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
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
areas 1,2,3
: post central gyrus – primary sensory regions
area 17
: occipital pole – primary visual cortex
areas 18, 19
: rostral to the occipital pole – visual association areas
Upper and Lower Motor Neurons
upper
: begins in cortex and terminates on motor neuron either in brain stem or spinal cord
lesions
: paralysis or paresis, Ý tone, Ý DTRs, ß 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
lesions
: paralysis/paresis, ß tone, ß all reflexes, no pathological reflexes present, marked atrophy, fasciculations and fibrillations present on EMG
Sensation
– all synapse in thalamus except for smell
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
touch: synapse in main sensory nucleus
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
Þ total facial paralysis
central facial palsy
: cerebral lesion Þ upper face is spared because of bilateral innervation
Effects of Lesions
Visual Pathways
retina and optic nerve
Þ monocular visual defects; usually associated with decreased visual acuity
(optic radiation within the temporal lobe) Þ contralateral superior quadrantanopsia
Hemispheric Lesions
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
left hemisphere
: same signs on contralateral side, but aphasia in all right-handers, and 60% of left-handers
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
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
Generalized
: decorticate state – destruction of cortex or disconnection from rest of nerv. system (white matter disease)
total bilateral destruction
Þ coma (although reticular formation destruction is a more common cause of coma)
: disruption of motor or sensory tracts is the same in any area; cranial nerves make localization possible
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)
Weber’s syndome
: midbrain lesion that causes 3rd nerve palsy and contralateral hemiparesis
Wallenberg’s syndrome
: lesion of nucleus ambiguous and fascicle
Þ 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
lateral syndrome
(involves hemisphere): ipislateral ataxia and incoordination
midline syndrome
(involves vermis): truncal unsteadiness and ataxia
Spinal Cord
: the important tracts Þ spinothalamic, lateral corticospinal, posterior columns
transection
: total paralysis and asesthesia below lesion; initial flaccid paralysis with spinal shock, later spastic paralysis
hemisection
(Brown-Sequard syndrome): ipsilateral weakness and touch sense, contralateral pain and temp loss
ALS
(amyotrophic lateral sclerosis): loss of anterior horn cells and demyelinization of corticospinal tracts
posterolateral sclerosis
: involves posterior columns, corticospinal tracts, and dorsal roots
vascular disease
: usually presents as anterior spinal artery syndrome involving the ventral 2/3 of the cord
Peripheral Nervous System
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
presents with proximal weakness, but no sensory or reflex loss
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