2010级神经病学专业试卷(专业课和专业外语).doc

大连医科大学硕士研究生专业课试卷
年级 （课程）试卷
学号 姓名
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一简单题：
1． 四肢瘫的诊断与鉴别诊断？
2． 青年脑卒中的常见病因？
3． 痴呆的诊断与鉴别诊断？
4． 脑血管造影阴性的蛛网膜下腔出血发病原因分析？
5． 痛性眼肌麻痹诊断和鉴别诊断？
6． 简述动静脉溶栓适应症、禁忌症、时间窗？

二 病案分析题
1． 女性，41岁，农妇。无外伤史，无高血压、糖尿病、心脏病史。否认吸烟、饮酒史。右侧上肢无力1周。查体：神清，语利，颅神经（-），右侧上肢远端肌力0级，伸和屈指不能，近端肌力4 级，手可及后脑，右侧下肢肌力正常，无感觉障碍，无病理征。头颅CT/MRI见下：

诊断和鉴别诊断？
2． 18岁男性，上课时突发抽搐，问诊时包括哪些内容？
3． 65岁男性，吸烟史30年，既往高血压病15年，脑梗死2个月，门诊复查血脂：Chol：6.5mmol/L，LDL：3.4mmol/L，颈部彩超提示：双侧颈动脉混合斑块，请问如何指导患者调脂，依据标准？
4． 男性，67岁，主诉：右侧肢体活动不灵1天入院。既往高血压病史，发病在看电视时，查头CT除外出血。查体：BP:170/100mmHg，混合性失语，右侧中枢性面舌瘫，右侧肢体肌力3级，右侧Babinski征（+），请做出诊断分析（提示：参照缺血性脑血管病诊治六步法）？

大连医科大学硕士研究生试卷
年级专业外语试卷
学号 姓名
考生须知
1、检查所发试卷是否和自己所报科目一致，试卷有无缺页、漏印、字迹模糊，如有可举手请求换卷。
2、必须将自己的学号、姓名、专业班级写在试卷指定位置上。
3、在试卷密封线以外填写姓名、学号或写有与答题内容无关的语句和作其它标记的试卷一律作废，后果自负。
命题单位： 教研室： 教研室主任审核签字：
阅卷人 ：

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(1) Genetic Basis of Migraine
The 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 penetrance, 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 subtype 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 mutations in a brain-expressed, voltage-gatedP/Q calcium channel gene) and two neighboring loci on Chr1q.
(2) The vascular Theory of Migraine
Intracranial vasoconstriction and extracranial vaaodilatation have long been held to be the respective causes of the aura headache phases of migraine. This theory received 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 in 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 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 adrenergic 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 Migraine
Fortification 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 metabolic 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 near 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 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 represent 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 Migraine
Serotonergic neurons ramify extensively throughout the brain, and 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 other 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 migraine attacks. Subsequently, it was found that platelet levels of 5-HT fall consistently at the onset of headache and that drugs that cause 5-HT to be released may trigger migrainous episodes. Such changes in circulating 5-HT levels proved to be pharmacologically trivial, however, and interest in the humoral role of 5-HT in migraine declined.
More recently, interest in the role of 5-HT in migraine has been renewed due to the introduction of the triptan class of antimigraine drugeThe triptans are designed to stimulate selectively a particular subpopulation of 5-HT receptors. At least 14 specific 5-HT receptors exist in humans.