Neuropath Flashcards
“watershed areas” of brain
areas of brain w/ little direct blood supply, but with potential collateral supply close by
(border areas btwn major supplying arteries).
–> could recruit collaterals if slow occlusive process, but 1st to become ischemic w/ acute occlusion.
Causes of cerebrovascular events (3)
(cerebrovascular event = stroke)
- Local vascular occlusion –> ischemia
- systemic hypoperfusion w/ O2 (hypoxemia)
- hemorrhage
Relative importance of vessels in cerebral circulation
- major (proximal) arteries = most important & most likely to get atherosclerosis.
- distal arteries/capillaries = less likely to be occluded; may spasm.
- venous circulation = least devastating w/ cerebrovascular events.
most common causes of arterial cerebral infarction
#1 & 2: embolism and thrombosis. Also: arterial dissection, HTN vasculopathy, arterial spasm/compression, decreased perfusion (systemically) --> watershed areas.
Atherosclerosis & cerebral infarction
- mostly in proximal arteries (internal carotids, MCA, vertebral aa, basilar a., etc.)
–> cause large areas of pale/non-hemorrhagic ischemia
(pale bc no reperfusion).
disease states causing cerebral thrombosis
- bc get hypercoagulable! **
1. Vasculitis (polyarteritis nodosa, etc.)- vasculopathy (SLE)
- granulomatous –> infectious, primary CNS…
- blood abnormalities (sickle cell, thrombocytopenia)
- bc get hypercoagulable! **
Characteristics of Embolic cerebrovascular infarction
–> hemorrhage, esp. petechial hemorrhage from damaged vessels (leak when reperfused)
Sources: heart or vasculature, small if not from atherosclerosis
transient ischemic attack(s) (“TIA”)
= small, temporary CNS artery occlusions, Sx last < 1 hr.
- -> may be symptomatic if affect important area, or asymptomatic.
- indicate increased risk of full stroke in (near) future!
arterial dissection & stroke
- Usually in younger ppl (NOT normal age demographic for stroke).
= false lumen forming in vessel wall –> blood redirects & compresses actual lumen => lose normal perfusion.
** esp. in trauma or chiropractic patients **
lacunar infarctions
small infarction (< 1.5 cm) caused by hypertension;
= abrupt change from large diameter vessel to small diameter vessel exacerbated by high P ==> low perfusion.
** may be asymptomatic OR symptomatic.
– Binswager Disease (dementia) = severe complication!
Pathology of Binswanger Disease
= dementia caused by Lacunar stroke.
HTN –> changes in vasculature (promotes hyaline membranes in vessel walls)
–> rarefraction of white matter –> dementia.
causes of mechanical occlusion – causing stroke/cerebral ischemia
(2)
- vasospasm (usually after subarachnoid hemorrhage)
2. uncal herniation (from increased ICP)
Types of watershed infarcts
- ACA-MCA boundary zone –> serious consequences!
2. SCA - PICA boundary –> typically asymptomatic.
Areas of selective susceptibility to ischemia
- Globus Pallidus (esp. w/ CO poisoning)
- hippocampus CA1
- Purkinje cells of cerebellum – usually die even despite person’s survival of stroke –> lasting symptoms.
consequences of global cerebral ischemia
(usually after severe hypotension or cardiac arrest)
– massive necrosis = poor/no survival (ie: not unless on ventilator) bc continue to infarct brain after initial damage.
Pathological changes from cerebral infarction
- Early stage (1-2 days): neuron death (eosinophilia and nucleus shrinks) + neutrophil infiltration
- Subacute stage (1-2 weeks): liquefactive necrosis, BBB breaks down, macrophage infiltration (to remove necrotic debris)
- astrocytosis & cavitation
- long term/resolution: Disappearance of brain tissue (NO fibrosis), degeneration of proximal/distal components of the neural tract.
characteristics of venous cerebral infarction
Causes: hypercoagulable states (pregnancy, etc.) –> thrombosis;
= VERY hemorrhagic, w/ deeper damage than arterial.
most common cause of subarachnoid hemorrhage
= ruptured saccular aneurysm
- --> diffuse, very bloody hemorrhage (difficult to localize) * *risk clot pressure causing secondary intracerebral hemorrhage! (dissection into parenchyma)
Common causes of intracerebral hemorrhage
- vascular malformations, hypertension
- tumors, trauma
- blood abnormalities (–> multifocal hemorrhage)
- mycotic aneurysms, amyloid angiopathies
most common sites for cerebral saccular aneurysms
1: Internal Cerebral a.
- MCA, AVA
- Basilar a.
Hypertensive Intracerebral hemorrhage
in very poorly controlled HTN, affects lenticulostriate arteries;
= caused by fibrinoid necrosis/degeneration of vessels.
–> often catastrophic damage, esp. to basal ganglia.
(difficult to surgically treat, may result in lasting paralysis if survive)
pathophysiology of arteriovascular malformations –> stroke.
make arteriovenous shunt(s) –> vessel walls thicken & rupture w/ high pressure.
- usually fatal if rupture!
- can also cause seizures (more likely to survive)
Amyoid angiopathy
amyloid build up in cerebral vessels –> can cause hemorrhage;
- may have amyloid pathology w/Out symptoms yet!
- this hemorrhage not AS fatal as AV malformations.
pathological mech for stroke from mycotic aneurysm
infection weakens vessel wall –> aneurysm + more weakening –> rupture = hemorrhage.
