大四下神经病3cvd英文

1、Cerebrovascular Disease （CVD，脑血管疾病）Jian W Department of Neurology Second affiliated Hospital Chongqing Medical UniversitylEmbolism 栓塞 embolus 栓子lThrombosis 血栓形成 thrombus 血栓lStroke 中风 atherosclerosis 粥样硬化lArteriosclerosis 小动脉硬化lAphasia 失语 Basal ganglia 基底节lPutamen 壳核 internal capsule 内囊lWatershed inf

2、arction 分水岭梗死lPenumbra 半暗带lTransient ischemic attack (TIA)短暂性脑缺血发作lCerebral infarction 脑梗死lHemiplegia 偏瘫lHemiparesis 轻偏瘫lHemianesthesia 偏身麻木lHemianopia 偏盲lAmaurosis fugax 一过性黑朦lDrop attack 跌倒发作lNeuroprotection 神经保护lAnticoagulant 抗凝剂lAntiplatelet drugs 抗血小板药物lDiabetes mellitus 糖尿病lHyperlipidemia 高脂血症

3、lHyperglycemia 高血糖lLenticulostriate branch 豆纹支lThrombocytosis 血小板增多症lHomocysteinemia 同型半胱氨酸血症lAtrial fibrillation 心房纤颤lAny abnormality of the brain resulting from a pathologic process of the blood vessels. lSudden loss of neurological function is the hallmark of CVD.lCerebrovascular accident or stro

4、ke may be defined as a sudden interruption of blood supply by embolism or thrombosis, or hemorrhage into the brain. lThe first leading cause of death in ChinalAbout 2 million/per year in ChinalHospitalization cost 9 billion annuallylAccording to WHO prediction, the stroke incidence in China increase

5、s by 9% annually.lIschemic transient ischemic attack (TIA)l cerebral thrombosisl cerebral embolism cerebral infarctionl lacunar infarctlHemorrhagic intracerebral hemorrhage (ICH)l subarachnoid hemorrhage (SAH)Internal carotid artery and vertebro-basilar arteryInternal carotid artery and vertebro-bas

6、ilar arterylOphthalmic arterylPosterior communicating arterylAnterior choroidal arterylAnterior cerebral arterylMiddle cerebral arterylpenetrating branch: lenticulostriate brancheslmost of the cerebral cortex (frontal, parietal, temporal lobe) and subcortical white matter, basal ganglia, internal ca

7、psule, optic nerve and retina.l Vertebral artery l Basilar artery lPosterior inferior cerebellar arterylAnterior inferior cerebellar arterylSuperior cerebellar arterylPosterior cerebral arterylbrain stem, cerebellum, thalamus and portions of the occipital and medial temporal lobe.Collateral circulat

8、ion (Willis Circle)Arteries in relation to the Willis circle include: Internal carotid artery (ICA) Anterior cerebral artery (ACA) Anterior communicating artery (ACoA) Posterior communicating artery (PCoA) Posterior cerebral artery (PCA) Basilar artery (BA)lAnastomosis branches between major arterie

9、s Controllable Uncontrollable hypertension age Diabetes mellitus sex hyperlipidemia race heart disease genetic factor atrial fibrillation heavy alcohol consumption cigarette smoking homocysteinemia oral contraceptive pill1.Vascular disorders: atherosclerosis, hypertensive arteriosclerosis, fibromusc

10、ular dysplasia, inflammatory disorders, carotid or vetebral artery dissection, drug abuse, moyamoya.2.Cardiac disorder: Mural thrombus, rheumatic heart disease (mitral stenosis and atrial fibrillation), arrhythmias, endocarditis, mitral valve prolapse, atrial myxomaThrombocytosis 血小板增多（症） Polycythem

11、ia 红血球增多症 Sickle cell disease 镰状细胞病 Leukocytosis 白血球增多症 Hypercoagulable states hypotension hypertension change of blood volume heart disease (cardiac insufficiency, arrhythmias ) lTIA is a focal disturbance of the cerebral circulation, frequently repetitive, resulting in acute loss of focal cerebral

12、 function.lSymptoms last less than 24 hours (often F characteristics:Abrupt onsetTransient ( middle anterior vertebral-basilarlArteritis: connective tissue diseaselrare cause: l congenital vascular malformationl polycythemial blood hypercoagulabilityl1-6 hour: super-early stage, tissue changes are n

13、ot obviousl12-24h: ischemic tissue swell / softenl7-14 days: Necrosis and liquefaction l3-4weeks: Necrotic tissue is cleared, glial scars or stroke capsule.lRed infarct: hemorrhagic infarctlMetabolism disturbance and acidosislexcitatory amino acid and calcium overloadlBreakdown of membranes lFree ra

14、dical lIschemic edemalNitric oxidelImmediate early gene, neurotrophic factors and heat shock protein lcytokineslapoptosislNeurons are sensitive to ischemial Central necrosis: irreversible damage l Ischemic penumbra: can be rescued!l the target of therapy Core of ischemic areaIschemic penumbraAt the

15、beginning Core of ischemic areaIschemic penumbra6 hours laterCore of ischemic areaIschemic penumbra24h laterlonset is rapid lusually occur in the rest and sleep lpremonitory symptoms such as weakness of a limb, transient ischemic attack lThe headache, vomit, and loss of consciousness may be absent o

16、r slight. lFocal signs often develop in several dayslreversible ischemic neurologic deficit, RIND (可逆性缺血性神经功能缺损) :minor stroke 3wlProgressive ischemic stroke (进展型缺血性脑卒中) 6h-2wlCompleted ischemic stroke (完全型缺血性脑卒中) 6h1. Internal carotid arteryMay have no signs (if the collateral supply from the other

17、 side is good )amaurosis fugax, uniocular blindnessHorners syndrome may present in the side of the occlusion. contralateral hemiplegia and hemianesthesia. 2. Middle cerebral arterycontralateral hemiplegia, hemianesthesia, hemianopiaaphasia (if the dominant hemisphere is affected)Disturbance of body

18、image (non-dominant hemisphere)3. Anterior cerebral artery Loss of use and / or feeling in the contralateral leg.paracentral lobule: regulation of sphincter function, retention or incontinencemental symptoms: apathy, euphoria(欣快） 4. Posterior cerebral arterycontralateral hemianopia or quadrantanopia

19、（象限盲）（象限盲） thalamic syndrome: contralateral hemianesthesia, thalamic pain, tremor, athetosis（手足徐动症）（手足徐动症）5. Vertebro-basilar artery(1) Main trunkvertigo, nausea, vomiting, tetraplegia, coma, death(2) Weber syndromeUnilateral lesion of midbrainSign: Ipsilateral oculomotor nerve paralysis, contralate

20、ral hemiplegia. (3) locked-in syndromeBilateral infarction in the basis ponsPatients remain conscious Tetraplegia, can not speak, can not swallow, only respond by eye movement.6. posterior inferior cerebellar artery Wallenbergs syndrome:Vertigo, vomiting, nystagmusCrossed sensory disturbance (ipsila

21、teral facial sensory deficit and contralateral impaired pain and temperature sensation)Ipsilateral Horners sign Dysphagia, dysarthriaIpsilateral cerebellar ataxia1. CTCT is usually preferred for initial diagnosis because it is widely available and rapid, it can readily make the critical distinction

22、between ischemia and hemorrhage.CT is often normal within 24h, especially within 6h.Low density focus after 24-48 hours2. Magnetic resonance imaging (MRI)lMRI is superior to CT scan for demonstrating early ischemic infarcts. lMRI (DWI) can find ischemic focus even within a few minutes after onset.23

23、h after stroke onset 8h after stroke onset MRA may detect stenosis of large cerebral artery, aneurysm, and other vascular lesion, but its sensitivity is generally inferior to that of conventional angiography.Magnetic resonance angiography (MRA) DSA is used to identify patients with vascular stenosis

24、 who are good surgical candidates. It also can be used for intra arterial thrombolysis.3.Cerebral Angiography (DSA)lafter middle or old age. loccurs in rest or sleeplpremonitory symptomslrapid onset and focal cerebral symptomslCT / MRI find cerebral infarction focuslIntracerebral hemorrhagelSubdural

25、 or epidural hematomalCerebral embolismlIntracranial tumorPrinciple:1. Restore the circulation and arrest the pathologic process: reperfusion therapy at super-early stageTime window: 34.5 hours Tissue-type plasminogen activator (rt-PA)2. Neuroprotective agents: keep neuron viable in the ischemic sta

26、teCalcium antagonist: nimodipineantioxidant: edaravone (依达拉奉） 3. Control brain edema and reduce intracranial pressure:Dehydrant: Mannitol, glycerin fructoseDecompressive craniectomy 4. Prevent and treat complications: infection, arrhythmia, upper gastrointestinal hemorrhage 5. Physical therapy and r

27、ehabilitation 6. Prophylactic treatmentControl risk factorsAspirin, Clopidogrella small subcortical infarction (50 years, history of hypertension, MFwith emotional excitement or active stateSudden onset, reach a peak within a few minutes or hours.Common manifestations: increased intracranial pressur

28、e; neurological deficits (paralysis of limbs, aphasia, etc.); blood pressure often increase significantly.Clinical manifestations depend on the site.About 3/4Site: putamen, thalamusputaminal hemorrhage results in a more serious motor deficit and thalamic hemorrhage results in a more significant sens

29、ory disturbance. 1.Deep cerebral hemorrhage10%. 40 years oldCauses: cerebral arteriovenous malformation, moyamoya disease, vascular amyloidosis, tumor, etc.Location: parietal other lobesManifestations: headache, vomiting focal symptoms, seizures are more frequent, while coma is rare.10%Small bleedin

30、g:Crossed paralysis; internuclear ophthalmoplegia, side-glance paralysis. No disturbance of consciousness large bleeding ( 5ml): rapid coma, quadriplegia, decerebrate rigidity, pinpoint pupils, central high fever and breathing problems, usually die within 48 hours.10%Symptom: headache, dizziness, at

31、axia, without limb paralysis.large hemorrhage leads to rapid coma and foramen magnum herniation (tonsillar herniation)3-5%rupture of choroid plexus artery or subependymal artery.Small hemorrhage: resembles SAHLarge hemorrhage: rapid coma, frequent vomiting, pinpoint pupils, quadriplegia, decerebrate

32、 rigidity, and rapid death. lCT: l (1)the most useful diagnostic procedure, since hematomas can be quickly identifiedl (2)high density, easily distinguishable from infarctionl (3)hematoma size, location, edema, tissue shift. lLumbar puncture: not routinely recommended lMRI: less value than CT in acu

33、te phaselDSA / MRA: search for the causel 50lhistory of high blood pressureloccurs in emotional excitement or active statelintracranial hypertension, focal neurological deficitlCT: final diagnosislCerebral infarctionlIntoxications and metabolic disease: coma, but lack focal signs, medical history an

34、d laboratory tests.lTraumatic intracranial hematomaprinciples:Prevent further bleedingLower intracranial pressure and control cerebral edemaAdjust blood pressurePrevent complications 1.General treatment:Nearest treatment, bed rest, keep quiet and reduce visitation.Keep the airway open.Close observat

35、ion of vital signs, pupil and altered consciousness.Note maintaining water and electrolyte balance and nutrition.2. Control cerebral edema (3-5d reach a peak):Mannitol, glycerin fructose.Pay attention to side effects. 3. Adjust blood pressure:AHA recommends blood pressure be maintained a mean arteri

36、al pressure of 130mmHg in persons with a history of hypertension.Overaggressive treatment of blood pressure may decrease cerebral perfusion presure and worsen brain injury-Gently lower! 4. Prevent and treat complications: similar to cerebral infarction lObjective: l remove the hematoma, relieve brai

37、n herniation, save lives, and to remove the cause (such as vascular malformations), to prevent the occurrence of complications (such as hydrocephalus)lIndications:l (1) sustained increase in intracranial pressure, brain herniation trend or early brain herniation.l (2) basal ganglia hemorrhage 30mll

38、(3) cerebellar hemorrhage 10 ml of (or 3cm) with brain stem compression and hydrocephalus.l (4) ICH due to vascular malformation or aneurysm. Surgical treatment Surgical methods: craniotomy (small bone window craniotomy)，minimally invasive puncture for removal of hematoma.Rehabilitation If condition

39、 permits, rehabilitation should be early. Subarachnoid hemorrhage (SAH)lDefinition: a clinical syndrome of blood flow into the subarachnoid space.lCategory:l Primary (vessel rupture in the surfacel Spontaneous or at the base of the brain ) l Secondary (from ICH) TraumaticlGenerally so-called SAH mea

40、ns primary SAHlcongenital aneurysmlAneurysms are mostly in the bifurcation and the nearby branch of the Willis Circle. Common site of intracranial aneurysms Uncommon causes:Cerebral vascular malformation (arteriovenous malformation, AVM)Hypertension atherosclerosisCerebral arteritisBlood diseasesaft

41、er thrombolytic or anticoagulant therapylAge: all age groups, young adults lOnset: sudden, some have prodromal symptomsl (small amount of bleeding or errhysis) lMain features: Severe headache, nausea, vomiting / seizureTransient loss of consciousness lSymptoms in elderly patients may be not typicall

42、signs:l Neck rigidity: main sign Focal signs: diplopia, limb paralysis (early / late onset), l vitreous hemorrhage Late-onset cerebral vasospasm1. CT1. CTThe first choice for The first choice for diagnosis.diagnosis.Find the bleeding, amount Find the bleeding, amount and distribution, and distributi

43、on, ventricle size, brain ventricle size, brain hematoma.hematoma.high density in sulci, high density in sulci, cisternal or lateral cisternal or lateral fissurefissureNote: CT may be negative Note: CT may be negative if amount of bleeding is if amount of bleeding is small or CT is done long small o

44、r CT is done long time after onset.time after onset.2.CSF2.CSFimportant basis for diagnosisimportant basis for diagnosisIndications: history is strongly suggestive, Indications: history is strongly suggestive, but CT can not be done or CT was negative.but CT can not be done or CT was negative.result

45、: ICP , bloody CSF or xanthochromiaresult: ICP , bloody CSF or xanthochromia3.DSA3.DSAFirst choice to find the cause, DSA should be First choice to find the cause, DSA should be done as soon as possible.done as soon as possible.Purpose: find the aneurysm, etc. determine its Purpose: find the aneurys

46、m, etc. determine its location, shows the vascular anatomy, location, shows the vascular anatomy, collateral circulation and vasospasm. collateral circulation and vasospasm. 4.MRI and MRAMRI is rarely used in acute phaseMRA can find aneurysms, but can not replace the DSA.5.TCDmonitoring cerebral vasospasmlSud