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Block 4 PATH Exam -- Cerebrovascular disease


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What is hypoxia?
Decreased OXYGEN supply and/or increased demand relative to supply
How long does neurologic deficit have to persist to qualify as stroke?
> 24 hours
Subarachnoid hemorrhage is often due to rupture of what?
Saccular aneurysm (cortico-meningeal arteries)
Intraparenchymal hemorrhage is often due to what?
Chronic hypertension

If due to trauma, they are commonly delayed (> 24 hrs after trauma)

NOTE: intraventricular extension can be deadly
What is the most common cause of cerebrovascular disease?
Infarction (due to athero. disease of carotid/cerebral arteries)

NOTE: In the U.S. infarction is more common than hemorrhage (10:1)
(In Japan, the ratio is 1:1)
Mnemonic for categorizing etiologic categories of disease

D -- drugs/toxins
I -- infections
G -- genetic/degenerative

I -- immunologic
T -- tumor

T -- trauma
O -- organ failure
M -- mechanical
Breakdown of % of CBF supplied by carotid and vertebral-basilar arteries
Internal carotid -- 70% of CBF
Vertebral-basilar -- 30% of CBF
Embolism to brain is most commonly of what origin?

NOTE: carotids are the next most common source
Embolism is usually assoc. w/ what type of infarction?

Infarction is presumed secondary to reperfusion injury
Thrombosis is usually assoc. w/ what type of infarction?
Bland (non-hemorrhagic) infarction
What is an infarction?
Irreversible tissue necrosis due to prolonged ischemia/hypoxia
How long does cerebral function continue after ischemia?
Only 10 seconds
How long after ischemia does irreversible damage set in?
6 - 8 minutes
Ranking of vulnerability to ischemic damage
(glia vs. neurons vs. vasculature)
Neurons > glia > vasculature
2 regions that are especially vulnerable to global hypoxia/ischemia
CA1 neurons of hippocampus (Sommer's sector)
Purkinje cells of the cerebellum
What is a TIA?
Transient Ischemic Attack

Focal neuro deficit resolving WITHIN 24 hours
What is amaurosis fugax?
Sudden, severe, transient loss of vision in one eye
What is the 2nd leading cause of dementia?
Multiple small, "silent" infarcts

Assoc. w/ HTN
Grossly, what has changed acutley after infarction (4)?
(1 - 2 days after)
Brain is swollen
Gyri are widened
Sulci are narrowed
Gray-white junction is blurred
Grossly, what becomes present sub-acutely after infarction?
(2 - 24 days)
Fluid-filled cysts
(Necrotic tissue has been liquefied and removed)
Grossly, what becomes present chronically after infarction?
(> 24 days)
Gliosis forms a wall around cystic infarcts
Lacunar infarcts often affect what brain structures (3)?
Basal ganglia
Deep white matter
What vessels supply the basal ganglia?
Lenticulostriate arteries
What vessels supply the thalami?
Perforant branches of the PCA
What areas do superficial penetrators provide blood to (2)?
Superficial cortex and deep white matter

NOTE: these are derived from pial branches of major cerebral arteries
What is the typical gross pattern of damage due to a venous infarct?
Bilateral frontal cerebral hemorrhagic necrosis
What are venous infarcts due to?

Where do they often happen?
Due to venous thrombosis

Often happens within dural venous sinuses
Hot spots for plaques (3)?
Bifurcation of carotid artery into external and internal
Origin of MCA
Origin of PCA
Arterial atherosclerotic disease typically affects what type of vessels?
LARGE vessels
Hypertensive vasculopathy usually affects what type of vessels?
SMALL vessels

i.e. deep perforating vessels supplying basal ganglia
(also, supply of deep white matter, and pons)
What is Moyamoya disease?
Progressive stenosis and eventual occlusion of intracerebral arteries
Entails severe intimal fibromuscular dysplasia

A rare, idiopathic condition
Presents w/ "puff of smoke" appearance on angio
What causes the "puff of smoke" appearance of Moyamoya disease?
(appearance on angiogram)
Compensatory dilatation of lenticulostriate arteries
What is the excitotoxic theory of brain injury?
Glutamate causes large Ca and Na influxes
Excessive intracellular Ca causes activation of proteases

BOTH of above lead to activation of pro-apoptotic pathways
Acute neuroprotective responses (4)
Vasodilation (via NO)
Activation of GABA-ergic interneurons
Depletion of extracellular Na and Ca
Activation of anti-apoptotic signaling
Explain how hemorrhagic lesions are ischemic lesions as well
Hemorrhage causes edema
Edema causes increased ICP
Increased ICP lowers perfusion, causing secondary ischemia
What are Charcot-Bouchard aneurysms?

What condition puts you at risk for these?
Microscopic, torturous aneurysms of small vessels

Form in the context of chronic HTN
Common sites of hypertensive hemorrhage (4)
Basal ganglia (60%)
Thalami (20%)
Cerebellum (10%)
Pons (10%)
Hot spots for berry (saccular) aneurysms (4)
Anterior communicating artery
Bifurcation of MCA and internal carotid
Proximal MCA
Origin of PCA from basilar artery

Generally, bifurcations in the Circle of Willis
What part of life do berry aneurysms most commonly rupture in?
5th decade of life
What are ruptured berry aneurysms often described as by patients?
(how is the symptom described?)
"Worst headache of my life"
2 major complications of blood in the subarachnoid space
Acute -- vasospasm, causing secondary ischemia

Chronic -- fibrosis/scarring, leading to obstruction of CSF flow
Where are most AVMs located?
90% are located in superficial cerebral hemispheres
What part of life do AVMs most commonly present in?

How do they present (2)?
Between the ages of 10 and 30

Often present w/ seizures and/or subarachnoid hemorrhage
What are cavernous angiomas commonly described as looking like?
What are cavernous angiomas?
Distended vascular channels w/ thin collagenized walls
Devoid of intervening brain tissue
Where do cavernous angiomas most commonly occur (3)?
Subcortical white matter of cerebral hemispheres
Internal capsule
What is CADASIL?

What pathology does it entail?
Cereb. aut. dom. arteriopathy w/ sub-cort. infarcts & leukoencephalopathy

Cerebral vessels show fibrosis
Media is replaced by EOSINOPHILIC granular material
What is the molecular defect in CADASIL?
(cerebral aut. dom. arteriopathy w/ sub. cort. infarcts and leukoenceph.)
NOTCH 3 mutations
What is MELAS?

What is the molecular defect in it?
Mitochondrial myopathy, encephalopathy, lac acid., and stroke-like episodes

Mitochondrial tRNA mutations
What is CCM?

What does CCM predispose you to?
Cerebral cavernous malformation

Predisposes people to hemorrhagic stroke
What group of people is CCM prominent amongst?
Hispanic Americans
Gene isolated as a candidate for susceptibility to stroke

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