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CNS > Prayson Vascular > Flashcards

Prayson Vascular Flashcards

1
Q

Carbon Monoxide

A

Bright pink edematous brain, necrosis of globus pallidus and substantia nigra, may show Grenker’s myelinopathy: demyelination and cerebral white matter destruction. Form of anemic/hypoxemic anoxia

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2
Q

Air embolism

A

spinal cord microinfarcts, “the bends” and cardiac bypass

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3
Q

Hypoglycemic damage

A

selective neuronal necrosis in superficial layers of the cortex, hippocampus (CA1 and dentate), and caudate. NO purkinje cell necrosis

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4
Q

Most common sites of venous thrombosis

A

Superior saggital sinus, lateral sinuses, and straight sinus

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5
Q

Most common site of Septic thrombosis

A

Cavernous sinus, ususally 2/2 contiguous spread from sinus/soft tissue infection

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6
Q

Berry aneurysm, how many bilateral / multiple?

A

Defective media and gap in internal elastic lamina85% occur in the circle of willis, 25% multiple, 20% bilateral. Most common sites: MCA trifurcation, anterior communicating and ACA jxn, Internal carotid-posterior communicating jxn

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7
Q

Berry aneurysm rupture risk

A

50% in aneurysms > 1cm

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8
Q

Berry aneurysm associations

A

Polycystic kidney, Ehlers-Danlos, NF1, coarctation of the aorta, fibromuscular dysplasia, Marfan’s, pseudoxanthoma elasticum

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9
Q

Wyburn-Mason synd

A

multiple AVMs, predominantly affecting brain (particularly midbrain), optic nerve/ retina, and face

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10
Q

AVM

A

Most supratentorial, superficial wedge-shaped w/ apex toward the ventricle, usually in MCA distribution, most common vascular association w/ hemorrhage. 4% of people have multiple. Most common vascular malformation and most common to casue hemorrhage. 2nd most common cause of SAH (after berry aneurysm)

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11
Q

Foix-Alajouanine synd (angiodysgenetic myelomalacia)

A

spinal cord A-V fistula/vascular malformation with thrombosis causing infarction and progressive myelopathy (areflexic parapersis, sensory disturbance, bladd, bowel, and sexual dysfxn) in middle aged men. Vessels with no internal elastic lamina which may be mineralized.

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12
Q

Cavernous malformation

A

Most supratentorial, CCM gene mutations. Seen on MRI, not angiography. Presents w/ siezures. Assoc w/ hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu)

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13
Q

Polyarteritis nodosa (PAN)

A

Necrotizing vasculitis with fibrinoid necrosis of small to medium sized vessels. M>F, 40-50 yoa, systemic (except lungs and spleen). CNS invloved in 60-80%

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14
Q

Wegner’s granulomatosis

A

Necrotizing granulomatous inflammation, cANCA directed agains proteinase 3, 40-60 yoa, systemic w/ respiratory component. Respiratory tract +/- glomerulonephritis. CNS effect in 20-40% of cases.

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15
Q

Giant cell arteritis

A

Granulomatous lymphoplasmacytic, Assoc. w/ polymyalgia rhuematica, F>M, >50yoa

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16
Q

Takayasu’s arteritis

A

Transmural granulomatous and lymphoplasmacytic inflammation of the media w/ fibrosis. Aorotic arch and descending aorta, younger (15-40 yoa) asian females

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17
Q

Churg-Stauss

A

necrotizing vasculitis with esoinophilia w/ fibrinoid necrosis in medium arteries, capillaries, and venules. Lung involvement

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18
Q

Primary angiitis of the CNS (PACNS)

A

M>F, 30-50 yoa, Leptomeninges is highest yeild area (bx temporal tip of non-dominant lobe leptomenignes, cortex and white matter), affetcts small and medium sized arteries, may be granulomatous.

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19
Q

what vasculitides typically involve the brain parencyma

A

Lupus and lymphomatoid granulomatosis

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20
Q

What vasculitides involve the vessels of the subrachnoid space, PNS, and extracranial vessels

A

PAN, Wegner’s granulomatosis, and giant cell arteritis

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21
Q

Binswanger’s (aka subcortical arterioclerotic encephalopathy)

A

5-60 yoa, evolves over 3-5 years. Intermittent HTN and stepwise/ progressive profound dementia (memory, mood and cognition). Widespread, vascular alterations and white matter changes, ventricular dilation, focal and diffuse myelin loss and astrocytosis in deep white matter most severe in temporal and occipital lobes. sparing of subarcuate U-fibers

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22
Q

CADASIL (Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencepholapathy)

A

NOTCH3 gene (EGFR), Slowly progressive (15-25 yr) strokes and dementia. Thickined vessels (media and adventicia) w/ basophilic PAS+ granules within smooth muscle. GRANULAR OSMIOPHILIC MATERIAL. Cortical and subcortical atrophy, astrocytosis, and lacunar infarcts/foci of encephalomalacia. Onset 45 yoa, systemic (can dectect osmophilic material by skin bx)

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23
Q

Charcot-Bouchard microaneurysms

A

aka miliary aneurysms, chronic HTN, dilations/ outpouchings 2/2 fibrinoid change and fragmentation of IEL. Usually basal ganglia and pons. Also seen in CAA and CADASIL

24
Q

Moyamoya Synd

A

Occlusion of the internal carotid, PCA, or Pcom arteries with the development of abnormal collateralization (dilation of lenticulostriate arteries), thrombus and intimal fibroplasia w/out atherosclerosis or inflammation. Hemiparesis and hemorrhage. Most pt.s <20 yoa, F>M

25
Q

Regions most vulnerable to ischemia in adults

A

Hippocampus (CA1), cerebral cortex (layers 3 and 5), purkinje cells, thalamus, basal ganglia, brainstem, hypothalamus, and spinal cord

26
Q

Regions most vulnerabtle to ischemia in infants

A

Thalamus, hippocampus, colliculi

27
Q

Cystic necrosis of globus pallidus

A

Carbon monoxide, cyanide, heroin overdose, global hypoxia/ischemia

28
Q

Red neurons occur when

A

First seen after survival for 4-6 hours and last for 2 weeks

29
Q

MELAS (mitochondrial encephalomyopathy, lactic acidosis, and stroke)

A

Infarct like lesions that don’t conform to vascular teritories. Muscle bx: Ragged red fibers with mitochondrial cytopathy. Due to several mutations in mitochondrial DNA leading to defective oxidative metabolism.

30
Q

Hereditary Hemorrhagic Telangiectasia (Osler-Webber-Rendu)

A

Vascular dysplasia and recurrent hemorrhages, AVMs, endoglin and ACVRL1 genes

31
Q

Doliechoectasia

A

Vertebral and basilar arteries, Increased diameter w/ fibrosis and degeneration of the internal elastic lamina. Can progress to fusiform aneuyrism, may casue compression of adjacent structures (hydrocephalus, CN palsy). Assoc w/ Fabry’s dx

32
Q

Large vessel vasculitidies

A

Giant cell arteritis and Takayasus

33
Q

Hemorrhagic conditons

A

Arteriosclerosis/arteriolosclerosis, lipohyalinosis, cerebral amyloid angiopathy

34
Q

Ischemic conditions

A

Vasculitis/angitis

35
Q

Infectious agents that cause CNS angiitis

A

HIV, CMV, VZV, Hep C, syphillis, Borrelia burgdorferi, TB, fungi

36
Q

CARASIL (Cerebral autosomal recessive arteriopathy with subcortical infarcts and leukoencephalopathy)

A

(aka MAEDA sydn) Mutations in HTRA1, very rare, Japan. 29-50 yoa, presenile dementia, alopecia, spondylosis, white matter infarcts, athero/arteriosclerotic changes

37
Q

Retinal vasculopathy and Cerebral Leukodystrophy (HERNS, cerebroretinal vascuolpathy, and hereditary vascular retinopathy)

A

Obliterative vasculopathy, mutations in TREX1. HERNS (hereditary endotheliopathy with retionpathy, nephropathy, and stroke): Lareas of ischemic necrosis and small unusual angiomatoid formations surrounded by calcifications. Visual impairment and dementia

38
Q

TREX1 mutations

A

Aicardi-Goutieres synd, HERNS/retinal vasculopathy with cerebral leukodystrophy, SLE, familial chilblain lupus

39
Q

COL4A1 mutations

A

vascuolpathy (affects small cerebral arteries and causes berry aneurysms), familal porenecephaly, hereditary angiopathy with nephropathy, aneurysms, and muscle cramps.

40
Q

MCA infarct

A

hemiparesis or complete hemiplegia, (face and arm, often leg), aphasia (if dominant hemisphere), hemisensory disturbance

41
Q

ACA infarct

A

Hemiparesis (leg consistently possibly face and arms), transcortical motor aphasia (halting speech), abulia (absence of willpower)

42
Q

PCA infarct

A

thalamic pain synd., hemianopia (cortical blindness if bilateral), and alexia (word blindness/can’t read, if dominant hemisphere)

43
Q

Date the infarct: red neurons, vacuolization of neuropil

A

1-4 days

44
Q

Date the infarct: endothelial proliferation and neovascularization, neutrophils around necrotic vessel, microglial activiation, and macs

A

5-12 days

45
Q

Date the infarct: neuronla ghosts, foamy macs, gliosis, neutrophils around necrotic vessel, microglial activiation

A

8-14 days

46
Q

Date the infarct: no red neurons, necrotic white matter w/ macs, axonal spheroids, early wallerian degen in non-infarcted white matter

A

15-30 days

47
Q

Epidural hemorrhage

A

Almost always caused by trauma, middle meningeal artery, lucid interval, temporal in adults, posterior in peds, () shape. Microscopic: usually only difuse axonal injury. 75-100 ml is fatal, Less common than subdural

48
Q

Subdural Hemorrhage

A

Concave (between dura and brain), bridging veins. Truama or spontaneous- can be acute or chronic (elderly)

49
Q

Subarachnoid hemorrhage

A

between arachnoid and pia, spontaneous or traumatic. Berry aneurysm is most common cause, also mycotic aneurysm, fusiform aneurysm

50
Q

Basis pontis hemorrhage

A

Locked in syndrome

51
Q

Thalamic hemorrhage

A

Hemiparesis, hemisensory loss, gaze abn, vomitting

52
Q

Cerebellar hemorrhage

A

Vomiting, HA, Tuncal/limb ataxia, cranial nerve abn, coma

53
Q

Large intrapontine hemorrhage

A

Coma, quadraplegia, small reactive pupils

54
Q

small intrapontine hemorrhage

A

gaze paresis, ataxia, contralateral sensorimotor defecit

55
Q

Putaminal hemorrhage

A

Hemiparesis, hemisensory loss, visual field deficits

56
Q

Cerebral Amyloid Angiopathy

A

APOE4, APOE2
Familial (ususally autosomal dominant):
HCHWA- Dutch type: mutation in APP, severe dementia, rare NFTs and plaques
Hereditary Cystatin C AA (HCHWA- Icelandic type): Mutation in cystatin C, young and middle aged adults, hemorrhage often lobar and fatal, no AD changes

57
Q

Capillary telangiectasia

A

Usually pons, vessels are smaller and have thinner walls than venous angioma, usually asymptomatic

CNS (17 decks)

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