Glossary of 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
- DIG IT TOM
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
- Where does laminar necrosis tend to occur?
- In cortical gray matter
Due to watershed effect @ anastamoses of pial penetrators and deep vessels
- 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%)
- Hot spots for berry (saccular) aneurysms (4)
- Anterior communicating artery
Bifurcation of MCA and internal carotid
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
- 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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