Lecture 2: Pathology & Imaging in Stroke.pdf

Lecture 2: Pathology & Imaging in Stroke Definition: ● Stroke: neurological deficit of cerebrovascular cause that persists > 24 hrs or is interrupted by death within 24 hours ○ Aka cerebrovascular accident (CVA): sudden onset of a neurologic deficit with clinical manifestations referable to anatomic...

Lecture 2: Pathology & Imaging in Stroke Definition: ● Stroke: neurological deficit of cerebrovascular cause that persists > 24 hrs or is interrupted by death within 24 hours ○ Aka cerebrovascular accident (CVA): sudden onset of a neurologic deficit with clinical manifestations referable to anatomic location of the lesion, due to disturbance in BF to the brain ○ A medical emergency & can cause permanent neurological damage & death ○ 3rd leading cause of death worldwide ○ Neurological damage can be due to: ■ Ischemia (lack of BF) ■ Generalized hypoxia ■ Focal ischemic necrosis/cerebral infarction ■ Hemorrhage (rupture of a bv or an abnormal vascular structure) ● TIA: related syndrome of stroke symptoms that resolve completely within 24 hrs ● Alternative concepts: ○ Brain attack & acute ischemic cerebrovascular syndrome ○ Reflect the urgency of stroke symptoms & the need to act swiftly ● Risk Factors: ○ Manageable: ○ Less Manageable: ■ ↑ BP ■ Age (risk 2x after each decade after 55) ■ Heart Disease (eg: AF) ■ Male (19% greater risk) ■ Cigarette Smoking ■ Race (African American have > risk) ■ TIA ■ DM (HBP Correlation) ■ ↑ RBC count ■ Heredity ■ Prior Stroke ● Neurologic Deficit: ○ As a result of stroke, the affected area of the brain cannot function, which might result in: ■ Inability to move one or more limbs on one side of the body ■ Inability to understand or formulate speech ■ Inability to see one side of the visual field ○ The deficit evolves over time ○ The outcome is either permanent or can slowly improve over a period of months Ischemic Stroke: Blood supply to part or all of the brain is ↓ → dysfunction of the brain tissue in that area Global cerebral Ischemia: ● Hypoxic encephalopathy ● Etiology: Systemic hypo-perfusion → General ↓ in blood supply → Hypotension ex: shock, hypoxemia, anemia ● Morphology: ○ 12-24 hrs: Red neurons: neurons show ischemic cell injury ○ Healing is by fibrosis ○ Cortical atrophy ○ Watershed or border zone infarcts (border zone between major vascular territories) ■ Brain: territory between anterior & MCA is most vulnerable ■ Spinal cord ● Clinical Features: ○ Mild transient confusion state to severe irreversible brain death ○ Flat EEG, Vegetative state ○ Coma Focal cerebral infarction: ● Caused by blockage of a blood vessel ● Can occur either from thrombotic or more frequently, embolic arterial occlusion Cryptogenic Stroke: ● No obv explanation (of unknown origin); 30-40% of all ischemic strokes Shock: ● ● ● ● Cardiogenic: Hypovolemic: Massive MI HF & CA Arrhythmias Cardiac tamponade ● Massive GI bleed eg ruptured varices, bleeding ulcer, carcinoma ● Ruptured aortic aneurysm ● Fluid loss: Vomiting, diarrhea, burns Septic: ● Overwhelming microbial infections ● Endotoxic shock Others: ● Neurogenic ● anaphylactic ● Acute Cerebral Infarction: ○ Infarction from obstruction of local blood supply causing focal cerebral ischemia (stroke): Thrombosis: ● Obstruction of a bv by a blood clot forming locally ● Usually due to atherosclerosis ● Extra-cerebral > intra-cerebral ○ Large-vessel (carotid, basilar, cerebral) ○ Small vessel (lacunar infarcts) ● Morphology: ISCHEMIC (bland or anemic) infarcts Embolism: Venous thrombosis: ● Obstruction due to an embolus from elsewhere in the body ● MC involves intracerebral arteries (esp MCA distribution) ● Embolus is most frequently a thrombus, it can also be other substances: fat, air (scu, cancer cells or clumps of bacteria (IE) ● Originate from: ○ Cardiac origin: mural thrombi, valvular disease, AF ○ Major arteries (fragments of thrombotic material break off from arterial mural thrombi ex carotid arteries) ● Morphology: ○ Ischemic vs Hemorrhagic infarcts ○ Emboli occlude bv → reperfusion injury → extravasated RBCs ● Cerebral venous sinus thrombosis → stroke due to locally ↑ venous pressure, which exceeds pressure generated by the arteries ● Infarcts are more likely to undergo hemorrhagic transformation (leaking of blood into the damaged area) than other types of ischemic stroke Infarct Stages: Immediate: Up to 24 hrs: ● 1-6 min: ischemic injury – vacuolation ● > 6 min: cell death ● 12-24 hrs: Red neurons Intermediate stage: 2 weeks: ● Demarcation, soft friable tissue, cysts ● Macrophages, liquefactive necrosis Acute stage: 2 days: ● Pale soft regions of edema ● Loss of gray/white matter border ● Inflammation: neutrophils Late stage: After 4 weeks: ● Fluid filled cysts containing mc is lined by gliosis ● loss of architecture Hemorrhagic Stroke: ● Intracranial hemorrhage: non-traumatic accumulation of blood within the skull vault Intracerebral: ● ● ● ● Subarachnoid: Intraparenchymal hemorrhage Leading cause of death in stroke patients HTN is a predisposing factor in 80% Blood can dissect into the ventricular system ● ● ● Mixed ● Rupture of congenital “Berry” aneurysms: ○ Most occur in anterior circulation, near arterial branch points ○ Multiple in 20-30% ○ Probability of rupture ↑ with size of aneurysm ○ Acute ↑ in ICP (ex: straining at stool, sex) ○ Mortality is ↑ re-bleeding is common in survivors ○ Resorption of blood may lead to meningeal fibrosis & hydrocephalus ● Atherosclerotic & mycotic aneurysms (rare) ● ex: in vascular malformations Vascular rupture is believed to result from arteriolar injury with formation of microaneurysms → Charcot-Bouchard aneurysms ○ The wall of a small intra-cerebral bv is weekend, forming a small aneurysm ○ Seepage of fibrin (red) into the wall Usually lethal In pts who survive, the hematoma is slowly resorbed over months with some restitution of function Hypertensive CVD: ↑ BP is the most important modifiable RF of stroke Intracerebral hemorrhage: ● Mc in the putamen, thalamus, pontine tegmentum, cerebellar hemispheres ● Lethal → serious impairment Lacunar infarcts: ● ● ● ● ● Basal Ganglia, thalamus, internal capsule Arteriolar occlusion of deep penetrating arterioles of pons Single or multiple cystic infarcts – lacunes Most common in BG, deep white matter & BS In the cystic space from resolved liquefactive necrosis → hemosiderin pigment Hypertensive encephalopathy ● Vascular Malformations: ○ Regarded as congenital in origin ○ Arteriovenous malformation: ■ Most important & most likely to bleed ■ May present at any age (commonly between 2nd - 4th decade) ■ Asymptomatic. Seizures. Hemorrhage ■ Contain tangles of arteries & veins with no intervening capillaries ■ Abnormal vessels of variable thickness ■ Frequently AVMs extend from the brain parenchyma into the subarachnoid space & when they bleed, give rise to mixed intracerebral & SAH ○ Cavernous hemangiomas ○ Capillary telangiectasias