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13 Cards in this Set

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CNS Vascular Disease
Name the 4 causes of obstruction of cerebral blood flow leading to ischemic/hypoxic/infarction
1) Arteriosclerosis/thrombosis (TIA)
2) Embolization from remote site
3) Venous thrombosis
4) Non occlusive necrosis (shock and brain death)
CNS Vascular Disease
Name the 5 causes rupture of cerebral vessels with of hemmorrhage
1) Hypertension
2) Saccular Aneurysm
3) Vascular Malformations
4) Cerebral amyloid angiopathy (CAA)
5) Bleeding dyscrasias
TIA
-Location
-What happens
-Treatment
-As a warning sign
-Arises from atheromas disrupting endothelial surface triggering thrombus formation

-typically in the vertebral and internal carotid arteries

-Shower of dislodged emboli into downstream arteries

-Treat with anticoagulants or carotid endarectomy

-SOS for impending thrombosis
Arteriosclerosis/thrombosis
-Vessel/tissue distribution
-Infarct size, number and type
-Infarcted tissue pathology
-Life threatening component
-Collateral circulation effects
-Usually affected tissue is confined to the territory supplied by large arterial vessels such as those in the C.O.W.

-Single, larger, pale infarcts from a "slow" occlusion

-Tissue is soft and swollen from necrosis and edema.

-Increasing edema over 7-10 days increases dysfunction and is a major cause of death.

-Severity dependent on collateral circulation
Infarction due to Embolization
-Vessel/tissue distribution
-Infarct size, number and type
-Infarcted tissue pathology
-Embolus from distant source such as heart valves lodge in bifurcations of mid sized distal arteries such as MCA

-Multiple, often bilateral sudden, hemmorhagic infarcts

-Tissue necrosis precedes edema contributes to hemorrhagic component. Multiple hemmorhages from small vessels are seen, distinguishing it from a hematoma.
???Infarction due to Venous thrombosis???
-Usually occurs during a hypercoagulative state
Non occlusive necrosis
*Watershed infarcts
-Cause
-Vessel/tissue distribution
*Watershed infarcts
-hypotension-->shock
-Occur in the vulnerable areas between the terminal distribution of distal arteries.

Ex: ACA/MCA watershed in the superior-lateral surface of the frontal lobes.
Non occlusive necrosis
*Brain death (respirator brain)
-Cause
-Vessel/tissue distribution
*Brain death (respirator brain)

-increased intracranial pressure (edema) causing cessation of blood flow to cerebrum

-Leads to diffuse hemispheric necrosis but brainstem is intact
Hypertensive Hemorrhage
-Cause
-Vessel/tissue distribution
-Microscopic appearance
-Hypertension leads to arteriosclerosis and weaking of microvasculature. Hemmorhage often expands

-75% occurs in the striatum. Can also occur in the cerebellum and pons. Can cause lacunar infarcts as well.

-The hematoma is well delineated from the parenchyma, distinguishing it from a hemorragic infarct.
Sacular/Berry Anneurysms
-Epidemiology
-Cause
-Vessel/tissue distribution
-Vasospasm complication
-Treatment
-sudden onset w/ no prodrome in 30 to 50 year olds

-massive subarachnoid hemmorhage b/c of defects in internal elastica/muscle

-Ruptures at arterial branching points, mainly in the anterior circulation ie: circle of willis, often the PComm and AComm aa.

-Vasospasm of neighboring arteries can lead to infarction in their distribution

-Early intervention has a bad prognosis and surgical clips are usually delayed.
CNS Vascular Malformations
-3 types
-cappillary telangiectasias are asymptomatic, venous angiomas are related to epilepsy, AVM's are related to hemmorhage
AVM associated hemmorhages
-Epidemiology
-Vessel/tissue distribution
-AVM's usually don't become apparent until adulthood. Account for 5-10% of spontaneous subarachnoid hemorrhage

-Usually extend from subarachnoid space into the underlying tissue
-80% supratentorial, but can also be in the brainstem
Cerbral Amyloid Angiopathy
-Epidemiology
-Cause
-Vessel/tissue distribution
-Microscopic examination
-Associated with Alzheimers; causes 20% of cerebral hemorrhage in the elderly

-Caused by beta-amyloid deposits in superficial small vessels of the cortex.

-Hemmorhages tend to be cortical/subcortical and may extend to subarachnoid space.

-Microscopic examination reveals hyalinized small vessels and thioflavin/congo red stained Beta-amyloid deposits.