精神发育迟滞合并精神分裂症的临床分析

目的　探讨精神发育迟滞 (MR)合并精神分裂症的临床特征。方法　 76例MR合并精神分裂症患者按智商 (IQ)≥ 5 0和IQ≤ 49分成两组进行临床特征分析 ,并与 76例智力正常的精神分裂症患者比较。结果　MR合并精神分裂症患者IQ≥ 5 0和IQ≤ 49两组间临床症状差异无显著性(P >0 0 5 ) ;MR合并精神分裂症组与正常智力的精神分裂症组的一级症状、逻辑推理障碍、妄想、情感平淡、思维贫乏的差异有非常显著性 (P <0 0 1)。结论　MR合并精神分裂症患者一级症状明显减少 ,有助于临床鉴别。     

精神发育迟滞合并精神分裂症的临床研究

目的探讨精神发育迟滞（MR）合并精神分裂症的临床特点。方法 48例MR合并精神分裂症患者按智商（IQ）≥50和IQ≤49分为两组进行临床特征分析,并与48例智力正常的精神分裂症患者比较。结果 MR合并精神分裂症患者IQ≥50和IQ≤49两组间临床差异无显著性（P≥0.05）;MR合并精神分裂症组与正常智力精神分裂症组的一级症状[1]、逻辑推理障碍、妄想、情感平淡、思维贫乏的差异有显著性（P〈0.01或P〈0.05）。结论 MR合并精神分裂症一级症状明显减少,有助于临床鉴别。     

难治性精神分裂症患者及亲属的临床特征和认知功能分析

目的探讨难治性精神分裂症患者及其亲属的临床特征及认知功能。方法:采用PANSS、数字广度和数字符号测验对符合DSM-IV精神分裂症诊断标准和难治性标准的139例患者,66例非难治性患者,以及118例难治性患者亲属,100例正常对照进行认知功能和临床症状的评定。结果:难治性精神分裂症患者在发病年龄、未治期、病程、阴性分量表评分与非难治性患者有显著性差异(P<0.05);在教育年限、数字广度、数字符号方面无显著性差异(P>0.05)。数字广度、数字符号比较,难治性患者、非难治性患者及一级亲属与正常组均有显著性差异(P<0.05)。数字广度和数字符号测验结果与难治性患者的病程、PANSS阴性量表评分和未治期呈显著负相关(P<0.05),与教育年限、起病年龄呈显著正相关(P<0.05)。结论:难治性精神分裂症患者有其特殊的临床特征,和其亲属都具有认知功能的损害。     

阿尼西坦改善慢性精神分裂症患者认知功能的临床研究

目的探讨阿尼西坦改善慢性精神分裂症患者认知功能的疗效。方法将64例慢性精神分裂症患者随机分为研究组32例和治疗组32例,分别予以奎的平(350±50)mg/d治疗8周,研究组同时合并阿尼西坦100mg/d,并于治疗前及治疗后分别进行阳性和阴性症状量表(PANSS)、简明精神状态量表(MMSE)、中国修订韦氏成人智力量表(WAIS-RC)、韦氏记忆量表(WMS)及威斯康星卡片分类测定(WCST)等评定,并与正常人组成的对照组进行比较。结果治疗前研究组和治疗组的MMSE、WMS及WAIS-RC均低于对照组,差异有显著性(P〈0.05),提示患者的认知功能有广泛性损害。治疗后研究组MMSE、WCST、WMS、WAIS-RC分数与治疗前比较差异有显著性(P〈0.05),而治疗后治疗组的WCST、WMS、WAIS-RC分数与治疗前比较无显著性差异(P〈0.05)。结论阿尼西坦改善慢性精神分裂症患者的认知功能疗效确切。     

精神分裂症患者的认知功能及其影响因素

目的 了解精神分裂症患者的认知功能及其影响因素。方法 对100例精神分裂症患者及79例正常对照进行韦氏智力测验（WAIS）评定，同时调查患者的临床特征。结果与正常对照比较发现，精神分裂症患者的IQ、言语智商和操作智商均显著低于正常对照，709／6患者的IQ低于平常，19％的患者智力缺损。多元逐步回归分析显示：①IQ与发病年龄有关，发病年龄越晚，IQ越高；②言语智商与发病年龄、诊断分型有关，发病年龄晚、偏执型患者，言语智商高；③操作智商与病程有关，病程越短，操作智商越高。结论精神分裂症的认知功能损害是明显的、广泛的，受多种因素的影响。     

精神分裂症及抑郁发作患者血清心肌酶的研究

目的探讨精神分裂症及抑郁发作患者血清心肌酶的变化与临床意义。方法动态监测281例精神分裂症和223例抑郁患者的心肌酶谱,正常对照50名。采用简明精神病量表(BPRS)或汉密顿抑郁量表(HAMD)评定病情。结果精神分裂症阳性症状组与阴性症状组及双相抑郁患者的血清心肌酶各指标均显著高于对照(P<0.01),阳性症状组心肌酶谱各项指标均高于阴性症状组(P<0.01)。各指标测定水平与精神分裂症及双相抑郁患者的病情严重程度呈正相关,且随着病情得到控制,各指标均逐渐下降并趋于正常。单相抑郁患者与对照比较,差异无显著性(P>0.05)。结论精神分裂症和双相抑郁患者的血清心肌酶活性明显增高与发病及病情严重程度有关,心肌酶谱检测对精神分裂症和双相抑郁的病情估计有一定的临床价值。单相抑郁患者治疗前后均无心肌酶活性明显增高。     

家族性与散发性精神分裂症患者认知功能的对比研究

目的探讨家族性与散发性精神分裂症患者认知功能损害的差异。方法 对符合CCMD-2-R精神分裂症诊断标准的26例家族性与64例散发性精神分裂症患者,应用中国修订韦氏成分智力量表(WAIS-RC)进行智力测验比较并与全国常模对照,同时比较其HR神经心理成套测验(HRB-RC)中的连线测验和范畴测验。结果 与散发组相比,家族组的智力分测验粗分和言语智商(VIQ)较低,VIQ与操作IQ(PIQ)的平衡性较差,退化商数(DQ)较大,连线测验时间较长,范畴测验错误数增多,有显著性差异(P<(0.01～0.05)]。结论 家族组的认知功能损害更严重,提示可能与其遗传学基础有关。     

首发精神分裂症患者及其一级亲属感觉门控P50研究

目的探讨首发精神分裂症患者及其未患病的一级亲属感觉门控电位P50的特征。方法采用条件-测试听觉刺激模式对50例首发精神分裂症患者(患者组)、40名未患病的一级亲属(亲属组)和50名正常人(正常对照组)进行P50检测,比较3组P50各成分之间的差异。结果患者组、亲属组和正常对照组3组之间P50潜伏期比较,差异无统计学意义(P>0.05);患者组和亲属组测试刺激所诱发的P50(S2-P50)波幅(中位数1.69uV和1.39uV)高于正常对照组(0.92uV),而2组条件与测试刺激P50波幅的差值(中位数0.16uV和0.44uV)与P50抑制率(中位数10.23%和19.10%)低于正常对照组(1.32uV与62.29%),差异均有统计学意义(P<0.01);正常对照组内男女性别组间P50各项指标比较差异无统计学意义(P>0.05)。结论精神分裂症患者及其未患病的一级亲属均存在P50感觉门控功能异常,提示P50可能是精神分裂症的遗传素质指标。     

利培酮与氯氮平治疗首发精神分裂症对认知功能的影响

目的 比较利培酮和氯氮平对首发精神分裂症患者认知功能的影响。方法 将符合入组标准的首发精神分裂症患者77例随机分为利培酮组与氯氮平组,分别进行8周系统治疗,用阳性与阴性症状量表(PANSS)、韦氏成人智力量表(WAIS-RC)、数字划销试验(CT)和临床记忆量表(CMS)进行检查,评估其疗效和对认知功能的影响。结果 脱落4例,73例患者在8周治疗后PANSS总分明显下降(P<0.01),两组之间差异无显著性(P>0.05)。利培酮组的WAIS-RC、CT、CMS总分均明显高于氯氮平组,差异有显著性(P<0.05～0.01)。结论 利培酮对首发精神分裂症患者认知功能的影响明显好于氯氮平。     

精神分裂症患者前驱症状的调查与分析

目的 调查与分析精神分裂症患者的前驱症状。方法 在有明显社会心理诱发因素的首发精神分裂症住院患者中，随机抽取100例作为精神分裂症组。在向危机干预中心求助的正常人群中，随机抽取100例作为危机干预组。并对两组的社会心理诱因和前驱症状进行比较分析。结果 正常人(危机干预组)在精神压力下产生的症状与有明显社会心理诱发的精神分裂症(精神分裂症组)的前驱症状元显著差异。结论 在危机干预过程中，警惕一些人群的症状表现可能就是精神分裂症的前驱症状。     

Childhood-onset schizophrenia and schizophrenia spectrum disorder

The concept, diagnosis and clinical picture of childhood-onset schizophrenia were presented. The cases with childhood-onset schizophrenia were classified into 4 groups according to their process of growth and development. Furthermore, it has been suggested that the progression of childhood-onset schizophrenia developed on the basis of neuro-developmenal hypothesis might contribute to the understanding of adult onset schizophrenia and early diagnosis and intervention of schizophrenia.     

Difference between treatment-resistant schizophrenia and clozapine-resistant schizophrenia

We read the impressive review article “Clozapine resistant schizophrenia: Newer avenues of management” with great enthusiasm and appreciation. The author believes that preventing clozapine resistance from developing may be the most effective treatment strategy for patients with clozapine-resistant schizophrenia (CRS), and optimizing clozapine treatment is a key component. Disentangling the differences between treatment-resistant schizophrenia and CRS is important for studies addressing treatment strategies for these difficult-to-treat populations.     

Mismatch negativity in chronic schizophrenia and first-episode schizophrenia

BACKGROUND: Mismatch negativity (MMN) is an event-related brain potential that is sensitive to stimulus deviation from a repetitive pattern. The MMN is thought primarily to reflect the activity of sensory memory, with, at most, moderate influences of higher-level cognitive processes, such as attention. The MMN is reported to be reduced in patients with chronic schizophrenia. However, it is unknown whether MMN is reduced in patients with first-episode schizophrenia (at first hospitalization). METHODS: Subject groups comprised patients with chronic schizophrenia (n = 16) and older control subjects (n = 13), and patients with first-episode schizophrenia (n = 21) and younger control subjects (n = 27). The MMN was visualized by subtracting the averaged event-related brain potential to standard tones (1 kHz [95% of all tones]) from the event-related brain potential to pitch-deviant tones (1.2 kHz [5% of all tones]). The MMN voltage was the mean voltage from 100 to 200 milliseconds. RESULTS: Pitch-deviant MMN was reduced by approximately 47% in patients with chronic illness along the sagittal midline relative to controls. The MMN was not reduced in patients with first-episode schizophrenia. All 4 groups showed approximately 64% larger MMN to pitch-deviant tones over the right hemisphere compared with the left hemisphere. CONCLUSIONS: The pitch-deviant MMN reductions present in patients with chronic schizophrenia are not present at first hospitalization. The sensory, echoic memory functions indexed by MMN seem unaffected early in the schizophrenia disease process. Reductions in MMN amplitude may develop over time and index the progression of the disorder, although that can only be definitively determined by longitudinal assessments.     

Cytokines and schizophrenia: Microglia hypothesis of schizophrenia

The etiology of schizophrenia remains unclear, while there has been a growing amount of evidence for the neuroinflammation and immunogenetics, which are characterized by an increased serum concentration of several pro-inflammatory cytokines. Despite the fact that microglia comprise only <10% of the total brain cells, microglia respond rapidly to even minor pathological changes in the brain and may contribute directly to the neuronal degeneration by producing various pro-inflammatory cytokines and free radicals. In many aspects, the neuropathology of schizophrenia has recently been reported to be closely associatedwith microglial activation. Previous studies have shown the inhibitory effects of some typical/atypical antipsychotics on the release of inflammatory cytokines and free radicals from activated microglia, both of which have recently been known to cause a decrease in neurogenesis as well as white matter abnormalities in the brains of patients with schizophrenia. The microglia hypothesis of schizophrenia may shed new light on the therapeutic strategy for schizophrenia.     

Early-onset schizophrenia

The study describes the psychopathological and social outcome of patients treated for schizophrenia in adolescence (mean age at onset 16.0 years/SD 1.52) after a mean follow-up period of 15.4 years (10.2-21.2 years). Out of 55 patients consecutively admitted to hospital, 47 (85 %) could be traced and 39 (71 %) could be re-examined.At follow-up, 33/39 patients (85 %) had had at least one readmission. Full remission of global psychopathological symptoms [Clinical Global Impression (CGI) 相似文献   

Treatment-refractory schizophrenia

Between one-third and one-half of the individuals who meet diagnostic criteria for schizophrenia remain actively ill despite optimal pharmacological treatment. These individuals tend to progressively deteriorate in terms of social and vocational functioning despite major public and private investments in their rehabilitation. For patients who do not respond to the first prescribed antipsychotic drug, current clinical practice is to switch to a second and a third drug, and eventually to clozapine, the only antipsychotic drug proven to be effective in treatment-refractory schizophrenia (TRS). Occasionally, two antipsychotics are given concomitantly or psychotropic drugs are added to antipsychotic drugs; however, very few empirical data exist to support this practice. Although there are many exceptions, patients who do not benefit from the first prescribed drug will not benefit from any pharmacological intervention. Therefore, efforts are under way to determine the reason for lack of response to available treatments and devise novel, more effective treatments. To be successful these efforts must result in a more specific definition of TRS, as well as in a better understanding of the illness pathophysiology and the mechanism of action of the drugs.     

Treatment-refractory schizophrenia

Treatment-refractory schizophrenia is common. Refinements in pharmacologic and psychosocial treatments of schizophrenia offer the expectation of superior outcomes for this disadvantaged patient group. This article critically reviews those articles that were published during the year 2000 that address this treatment-refractory population.