Chapter 16： Disease of Central Nervous System Cerebral Vascular Disorders,Zhu keqing 竺可青 Department of pathology Department of Neuroscience ZJUCBB,Hemodynamic Derangement & Cerebral Vascular Disorders 406,Circulation disturbances: 1. ischemic encephalopathy 2. infarction( thrombotic or embolitic) 3. hemorrhage Vascular disorders: arterosclerosis, atherosclerosis, arteritis, aneurysm, ateriovenous malformation(AVM),Cerebral injury caused by hypertension, cardiac arrest, hemorrhage and shock. Predisposing factors： higher metabolic rate：more susceptible NeuronAsOligoEndo Gray MatterWhite Matter 3rd、5th、6th layers of cortex are most vulnerable,1. Ischemic Encephalopathy,4,Focal ischemic insults,Focal blockage of cerebral artery Typically embolic (cardiac, atherosclerotic carotid disease) Can be thrombotic (venous thrombosis),Persistence and severity of ischemia mild ischemia: no remarkable change severe ischemia, survive few hours before death: not remarkable moderate ischemia, survive more than 12 hours：typical changes Architecture of cerebral arteries the location at the border zone of cerebral arteries is much more vulnerable.,Ischemic Encephalopathy,Changes: 1. laminar cortical necrosis : neurons in 3rd, 5th, 6th layers of cortex involved 2. hippocampal sclerosis ：pyramidal neuron death 3. border zone infarction ： early stage： “C” shaped infarct later stage: astrogliosis (granular atrophy) cardiopetal developmentglobal necrosis(respirator brain) CPC：weakness sensation abnormalities coma, vegetable status death,1. Ischemic Encephalopathy 小结,Cause： thrombosis, embolism, space occupying lesion, local vessels compressed by hernia Types: 1. thrombotic: on the sites of atherosclerosis the symptoms: from weakness of muscles to semiplegia or coma 2. embolic: the emboli often are cardiogenic , or from atherosclerotic plaque, with sudden onset and poor prognosis.,2. Cerebral Infarction 408,Types: white infarct red infarct: incomplete occlusion or frangible emboli going further to small vessels, resulting in blood escape from injured vascular wall. Morphology changes: first 412h: normal then: ischemic neuronal changes 36-48h: swollen and soft; demarcation between gray and white matter becomes blurred due to edema the third day: macrophage, progressive marked demarcation of the lesion 1 month: liquefaction, irregular cavities 6 month: completely liquefied,Brain infarction,Lacunae腔隙状坏死: necrosis less than 1.5cm in diameter. TIAs( transient ischemic attacks) 一过性脑缺血症 transient episode of neurologic dysfunction lasting several minutes24 hours an important predictor of subsequent infarcts 1/3 patients with TIA developing clinically significant infarcts within 5 years/ 预后不好,10,Cerebral infarction,A, At low magnification, it is possible to see the demarcated areas of an acute infarction. In the underlying white matter, the areas of infarction are well shown by the myelin stain. B, Acute ischemic injury causes diffuse eosinophilia of neurons, which are beginning to shrink. C, Infiltration of a cerebral infarct by neutrophils begins at the edges of the lesion where vascular supply has remained intact. D, After about 10 days, an area of infarction is characterized by the presence of macrophages and surrounding reactive gliosis. E, Remote small intracortical infarcts are seen as areas of tissue loss with a small amount of residual gliosis.,11,Sequential organization of cerebral infarcts 小结,24 hours well-circumscribed area of necrosis, softening, discoloration in an arterial territory. Circumscribed penumbral zone. Days 1-2 Minimal polymorphonuclear leukocyte infitrate Days 2-5 Blood-brain barrier breakdown and cerebral edema Days 3-5 Axonal retraction balls at the edge of infarct , usually in white matter Days 5-7 Appearance of lipid-laden macrophages at periphery; hyperplastic blood vessels Day 14 Sheets of lipid-laden macrophages Days 10-20 Surrounding rim of gemistocytic astrocytes 3 months Cystic space surrounded by fibrillary astrocytes,3. Brain Hemorrhage 409,Intracerebral Hemorrhage Cause: hypertension * congenital saccular aneurysms, tumors, vasculitis, AVM, trauma, CAA, CADASIL 410 Pathogenesis:,anoxia of vascular wall,anoxia of perivascular tissue,Charcot Bounchard microaneurysms,micro-softening foci,vessels ruptured,spasm of vessels B.P,hemorrhage,Changes: In the center of foci, normal structure is destroyed and filled with RBC，at periphery multifoci of hemorrhage The old hemorrhage foci becomes cavitated & with hemosiderin.,Brain Hemorrhage,1. B.G hemorrhage:directed to insular contralateral semiplegia directed to ventricle , thalamus death 2. Pons hemorrhage: pin-like pupils, persistent high fever or sudden death 3. Cerebellar hemorrhage: severe occipital headache, frequent vomiting,Brain Hemorrhage,Vascular malformation,Abnormalities in angiogenesis in the developing brain AVM: the most common caused vessels of variable caliber including A,V Hemorrhagic, calcification, r