精神障碍中的失眠研究进展

失眠是精神科最常见的睡眠障碍。大多数的慢性失眠患者出现睡眠问题是因为存在精神障碍。现重点介绍临床常见的抑郁、精神分裂症等精神障碍中的失眠的相关研究情况。     

精神分裂症患者复发的早期表现调查分析

目的　探讨精神分裂症患者复发的早期表现 ,提出预防复发的干预措施。方法　采用匹兹堡睡眠质量指数 (PSQI)等工具 ,调查符合CCMD 2 R的精神分裂症再次住院的患者及家属 ,内容包括本次复发的早期睡眠、情绪、植物神经功能、行为等表现。结果　 88%的患者有睡眠障碍、情绪障碍、植物神经功能障碍、行为障碍等 11种症状最多见。结论　精神分裂症患者复发的早期症状为精神病性与非精神病性症状的混合表现 ,其中以睡眠障碍和情绪障碍占重要地位。依据此结果提出预防精神分裂症复发的早期干预措施。     

精神疾病睡眠障碍研究的近况

精神疾病睡眠障碍研究的近况雷声睡眠有提高人类生活质量的基本作用，而关于睡眠及其相关问题，却有很多内容尚未阐明。各种精神疾病都会发生睡眠障碍（Ｆｏｒｄ，等．１９８９），如精神分裂症患者常有失眠（今井，等．１９７４），而睡眠障碍又几乎是抑郁症的必有症状。...     

益生菌治疗抗精神病药物所致糖脂代谢紊乱的研究进展

对抗精神病药物引起的糖脂代谢紊乱的相关管理及治疗，是近几年来临床医生一直关注的问题。抗精神病药物可导致肠道菌群失调，使得机体出现糖脂代谢紊乱，而益生菌能够维持肠道菌群稳态。现对使用益生菌治疗抗精神病药物所致糖脂代谢紊乱的相关研究进行综述，以期为治疗抗精神病药物引起的糖脂代谢紊乱提供思路。     

精神分裂症的睡眠脑电图研究进展

精神分裂症是一组病因未明的精神疾病,多起病于青壮年,常有感知、思维、情感、行为等多方面的障碍和精神活动不协调,病程多迁延［1］。睡眠障碍往往是精神分裂症的先兆症状和伴随症状,睡眠质量的好坏也常常影响病情的转归［2］。多导睡眠图（Polysomnogram ,PSG ）是评估睡眠质量的重要手段,可以用来探讨药物、心理治疗、物理治疗等治疗手段对睡眠的影响［3］。既往研究对精神分裂症患者睡眠脑电图的改变进行了探讨,主要包括睡眠结构、慢波睡眠（SWS ）、睡眠纺锤波、K 复合波和睡眠δ波,希望找到精神分裂症患者睡眠参数的改变与神经生理学、精神病理学之间的关系,继而确定睡眠脑电图改变与精神分裂症之间的相关性,找到精神分裂症的生物学标记,为精神分裂症的诊断和治疗提供依据。     

伴与不伴睡眠障碍的精神分裂症高危人群的认知功能差异

目的 评估伴与不伴睡眠障碍的精神分裂症超高危患者的认知功能,探讨睡眠质量对该人群认知功能的影响.方法 选取精神分裂症超高危患者97例,用匹兹堡睡眠质量指数量表评估睡眠情况,将被试分为伴睡眠障碍组46人,不伴睡眠障碍组51人,采用重复性成套心理测验评估认知功能.结果 伴有睡眠障碍组在即刻记忆、注意、视觉广度、认知总分上均...     

睡眠纺锤波在精神分裂症患者中的改变及其在记忆巩固中的作用

精神分裂症是一种常见的精神疾病,睡眠障碍在精神分裂症患者中也比较常见,本文就睡眠纺锤波在精神分裂症患者中的改变及其在记忆巩固中的作用作一综述。     

精神分裂症患者有无不眠临床特征分析

精神分裂症患者常伴有睡眠障碍，尤其是不眠，我们对有无不眠的精神分裂症患者的临床特征进行研究，现将结果报告如下。     

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。     

精神分裂症复发的相关因素研究进展

精神分裂症是一种常见的、病因不明的、往往累及终身的重性精神疾病，具有高患病率、 高复发率、高致残率等特点。精神分裂症的反复发作会导致患者认知功能障碍、社会功能受损、生活质 量下降等严重后果。近些年的研究对于精神分裂症复发相关因素的探讨相对零散，现就精神分裂症复 发的定义及其相关因素进行梳理及综述。     

Obsessive-compulsive spectrum disorders and anxiety disorders

Although obsessive-compulsive disorder (OCD) is classified as an anxiety disorder in the DSM-IV, recent considerations for a reclassification into an obsessive-compulsive spectrum disorders (OCSDs) cluster are gaining prominence. Hollander and colleague indicate that similarities in symptomatology, course of illness, patient population, and neurocircuitry of OCD and OCSD are supported by comorbidity, family, and neurological studies, which also offer a critical re-evaluation of the relationship between OCD and anxiety disorders. In February 2010, as a consequence, members of the DSM-5 Task Force and Work Groups have updated draft DSM-5 and have added many diagnostic-specific severity measures, including the Anxiety, Obsessive-Compulsive-Related, and Trauma-Related Disorders. Recently, however, there are some results indicated that support the current association of OCD with other anxiety disorders rather than with OCSDs. Thus, controversy surrounds the classification of OCSD symptoms. In this review, we investigated the relationship of OCD, OCSDs, and anxiety disorders to answer the question of where OCD should be located in the diagnostic system.     

CNS disorders caused by metabolic disorders

A guideline for early diagnosis of metabolic disorders affecting central nervous system during neonatal and early infancy was presented. Clinical manifestations associated with inborn errors of metabolism in the neonatal period are poor feeding, vomiting, diarrhea, abnormalities in muscle tonus, dyspnea, convulsion, coma and so on, and these are not specific to each disorder. However, such symptoms or signs as described below have often intimate relation to metabolic disorders: (1) previous children died of undetermined causes during early infancy; (2) complication of sepsis; (3) onset in the early neonatal period; (4) developmental and growth retardation. When newborns and infants have these symptoms or signs, we should start simple screening studies immediately for metabolic disorders, including CBC, hepatic function tests, blood glucose, lactate, pyruvate, ketone bodies, ammonia, blood gas analysis, urinalysis (including non-glucose reducing substance tests and FeCl3 reaction) and so on. As for CBC, we have to make our own effort to find spherocytosis and vacuoles in lymphocytes. Family history, especially the mother's personal history, is indispensable. During physical examinations, we must pay attention to facial appearance, skin color, macroglossia, hair abnormalities, peculiar odor of the urine and hepatosplenomegaly. When abnormality is found in these clinical signs or simple laboratory examinations, we should not hesitate to start dietary treatment even if special examinations for differential diagnosis are on the way.     

Schizoaffective disorders are psychotic mood disorders; there are no schizoaffective disorders

Schizoaffective disorder (SA D/O), introduced in 1933 by Dr. Jacob Kasanin, represented a first, modest change in our concept about the diagnoses of psychotic patients away from the beliefs of E. Bleuler, i.e., that hallucinations and delusions define schizophrenia, and toward the recognition of a significant role for mood disorders. SA D/O established a connection between schizophrenia and mood disorders, traditionally considered mutually exclusive, a connection that has strengthened progressively toward the diagnostic unity of all three disorders. A basic tenet of medicine holds that if discrepant symptoms can be explained by one disease instead of two or more, it is likely there is only one disease. The scientific justification for SA D/O and schizophrenia as disorders distinct from a psychotic mood disorder has been questioned. The "schizo" prefix in SA D/O rests upon the presumption that the diagnostic symptoms for schizophrenia are disease specific. They are not, since patients with severe mood disorders can evince any or all of the "schizophrenic" symptoms. "Schizophrenic" symptoms mean "psychotic" and not any specific disease. These data and a very low interrater reliability for SA D/O suggest that the concepts of SA D/O and schizophrenia as valid diagnoses are flawed. Clinically SA D/O remains popular because it encompasses both schizophrenia and psychotic mood disorder when there is a diagnostic question. We present a review of the literature in table form based on an assignment of each article assigned to one of five categories that describe the possible relationships between SA D/O, schizophrenia and psychotic mood disorders. We conclude that the data overall are compatible with the hypothesis that a single disease, a mood disorder, with a broad spectrum of severity, rather than three different disorders, accounts for the functional psychoses.     

Autism spectrum disorders: concurrent clinical disorders

Individuals with autism spectrum disorder are heterogeneous in clinical presentation, concurrent disorders, and developmental outcomes. This study characterized the clinical co-occurrences and potential subgroups in 160 children with autism spectrum disorders who presented to The Autism Center between 1999 and 2003. Medical and psychiatric co-occurrences included sleep disorders, epilepsy, food intolerance, gastrointestinal dysfunction, mood disorder, and aggressive and self-injurious behaviors. Sleep disorders were associated with gastrointestinal dysfunction (P < .05) and mood disorders (P < .01). Food intolerance was associated with gastrointestinal dysfunction (P = .001). Subjects with mood disorder tended to develop aggressive or self-injurious behaviors (P < .05). Developmental regression was not associated with increased co-occurrence of medical or psychiatric disorders. Medical co-occurrence did not present as a risk factor for psychiatric co-occurrence, and vice versa. These results showed a high prevalence of multiple medical and psychiatric co-occurrences. There may be common pathophysiologic mechanisms resulting in clinical subgroups of autism spectrum disorders. Recognition of the co-occurrence of concurrent disorders may provide insight into the therapeutic strategy.     

Managing mood disorders and comorbid personality disorders

PURPOSE OF REVIEW: To examine the influence of personality disorder comorbidity on the general treatment of mood disorders. RECENT FINDINGS: Personality disorders generally have a negative influence on outcome of mood disorders, both unipolar and bipolar. When the personality features are addressed, however, the outcome is less negative. Recent studies suggest a special role for psychological and educational therapies in the treatment of these comorbid disorders. SUMMARY: The assessment of, and attention to, the management of personality disorder as well as concurrent mood disorder may improve outcome.