級神經(jīng)病學專業(yè)試卷專業(yè)課和專業(yè)外語

1、大連醫(yī)科大學碩士研究生專業(yè)課試卷 年級 （課程）試卷 學號 姓名 考生須知1、檢查所發(fā)試卷是否和自己所報科目一致，試卷有無缺頁、漏印、字跡模糊，如有可舉手請求換卷。2、必須將自己的學號、姓名、專業(yè)班級寫在試卷指定位置上。3、在試卷密封線以外填寫姓名、學號或寫有與答題內容無關的語句和作其它標記的試卷一律作廢，后果自負。命題單位： 教研室： 教研室主任審核簽字： 閱卷人 ： 一二三四五總分分數(shù)一簡單題：1 四肢癱的診斷與鑒別診斷？2 青年腦卒中的常見病因？3 癡呆的診斷與鑒別診斷？4 腦血管造影陰性的蛛網(wǎng)膜下腔出血發(fā)病原因分析？5 痛性眼肌麻痹診斷和鑒別診斷？6 簡述動靜脈溶栓適應癥、禁忌癥、時間

2、窗？二 病案分析題1 女性，41歲，農(nóng)婦。無外傷史，無高血壓、糖尿病、心臟病史。否認吸煙、飲酒史。右側上肢無力1周。查體：神清，語利，顱神經(jīng)（-），右側上肢遠端肌力0級，伸和屈指不能，近端肌力4 級，手可及后腦，右側下肢肌力正常，無感覺障礙，無病理征。頭顱CT/MRI見下： 診斷和鑒別診斷？2 18歲男性，上課時突發(fā)抽搐，問診時包括哪些內容？3 65歲男性，吸煙史30年，既往高血壓病15年，腦梗死2個月，門診復查血脂：Chol：6.5mmol/L，LDL：3.4mmol/L，頸部彩超提示：雙側頸動脈混合斑塊，請問如何指導患者調脂，依據(jù)標準？4 男性，67歲，主訴：右側肢體活動不靈1天入院。既往

3、高血壓病史，發(fā)病在看電視時，查頭CT除外出血。查體：BP:170/100mmHg，混合性失語，右側中樞性面舌癱，右側肢體肌力3級，右側Babinski征（+），請做出診斷分析（提示：參照缺血性腦血管病診治六步法）？大連醫(yī)科大學碩士研究生試卷 年級專業(yè)外語試卷 學號 姓名 考生須知1、檢查所發(fā)試卷是否和自己所報科目一致，試卷有無缺頁、漏印、字跡模糊，如有可舉手請求換卷。2、必須將自己的學號、姓名、專業(yè)班級寫在試卷指定位置上。3、在試卷密封線以外填寫姓名、學號或寫有與答題內容無關的語句和作其它標記的試卷一律作廢，后果自負。命題單位： 教研室： 教研室主任審核簽字： 閱卷人 ： 一二三四五總分分數(shù)(

4、1) Genetic Basis of MigraineThe aggregation of migraine within families has long beeen recognized, although consistent mendelian patterns of inheritance have not been found among the collective group of familial migraineurs. Presumably this reflects a variety of inheritance patterns, variable penetr

5、ance, and possibly multiple genes interacting with enviromental factors in the multigenic/multifactorial pattern charateristic of complex disease. Concordance rates in monozygotic twins of only 28-52 attest to the genetic component, but also predict a significant environmental contrivution.A rare su

6、btype of migraine with aura, familial hemiplegic migraine, has a straightforward autosomal dominant, highly penetrant inheritance pattern indicative of a strong genetic component. Three genetic loci for familial hemiplegic migraine have been identified:one on Chr19p13(associated with missense mutati

7、ons in a brain-expressed, voltage-gatedP/Q calcium channel gene) and two neighboring loci on Chr1q.(2) The vascular Theory of MigraineIntracranial vasoconstriction and extracranial vaaodilatation have long been held to be the respective causes of the aura headache phases of migraine. This theory rec

8、eived support from the efficacy of vasoconstrictive ergot alkaloids (eg,ergotamine) in aborting the acute migraine attack and vasodilators such as amyl nitrite in abolishing the migraine aura. More recent studies of regional cerebral blood flow during migraine attacks have demonstrated a reduction i

9、n regional flow,which begins in the occipital region, during the aura phase. The “spreading depression” in cerebral blood flow, however, proceeds according to cytoarchitectural patterns in the cerebral cortex and does not reflect the distribution of major vascular territories.In addition, the areas

10、of decreased blood flow may remain depressde after focal neurologic symptoms have resolved and headache has begun. Later in the headache phase, blood flow increases to parts of the cortex (cingulate, auditory, and visual association areas) and the brainstem (serotonergic dorsal raphe nucleus and adr

11、energic nucleus ceruleus); treatment with effective agents (sumatriptan, ergotamine) attenuates the cortical but not brainstem changes.These date imply that vascular abnormalities in migraine may be secondary to a primary disturbance in neuronal function in the brainstem.(3) The Neuronal Theory of M

12、igraineFortification spectrum is a migraine aura characterized by a slowly enlarging visual scotoma with luminous edges.It is believed to result from spreading depression a slowly moving(2 to 3 mm/min), potassium-liberating depression of cortical activity,preceded by a wavefront of increased metabol

13、ic activity. Spreading depression can be produced by a variety of expermental stimule,including hypoxia, mechanical trauma, and the topical application of potassium. These observations suggest that neuron abnormalities could be the cause of a migraine attack.Physiologically,electrical stimulation ne

14、ar dorsal raphe neurons the upper brainstem can result in migraine-like headaches.Blood flow in the pons and midbrain increase focally during migraine headache episodes;this alteration probably results from increased activity cell in the dorsal raphe and locus coeruleus . There are projections from

15、the dorsal raphe that terminate on cerebral arteries and alter cerebral blood flow.There are also major projections from the dorraphe to important visual centers, including the lateral geniculate body, superior colliculus, retina, and visual cortex. These various serolo nergic projections may repres

16、ent the neural substrate for the circulate and visual characteristics of migraine;antimigraine prophylactic drugs also inhibit activity of the dorsal ray cell through a diect or indirect agonist effect.(4) 5-Hydroxytryptamine in MigraineSerotonergic neurons ramify extensively throughout the brain, a

17、nd many effective antimigraine drugs act as antagonists or partial agonists at central serotonin receptors. Serotonin in platelets decreases and urinary serotonin increases during theacute phase of a migraine attack. Depletion of serotonin by reserpine may precipitate migraine, The headache and othe

18、r manifestations of migraine may thus reflect a disorder of central serotonergic neurotransmission. The link between neuronal initiation and trigemino-vascular-mediated pain may be calcitonoin gene-related peptide(CGRP).which is a potent vasodilator in venous blood during migraine and decreased by serotonin antagonists(sumatriptan)Pharmacologic and other data point to the involvement of the neurotransmitter 5-HT in migraine.Approximately 40 years ago,methysergide was found to antagonize certain peripheral action of 5-HT and was introduced as the first drug capable of preventing mig