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Cerebrovascular Disease Pathology

Terms in this set (57)

limiting factor to neuron function
OXYGEN
how much of the total oxygen in the body does the brain use
20%
homeostatic mechanisms maintain cerebral blood flow regardless of...
CNS and blood pressure
Cerebrovascular disease
1. prevalence
2. death rate
3. lay term
1. most prevalent of the CNS disorders and diseases
2. third leading cause of death in the US
3. stroke
Any vascular disorder with acute onset and permanent neurologic sequelae
stroke
non-traumatic hemorrhages are related to
hypertension, vascular abnormalities
hypoxia, ischemia, and infarctions cause..
global or focal, thrombotic or embolic, symptoms related to area of CNS affected
hypoxia
causes of hypoxia
low partial pressure of oxygen
high altitude, lung disease, anemia, CO poisoning
ischemia
causes of ischemia
decreased/interrupted blood flow
decreases oxygen tension, increases CO2 and acidosis, decreased nutrients
infarction
irreversible tissue damage (necrosis) due to variations in blood flow or severe hypoxemia
most ischemia sensitive CNS cells
neurons
what areas would you find ischemic affected neurons (2)
sommer section of Hippocampus, purkinje cells of cerebellum
how long can neurons withstand ischemia
3-4 minutes
Diffuse Ischemic/hypoxic encephalopathy
1. cause
2. diseases causing this
3. clinical presentation (transcient)
4. clinical presentation (persistent)
1. generalized reduction in CNS perfusion or severe hypoxia
2. severe hypotension***, cardiopulmonary arrest, CO poisoning, severe anemia
3. post-ischemic confusional state with complete recovery
4. severe, diffuse neurologic injury (infarction) --brain death, vegetative state
CNS infarction
1. first change seen
2. second change seen
3. third change seen
4. pattern seen with infarction
1. red neurons requires 12-24 hours of survival
2. subacute changes (24 hr - 2 wks), extensive necrosis and inflammation with phagocytosis
3. repair (2 wks onward) - gliosis, removal of necrotic tissue
4. psudolaminar necrosis due to variable neuron death in the layers of the gray matter
Common site of infarction in the CNS
Border zone (watershed) infarcts
1. description
2. location
3. cause
1. infarcts at junctional zones between arterial distributions
2. mainly between ACA and MCA, sometimes in the spinal cord
3. generalized perfusion deficits (hypotension)
Focal CNS ischemia
1. causes
2. rare causes
3. clinical presentation
4. severity
1. arterial thrombosis or embolism
2. vascular compression due to mass effect or herniation, arterial dissections
3. infarcts of the cerebellum, cerebrum, brain stem, spinal cord
4. depends on collateral flow, amount of tissue by involved vessel, etc.
Thrombotic Infarctions
1. class
2. disease causing this
3. associated diseases
4. clinical presentation
1. Focal CNS ischemia with necrosis -CNS infarction
2. most commonly artherosclerosis disease due to plaque rupture
3. hypertension, diabetes
4. tend toward slower onset, may be associated with prior transcient ischemic attacks

Single major vessel seldom causes infarct because of collateral circulation
uncommon causes of thrombotic infarctions
infectious vasculitis, non-infectious vasculitis, hypercoagulable states
Transcient ischemic attacks
1. description
2. how long do they last
3. location
4. cause
1. episode of transcient neurologic dysfunction without infarction of parenchymal tissues (no permanent residual effect)
2. minutes up to 24 hours
3. brain, spinal cord, or retina
4. ischemia and same etiology as ischemic infarcts


These make you at risk for future infarctions***
Reversible ischemic neurologic deficit or RIND
longer episodes of transcient ischemic attacks
Embolic infarction
1. class
2. causes (7)
1. focal CNS ischemia with necrosis - CNS infarctions
2.
--atherosclerosis (from carotid plaques)
--cardiac abnormalities (mural thrombi, endocarditis)
--Fat emboli (fracture)
--Tumor emboli
--Iatrogenic materials (doctors messed up)
--air emboli
--amniotic fluid emboli
Embolic infarction
1. class
2. clinical pattern
3. location
4. when would a patient show up?
1. Focal CNS ischemia with necrosis -CNS infarction
2. lodged at bifurcation points, fat/bone marrow emboli shower and cause generalized CNS dysfunction
3. middle cerebral artery (b/c it's directly from the IJ)
4. sudden in onset, bilateral, CSF may be bloody
Focal CNS ischemia with necrosis -CNS infarctions
1. gross pathology findings
1. same as global ischemia, but FOCAL
Hemorrhagic and anemic infarcts
Hemorrhagic (red) infarct
embolic infarction with reperfusion resulting in bleeding
Anemic (bland) infarct
thrombotic infarction with no reperfusion
How would you treat hemorrhagic and anemic infarcts differently
Imaging studies to distinguish them.
anti-coagulation therapy for ischemic infarcts, but not in hemorrhagic infarcts
6 microscopic changes for focal CNS ischemia with necrosis
1. ischemic changes - red neurons, edema
2. liquifactive necrosis with neutrophils
3. "gitter cells" of microglia
4. astrocytic gliosis
5. hemosiderin deposition in hemorrhagic infarctions
6. cyst formation
Venous cerebrovascular infarcts
1. class
2. prevalence
3. when do these show up
4. cause
5. nature of the infarct
1. focal CNS ischemia with necrosis
2. rare, less than 1% of strokes
3. females, up to 50% in pregnancy
4. venous thrombosis from occlusion of venous sinus or cortical vein
5. hemorrhagic
risk factors for venous cerebrovascular infarcts
oral contraceptives, pregnancy, cyanotic congenital heart disease, dehydration, neoplasia, hematologic disease, hypercoagulable states
Spinal cord infarctions
1. class
2. prevalence
3. cause
4. symptoms
1. focal CNS ischemia with necrosis
2. less common than cerebral infarctions
3. hypoperfusion or interruption of feeder vessels from aorta
4. depends on location in cord (EX:surfer's myelopathy)
Cerebral incomplete infarction
RARE focal ischemia with relative sparing of glia and vessels --just lose the neurons
Multi-infarct (vascular) dementia
1. description
2. associated with
3. note
4. clinical presentation
1. multiple, bilateral infarcts are seen
2. cerebral atherosclerosis, embolization from carotids or heart, hypertension diseases
3. may complicate and worsen other forms of dementia
4. dementia in step like manner, gait issues, pseudobulbar signs (facial movement), focal neurologic signs
Binswanger disease
1. description
2. pattern
1. sub-set of vascular dementia
2. preferentially involves large areas of subcortical white matter with myelin and axon loss
Intracerebral (intraparenchymal) hemorrhage
1. cause
2. peak age
3. description
4. size
1. non-traumatic by nature
2. peak at 60 years
3. diffuse extravasation into the neural parenchyma defines this type
4. very large!!!! (25-80% of hemisphere in nonvascular dstribution)
Intracerebral (intraparenchymal) hemorrhage
1. gross view
2. may cause
1. hemorrhage may extend into ventricles --see blood tinged CSF with increased RBC count
later have discolored CSF (xanthochromia) minus the RBC
2. herniation
Intracerebral (intraparenchymal) hemorrhage
1. two types
2. locations
3. micro
4. cause
1. ganglionic (basal ganglia or thalamus), versus lobar (cerebral hemisphere)
2. 55% Putamen
15% cerebral cortex
thalamus, pons 10%
3. clotted blood with anoxic neurons/edema, influx of macrophages that digest RBC, hemosiderin end result
4. hypertension for 50%
cause of death in 15% of chronic hypertensives
most common location for hypertensive bleeds
deep white and gray matter, then brainstem and cerebellum
Charcot-Bouchard microaneurysms (<300um)
1. class
2. location
3. lesion location
1. intracerebral hemorrhage
2. basal ganglia
3. cerebral hemorrhage is common site
other causes of intracerebral hemorrhage (5)
neoplasms, amyloid angiopathy, drug abuse, infections, hereditary disorders
Cerebral amyloid angiopathy
1. description
2. cause
3. class
4. association
1. amyloid deposited in medium and small vessels of cerebral cortex and meninges
2. vessel walls weakened by amyloid, predisposing to numerous small bleeds
3. intracerebral hemorrhage
4. alzheimer's and Apo E ...familial forms
CADASIL
1. class
2. full name
3. description
4. gene mutation
1. intracerebral hemorrhage
2. cerebral autosomal-dominant arteriopathy with subcortical infarcts and leukoencephalopathy
3. hereditary form of strokes with recurrent infarcts and sometimes development of dementia
4. notch 3 gene
Subarachnoid hemorrhage
1. description
2. cause
3. less common causes
4. gross exam
1. bleeding into subarachnoid space
2. ruptured saccular (berry) aneurysms (85%)
3. trauma, ventricular bleeding
4. hemorrhagic CSF with RBC's acutely.. later CSF displays xanthochromia
saccular aneurysms
1. description
2. cause
3. risk factors
4. rupture
5. what alerts you of this
1. seen in 2-3% of autopsies
frequently multiple (20-30%)
occur at bifurcation sites in cerebral circulation
2. can be congenital or acquired.. some genetic predispositions are Ehler Danlos and Marfan's
3. cigarette smoking and hypertension in 54% of patients
4. entire subarachnoid space filled with blood, may cause purely intraparenchymal hemorrhage(depends on location of aneurysm and point of wall disruption)
5. "thunderclap headache"-worst ever, developing over seconds or minutes
what size are saccular aneurysms when they rupture?
what population has these?
9-14mm
younger population than strokes...peak incidence in the 40s
What can cause saccular aneurysm rupture? (3)
female > male
rupture risk parallels size
1/3 of cases associated with acute increases in intracranial pressure (on the toilet, orgasm)
Complications of saccular aneurysms (4)
1. rebleeding - common and worsens prognosis with each episode of hemorrhage
2. vasospasm (constriction) - can lead to ischemic injury
3. arachnoid fibrosis and scarring (may lead to comm hydrocephalus)
4. herniation
5. death (25-50% with first rupture)
Arteriovenous malformations
1. description
2. association
3. prevalence
4. significance
5. age
1. direct arterial to venous flow (because of tangles of abnormal arteries)
2. epilepsy, intraparenchymal bleeds, subarachnoid bleeds
3. males > females (2:1)
4. most significant CNS vascular malformation
5. 30s and 40s with seizures at earlier ages
Arteriovenous malformations
1. location
2. artery
3. treatment
1. cerebral and superficially located (subarachnoid space or within brain barely)
2. MCA most commonly involved
3. intra-arterial embolization

Disease of senator tim johnson
Cavernous hemangiomas
1. description
2. location
3. clinical
4. cause
1. dilated thin walled vessels with no intervening neural tissue
2. cerebellum, pons, and subcortical regions
3. rarely bleed significantly, but surrounded by gliosis and old hemorrhage that may cause seizures
(stokes rare)
4. most are sporadic, but some are familial
Venous angioma (varix)
1. description
2. clinical
3. when is it found
1. thin walled, dilated veins most often found in subcortical white matter with normal brain around them
2. rarely bleeds, except in cerebellum
3. autopsy most common
Capillary telangiectasias
1. description
2. distinguished from venous
3. clinical
4. location
1. microscopic foci of dilated thin walled vessels separated by relatively normal brain (no surrounding change)
2. smaller vessels only with endothelium
3. incidental finding at autopsy, almost NEVER hemorrhagic
4. pons
Foix-Alajouanine disease
1. class
2. another name
3. description
4. location
5. association
1. spinal vascular malformation
2. angiodysgenetic necrotizing myelopathy
3. venous angiomatous malformation of spinal cord and overlying meninges
4. lumbosacral region
5. ischemic myelomalacia and slowly progressive neurologic symptoms
Lacunar infarcts
1. class
2. description
3. gross exam
4. size
5. clinical
1. hypertensive cerebrovascular disease
2. arteriolar sclerosis of deep penetrating vessels of basal ganglia and white matter
3. small cavity infarcts in lenticular nucleus, internal capsule, deep white matter with surrounding gliosis and "gitter cells"
4. <15mm (important)
5. clinically silent or not depending on location
slit hemorrhages
1. description
2. gross exam
3. class
4. micro
1. rupture with small hemorrhages along small caliber penetrating vessels of the brain
2. after resorption of blood, one sees slit like spaces with brown (due to hemosiderin deposition) discoloration
3. hypertensive cerebrovasc disease
4. gliosis, gitter cells, hemosiderin deposition
acute hypertensive encephalopathy
1. class
2. cause
3. clinical
4. result
5. gross exam
1. hypertensive cerebrovasc disease
2. follows acute onset of significant hypertension - hypertensive emergency
3. diffuse cerebral dysfunction with headache, confusion, vomiting, convulsions, coma
4. herniation and death possible
5. edema, arteriolar fibrinoid necrosis, petechiae, frank hemorrhage, herniation
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