神經病學英文課件：08腦血管

1、CEREBRAL VASCULAR DISEASE (CVD,Outline Epidemiology 8: 34554,the 3rd national death cause retrospective investigation 2008,死亡原因排序,腦血管病，中國頭號殺手 136.64 /100,000/ y,1) Data from: Z Chen. Report of the third national death cause retrospective investigation. Xiehe Medical University Press of China, Beijin

2、g 2008,2) Liu M, et al. Lancet Neurol 2007; 6: 45664,Etiology,Localized injury to the endothelium: Atherosclerosis ; Hypertensive fibrinoid necrosis hyalinosis microaneurysm of arterials; Infective or non-infective arteritis; Vascular defects which secondary to toxic, metabolic diseases ; Congenital

3、 vascular diseases: aneurysms; vascular malformations,Etiology,Heart diseases and hemodynamic changes: Atrial fibrillation; Rheumatic valvular diseases; Congenital cardiac diseases; Bacterial endocarditis,Etiology,Intravascular embolisms: air, fat, carcinomatous embolisms Unknown(cryptogenic,Stroke:

4、 Multiple Etiological Clinical Syndrome,Risk factors,Nonmodifiable: Age Gender Race/ethnicity Family history Genetics,Modifiable: systolic or diastolic hypertension Diabetics Heart diseases hypercholesterolemia cigarette smoking Oral contraceptive use heavy alcohol consumption Carotid stenosis,Risk

5、Factor: Hypertension,血清膽固醇mg/dL (mmol/L,缺血性卒中死亡相對危險,350977,M,F/U6y,對多種混雜因素校正后,Iso H, et al. N Engl J Med. 1989;320:904-910,Risk Factor: Hypercholesterolemia,major types of CVD,Cerebral ischaemia and infarction Transient Ischemic Attacks, TIA Cerebral thrombosis Lacunes Embolism Hemorrhage Hypertensi

6、ve hemorrhage Subarachnoid hemorrhage Others Cerebral venous thrombosis,infarction,Anatomy of cerebral vessels,Carotid artery (anterior circulation,Vertebral Dyslexia; Dysgraphia; Dyscalculia; Loss of use of contralateral face and arm; Loss of feeling in contralateral face and arm,Neurological sympt

7、oms and signs,The following suggests anterior cerebral territory(ACA):Loss of use and/ or feeling in the contralateral leg. The following suggests posterior cerebral territory(PCA):Development of a contralateral homonymous hemianopia,Neurological symptoms and signs,The following suggests a deep-seat

8、ed lesion affecting the internal capsule which is supplied by small perforating branches of the middle and posterior cerebral arteries close to their origins: Complete loss of motor and sensory function throughout the whole of the contralateral side of the body with a homonymous hemianopia,Neurologi

9、cal symptoms and signs,The following suggests ophthalmic artery territory (the ophthalmic artery arises from the internal carotid artery just below the Circle of Willis): Monocular loss of vision,Neurological symptoms and signs,The following suggest vertebro-basilar territory:double vision( 3,4,6);f

10、acial numbness(5);facial weakness(7);vertigo (8);dysphagia (9, 10);dysarthria ( 9, 10, 12);ataxia;drop attacks;motor or sensory loss in both arms or legs,1. Transient Ischemic Attacks(TIA,Definition TIAs are brief, reversible episodes of focal, nonconvulsive ischaemic neurologic disturbance. Consens

11、us has been that their duration should be less than 24 h,Clinical picture,TIA can reflect the involvement of any cerebral artery. The loss of function entirely depends on the influenced artery. It may last a few seconds or up to 12 to 24 h, Most of them last 2 to 15 min. There are only a few attacks

12、 or several hundred.Between attacks, the neurologic examination may disclose no abnormalities. A stroke may occur after numerous attacks have occurred over a period of weeks or months,Carotid TIA: Ophthalmic ischemia with contralateral paralysis; Horners syndrome with contralateral paralysis, etc,Sy

13、mptoms suggestive of carotid TIA: Transient ipsilateral monocular blindness (amaurosis fugax) Contralateral body weakness or clumsiness Contralateral body sensory loss or paresthesias Aphasia with dominant hemisphere involvement Various degrees of contralateral homonymous visual field defects Dysart

14、hria(not in isolation,Vertebrobasilar TIA: transient global amnesia, TGA ; drop attack, etc,Symptoms suggestive of Vertebra-basilar TIA: Usually bilateral weakness or clumsiness, but may be unilateral or shifting Bilateral, shifting, or crossed(ipsilateral face and contralateral body) sensory loss o

15、r paresthesias Bilateral or contralateral homonymous visual field defects or binocular vision loss Two or more of the following symptoms: vertigo diplopia dysphagia dysarthria ataxia,Differential diagnosis of TIAs,Seizure; Migraine; Syncope; Meniere disease Others: multiple scelerosis; incranial neo

16、plasms; hypoglycemia,etc,2. Cerebral thrombosis,Most CVD can be attributed to atherosclerosis and chronic hypertension; until ways are found to prevent or control them, vascular disease of the brain will continue to be a major cause of morbidity,大腦中動脈狹窄-腦梗塞,Clinical picture,The loss of function enti

17、rely depends on the area of brain tissue involved in the ischaemic process.(above,Laboratory Findings,CT Scan or MRI: A CT scan or MRI should be obtained routinely to distinguish between infarction and hemorrhage as the cause of stroke, to exclude other lesions (eg, tumor, abscess) that can mimic st

18、roke, and to localize the lesion. CT is usually preferred for initial diagnosis because it is widely available and rapid and can readily make the critical distinction between ischaemia and hemorrhage,Several hours,48 hours,120 hours,Dynamic changes of CT scans,MRI 表現(T2W,Laboratory Findings,Cerebral

19、 Angiography: Intra-arterial angiography is used to identify operable extracranial carotid lesions in patients with anterior circulation TIAs who are good surgical candidates,Carotid stenosis,MRI subdural or epidural hematoma; subarachnoid hemorrhage): Distinguished by a history of trauma ; excrucia

20、ting headache at onset; a more marked depression of consciousness; or by the presence of neck stiffness on examination; can be excluded by CT or MRI,Differential Diagnosis,tumor or abscess Brain abscess is suggested by concurrent fever, and both abscess and tumor can usually be diagnosed by CT scan

21、or MRI. stroke-like fashion :(Metabolic disturbances as hypoglycemia and hyperosmolar nonketotic hyperglycemia) Glucose level should therefore be determined in all patients with apparent stroke,3.Embolic infarction,Cerebral embolism comes from a thrombus within the heart (cardiac origin) - in most c

22、ases; Embolism due to fat, tumor cells, fibrocartilage, amniotic fluid, or air (non-cardiac origin) - rarely Undetermined origin (Cryptogenic,Clinical Picture,Of all strokes, cerebral embolism develops most rapidly. The embolus strikes at any time of the day or night. The neurologic picture will dep

23、end on the artery involved and the site of obstruction,Laboratory Findings,It is advisable that an ECG and echocardiogram be obtained in all patients with stroke of uncertain origin.Prolonged study of heart rhythm with Holter monitoring should be undertaken,Course and prognosis,The eventual prognosi

24、s is determined by the occurrence of further emboli and the gravity of the underlying illness- cardiac failure myocardial infarction, bacterial endocarditis and so on,Treatment of Cerebral Ischemia,Principles of treatment: emergent ; individualized; integralized General medical management in the acu

25、te phase: management of blood pressure;internal environment; prevention of infections，pulmonary embolisms and DVT, etc. treatment of cerebral edema and raised intracranial pressure; control of seizures and post-stroke depression /anxiety,Measures to restore the circulation and arrest the pathologic

26、process Thrombolytic agents ( t-PA only for completed stroke ); Anticoagulant drugs ( Heparin Neuroprotective agents: No high level evidences,Treatment and prevention,Three phases of therapy :General medical management in the acute phase;Measures directed to restoring the circulation;Physical therap

27、y and rehabilitation,Current Status of Antithrombotic Therapy of Cerebral Ischemia: Therapy Conclusion Aspirin + Clopidogrel + Ticlopidine + Slow-release dipyridamole intra-arterial use) Hemorheological therapy Hemodilution - Pentoxifylline - Ancrod + ( in one study only with 3 hr of onset, intraven

28、ous use,Images in a 47-year-old woman with a sudden onset of left hemiplegia, which occurred while she was in the ICU. She was excluded from the intravenous tissue-type plasminogen activator (tPA) protocol because she had recently undergone heart-lung transplantation. Image A is an angiogram of the

29、right internal carotid artery that demonstrates an occlusion of the right middle cerebral artery. Image B shows that flow in the right middle cerebral artery is reestablished at 28 minutes during a selective infusion of urokinase into the right middle cerebral artery. The patient recovered her forme

30、r neurologic function while she was on the angiography table,Current Status of Neuroprotection of Cerebral Ischemia Nimodipine - Neurotrophins - Calpain inhibitors - Excitatory aa antagonists -,Cerebral edema: Medical intervention: Mannital;furosemide; Surgical intervention : strokectomy-removing in

31、farcted tissue and replacing the cranial bone flap,Physical therapy and rehabilitation,Secondary prevention,Measures to prevent further strokes and progression of vascular disease: Antiplatelets : Aspirin, Clopidogrel(Plavix) Anticoagulants: warfarin Agents for risk factors: hypertension; diabetes;

32、hyperlipidemia, etc. Surgery for carotid stenosis : Carotid endarterectomy; intralumenal stents; extracranial-intracranial bypass,In a patient who presented with hemiplegia, an embolus to the middle cerebral artery likely originated at this severe stenosis of the internal carotid artery (Image A). T

33、he stenosis was successfully treated with angioplasty and stents (Image B). Afterward, the middle cerebral artery was safely catheterized and the embolus lysed (Image C). The patient fully recovered over the following week,II. Intracranial Hemorrhage,It is due predominantly to chronic hypertension a

34、nd degenerative changes in cerebral arteries. Hemorrhage may interfere with cerebral function through a variety of mechanisms, including destruction or compression of brain tissue and compression of vascular structures, leading to secondary ischaemia and edema,Intracranial Hemorrhage,Intracranial he

35、morrhage is classified by its location as intracerebral, subarachnoid, subdural, or epidural, all of which- except subdural hemorrhage- are usually caused by arterial bleeding,SAH,Epidural,Intracerebral,1. Intracerebral Hemorrhage,Clinical Picture,Headache and vomiting are cardinal features.Very sma

36、ll hemorrhages in “silent” regions of the brain may escape clinical detection,Clinical Picture,Clinical features vary with the site of hemorrhage: Deep cerebral hemorrhage The two most common sites of hypertensive hemorrhage are the putamen and the thalamus, which are separated by the posterior limb

37、 of the internal capsule. This segment of the internal capsule is traversed by descending motor fibers and ascending sensory fibers, including the optic radiations,Clinical Picture,Lobar hemorrhage Hypertensive hemorrhages also occur in subcortical white matter underlying the frontal, parietal, temp

38、oral, and occipital lobes. Symptoms and signs vary according to the location,Hyperdensity in the left temporal parietal region consistent with an acute parenchymal hemorrhage with intraventricular depression,Clinical Picture,Pontine hemorrhage With bleeding into the pons, coma occurs within seconds

39、to minutes and usually leads to death within 48 hours. Ocular findings typically include pinpoint pupils. Horizontal eye movements are absent or impaired, but vertical eye movements may be preserved,Clinical Picture,Cerebellar hemorrhage The distinctive symptoms of cerebellar hemorrhage (headache, d

40、izziness, vomiting, and the inability to stand or walk) begin suddenly, within minutes after onset of bleeding,Laboratory Findings,In CT scans, fresh blood is visualized as a white mass as soon as it is shed. The mass effect and the surrounding extruded serum and edema are hypodense,Differential Dia

41、gnosis,Infarctions: To some extent, the presence of severe headache, nausea and vomiting, and impairment of consciousness are useful clues that a hemorrhage may have occurred; CT scan or MRI is the most useful diagnostic procedure, since hematomas can be quickly and accurately localized,Treatment,th

42、e maintenance of adequate ventilation, use of controlled hyperventilation to a Pco2 of 25 to 30 mmHg monitoring of intracranial pressure (ICP) in some cases and its control by the use of tissue-dehydrating agents such as mannitol and limiting intravenous infusions to normal saline,Treatment,Sustaine

43、d mean BP around 100mmHg : The use of beta-blocking drugs(esmolol, labetalol) or angiotensin-converting enzyme inhibitory drugs is recommended,Treatment,In contrast to cerebral hemorrhage, the surgical evacuation of cerebellar hematomas is a generally accepted treatment and is a more urgent matter b

44、ecause of the proximity of the mass to brainstem and the risk of abrupt progression to coma and respiratory failure,Course and Prognosis,A volume of 30 ml or less, calculated from the CT scan, predicted a generally favorable outcome. In patients with clots of 60 ml or larger and an initial Glasgow C

45、oma Scale score of 8 or less, the mortality was 90 percent. As remarked earlier, it is the location of the clinical effects,2.Spontaneous Subarachnoid Hemorrhage,Saccular aneurysms are also called berry aneurysms; actually they take the form of small, thin-walled blisters protruding from arteries of

46、 the circle of Willis or its major branches. Their rupture causes a flooding of the subarachnoid space with blood under high pressure. Aneurysms are multiple in 20 percent of patients,SAH,Aneurysm,Clinical picture,Prior to rupture, saccular aneurysms are usually asymptomatic or exceptionally cause l

47、ocalized cranial pain. The presence of a partial oculomotor palsy with dilated pupil may be indicative of an aneurysm of the posterior communicating- internal carotid junction. With rupture of the aneurysm, blood under high pressure is forced into the subarachnoid space(where the circle of Willis lies,Clinical picture,SAH usually occurs while the patient is active rather than during sleep. There are few or no focal neurologic signs. Convulsive seizures, usually brief and generalized,Clinica