8.8 Cerebrovascular Disease Flashcards
- due to cardiac arrest, hypotension, suffocation, posisoning
- neurons most vulnerable, can occur in watershed areas
- CA1 of hippocampal formation, purkinje cells, pyramidal neurons
global ischemia
12-24 hours after ischmia, microscopically see?
red neurons, microvacuolization, nuclear pyknosis
12-48 hours after ischemia, microscopically see?
neutrophils
48 hours to 2 weeks after ischemia, microscopically see?
macrophages, necrosis
1 week to months after ischmia, microscopically see?
astrocytic proliferation
chronic damage after ischemia, microscopically see?
glial scar, cyst, Wallerian degeneration
gross changes in brain 48 hours after ischemia?
pale, soft, swollen
gross changes 2-10 days after ischemia?
friable, demarcation
gross changes 10-21 days after ischemia?
liquefaction
in situ blood clot, majority due to atherosclerosis and plaque rupture, common sites are carotid bifurcation, MCA, and top/bottom of basilar artery
thrombosis
mural thrombosis, valves, a. fib, carotid arteries, paradoxical, or fat/tumor/air
- lodge in branchpoints, mostly MCA
- petechial hemorrhages upon reperfusion
emboli
- rigid encasement of brain or spinal cord
- can be vasogenic, cytotoxic, or interstitial
- due to tumor/infarct/hemorrhage/abscess/difffuse axonal injury
cerebral edema
unilateral or asymmetric expansion of cerebral hemisphere displaces the cingulate gyrus under the falx, compresses ACA
subfalcine (cingulate) herniation
medial aspect of temporal lobe is compressed against free margin of tentorium, CN III compression, PCA compression and occipital lobe infarct, midbrain and pons duret hemorrhage
transtentorial (uncal) herniation
displacement of cerebellar tonsils through foramen magnum, brainstem compression compromising vital respiratory and cardiac centers in medulla
cerebellar tonsillar herniation
CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy) due to mutation in _________, leads to dementia, depression, migraine w/ aura, and recurrent stroke
NOTCH3
in CADASIL, the MRI shows ________ changes, and skin shows _________ changes and concentric thickening of media
white matter, basophilic PAS deposits
arteriolar sclerosis due to HTN in deep nuclei, white matter, and brainstem; get lacunes in putamen, globus pallidus, deep white matter, caudate and pons
hypertensive CV disease
-commonly due to HTN, leading to accelerated atherosclerosis, hyaline arteriolarsclerosis, and Charcot Bouchard aneurysms
intraparenchymal hemorrhage
- lobar hemorrhages
- amyloid peptides deposited in walls of small vessels
- stains with Congo red
cerebral amyloid angiopathy
tangled network of wormlike vascular channels, prominent pulstile AV shunting with high blood flow
AV malformation
distended, loosely organized vascular channels arranged back to back with collagenized walls of variable thickness and no brain parenchyma b/w vessels
-low flow channels, foci of old hemorrhage, infarction, and calcification
cavernous angioma
-microscopic, thin walled vascular channels separated by relatively normal brain parenchyma, usually in pons
capillary telangiectasia
rupture of a saccular berry aneurysm in a cerebral artery, near major arteriolar branch point in anterior circulation (ACA and MCA)
- associated with ADPKD, NF1, marfan, ehler danlos
- risks: smoking and HTN
subarachnoid hemorrhage
middle meningeal artery tear due to temporal skull fracture, extravasation of blood under arterial pressure can cause dura to separate from inner surface of skull, compression of brain
epidural hematoma
- subdural space lies between the inner surface of dura and outer arachnoid layer
- bridging veins tear at any place they meet the dura
- lysis of clot in 1 week, growth of fibroblasts from dural surface into hematoma, development of hyalinized connective tissue
subdural hematoma
