神经病学：脑血管疾病

1、Cerebrovascular Disease （CVD，脑血管疾病）,Special words,Embolism 栓塞 embolus 栓子 Thrombosis 血栓形成 thrombus 血栓 Stroke 中风 atherosclerosis 粥样硬化 Arteriosclerosis 小动脉硬化 Aphasia 失语 Basal ganglia 基底节 Putamen 壳核 internal capsule 内囊 Watershed infarction 分水岭梗死 Penumbra 半暗带,Transient ischemic attack (TIA)短暂性脑缺血发作 Cereb

2、ral infarction 脑梗死 Hemiplegia 偏瘫 Hemiparesis 轻偏瘫 Hemianesthesia 偏身麻木 Hemianopia 偏盲 Amaurosis fugax 一过性黑朦 Drop attack 跌倒发作 Neuroprotection 神经保护 Anticoagulant 抗凝剂 Antiplatelet drugs 抗血小板药物,Diabetes mellitus 糖尿病 Hyperlipidemia 高脂血症 Hyperglycemia 高血糖 Lenticulostriate branch 豆纹支 Thrombocytosis 血小板增多症 Hom

3、ocysteinemia 同型半胱氨酸血症 Atrial fibrillation 心房纤颤,Conception,Any abnormality of the brain resulting from a pathologic process of the blood vessels. Sudden loss of neurological function is the hallmark of CVD. Cerebrovascular accident or stroke may be defined as a sudden interruption of blood supply by

4、embolism or thrombosis, or hemorrhage into the brain.,Epidemiological investigation,The first leading cause of death in China About 2 million/per year in China Hospitalization cost 9 billion annually According to WHO prediction, the stroke incidence in China increases by 9% annually.,Classification,

5、Ischemic transient ischemic attack (TIA) cerebral thrombosis cerebral embolism cerebral infarction lacunar infarct Hemorrhagic intracerebral hemorrhage (ICH) subarachnoid hemorrhage (SAH),Cerebrovascular Anatomy,Internal carotid artery and vertebro-basilar artery,Carotic and vertebral arteries,Inter

6、nal carotid artery and vertebro-basilar artery,Internal carotid artery,Ophthalmic artery Posterior communicating artery Anterior choroidal artery Anterior cerebral artery Middle cerebral artery penetrating branch: lenticulostriate branches,Anterior circulation dominated area,most of the cerebral cor

7、tex (frontal, parietal, temporal lobe) and subcortical white matter, basal ganglia, internal capsule, optic nerve and retina.,Brain arteries: lateral and medial aspects,Brain arteries lateral view,Basilar-vertebral artery,Vertebral artery Basilar artery,View to medulla, brainstem and inferior brain

8、vessels,Basilar-vertebral artery,Posterior inferior cerebellar artery Anterior inferior cerebellar artery Superior cerebellar artery Posterior cerebral artery,Posterior circulation dominated area,brain stem, cerebellum, thalamus and portions of the occipital and medial temporal lobe.,Collateral circ

9、ulation (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),Collateral circulation,Anastomosis br

10、anches between major arteries,Risk factors of CVD,Controllable Uncontrollable hypertension age Diabetes mellitus sex hyperlipidemia race heart disease genetic factor atrial fibrillation heavy alcohol consumption cigarette smoking homocysteinemia oral contraceptive pill,Essential causes,1.Vascular di

11、sorders: atherosclerosis, hypertensive arteriosclerosis, fibromuscular 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, mit

12、ral valve prolapse, atrial myxoma,3.Haematological disorders :,Thrombocytosis 血小板增多（症） Polycythemia 红血球增多症 Sickle cell disease 镰状细胞病 Leukocytosis 白血球增多症 Hypercoagulable states,4.Hemodynamic factors:,hypotension hypertension change of blood volume heart disease (cardiac insufficiency, arrhythmias ),T

13、ransient Ischemic Attack (TIA),Definition,TIA is a focal disturbance of the cerebral circulation, frequently repetitive, resulting in acute loss of focal cerebral function. Symptoms last less than 24 hours (often 1h). Attacks can occur in the carotid or vertebral artery territories.,Etiology and pat

14、hogenesis,Micro embolism Hemodynamic change Others: cerebral vasospasm; compression of vertebral artery; subclavian steal syndrome,Clinical feature,1. age: 50-70 years, MF characteristics: Abrupt onset Transient ( 24 hours ) Complete recovery (without any residual) Recurrent attack,2. Transient caro

15、tid ischemic attacks (1) Common symptom: Weakness of the contralateral arm and/or leg. (2) Characteristic symptoms: Transient monocular blindness caused by ipsilateral retinal artery ischemia (3) Symptoms may present: Aphasia is present with dominant hemisphere involvement Paraesthesia or numbness i

16、n the contralateral limbs. hemianopia,Clinical feature,3. Transient vertebral basilar ischemic attack (1) Common symptoms Vertigo, nausea, vomiting (2) Characteristic symptoms: Drop attack (sudden collapse without loss of consciousness) Transient global amnesia (TGA): Loss of memory, without other a

17、bnormal symptoms. Cortical blindness Crossed paralysis or sensory disturbance (affect the face on one side of the body and the limbs on the other side),Clinical feature,(3) Symptoms may present: Dysphagia, dysarthria Ataxia Disturbance of consciousness Diplopia,Clinical feature,Assist examination,CT

18、 scan or MRI: show no fresh focus TCD (transcranial doppler): arterial stenosis or micro-embolus DSA (digital subtraction angiography) : vasculopathy (stenosis, plaque),Diagnosis,Depend on history (4 clinical features) Risk factors,Differential diagnosis,Meniere disease: The attack can last several

19、days, with tinnitus, hearing loss after several episodes. Partial epilepsy: Short duration, convulsions, EEG shows epilepsy waves. Others: Migraine, hypoglycemia, hypotension,Treatment,1. Etiologic treatment Control blood pressure, blood glucose, blood lipid Treat cardiac disease Operation treatment

20、: moderate (50-70%) or high-grade (70-90%) carotid stenosis: Carotid endarterectomy, intraluminal stents,2. Prophylactic treatment Anti-platelet aggregation drugs: Aspirin 100mg Qd Po clopidogrel 75mg Qd Po Anticoaguation: Warfarin orally 3. Brain protective agents Calcium antagonist: nimodipine 20-

21、40mg tid po flunarizine (Sibelium) 5mg Qn po,Treatment,Prognosis,1/3 continue to repetitive attack 1/3 remission 1/3 cerebral infarction (within 5 years),Cerebral infarction,Atherothrombotic cerebral infarction,Definition,The formation of an area of necrosis in the cerebrum caused by an insufficienc

22、y of arterial blood flow. Vascular stenosis, slow blood flow, blood components abnormal or blood viscosity increase, leading to the formation of thrombus which occludes vascular.,Etiology,Atherosclerosis: often associated with high blood pressure, DM and hyperlipidemia. Thrombosis incidence: carotid

23、 middle anterior vertebral-basilar Arteritis: connective tissue disease rare cause: congenital vascular malformation polycythemia blood hypercoagulability,Pathology,1-6 hour: super-early stage, tissue changes are not obvious 12-24h: ischemic tissue swell / soften 7-14 days: Necrosis and liquefaction

24、 3-4weeks: Necrotic tissue is cleared, glial scars or stroke capsule. Red infarct: hemorrhagic infarct,Pathophysiology:Ischemic neuronal damage,Metabolism disturbance and acidosis excitatory amino acid and calcium overload Breakdown of membranes Free radical Ischemic edema Nitric oxide Immediate ear

25、ly gene, neurotrophic factors and heat shock protein cytokines apoptosis,Pathophysiology,Neurons are sensitive to ischemia Central necrosis: irreversible damage Ischemic penumbra: can be rescued! the target of therapy,Ischemic stroke,Core of ischemic area,Ischemic penumbra,At the beginning,Ischemic

26、stroke,Core of ischemic area,Ischemic penumbra,6 hours later,Ischemic stroke,Core of ischemic area,Ischemic penumbra,24h later,Clinical feature,onset is rapid usually occur in the rest and sleep premonitory symptoms such as weakness of a limb, transient ischemic attack The headache, vomit, and loss

27、of consciousness may be absent or slight. Focal signs often develop in several days,Clinical type,reversible ischemic neurologic deficit, RIND (可逆性缺血性神经功能缺损) :minor stroke 3w Progressive ischemic stroke (进展型缺血性脑卒中) 6h-2w Completed ischemic stroke (完全型缺血性脑卒中) 6h,Clinical syndrome,1. Internal carotid

28、artery May have no signs (if the collateral supply from the other side is good ) amaurosis fugax, uniocular blindness Horners syndrome may present in the side of the occlusion. contralateral hemiplegia and hemianesthesia.,2. Middle cerebral artery contralateral hemiplegia, hemianesthesia, hemianopia

29、 aphasia (if the dominant hemisphere is affected) Disturbance of body image (non-dominant hemisphere),Clinical syndrome,3. Anterior cerebral artery Loss of use and / or feeling in the contralateral leg. paracentral lobule: regulation of sphincter function, retention or incontinence mental symptoms:

30、apathy, euphoria(欣快）,Clinical syndrome,4. Posterior cerebral artery contralateral hemianopia or quadrantanopia（象限盲） thalamic syndrome: contralateral hemianesthesia, thalamic pain, tremor, athetosis（手足徐动症）,Clinical syndrome,5. Vertebro-basilar artery (1) Main trunk vertigo, nausea, vomiting, tetraple

31、gia, coma, death (2) Weber syndrome Unilateral lesion of midbrain Sign: Ipsilateral oculomotor nerve paralysis, contralateral hemiplegia.,Clinical syndrome,(3) locked-in syndrome Bilateral infarction in the basis pons Patients remain conscious Tetraplegia, can not speak, can not swallow, only respon

32、d by eye movement.,Clinical syndrome,6. posterior inferior cerebellar artery Wallenbergs syndrome: Vertigo, vomiting, nystagmus Crossed sensory disturbance (ipsilateral facial sensory deficit and contralateral impaired pain and temperature sensation) Ipsilateral Horners sign Dysphagia, dysarthria Ip

33、silateral cerebellar ataxia,Clinical syndrome,Assist examination,1. CT,CT is usually preferred for initial diagnosis because it is widely available and rapid, it can readily make the critical distinction between ischemia and hemorrhage. CT is often normal within 24h, especially within 6h.,Low densit

34、y focus after 24-48 hours,2. Magnetic resonance imaging (MRI),MRI is superior to CT scan for demonstrating early ischemic infarcts. MRI (DWI) can find ischemic focus even within a few minutes after onset.,23h after stroke onset,8h after stroke onset,MRA may detect stenosis of large cerebral artery,

35、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 who are good surgical candidates. It also can be used for intra arterial thrombolysis.,Inve

36、stigation,3.Cerebral Angiography (DSA),Diagnosis,after middle or old age. occurs in rest or sleep premonitory symptoms rapid onset and focal cerebral symptoms CT / MRI find cerebral infarction focus,Differential diagnosis,Intracerebral hemorrhage Subdural or epidural hematoma Cerebral embolism Intra

37、cranial tumor,Treatment,Principle: 1. Restore the circulation and arrest the pathologic process: reperfusion therapy at super-early stage Time window: 34.5 hours Tissue-type plasminogen activator (rt-PA) 2. Neuroprotective agents: keep neuron viable in the ischemic state Calcium antagonist: nimodipi

38、ne antioxidant: edaravone (依达拉奉）,3. Control brain edema and reduce intracranial pressure: Dehydrant: Mannitol, glycerin fructose Decompressive craniectomy 4. Prevent and treat complications: infection, arrhythmia, upper gastrointestinal hemorrhage 5. Physical therapy and rehabilitation 6. Prophylact

39、ic treatment Control risk factors Aspirin, Clopidogrel,Treatment,Lacunar infarct,Defination,a small subcortical infarction (15mm) that results from the occlusion of a penetrating end artery (100-200m). Lacuna predominate in the basal ganglia, thalamus, brainstem and internal capsule. Often multiple

40、- lacunar state,Etiology and pathology,Hypertension: the main etiological factor The cerebral arteriosclerosis with micro atheroma, lipohyalinosis, and fibrinoid necrosis stenosis secondary thrombosis lacunar infarction.,Clinical feature,40-60 years of age Always with history of hypertension Lacunar

41、 syndrome and localization: 1. Pure motor hemiparesis: posterior internal capsule, pons 2. Pure sensory stroke: thalamus 3. Ataxic-hemiparesis: pons, corona radiata 4. Dysarthric-clumsy hand syndrome: pons, anterior branch and genu of the internal capsule,Lacunar state: Multiple lacunar infarcts Oft

42、en involving the bilateral corticospinal tracts and corticobulbar tracts Pseudobulbar palsy, dementia, parkinson syndrome.,Clinical feature,Assist examination,CT scan: low density MRI: small infarction can be found,Diagnosis,Middle or old age Hypertension history Focal neurological dysfunction CT /

43、MRI: final diagnosis,Treatment,The same as cerebral infarction Prevention of recurrence, treatment of risk factors.,Cerebral embolism,Definition,15%-20% of stroke Cerebral arteries are occluded by an embolus from the heart, aortic arch, or large cerebral arteries, etc., resulting in brain tissue isc

44、hemic necrosis and focal neurological deficit.,Etiology,Source of embolus: Cardiac origin: the most common atrial fibrillation, rheumatic valve disease, endocarditis, atrial myxoma, myocardial infarction. Non-cardiac origin: atherosclerosis plaque, air embolus, fat embolus, cancer embolus Embolus of

45、 unknown origin,Clinical feature,Age of onset: underlying disease At any time of the day or night Left middle cerebral artery Abrupt onset - the fastest stroke type Most are complete stroke; half of the patients have transient disturbance of consciousness; the symptoms depend on the site. The corres

46、ponding symptoms of primary disease: cardiogenic embolism has atrial fibrillation.,Assist examinationCT or MRI is helpful,Diagnosis,Rapid-onset Evidence of embolus sources Focal neurological signs: hemiplegia, aphasia CT or MRI,Treatment,Treatment of brain lesions: basically the same as cerebral thr

47、ombosis improve cerebral circulation (thrombolytic therapy should be cautious!) control cerebral edema: dehydrant, decompressive craniectomy Treatment of the primary disease:- eradicate the source of embolus to prevent recurrence Prevention of recurrent stroke: Anticoagulant,Intracerebral hemorrhage

48、（ICH）,Definition,ICH is non-traumatic intracerebral hemorrhage, accounting for 20% -30% of stroke.,Etiology,Hypertension: the most common cause Atherosclerosis Other: blood disease, cerebral amyloid angiopathy, aneurysms and vascular malformations, hemorrhage into tumors, hemorrhagic infarction, ant

49、icoagulant or thrombolytic therapy.,Clinical Findings,General characteristics: 50 years, history of hypertension, MF with emotional excitement or active state Sudden onset, reach a peak within a few minutes or hours. Common manifestations: increased intracranial pressure; neurological deficits (para

50、lysis of limbs, aphasia, etc.); blood pressure often increase significantly. Clinical manifestations depend on the site.,About 3/4 Site: putamen, thalamus putaminal hemorrhage results in a more serious motor deficit and thalamic hemorrhage results in a more significant sensory disturbance.,1.Deep ce

51、rebral hemorrhage,2. Lobar hemorrhage,10%. 40 years old Causes: cerebral arteriovenous malformation, moyamoya disease, vascular amyloidosis, tumor, etc. Location: parietal other lobes Manifestations: headache, vomiting focal symptoms, seizures are more frequent, while coma is rare.,3.Pontine hemorrh

52、age,10% Small bleeding: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.,4.Cerebellar

53、hemorrhage,10% Symptom: headache, dizziness, ataxia, without limb paralysis. large hemorrhage leads to rapid coma and foramen magnum herniation (tonsillar herniation),5.Intraventricular hemorrhage,3-5% rupture of choroid plexus artery or subependymal artery. Small hemorrhage: resembles SAH Large hem

54、orrhage: rapid coma, frequent vomiting, pinpoint pupils, quadriplegia, decerebrate rigidity, and rapid death.,Assist examination,CT: (1)the most useful diagnostic procedure, since hematomas can be quickly identified (2)high density, easily distinguishable from infarction (3)hematoma size, location,

55、edema, tissue shift. Lumbar puncture: not routinely recommended MRI: less value than CT in acute phase DSA / MRA: search for the cause,Diagnosis, 50 history of high blood pressure occurs in emotional excitement or active state intracranial hypertension, focal neurological deficit CT: final diagnosis

56、,Differential Diagnosis,Cerebral infarction Intoxications and metabolic disease: coma, but lack focal signs, medical history and laboratory tests. Traumatic intracranial hematoma,Treatment,principles: Prevent further bleeding Lower intracranial pressure and control cerebral edema Adjust blood pressu

57、re Prevent complications,Medical treatment,1.General treatment: Nearest treatment, bed rest, keep quiet and reduce visitation. Keep the airway open. Close observation of vital signs, pupil and altered consciousness. Note maintaining water and electrolyte balance and nutrition.,2. Control cerebral ed

58、ema (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 arterial pressure of 130mmHg in persons with a history of hypertension. Overaggressive treatment of blood pressure may decrease cerebral per

59、fusion presure and worsen brain injury-Gently lower! 4. Prevent and treat complications: similar to cerebral infarction,Objective: remove the hematoma, relieve brain herniation, save lives, and to remove the cause (such as vascular malformations), to prevent the occurrence of complications (such as hydrocephalus) Indications: (1) sustained increase in intracranial pressure, brain herniation trend or early brain herniatio