精神病學課件：Cerebrovascular Diseases

1、 Cerebrovascular DiseasesOutlineIntroductionTransient Ischemic Attacks (TIA)Ischemic strokeIntracerebral HemorrhageSubarachnoid HemorrhageIntroductionDefinitiona group of brain dysfunctions related to disease of the blood vessels supplying the brainStroke: cerebrovascular accidentsudden loss of bloo

2、d circulation to an area of the brain, with corresponding loss of neurologic function.As if “struck by the hand of God”EpidemiologyThird leading cause of death Approximately 2 million new strokes each year in chinaAssociated with risk factors (see below)Blood supply of the Braininternal carotid arte

3、ry vetebral-basilar arterythey are interconnected by an arterial circle (of Willis)INTERNAL CAROTID ARTERYINTERNAL CAROTID ARTERYEnters cranium via the carotid canal of the temporal boneSupplies dura, hypophysis, tympanic cavity and trigeminal gangliaProvide direct branches to the optic nerve, optic

4、 chiasm, hypothalamus and genu of internal capsulTerminal branches are the anterior and middle cerebral arteriesAnterior cerebral artery (ACA)Anterior cerebral arteryCortical branches supply all the medial surface of the cerebral cortex (basal ganglia, corpus callosum) as far back as the parieto-occ

5、ipital sulcus.Key functional areasPrimary motor cortex for leg and footMotor planning in medial frontal lobeMiddle and anterior corpus callosumMiddle cerebral arteryMiddle cerebral artery (MCA)Largest branch, Runs in the lateral sulcusDivides into superior and inferior branchSuperior MCA lateral and

6、 inferior frontal, anterior part of parietal Inferior MCA lateral temporal, posterior parietal, lateral occipital.Central perforating branches supply the lentiform and the caudate nuclei and the internal capsuleDeep branches of MCAKey functional areas of MCAPrimary motor cortex for face, arm, legPri

7、mary sensory cortex for face, arm, legBrocas language area (superior MCA)Wernickes area (inferior MCA)Perception of own body, outside world and ability to express emotionsArea of supply of cerebral arteriesVERTEBROBASILAR SYSTEMEnter the cranial cavity through the foramen magnum.Just inferior to the

8、 pons, fuse to form the basilar artery. Key functional areas1/3 of posterior braincerebellumSpinal cord tracts pyramidal and spinothalamicCranial nerves 3 - 12VERTEBROBASILAR SYSTEMVertebral artery branchesThe meningeal branchesThe posterior spinal arteryThe anterior spinal arteryPosterior inferior

9、cerebellar artery (PICA)Small medullary arteriesBASILAR ARTERY BRANCHESPontine arteriesLabyrinthine artery (Supplies the internal ear)Anterior inferior cerebellar artery (AICA)Superior cerebellar artery (SCA)Anterior and posterior spinal arteryPosterior cerebral artery (PCA)Posterior cerebral artery

10、 (PCA)Blood supply for midbrain, half thalamus, geniculate bodiesoccipital lobe, visual cortex, inferior temporal lobe, including the hippocampusKey functional areasPrimary visual cortex3rd nerve in midbrainSensory control temperature, pain, sleepCIRCLE OF WILLIS-Bridges ICA and vertibrobasilar arte

11、ryCIRCLE OF WILLISFormed by anastomosis between two internal carotid and two vertebral arteriesThe contributing arteries areThe anterior communicatingThe anterior cerebralThe internal carotidThe posterior communicatingThe posterior cerebralThe basilarCerebral blood flow(CBF)The brain accounts for 2%

12、3% of body weight but utilizes 20%25% of glucose and energy.Regulation of CBFBlood pressure: CBF is automatically regulated when mean arterial pressure (MAP) is between 60-160mmHg (Bayliss effect). Autonomic regulation will not be effective when MAP is below 60mmHg or above 160mmHg (hypertension).Ch

13、emicals: O2, CO2 and pH in blood and CSF.Common forms of CVDTIAIschemia（缺血性,8590%）Thrombosis（腦血栓形成）Embolism（腦栓塞） Hemorrhage（出血性,1015%）Intracranial hemorrhage（腦出血） Subarachnoid hemorrhage （蛛網(wǎng)膜下腔出血）Risk factors of CVDNon-modifiable risk factorsAge, Sex , Race, GeneticsModifiable: TIAsHigh blood pressu

14、reAtrial fibrillationDiabetesCholesterolOthers: smoking, alcohol, drugs (contraceptive, cocaine, amphetamines), lack of physical activities, obesityPrimary preventionTreatment of risk factors in individuals with no previous history of strokeHypertension: blood pressure to 140/90mmHgAtrial fibrillati

15、on: 1/6 of stroke in patients 60 years oldWarfarin +statins(lipid reduction)DiabetesSecondary preventionRisk factor treatment for those who have experienced a strokeBlood pressure lowering:Recommended even for normal blood pressure without stenosisCholesterol loweringLow dose of statins is suggested

16、 even for normal cholesterol levelAntiplatelet agents aspirin + dipyridamole (雙嘧達莫) is better than aspirin aloneClopidogrel: aspirin allergy, or with coronary artery diseaseAnticoagulants: Atrial fibrillation, or TIACarotid intervention: Stenosis of 50%: Endarterectomy(proven beneficial for symptoma

17、tic, applied within 2 weeks), stenting (angioplasty, 支架成形術(shù), recommended in younger patients of 70 years old). Aneurysms: clipping or coilingSupposed to know in this sectionRisk factors Concepts of primary and secondary prevention of CVDOutlineIntroductionTransient Ischemic Attacks (TIA)Ischemic stro

18、keIntracerebral HemorrhageSubarachnoid HemorrhageTransient Ischemic Attacks (TIAs)Are episodes of stroke symptoms that only last briefly, with average duration of 12min. Without evidence of infarction50% of TIA recovered within the first hour, 90% recovered within 4 hours. Infarcts do occur in 15 to

19、 40% of TIAs even though neurologic signs and symptoms are absentUrgent risk stratification is requiredCauses and pathophysioloyCauses are similar to all strokePathophysiologyBlood flow dynamics: Atherosclerosis or stenosis + blood pressure fluctuation, or with high coagulative stateMicro-emboli: At

20、herosclerosis, arterial or vetricular sourcesOthers: Arteritis, arterial steal syndrome (ASS) Clinical presentationsAge: 5070 years oldWith risk factors: hypertension, heart disease, diabetes, abnormal blood lipidAbrupt onsetBrief neurologic deficitsInternal carotid systemVertibro-basal systemIntern

21、al carotid TIAsCommon features: contralateral hemiplegia, sensory loss or numbnessCharacteristic presentations: transient monocular blindness(ophthalmic artiery), with contralateral hemiplegia or sensory disturbanceHoners sign (hypothalamus) with contralateral hemiplegiaAphasia (MCA occlusion)Vertib

22、ral-basal TIAsCommon features: Vertigo, usually without tinnitus (耳鳴); nausea, vomiting Characteristic featuresDrop attack: brain stemTransient global amnesia: temporal lobe, the hippocampusPossible symptoms: Diplopia (復(fù)視), nystagmus, dysarthria(構(gòu)音障礙), dysphgia(吞咽困難),ataxia, disturbance of conscious

23、nessCrossed sensory disturbance: Wallenberg syndrome Crossed paralysis: cranial nerves (brain stem syndromes), will be discussed in detail in next sectionDiagnostic testsRisk factors:Blood pressure, serum lipid and sugar, coagulation (ESR, Erythrocyte sedimentation rate; Thrombin time),artery diseas

24、es(atherosclerosis, arthritis), heart disease (atrial fibrillation, patent foramen ovale),TCD (transcranial Dopplar):Large artery blood flow dynamicsArterial stenosis: MRA, CTA, sometimes DSADiagnosisHeavily relies on historyAged peopleTransient signs or symptomsInternal carotid or vertibral-vasal s

25、ystemlast for min and are recovered in 24 hrsImage study fails to show any lesionsDifferential diagnosisEpilepsy: symptoms last for seconds(5min), stereotyped, loss of consciousness (events can not be recalled), EEG abnormalityMeniere Disease: vertigo/nausea several hrs, with hearing impairment, ves

26、tibular dysfunctionMigraine: vertigo sometimes, younger in age (60 years old; duration 10minSymptoms: unilateral motor weakness, speech disturbanceHypertension 140/95mmHgDiabetes Treatment: Hospitalization suggestedAspirin or aspirin + clopidagrel for 2 weeksBlood pressure controlLowering blood suga

27、rDrug treatment for TIAsAntipletlets: Aspirin 50300mg qd.Or aspirin 100mg qd + dipyridamole 2550mg tidOr aspirin 100mg qd + clopidagrel 75mg qd (in acute phase 5070%)Endarterectomy or angioplastyHeart diseasesHypertensionDiabetesHyperlipidaemiastatinsImportant notes in TIAsDiagnosis of TIAsAged peop

28、le brief presentation (minutes), recovered within 24hrsNo positive image findingsDifferential diagnosis of TIAsTreatment principlesIdentify high risk TIAsDrug choiceUnderlying pathology controlOutlineIntroductionTransient Ischemic Attacks (TIA)Ischemic stroke (cerebral infarction)Intracerebral Hemor

29、rhageSubarachnoid HemorrhageCerebral infarction(cerebral ischemic stroke)Major forms of ischemic strokeAtherosclerotic thrombotic cerebral infarctionCerebral embolismLacunar infarction (small-vessel stroke)Border zone infarction (cerebral watershed infarction)They share common pathophysiology and th

30、erefore the treatment is similar.EtiologyCommon: Thrombus: Atherosclerosis, dehydrationEmbolus: artery-to-artery, cardioembolic, valvular lesions, patent foremen ovaleLess common: Hypercoagulable disorders: sickle cell anemia, SLE, homocysteinemia, oral contraceptivesVenous sinus thrombosisVasculiti

31、sVasospasm after subarachnoin hemorrhageDrugs:coccaine, amphatamine,Moyomoya diseaseCBF in ischemiaNormal CBF is approximately 5060 ml/100 g /minPermanent ischemia 17 - 18 ml/100g/min histological changes2 hours ischemia 12 ml/100g/min histological changesReduction of CBF of less than 10 ml/100 g/mi

32、n results in irreversible neuronal injuryIschemic cascadeLack of oxygen supply to ischemic neuronesATP depletionMembrane ions system stops functioningDepolarisation of neuroneInflux of calciumRelease of neurotransmitters, including glutamate, activation of N-metyl -D- aspartate and other excitatory

33、receptorsat the membrane of neuronesFurther depolarisation of cellsFurther calcium influxCarrol and Chataway,2006Energy failure / depolarisationTransmitter releaseand receptor activation Ca2+Lipolysis (DAG PKC) ProteinphosphorylationProteolysisDisaggregationof microtubuli(FFAs.LPLs)EnzymeconversionB

34、reakdown ofcytoskeletonDamage to membranestructure and functionDysfunction ofreceptors andion channelsFree radicalformationInhibition of axonaltransportCosequences of brain ischemiaIschemic penumbraRing-like area around ischemic centerBlood flow range between the thresholds of transmitters release a

35、nd cell membranes failureFunctional activity of the neurons is suppressed although structural integrity of the cell is still preserved - neurons are injured but still viableIt provides a rational basis for functional improvements in injured brain tissue occurring long after the onset of stroke MRI o

36、f ischemic penumbraDWI/PWI mismatch is increasingly being used to identify patients who are most likely to benefit from new interventions in acute ischaemic strokeCell death and tissue edemaTwo types of cell deathNecrosis: core of infarctApoptosis: may exists in penumbraBrain edema: leading cause of

37、 death especially in the first weekMixture of cytotoxic and vasogenic edemaCytotoxic occurs early due to cell energy failure Vasogenic edema occurs latter due to disrupted blood-brain barrierThe concept of diaschisis(失聯(lián)絡(luò))Remote disturbances of brain cells due to the suppression of neurons connected

38、to the injured (ischemic) region The remote focus of brain suffer a kind of shock when deprived from afferent input comming from ischemic focus Disturbed neurotransmitter metabolism Appears within 30 min after the onset of ischemia; reverses after a few month Also seen in spinal shock after acute my

39、elitisAtherosclerotic thrombotic cerebral infarctionAtherosclerotic thrombotic cerebral infarctionTypes: complete stroke develops within 6 hrs, progressive stroke develops in 6hrs to several daysMiddle to old ageRisk factorsNeurologic defects: hemiplegia, hemianesthesia, aphasia, ataxia. Sometimes v

40、omiting and coma, and , death.Stroke syndromesInternal carotid arteryMCA, ACAMotor, sensory and advanced brain functionVetebrobasilar arteryBrain stem, cerebellum, part of hypothalamus, thalamusCranial nerve, cerebellar dysfunction with crossed characteristicsACA occlusionUsually without neurologic

41、deficitCollaterals from MCA,PCA, or anteriaior communicating arteryParalysis and sensory loss of opposite foot and legUrinary incontinence (paracentral lobule)Contralateral gasp and sucking reflexAbbulia (akinetic mutism), slownessMCA occlusionComplete block: 3 HEMIs: contralateral hemiplegia, hemia

42、nesthesia, homonymous hemianopia Gaze preferance to ipsilateral sideAdvanced brain functionAphaia, anosognosia (病覺缺失), constructional apraxia (結(jié)構(gòu)性失用)Vertibral arteries occlusionWallenberg Syn.(lateral medullary syn.)VIII, IX, X cranial nerve: Vertigo, hoarseness, dysarthria, disphagia,Crossed surfac

43、e sensory loss: ipsilateral face and contrlateral trunk and limbHorners sign (ipsilateral) Ataxia (ipsilateral)Cerebellar infarctionGait unsteadiness,nausea, vomitting, with headache, neck stiffnessEdema can lead to sudden respiratory arrestBasilar artery occlusionThree groups: paramedian (7-10 bran

44、ches), short circumferential (5-7) and bilateral long circumferential (SCA and AICA)Affects corticospinal and corticobulbar tracts, ascending sensory tracts and cranial nerve nuclei (sensory + motor+ cranial nerves+cerebellum)Complete block usually causes bilateral signsCommon syndromes: basilar art

45、ery occlusionMedial inferior pontine syn.(Millard-Gubler Syn.)Ipsilateral facial and abdunct nerve palsyContrlateral hemiparalysisLock-in syn (bilateral pontine infarction)Preserved consciousnessQuapledia and lower cranial nerve signsTop of the basilar syn(TOBS, SCA+PCA)Rostral brain stem: dysfuncti

46、onal eye movement and pupil(anisocoria,瞳孔不等), disturbance of consciousness, hypersomnia (嗜睡)PCA: memory loss, homonymous hemianopia Hallucination of cerebral peduncle: animated, vivid charateristicsTOBSPCA occlusionCortical branches: contralateral homonymous hemianopia with macula sparing , acute di

47、sturbance of memoryPenetrating branches:3rd nerve palsy with contralateral hemiplegia (Weber syndrome), or contralateral ataxia or dyskinesia(Benedikt Syndrome, red nucleus)Thalamic syndrome: contralateral hemisensory loss or burning painImaging studiesCTuseful for identifying ischemia from hemorrha

48、gesensitive to ischemia in brain hemisphere after 24hrsMRICan find small and posterior fossa ischemiaSensitive in several min, but time consumingAngiographyCTA, DSA and MRAHelpful in finding vesculopathiesExamples of CT and MRI (MCA occlusion)a Magnetic resonance angiography, b diffusion-weighted im

49、aging and c perfusion-weighted imaging performed in a patient 2.5 hours after onset of aphasia and right hemiparesis. Occlusion of the left middle cerebral artery trunk (arrow) is seen, with a small diffusion abnormality and a large perfusion abnormality indicative of a large ischemic penumbra (tiss

50、ue potentially salvageable with thrombolysis).DiagnosisMiddle to old ageRisk factors including previous TIAsSymptoms peak within min to several daysNeurologic deficits correspond to occluded brain areasPositive image findingsDifferential diagnosisThrombotic vs. embolicAge, heart disease, TIAs, onset

51、Ischemic vs. hemorrhagicAge, TIAs, background activity, symptom onset, sings of intracranial hypertension, imaging studySubdural/epidural hematomaHistory of head injury, sings of intracranial hypertension, CT findingSpace occupying lesionsBroken tumor or abscessPrinciples of treatment General manage

52、ment: very importantManagement of brain edemaTargeting on thrombosisThrombolysis, fibrinolytics, anticoagulants, antipltelets (Avoid combined use of these drugs)NeuroprotectionSurgeryRehabilitation General managementAirwayHypertension(200/110mmHg) Blood sugar HyperthermiaUpper gastrointestinal bleed

53、ingFluid and electrolyte imbalanceHeart diseaseEpilepsyBrain edemaElevation of the head end of the bed to a 2030 degree angle to improve venous drainage.Hypoxia, hypercapnia, hyperthermia, hyperglycemia, and antihypertensive drugs, particularly those that can cause cerebral vasodilatation, should be

54、 avoided.Osmotherapy (manitol, glycerol fructose, corticosteroids). Surgical: decompressive surgery, ventricular drainage.Thrombolysis IndicationsTime window: 4.5 hrs for rt-PA, 6hrs for urokinase(UK)No known intracranial hemorrhageContraindicationsBleeding tendency (history of bleeding, anticoagula

55、nts, low plasma platelets), Recent (3months) cerebral or cardiac infarction,Special conditions: Pregnant, severe systemic diseases, hypertension, hypoglycemiaUsage of thrombolysisrt-Pa: 0.9mg/kg (maximum 90mg)/ iv. gtt (in 100ml NS)Urokinase(UK)11.5 million IU /iv. Gtt (in 100ml NS)Anticoagulants Not rec