精神分裂症患者的脑结构及其认知功能损害

精神分裂症患者的脑结构变异与认知功能损害有密切关系。以脑病理学为依据，在临床研究基础上，分别探讨了精神分裂症患者的脑结构变异、认知功能损害及两者之间的关系。最后，对广为应用的言语流畅性测验在精神分裂症评测上的作用作了分析，旨在深入理解该病的病理机制，有利于精神分裂症的临床预防与治疗。     

精神分裂症脑电在不同认知作业下的复杂度分析

为探讨在不同认知作业状态下精神分裂症患者脑电复杂性测度的变化规律,本文利用Lempel-Ziv复杂性测度方法对62例精神分裂症患者和26例正常人群在三种不同精神状态安静闭目、闭眼心算连减和数字划消下的16导联脑电数据进行了分析.实验结果得出:精神分裂症患者和正常在三种精神状态下某些导联复杂性测度的大小有明显差异,复杂度的空间分布规律相似;与安静闭目状态下相比,完成认知作业的两种状态下EEG的复杂度都偏低(a=0.01).认为复杂性测度分析适合研究认知过程中大脑功能活动的变化规律,有助于了解认知过程中大脑的工作机制.     

精神分裂症有暴力行为患者脑电图特征

精神分裂症暴力攻击行为是复杂的反社会行为,其产生机制尚不清楚。攻击行为与脑功能紊乱之间关系备受关注。脑电图在暴力行为研究中得到一定运用。研究显示脑电图检测有助于对精神分裂症暴力攻击行为进行评估和预测。作者在血清皮质醇,醛固酮水平在伪装精神病司法鉴定中的作用研究过程中,对精神分裂症有暴力行为患者脑电图特征文献进行了回顾,现综述如下。     

首发未服药精神分裂症患者河内塔任务时的脑电图信号特征

目的:探讨首发未服药精神分裂症患者在冷执行任务执行过程中的认知生理特征。方法:纳入符合美国精神障碍诊断与统计手册第4版(DSM-IV)诊断标准的精神分裂症患者18例和正常对照18例,冷执行功能任务选择经典的河内塔测验(3层),记录反应速度和执行步骤,同时采集执行任务过程中的脑电图数据。结果:患者组每一任务步骤反应时较正常对照组长(P<0.05),两组操作步骤数差异无统计学意义(P>0.05)。两组被试在测验中均主要激活0.01～10 Hz频段;与对照组相比,患者组在河内塔任务中额-枕和额-顶区域存在功能连接增强(P<0.05),对应的脑网络聚类系数值低,特征路径长度长(P<0.05)。患者组的阳性症状分与其脑网络的聚类系数呈负相关(r=-0.66,P<0.01),与特征路径长度呈正相关(r=0.60,P<0.05)。结论:精神分裂症患者的冷执行功能呈现一定程度的损害,特别是流畅性受损;脑网络效率下降,可能与精神分裂症阳性症状严重程度有关。     

首发精神分裂症患者脑电图与脑电地形图结果相关性探讨

脑电图(EEG)是20世纪30年代开始应用于临床的[1],是一项传统的脑功能评价方法,脑地形图(BEAM)是20世纪80年代应用于临床的[2],是一项新的定量脑功能评价方法,采用脑电图与脑地形对比分析评价脑功能状态成为一种常用的临床研究方法,本文收集北京回龙观医院1995年8月~2002年1月首发精神分裂症患者脑电图与脑地形图资料,并进行对比分析,以探讨脑电图与脑地形图对首发精神分裂症患者脑功能的评价作用,结果报告如下。一、资料与方法病历资料200例病例均来自于北京回龙观医院1995年8月~2002年1月间住院和门诊首发精神分裂症患者,男101例,女99例…     

精神分裂症患者认知功能损伤的神经生物学基础和电生理表现

精神分裂症患者存在严重的认知功能损伤,认知功能损伤的重要神经生物学基础是患者脑内神经递质水平异常,这会导致患者出现异常神经元电活动,脑电图指标可以客观、定量反映神经递质导致的异常神经元电活动。本文主要对国内外精神分裂症患者认知功能损伤的神经生物学和电生理学等研究情况进行综述,回顾了认知功能损伤相关神经递质的生物学机制,梳理了与之相关的异常神经生物电指标,为精神分裂症的发病原理和辅助诊断提供相应参考。未来的研究应更多关注疾病的致病基因、神经影像学等生物学标记物,建立精神分裂症辅助诊断的指标体系。     

精神分裂症患者治疗前后认知功能的对照研究

目的进一步了解药物治疗精神分裂症病人认知功能的影响及认知功能与阳性和阴性症状的关系.方法对30例精神分裂症或分裂样精神病患者,在利培酮治疗前后进行威斯康星卡分类测验(WCST).结果治疗后WCST总测验次数,持续错误数,非持续错误数均少于治疗前,差异有显著性,P分别小于0.01及0.05.结论经利培酮治疗后,精神分裂症病人在主症状改善的同时,认知功能也有明显提高,且认知功能的提高与阳性症状的改善存在着明显相关性,而与阴性症状的改善关系不大.     

神经症与精神分裂症患者脑电图对照分析

为了进一步探讨神经症患者脑电图改变，以及神经症与精神分裂症患者脑电图改变有无区别，为临床诊断提供客观资料．对我院1990～2003年临床诊断为神经症且未服精神药物患者的脑电图进行分析．并与同期未服精神药物的精神分裂症患者的脑电图进行对照分析，现报道如下。     

精神分裂症患者的脑电图与CT检查分析

目的:用脑电图(EEG),计算机断层扫描(CT)检查,对精神分裂症患者脑电活动和大脑结构特征与规律进一步认识。方法:86例精神分裂症患者均在安静状态下进行EEG常规参考导联,双极导联描记,描记时间20~30分钟,86例患者中52例作脑CT扫描。结果:本组86例精神分裂症患者中,EEG检查结果24例异常,异常率28.6%,均为轻度异常。86例中52例作脑CT检查,检查结果13例异常,异常率25%。结论:精神分裂症患者中,少部分有一定程度的大脑功能障碍与脑结构改变的表现。     

心理健康对精神分裂症患者认知功能的影响

目的观察心理健康对精神分裂症患者认知功能的影响。方法采用入院顺序分层随机法，将120例慢性精神分裂症患者分为研究组（心理健康＋奋乃静）和对照组（单用奋乃静）治疗。在治疗前，治疗后4、8、12周末分别以阳性症状和阴性症状量表（PNASS？评定疗效，用韦氏成人智力量表（WAIS—R）、韦氏记忆量表（WMS）和威斯康星卡片分类测验（wCST）评定治疗前后患者认知功能的改变。结果治疗12周后，研究组的言语量表、操作量表、全量表和记忆量表分分别为84．97±3．73、80．41±5．93、83．37±5．81、77．26±13．31；对照组分别为75．41±3．95、72．43±5．56、75．87±5．34、72．15±13．19，两组有显著差异（P〈0．01）。PANSS总分、阴性因子分比治疗前明显降低。结论心理健康治疗对精神分裂症患者认知功能有明显改善。     

Dysbindin基因在精神分裂症中的研究进展

位于染色体6p22.3区域的Dysbindin基因是精神分裂症的易感基因之一.在大脑中,其功能主要是通过复杂的突触后或前机制影响谷氨酸神经递质的释放,现就Dysbindin基因在精神分裂症中的研究情况进行综述,包括Dysbindin基因及其产物,可能的致病机制,与精神分裂症的关联研究以及该基因变异对精神分裂症患者认知功能可能造成的损害.     

Interaction of dopamine system genes and cognitive functions in patients with schizophrenia and their relatives and in healthy subjects from the general population

Linkage between the DRD4 and COMT genes and cognitive measures characterizing verbal memory, executive functions, and associative processes was studied in 150 patients with schizophrenia, 83 of their relatives, and 118 mentally healthy subjects without any family history of psychoses, with the aim of detecting the main effects of the polymorphic markers −809G/A and −521C/T (DRD4) and Val158Met (COMT) when present individually and together. The group of patients showed a main effect for polymorphism −521C/T on verbal fluency and an effect of the interaction of this polymorphism and the COMT gene on this cognitive trait. The highest level of verbal fluency was seen among carriers of the Val/Val+CC and Met/Met+TT genotypes. In the combined group of unaffected individuals, the interaction of the COMT and DRD4 −521C/TT genotypes had an effect on the standardness of speech associations due to a decrease in the standardness of associations in carriers of the Met/Met+CC genotype. Finally, both patients and unaffected individuals showed an effect for the interaction between the COMT and DRD4 −809G/A genotypes on working memory. Patients and healthy subjects showed similar features: the highest values were seen in subjects homozygous for the Val and G alleles, while the lowest values were seen in homozygotes for the Met and A alleles. These data provide evidence for a relationship between the DRD4 and COMT genes and different aspects of executive functions and the absence of such a relationship in relation to verbal memory. __________ Translated from Zhurnal Nevrologii i Psikhiatrii imeni S. S. Korsakova, Vol. 106, No. 7, pp. 57–63, July, 2006.     

Cognitive adaptation training for outpatients with schizophrenia

Schizophrenia is a complex neurodevelopmental disorder characterized by cognitive deficits. These deficits in cognitive functioning have been shown to relate to a variety of functional and treatment outcomes. Cognitive adaptation training (CAT) is a home‐based, manual‐driven treatment that utilizes environmental supports and compensatory strategies to bypass cognitive deficits and improve target behaviors and functional outcomes in individuals with schizophrenia. Unlike traditional case management, CAT provides environmental supports and compensatory strategies tailored to meet the behavioral style and neurocognitive deficits of each individual patient. The case of Ms. L. is presented to illustrate CAT treatment. © 2009 Wiley Periodicals, Inc. J Clin Psychol: In Session 65:1–12, 2009.     

The impact of cognitive training on spontaneous gamma oscillations in schizophrenia

Schizophrenia patients exhibit less gamma‐frequency EEG/MEG activity (>30 Hz), a finding interpreted as evidence of poor temporal neural organization and functional network communication. Research has shown that neuroplasticity‐oriented training can improve task‐related oscillatory dynamics, indicating some reorganization capacity in schizophrenia. Demonstrating a generalization of such task training effects to spontaneous oscillations at rest would not only enrich understanding of this neuroplastic potential but inform the interpretation of spontaneous gamma oscillations in the service of normal cognitive function. In the present study, neuromagnetic resting‐state oscillatory brain activity and cognitive performance were assessed before and after training in 61 schizophrenia patients, who were randomly assigned to 4 weeks of neuroplasticity‐oriented targeted cognitive training or treatment as usual (TAU). Gamma power of 40–90 Hz increased after training, but not after TAU, in a frontoparietal network. Across two types of training, this increase was related to improved cognitive test performance. These results indicate that abnormal oscillatory dynamics in schizophrenia patients manifested in spontaneous gamma activity can be changed with neuroplasticity‐oriented training parallel to cognitive performance.     

Altered cerebrocerebellar functional connectivity in patients with obstructive sleep apnea and its association with cognitive function

Study ObjectivesPrevious functional MRI studies have reported altered brain networks in patients with obstructive sleep apnea (OSA). However, the extent and pattern of abnormal connectivity were inconsistent across studies, and cerebrocerebellar connections have been rarely assessed. We investigated functional network changes in cerebral and cerebellar cortices of OSA patients.MethodsResting-state functional MRI, polysomnography, and neuropsychological (NP) test data were acquired from 74 OSA patients (age: 45.8 ± 10.7 years) and 33 healthy subjects (39.6 ± 9.3 years). Connectivity matrices were extracted by computing correlation coefficients from various regions of interest, and Fisher r-to-z transformations. In the functional connections that showed significant group differences, linear regression was conducted to examine the association between connectivity and clinical characteristics.ResultsPatients with OSA showed reduced functional connectivity (FC) in cerebrocerebellar connections linking different functional networks, and greater FC in cortical between-network connections in prefrontal regions involving the default mode network (DMN) and the control network. For OSA group, we found no correlation between FC and sleep parameters including lowest SaO₂ and arousal index in the connections where significant associations were observed in healthy subjects. FC changes in DMN areas were related to reduced verbal fluency in OSA. Lower local efficiency and lower clustering coefficient of the salience network in the left cerebellum were also observed in OSA.ConclusionsOSA affects mainly the cerebrocerebellar pathway. The disruption of function in these connections are related to sleep fragmentation and hypoxia during sleep. These abnormal network functions, especially DMN, are suggested to participate in cognitive decline of OSA.     

The stop null mice model for schizophrenia displays cognitive and social deficits partly alleviated by neuroleptics

Recently evidence has accumulated that schizophrenia can arise from primary synaptic defects involving structural proteins particularly, microtubule associated proteins. Previous experiments have demonstrated that a STOP (stable tubule only peptide) gene deletion in mice leads to a phenotype mimicking some aspects of positive symptoms classically observed in schizophrenic patients. In the current study, we determined if STOP null mice demonstrate behavioral abnormalities related to the social and cognitive impairments of schizophrenia. Compared with wild-type mice, STOP null mice exhibited deficits in the non-aggressive component of social recognition, short term working memory and social and spatial learning. As described in humans, learning deficits in STOP null mice were poorly sensitive to long term treatment with typical neuroleptics. Since social and cognitive dysfunction have consistently been considered as central features of schizophrenia, we propose that STOP null mice may provide a useful model to understand the neurobiological correlates of social and cognitive defects in schizophrenia and to develop treatments that better target these symptoms.     

Sleep efficiency and neurophysiological patterns in middle‐aged men are associated with cognitive change over their adult life course

Disrupted sleep is a contributing factor to cognitive ageing, while also being associated with neurodegenerative disorders. Little is known, however, about the relation of sleep and the gradual cognitive changes over the adult life course. Sleep electroencephalogram (EEG) patterns are potential markers of the cognitive progress. To test this hypothesis, we assessed sleep architecture and EEG of 167 men born in the Copenhagen Metropolitan Area in 1953, who, based on individual cognitive testing from early (~18 years) to late adulthood (~58 years), were divided into 85 subjects with negative and 82 with positive cognitive change over their adult life. Participants underwent standard polysomnography, including manual sleep scoring at age ~58 years. Features of sleep macrostructure were combined with a number of EEG features to distinguish between the two groups. EEG rhythmicity was assessed by spectral power analysis in frontal, central and occipital sites. Functional connectivity was measured by inter‐hemispheric EEG coherence. Group differences were assessed by analysis of covariance (p < 0.05), including education and severity of depression as potential covariates. Subjects with cognitive decline exhibited lower sleep efficiency, reduced inter‐hemispheric connectivity during rapid eye movement (REM) sleep, and slower EEG rhythms during stage 2 non‐REM sleep. Individually, none of these tendencies remained significant after multiple test correction; however, by combining them in a machine learning approach, the groups were separated with 72% accuracy (75% sensitivity, 67% specificity). Ongoing medical screenings are required to confirm the potential of sleep efficiency and sleep EEG patterns as signs of individual cognitive progress.     

Differences in and correlations between cognitive abilities and brain volumes in healthy control,mild cognitive impairment,and Alzheimer disease groups

The purpose of this study is to investigate differences in and correlations between cognitive abilities and brain volumes in healthy control (HC), mild cognitive impairment (MCI), and Alzheimer's disease (AD) groups. The Korean Version of the Consortium to Establish a Registry for Alzheimer's Disease (CERAD‐K), which is used to diagnose AD, was used to measure the cognitive abilities of the study subjects, and the volumes of typical brain components related to AD diagnosis—cerebrospinal fluid (CSF), gray matter (GM), and white matter (WM)—were acquired. Of the CERAD‐K subtests, the Boston Naming Test distinguished significantly among the HC, MCI, and AD groups. GM and WM volumes differed significantly among the three groups. There was a significant positive correlation between Boston Naming Test scores and GM and WM volumes. In conclusion, the Boston Naming Test and GM and WM brain volumes differentiated the three tested groups accurately, and there were strong correlations between Boston Naming Test scores and GM and WM volumes. These results will help to establish a test method that differentiates the three groups accurately and is economically feasible. Clin. Anat. 29:473–480, 2016. © 2016 Wiley Periodicals, Inc.