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

Ch 2 Vascular Flashcards

1
Q

What is the ABCD2 score?

A

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)
Diabetes

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2
Q

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

A

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

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3
Q

dose of tpa

A

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

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4
Q

etiology of locked-in syndrome?

A

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

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5
Q

venous sinus thrombosis presents with (3)?

A

HA 90%
seizures 40%
IIH

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6
Q

Lateral medullary infarct is caused by occlusion of what vessel?

A

PICA (often associated w occlusion of vertebral a)

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7
Q

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

A

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

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8
Q

How does Wallenberg syndrome present?

A

(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

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9
Q

Medial medullary syndrome is caused by occlusion of what vessel?

A

the vertebral artery or one of its medial branches

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10
Q

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

A

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

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11
Q

How does medial medullary syndrome present?

A

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

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12
Q

GCA/temporal arteritis p/w (7)?

A

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

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13
Q

What is Millard-Gubler syndrome?

A

-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)

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14
Q

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

A

(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

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15
Q

What is the most common site of vertebral a dissection?

A

level of C1-C2

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16
Q

What are the benefits of tpa given in 3 hours?

A

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

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17
Q

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

A

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

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18
Q

Left sided occipital strokes will present with?

A

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

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19
Q

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

A

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

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20
Q

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

A

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

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21
Q

What were the results of the WASID trial?

A

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

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22
Q

What were the results of the SPARCL trial?

A

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

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23
Q

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?

A

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

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24
Q

What is the ASPECTS score?

A

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.

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25
Q

Where does the anterior choroidal artery arise from?

A

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

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26
Q

What are the segments of the ICA? (4)

A

cervical segment, petrous segment, cavernous segment, supraclinoid segment

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27
Q

What were the results of the NASCET trial?

A

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
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28
Q

When is the highest risk for stroke after TIA?

A

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

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29
Q

What are the two most common causes of spontaneous ICH?

A

HTN in 75% of cases followed by cerebral amyloid angiopathy

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30
Q

Where is hypertensive ICH commonly seen in the brain?

A

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

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31
Q

What is a characteristic finding of patients with cerebral hemorrhages from anticoagulation?

A

Pts on AC may have hemorrhages showing a fluid-fluid level.

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32
Q

What is Moyamoya disease?

A

It’s a noninflammotory, nonatherosclerotic vasculopathy.
progressive bilateral stenosis of the distal ICAs extending to proximal MCAs and ACAs, and development of extensive collateral circulation at the base of the brain, with the “puff of smoke” appearance

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33
Q

Clinical manifestations of Moyamoya? (7)

A

TIAs, strokes, ICH. Can also present with HA, sz, movement disorders, cognitive deterioration

34
Q

Txt options for Moyamoya?

A

APTs, vasodilators, CCB, steroids have been used with equivocal results. Avoid AC given risk of hemorrhagic complications

35
Q

what is Dejerine-Roussy syndrome?

A

caused by thalamic infarct, in which the lesion affects the sensory relay nuclei. These patients present with severe deep and cutaneous sensory loss of teh contralateral hemibody, usually the entire hemibody and up to midline

36
Q

describe the segments of the vertebral arteries?

A

V1 segment: from subclavian artery to C6
V2 segment: C6 to C2
V3 segment: transverse foramen of C2 to around arch of C1 btwn the atlas and occiput
V1 to V3 are extracranial
V4 segment (intracranial): from dura at the foramen magnum to where it joins the contralateral VA to form basilar artery

37
Q

What was the WASID trials and what were the results?

A

The Warfarin-Aspirin Symptomatic Intracranial Disease trial randomized pts with recent TIA/stroke with 50-99% stenosis of a major intracranial artery to warfarin or ASA. Warfarin had higher rates of adverse events with no greater benefit than ASA.

38
Q

What is Claude’s syndrome

A

ipsilateral CN 3 palsy, contralateral ataxia and tremor; lesion of the red nucleus and 3rd nerve fascicle; it’s the DORSAL midbrain tegmentum (unlike Benedikt’s syndrome which is ventral mesencephalic tegmental lesion and has the same symptoms with the addition of involuntary choreoathetotic movements

39
Q

What does the cavernous sinus drains into?

A

drains into the superior and inferior petrosal sinuses. The inferior petrosal sinus connects the cavernous sinus with the sigmoid sinus or the jugular bulb

40
Q

What is the superior anastomotic vein that connects th Sylvian vein to the superior sagittal sinus?

A

vein of Trolard

41
Q

What is the inferior anastomotic vein that connects the Sylvian vein to the transverse sinus?

A

vein of Labbe

42
Q

How does CADASIL occur?

A

missense mutation in gene NOTCH3 on chromosome 19. The gene product is a transmembrane receptor expressed mainly in vascular smooth muscle, mutation leads to accumulation of this protein in the vascular walls, especially in small arteries and capillaries

43
Q

What is Weber syndrome?

A

midbrain lesion/infarct causing ipsilateral CN 3 palsy and contralateral hemiplegia

44
Q

Appearance of cavernous malformation on MRI?

A

popcorn like appearance with a dark rim on T2 consistent with hemosiderin

45
Q

What are AVMs?

A

congenital vascular lesions consisting of a tangle of dilated vessels in which arteries and veins communicate without an intervening capillary bed. Can be seen on CT and CTA. MRI will show slow voids and prior hemorrhage. Diagnostic angiography = gold standard

46
Q

What are DAVFs?

A

acquired vascular lesions in which there is arteriovenous shunting typically from meningeal or dural arterial branches with drainage toward a dural venous sinus. Associated with increased venous pressure and arterialization of the draining veins

47
Q

The common carotid artery divides into external and internal carotid arteries at what level?

A

C4 (below the angle of the jaw)

48
Q

What is the most common type of spinal vascular malformation?

A

spinal DAVF

49
Q

What is a spinal DAVF?

A

acquired AV shunting within the dura mater where a radiculomeningeal artery connects with a radicular vein. This arterialization leads to increased venous pressure, venous congestion, intramedullary edema, and progressive myelopathy

50
Q

How does a spinal DAVF appear on MRI?

A

enlargement of the cord with hyperintensity on T2 seen on several levels, with perimedullary flow voids

51
Q

Treatment of spinal DAVFs?

A

endovascular embolization and/or surgical disconnection of the lesion

52
Q

Describe MRI findings for hyperacute (<12 hours) hemorrhage? What is the predominant blood product?

A

predominant blood product: oxyhemoglobin

T1 isointense, T2 hyperintense

53
Q

Describe MRI findings for acute (12 hours to 2 days) hemorrhage? What is the predominant blood product?

A

predominant blood product: deoxyhemoglobin

T1 isointense, T2 hypointense

54
Q

Describe MRI findings for early subacute (2 to 7 days) hemorrhage? What is the predominant blood product?

A

predominant blood product: intracellular methemoglobin

T1 hyperintense, T2 hypointense

55
Q

Describe MRI findings for late subacute (8 days to 1 month) hemorrhage? What is the predominant blood product?

A

predominant blood product: extracellular methemoglobin

T1 hyperintense, T2 hyperintense

56
Q

Describe MRI findings for chronic (>1 month to years) hemorrhage? What is the predominant blood product?

A

hemosiderin

T1 isointense or hypointense; hypointense T2

57
Q

What are the most frequent locations of intracranial saccular aneurysms in order of their frequency? (7)

A

ACOMM, PCOMM, MCA bifurcation, ICA bifurcation, basilar apex, pericallosal artery, and PICA

58
Q

The most common cause of nontraumatic SAH?

A

intracranial saccular aneurysms (1 in 200-400 will rupture, but makes up 85% of nontraumatic SAH)

59
Q

What is a carotid cavernous fistula? How does it present?

A

A tear in the cavernous segment of the ICA (most commonly caused by trauma) that allows AV shunting between the ICA and the cavernous sinus. This causes increased pressure in the cavernous sinus (with CN involvement and ophthalmoplegia), increased pressure in the venous system draining the eye, impairing venoous drainage (chemosis, proptosis, increased IOP, retinal ischemia, vision loss). increased ICP can occur which can lead to ICH or SAH.

60
Q

Treatment of a direct carotid-cavernous fistula?

A

Endovascular embolization = treatment of choice. Surgical ligation of ICA if endovascular txt is not possible or successful.

61
Q

What are DAVF?

A

acquired vascular lesions in which there is AV shunting supplied by meningeal or dural arterial branches, with drainage toward a dural venous sinus.

62
Q

What is the etiopathogenesis behind DAVFs?

A

May be related to venous sinus occlusion (ie venous sinus thrombosis) leading to increased venous pressure and eventual formation of the arteriovenous shunt

63
Q

What types of DAVFs are associated with increased risk of intracranial hemorrhage and nonhemorrhagic neurological symptoms?

A

Type II and III which have cortical venous drainage and are considered aggressive

64
Q

Brand name of Dabigatran and mechanism of action? Metabolism?

A

Pradaxa; direct thrombin inhibitor; poor bio availability and 80% renally cleared, with the rest being metabolized in the liver

65
Q

Results of RE-LY study regarding Dabigatran?

A

Dabigatran (Pradaxa) 110mg BID was noninferior to warfarin for prevention strokes and systemic embolism in nonvalvular atrial fibrillation with lower rates of major hemorrhage. Side effects: dyspepsia and increased risk if GI hemorrhage

66
Q

Which is the only NOAC agent that has an FDA approved reversal agent?

A

For Dabigatran, the reversal agent Idarucizumab has been approved

67
Q

Brand name of Rivaroxaban and mechanism of action? Metabolism?

A

Xarelto; factor Xa inhibitor; 2/3 are metabolized in the liver with 1/3 excreted in the urine

68
Q

What is the only NOAC in the treatment of stroke prevention in afib that has once a day dosing?

A

Rivaroxaban (because it’s 95% protein bound)

69
Q

Results of ROCKET AF trial regarding Rivaroxaban?

A

Rivaroxaban (Xarelto) was noninferior to warfarin for preventing stroke and systemic embolism in nonvalvular atrial fibrillation with similar risks of bleeding, but lower risks of intracranial and fatal hemorrhage

70
Q

Brand name of Apixaban and mechanism of action? Metabolism?

A

Eliquis; factor Xa inhibitor; metabolized in the liver and 25% renally excreted

71
Q

Results of ARISTOTLE trial regarding Apixaban?

A

Apixaban 2.5mg or 5mg BID was superior to warfarin for preventing stroke and systemic embolism in nonvalvular afib. Also associated with lower risk of major bleeding including intracranial hemorrhage and lower mortality rates.

72
Q

What are some categorical causes of secondary CNSV? (3)

A

(1) idiopathic systemic vasculitides, (2) systemic vasculides associated with autoimmune disease, (3) systemic vascultides secondary to nonautoimmune conditions such as infections drugs or cancer

73
Q

What is PACNS?

A

inflammation of small and medium sized parenchymal and leptomengingeal arteries involving the brain and/or spinal cord.

74
Q

What are common presenting symptom of PACNS? (3)

A

(1) headache which is usually insidious and/or chronic; thunderclap is rare (distinguishing from RCVS).
(2) ischemic strokes
(3) altered cognition

75
Q

diagnostic criteria for PACNS

A

(1) Acquired otherwise unexplained neurologic or psychiatric deficit
(2) Classic angiographic or histopathologic features of CNS angitis
(3) no evidence of systemic vasculitis or any disorder that could mimic the angiographic or pathologic features

76
Q

How to definitively diagnose PACNS?

A

high probability with cerebral angiogram and with abnormal MRA and abnormal CSF. A definite diagnosis requires brain biopsy of vessel wall inflammation.

77
Q

Three main histopathologic patterns of PACNS?

A

(1) Granulomatous angiitis of the CNS
(2) lymphocytic PACNS
(3) necrotizing CNSV

78
Q

Treatment of PACNS?

A

high dose steroids with or without cyclophosphamide. Once remission is achieved, azathioprine or mycophenolate can be used for maintenance

79
Q

What is RCVS?

A

characterized by thunderclap headaches, +/- FND, with vasoconstriction of cerebral arteries that resolve spontaneously within 12 weeks

80
Q

RCVS can occur spontaneously, but what are common precipitating factors?

A

(1) Vasocative drugs: amphetamines, cocaine, cold medicines with decongestants, triptans, ergot alkaloid derivatives, other adrenergic and serotoninergic drugs
(2) triggers: strenuous activity, sexual activity, Valsalva, and/or stressful or emotional situations

81
Q

How is the diagnosis of RCVS confirmed?

A

Noninvasive or cerebral angiography show beading pattern with areas of narrowing and dilatation representing vasoconstriction. The diagnosis is confirmed with the reversibility of angiographic findings, which occur within 12 weeks. Brain biopsy is NOT indicated.

82
Q

Treatment of RCVS?

A

CCB and magnesium sulfate. Inciting factors and drugs should be avoided. Steroids are not indicated (and can worsen clinical course).

Dr. Cheng neuro review Qs (9 decks)

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