neuro-path Flashcards

1
Q

what symptom might be expected from transtentorial herniation of the uncus secondary to expanding space occupying lesions within the temporal lobe?

A

elevated ICP

ipsilateral oculomotor nerve palsey due to compression of CNIII as it exits the midbrain

fixed dilated pupil (due to damage to the preganglionic parasympathetic fibers running on the outer portion of CNIII)

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2
Q

what brain herniation is most likely to cause impaired lateral eye movement (or medially drifting eye) with double vission due to damage to lateral rectus muscle?

A

downward displacement of the brainstem (central herniation)

uncal herniation is more likely to cause 3rd nerve palsy with fixed dilated pupil and alevated ICP

abducens/CN VI palsey (described in this question) is due to nerve traction along the clivus

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3
Q

what is the effect on reflexes from uncal herniation that causes compression of the cerebral peduncles and indury to the corticospinal tract?

A

initial flacid paralysis and hyporeflexia (ie spinal shock) followed by spasticity/hyperreflexia (develops days to weeks after acute UMN damage)

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4
Q

lesion to what regions can cause horners syndrome?

A

lateral hypothalamus
lateral medulla - sypathetic tracts in the brain stem

ipsilateral eye droop (ptosis), ipsilateral contracted pupil (miosis), ipsilateral loss of sweating (anhidrosis)

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5
Q

what symptom might be expected from bilateral pontine lesions?

A

pin-point pupils due to damage to the descending sypathetic tracts

frist order neurons have cell bodies in lateral hypothalamus and travel down the lateral brain stem and synapse at the intermediolateral horn of the spinal cord at level of ciliospinal center of Budge C8-T2). Second order nervons exit the spinal cord and ascend along the sympathetic chain, near lung apex and subclavian vessels, to synapse at the cervical ganglia at the level of C2 - 3rd neurons are post-ganglionic noradrenergic fibers that form plexus and ascend along the internal corotid through the cavernous sinus and branch off to enter the orbit as the long ciliary nerve (run along the opthalmic division of the trigeminal nerve) to innervate the pupilary dilator muscle

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6
Q

what is the effect of hydrocephalus on extra-occular muscles and vision?

A

impaired upward gaze due to dialtion of the third ventrical with compression of the dorsal midbrain (pretectal area - pretectal nucleus => problem’s w/ CN III)

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7
Q

pt presents with cape like distribution of bilateral loss of pain and temperature sensation in the upper extremities with spared fine touch sensation. What was the cause (where was the lesion)?

A

damage to the anterior white commisure spinothalamic tract - often consequence of syringomyelia

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8
Q

where are lesions most commonly found in wenicke-korsakoff syndrome?

A

paraventricular and commonly involve mamillary bodies

administration of glucose before thiamine can worsen symptoms!

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9
Q

what is karsakoff syndrome?

A

damage to the bilateral temporal lobes, anterior and dosomedial thalamic nuclei – permanant memory/leaning impairment from chronic alcohol or thiamine deficiency

inability to form new memories (anteriograde amnesia)

confabulations - pt. can’t remember a memorie so that replace it with fabricated story they beleive to be true

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10
Q

chronic alcoholic develops coarse, rythmic, postural tremor affecting fingers and arms. What is the most likely affected brain structure?

A

cerebellum

loss of purkinje cells in teh anterior lobes of the cerebellar vermis

eventually leads to trunkal ataxia, intention tremor of hands and fingeers and rythmic postural parkansoniansm

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