昼夜节律失调性睡眠障碍的临床特点与处理

生物之所以形成并维持24 h周期性节律,主要是由于受到因地球自转产生昼夜明暗变化的影响,当生物使这种节律变成自身固有节律后,生物本身就好像具有了感知时间的能力,这一机制被形象地称为"生物钟",其专门负责从时间上调节机体的生理功能[1].     

双相障碍合并睡眠障碍的发病机制及治疗进展

双相障碍中普遍存在睡眠障碍,睡眠障碍可能是双相障碍首发和复发的预测因素,同时 睡眠障碍对双相障碍患者造成诸多不利影响。目前双相障碍中睡眠障碍的发病机制尚不完全明确,且 治疗方法较少。现综述双相障碍中睡眠障碍的发病机制和治疗现状,以期为优化双相障碍睡眠治疗方 法提供临床借鉴。     

音乐电针治疗与磁疗对脑卒中后睡眠障碍的影响

目的探究音乐电针治疗与磁疗对脑卒中后睡眠障碍患者的影响。方法随机选取2012-03—2014-10来我院接受治疗的50例脑卒中患者为研究对象,根据入院时间先后将患者分为观察组和对照组,观察组采用音乐电针治疗,对照组采用电磁疗法治疗,对比2组PSQI评分和临床治疗效果。结果观察组平均PSQI评分为(3.51±1.42)分,对照组为(9.25±2.73)分,对照组平均入睡时间相对较长,2组比较差异有统计学意义(P0.05)。观察组总有效率92.31%,对照组为66.67%,观察组临床有效率明显高于对照组,差异有统计学意义(u=2.3116,P=0.020 8)。对照组接受治疗后仍有16.67%的患者出现重度睡眠障碍,而观察组无重度睡眠障碍患者,2组比较差异有统计学意义(P0.05)。经治疗后,观察组神经功能重度缺损2例(7.69%),对照组重度缺损9例(37.50%),2组比较差异有统计学意义(P0.05)。结论音乐电针疗法治疗脑卒中后发生睡眠障碍的患者临床疗效较好,安全性高,对体质较差的老年人也同样适用,患者PSQI评分低,睡眠质量较好,睡眠时间明显增加,失眠现象得到改善,有利于患者恢复健康,提高生活质量,值得临床应用。     

脑卒中后癫痫的临床特点

脑卒中后继发癫痫是脑血管病的常见并发症，我院自1994-01—2004-01收治经CT证实的脑卒中住院患者1250例，其中105例继发癫痫，现对其临床资料进行分析，以探讨其临床特点和发病机制。     

生物反馈治疗对150例脑卒中后睡眠障碍患者的临床观察

目的观察生物反馈治疗脑卒中后睡眠障碍的临床疗效。方法将150例脑卒中后睡眠障碍患者随机分为治疗组和对照组各75例,全部患者常规治疗原发病及进行康复训练,治疗组接受生物反馈治疗,对照组进行药物治疗,治疗前后进行匹兹堡睡眠质量指数量表（PSQI）评定及使用睡眠多导仪监测,比较两组疗效。结果治疗后,治疗组PSQI总分及睡眠潜伏期、觉醒次数较治疗前显著降低,睡眠总时间、睡眠效率、深睡眠时间、REM时间明显增加;与对照组比较,治疗组治疗后睡眠潜伏期、觉醒次数、深睡眠时间等的改善更明显。差异有统计学意义（P〈0．05）。结论生物反馈治疗可以明显改善脑卒中后的睡眠障碍,疗效优于传统药物治疗。     

卒中后癫痫发病机制及临床特点的探讨

卒中和癫痫都是神经科常见疾病,而这两种疾病之间有着十分密切的联系。卒中患者经 常会继发痫性发作,而卒中后痫性发作或癫痫又可能影响卒中患者的预后以及生活质量,因此,关于 卒中后癫痫的研究越来越受到重视。虽然迄今关于卒中后痫性发作的研究数据受到各种因素的干扰 而并不一致,但是近些年来在影响因素、发病机制以及临床特点方面仍然取得了一些进展。对卒中后 痫性发作的深入了解有助于制定正确的诊治方案,改善患者的预后,提高生存质量。     

脑桥中央髓鞘溶解症的流行病学、发病机制和临床特点

脑桥中央髓鞘溶解症（central pontine myelinolysis,CPM）是并不多见的脱髓鞘疾病,以往仅见于尸解病理诊断,部分患者预后良好.目前随着影像技术的发展,本病得以更多地在患者生前诊断.由于CPM发生在许多基础疾病之上,临床医生应加强对该病的认识并重视其预防。     

脑卒中后认知功能障碍及其康复治疗的研究进展

脑卒中已位于现代社会发病率最高的疾病之列,它不仅引起感觉、运动功能障碍,更严重的是导致脑的认知功能障碍.卒中后认知功能障碍已成为影响老年人健康和生活质量的常见原因.     

脑卒中后睡眠障碍的病因及治疗研究进展

脑卒中后睡眠障碍发病率高,对卒中后康复治疗及日常生活能力影响较明显。脑卒中后睡眠障碍的发病机制复杂,不能完全明确,同时治疗方法较多,需要个体评估,给予相应的治疗方法才能得到较满意的结果。     

Clinical features of circadian rhythm sleep disorders in outpatients

The clinical data of 86 cases of primary circadian rhythm sleep disorder (primary CRSD) were retrospectively examined and compared to 40 cases of secondary circadian rhythm sleep disorder (secondary CRSD), who had presented with some kind of psychiatric or medical disorder, and had exhibited sleep-wake rhythm disorders that were judged to be secondary CRSD based on sleep logs. The comparison of cases found that: (i) the mean age at first presentation to the clinic was significantly younger for primary CRSD compared to secondary CRSD; (ii) more secondary CRSD cases were unemployed than were Primary CRSD cases; (iii) more cases in the secondary CRSD group had a clear trigger for sleep-wake rhythm disorder onset than cases in the primary CRSD group; and (iv) the types of sleep-wake rhythm disorders in the primary CRSD group consisted of delayed sleep phase syndrome (DSPS), 72 (83.7%), non-24 pattern, 11 (12.8%), and irregular, 3 (3.5%). In the secondary CRSD group there were 25 (62.5%) cases of DSPS pattern, 1 (2.5%) of non-24 pattern and 14 (35.0%) with irregular pattern. The 56 (65.1%) cases with primary CRSD showed good response to vitamin B12 and bright light therapy; however, 28 (70.0%) cases with secondary CRSD did not respond to such therapies.     

Clinical spectrum of movement disorders after stroke in childhood and adulthood

Although rare, many different types of hyperkinetic and hypokinetic movement disorders have been described after both ischemic and hemorrhagic stroke in children and in adults. Current knowledge about these disorders comes from single case reports or small series of cases compiled from retrospective studies. Data from hospital-based studies suggest a prevalence of poststroke movement disorders ranging from 1.1 to 3.9%. However, despite the development of emergency care for stroke, these clinical syndromes remain insufficiently recognized. Poststroke movement disorders take place in the acute phase or following a variable delay after stroke onset, and could be transient or persistent. Dystonia is the most frequent movement disorder, occurring after a delay of several months, while chorea and hemiballism are most frequent in the acute stages. Amongst transient movement disorders, limb shaking is associated with high-grade stenosis or occlusion of the internal carotid artery, while myoclonus and asterixis are rare. From a pathophysiological point of view, most of these symptoms are induced by a lesion involving the basal ganglia, the thalamus, or the frontal subcortical pathways. In this article, we updated the clinical spectrum, neuropathophysiological mechanisms, and prognosis of stroke-induced movement disorders in adults and children.     

Clinical neuropharmacology of sleep disorders

Within the context of the comprehensive treatment of sleep disorders, which includes medical, neurologic, psychiatric, and social interventions, use of medication is often indicated. Among the three benzodiazepine hypnotics that are available in the United States for the treatment of insomnia, flurazepam is effective for both sleep induction and maintenance, and it retains most of its efficacy over a 4-week period of nightly administration; temazepam is effective only for sleep maintenance, and triazolam improves both sleep induction and maintenance with initial but not with continued administration. Rebound phenomena are more frequent and intense with the more rapidly eliminated drug, triazolam, and to a lesser degree with temazepam. Also, with triazolam, certain behavioral side effects, such as amnesia and psychotic-like symptoms, have been reported. With flurazepam, which is a slowly eliminated benzodiazepine, daytime sedation is more frequent than with the other two drugs. When insomnia is secondary to major depression, antidepressant medication should be administered. Methylphenidate, amphetamines, or other stimulant medications are used for the symptomatic treatment of the sleepiness and sleep attacks of narcolepsy and hypersomnia. For cataplexy and the other two auxiliary symptoms of narcolepsy, imipramine or other tricyclics are the drugs of choice. Protriptyline and medroxyprogesterone have been used in treating mild cases of obstructive sleep apnea, but their efficacy is limited. Similarly, for the treatment of central sleep apnea, medroxyprogesterone and acetazolamide have shown only limited effects. Medication for patients with sleepwalking, night terrors, or nightmares should be prescribed judiciously, and primarily when treatment of an underlying psychiatric condition is desired. The neuropharmacology of sleep should also consider drugs that may cause sleep disorders. Medications with sleep disturbing effects include various antihypertensives, bronchodilators, and the energizing antidepressants. Withdrawal of REM-suppressant drugs, such as the barbiturates, may cause nightmares in association with a REM rebound. Occasionally, a drug or a combination of drugs may produce somnambulistic-like activity in some patients.     

Early investigation and treatment of obstructive sleep apnoea after acute stroke.

Obstructive sleep apnoea (OSA) is an independent risk factor for hypertension, which is a major cause of stroke. The prevalence and associations of OSA in a cohort of stroke patients were studied. The safety and tolerability of early treatment with nasal continuous airways pressure (nCPAP) was also assessed. Consecutive subjects admitted with acute stroke were assessed clinically, radiologically and with scales assessing prior OSA risk, dysphagia and disability. Sleep studies were performed within the first few days of admission using a portable diagnostic system. Twenty-nine of 55 (53%) subjects had evidence of OSA, using an apnoea-hypopnoea index (AHI) of 10 or greater. The AHI was significantly associated with an index of prior OSA symptoms, but not with history of hypertension, degree of dysphagia, or type and severity of stroke. Use of a portable diagnostic system for detecting OSA in the acute stroke setting was well tolerated. OSA is common after acute stroke and exceeds rates seen in control populations of similar age (53% vs. 11%). Early treatment with nCPAP was effective and well tolerated.     

痴呆相关性睡眠障碍的发生机制和处理

多数痴呆患者存在不同程度的睡眠障碍。但目前人们对痴呆相关性睡眠障碍的了解甚少。本文综述了痴呆相关性睡眠障碍的临床表现、发病机理和治疗方法。褪黑素治疗和其他一些方法能改善痴呆患者的睡眠障碍。     

急性脑卒中患者睡眠障碍的特点

目的探讨急性脑卒中患者睡眠障碍的特点。方法采用匹兹堡睡眠质量指数量表(PSQI)对168例急性脑卒中患者与98例正常对照者的睡眠状况进行测评分析,同时采用Barthel指数(BI)与NIHSS分别评价脑卒中患者的日常生活活动能力与神经功能缺损程度。结果脑卒中组睡眠障碍发生率、PSQI总分以及睡眠质量、入睡时间、睡眠障碍、催眠药物、日间功能障碍的得分均显著高于正常对照组(P0.05~0.01)。脑卒中组男性睡眠障碍发生率显著低于女性(P0.05),正常对照组男性及女性睡眠障碍发生率差异无统计学意义。脑卒中组女性睡眠障碍发生率显著高于正常对照组(P0.05)。脑卒中组年龄50岁患者的PSQI总分显著高于脑卒中组50~59岁、60~69岁、≥70岁的患者及对照组各年龄段患者(均P0.01)。与无睡眠障碍患者比较,脑卒中组睡眠障碍患者的BI显著降低,NIHSS评分显著升高(均P0.001)。结论急性脑卒中患者更易伴发睡眠障碍,在年龄50岁伴神经功能缺损的女性患者中更明显。     

发作性运动障碍的临床特征及发病机制

目的 探讨发作性运动障碍（PMD）的临床特征及发病机制。方法 回顾性分析5例发作性运动诱发舞蹈手足徐动症（PKC）和2例发作性持续运动诱发肌张力障碍（PED）患者的临床资料。结果 5例PKC发作均南突然运动诱发,表现肌肉僵直、肌张力增高3例,表现肢体扭动、肌张力不全3例（其中1例先为肢体僵直后扩展为周身扭动）。2例PED由持续运动诱发,表现为肢体不自主运动,持续数秒至数分钟缓解。脑电图（EEG）或动态脑电图（AEEG）示痫样放电5例,头部CT或MRI检查正常5例,异常2例。4例PKC予卡马西平治疗有效,1例PED予较大剂晕丙戊酸钠有效。结论PMD表现为发作性锥体外系症状,多由突然运动诱发。大部分病例的EEG有痢样放电,抗癫痫药物治疗有效。提示PMD的发病机制可能与癫痫类似或相同。