高血压共病性失眠患者血浆皮质醇测定及临床意义

目的检测高血压共病性失眠症患者血浆皮质醇水平,评估其临床意义及对失眠症过度觉醒的预测价值,探讨两者可能的病理生理机制。方法纳入高血压共病性失眠症患者25例(高血压共病性失眠组)、原发性失眠症患者25例(原发性失眠组)和对照组25例(正常睡眠),分别检测清晨血浆皮质醇水平,比较3组匹兹堡睡眠质量指数(PSQI)、过度觉醒量表(HAS)评分,分析各量表评分与皮质醇水平的相关性。结果高血压共病性失眠组患者的PSQI、HAS评分、血浆皮质醇水平均较原发性失眠组和对照组增高,且血浆皮质醇水平与两个量表总分及各因子分呈正相关。结论过度觉醒机制可能是失眠症发生的重要机制,血浆皮质醇水平可视为代表觉醒水平的重要指标,高血压病和失眠可能通过共同的下丘脑-垂体-肾上腺轴的病理生理机制相互作用,相互影响。     

右美托咪定诱导睡眠平衡术对慢性顽固性原发性失眠症患者的疗效观察

目的:探讨右美托咪定诱导睡眠平衡术(DISBT)对慢性顽固性原发性失眠症患者的临床疗效。方法:将42例慢性顽固性原发性失眠症患者随机分为DISBT组(21例)给予DISBT治疗和对照组(21例)给予常规治疗。DISBT治疗时间为3 d,共行3次治疗。于治疗前、治疗后1周分别对两组进行匹兹堡睡眠质量指数、过度觉醒量表和汉密尔顿焦虑量表评估,并检测治疗前后睡眠结构和脑电频谱差异。结果:①两组治疗后匹兹堡睡眠质量指数、汉密尔顿焦虑量表分值均较治疗前降低(P<0.05);降低程度DISBT组>对照组(P<0.05)。②DISBT组睡眠结构中2期睡眠比例、脑电频谱β、γ频段相对功率值较治疗前减少(P<0.05),对照组则较冶疗前上升(P<0.05);DISBT组冶疗后3期睡眠比例及6频段相对功率值较治疗前上升(P<0.05);对照组则较治疗前下降(P<0.05)。③两组治疗后,过度觉醒量表总分较治疗前下降(P<0.05),降低程度DISBT组>对照组(P<0.05);对照组过度觉醒量表中极限数个数总和、反应因子及自省因子评分与治疗前相比差异无统计学意义(P>0.05),DISBT组则均较治疗前下降(P<0.05)。结论:右美托咪定诱导DISBT能有效降低失眠患者的脑皮质过度觉醒水平,纠正紊乱的睡眠-觉醒通路,改善患者失眠症状,是治疗慢性顽固性原发性失眠症的有效方法。     

盐酸右美托咪定诱导睡眠平衡术治疗失眠的临床观察

目的探讨右关托咪定治疗失眠症的疗效以及该治疗方法对失眠症过度觉醒的影响。方法对本科室22例失眠症患者行睡眠监测、血清皮质醇检测、相关量表评估及各系统检查,并行盐酸右美托咪定诱导睡眠平衡术,术后复查睡眠监测、血清皮质醇进行疗效评估。结果行盐酸右美托咪定诱导睡眠平衡术后,失眠症患者较术前睡眠潜伏期缩短（P〈0．05）,睡眠总时间延长（P〈0．05）,睡眠效率增高（P〈0．05）,觉醒次数及入睡后清醒时间无明显减少（P〉0．05）,清晨8：00血皮质醇降低（P〈0．05）。结论盐酸右美托咪定诱导睡眠平衡术可缩短失眠症患者的睡眠潜伏期,延长睡眠总时间,改善睡眠效率,但对睡眠维持状态无明显改善,并可降低血皮质醇抑制过度觉醒状态。     

失眠症患者应用个性化睡眠护理干预的临床效果分析

目的探讨个性化睡眠护理干预对失眠症患者的效果。方法收集2014年1月至2015年6月,我院住院失眠症患者112例,采用随机数字表法分为观察组与对照组,每组各56例。对照组接受常规护理,观察组在对照组的基础上加行个性化睡眠护理干预,对比两组的睡眠进程以及匹兹堡睡眠质量指数(PSQI)变化。结果两组患者干预前睡眠进程及PSQI评分,组间比较无明显差异(P0.05);干预后两组的睡眠时间均延长,入睡潜伏期、觉醒时间及觉醒次数均减少,PSQI评分均著降低(P0.05)干预后,观察组的各个睡眠进程指数及PSQI评分结果均优于对照组(P0.05)。结论在常规护理的基础上增加个性化睡眠护理干预,可更有利于改善失眠症患者的睡眠质量,值得推广应用。     

右美托咪定对顽固性原发性失眠患者的脑电超慢涨落图的影响

目的 观察右美托咪定睡眠诱导平衡治疗后顽固性原发性失眠患者脑内神经递质活动的变化.方法 对23例顽固性原发性失眠且内科治疗效果不佳的患者实施右美托咪定睡眠诱导平衡治疗,每日1h,持续3d,对照组23例患者采用常规方案治疗.采用阿森斯失眠量表及过度觉醒量袁评估患者治疗前后的主观症状变化,并采用脑电超慢涨落技术对治疗前后的脑内神经递质分别进行检测.结果 治疗后治疗组阿森斯失眠量表及过度觉醒量表指标分值明显改善,治疗前患者脑内5-羟色胺活动水平偏低,去甲肾上腺素活动水平偏高,经睡眠诱导平衡治疗后5-羟色胺活动水平升高,去甲肾上腺素活动水平降低,差异具有统计学意义（P＜0.05）,余神经递质活动水平无明显变化,差异无统计学意义（P＞0.05）,且无严重治疗不良反应.结论 顽固性原发性失眠患者脑内神经递质存在5-羟色胺活动水平偏低,去甲肾上腺素活动水平偏高,右美托咪定睡眠诱导平衡术治疗可以调节它们的活动水平,同时患者的失眠症状及过度觉醒表现也有所改善.     

抑郁症患者睡眠障碍与血浆增食欲素A的关系

目的 探讨抑郁症患者睡眠障碍与血浆增食欲素A的关系,以期为抑郁症睡眠障碍的干预提供理论基础.方法 67例抑郁症患者行24项汉密尔顿抑郁量表(HAMD-24)及匹兹堡睡眠质量指数量表(Pittsburgh sleep quality index,PSQI)评定,根据睡眠情况分为睡眠障碍组(研究组,n=37)及非睡眠障碍组(阳性对照组,n =30),多导睡眠图检测睡眠情况,放射免疫法检测血浆增食欲素-A水平,并与26例健康体检者进行对比(阴性对照组).结果 与正常对照组及非睡眠障碍组比较,抑郁症睡眠障碍组患者HAMD抑郁量表评分及血浆Orexin-A水平均明显增加(P＜ 0.05,P＜0.01);总睡眠时间减少,睡眠潜伏期长,觉醒次数及时间增多,睡眠效率及维持率明显下降,浅睡(S1期睡眠)增加而深睡(S3、S4期睡眠)减少(P＜0.05,P＜ 0.01);REM潜伏期缩短,REM睡眠时间增多,REM活动度、强度及密度明显增强(P＜0.05,P＜0.01);相关性分析表明,血浆Orexin-A水平与睡眠潜伏期、觉醒时间、觉醒次数均呈正相关(r分别为0.447、0.591、0.670,P＜0.01),与S3％+S4％呈负相关(r=-0.872).结论 睡眠障碍者抑郁程度较非睡眠障碍者更高,血浆Orexin-A水平升高可能是引起抑郁症睡眠障碍的一项重要因素,其机制可能与其促进觉醒有关.     

肝豆状核变性睡眠障碍初步研究

目的探讨肝豆状核变性(HLD)患者睡眠障碍特点及其潜在发生机制。方法采用帕金森病睡眠量表(PDSS)、Epworth嗜睡量表(ESS)和匹兹堡睡眠质量指数(PSQI)评价26例肝豆状核变性患者的睡眠障碍。结果 HLD组患者PDSS总评分低于对照组(P=0.000),其中,夜间总体睡眠质量(P=0.010)、入睡困难(P=0.009)、睡眠维持困难(P=0.013)、震颤(P=0.005)、清晨醒后感觉困倦欲睡(P=0.042)和白天过度嗜睡(P=0.028)等分评分亦低于对照组;而ESS(P=0.009)和PSQI(P=0.005)评分高于对照组。进一步分析肝豆状核变性各亚组患者睡眠障碍,脑型HLD组PDSS总评分低于肝型HLD组和无症状型HLD组(P=0.046),其中,夜间总体睡眠质量(P=0.021)、入睡困难(P=0.009)和睡眠维持困难(P=0.002)等分评分亦低于肝型HLD组和无症状型HLD组。结论肝豆状核变性患者常合并睡眠障碍且以入睡困难、夜间觉醒和白天过度嗜睡为主,其中脑型肝豆状核变性患者睡眠质量差于肝型和无症状型患者。肝豆状核变性睡眠障碍的发生机制尚待进一步研究。     

卡比多巴-左旋多巴控释片治疗帕金森病合并睡眠障碍的疗效观察

目的探讨卡比多巴-左旋多巴控释片对治疗帕金森病(Parkinson′s disease,PD)合并睡眠障碍患者睡眠障碍的疗效。方法选取符合英国脑库原发性帕金森病临床诊断标准确诊为原发性帕金森病的患者96例,并随机分成卡比多巴-左旋多巴控释片及左旋多巴组各48例,分别进行3个月药物治疗后,通过睡眠量表(PDSS)、匹兹堡睡眠质量指数(PSQI),及用ESS评分评价2组睡眠质量。结果与左旋多巴组比较,卡比多巴-左旋多巴控释片治疗后能明显改善患者的PDSS量表在PDSS-1、3、4、5、6、8、10、11、13、15项目上得分明显增高(P0.05);卡比多巴-左旋多巴控释片组患者较左旋多巴组能明显降低PSQI及ESS评分(P0.05);同时,多导睡眠图监测实验显示患者卧床时间、总睡眠时间、睡眠效率明显升高、觉醒次数明显下降,差异有统计学意义(P0.05)。结论与左旋多巴比较,卡比多巴-左旋多巴控释片在改善PD合并睡眠障碍患者的睡眠状况方面有更好的优势。     

低频重复经颅磁刺激对原发性失眠的疗效及神经内分泌的影响

目的探究低频重复经颅刺激(rTMS)治疗对原发性失眠患者的临床效果及对患者神经内分泌的影响。方法选取2019年5月～2020年4月期间本院收治原发性失眠患者70例,按随机数字表法将研究对象随机分为观察组和对照组,对照组(35例)采用交变磁场疗法,观察组(35例)采用低频重复经颅磁刺激疗法。观察比较两组患者的匹茨堡睡眠质量指数量表(PSQI)评分、神经内分泌指标和临床疗效。结果治疗后,观察组患者的PSQI评分低于对照组(P0.05);观察组患者的Glu水平较对照组降低,皮质醇和Gly水平较对照组升高(P0.05);对照组的治疗有效率低于观察组(P0.05)结论低频重复经颅刺激治疗原发性失眠疗效显著,可改善患者睡眠质量及神经内分泌水平,值得临床推广应用。     

集束化护理干预在心内科住院失眠老年患者中的应用效果研究

目的探讨集束化护理干预应用于心内科住院失眠老年患者的临床效果。方法选择心内科住院且有明确失眠症的老年患者146例,随机分为观察组与对照组,每组73例,均服用一片阿普唑仑助眠。对照组实施常规护理,观察组则在此基础上实施集束化护理干预,对比两组护理前后睡眠进程参数、匹兹堡睡眠质量指数(PSQI)及汉密尔顿焦虑和抑郁量表(HAMA、HAMD)评分和临床疗效。结果观察组的总有效率为94.52%,显著高于对照组的80.82%(P0.05);干预后观察组的入睡潜伏时间、觉醒次数及觉醒时间均显著低于对照组,实际睡眠时间及睡眠维持率均显著高于对照组(P0.05);干预后观察组的PSQI量表各维度评分、HAMA及HAMD评分均显著低于对照组(P0.05)。结论集束化护理干预合并助眠药物能够改善心内科失眠老年患者的精神心理状态及失眠症状,提高其睡眠质量并促进病情康复。     

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.     

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.     

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.     

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.     

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.