Neurologic Localization
Introduction
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the goal is to try to explain neurological signs by a single lesion
should be able to localize signs from the physical exam to cerebral, brainstem, spinal cord, nerve,
or muscle
Brodman’s areas – the basics
o area 4: precentral gyrus – primary motor cortex
 corticospinal tract: nerve fibers decussate at the pyramids and terminate at the
ventral horn of the spinal cord
 corticobulbar tract: fibers dessucate immediately rostral to where they
terminate at brain stem nucleii
o areas 1,2,3: post central gyrus – primary sensory regions
o area 17: occipital pole – primary visual cortex
o areas 18, 19: rostral to the occipital pole – visual association areas
Upper and Lower Motor Neurons
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upper: begins in cortex and terminates on motor neuron either in brain stem or spinal cord
o lesions: paralysis or paresis,  tone,  DTRs,  cutaneous reflexes, pathological reflexes
present (Babinski), minimal atrophy, normal EMG
lower: begins at the nucleus in the brainstem or anterior horn of the spinal cord; proceeds
peripherally as a nerve
o lesions: paralysis/paresis,  tone,  all reflexes, no pathological reflexes present, marked
atrophy, fasciculations and fibrillations present on EMG
Sensation – all synapse in thalamus except for smell
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pain and temperature: ascend in contralateral spinalthalamic tract after decussation several
segments above where the root enters; synapse in VPL of thalamus; pass through posterior limb
of internal capsule to sensory cortex
touch: ascend in ipsilateral DCML, decussate in the medulla and continue to VPL of thalamus
sensation of the face: all via CN V
o touch: synapse in main sensory nucleus
o pain/temperature: descend in trigeminal tract and terminate in trigeminal nucleus
according to ‘onion skin’ face model (peri-oral region highest, regions near ears most
caudal); after synapse, fibers decussate and ascend in contralateral trigeminal tract to
VPM
peripheral facial palsy: in CN VII or nucleus  total facial paralysis
central facial palsy: cerebral lesion  upper face is spared because of bilateral innervation
Effects of Lesions
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Visual Pathways
o retina and optic nerve  monocular visual defects; usually associated with decreased
visual acuity
o optic chiasm  bitemporal hemianopsia
o optic tract, lateral geniculate body, optic radiation, visual cortex  contralateral
homonymous hemianopsia
Meyer’s Loop (optic radiation within the temporal lobe)  contralateral superior
quadrantanopsia
Hemispheric Lesions
o right hemisphere: left hemiplegia or paresis with upper facial sparing; contralateral
anesthesia; left homoynmous hemianopsia; speech is normal in right-handers, aphasia in
40% of left-handers; UMN lesion reflex manifestations; normal consciousness, fund of
info and orientation, hearing, taste, smell
o left hemisphere: same signs on contralateral side, but aphasia in all right-handers, and
60% of left-handers
o capsular triad: a lesion in the posterior limb of the internal capsule can produce the
same signs of hemiplegia, hemianopsia, and hemianesthesia (but not aphasia)
Cortical Lesions
o Focal: depends on location of lesion
 motor or sensory loss from contralateral motor or sensory cortex
 aphasia from peri-Sylvian lesions in the dominant hemisphere
 ‘silent’ areas such as the anterior frontal lobes do not produce neurological signs
 lesions of the cortex can become epileptic foci
o Generalized: decorticate state – destruction of cortex or disconnection from rest of nerv.
system (white matter disease)
 total bilateral destruction  coma (although reticular formation destruction is a
more common cause of coma)
 partial cortical destruction  acute: delerium; chronic: dementia
o
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Basal Ganglia Disease
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sustantia nigra  parkinsonism (resting tremor, rigidity, bradykinesia)
subthalamic nucleus  hemiballismus
caudate, putamen, globus pallidus  chorea and athetosis
Brain Stem: disruption of motor or sensory tracts is the same in any area; cranial nerves make
localization possible
o general rules: first two nuclei are outside brainstem; next two are midbrain, next four are
pons, last four are medulla
 lesions of nuclei cause ipsilateral signs except for CN IV (which crosses the
midline)
o Weber’s syndome: midbrain lesion that causes 3rd nerve palsy and contralateral
hemiparesis
o Wallenberg’s syndrome: lesion of nucleus ambiguous and fascicle  ipsilateral palatal
and vocal cord weakness
 other signs (variable depending on extent of lesion): sensory loss of ipsilateral
face and contralateral body, ipsilateral Horner’s syndrome, ataxia, nystagmus; no
extremity weakness if lesion is limited to lateral medulla
Cerebellum: difficult to separate from brainstem lesions of cerebellar pathways
o lateral syndrome (involves hemisphere): ipislateral ataxia and incoordination
o midline syndrome (involves vermis): truncal unsteadiness and ataxia
Spinal Cord: the important tracts  spinothalamic, lateral corticospinal, posterior columns
o transection: total paralysis and asesthesia below lesion; initial flaccid paralysis with
spinal shock, later spastic paralysis
o hemisection (Brown-Sequard syndrome): ipsilateral weakness and touch sense,
contralateral pain and temp loss
o ALS (amyotrophic lateral sclerosis): loss of anterior horn cells and demyelinization of
corticospinal tracts
o posterolateral sclerosis: involves posterior columns, corticospinal tracts, and dorsal
roots
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vascular disease: usually presents as anterior spinal artery syndrome involving the
ventral 2/3 of the cord
Peripheral Nervous System
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may be mononeuropathy, mononeuropathy multiplex (two or more nerves affected),
polyneuropathy (all nerves)
presents with distal weakness and sensory loss (glove-stocking sensory loss), hyporeflexia
Myopathies: primary disease of muscle
o presents with proximal weakness, but no sensory or reflex loss
o muscular dystrophy: myopathy that is genetically determined
Note: despite standard texts, position and vibration do not only travel in the posterior columns;
ascending pathways seem to be located throughout the spinal cord, but we do not know exactly
where