脑卒中后睡眠障碍的研究进展

睡眠占人生1/3的时间,是维持人体健康必不可少的生理过程,良好的睡眠是高质量的生活及完成各种社会活动的基础,常见的障睡眠障碍性疾病有失眠症、睡眠的发动与维持困难、白天过度睡眠、24h睡眠-觉醒周期紊乱、阻塞性睡眠呼吸暂停综合征、不安腿综合征、发作性睡病、Kleine-Leyin综合征、睡眠中的异常活动或行为、梦游、夜惊及夜尿症。脑卒中后患者常出现失眠、嗜睡、睡眠颠倒等症状,部分患者夜间入睡后常伴精神症状等,直接影响脑卒中患者的康复及生活质量[1]。脑卒中后睡眠障碍的发病原因及发病机制十分复杂。本文拟开展脑卒中后睡眠障碍的发生机制以及对目前脑卒中后睡眠障碍多种治疗方法的综合研究,为临床诊治此类疾病提供一定的参考,现结合文献综述如下。     

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。     

自主神经功能障碍对卒中后睡眠障碍的影响

目的 探讨急性脑卒中睡眠觉醒障碍的早期诊断与自主神经系统(ANS)功能障碍的关系。方法 本研究是一项横断面观察研究,使用Ewing试验评估ANS功能障碍的严重程度,并应用PSQI评分评估脑卒中后3个月的失眠程度。分析首次缺血性脑卒中后自主神经系统功能变化与睡眠障碍的相关性。将缺血性卒中患者的脑成像标志物与自主神经系统(ANS)功能障碍联系起来,分析缺血性卒中合并ANS功能障碍、睡眠障碍对预后的影响以及相关因素。结果 本研究共纳入52例急性缺血性脑卒中患者,其中男44例(84.6%),年龄(58.85±9.52)岁。ANS功能障碍的比例高达90.4%,10例(19.2%)严重ANS功能障碍患者在脑干卒中患者中睡眠障碍的发生率最高。经过3个月的随访,发现与非严重ANS功能障碍组相比,严重ANS功能障碍组的神经功能障碍和日常生活能力受损更严重,但未发现严重的ANS功能障碍与睡眠障碍之间的联系。结论 急性缺血性脑卒中普遍存在ANS功能障碍,尚未发现严重的ANS功能障碍与睡眠障碍之间的关系。ANS调节可能是急性缺血性脑卒中的一个治疗方向。     

脑卒中病人睡眠-觉醒昼夜节律紊乱的影像学研究

目的探讨睡眠-觉醒昼夜节律紊乱脑卒中患者的脑结构改变,了解生物钟系统与其他脑组织之间可能的联系。方法收集存在睡眠-觉醒昼夜节律紊乱脑卒中患者(观察组)21例和无睡眠-觉醒昼夜节律紊乱脑卒中病人(对照组)92例影像学资料,比较两者之间的差别,寻找最可能引起睡眠-觉醒昼夜节律紊乱的脑区损害。结果通过比较发现,位于侧脑室枕角前部、丘脑外侧、岛叶后方、颞叶内侧的脑区脑组织损害可能与睡眠-觉醒昼夜节律紊乱有关。结论脑卒中病人中睡眠-觉醒昼夜节律紊乱的出现可能与特定的脑区损害有关。     

脑卒中后睡眠障碍的相关因素分析

目的调查分析脑卒中后睡眠障碍的发生情况。方法对2006-06~2007-12在本院住院的脑卒中患者286例,分析脑卒中后睡眠障碍的发病率及危险因素。计数资料以百分率(%)表示,数据采用χ2检验。结果脑卒中后睡眠障碍的发病率为58.74%,不同性别、不同类型脑卒中后睡眠障碍的发病率无显著差异(P>0.05),不同年龄组、不同部位、初发和复发组及不同程度神经功能缺损组发病率有显著差异(P<0.05)。结论脑卒中后睡眠障碍的发病率极高,与患者的性别、卒中类型无关,与患者的年龄、脑卒中部位、脑卒中次数及神经功能缺损程度有关。     

轻度认知障碍患者睡眠障碍的研究进展

<正>轻度认知障碍(Mild Cognitive Impairment,MCI)常常伴发多种睡眠-觉醒障碍疾病,包括失眠、睡眠相关的呼吸障碍、REM期睡眠行为障碍、昼夜节律失调性睡眠-觉醒障碍、日间过度思睡、不宁腿综合征。MCI患者的睡眠障碍会影响患者的生活质量、加重认知功能障碍、增加照料者负担。对MCI的睡眠-觉醒障碍应该进行常规和全面的评估,了解MCI睡眠障碍类型和影响因素,才能给予患者个体化的治     

卒中后抑郁心理干预治疗观察

脑卒中后抑郁(post-stroke depression PSD)是以情绪低落、睡眠障碍、思维迟缓、自我评价过低等为特征的脑卒中后常见并发症,严重影响患者神经功能障碍的恢复,降低患者的生存质量.我们采取心理干预治疗脑卒中后抑郁,取得良好效果,报告如下.     

脑卒中患者的睡眠障碍及其相关因素分析

目的探讨脑卒中患者睡眠障碍的情况及其影响因素。方法选择526例脑卒中急性期住院病人,采用匹兹堡睡眠质量指数问卷(PSQI)、神经功能缺损程度评分(NDS)、症状自评量表(SCL-90)、日常生活能力量表(ADL)进行调查。结果在526例脑卒中患者中,睡眠障碍患者(PSQI总分>7分者)341例(64.8%)。睡眠障碍患者与非睡眠障碍患者在性别、年龄、SCL-90、NDS和ADL评分方面比较,差异均有统计学意义(P<0.05或P<0.01)。多元逐步回归分析显示,睡眠障碍与患者的性别、年龄、精神状态、神经功能缺损程度、日常生活能力、脑卒中的部位及病变范围大小密切相关。结论脑卒中患者睡眠障碍的发生率较高,要改善脑卒中后的睡眠障碍,除了防止脑卒中外,还需要患者自身有良好的心理状态,改善睡眠有助于患者神经功能缺损的康复和生存质量的提高。     

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。     

脑卒中并发睡眠障碍研究进展

脑卒中是一种高发病率高致残率的疾病,睡眠障碍是脑卒中后常见的并发症,这严重影响患者的神经功能恢复和身心健康,并且可能诱发高血压和卒中复发等危险。本文就脑卒中患者常见睡眠障碍类型如失眠、睡眠相关呼吸障碍、昼夜节律紊乱、睡眠相关运动障碍的概念、发病机制和治疗的研究进展进行概述。     

Epilepsy and anomalies of neuronal migration: MRI and clinical aspects

Neuronal migration disorders are the result of disturbed brain development. In such disorders, neurons are abnormally located. In diagnosing these conditions, magnetic resonance imaging is superior to any other imaging technique. This enables us to improve our knowledge of the clinical correlates of neuronal migration. With reference to migrational disorder, a retrospective study of all 303 patients with epileptic seizures referred for magnetic resonance imaging during a 3-year period was performed, 13 patients (aged 12-41, mean age 27) were identified. They represent 4.3% of the entire study group. Of the patients with known epilepsy, 6.7% and of the mentally retarded, 13.7% had migrational disorders. Four patients had schizencephaly as the dominant finding, one was classified as hemimegalencephaly, 2 had isolated heterotopias, and 6 had localized pachy- and/or poly-microgyria. The clinical pictures are complex. Ectopias of grey matter are recognised foci of epilepsy, but from an epileptological and a clinical viewpoint little attention has been given to these disorders. The present study shows that malmigration is not rare in epilepsy patients, especially not in the mentally retarded.     

Hepatic Considerations in the Use of Antiepileptic Drugs

Summary: Virtually all of the major antiepileptic drugs (AEDs) can cause hepatotoxicity, although fatal hepatic reactions are rare. The mechanisms, incidences, and risk profiles for such reactions differ from drug to drug. With carbamazepine and phenytoin, hepatotoxicity may be due to drug hypersensitivity. Although the profiles of patients at risk have not been well-defined for these two antiepileptic drugs, it would appear from reports in the literature that older adolescents and adults are at higher risk than children of developing serious or fatal hepatotoxicity. Once hepatotoxicity develops, mortality rates are 10–38% with phenytoin and 25% for carbamazepine. The risk profile for valproate fatal hepatotoxicity has been more clearly defined. Those at primary risk of fatal hepatic dysfunction are children under the age of 2 years who are receiving multiple anticonvulsants and also have significant medical problems in addition to severe epilepsy. The risk is considerably lower for patients over the age of 2 years on valproate monotherapy. In contrast to the risk profile with other AEDs, adults receiving valproate as monotherapy have the lowest risk of hepatotoxicity. Fatal hepatic dysfunction coincident with valproate may be the result of aberrant drug metabolism. Concomitant use of AEDs that induce microsomal P450 enzymes (e.g., phenytoin and phenobarbital) may enhance the production of a toxic metabolite, and hence the greater risk of hepatotoxicity with polypharmacy.     

Vascular Malformations and Epilepsy: Clinical Considerations and Basic Mechanisms

Summary: Vascular malformations (VMs) are associated with epilepsy. The natural history of the various VMs, clinical presentation, and tendency to provoke epilepsy determine treatment strategies. Investigations have probed the mechanisms of epileptogenesis associated with these lesions. Electrophysiologic changes are associated with epileptogenic cortex adjacent to VMs. Putative pathophysiologic mechanisms of epileptogenesis include neuronal cell loss, glial proliferation and abnormal glial physiology, altered neurotransmitter levels, free radical formation, and aberrant second messenger physiology.     

Classification of methods in transcranial Electrical Stimulation (tES) and evolving strategy from historical approaches to contemporary innovations

Transcranial Electrical Stimulation (tES) encompasses all methods of non-invasive current application to the brain used in research and clinical practice. We present the first comprehensive and technical review, explaining the evolution of tES in both terminology and dosage over the past 100 years of research to present day. Current transcranial Pulsed Current Stimulation (tPCS) approaches such as Cranial Electrotherapy Stimulation (CES) descended from Electrosleep (ES) through Cranial Electro-stimulation Therapy (CET), Transcerebral Electrotherapy (TCET), and NeuroElectric Therapy (NET) while others like Transcutaneous Cranial Electrical Stimulation (TCES) descended from Electroanesthesia (EA) through Limoge, and Interferential Stimulation. Prior to a contemporary resurgence in interest, variations of transcranial Direct Current Stimulation were explored intermittently, including Polarizing current, Galvanic Vestibular Stimulation (GVS), and Transcranial Micropolarization. The development of these approaches alongside Electroconvulsive Therapy (ECT) and pharmacological developments are considered. Both the roots and unique features of contemporary approaches such as transcranial Alternating Current Stimulation (tACS) and transcranial Random Noise Stimulation (tRNS) are discussed. Trends and incremental developments in electrode montage and waveform spanning decades are presented leading to the present day. Commercial devices, seminal conferences, and regulatory decisions are noted. We conclude with six rules on how increasing medical and technological sophistication may now be leveraged for broader success and adoption of tES.     

Carbamazepine Efficacy and Utilization in Children

Summary: Carbamazepine is effective for preventing partial and generalized tonic-clonic seizures in children. Although absence epilepsies are more common in children than adults, an estimated 80% of children with epilepsy have seizure types or epilepsies that are potentially responsive to carbamazepine. The differential diagnosis of ictal staring is an especially important issue in children because absence and atypical absence seizures are more prevalent in children than adults. Age-related pharmacokinetic differences and drug interactions are major considerations in children. On average, children have higher clearance rates of carbamazepine, shorter half-lives, and higher ratios of carbamazepine-10, 11-epoxide to carbamazepine than adults. In addition, children with severe epilepsy are more likely to require multiple-drug therapy, which can lead to complex drug interactions. When carbamazepine is administered along with valproate, drug protein binding interactions can cause intermittent side effects.     

Neonatal Seizures: Problems in Diagnosis and Classification

Summary: The clinical identification of neonatal seizures is critical for the recognition of brain dysfunction; however, diagnosis is often difficult because of the poorly organized and varied nature of these behaviors. Current classification systems are limited in their ability to communicate motor, autonomic, and electroencephalo-graphic features of seizures precisely and to provide a basis for uniform effective diagnosis, therapy, and determination of prognosis. Recent investigations of neonates, utilizing bedside electroencephalographic/polygraphic/ video monitoring techniques, have provided the basis for improved diagnosis and classification of seizures in the newborn. These studies have demonstrated that not all clinical phenomena currently considered to be seizures require electrocortical epileptiform activity for their initiation or elaboration. In addition, the specific clinical character of the phenomena considered to be seizures, the clinical state of the infant, and the character of the EEG indicate the probable pathophysiological mechanisms involved and suggest probable etiologies, prognosis, and therapy. Similarities between animal models that demonstrate reflex physiology and neonates with motor automatisms and tonic posturing suggest that these clinical behaviors may not be epileptic in origin but, rather, primitive movements of progression and posture mediated by brainstem mechanisms. Although not all clinical behaviors currently considered to be neonatal seizures may have similar pathophysiological mechanisms, they are clinically significant because they all indicate brain dysfunction.     

Valproate Monotherapy in the Management of Generalized and Partial Seizures

Summary: For decades, therapeutic tradition has promoted the concept of polypharmacy in the management of epilepsy. In recent years, however, studies have shown that, for most patients, monotherapy can provide comparable or better seizure control than administration of multiple anticonvulsants, while diminishing the potential for adverse reactions, drug interactions, and poor compliance. Valproate is an important monotherapeutic agent that is highly effective in the control of idiopathic primary and secondarily generalized epilepsies, and partial seizures that do not generalize. Comparative studies have found that valproate is at least as effective as phenytoin and carbamazepine in the treatment of generalized and partial seizures. Given the similar efficacy, other factors such as pharmacokinetics and side effects may therefore determine anticonvulsant selection for monotherapy.     

Un nouveau cadre conceptuel de travail pour la psychiatrie

In an attempt to place psychiatric thinking and the training of future psychiatrists more centrally into the context of modern biology, the author outlines the beginnings of a new intellectual framework for psychiatry that derives from current biological thinking about the relationship of mind to brain. The purpose of this framework is twofold. First, it is designed to emphasize that the professional requirements for future psychiatrists will demand a greater knowledge of the structure and functioning of the brain than is currently available in most training programs. Second, it is designed to illustrate that the unique domain which psychiatry occupies within academic medicine, the analysis of the interaction between social and biological determinants of behavior, can best be studied by also having a full understanding of the biological components of behavior.