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Neuro Clerkship > Cerebrovascular Disease > Flashcards

Cerebrovascular Disease Flashcards

1
Q

sudden onset, cortical symptoms, afib, subtheraputic INR-Which kind of stroke and etiology

A

cardioembolic stroke, ischemic

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2
Q

tx for cardioembolic stroke–what must be checked first

A

tPA/heparin; check INR, CT head + CTA

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3
Q

Contraindication to tPA

A
  1. elevated INR
  2. > 4.5 hours after onset of sx
  3. intercranial bleed
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4
Q

What is atherosclerotic plaque made of?

A

Subintimal proliferation of smooth muscle, fatty deposits of intima, inflammatory cells, and excessive elaboration of tissue matrix in vessel wall

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5
Q

How common is fibromuscular dysplasia in causing cranial vessel occlusion? Mechanism?

A

relatively uncommon; segmental overgrowth of fibrous & muscular tissue in media

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6
Q

Causes of meningovascular inflammation

A

syphilis, TB meningitis, sarcoid

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7
Q

Pure motor deficit, where’s the lesion/ what type of stroke

A

lacunar stroke/infarction

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8
Q

Lacunar stroke presentation

A

hemiplegia; no cognitive, sensory, visual deficits

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9
Q

Usual site of injury for lacunar stroke

A

posterior limb of internal capsule

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10
Q

How does lacunae form

A

occlusive lesion in arteriole that supplies injured structure

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11
Q

Presentation of cerebellar lesion

A

impaired coordination, strength preserved

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12
Q

Presentation of caudate or putamen lesion

A

grossly asymptomatic, does not cause weakness, subtle cognitive/motor deficits

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13
Q

Amygdala lesion presentation

A

memory formation and emotion changes

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14
Q

Pure sensory stroke, where’s the lesion/what type of stroke?

Where would eyes be deviated?

A

thalamus (specifically posteroventral nucleus of the lateral thalamus); infarct 2/2 emboli

Eyes deviated towards lesion

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15
Q

What might people feel while recovering from thalamus stroke? What is it called?

A

Paradoxical pain in the area of sensory impairment; “Thalamic pain syndrome”

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16
Q

Wallenberg is also known as ____

A

Lateral medullary infarction

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17
Q

Presentation of lateral medullary infarction

A
  1. ipsilateral ataxia
  2. ipsilateral Horner syndrome
  3. Trigeminal tract damage: ipsilateral loss of facial pain and temp perception & ipsilateral impairment of corneal reflex
  4. Lateral spinothalamic damage: contralateral pain and temp disturbance, contralateral to injury in limbs and trunk
  5. Dysphagia and dysphonia (9th nerve)
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18
Q

Nucleus Ambiguus lesion

  • location
  • what it innervates
  • presentation
A

Location: ventrolateral medulla, contributes to glossopharyngeal 9th nerve and vagus nerve.

Innervates: striated muscles of larynx and pharynx + preganglionic para-sympathetic supply of thoracic organs (esophagus, heart, lungs)

Presentation: dysphagia & hoarseness

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19
Q

Nucleus solitarius, what does it do?

A
  1. combines afferents from CN VII, IX, and X responsible for visceral sensation
  2. Projections are to parasympathetic and sympathetic preganglionic neurons in medulla and spinal cord
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20
Q

What are cerebellar peduncles

A

fibers connecting cerebellum to brain stem

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21
Q

Wallenberg is caused by occlusion of which artery?

A

Most common: vertebral artery

Less common: PICA (largest branch of vertebral artery)

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22
Q

What are the structures that might be involved in lateral medulla infarction (Wallenberg)?

A
  1. lateral medulla
  2. nucleus of lateral medulla
  3. descending tract of 5th nerve
  4. nucleus ambiguus
  5. lateral spinothalamic tracts (pain+temp)
  6. inferior cerebellar peduncle
  7. descending sympathetic fibers
  8. vagus
  9. glossopharyngeal nerves
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23
Q

What does the basilar artery supply

A

ENTIRE posterior brain circulation (huge stroke if occluded)

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24
Q

What does the superior cerebellar artery supply?

A

superior portions of cerebellum

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25
Q

What does AICA supply

A

portions of the cerebellum and lower cranial nerves

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26
Q

Most common cause of lobar hemorrhage in elderly patients (>70yo) w.out HTN

A

Cerebral amyloid angiopathy

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27
Q

Which protein is deposited in vessel walls in cerebral amyloid angiopathy

A

beta-amyloid protein

28
Q

Cerebral amyloid angiopathy presentation

A

multiple cortical hemorrhage, w. or w.out dementia

29
Q

Gliomatosis Cerebri

A

related to glioblastoma multiforme, arises form glial cels, rare, threads that penetrates deep, invasive and aggressive

30
Q

Mycotic aneurysm

A

infected aneurysm from bacterial infection of arterial wall. Orgs usually low virulence, but the more virulent types can cause meningitis or abscess.

31
Q

Risk of mycotic aneurysm

A

Bleeding during exertion (like sexual activity or defecation)

32
Q

Hematoma on CT

A

does not change b/w enhanced or unenhanced

33
Q

CSF finding in SAH

A

xanthochromic, many RBCs, grossly bloody

34
Q

Mycotic aneurysm appearance on CT

A

multiple, sometimes can’t see on CT

35
Q

Tx of post hemorrhage seizure

A

levetiracetam (keppra)

36
Q

Focal weakness following 24h after motor seizure

A

Todd paralysis

37
Q

Sturge-Weber syndrome is also known as ___

A

encephalofacial angiomatosis

38
Q

People with Sturge-Weber might have:

A

Facial cutaneous angiomas with intracranial abnormalities like leptomeningeal angiomas

39
Q

Sturge-Weber/ Encephalofacial angiomatosis presentation

A
  1. Port-wine nevus (sensory distribution of 1st trigem nerve)
  2. Mental retardation
  3. Hemiparesis
  4. Hemiatrophy (opposite nevus)
  5. Angioma of choroid in eye

–Intracranial angioma unlikely if nevus doesn’t involve upper face–

40
Q

Mechanism of neurologic deficit in Sturge-Weber

A

focal ischemia in cerebral cortex that underlies leptomeningeal angioma

41
Q

Charcot-Bouchard aneurysms: what is it and where?

A

small and microscopic aneurysms in ppl with CHRONIC HTN; appear in perforating arteries of the brain (lenticulostreiate arteries); hematomas commonly appear in putamen.

Supplies:

  1. caudate
  2. nucleus
  3. thalamus
  4. pons
  5. cerebellum (dentate nucleus)
42
Q

Difference between charcot-bouchard (CBA) and berry aneurysms (BA)

A

CBA: assoc. w/ chronic HTN, small vessel (<1mm) internal capsule and basal ganglia , SUDDEN onset of focal deficits

BA: assoc. w/ ADPKD, marfan’s, ehler danlos, large vessel (2-25mm) esp. Circle of Willis (anterior and posterior communicating arteries), SAH affecting bridging veins, sudden onset HA, altered mental status, neurologic deficits occur later

43
Q

hemangioblastomas are ____ associated with ____ & _____

A

vascular tumors

APKD and telangiectasias of the retina (von Hippel-Lindau)

44
Q

Fusiform aneurysm character and cause

A

widened arteries with evaginations along walls without stalks (which would be seen in typical berry-shaped structures in saccular aneurysm)

arteriosclerotic damage to artery wall

45
Q

Optic radiation loops through which lobe on its way to the occipital cortex?

A

Temporal lobe

46
Q

Posterior aphasia is also known as

A

fluent aphasia or wernicke’s aphasia or sensory aphasia

47
Q

Wernicke’s aphasia vascular lesion, which vessel

A

posterior cerebral artery

48
Q

Common etiology of hemorrhage if <40yo

if >40?

A

<40 yo: AV malformation

>40 yo: aneurysm (in 40s-50s F>M, especially internal carotid artery inside cavernous sinus)

49
Q

Dull pain behind eye, diplopia intermittent, papillary edema, color separation…think about lesion where ___

A

cavernous sinus

50
Q

CN III deficit, HA, pupillary dilation. What’s the mechanism and location of the lesion?

A

Posterior communicating artery aneurysm (compressing oculomotor nerve and pupilloconstrictor fibers

51
Q

Complications after subarachnoid hemorrhage

A

vasospasm, seizures

52
Q

Treatment/ppx for post SAH vasospasm

A

CCB (nimodipine)

53
Q

Workup of TIA/amaurosis fugax

A

Doppler of carotids
lipid panel
HA1c

54
Q

transient visual loss etiology

A

central retinal artery ischemia

55
Q

Presentation of retinal vein thrombosis

A

rapidly progressive loss of vision, funduscopic exam with hemorrhages in retina

56
Q

Indication for carotid endarterectomy (CEA)

A

symptomatic disease of internal carotid artery

57
Q

Best way to prevent future stroke for symptomatic 90% sttenosis of R intercal carotid artery at bifurcation

A

CEA

not ASA, warfarin, carotid artery angioplasty or extracranial-intracranial bypass

58
Q

Explain stroke p/w:

  1. left eye deviation,
  2. right dense hemiplegia,
  3. R visual field cut, & intact pain sensation on L

Where’s the lesion, what’s affected, and what kind of aphasia?

A

Global Aphasia–impaired comprehension, repetition, fluency

  1. Left eye deviation: Left lesion affecting left frontal eye fields (overriding signal from right pushes eyes to left)
  2. R Hemiplegia: Left cortex lesion, contralateral hemiplegia
  3. R Field cut: Optic radiation damage on L hemisphere
59
Q

What type of aphasia p/w:

  1. language comprehension deficit
  2. Ability to produce intelligible phrases & sound fluently
  3. unable to follow simple instructions
  4. unable to repeat simple phrases
  5. agraphia*
  6. MRI + for lesion on L temporal lobe extending into superior temporal gyrus
A

Wernicke aphasia (fluent aphasia)

60
Q

What is the arcuate fasciculus and where does it travel?

A

connects expressive language centers in frontal lobe and receptive centers in temporal lobe, travels through temporal and parietal lobes

61
Q

Presentation of conduction aphasia, and what is the lesion

A

problems with repetition
speech does not sound fluent

lesion: arcuate fasciculus in temporal/parietal lobe

62
Q

Broca’s aphasia prognosis

A

will regain ability to produce meaningful language if infarction is less than a few cms across. Usually with permanent loss of syntax

63
Q

Mixed transcortical aphasia, presentation and probable type of stroke.

A

Presentation: after profound hypotension; speech limited to repetition of words and sounds; no comprehension of language and produces few sounds spontaneously.

Type of stroke: watershed infarction

64
Q

Anomic aphasia presentation and localization

A
  • naming impaired, duh. word-finding deficit.
  • comprehension, repetition and fluency relatively maintained
  • least localizable of major aphasias (common with diffuse brain dysfunction)
65
Q

Transcortical motor aphasia

presentation and location of lesion

A

similar to broca’s but PRESERVED REPETITION

Location: L frontal white matter, spares overlying cortex (broca’s)

66
Q

Transcortical sensory aphasia

presentation & location of lesion

A

similar to Wernicke’s but PRESERVED REPETITION

Location: white matter underlying cortex of wernicke area
Prognosis better than wernicke aphasia

Neuro Clerkship (7 decks)

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