Ischemic Disorders Flashcards
Occlusion of internal carotid commonly presents as
Infarct of MCA because anterior cerebral artery receives blood via anterior communicating artery
Stroke definition
Sudden neurological deficit due to vascular disease
Ischemia biochemical changes
Depletion of energy
Excessive release of glutamate which interact with NMDA receptors on post synaptic membranes to permit influx of calcium ions triggering cell death through necrosis
Penumbra
Between necrotic area and normal brain parenchymal tissue there is “at risk” tissue called penumbra which may undergo apoptosis
Possible to facilitate recovery
Watershed infarcts
Border zone infarcts
Failing myocardium inadequately perfumes a an already occlusive vascular system
Junctions of major arterial supplies
E.g. Lateral cortex at borders of anterior and middle cerebral arteries would affect the arm and sensory cortex-bilaterally
Hypoxic encephalopathy
Caused by CO, cyanide, carbon disulfide, hypoglycemia, and ischemia
Affects
Pyramidal neurons in the deep layers of cerebral cortex, purkinje cells of cerebellum, hippocampal pyramidal cells, globus pallidus neurons
Genrally leads to vegetative state, brain death or death
Most common cause of stroke and common origin sites
Atherosclerosis
Internal carotid arteries, vertebral arteries and middle cerebral
Cerebral autosomal dominant arteriopathy with sub cortical infarcts and leukoencepnalopathy (CADASIL)
Rare hereditary form of stroke caused by mutations in the Notch3 gene
Transient ischemic attacks
Warning of possible impending stroke
Numbness weakness and blindness
Symptoms last an hour or less
Multiple TIAs indicate a critical narrowing of the lumen of the involved artery by an atherosclerotic plaque with superimposed thrombus
Middle cerebral artery infarct symptoms
Sudden
Paralysis of contralateral face, arm and leg
Sensory impairment over contralateral face arm and leg
Homonymous hemianopsia or homonymous quadrantanopsia
Paralysis of conjugate gaze to opposite side
Aphasia if on dominant side (left mainly)
Unilateral neglect and agonist for half of external space if on non dominant side (right mainly)
Anterior cerebral artery infarct
Paralysis of contralateral foot and leg
Sensory loss over toes, foot and leg
Impairment of gait and stance
Posterior cerebral artery infarct
Homonymous hemianopsia
Sensory loss and spontaneous pain-if thalamus is involved
Third nerve palsy
Contralateral hemipenis (if midbrain is involved)
Posterior inferior cerebellar artery infarct
Dorsolateral medulla Pain, numbness, impaired sensation to face on ipsilateral side Impaired pain and temp sensation on body contralateral to lesion Ataxia of limbs Falling to side of lesion Nystagmus Vertigo Horners syndrome Dysphasia Hoarseness
Gross pathology of infarct
6-12 hours tissue difficult to discern at autopsy
48 hours- pale soft and swollen, gray white matter junction becomes I distinct
2-10 days friable
10 days-3 weeks tissue liquefies and leaves a cavity
Edema-reaches max at 4-5 days
Cell loss, myelin breakdown, phagocytic and glial scad result in shrinkage
Cysts may form in large infarcts leading to ventricular enlargement, wallerian degeneration
Embolic ischemia
Pathogenesis: circulating bodies lodge in vessels
Most common is thrombotic embolus in the MCA
Tissue undergoes infarction and the distal portion of vessel becomes necrotic
Embolus can move and blood flows through weakened wall causing hemorrhage
Atrial fibrillation can be contributing factor
Types: most common is thromboemboli most frequently from the heart, artheromatous plaques on carotid and vertebral-basilar arteries. Fat emboli occur during lung injury or surgery. Nitrogen bubbles occur in deep sea divers
Clinical: sudden onset of focal impairment. Distribution of the MCA is most commonly involved. Most patients survive
Pathological: emboli often produce small hemorrhagic infarcts in cerebral cortex
Macroscopically by multiple, sometimes co fluent petechial hemorrhages
