Cerebrovascular diseases
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- 3 categories of cerebrovascular disease
- 1. thrombosis 2. embolism 3. hemorrhage
- most common cerebrovascular disorders
- global ischemia, embolism, hypertensive intraparenchymal hemorrhage and ruptured aneurysm.
- cardiac output to the brain
- 1-2% of body weight. 15% of resting cardiac output 20% of total body oxygen consumption
- Determinants for brain lesions
- - presence of collateral circulation - hypotension vs. large vessel obstruction - duration of ischemia - magnitude and rapidity of flow reduction.
- Global cerebral ischemia
- ischemic/hypoxic encephalopathy. generalized reduction of cerebral perfusion (ex/ cardiac arrest, shock and severe hypotension).
- Focal cerebral ischemia
- reduction/cessation of blood flow to a localized area of the brain due to large vessel disease (ex/ thrombotic or embolic arterial occlusion). majority of thrombotic occlusions are due to atherosclerosis.
- Biochemistry of ischemia
- - depletion of energy --> inappropriate release of excitatory amino acid NT's - influx of calcium ions through NMDA glutamate receptors. - inappropriate trigger of signal cascades - free radical generation - mitochondrial injury
- Penumbra
- region of transition between necrotic tissue and normal brain is the "at risk" tissue. can be rescued from injury.
- selective vulnerability of CNS
- short duration global ischemia - pyramidal cells in CA1 of hippocampus - purkinje cells of cerebellum - cortical pyramidal neurons
- Brain death
- evidence of irreversible diffuse cortical injury, flak EEG and brainstem damage. - absent reflexes - absent respiratory drive
- watershed infarcts
- regions of brain or spinal cord that lie at most distal reaches of arterial blood supply. border zones between arterial territories.
- Most common sites of thrombosis
- - carotid bifurication - origin of middle cerebral artery - basilar artery
- most common origins of brain embolism
- - cardiac mural thrombi ( MI or A-fib) - valvular disease - atheromatous plaques of the carotid artieries. - paradoxical emboli (children with cardiac anomalies)
- Shower embolization
- fat embolism after long bone fx. affected poeple have general cerebral dsyfunction with distrubances of higher cortical function and conciousness. - widespread hemorrhagic lesions of white matter
- Polyarteritis nodosa
- vasculatide that can involve cerebral vessels, causing mulitple infarcts throughout the brain.
- primary angiits of the CNS
- inflammatory disorder involving multiple small to medium sized parenchymal and subarachnoid vessels. - giant multinucleated cells - destruction of vessel walls. - granulomas cognitive dysfunction that improves with steroid immunosuppressive treatmenkt.
- Hemorrhagic (red) infarct
- characterized by multiple, confluent petechial hemorrhages. associated with embolic events. hemorrhage presumed secondary to reperfusion of damaged vessels and tissue through collaterals. *thrombolytic therapy contraindicated*
- nonhemorrhagic (pale, bland, anemic) infarcts
- associated with thrombosis. treated with thrombolytic therapy.
- nonhemorrhagic infarct
- 6 hrs - no change 48 hrs - pale, soft, swollen tissue. corticomedullary junction becomes indistinct 2-10 days - gelatinous, friable and distinct borders between normal and abnormal tissue. 10 days -3 weeks - tissue liquefies, leaving fluid-filled cavity lined by dark gray tissue.
- spinal cord infarction
- seen with hypoperfusion or with interrption of feeding tributaries from the aorta. (occlusion of anterior spinal artery).
- Lacunar infarcts
- hypertensive cerebrovascular disese -- affecting deep penetrating arteries and arterioles of the basal ganglia and hemispheric white matter, brainstem. - arteriolar sclerosis --> occlusion - contributes to development of multiple, small cavitary infarcts or lacunae. (<15mm wide) - occur in lenticular nucleus, thalamus, internal capsule, deep white matter, caudate nucleus and pons
- slit hemorrhages
- HTN that results in rupture of small caliber penetrating vessels and small hemorrhage. - hemorrhages resorb, leaving slitlike cavity - surrounded by brownish discoloration - pigment laden macrophages and gliosis.
- Hypertensive encephalopathy
- arises with malignant HTN -- diffuse cerebral dysfunction - headache, confusion, n/v - convulsions --> coma petechiae and fibrinoid necrosis of arterioles in the gray and white matter seen microscopically.
- vascular dementia
- multi infarct - dementia, gait abnormaltiies and pseudobulbar signs sufperimposed with focal neuro defecit. 3 types
- 3 types of vascular dementia
- 1. cerebral atherosclerosis 2. vessel thrombosis or embolization from carotid vessels 3. cerebral arteriolar sclerosis from chronic HTN
- Binswanger disease
- HTN vascular injury that involves large ares of subcortical white matter with myelin and anxon loss.
- Intraparenchymal hemorrhage
- occur in middle-late adult life caused: rupture of small intraparenchymal vessel. etiology: HTN and cerebral amyloid angiopathy (CAA)
- HTN
- most common underlying cause of primary brain parenchymal hemorrhage accounting for >50% of clinically significant hemorrhages. - hyaline arteriosclerosis - weakens vessel walls.
- Charcot-bouchard microaneurysms
- chronic HTN and subsequent development of minute aneurysms which can rupture --> intraparenchymal hemorrhage.
- Hypertensive intraparenchymal hemorrhage
- putamen (50-60% of the time) thalamus pons cerebellar hemispheres (rarely) extravasation of blood with compression of adjacent parenchyma. cavitary destruction with rim of brown discoloration.
- CAA
- amyloidgenic peptides (similar to alzheimers) deposit in walls of mediumand small caliber meningeal and cortical vessels. - lesions are restricted to leptomeningeal and crebral cortical vessels. - weakens vessel walls --> hemorrhage. - polymorphiism of gene encoding apolipoprotein E (ApoE). e2 or e4 allele increases risk of repeat bleeding.
- Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy
- CADASIL - hereditary form of stroke. - mutated gene for Notch 3 receptor - recurrent strokes (infarct >hemorrhage) - dementia concentric thickening of media and adventitia of vessels. basophilic PAS + depsits in osmiophilic compact granular material.
- Subarachnoid hemorrhage
- most common cause = rupture of saccular (berry) aneurysm. - also extension fo traumatic hematoma, rupture of hyeprtensive hemmorhage into ventricular system. -
- saccular aneuysm
- most common type of intracranial aneurysm. cause subarachnoid hemorrhage. - autsomal dominant polycystic kidney disease - ehlers-danlos syndrome type IV - neurofibromatosis type 1 - marfan syndrome risk factors: cigarette smoking and HTN.
- subarachnoid hemorrhage
- (if related to ruptured aneurysm) - acute increased intracranial pressure (pooping or sexing) - sudden excruciating headache - rapid LOC
- vascular malformations
- four principal groups: 1. arteriovenous malformations 2. cavernous malformations 3. capillary telangiectasias 4. venous angiomas.
- Arteriovenous malformation
- vessels of subarachnoid space extending into parenchyma. tangled network of wormlike vascular channels with prominent pulsatile AV shunting with high blood flow. - enlarged blood vessels separated by gliotic tissue *most common vascular malformation*
- cavernous malformations
- distended, loosely organized vascular channels with thin, collagenized walls devoid of intervening nervous tissue. - occur in cerebellum, pons and subcortical regions - low flow, no AV shunting.
- Capillary telangiectasia
- microscopic foci of dilated, thin walled vascular channels separated by relatively normal brain parenchyma and ocurring most frequently in pons.
- venous angiomas
- aggregates of ectatic venous channels.
- Foix-alajouanine disease
- angiodysgenetic necrotizing myelopathy - venous angiomatous malformation of the spional cord and overlying meninges (often in lubosacral region)
- AVM sx
- age 10-30 - seizure disorder and intracerebral hemorrage/subarachnoid hemorrhage. - m,ost common in middle cerebral artery (posterior branches)