腦儲蓄英文 ppt課件

1、Cerebrovascular Diseases,Xue QunDepartment of NeurologyThe First Affiliated Hospital of Soochow University,第一節(jié),outline（ 概述 ）,key concepts,Cerebrovascular diseases: the focal or diffused function disorders of

2、the brain , on the basic disorder of the cerebral vascular wall or of the blood flowType:Accute:TIA (transient ischemic attack)Stroke Chronic:Cerebrovascular dementia,Stroke（apoplexy/cerebrovascular accident）:

3、 a syndrome characterized by the acute onset of a neurologic deficit that persists for at least 24 hours, reflects focal involvement of the central nervous system, and is the result of a disturbance of the cerebral circ

4、ulation. Types: ischemia : local thrombosis or embolization from a distant site hemorrhage：,Stroke,ischemia : Cerebral ischemic stroke (cerebral infarction) arterothrombotic infarctionCereb

5、ral embolismLacunar infarctionhemorrhage： Cerebral hemorrhage Subarachnoid hemorrhage,,,Territories of the principal cerebral arteries,Anterior circulationInternal carotid arteryOphthalmic arteryposterior commun

6、icating arteryAnterior choroidal artery (hippocampus, globus pallidus, lower internal capsule)Anterior cerebral artery(medial frontal 額葉and parietal 頂葉cortex and subjacent white matter,anterior corpus callosum胼胝體)Midd

7、le cerebral artery(lateral frontal, parietal , occipital,and temporal 顳葉cortex and subjacent white matter) Lenticulostriate branches (caudate nucleus尾狀核, putamen殼核, upper internal capsule),Territories of the principal

8、 cerebral arteries,Posterior circulationVertebral artery Posterior inferior cerebellar (medulla,lower cerebellium)Basilar artery Anterior inferior cerebllar(lower and midpons, mid cerebellium) Superior cerebell

9、ar (upper pons,lower mid cerebellum) Posterior cereballar (medial occipital and temporal cortex and subjacent white matter,posterrior corpus callosum胼胝體,upper midbrain)Thalamoperforate branches丘腦穿通動脈(thalamus)Thalamo

10、geniculate branches丘腦膝狀體動脈 (thalamus),Pathology, physiology and blood circulation regulation,Weight of brain is 1.5kg , about 2~3%of body weightCBF 750~1000ml/min (CBF∞CPP/CVR) Cerebral blood flow ∞cerebral

11、perfusion pressure / cerebral vascular resistance CBF=(MAC-ICP)πr4/(8η*L) MAC(平均動脈壓)，ICP（顱內壓), r (caliber管徑)， η（blood viscosity血黏度），L（血管長度）,,第二節(jié)Epidemiology and prevention(流行病學和預防),Etiologic factors,Va

12、scular disorders Atherosclerosis / inflamatory disorder/cerebral amyloidosis(淀粉樣變)/ Vascular malformations /aneurysm…Cardiac and hemodynomics disordersMural thrombus / rheumatic heart disease/ arrhythmias / endoca

13、rditis…Hematologic disorders(blood constituent and hemorheology disorders)Hypercoagulable state / leukocytosis / thrombocytosis / polythemia(紅細胞增多)others,Risk factors,HypertensionDiabetes mellitusCardiac disorderH

14、yperhomocysteinemiaTIA or stroke historySmoking or alcohol abuseHyperlipemiaOthers: obesity, age, contraceptive（避孕）, high fibrinogen …,Primary prevention (一級預防),HypertensionCardiac disorderDiabetes mellitusHyperli

15、pemiaSmoking or alcohol abuseWeight controlCarotid artery stenosisHyperhomocysteinemia (>16umol/l)high fibrinogenExercise, diet,Secondary prevention (二級預防),Hypertension, Cardiac disorder, Diabetes mellitus, Hype

16、rlipemia,Smoking or alcohol abuse, Weight control, Carotid artery stenosis, Hyperhomocysteinemia (>16umol/l), high fibrinogen, Exercise, diet…Anti-platelet aggregationpost-stroke cognitive handicap intervention pos

17、t-stroke depression intervention,,第三節(jié)transient ischemic attack （短暫性腦缺血發(fā)作）,transient ischemic attack (TIA),Transient, repeatedly, episode（發(fā)作性）,Last a few minutes ~1 hour, oft

18、en completely recover within 30min,never last over 24 hours, leave no symptom , physical sign or sequela（后遺癥）,Etiological factors and pathogenesis,Mini-embolismCerebral vascular spasmBlood constituent and hemodynamic（

19、血液動力學） alterationOthers: vasculitis, cervical syndrome,（頸椎病）,Clinical situation,Middle-age or senium, male>female,Company with hypertension, diabetes, cardiac disease, hyperlipemiaAcute onset, usually reach to the

20、peak within 5min, recover within 30min,never last over 24 hours, leave no symptom , physical sign or sequelaRelative fixed symptom,relapse,Clinical situation,Internal carotid artery TIAOphthalmic artery crossing paraly

21、sisHorner sign crossing paralysisAphasia失語( dominant hemisphere)Vertebral-Basilar artery TIADrop attack: reticular formation of brain stem (腦干網(wǎng)狀結構)Transient global amnesiaBinocular vision disorder attack（雙眼視力障礙）ve

22、rtigo(眩暈), nausea(惡心),vomiting(嘔吐), diplopia(復視),dysequilibrium(平衡失調), dysphagia(吞咽困難),Diagnosis,Case historyPlatelet counting and aggregation rateBlood sugar and blood lipid on an empty stomachProthrombin time and pa

23、rtial thromboplastin timeErythrocyte sedimentation（血沉）EEG,TCDCT,MRA,CTA,DSA,differential diagnosis,Partial epilepsiaMeniere’s diseaseCardiac disorderRIND(reversible ischemic neurologic deficit)Migraine headache( 偏

24、頭痛)Tumor,treatment,Etiological treatmentProphylactic drugs(預防用藥)Anti-platelet aggregation drugsAnticoagulant drugsBrain conservancySurgery prognosis,第四節(jié) cerebral infarction

25、 （腦梗死）,,cerebral infarction,Prolonged interruption of blood flow leads to irreversible injury and persistent neurologic deficitsclinic category RIND(reversible ischemic neurologic deficit):<3wProgr

26、essive ischemic stroke :6h~2wCompleted ischemic stroke:6hPathologic categoryAtherothrombotic cerebral infarction (artery to artery embolism/thromboembolism & cerebral thrombosis)Cerebral embolismLacunar infarcti

27、onCerebral watershed infarction,Part one,Atherothrombotic cerebral infarction,Arterothrombotic cerebral infarction,Thrombus forms in the artery basing on the cerebral atherosclerosis or other disorder of the vasc

28、ular wall, leads to the prolonged interruption of blood flow , irreversible injury and persistent neurological deficits.etiologic factorCerebral atherosclerosis,PathogenesisEndothelial injuryadherence of monocyto/ma

29、crophages/T-lymphocytemigration and subendothelial localization of the cellsformation of platelet thrombusproliferative lesion (fibrous plaque)Energy,excitatory amino acid,calcium overload, ischemic cerebral edema,ni

30、tric oxide,immediate early genes, neurotrophic factors,heat shock protein, CK, apoptosisIschemic penumbra(缺血半暗帶)CBF~20 ml/100g.min electric failure thresholdCBF~10 ml/100g.min membrane failure thresholdReperfusi

31、on damage,hemorrhagic infarctionTTW (therapeutic time window), RTW (reperfusion time window), CTW (cytoprotective time window)Pathology,Clinical findings,elder person with atherosclerosis, hypertension,diabetes,cardiac

32、 disorderStepwise incremental neurologic deficitsAssociated symptoms(often without seizures,headache,vomiting,dementia)In quiet status,Internal carotid artery,SyndromeTransient monocular blindness(retinal artery isch

33、emia)the severity is highly variableSymptomatic similar to the MCA occlusion or asymptomatic,Middle cereberal artery occlusion,Anatomy: supplies most of the cerebral hemisphere and deep subcortical structuressuperior

34、 division: the entire motor and sensory cortical representation of the face,hand, and arm;and the expressive language area of the dominant hemisphere; inferior division: the visual radiations,the region of visual corte

35、x related to macular vision; the receptive language area of the dominant hemispherelenticulostriate branches:the basal ganglia and the posterior limb of the internal capsule (the motor fibers related to the face,hand, a

36、rm, and leg),Middle cereberal artery occlusion,Syndrome:superior division stroke: contralateral hemiparesis that affects the face, hand, and arm but spares the legContralateral hemisensory deficit in the same distribu

37、tionNo homonymose hemianopia(偏盲）Brocar’s aphasia ( the dominant hemisphere is involved), which is characterized by impairment of language expression with intact comprehension,Middle cereberal artery occlusion,Syndrome:

38、Inferior division stroke:Contralateral homonymose hemianopia ,may be denser inferiorlyImpairment of cortical sensory functionsDisorders of spatial thoughtWernicke’s aphasia(dominant hemisphere),manifested by impaire

39、d comprehension and fluent but often nonsensasiacal speechAcute confusional state(non domonant hemisphere),Middle cereberal artery occlusion,Syndrome:the bifurcation or trifurcation of MCAContalateral hemiparesis and

40、hemisensory deficit involving the face and arm far more than the legHomonymous hemianopiaGlobal(dominant hemisphere) aphasia,characterized by combined expressive and receptive,Middle cerebral artery occlusion,Syndrome:

41、the stem of MCAContalateral hemiparesis and hemisensory deficit involving the face ,hand,arm and the legHomonymous hemianopiaGlobal(dominant hemisphere) aphasia,anterior cerebral artery occlusion,Anatomy: supplies th

42、e parasagittal 矢狀旁cerebral cortex—includes portions of motor and sensory cortex related to the leg and micturition排尿 centerSyndrome: Contralateral paralysis and sensory loss affecting leg ,voluntary control of micturit

43、ion may be impaired,Basilar Artery system,Anatomy:branches of BA supply the occipital and medial temporal ， medial thalamus, the posterior limb of the internal capsule,and the entire brain stem and cerebellumClinical s

44、yndromes:a serious event that is often incompatible with survival, produces bilateral neurologic signs referable to involvement of both vertebral artery (VA) or of a lone unpaired VA Ipsilateral cerebellar ataxia共濟失調,

45、vertigo, nausea, vomiting, dysphagia吞咽困難,dysarthria構音障礙?coma,constricted pupils, high temperature,locked in syndrome, hemiplegia or quadriplegia四肢癱,even death,Basilar Artery system,Locked in syndrome:with basilar occlus

46、ion,the ventral portion of the pons (basis pontis) is infarcted and the tegmentum is spared,such patients remain conscious but quadriplegic.They may open their eyes or move their eyes vertically on command.Weber syndrom

47、e: ipsilateral III nerve palsy, contralateral hemiparesisParinaud syndrome:unable to move eyes verticallyBenedikt syndrome: ipsilateral III nerve palsy, involuntary movement不自主運動 on the contralateral,Basilar Artery sys

48、tem,Millard-Gubler syndrome: ipsilateral facial nerve, abducent nerve paralysis, contralateral hemiplagiaFoville syndrome: syntropy gaze paralysis to the focus, ipsilateral facial nerve, abducent nerve paralysis, contr

49、alateral hemiplagiaWallenberg syndrome: ipsilateral cerebellar ataxia,Horner’s syndrome,facial sensory deficit;contrlateral impaired pain and temperature sensation; nystagus(眼震), vertigo，nausea, vomiting, dysphagia, dy

50、sarthria, and hiccupTop of the basilar artery syndrome: abnormal eye movement, pupil, consciousness and behavior, lose of rememberance, contralateral hemiablepsia or cortexablepsia,Posterior artery,Anatomy:supply the o

51、ccipital cerebral cortex,medial temporal lob,thalamus,and rostral midbrain(中腦腳)Clinical syndrome:homonymous hemianopia affecting contralateral visual field,vertical gaze palsy; oculomotor nerve palsy,internuclear ophth

52、almoplegia,vertical skew deviation of the eyes;anomic aphasia,visual agnosia(失認)；cortical blindness,memory impairment,inability to recognize familiar things,exotonic visual and behavioral syndrome.,Investigative studies,

53、Blood testsComplete blood count (to find possible cause of stroke as thrombocytosis, polycythemia, anemia,and leukocytosis)Erythrocyte sedimentation rate(血沉)（to detect giant cell arteritis or other vasculitides）Serol

54、ogic assay for syphilis(梅毒)（FTA-ABS /CSF VDRL）Serum glucose (to detect hypoglycemia or hyperosmolar nonketotic hyperglycemia高滲性非酮癥性高血糖)Serum cholesterol and lipids,Investigative studies,Electrocardiaogram(to detect unr

55、ecognized myocardial infarction or cardiac arythmias, such as fibrillation)CT:low densityMRI:T1-weighted MRI scan shows decreases signal,T2 -weighted MRI scan shows increases signalLumbar puncture(腰穿) Cerebral angiog

56、raphyUltrasonography / transcranial doppler/ Echocardiography(心超)ElectroencephalogramSPECT，PET,Diagnosis and differential diagnosis,Onset and course: neurologic deficits progress over seconds to hours / occasionally

57、days,happened in quiet status or in sleepDuration of deficits: persist for at least 24 hrRIND (almost completely resolve in a few days, <3weeks)History: artherosclerosis, hypertension, diabetes mellit

58、us,coronary artery disease, TIAs,Associated symptoms:without headache, vomiting, seizures, or coma.CT scan and MRI: T1 short, T2 long,Treatment,Thrombolytic therapy:tissue plasminogen activator(tPA) 0.9mg/kg within 3h

59、r,urokinase,major complication is hemorrhage affecting brain or other tissues。Contraindication:time has over 3h,CT scan has shown evidence of a large ischemic stroke or of hemorrhage,coagulation function has been compro

60、mised by the administration of warfarin or heparin or by throbocytopenia (platelet 180/110mmHg, elder than 75y Within the first 24h after t-PA,anticoagulant and antiplateletagents should not be given.,Treatment,Acute p

61、eriodAntiplatelet agents: Asprin, ticlopidine, clopidogrelBlood diluteExpand blood vesselDefibrase: batoxobin, ancrodAnticoagulation: heparin, warfarinAntihypertensive agents（Bp>220/120mmHg）Antiedema agents: ma

62、nnitol, furosemideNeuroprotective agents: barbiturates,the opioid antagonist naloxone, calcium channel antagonists, excitatory amino acid receptor antagonistsSymptomatic treatment 對癥治療：blood pressure, temperature, hyp

63、erglycemia, pneumonia, bedsore, upper gastrointestinal hemorrhage, dysphagia, electrolyte disturbanceSurgeryconvalescent treatmentSecondary prevention,prognosis,Mortality 10%Multilation rate 50%about 40% patients

64、who survived the acute period would recidivism,Part two,Cerebral embolism （腦栓塞）,Cerebral embolism,All kinds of emboli enter the cerebral vascular,break down blood flow,induce the district brain necrosis,and turn up

65、 relevant neurological deficiency.Etiological factors and pathogenesisCardiac genesis (70%)Mural thrombus(附壁血栓) / rheumatic heart disease/ arrhythmias （心律失常）/ endocarditis…Non cardiac genesisFracture, cancer, air

66、Red infarction(hemorrhagic infarction),Clinic finding,Onset : begin abruptly,usually within a few seconds or minutes, neurologic deficits may be maximal at onset, happened in quiet or in active status Age: young as wel

67、l as oldHistory: TIAs, Mural thrombus/ rheumatic heart disease/ arrhythmias / endocarditis/ fractureAssociated symptoms:headache, vomiting, seizures, or disorders of consciousness can be found in some patients.Symp

68、toms relate with the emboli original diseases or emboli signs in other tissues,Syndromes:,Internal carotid artery system:Contralateral hemiparesis and hemisensory lossContralateral homonymous hemianopiaaphasia(dominan

69、t hemisphere), characterized by combined expressive and receptivevertebral-basilar artery system:Ipsilateral cerebellar ataxia, vertigo, nausea, vomiting, dysphagia, dysarthria ?coma, constricted pupils, high temperat