaneous muscle activity
-signs of UPPER motor neuron injury include muscle weakness and combination of increased
muscle tone and hyperreflexia sometimes called spasticity; also abnormal reflexes may be
present, such as Babinski’s sign, hoffmann’s sign, etc…
-with acute upper motor neuron lesions, decreased tons/reflexes can cause spastic
paresis (partial paralysis)
-palsy = weakness/no movement; plegia/paralysis = no movement; hemi = one side of body;
para = both legs; mono = one limb; di = both sides of body; quadri/tetra = all 4 limbs
Unilateral Face, Arm and Leg Weakness or Paralysis (hemiparesis or hemiplegia)
1. No associated sensory deficits = Pure motor hemiparesis
a. Locations possible: corticospinal/corticobulbular tract fibers below cortex and
above medulla to cause motor but not sensory deficits
b. Side of Lesion: contralateral to weakness (above pyramidal decussation)
c. Common Cause: lacunar infarct of internal capsule (lenticulostriate branches of
middle cerebral artery) or of pons, cerebral peduncle is less common, tumor
d. Ass. Symptoms: upper motor neuron signs, dysarthria (dysarthria-pure motor
hemiparesis), ataxia of affected side (ataxia-hemiparesis)
2. Associated with Somatosensory, Oculomotor, Visual, or Cortical Defects
a. Locations: entire primary cortex, including face, arm, leg representations of
precentral gyrus, or corticospinal and corticobulbular tract fibers above medulla
b. Side of Lesion: contralateral to weakness (above pyramidal decussation)
c. Ass. Symptoms: sensory defects, aphasia, dysarthia, ataxia, upper motor lesions
d. Causes: infarct, hemorrhage, tumor, trauma, herniation, etc…
3. Unilateral Arm and Leg Weakness or Paralysis (Hemiplegia, hemiparesis, brachiocrural
plegia)
a. Locations: arm and leg area of motor cortex; corticospinal tract from lower medulla
to C5 level of cord
b. Side of Lesion: motor cortex/medulla= contralateral; lower medulla/C5= ipsilateral
c. Associated Features: often in watershed distribution, sparing face, affecting
proximal more than distal muscles, may be associated with aphasia; brown sequard
syndrome may be present in lesions of spinal cord. Lesions extending to lateral
medulla may cause lateral medullary syndrome
d. Causes: anterior cerebral-middle cerebral watershed, MS, medullary infarct, lat
trauma
4. Unilateral Face and Arm Weakness or Paralysis (faciobrachial paresis or plegia)
a. Locations: face and arm areas of primary motor cortex; lateral frontal convexity
b. Side of Lesion: Contralateral to weakness (above pyramidal decussation)
c. Associated Features: upper motor neuron lesion, dysarthria, broca’s aphasia,
hemineglect, sensory loss if lesion extends into parietal lobe
d. Causes: middle cerebral artery superior division infarct
5. Unilateral Arm Weakness or Paralysis (Brachial monoparesis/monoplegia)
a. Locations: arm area of primary motor cortex or peripheral nerves supplying arm
b. Side of Lesion: Motor cortex = contralateral, peripheral nerve = ipsilateral
c. Ass Features:
i. Motor Cortex: upper motor neuron signs, cortical sensory loss, aphasia,
symptoms not associated with peripheral nerve lesion, such as weakness of
all finger, hand, wrist muscles without sensory loss
ii. Peripheral nerve Lesion: lower motor neuron signs, weakness/sensory loss
d. Common Cause: if motor cortex= infarct of small cortical branch of mid cerebral art.
If peripheral nerve lesion = compression injury, diabetic neuropathy
6. Unilateral Leg Weakness or Paralysis (crural monoparesis/monoplegia)
a. Locations: leg area of primary motor cortex along medial surface of frontal lobe,
lateral corticospinal tract bwloe T1, or peripheral nerves supplying leg
b. Side of Lesion: motor cortex= contralateral, spinal cord/peripheral nerve= ipsilateral
c. Ass Features:
i. Motor Cortex: upper motor signs, cortical sensory loss, frontal lobe signs,
grasp reflex, subtle involvement of arms/face
ii. Spinal Cord: upper motor signs, Brown-Sequard syndrome, sensory level,
subtle spasticity of contralateral leg
iii. Peripheral Nerve: lower motor signs, weakness/sensory loss
d. Cause: cortex= infarct of ant cerebellar art. spinal cord= unilateral cord trauma, MS,
peripheral nerve: compression injury, diabetic neuropathy
7. Unilateral Facial Weakness or Paralysis (Bell’s palsy) –
a. Locations: facial nerve VII, facial area of primary motor cortex or genu of int capsule
b. Side of Lesion: facial nerve VII = ipsilateral; motor cortex = contralateral
c. Ass Features: Facial nerve= forehead/orbicularis ori NOT spared, hyperacusis,
decreased taste, decreased lacrimation, pain behind ear and on affected side; in
facial nucleus lesions in pons – deficits to VI, V or corticospinal tract
i. Motor cortex or capsular genu lesions: forehead is SPARED, dysarthria and
unilateral tongue weakness is common
d. Causes: facial nerve: bell’s palsy; motor cortex, genu, pons, medulla: infarct
i. Only cases of isolated facial weakness of lower motor neuron pattern with
some hyperacusus, loss of taste, dry eye or retroauricular pain can be
localized to peripheral facial nerve
1. Sensory loss indicative of CNS lesion
ii. If it occurs bilaterally, it is called facial diplegia, weakness = symmetrical
8. Bilateral Arm Weakness or Paralysis – (Brachial diplegia)
a. Locations: medial fibers of both lateral corticospinal tracts; bilateral C spine ventral
horns, peripheral nerve/muscle disorders in both arms
b. Features: central cord syndrome or anterior cord syndrome
c. Causes: central cord syndrome= syringomyleia, tumor, myelitis… anterior cord
syndrome= anterior spinal artery infarct; peripheral nerve= bilateral carpal tunnel
9. Bilateral Leg Weakness or Paralysis – (Parapesis/paraplegia)
a. Locations: bilateral leg areas of primary cortex along medial surface of frontal lobes;
lateral corticospinal tractsbelow T1, cauda equine syndrome
b. Features: Bilateral medial frontal lesions: upper motor neuron signs, frontal lobe
dysfunctions, confusion, apathy, grasp reflexes
i. Spinal cord lesions: upper motor signs, sphincter dysfunction, autonomic
dysfunction
ii. Bilateral peripheral nerve: cauda equina syndrome= sphincter/erectile
dysfunction, sensory loss, lower motor neuron signs
c. Causes: spinal cord lesions are common and serious cause of paraplegia/weakness
i. Bilateral medial frontal lesion: parasagittal meningioma, infarcts, palsy
ii. Spinal cord: numerous; trauma, tumor, myelitis
iii. Bilateral peripheral nerve: cauda equine syndrome, tumor, disc herniation
10. Bilateral Arm and Leg Weakness or Paralysis (quadriparesis/plegia/tetraplegia)
a. Locations: bilateral arm and leg areas of motor cortex, bilateral lesions of
corticospinal tracts from lower medulla to C5
b. Features:
i. Bilateral motor cortex lesions: cortical lesions sparing the face are often in
watershed distribution affecting proximal over distal msucles
ii. Bilateral upper C spine lesions: upper motor neuron signs, sensory level,
sphincter dysfunction, bladder atony
iii. Lower medullary lesions: upper motor neuron signs, occipital headache,
tongue weakness
iv. Peripheral nerve: lower motor neuron signs
c. Causes:
i. Motor Cortex = bilateral watershed infarcts
ii. Upper cervical cord/lower medullary lesion: tumor, infarct, trauma
iii. Peripheral nerve: numerous
11. Generalized Weakness or Paralysis
a. Locations: bilateral lesions of entire motor cortex, corticospinal/corticobulbular
tracts, diffuse disorders from corona radiate to pons, all lower motor neurons,
peripheral axons, neuromuscular junctions or muscles
b. Features: bilateral cerebral lesions can cause upper motor neuron signs, lesions of
peripheral nerves can cause lower motor neuron signs
i. Sensory loss, eye movement abnormalities, pupillary abnormalities
c. Causes: global cerebral anoxia, pontine infarct or hemorrhage, ALS, Guillain-Barre
Detecting Subtle Hemiparesis at the Bedside – the following tests help determine damage:
1. Pronator Drift – patient holds arm extended, palm up, closes eyes; slight inward rotation of
one forearm is abnormal
2. Finger Extensors – pt extends fingers + resists examiner trying to flex them (flexors spared)
3. Fine Movements – pt rapidly taps index + thumb together, taps each finger + thumb in
sequence, rapidly pronates/supinates; taps foot on floor; dominant hand slightly faster
4. Isolated Finger Movement – pt holds fingers abducted/extended + moves 1 finger at a time
5. Spastic Catch – feel for catch on one side when holding pt’s hand in handshake position and
rapidly supinating forearm
6. Subtle Decreased Nasolabial Fold – observe face in several settings: rest, smile, grimace
7. Careful Gait Testing – look for slight circumduction of one leg or decreased arm swing
8. Forced Gait – patient walks on outsides of feet, observe the hands for dystonic posturing
9. Silent Plantar – if normal flexor plantar response is present on one side, a silent plantar
response on other side may represent subtle BABINSKY’S sign
10. Quantitative Testing – testing of motor power and speed may be helpful
Unsteady Gait – gait disorders can be caused by abnormal function of many nervous system
parts, here are a few of the common gait disorders
1. Spastic Gait – uni/bilateral stiff-legged, circumduction, sometimes with scissoring, < arm
swing, unsteady, falling TOWARD side of greater spasticity
a. Localization – unilateral/bilateral corticospinal tracts
2. Ataxic Gait – wide based, unsteady, staggering side-side, falling toward worse pathology
a. Localization – cerebellar vermis/other midline cerebellar structures
3. Vertiginous Gait – wide based and unsteady; patients sway and fall when attempting to
stand with feet together and eyes closed (ROMBERG SIGN)
a. Localization – vestibular nuclei, vestibular nerve, semicircular canals
4. Frontal Gait – slow, shuffling, narrow or wide base, magnetic (barely raising foot off
ground), resembles Parkinsonian gait, some ppl perform cycling movement of back better
than they can walk, calling it gait apraxia
a. Localization – frontal lobes or frontal subcortical white matter
5. Parkinsonian Gait – slow, shuffling, narrow; difficulty initiating walking, stooped forward,
decreased arm swing, en bloc turning, unsteady (retropulsion), taking several rapid steps to
regain balance when pushed backward
a. Localization – substantia nigra or other regions of basal ganglia
6. Dyskinetic Gait – uni/bilateral dancelike, flinging, or writhing movements during walking
a. Localization – subthalamic nucleus, other regions of basal ganglia
7. Tabetic Gait – high-stepping, foot-flapping gait, difficulty walking in dark or uneven surfaces,
positive Romberg sign
a. Localization – posterior columns or sensory nerve fibers
8. Paretic Gait – w/ proximal hip weakness there may be waddling, trendelenburg gait; severe
thigh weakness may cause sudden knee buckling; foot drop can cause high-stepping,
slapping gait
a. Localization – nerve roots, peripheral muscles, NMJ, muscles
9. Painful (antalgic) Gait – pain may be obvious from facial expression, pt’s avoid putting
pressure on affected limb
a. Localization – peripheral nerve or orthopedic injury
10. Orthopedic Gait Disorder – depends on nature; peripheral nerve injury/spinal cord = deficit
a. Localization – bones, joints, tendons, ligaments, muscles
11. Functional Gait Disorder – patients say they have poor balance, destabilizing swaying
movements while walking without falling
a. Localization – psychologically based
Multiple Sclerosis – autoimmune inflammatory disorder affecting CNS myelin caused by T
lymphocyte activation through genetic/environmental factors to react against oligodendroglial
myelin; PNS myelin NOT affected
-plaques of demyelination and inflammatory response can appear in CNS, forming scars
-demyelination causes slowed conduction velocity, dispersion of action potential, and
conduction block; patients have WORSE symptoms when they are warm
-classic definition of multiple sclerosis is two or more deficits separated in neuroanatomical
space and time
-diagnosis is based on presence of clinical features with MRI evidence of white matter lesions
and presence of oligoclonal bands in CSF
Oligoclonal bands – abnormal bands seen on CSF gel electrophoresis resulting from large
amounts of immunoglobulin by plasma cell clones in CSF
-MRI findings including T2-bright areas, representing demyelinative plaques in white matter,
plaques extend into white matter from periventricular locations (“Dawson’s Fingers”) and occur
in both supratentorial and infratentorial structures
-50% of patients have optic neuritis or transverse myelitis
-course of MS is relapsing-remitting at onset but may evolve into chronic progressive phase
-high dose-steroids can treat acute exacerbations
-for first-line relapsing-remitting treatment, use beta-interferon and copolymer
-second line treatments for relapsing disease include antibodies such as cyclophosphamide,
mitoxantrone
Motor Neuron Disease – most disorders affecting upper/lower motor neurons produce deficits
without sensory abnormalities
-classic example is amyotrophic lateral sclerosis (ALS) or Lou Gehrig’s Disease, characterized by
progressive degeneration of both upper and lower motor neurons, leading to respiratory failure
and death
-initial symptoms are weakness/clumsiness, begins focally and spreads to adjacent muscles with
cramping and fasciculations
-some patients present with dysarthria and dysphagia or respiratory symptoms; on neuro exam,
upper motor neuron findings are increased tone and brisk reflexes; lower motor neuron findings
are atrophy and fasciculations (in tongue); extraocular muscles are spared
-Riluzole is a blocker of glutamate release can prolong survival
-similar disorders are lead toxicity, dysproteinemia, thyroid dysfunction, B12 deficiency
-Primary Lateral Sclerosis is an upper motor neuron disease exclusively
-Spinal Muscular Dystrophy affects lower motor neurons (Werdnig-Hoffmann Disease in
infancy leading to death in 2 years)