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Neuro | Howard Slides > CNS Vascular Disease > Flashcards

CNS Vascular Disease Flashcards

1
Q

Which vascular structure is damaged in an epidural hematoma?

A

middle meningeal artery

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2
Q

If epidural patient herniates (uncal), what complications can occur?

A

CN III compression causes ipsilateral pupillary dilation and “down and out.”PCA compression causes ischemia of ipsilateral visual cortex and contralateral VF deficitBrainstem compression causes Duret hemorrhageCompression of contralateral cerebral peduncle causes ipsilateral hemiparesis (FALSE LOCALIZING SIGN!)

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3
Q

A sub dural bleed is caused by damage to what structures?

A

The bridging veins draining into the venous sinuses.

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4
Q

Where are Berry aneurysms located?

A

80% in the anterior circulation, 20% in the posterior circulation.

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5
Q

Stroke after SAH is due to what? How is it treated?

A

Vasospasm. Treated with nimodipine, a calcium channel blocker, delivered directly to the site of vasospasm via angiography.

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6
Q

If suspected SAH and CT is normal, what next?

A

LP to detect blood.

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7
Q

What is xanthochromia in CSF?

A

The yellow tinge that occurs 6-12 hours after SAH due to breakdown of RBCs in CSF.

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8
Q

Why does ICH of the cerebellum need emergency neurosurgical intervention?

A

Any mass lesion or swelling of the cerebellum can lead to occlusion of the 4th ventricle and obstruction of CSF, leading to hydrocephalus and death if not treated.

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9
Q

What is the main risk factor of ICH?

A

Hypertension

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10
Q

Diagnosis of elderly patient that suffers repeated ICH in lobes of brain is what?

A

Cerebral amyloidosis

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11
Q

Other causes of ICH

A

Bleeding into an ischemic infarct, bleeding into a tumor, bleeding into intrinsic AVM, bleeding into cavernomas, head trauma

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12
Q

What looks like a “popcorn” mass on imaging?

A

Cavernoma. A malformation made of masses of abnormal vessels without any recognizable intervening neural tissue.

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13
Q

Common locations for ICH

A

Putamen, pons, cerebellum, thalamus

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14
Q

Where is the stroke: contralateral motor/sensory deficits, leg > arm/face

A

Anterior Cerebral Artery

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15
Q

Where is the stroke: frontal lobe behavioral abnormalities, akinetic mutism

A

Anterior Cerebral Artery

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16
Q

Where is the stroke: transcortical motor aphasia (left side), neglect syndrome (right side)

A

ACA

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17
Q

Where is the stroke: urinary incontinence to which the patient is often apathetic

A

ACA

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18
Q

Where is the stroke: contralateral motor/sensory deficits of face/arm > leg, visual field deficits

A

MCA

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19
Q

Where is the stroke: aphasia for left-sided strokes, neglect for right-sided strokes

A

MCA

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20
Q

Where is the stroke: eyes deviate toward the lesion

A

MCA

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21
Q

Where is the stroke: contralateral hemianopsia (visual field deficit)

A

MCA

22
Q

Where is the stroke: contralateral hemianopsia, alexia without agraphia for left-sided strokes. Patients may be unaware of the visual field loss, or perceive it as coming from only one eye

A

PCA

23
Q

Where is the stroke: large lesions may cause contralateral motor/sensory deficits

A

PCA

24
Q

Common locations of lacunar strokes:

A

sub-cortical white matter, cerebellum, thalamus, pons, internal capsule, basal ganglia

25
Q

Pure motor lacunar stroke localizes where?

A

Internal capsule

26
Q

Pure sensory lacunar stroke localizes where?

A

Thalamus

27
Q

Other clinical presentations of lacunar stroke:

A

Ataxic hemiparesis, clumsy-hand/dysarthria

28
Q

In brainstem strokes, on which sides do you find cranial nerve findings and motor/sensory findings?

A

Cranial nerve ipsilateral; motor/sensory contralateral

29
Q

What are typical signs and symptoms of brainstem disease?

A

dizziness, vertigo, ataxia, nausea, imbalance, double vision, nystagmus, dysarthria, and dysphagia

30
Q

What is Wallenberg (lateral medullary) syndrome and what are features of it?

A

Due to occlusion of the vertebral artery or the posterior inferior cerebellar artery. Dysphagia, hoarseness, dizziness, n/v, nystagmus, balance/gait coordination, intractable hiccups. Loss of contralateral body pain/temp and ipsilateral face. Horner’s syndrome.

31
Q

Presentation of lateral cerebellar strokes:

A

ataxia of ipsilateral arm/leg

32
Q

Presentation of medial cerebellar strokes:

A

axial muscle symptoms and gait and balance problems

33
Q

3-5 days after cerebellar stroke there is a risk for what?

A

Swelling peaks, risk for hydrocephalus due to occlusion of 4th ventricle.

34
Q

What presents as “man in a barrel?”

A

A watershed stroke in the overlap of ACA/MCA, proximal arm/leg weakness with preservation of distal strength.

35
Q

Cord sign and delta sign on imaging is what? Treat how?

A

Sinus venous thrombosis. Give heparin, despite bleeding.

36
Q

Curtain coming down over one eye:

A

Amaurosis fugax - temporary central retinal artery occlusion

37
Q

Where is the lesion in locked-in syndrome?

A

Aware and awake but can only move the eyes. Lesion in the ventral pons, either ischemic or hemorrhagic.

38
Q

What is the “dense MCA” sign?

A

On CT, a massive stroke may be normal for hours, though a clot within the affected vessel may be seen (dense MCA sign).

39
Q

What 2 things appear bright on non-contrast CTs?

A

Blood and calcium

40
Q

When is tPA contraindicated?

A

In patients with minor or rapidly resolving deficits, blood glucose < 50, recent trauma/surgery, hemorrhage, BP > 185/1120, INR > 1.7, or platelets < 100K

41
Q

T1 MRI

A

White matter is white; gray matter is gray; CSF is dark

42
Q

T2 MRI

A

White matter is gray; gray matter is white, CSF is bright

43
Q

FLAIR MRI

A

Same as T2, but CSF signal is voided (dark)

44
Q

CADASIL

A

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy. Presents with migraines, dementia, and multiple lacunar strokes.

45
Q

MELAS

A

Mitochondrial encephalopathy with lactic acidoses and stroke. Maternal inheritance, mitochondrial disorder, stroke-like episodes often in the occipital region. Presents with seizures and dementia in adolescence.

46
Q

Autosomal recessive disease in AA population, increases stroke incidence.

A

Sickle-cell disease

47
Q

What is the treatment of choice for stroke patients not eligible for tPA that has been shown to reduce mortality if given acutely?

A

Aspirin

48
Q

Antiplatelet agents used in stroke:

A

ASA, ASA/dipyridamole (aggrenox), Clopidogrel

49
Q

Anticoagulants used in stroke:

A

Dabigatran (Pradaxa) or Warfarin

50
Q

What is the 90-day stroke risk in TIA?

A

nearly 20%

51
Q

Inherited coagulation cascade disorders, most of which present with strokes before age 30, causing venous infarctions:

A

antithrombin II deficiency, protein C/S deficiency, factor V Leiden mutation, and prothrombin gene mutation.

Neuro | Howard Slides (9 decks)

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