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Dr. Cheng neuro review Qs > Ch 2 Vascular > Flashcards

Flashcards in Ch 2 Vascular Deck (82)
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What is the ABCD2 score?

Evaluates the risk of stroke after TIA.
Age of 60+
Blood pressure 140/90+
Clinical sx (1pt speech impairment, 2 pt focal weakness)
Duration of sx (1pt for 10-20mins, 2pts for 60+ mins)


Extensive infarcts of b/l pons presents with (6)?

locked in syndrome: (1) awake (2) preserved consciousness (3) can blink/move eyes vertically (4) quadraplegic (5) unable to speak (6) impairment of horizontal gaze


dose of tpa

0.9mg/kg, 10% bolus over 1 hr, max dose of 90mg


etiology of locked-in syndrome?

basilar occlusion --> b/l infarcts at base of the pons, affecting the long tracts but preserving the reticular activating system


venous sinus thrombosis presents with (3)?

HA 90%
seizures 40%


Lateral medullary infarct is caused by occlusion of what vessel?

PICA (often associated w occlusion of vertebral a)


What structures (nuclei/tracts) are affected in Wallenberg's syndrome? (7)

vestibular n, CN 5 n, spinothalamic tract, sympathetic tract, CN 9 and 10 fibers, cerebellum and cerebellar tracts, nucleus of tractus solitarius


How does Wallenberg syndrome present?

(1) Vestibular n --> vertigo, nystagmus, N/V
(2) n of CN 5 --> impaired sensation ipsilateral hemiface
(3) spinothalamic tract --> impaired pain/temperature sensation in contralateral hemibody
(4) sympathetic tract --> ipsilateral Horner's syndrome
(5) fibers of CN 9 and 10 --> hoarseness, dysphagia, ipsilateral paralysis of palate and vocal cord, decreased gag reflex
(6) cerebellum --> ipsilateral ataxia and lateropulsion
(7) nucleus of tractus solitarius --> loss of taste


Medial medullary syndrome is caused by occlusion of what vessel?

the vertebral artery or one of its medial branches


What structures are affected in medial medullary syndrome (3)?

infarct of the pyramid, medial lemniscus, and emerging hypoglossal fibers?


How does medial medullary syndrome present?

corticospinal tract prior to decussation --> contralateral arm and leg weakness/sparing the face
medial lemniscus --> contralateral loss of position and vibration
hypoglossal fibers --> ipsilateral tongue weakness


GCA/temporal arteritis p/w (7)?

pts >50 years old, HAs, constitutional sx, jaw claudication, tenderness of scalp around temoporal artery
labs: leukocytosis, elevated ESR and CRP


What is Millard-Gubler syndrome?

-lesion of the pons that affects corticospial tract before decussation as well as CN 7 nucleus
-p/w contralateral hemiplegia with ipsilateral facial palsy
(if there is also conjugate gaze towards brainstem lesion - it's called Foville syndrome)


What factors lead to increase risk of aneurysmal rupture (6)?

(1) diameter of 7mm or higher
(2) aneurysmal growth
(3) location! posterior circulation aneurysms have higher chance of rupture than anterior circulation aneurysms
(4) smoking
(5) uncontrolled HTN
(6) hx of previous aneurysmal rupture


What is the most common site of vertebral a dissection?

level of C1-C2


What are the benefits of tpa given in 3 hours?

increase chance by 30% of minimal or no disability at 3 months


What is the exclusion criteria for tpa for patients who arrive within 3hr- 4.5 hr window (4)?

(1) NIHSS > 25
(2) age > 80
(3) hx of both stroke and diabetes
(4) any AC use


Left sided occipital strokes will present with?

(1) alexia without agraphia
(2) anomia
(3) visual agnosia
(4) contralateral homonymous hemianopia


Why is it that a left occipital stroke will present with anomia and alexia (without agraphia)?

the pt cannot see what's in the right visual field and whatever can be seen in the left visual field will be represented in the right occipital cortex. Due to corpus collosum involvement, this information cannot be connected with language centers in the left hemisphere


What is Benedikt's syndrome (etiology and presentation (3))?

infarction in the mesencephalic tegmentum involving ventral part of red n, the brachium conjunctivum, and fascicle of the 3rd CN
-p/w ipsilaterl CN 3 palsy, contralateral tremors and coreoathetosis


What were the results of the WASID trial?

Warfarin-Aspirin Symptomatic Intracranial Disease.
Oral AC with warfarin was associated with more adverse events and provided no benefit over aspirin in the prevention of cerebrovascular events in the setting of intracranial atherosclerotic disease


What were the results of the SPARCL trial?

The Stroke Prevention by Aggressive Reduction in Cholesterol Levels
Atorvastatin 80mg daily reduces overall incidence of strokes and CV events in pts with recent (within 6 mo) TIA or stroke with LDL btwn 100-190


Patient with supranuclear paralysis of eye elevation, defect in convergence, convergence-retraction nystagmus, light-near dissociation, lid retraction and skew deviation. Where is the lesion?

This is Parinaud's syndrome, seen commonly with pineal tumors compressing the quadrigeminal plate. It can also occur from midbrain infarcts


What is the ASPECTS score?

provides a grading system to assess early ischemic changes in patients with AIS of the anterior circulation. Two axial cuts are needed, one at the BG and thalamus and one more cranial cut. 10 points = normal head CT. 0 = diffuse ischemic injury of the entire MCA territory. Low scores should not get tpa. ASPECTS < 7 or less correlates with increased dependence and death.


Where does the anterior choroidal artery arise from?

branch of ICA that arises from the communicating segment or supraclinoid ICA segment


What are the segments of the ICA? (4)

cervical segment, petrous segment, cavernous segment, supraclinoid segment


What were the results of the NASCET trial?

NASCET trial (North American Symptomatic Carotid Endarterectomy Trial)
-in patients with 70-99% symptomatic carotid stenosis, 2 yr stroke rate was 26% with medical txt vs 9% with CEA
-symptomatic stenosis 50-69% may also benefit from CEA, with greater impact on men vs women, in those with precious strokes vs TIAs, and with hemispheric vs retinal sx


When is the highest risk for stroke after TIA?

risk is higher soon after TIA, with 50% of strokes occurring within 48 hours


What are the two most common causes of spontaneous ICH?

HTN in 75% of cases followed by cerebral amyloid angiopathy


Where is hypertensive ICH commonly seen in the brain?

deep subcortical structures (putamen, caudate, thalamus) and pons, cerebellum, and periventricular WM.