多巴胺D3受体对精神分裂症患者认知功能的影响

认知功能障碍是精神分裂症患者核心症状之一,对患者的生活质量和日常功能有重要影响。研究发现多巴胺D3受体(DRD3)主要与注意、记忆及执行功能等认知功能相关。本文从DRD3与精神分裂症认知功能的相关性及其具体机制以及相关治疗进展进行综述,为改善精神分裂症患者相关认知功能障碍提供依据。     

精神分裂症患者认知功能障碍与微小RNA调控表达的研究进展

本文对精神分裂症患者认知功能障碍相关的微小RNA(microRNA)的种类及表达特点进行综述,为更深入地研究精神分裂症患者认知功能障碍症状特点和分子机制、并为后续精准治疗及预后评估开辟新思路。     

精神分裂症患者认知功能损伤的研究进展

为进一步了解精神分裂症神经生物学机制并为未来的相关研究及诊疗提供新思路,故对精神分裂症认知功能损伤的研究进行综述。认知功能受损是精神分裂症的重要临床表现之一。目前使用蒙特利尔认知评估量表(MoCA)及精神分裂症认知功能成套测验共识版(MCCB)评定精神分裂症患者的认知功能均发现患者存在严重的工作记忆障碍。工作记忆是大脑前额叶皮质的主要功能之一,而纹状体突触前合成和分泌的多巴胺(DA)含量与认知功能损伤程度及前额叶皮质功能存在相关性。对认知功能损伤的治疗有助于改善精神分裂症患者的预后、减轻社会负担。目前已有多种治疗方式可供选择。     

精神分裂症认知功能障碍的研究进展

认知功能障碍严重影响精神分裂症患者的社会功能和生活质量，这一核心症状稳定、持 久地存在于精神分裂症的不同病程中。研究认知功能障碍的特征有助于疾病机制的探索，加深对疾病 发展进程的理解并提供有针对性的干预策略。现就精神分裂症认知功能障碍的特征及机制展开综述。     

精神分裂症、抑郁症的认知功能障碍研究进展

认知功能是指大脑对信息加工处理的能力,即中枢神经系统分辨、整合信息并解决问题和完成任务的综合能力。通过威斯康星卡片分类测验等评估工具评估及SPECT等影像学研究,发现精神分裂症患者认知功能障碍以工作记忆为核心,伴有执行功能等障碍和影像学改变,抑郁症患者则以执行功能障碍为主,且和老年痴呆及血管性痴呆有着机制上的区别。     

精神分裂症患者认知功能障碍的神经生化研究进展

近年来,精神分裂症患者的认知功能损害受到了广泛的关注,逐步成为研究热点。但影响精神分裂症患者认知功能的病因多样,本文仅就神经生化方面与精神分裂症患者认知功能障碍的关系进行综述。精神分裂症存在认知功能损害的机制至今尚未完全阐明,但大多数学者认为可能与前额叶和颞叶的多巴胺（DA）功能下降及五羟色胺（5-HT）能、去甲肾上腺素（NE）能、     

早发性精神分裂症患者认知功能损伤临床分析

目的评测早发性精神分裂症患者认知功能,以期为临床早发性精神分裂症的诊疗提供借鉴。方法以2009-06—2011-12我院治疗确诊为早发性精神分裂症的患者为研究对象,以正常人为对照组,采用神经心理学测评工具RBANS、Stroop、WCST量表分析早发性精神分裂症患者认知功能损伤的特点,并以PANSS为测量工具,分析精神病性症状指标与认知功能损害的相关性。结果纳入232例患者,阳性症状组、阴性症状组与正常对照组在RBANS各个维度上,除颜色干扰时外Stroop各因子、除WCST_13外WCST各个因子均存在显著差异(P0.05)。其中,阳性症状组与阴性症状组比较,除视觉广度和注意外RBANS评分,除字义干扰时和颜色干扰时外,其余Stroop各因子各维度,除WCST_4、WCST_10、WCST_13外WCST各因子等均存在显著性差异(P0.05)。回归分析结果显示,早发性精神分裂症患者认知功能损害的影响因素有性别、年龄、文化程度和家族史等(P0.05)。结论早发性精神分裂症患者存在不同程度的认知功能损害,特别是在注意、言语记忆和执行功能方面,早发性精神分裂症患者认知功能损害可能受性别、年龄、文化程度和家族史等因素影响。     

精神分裂症认知功能（下）

3.3　病理目前的研究结果多数显示 ,精神分裂症患者的认知功能损害是静止性的 ,而不是渐进性的病程。年轻患者的认知成绩与老年患者比较在排除年龄老化因素后没有差异。精神分裂症的认知损害不是进行性痴呆障碍 (不同于 AD) ,与局部脑损害时出现的认知功能障碍非常相似而且稳定。Hoff等对首发精神分裂症患者和慢性精神分裂症患者进行研究后发现 ,认知功能损害在病前及疾病开始时就已出现 ,所有的认知测验均显示首发患者和慢性精神分裂症患者在认知损害的程度上是一致的 ,首发者和慢性患者的执行功能、瞬时记忆、言语空间记忆的检测结果明…     

精神分裂症的认知功能障碍

认知功能障碍是精神分裂症患者主要功能缺陷之一[1],严重影响到患者的社会功能及生活质量,近年来越来越受到人们的关注.精神分裂症的认知功能损害涉及注意、记忆和执行功能等多个方面.许多患者在缓解期仍表现出一定的认知功能障碍,严重影响病情的康复和社会功能的恢复.现将近年来关于精神分裂症认知功能障碍的研究综述如下.     

精神分裂症认知功能障碍研究进展

近年来精神分裂症病人的认知功能已成为精神科临床及心理学研究的热点问题之一,除传统的心理测验方法,随着功能影像学的发展,功能磁共振(fMRI),正电子发射断层扫描(PET)等应用于精神分裂症认知功能研究,得到了一些有意义的结果。目前对认知功能障碍的研究已基本统一观点,即认知功能障碍在首发精神分裂症发病前或发病时就已经存在,认知功能障碍是精神分裂症的独立症状,至少85%的精神分裂症患者存在持久而严重的认知障碍,特别是在注意、言语记忆和执行功能方面[1]。1认知功能障碍的表现1.1记忆障碍最近的研究结果显示,记忆障碍和注意障碍是…     

Pathways to similar executive impairment: Comparison of schizophrenia patients and healthy aging individuals

Executive impairment is prominent in schizophrenia, in conditions such as Parkinson's disease and dementia and in healthy aging. Identifying processes that critically constrain executive function can advance investigation of their biological basis and treatment planning. Recent findings that elderly healthy individuals showed similar impairment on conditional exclusion task as schizophrenia patients raised the question whether similar processes are impaired. To test this we compared 56 schizophrenia patients, 57 elderly and 77 young healthy individuals on three executive tests: conditional exclusion, abstraction and inhibition and tests of working memory and psychomotor speed. Schizophrenia patients performed worse than elderly healthy on abstraction, inhibition and verbal working memory. They were similarly impaired on Penn Conditional Exclusion Test (PCET) outcome measures but differed in performance characteristics. Schizophrenia patients needed relatively more trials to learn the first PCET category than the second or the third. This correlated with other cognitive impairments, particularly in working memory. Elderly healthy individuals found it most difficult to learn the last category. The two groups showed different error patterns. We propose that schizophrenia patients have particular difficulty in early (probabilistic) learning (“what to do”) while aging individuals have selective impairment in executive integration. These constitute distinct targets for customized treatment in the two conditions.     

Executive function in schizophrenia

Many domains of executive function are impaired in patients with schizophrenia including forward planning, concept formation, initiation, self-monitoring, and the ability to direct attention and memory. These impairments are noticeable against a background of generalized cognitive deficits, and many affect 40% to 95% of individuals with this disorder. Specific executive deficits appear to be related to specific symptom clusters and are linked to structural and functional brain abnormalities. Executive impairment predicts multiple domains of functional outcome in schizophrenia patients. Atypical antipsychotic agents and cognitive rehabilitation may be promising new approaches for the treatment of cognitive and functional impairment in schizophrenia.     

Neurocognitive function in clinically stable men with bipolar I disorder or schizophrenia and normal control subjects.

BACKGROUND: Patients with bipolar disorder and schizophrenia have been shown to have neurocognitive deficits when compared with control subjects. The degree and pattern of impairment between psychiatric groups have rarely been compared, especially when subjects are psychiatrically stable. METHODS: Using a standard neurocognitive battery, we compared euthymic outpatients with bipolar disorder (n = 40), stable patients with schizophrenia (n = 20), and subjects with no psychiatric disorder (n = 22). The neurocognitive domains assessed included executive functioning, verbal memory, visual memory, procedural learning, visuoconstructive ability, and language functions. Effect sizes were calculated for each cognitive domain across groups. RESULTS: Stable schizophrenic subjects demonstrated a generalized cognitive impairment across most domains compared with control subjects, with average effect sizes of .9. Euthymic bipolar subjects were significantly impaired compared with control subjects only in executive functioning (Wisconsin Card Sorting Task) and verbal memory (California Verbal Learning Test) domains (effect sizes in the .8-.9 range). Performance on the executive function measures was bimodal among bipolar subjects, suggesting two subgroups: one with relatively normal and one with impaired executive functioning. No significant differences between the bipolar patient group and control subjects were observed in visuoconstructive ability, procedural learning, or language function. CONCLUSIONS: Both euthymic bipolar subjects and relatively stable schizophrenic subjects differed from control subjects in neurocognitive function. Among schizophrenic subjects, a generalized cognitive impairment was observed, and the degree of impairment was greater in the schizophrenic compared with the bipolar subjects. Subjects with bipolar disorder were impaired in two specific domains (verbal memory and executive function). Furthermore, within the bipolar group there was a subset with relatively normal executive functioning and a subset with significant impairment. Possible reasons for the persistence of these neurocognitive deficits in some subjects with bipolar disorder during periods of euthymia are reviewed.     

Blood DHEAS concentrations correlate with cognitive function in chronic schizophrenia patients: a pilot study

There is evidence that neurosteroids such as DHEA and its sulfated form DHEAS can modulate cognitive function. We hypothesize that DHEA/S concentrations may be linked to cognitive impairment in schizophrenia. The aim of this pilot study was to test this hypothesis by examining the relationship between blood levels of DHEAS and cognitive function. The performance of 26 stable medicated chronic schizophrenia patients in a range of neuropsychological domains including verbal memory (Wechsler Memory Scale), executive function (AIM), memory of faces (PFMT), memory for objects (VOLT) and identification of facial emotional expressions (PEAT) was assessed. Single morning blood samples were assayed for levels of DHEAS and cortisol. Significant associations were found between DHEAS levels and DHEAS/Cortisol ratio and verbal memory, executive function and memory for faces. The relationship was independent of the age related reduction in DHEAS levels. These preliminary results suggest that DHEAS may be associated with cognitive impairment in schizophrenia.     

Childhood trauma and cognitive functioning in mood disorders: A systematic review

Background

Cognitive impairment is a core feature of mood disorders and has been identified as an important treatment target. A better understanding of the factors contributing to cognitive impairment in mood disorders would be beneficial in developing interventions to address cognitive impairment. One key factor is childhood trauma. The aim of this review was to systematically synthesise and review research examining associations between reported childhood trauma and cognitive functioning in mood disorders.

Methods

Studies in adult samples examining the relationship between objective cognitive function and reported childhood trauma in major depressive disorder and/or bipolar disorder (in-episode or euthymia) were identified. Searches were conducted on PubMed, Embase and PsycINFO until January 2022. A narrative review technique was used due to the heterogeneity of group comparisons, cognitive tests and data analysis across studies.

Results

Seventeen studies met the criteria for inclusion (mood disorders N = 1723, healthy controls N = 797). Evidence for childhood trauma being related to poorer cognitive functioning was consistent across global cognitive functioning and executive function domains for euthymic patients and psychomotor speed for in-episode patients. There was mixed evidence for verbal learning and memory and executive function for in-episode patients. Identification of patterns within other domains was difficult due to limited number of studies.

Conclusion

Findings from this review suggest childhood trauma is associated with poorer cognitive functioning in people with mood disorders. Targeted interventions to improve cognition may be warranted for this group.     

Cognitive impairment 3 years after neurological Varicella-zoster virus infection: a long-term case control study

Varicella-zoster virus (VZV) is one of the most common viruses causing central nervous system (CNS) infection, sometimes with severe neurological complications and sequelae despite appropriate antiviral treatment. Whether the neurological sequelae of VZV CNS infections include long-term cognitive impairment and how this impairment might affect the patients is still largely unknown. In this study, 14 patients with predominant CNS manifestations caused by VZV infection underwent cognitive testing 3 years (median 39.5 months, range 31–52 months) after acute disease. The results were compared with those for 28 controls, matched for age and gender. The tests covered the cognitive domains of speed and attention, memory and learning, visuospatial function, language and executive function. To further assess the cognitive dysfunction caused by neurological VZV infection, patients were classified into the concept of mild cognitive impairment (MCI), which is associated with development of dementia in other pathologies. The VZV patients performed significantly worse than controls on four tests covering the domains of speed and attention, memory and learning and executive function. The cut-off was set at 1.5 SD below mean age. In addition, a greater proportion of VZV patients were classified with MCI as compared with controls. In conclusion, patients with previous VZV infection affecting the brain had signs of long-term cognitive impairment in the domains of speed and attention, memory and learning and executive function. However, larger study populations are needed to confirm these results.     

Posttraumatic stress disorder, cognitive function and quality of life in patients with schizophrenia

The purpose of the present study was to assess posttraumatic stress disorder (PTSD), cognitive function, and quality of life in patients with schizophrenia who had a self-reported history of trauma exposure. Outpatients diagnosed with schizophrenia or schizoaffective disorder were referred to the study. Each patient was assessed with the Positive and Negative Syndrome Scale (PANSS), the Harvard Trauma Questionnaire (HTQ), a cognitive assessment battery, Heinrich's Quality of Life Scale (QLS), and the Behavior and Symptom Identification Scale (BASIS). Eighty-seven subjects who reported experiencing at least one traumatic event were included in the study. Fifteen of 87 (17%) met the DSM-IV criteria for PTSD. The PTSD group had significantly worse overall cognitive performance than the non-PTSD group, especially in the domains of attention, working memory and executive function. In addition, the PTSD group showed significantly worse self-rated quality of life as measured by the BASIS total score. The development of PTSD is associated with poor cognitive function and subjectively, but not objectively, rated low quality of life in patients with schizophrenia. Evaluating PTSD in patients with schizophrenia could have important implications from both clinical and research perspectives.     

Pharmacological and non-pharmacological interventions to improve cognitive dysfunction and functional ability in clinical depression – A systematic review

Cognitive dysfunction is of clinical significance and exerts longstanding implication on patients? function. Pharmacological and non-pharmacological treatments of cognitive dysfunction are emerging. This review evaluates pharmacological and non-pharmacological treatments of cognitive impairment primarily in the domains of memory, attention, processing speed and executive function in clinical depression. A total of 35 studies were retrieved from Pubmed, PsycInfo and Scopus after applying inclusion and exclusion criteria. Results show that various classes of antidepressants exert improving effects on cognitive function across several cognitive domains. Specifically, studies suggest that SSRIs, the SSRE tianeptine, the SNRI duloxetine, vortioxetine and other antidepressants such as bupropion and moclobemide may exert certain improving effects on cognitive function in depression, such as in learning and memory and executive function. Class-specific cognitive domains or specific dose–response relationships were not identified yet. The few non-pharmacological studies conducted employing cognitive orientated treatments and cognitive remediation therapy show promising results for the improvement of cognitive impairment in depression. However, several methodological constraints of studies limit generalizability of the results and caution the interpretation. Future direction should consider the development of a neuropsychological consensus cognitive battery to support the discovery, clinical assessment, comparison of studies and registration of new agents in clinical depression.     

奥氮平和氯氮平对慢性精神分裂症的认知功能的影响

目的了解奥氮平和氯氮平对慢性精神分裂症患者的认知功能的影响。方法78例经典型抗精神病药物治疗疗效不显著或不能耐受不良反应的慢性精神分裂症患者随机替换为奥氮平及氯氮平治疗,分别在入组前、12周、6个月进行PANSS量表评定、认知功能测定,包括言语学习、记忆、注意、执行功能、精神运动。结果奥氮平组32例和氯氮平组34例完成了6个月的治疗,这些患者疗程结束时均显示精神症状显著改善,认知功能显著提高,表现为言语流畅性、言语学习、言语视觉记忆、执行功能方面。二者之间无显著差异。结论奥氮平和氯氮平均可改善慢性精神分裂症的认知功能,且二者的疗效相似。     

A systematic review of the effect of cannabidiol on cognitive function: Relevance to schizophrenia

Background and objectivesCognitive impairment is a core symptom domain of schizophrenia, neurological disorders and substance abuse. It is characterised by deficits in learning, memory, attention and executive functioning and can severely impact daily living. Antipsychotic drugs prescribed to treat schizophrenia provide limited cognitive benefits and novel therapeutic targets are required. Cannabidiol (CBD), a component of the cannabis plant, has anti-inflammatory and antipsychotic-like properties; however, its ability to improve cognitive impairment has not been thoroughly explored. The aim of this systematic review was to evaluate preclinical and clinical literature on the effects of CBD in cognitive domains relevant to schizophrenia.MethodsA systematic literature search was performed across numerous electronic databases for English language articles (January 1990–March 2016), with 27 articles (18 preclinical and 9 clinical studies) included in the present review.ResultsCBD improves cognition in multiple preclinical models of cognitive impairment, including models of neuropsychiatric (schizophrenia), neurodegenerative (Alzheimer’s disease), neuro-inflammatory (meningitis, sepsis and cerebral malaria) and neurological disorders (hepatic encephalopathy and brain ischemia). To date, there is one clinical investigation into the effects of CBD on cognition in schizophrenia patients, with negative results for the Stroop test. CBD attenuates Δ⁹-THC-induced cognitive deficits.ConclusionsThe efficacy of CBD to improve cognition in schizophrenia cannot be elucidated due to lack of clinical evidence; however, given the ability of CBD to restore cognition in multiple studies of impairment, further investigation into its efficacy in schizophrenia is warranted. Potential mechanisms underlying the efficacy of CBD to improve cognition are discussed.