Dexamethasone suppression and multiple hormonal responses (TSH,prolactin and growth hormone) to TRH in some psychiatric disorders

Summary Baseline and TRH-induced changes of thyroid stimulating hormone (TSH), prolactin (PRL), and growth hormone (GH) were measured in 15 healthy control subjects and 63 psychiatric inpatients with DSM-III diagnoses of major depression (n = 19), schizophrenic disorder (n = 20), alcohol dependence (n = 10), and adjustment disorder (n = 14); baseline and postdexamethasone cortisol (CS) were also determined 3–6 days after the TRH-challenge. All patients and controls were women of similar mean age, weight, height, and they were free from interfering illness or drugs.Baseline TSH and PRL were lower in depression, TRH-induced TSH and PRL responses were lower in the whole patient group, but most markedly in depression and alcohol dependence. Postdexamethasone CS was significantly higher in depression, schizophrenia and alcohol dependence. Basal GH did not differentiate the subgroups; TRH-induced pathological GH responses were sometimes found in the patient groups. The differences were most marked quantitatively in major depression: a multivariate analysis of variance showed that TSH, postdexamethasone CS and PRL were the most important variables in separating patients from controls. A discriminant function derived from these variables classified all controls and 18 of 19 depressed patients correctly; however, 25 of the 44 other patients were also classified with depression.It was confirmed that psychiatric patients show significantly more endocrine disturbances than controls, and this was seen not only in major depression but also in at least three other conditions. Further work is needed to identify other neuroendocrine patterns more specific to depressive disorder.     

Abnormal seasonality of schizophrenic births A specific finding?

Summary The unusual finding of an abnormal seasonal distribution of schizophrenic births, showing an excess of 10% in the winter or spring months and an equal deficit in the summer or autumn months, cannot be explained by artefacts. It has not yet been established whether the finding is specific to schizophrenia. We observed an excess of schizophrenic births of some 10% in March to May, significant at the 5% level, and a deficit of approximately the same size in June to August on the birth data of first-admission patients with the clinical diagnosis of schizophrenia. The data, obtained from the Mannheim Psychiatric Case Register, were compared with those of the Mannheim population and a control group matched by birth year and sex. The total population of mentally retarded children aged 7 to 16 years from the Mannheim population showed an excess of some 20% in April to June and an equal deficit in the last two quarters of the year, compared with the Mannheim population of the same birth years. The finding was not significant, but allowance must be made for the low case number of 415. We also compared 3409 first-admission patients with depressive syndromes (ICD 296 and 300.4) and 5615 first-admission patients with the diagnosis of neurosis and personality disorders (ICD 300–302, except 300.4, and 305–309) from the Mannheim Case Register with a control population and a parallel control group. Depressed males showed an excess of births in March to May, which was significant at the 1% level; the birth peak for females was smaller and not significant. The same findings were obtained for the category of neurosis and personality disorders, i.e. an excess of about 10% in March to May for males, significant at the 1% level, and a non-significant excess for females. Our findings are awaiting replication. Causal explanations will be discussed with great reservation. The procreational hypothesis, assuming those factors that lead to an equidirectional seasonal pattern of births with a slight deviation from the average of a year in the general population, to be reinforced in the disease categories mentioned, is regarded as the most simple and plausible explanation. It is based on the assumption that some of the parents of individuals suffering from schizophrenia, mental retardation or probably also some other mental disorders running from generation to generation, have a higher threshold in partner-seeking behaviour, which is overcome more easily in the summer months with the consequence of increased pregnancies.     

Examining the feasibility,acceptability, validity and reliability of physical activity,sedentary behaviour and sleep measures in people with schizophrenia

BackgroundSchizophrenia is associated with a more than doubled risk of death from cardiovascular disease (CVD). Risk factors for CVD include low levels of physical activity, sedentary behaviour and sleep problems. These risk factors are not systematically assessed by health services.AimsExamine the feasibility, acceptability, validity and reliability of tools measuring physical activity, sedentary behaviour and sleep.MethodsThirty participants with schizophrenia measured their physical activity, sedentary behaviour and sleep by wearing ActiGraph wGT3X-BT accelerometers on their wrist and waist, and recorded their sleep using the SleepBot smartphone app for 7 days. After 7 days they completed the 5-item Simple Physical Activity Questionnaire (SIMPAQ) to retrospectively measure their physical activity and sedentary behaviour over the study period. Concurrent SIMPAQ and SleepBot validity and inter-rater reliability were assessed against accelerometer-derived measures of physical activity, sedentary behaviour and sleep. A qualitative interview was conducted at the end of the study to assess acceptability.ResultsThe tools were feasible: 93% of participants provided valid wear-time accelerometry data and 83% provided SleepBot data. The SIMPAQ showed moderate concurrent validity but poor agreement for moderate-vigorous physical activity (MVPA) and moderate validity and agreement as a measure of sedentary behaviour. The SleepBot app showed poor concurrent validity and agreement for measures of sleep. The qualitative interviews demonstrated the tools were acceptable.ConclusionMonitoring physical activity, sedentary behaviour and sleep by accelerometry, smartphone and questionnaire was feasible and acceptable to people with schizophrenia. The SIMPAQ could be a valid and appropriate tool for routine clinical use.     

住院精神分裂症患者自测健康的对照研究

目的：比较住院精神分裂症患者和躯体疾病患者的健康状况,及了解影响精神分裂症患者健康的因素。方法：采用“自测健康评定量表”（SRHMS）对81例慢性精神分裂症康复期患者和82例躯体疾病病人作自我评定,进行对照研究,并对相关因素作多元逐步回归分析。结果：两组间SRHMS总分、心理健康子量表总分比较不存在显著性差异;（P＝0．39）;生理及健康子量表及总分,社会健康子量表总分两组间的差异均有非常显著性差异（P＝0．00）。经多元逐步回归分析,精神分裂症组病程,IPROS总分、服药剂量影响SRHMS的评分。结论：自测健康评定量表是健康测定的一个有效工具,测试结果反映了两组人群实际健康状况。     

社区精神分裂症综合式家庭干预对照研究

目的：了解综合式家庭干预对社区精神分裂症患者和家属的效果。方法：在宝山区随机抽取186例精神分裂症进行一年的综合式家庭干预对照研究,干预组86例接受综合式家庭干预和常规社区服务,对照组100例仅接受常规社区服务。结果：干预组患者年复发率下降47．3％,社区功能明显改善,干预组家庭对有关疾病知识增长,心理状况改善,照料负担减轻,与对照组比较效果显著。结论：综合式家庭干预对精神分裂症患者家属有良好的效果,应纳入常规社区服务。     

利培酮治疗精神分裂症2484例临床研究

目的了解利培酮在中国的应用概况.方法在2484名使用利培酮的精神分裂症病人中,采用<临床总体印象量表>(CGI)、<阳性与阴性综合征量表>(PANSS)及不良反应量表,在利培酮治疗8周前后进行评定分析.结果在治疗第8周末继续服用利培酮者占97.02%,其中96.60%服用剂量≤6mg·     

精神分裂症患者血浆精氨酸加压素含量的研究

目的研究精神分裂症患者血浆精氨酸加压素(AVP)的变化。方法采用放射免疫法测定38例精神分裂症患者和22例正常对照者的血浆AVP含量。结果精神分裂症患者血浆AVP含量较对照组低,差异非常显著(t=9.59,P<0.01);给精神分裂症患者氯氮平治疗4周后其血浆AVP含量较治疗前显著增高(t=2.21,P<0.05)。结论精神分裂症患者AVP含量降低,抗精神药物氯氮平对体内AVP代谢有一定的影响。     

住院精神分裂症患者十年前后用药情况对比分析

目的对十年前后精神分裂症患者用药情况的变化进行调查分析.方法对十年前后两个五年段的各500份符合精神分裂症诊断标准的病历进行回顾性调查,并对各项指标进行对比分析.结果两组折算用药剂量经t检验差异无显著性(P>0.05);两组合并用药、合并抗胆碱药及疗效经χ2检验差异有显著性(P<0.01);十年后非典型抗精神病药物氯氮平在临床上的应用比例明显增大并上升为首位.结论十年前后两组抗精神病药的应用发生了明显变化,疗效好、副作用轻的非典型抗精神病药的应用比例明显增加.     

多巴胺D2受体基因启动子A-241G多态性在精神分裂症家系中的连锁不平衡传递

目的:探讨多巴胺D2受体基因(dopamine D2 receptor,DRD2)启动子A-241G多态性与精神分裂症的关系.方法:采集101个家系,每家有2名或2名以上符合ICD-10精神分裂症诊断标准患病同胞且父母存活.对DRD2启动子的A-241G多态性进行检测.结果:(1)DRD2启动子的A-241G等位基因频度和基因型频度在父母组、非患病同胞组和患病同胞组之间差异无显著性,在3组不同性别之间以及在精神分裂症不同亚型之间基因型频度和等位基因频度的分布差异亦无显著性;(2) 传递不平衡检验发现在患病同胞(χ2 =0.94,P>0.05,OR=0.83,95%可信区间0.57～1.21)中未表现传递不平衡性,而在非患病同胞(χ2 =6.76,P<0.01,OR=3.17,95%可信区间0.41～24.71)中存在传递不平衡性,其中-241A等位基因在非患病同胞中传递较多;(3) 基因型与妄想总分、幻觉总分、思维形式障碍、情感障碍、精神性失语及症状持续时间等临床特征相关.结论:DRD2启动子的A-241G多态性对精神分裂症的发病和临床表现具有一定影响.