病变疾病,脱髓鞘疾病精神病

Chapter 16：Disease of Central Nervous System Cerebral Vascular Disorders,Zhu keqing 竺可青Department of pathologyDepartment of NeuroscienceZJUCBB,Hemodynamic Derangement & Cerebral Vascular Disorders 406,Circulation disturbances: 1. ischemic encephalopathy 2. infarction( thrombotic or embolitic) 3. hemorrhageVascular 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 arteryTypically 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 changesArchitecture 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 involved2. hippocampal sclerosis ：pyramidal neuron death3. 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 herniaTypes: 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 infarctred 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 infitrateDays 2-5 Blood-brain barrier breakdown and cerebral edemaDays 3-5 Axonal retraction balls at the edge of infarct , usually in white matterDays 5-7 Appearance of lipid-laden macrophages at periphery; hyperplastic blood vesselsDay 14 Sheets of lipid-laden macrophagesDays 10-20 Surrounding rim of gemistocytic astrocytes3 months Cystic space surrounded by fibrillary astrocytes,3. Brain Hemorrhage 409,Intracerebral HemorrhageCause: hypertension * congenital saccular aneurysms, tumors, vasculitis, AVM, trauma, CAA, CADASIL 410Pathogenesis:,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 death2. Pons hemorrhage: pin-like pupils, persistent high fever or sudden death3. 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, reactive gliosis可导致脑内和蛛网膜下腔的混合出血。,16,CASE 1,病史摘要：死者被人用塑料凳子打伤头部而入院，晚上突然死亡。,17,病 理 诊 断1. 弥漫性蛛网膜下腔出血伴二侧脑室小凝血块；2大结节性肝硬变伴胆管增生扩张慢性炎；脾缺如；3肺水肿。讨论1 死者的内脏经病理学检查证实，其生前主要患有大脑、脑干及小脑弥漫性蛛网膜下腔出血，但脑基底动脉未见畸形或血管瘤等病变，故此蛛网膜下腔出血应考虑系由外力作用引起。2 死者生前患有严重的大结节性肝硬变。肝硬变可导致患者凝血功能降低，在外伤情况下，易诱发出血。,18,CASE 2,死者在劳动时突发右侧头部抽动感，四肢及全身抽搐，伴呕吐。当时体检：“血压130/82mmHg，神志欠清，瞳孔对光反射迟钝，颈部有抵抗，四肢及全身肌肉抽搐。”予安定等处理，于当天因抢救无效死亡。,19,病 理 诊 断1. 右大脑基底节及中脑灶性出血伴右侧脑室出血；（后枕部硬膜外血肿）；2心脏肥大，左冠状动脉粥样硬化狭窄级； 3肺水肿。讨论1死者生前主要患有右大脑基底节及中脑灶性出血，右侧脑室出血；同时当地解剖时尚发现死者有硬膜外血肿。结合病史中死者突发右侧头部抽动感，四肢及全身抽搐，伴呕吐，迅速死亡，故我们认为其死因主要系由于上述脑出血病变导致颅内压高压，脑干生命中枢功能障碍所致。2死者脑出血的原因，由于病史资料有限，难以明确认定，请结合临床全面分析后加以认定。其硬膜外血肿应属外伤性。,20,CASE 3,因头痛伴发热七天。医院头颅CT示：右侧颞顶枕区见低密度区。一个月前有“肺炎”史。后出现嗜睡昏迷。考虑颅内压增高，