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
Venous or dural sinus thrombosis
Least common pattern of cerebral infarction
Hemorrhagic infarction occurs when blood stasis in large veins leads to infarction.
Increased pressure disrupts capillaries causing blood to enter infected areas
Abrupt occlusion of several cerebral veins is necessary to produce a large hemorrhagic infarct
Factors: dehydration in kids, spread of infection from nasal sinus or middle warm disorders that cause hypercoagulability of blood
Superior sagital sinus hemorrhage can cause bilateral hemorrhagic infarcts
Intracerebral hemorrhage
More lethal than infarction
Hypertension is the most important risk factor
Arteriolosclerosis of small arteries & arterioles
Changes In small vessels: Thickening of vessel wall with increased cellularity, hylanizarion of the medium formation of aneurysms
Hypertension causes spontaneous rupture of small penetrating vessels
Most common sites are basal ganglia/thalamus, pons and cerebellum (all supplied by penetrating arteries) lateral striate supply basal ganglia and internal capsule
Incidence: greater than 50, chronic hypertension. Increases with age
Clinical: acute onset of headache, rapid development of stupor followed by coma. Signs and symptoms depend on location of the hematoma.
CT Adam reveals presence
Not instantly fatal takes 6-36 hours
Pathological changes: hemorrhage produces large cavity filled with clot. Highly destructive space occupying lesion.
May cause uncal herniation with brainstem compression and secondary brainstem hemorrhages
Subarachnoid hemorrhage/intracranial aneurysms
Aneurysms are abnormal lock sized dilatations arteries-berry or saccule or congenital
Most common to cause subarachnoid hemorrhage is rupture of berry aneurysm
Berry aneurysms: walls composed of Adventitia and intima only, muscular and elastic coats are absent
Most common sites are bifurcations of vessels at the base of the brain especially in the anterior circulation
Sequelae: rupture, may exert pressure on local structures
Incidence: may occur at any age
Clinical: rapidly developing headache, nuchal rigidity, unconsciousness
CAT scan, arteriography and bloody CSF on lumbar puncture are helpful in diagnosis
After 3 weeks CSF becomes yellow
Prognosis: 1/3 die
Complications: localized vasospasm due to blood and it’s breakdown products in the subarachnoid space
Hydrocephalus from subarachnoid hemorrhage and reactive meningitis
Arteriovenous malformation
Rupture Causes 2% of strokes, most likely cause of intracerebral hemorrhage in a child
Generally asymptomatic
Characteristics: tangles of abnormal vessels, absence of capillary bed, separated by gliosis neural parenchyma, walls have a deficiency of smooth layer
Developmental origin
First hemorrhage occurs between 20 and 40 years
Clinical: seizures, headaches focal neurological signs
Consequences: hemorrhage-subarachnoid or intracerebral, ischemic necrosis of tissue surrounding malformation, hypoperfusion of adjacent structures
Arteriovenous shunt
Large brain arteriovenous malformation that is a common cause of cardiomegaly and congestive heart failure on first day of life
Causes high output cardiac failure
Occur between vein of Galen and middle or posterior cerebral artery
Surgical intervention can be successful
Lacunar infarcts
Arteriolar pathology associated with hypertension
Most affected arteries are penetrating arteries and arterioles that supply the basal ganglia, thalamus, deep cortical white matter and pons
Can develop single or multiple small cavity infarcts
Areas of tissue loss with scattered lipid laden macrophages and surrounding gliosis
Slit hemorrhages
Rupture of penetrating arterioles with small intracerebral hemorrhages
Resoprtion leaves a slit like cavity
Hypertensive encephalopathy
Rapidly evolving syndrome of severe hypertension associated with headache, nausea and vomiting
