精神分裂症患者在听觉掩蔽环境下的言语识别

深入研究精神分裂症患者特异性的认知障碍有助于精神分裂症的早期发现、早期诊断和早期治疗.本综述在总结精神分裂症患者的听觉和言语识别异常以及听觉注意和听觉工作记忆缺陷的同时,重点阐述了精神分裂症患者完成言语听觉任务时的对掩蔽刺激特别信息掩蔽刺激的异常易感性.本文还特别指出,精神分裂症患者仍然具有利用言语内容启动线索来提高掩蔽下言语识别的能力.本文所总结的研究成果对探讨精神分裂症的病因学基础、寻找新的临床诊断以及治疗和康复手段都具有参考价值.     

孤独症碎镜理论述评

孤独症是泛指一大类在社会交往、沟通方面存在功能缺陷的疾病, 至今病因尚未阐明。“碎镜理论”作为孤独症研究领域的新兴理论, 在神经—认知层面较先前理论更为全面地解释了孤独症的各种临床行为表现, 并为这些异常行为间的相互关系提供了一种统一性的研究视角。文章首先对镜像神经元的发现进行了简介, 在此基础上对碎镜理论的由来及其与孤独症相关功能(包括动作识别与模仿、心理理论、共情以及语言理解)缺陷的关系进行了综述, 最后通过区分主动模仿和自动模仿, 就镜像神经元系统及其调控系统与孤独症关系中存在的问题进行了反思与展望。     

急性期精神分裂症返回抑制的时间进程

利用线索-靶子模式研究急性期精神分裂症返回抑制的时间进程.研究对象包括健康对照组、早期精神分裂症组和慢性精神分裂症组.结果表明:(1)健康志愿者和早期精神分裂症患者均有完好的返回抑制现象,而慢性精神分裂症患者存在返回抑制缺陷,返回抑制出现时间延迟,持续时间缩短.(2)精神分裂症的返回抑制缺陷与疾病慢性化指标(病程、既往发作次数和住院次数)之间存在相关性.结果支持早期精神分裂症和慢性精神分裂症在急性期存在不同的返回抑制特征,早期精神分裂症的返回抑制保存完好,而慢性精神分裂症的返回抑制存在缺陷;精神分裂症返回抑制缺陷可能发生发展于疾病的慢性过程中,而不是发生于疾病初期;精神分裂症的注意缺陷是独立的缺陷症状.     

NMDA受体的结构与药理学特性

NMDA受体是一类离子型谷氨酸受体,其功能主要参与发育过程中神经回路的细化及触发多种形式的突触可塑性。近年来的证据表明,组成NMDA受体的亚单位有着复杂的生理学和药理学特性;NMDA受体的数量、分布和亚单位组成并非一成不变,而是在发育过程中、神经元活动时,以一种细胞特异性和突触特异性的方式变化着。这种NMDA受体的双向变化是突触可塑性重塑的基础,而其调节的异常又可导致神经-精神疾病的发生,如可卡因成瘾、精神分裂症等     

精神分裂症患者的语音感知

精神分裂症是一种常见的精神疾病, 表现为多方面的症状, 其中, 语言异常是精神分裂症患者认知损伤的核心症状之一。本文关注精神分裂症患者的语音感知, 从音段和超音段两方面简述国内外对精神分裂症患者语音感知开展的行为和神经科学实验, 指出中国应加大对中国精神分裂症患者的汉语语音感知探索。     

自闭症碎镜理论之迷思:缘起、问题与前景

自闭症患者在社会沟通和交往障碍上主要涉及社会情感互动缺陷、非语言行为交流缺陷、发展维持和理解人际关系的缺陷。该群体在社会认知过程中潜在自动的直觉成分受损被视为其独特的临床症状。鉴于镜像神经元系统在社会认知的直觉成分上扮演的重要角色,该系统的功能障碍假说(或称"碎镜"理论)被提出并用以解释自闭症的成因及其异常表现。然而,在经历了10年的发展与证据检验后,该理论潜在的问题逐渐暴露。当前的研究显示,迄今为止人类镜像神经元系统的研究存在内在缺陷,镜像神经元系统至多是社会认知的附带原因,该系统功能障碍也并非自闭症患者社会认知障碍的必要条件。碎镜理论面临来自临床行为研究与认知神经科学实验证据的广泛质疑。未来,伴随自闭症研究对象的变化,镜像神经元的社会响应学说的提出,双个体范式、第二人称神经科学范式与计算精神病学的兴起,镜像神经元与自闭症的真正关系将有望得以阐明。     

科学院畜牧兽医研究所,军事医学科学

1　引言精神分裂症是最常见的精神疾病之一。多年来 ,大量生物医学研究成果给精神分裂症的预防及治疗带来了希望。但这些研究成果尚未就精神分裂症的病理心理学基础达成统一明确的意见。就本质上来说 ,精神分裂症是一种心理现象的异常 ,表现为患者心理过程及个性心理特征的异常。因此 ,对精神分裂症进行神经心理学的研究籍以阐明其心理机制是必要的 ,也是可行的。除了探讨脑神经细胞病变对心理活动的影响外 ,从宏观角度即大脑两半球的功能特点及其相互关系了解心理活动的神经机制也是众多学者关注的焦点。2　大脑两半球关系研究的历史2 .1　…     

精神分裂症的潜伏抑制动物模型

精神分裂症动物模型的建立,是当前研究精神分裂症的神经生物学机制以及开发新的抗精神病药物的一个重要课题。文章系统地阐述了以潜伏抑制为行为模式的精神分裂症动物模型的理论以及神经机制,并重点介绍了精神分裂症的潜伏抑制动物模型的建立方法,包括（1）调节某些与精神分裂症相关的中枢神经递质的传递活动;（2）对与精神分裂症有关的中脑-伏隔核神经环路进行结构损伤或药物性干预;（3）在发育早期给予免疫刺激或环境应激     

精神分裂症患者的记忆损害

摘 要 目的 探讨精神分裂症患者记忆损害状况。方法 采用修正的加工分离记忆实验程序,分别测试精神分裂症患者和正常对照组的记忆能力。结果 （1）精神分裂症患者外显记忆功能存在广泛的缺陷,而内隐记忆功能缺陷只在概念驱动下的测验中出现。（2）以阳性症状为主的精神分裂症患者的外显记忆成绩均高于以阴性症状为主的精神分裂症患者。(3)阴性症状严重程度与外显记忆成绩呈显著负相关。结论 精神分裂症患者的内隐记忆功能相对完整,而外显记忆障碍在以阴性症状为主的精神分裂症患者尤为突出。     

正常和精神分裂患者脑电图对照研究

本研究发现精神分裂症患者异常脑电图(40.6%)显著多于正常对照组(7.5%),并以轻—中度异常为主,偶见局灶性棘波。精神分裂症年龄组的异常率随年龄增大而增高。简易精神病量表分与精神分裂症脑电图检查结果之间存有一定关系。作者最后认为,现阶段在精神分裂症实验室辅助诊断中,脑电图仍起某种作用。     

Different corticostriatal patterns of L-DOPA utilization in patients with untreated schizophrenia and patients treated with classical antipsychotics or clozapine

Positron emission tomography (PET) has been shown to be of great importance in elucidating the mechanism of action of antipsychotic drugs. In psychotic patients L-[11C]DOPA PET has been used to demonstrate some differences in dopaminergic activity compared with that in healthy volunteers. Ten healthy volunteers were investigated with PET and L-[11C]DOPA. Ten drug-free patients with psychosis, nine stable schizophrenics treated with clozapine, and nine stable patients treated with classical antipsychotics were also investigated with L-[11C]DOPA. Principal-component analysis was employed for the analysis of L-[11C]DOPA Ki values across a number of corticostriatal brain regions. These data revealed a significant three-component model with clear-cut separation between healthy controls and patients with unmedicated schizophrenia. Stable optimal treatment with either classical neuroleptics or clozapine partially, albeit differentially, reversed the aberrant patterns seen in drug-free schizophrenia. It can thus be concluded that schizophrenia is associated with abnormal patterns of L-[11C]DOPA utilization in corticostriatal systems. Treatment with clozapine or classical neuroleptics induces partial, albeit differential, normalization of the abnormal patterns seen in untreated schizophrenia.     

Coordinate high-frequency pattern of stimulation and calcium levels control the induction of LTP in striatal cholinergic interneurons

Current evidence appoints a central role to cholinergic interneurons in modulating striatal function. Recently, a long-term potentiation (LTP) of synaptic transmission has been reported to occur in these neurons. The relationship between the pattern of cortico/thalamostriatal fibers stimulation, the consequent changes in the intracellular calcium concentration ([Ca2+]i), and the induction of synaptic plasticity was investigated in striatal cholinergic interneurons from a rat corticostriatal slice preparation by means of combined electrophysiological intracellular recordings and microfluorometric techniques. Different protocols of stimulation were considered, varying both the frequency and the duration of the train of stimuli. High-frequency stimulation (HFS) (three trains at 100 Hz for 3 sec, 20-sec interval) induced a rise in [Ca2+]i, exceeding by fivefold the resting level, and caused a LTP of synaptic transmission. Tetanic stimulation delivered at lower frequencies (5-30 Hz) failed to induce long-term changes of synaptic efficacy. The observed elevation in [Ca2+]i during HFS was primarily mediated by L-type high-voltage activated (HVA)-Ca2+ channels, as it was fully prevented by nifedipine. Conversely, blockade of NMDA and AMPA glutamate receptor did not affect either LTP or the magnitude of the [Ca2+]i rise. Interestingly, the pharmacological analysis of the post-tetanic depolarizing postsynaptic potential (DPSP) revealed that LTP was attributable, to a large extent, to the potentiation of the GABA(A)-mediated component. In conclusion, the expression of LTP in striatal cholinergic interneurons is a selective response to a precise stimulation pattern of induction requiring a critical rise in [Ca2+]i.     

Motivation and learning: Neurophysiological mechanisms in a “model” system

The neurophysiological mechanisms underlying behavioral motivation and associative learning are described in an invertebrate “model” system, the carnivorous marine mollusc Pleurobranchaea. Feeding motivation can be controlled via nutritional history and is represented centrally in the feeding motor network as a change in the balance of synaptic excitation and inhibition at the level of interneurons that initiate feeding behavior, i.e., feeding “command” interneurons. Associative learning, induced by avoidance conditioning of feeding behavior, manifests identically at the level of the command interneurons, but is distinguished from non-associative motivational changes by processes that occur in identified neurons and pathways presynaptic to the command interneurons. Motivation and learning are therefore linked mechanistically by convergent neurophysiological mechanisms at the level of central neurons that initiate behavior.     

Preliminary evidence for impaired rapid verb generation in schizophrenia

It has been hypothesized that nouns and verbs are processed within relatively separable semantic memory networks. Although abnormal semantic processing is a common feature of schizophrenia-spectrum disorders, no prior studies have specifically examined the comparability of noun and verb generation deficits in schizophrenia. In the current study, verb (action), noun (animal), and letter (f) fluency performance was evaluated in 22 inpatients with schizophrenia and 27 healthy comparison subjects. On average, individuals with schizophrenia performed approximately one standard deviation below the healthy comparison subjects on action, animal, and letter fluency. Action fluency-but not letter or animal fluency-was moderately correlated with tests of working memory, response inhibition, semantic memory, and cognitive flexibility. Findings suggest that verb- and noun-based fluency deficits are of comparable severity in schizophrenia, but that the impairment in verb generation may be driven by different underlying cognitive mechanisms. Further, hypothesis-driven research on the nature and extent of verb network disruption in schizophrenia appears warranted.     

Neural correlates of Pavlovian conditioning in components of the neural network supporting ciliary locomotion in Hermissenda

Pavlovian conditioning in Hermissenda consists of pairing light, the conditioned stimulus (CS) with activation of statocyst hair cells, the unconditioned stimulus (US). Conditioning produces CS-elicited foot shortening and inhibition of light-elicited locomotion, the two conditioned responses (CRs). Conditioning correlates have been identified in the primary sensory neurons (photoreceptors) of the CS pathway, interneurons that receive monosynaptic input from identified photoreceptors, and putative pedal motor neurons. While cellular mechanisms of acquisition produced by the synaptic interaction between the CS and US pathways are well-documented, little is known about the mechanisms responsible for the generation or expression of the CR. Here we show that in conditioned animals light reduced tonic firing of ciliary activating pedal neurons (VP1) below their pre-CS baseline levels. In contrast, pseudorandom controls expressed a significant increase in CS-elicited tonic firing of VP1 as compared to pre-CS baseline activity. Identified interneurons in the visual pathway that have established polysynaptic connections with VP1 were examined in conditioned animals and pseudorandom controls. Depolarization of identified type I_e interneurons with extrinsic current elicited a significant increase in IPSPs recorded in VP1 pedal neurons of conditioned animals as compared with pseudorandom controls. Conditioning also enhanced intrinsic excitability of type I_e interneurons of conditioned animals as compared to pseudorandom controls. Light evoked a modest increase in IPSP frequency in VP1 of conditioned preparations and a significant decrease in IPSP frequency in VP1 of pseudorandom controls. Our results show that a combination of synaptic facilitation and intrinsic enhanced excitability in identified components of the CS pathway may explain light-elicited inhibition of locomotion in conditioned animals.     

Habit and skill learning in schizophrenia: evidence of normal striatal processing with abnormal cortical input

Different forms of nondeclarative learning involve regionally specific striatal circuits. The motor circuit (involving the putamen) has been associated with motor–skill learning and the dorsolateral prefrontal cortex (DLPFC) circuit (involving the caudate) has been associated with cognitive–habit learning. Efforts to differentiate functional striatal circuits within patient samples have been limited. Previous studies have provided mixed results regarding striatal-dependent nondeclarative learning deficits in patients with schizophrenia. In this study, a cognitive–habit learning task (probabilistic weather prediction) was used to assess the DLPFC circuit and a motor–skill learning task (pursuit rotor) was used to assess the motor circuit in 35 patients with schizophrenia and 35 normal controls. Patients with schizophrenia displayed significant performance differences from controls on both nondeclarative tasks; however, cognitive–habit learning rate in patients did not differ from controls. There were performance and learning-rate differences on the motor–skill learning task between the whole sample of patients and controls, however, analysis of a subset of patients and controls matched on general intellectual level eliminated learning rate differences between groups. The abnormal performance offset between patients with schizophrenia and controls in the absence of learning rate differences suggests that abnormal cortical processing provides altered input to normal striatal circuitry.     

Exploring self-defining memories in schizophrenia

Previous studies have shown that patients with schizophrenia are impaired in recalling specific events from their personal past. However, the relationship between autobiographical memory impairments and disturbance of the sense of identity in schizophrenia has not been investigated in detail. In this study the authors investigated schizophrenic patients’ ability to recall self-defining memories; that is, memories that play an important role in building and maintaining the self-concept. Results showed that patients recalled as many specific self-defining memories as healthy participants. However, patients with schizophrenia exhibited an abnormal reminiscence bump and reported different types of thematic content (i.e., they recalled less memories about past achievements and more memories regarding hospitalisation and stigmatisation of illness). Furthermore, the findings suggest that impairments in extracting meaning from personal memories could represent a core disturbance of autobiographical memory in patients with schizophrenia.     

Schizotypy and hemisphericity

There is considerable evidence that schizophrenia spectrum disorders are associated with a variety of abnormal asymmetries of brain structure, function, and behavior. Schizotypy is a personality trait dimension extending into the normal range, which at its extreme, is associated with a vulnerability to schizophrenia spectrum disorders. Schizotypy in the normal range is also associated with a variety of neurobiological characteristics associated with schizophrenia spectrum disorders, including abnormal brain and behavioral asymmetries. Previous studies have suggested that normal schizotypy (as well as belief in the paranormal) is associated with an increased reliance on the right hemisphere in a variety of tasks. Hemisphericity is a trait-related characteristic preference for the cognitive mode of one or the other cerebral hemispheres, putatively related to hemispheric activation asymmetry. A sample of 256 undergraduates was administered five schizotypy scales, as well as three hemisphericity measures. Higher schizotypy scores were associated with an increase in right hemisphericity and a decrease in integrated hemisphericity. Although the construct of hemisphericity has been criticized, there is evidence to suggest that questionnaire and eye movement measures of hemisphericity may yet have construct validity, and further research on hemisphericity may be warranted.     

Brain Networks in Schizophrenia

Schizophrenia—a severe psychiatric condition characterized by hallucinations, delusions, loss of initiative and cognitive function—is hypothesized to result from abnormal anatomical neural connectivity and a consequent decoupling of the brain’s integrative thought processes. The rise of in vivo neuroimaging techniques has refueled the formulation of dysconnectivity hypotheses, linking schizophrenia to abnormal structural and functional connectivity in the brain at both microscopic and macroscopic levels. Over the past few years, advances in high-field structural and functional neuroimaging techniques have made it increasingly feasible to reconstruct comprehensive maps of the macroscopic neural wiring system of the human brain, know as the connectome. In parallel, advances in network science and graph theory have improved our ability to study the spatial and topological organizational layout of such neural connectivity maps in detail. Combined, the field of neural connectomics has created a novel platform that provides a deeper understanding of the overall organization of brain wiring, its relation to healthy brain function and human cognition, and conversely, how brain disorders such as schizophrenia arise from abnormal brain network wiring and dynamics. In this review we discuss recent findings of connectomic studies in schizophrenia that examine how the disorder relates to disruptions of brain connectivity.     

Dynamics of alpha oscillations elucidate facial affect recognition in schizophrenia

Impaired facial affect recognition is characteristic of schizophrenia and has been related to impaired social function, but the relevant neural mechanisms have not been fully identified. The present study sought to identify the role of oscillatory alpha activity in that deficit during the process of facial emotion recognition. Neuromagnetic brain activity was monitored while 44 schizophrenia patients and 44 healthy controls viewed 5-s videos showing human faces gradually changing from neutral to fearful or happy expressions or from the neutral face of one poser to the neutral face of another. Recognition performance was determined separately by self-report. Relative to prestimulus baseline, controls exhibited a 10- to 15-Hz power increase prior to full recognition and a 10- to 15-Hz power decrease during the postrecognition phase. These results support recent proposals about the function of alpha-band oscillations in normal stimulus evaluation. The patients failed to show this sequence of alpha power increase and decrease and also showed low 10- to 15-Hz power and high 10- to 15-Hz connectivity during the prestimulus baseline. In light of the proposal that a combination of alpha power increase and functional disconnection facilitates information intake and processing, the finding of an abnormal association of low baseline alpha power and high connectivity in schizophrenia suggests a state of impaired readiness that fosters abnormal dynamics during facial affect recognition.