早发型与晚发型抑郁症遗传效应比较

目的:了解早发型与晚发型单相抑郁症之间是否存在遗传效应的差异. 方法:对符合中国精神障碍分类与诊断标准第3版抑郁发作诊断标准的115例单相抑郁症患者,以初发病年龄30岁为界,分为早发组47例和晚发组68例.对照组230名,无精神疾病,与患者组无血缘关系.对所得资料行单因素分析,用多基因阈值理论进行遗传率的估算. 结果:早发组有精神疾病家族史者为55.3%(26/47),显著高于晚发组35.3%(24/68);早发组一级亲属心境障碍和单相抑郁症发生率分别为9.1%(23/252)和7.9%(20/252),显著高于晚发组一级亲属的4.8%(23/479)和3.6%(17/479);两组一级亲属单相抑郁症发生率均显著高于对照组一级亲属的0.2%.早发组加权平均遗传率及标准误(96.3±1.3)%高于晚发组(75.7±1.2)%,脑部CT器质性改变亦少于晚发组(P<0.05或P<0.01). 结论:早发型及晚发型单相抑郁症均有明显的遗传效应,但二者的遗传效应存在差异.     

晚发型单相抑郁症遗传方式的研究

目的 探讨晚发型单相抑郁症的遗传实方式.方法 采用严格的纳入标准,对符合中国精神疾病分类方案与诊断标准第3版（CCMD-3）抑郁发作诊断标准,首次发病年龄＞30岁的68例单相抑郁症患者用医学遗传数学方法中分离分析和多基因阈值理论进行遗传实方式的研究.结果 晚发型一级亲属单相抑郁症加权平均遗传率及标准误为（75.7±1.2）%,预期发病率为5.0%,与实际发病率3.6 %相比较无显著性差异（u=1.5,P＞0.05）.结论 晚发型单相抑郁症的遗传方式符合多基因遗传.     

Ⅰ型和Ⅱ型精神分裂症的遗传效应比较

目的：了解Ⅰ型和Ⅱ型精神分裂症间是否存在遗传效应的差异．方法：调查了精神分裂症Ⅰ型（１８６例）和Ⅱ型（９９例）患者亲属中精神疾病病的患病情况。结果：Ⅱ型组有精神疾病家族史多，一级亲属中精神分裂症的发病的发病风险率高。一级亲属的遗传率高，与Ⅰ型组比较，差异均有显著性。结论：Ⅰ型和Ⅱ型精神分裂症间存在着遗传效应差异。     

晚发性和早发性精神分裂症的遗传差异

目的：了解晚发性和早发性精神分裂症在遗传效应上的差异。方法：调查精神分裂症晚发组和早发组患者亲属中精神病的患病情况。结果：早发组有精神病家族史多,一级亲属中精神分裂症的发病风险率高,一级亲属的遗传率高,与晚发组比较,有明显的差异性。结论：晚发性和早发性精神分裂症间有遗传效应上的差异。     

早发型单相抑郁症患者遗传方式的研究

目的:探讨早发型单相抑郁症患者的遗传方式. 方法:采用严格的纳入标准,对符合中国精神障碍分类与诊断标准第3版抑郁发作诊断标准、首次发病年龄≤30岁的47例单相抑郁症患者采用医学遗传数学方法中分离分析和多基因阈值理论进行遗传方式的探讨. 结果:早发型一级亲属单相抑郁症加权平均遗传率及标准误为(96.3±1.3)％；预期发病率为9.37％,与实际发病率7.94％相比较差异无统计学意义(u=0.7814,P＞0.05). 结论:早发型单相抑郁症患者遗传方式符合多基因遗传.     

高发情感性障碍的遗传方式探讨

目的 探讨４５个高发情感性障碍的家系的遗传方式。方法 按中国精神疾病分类方案与诊断标准第二版（ＣＣＭＤ－２）及美国精神障碍诊断和统计手册第三版修订本（ＤＳＭ－Ⅲ－Ｒ）的情感障碍诊断标准，均符合者选为样本进行家系调查。结果 其遗传方式为多基因遗传，其加权平均遗传率为１３２．２７％，结论 认为本病可能具有一个显性主基因的多基因遗传。     

单相抑郁症遗传效应的性别差异

目的探讨男性和女性抑郁症的遗传效应及差异。方法采用严格的纳入标准,对符合中国精神障碍分类方案与诊断标准第3版(CCMD-3)抑郁发作诊断标准的单相抑郁症患者115例(男38例,女77例)应用家族史法进行研究,用多基因阈值理论进行遗传率的估算。结果女性和男性患者组有精神疾病家族史者分别为46.75%(36/77)和36.84%(14/38),而两组一级亲属心境障碍发生率分别为7.21%(38/527)和3.92%(8/204),但上述差异均无统计学意义(P>0.05)。女性患者组一级亲属单相抑郁症发生率(6.07%)较男性患者组一级亲属(2.45%)高,二者均较对照组一级亲属(0.24%)高;女性单相抑郁症加权平均遗传率及标准误(86.77±5.77)%较男性(60.10±12.24)%高;上述差异均有统计学意义(P<0.05)。结论男、女性单相抑郁症均有明显的遗传效应,但二者的遗传效应存在差异。     

晚发型情感性障碍的遗传方式探讨

目的探讨晚发型情感性障碍的遗传方式。方法对６７例３０岁以后首次发病的情感性障碍家系采用分离分析和多基因阈值理论进行遗传方式的探讨。结果加权平均遗传率为５３０％±１１６％，预期发病率为１４６％，与实际发病率１２７％比较无显著性差异。结论提示晚发型情感性障碍的遗传方式为多基因遗传方式。     

抑郁症患者自杀的遗传效应研究

目的：了解抑郁症患者自杀行为与遗传的关系，提供有关遗传预测的资料。方法：对近二年连续住我院符合ＣＣＭＤ－２－Ｒ抑郁症诊断标准的６３例抑郁症患者及其一级亲属进行了遗传效应的研究，以无精神疾病者２６９人为对照组。所得资料行单因素分析，用多基因阈值理论估算自杀行为的遗传率。结果：索引病例中有自杀行为者较其一级亲属高（Ｐ〈０．００１）。一级亲属中发生自杀行为的危险性较对照组高（Ｐ〈０．０１），有自杀行为的     

SADS／RDC对分裂情感性障碍诊断的应用

４２例患者按情感性障碍和精神分裂症检查提纲（ＳＡＤＳ）／研究用诊断标准（ＲＤＣ）测查结果均符合分裂情感性障碍。ＳＡＤＳ各症状症状量表在分裂憎感性障碍中均呈高度相关。联合检查和检查一再检查一致率均高，显示ＳＡＤＳ／ＲＤＣ诊断分裂情感性障碍可靠性良好，ＳＡＤＳ／ＲＤＣ与中国精神疾病分类方案与诊断标准（ＣＣＭＤ－２）之间有显著差异。     

Age-of-onset and genetic transmission in affective disorders

Age-of-onset data were gathered on first-degree relatives of 252 probands with bipolar and unipolar affective disorders. Early onset probands (younger than 40 at onset) had more early onset relatives and a greater risk for affective disorder among their relatives than late onset probands (40 or older). This indicates that age-of-onset is a familial factor correlated with the liability to affective illness. Multiple threshold models of inheritance were applied to the data using age-of-onset as a liability-threshold determinant. The hypothesis of autosomal single-major locus was ruled out. Multi-factorial-polygenic inheritance provided a better fit to the data. The data suggest that early and late onset affective disorders can be placed at different thresholds on a genetic environmental continuum and that the early onset form is more deviant genetically than the late onset type. The implications for genetic research in affective disorder are discussed.     

The role of vascular risk factors in late onset bipolar disorder

BACKGROUND: The association between late life depression and cerebro-vascular risk and cerebro-vascular disease is well established. Do similar links exist with late onset bipolar disorder? AIMS AND OBJECTIVES: Patients with early onset (less than 60 years of age) bipolar disorder were compared with those of late onset (aged 60 and above) in relation to cognitive function, physical health and vascular risk factors. METHOD: Cross-sectional survey of elderly bipolar disorder patients (above 65 years) involved with secondary care mental health services. Thirty patients with early onset were compared with 20 patients with a late onset bipolar disorder. Diagnosis of bipolar disorder was according to ICD-10 criteria and without an associated clinical diagnosis of dementia. Assessment of cognition included tests of frontal-executive function, and cerebro-vascular risk was quantified with the Framingham stroke risk score. RESULTS: The late onset group had a higher stroke risk score than the early onset group, this difference persisting despite taking age and gender differences into account. However, late onset patients' cognitive function (including frontal lobe tests) and physical health status was no different to the early onset group. CONCLUSION: There is higher 'cerebrovascular risk' in elderly patients with late onset bipolar disorder, compared to patients with an early onset. This suggests that cerebrovascular risk may be an important factor for the expression of bipolar disorders in later life, and has significant management implications for older bipolar patients.     

Mode of onset and two years outcome of a broad spectrum of affective disorders]

In recent years emphasis has tended to be placed on assessing and diagnosing low-grade affective disorders. If mild affective symptoms are also considered a broad spectrum of affective disorders, this spectrum can be seen, not only in the manifestation of major symptoms of such illnesses as manic-depressive illness, but also in symptoms of various mental disorders. The present study was undertaken to analyze the clinical features of a broad spectrum of affective disorders in a prospective follow-up study. Ninety mentally ill patients who visited our outpatient clinic were followed for 2 years, to investigate the mode of onset, the course and outcome of their disorders. Using a semistructured interview method specially developed for this survey, these patients were divided into a broad spectrum of affective disorder group and the other groups. Forty-nine patients were allocated to a spectrum of affective disorder group characterized by four-day (or longer) persistence of at least one of the following symptoms, depressed mood, loss of interest or elevated, expansive, or irritable mood. Of the forty-nine patients there were only two patients with manic symptoms. And the forty-seven patients with depressive symptoms were compared with the other groups as a main subject. The other groups were composed of eighteen patients with psychotic symptoms (the psychotic group) and 23 patients with neurotic symptoms (the neurotic group). The psychotic and neurotic groups did not satisfy the criteria shown above. There was no significant differences in male-to-female ratio or age between these three groups. When the mode of onset of symptoms were compared, the percentage of cases in whom symptoms could be identified early (within 10 days after onset) was 64.4% in the depressive group, 41.2% in the psychotic group and 30.4% in the neurotic group. The percentage of cases who remitted 2 years later was 70.2%, 38.9%, 45.5% in the depressive group, psychotic and neurotic groups, respectively. The GAS score (mean +/- SD), assessed 2 years later, was 76.2 +/- 12.5, 62.8 +/- 11.7, 78.2 +/- 9.9 points for these three groups, respectively. These results suggest that a broad spectrum of depressive disorders develops more acutely and patients with this spectrum are more likely to recover from symptoms and in function. Thus, the course of disorders was more favorable in the depressive group than in the psychotic group or the neurotic group.     

Clinical characteristics of bipolar I patients according to their family history of affective disorders

BACKGROUND: The familial nature of bipolar disorder has been well described and multiple genes are probably involved in most or all cases. Each gene contributes equally to a bipolar phenotype and it may contribute to clinical characteristics. However, the genetic transmission of bipolar disorder remained undetermined up to now, partly due to clinical and genetically heterogeneity. In Tunisia, genetic study will profit from specific interests and advantages: the high rates of consanguinity, the existence of large families, and the relative geographical stability of the population. OBJECTIVE: The aim of this study was to compare clinical characteristics of familial and nonfamilial bipolar I disorder. METHOD: One hundred and thirty subjects met DSM-IV criteria for a bipolar I disorder; they were recruited and divided into groups according to their family history of affective disorders. Group 1 with a familial history group, comporting bipolar I patients with a family history of affective disorders in first and second degree relatives (n = 76; 52 males and 24 females, mean age = 37.2 +/- 10.7 years) was compared to group 2 (nonfamilial history group), comporting bipolar I patients without a family history of affective disorders (n = 54; 29 males and 25 females, mean age = 38.1 +/- 10.9 years). Available information was obtained from a structured clinical interview, collateral history, and medical records. The family investigation permitted completion of genealogies over three generations. The comparison of the two groups was based on the clinical characteristics (age at onset, numbers of affective episodes, nature and severity of the last affective episode,...). RESULTS: There were no significant differences between the two groups concerning demographic and social features, with the exception of professional activity. Indeed 30.2% of patients with a family history of affective disorders were unemployed versus 12.9% of patients without a family history of affective disorders (p = 0.02). Bipolar I patients with a family history of affective disorders were characterised by an early age at onset of the first episode (before 20 years) (48.7 versus 24.0%; p = 0.004), a high frequency of affective episodes (8.1 +/- 3.6 versus 6.0 +/- 3.5; p = 0.002) and had been more often hospitalised than patients without a family history of affective disorders (5.7 +/- 3.0 versus 4.7 +/- 3.0; p = 0.06). No significant differences were found concerning the nature of the first affective episode in bipolar I patients with or without a family history of affective disorders. Eleven women had developed their first affective episode during the puerperal period; eight of whom had a family history of affective disorders (p = 0.07). The last affective episode was significantly more severe (94.8 versus 77.8%; p = 0.003) and more often associated with psychotic features (55.3 versus 35.2%; p = 0.02) in patients with a family history of affective disorders. After multiple regression, the high frequency of affective episodes and the severity of last episode were more related with a family history of affective disorders. CONCLUSION: The results of our study provide evidence of familiality for some clinical characteristics which can be useful as phenotypic measures in future molecular genetic studies.     

Heritability of schizophrenia and major affective disorder as a function of age, in the presence of strong cohort effects

It remains unclear whether age at onset for major psychiatric disorders is a useful marker of etiologic and genetic heterogeneity. The authors examined how heritability of schizophrenia and major affective disorders varied with age at onset. The sample was drawn from a large archival data set collected by Lionel Penrose, comprising 3,109 families with two or more members first hospitalized in Ontario between 1874 and 1944. The authors studied 1,295 sibships with schizophrenia (n = 487), major affective disorder (n = 378), both (n = 234) or neither (n = 196) of these disorders. Proportional hazards models were used to estimate how the hazard of hospitalization for each disorder (schizophrenia or major affective disorder) varied with proband age at onset, adjusted for changes in age at onset distribution between 1874 and 1944. A sibling's risk of hospitalization for the same illness significantly increased for each 10–year decrease in age at onset of the proband both for schizophrenia (hazard ratio = 1.21, 95 % confidence interval: 1.06, 1.39), and for affective disorder (hazard ratio = 1.29,95 % CI: 1.14, 1.45). Gender of proband was unrelated to sibling risk of the same illness, and tests of interaction effects between proband age at onset and gender on sibling risk were nonsignificant.     

101例惊恐发作患者诊断归属及发作场所调查

目的:分析101例惊恐发作患者诊断归属及发作场所变化。方法:对101例惊恐发作患者以美国精神障碍诊断与统计手册第4版(DSM-Ⅳ)轴Ⅰ障碍用定式临床检查-临床版(SCID-CV)进行诊断;采用自制问卷调查发作情况。结果:符合DSM-Ⅳ惊恐障碍90例(89.1%),广泛性焦虑障碍6例(5.9%),抑郁障碍3例(2.9%),强迫障碍及精神分裂症各1例。90例惊恐障碍患者中,首次发作场所为家中50例,公共场所31例,途中9例;76.6%患者常在初次发生发作的场所发作,23.4%发作场所没有倾向性,仅1例发作场所固定。11例非惊恐障碍患者首发场所为家中3例,公共场所8例;此后发作场所均不固定。结论:约90%惊恐发作患者诊断为惊恐障碍,首次多发作于家中,并且倾向于在初次发作的场所发作;非惊恐障碍患者发作场所不固定。     

昆明市焦虑障碍现况调查及相关因素分析

目的 调查昆明市焦虑障碍的患病情况.方法 2005年11月至2006年1月采用分层容量比例概率随机抽样法,应用中文版复合性国际诊断交谈检查2.1版(CIDI-2.1)对昆明市≥15岁的居民5033人进行访谈,调查焦虑障碍的患病率,分析影响焦虑障碍的相关因素、起病年龄及共病情况.结果 (1)焦虑障碍的加权终生患病率为7.05%(324例),其中,男性为5.34%(100例),女性为8.89%(224例);城镇人口为7.81%(189例),农村人口为5.33%(135例);以特殊恐怖障碍患病率最高(5.64%,236例),惊恐障碍患病率最低(0.14%,6例).(2)女性患病风险[相对危险度(OR)=1.00]高于男性(OR=0.61;P<0.01);各类焦虑障碍的起病年龄中位数为16岁;焦虑障碍与美国精神障碍诊断与统计手册第4版诊断的物质使用障碍,情感障碍及疼痛障碍存在共病情况.结论 昆明市焦虑障碍患病率较高,焦虑障碍是一类起病年龄早、呈慢性病程且普遍存在与其他精神障碍共病状况的精神障碍,有必要加强对焦虑障碍的防治.     

A cluster-analytically derived subtyping of chronic affective disorders.

This article aims to propose a mathematically legitimate and externally validated subclassification of chronic affective disorders. Three subtypes emerged from the cluster analysis of the symptom data of 40 patients with chronic affective disorder that had been present without remission for more than 2 years; the subtypes were then validated by psychosocial variables. The first cluster, a predominantly male group with young onset, is characterized by past history of psychotic features and is named psychotic subtype. The second cluster, a predominantly female group with late onset, is tentatively called late-onset female subtype. The third cluster has the youngest onset and the longest duration, and is characterized by early object loss and high neuroticism score: depressive personality subtype.     

Transmitted factors in the morbid risk of affective disorders: A controlled study

Data on psychiatric disorders were collected on first-degree relatives and spouses of 70 patients with primary affective disorder and 75 patients admitted to a general hospital without psychiatric disorder, from the Jewish population of Jerusalem, Israel. Bipolar patients tended to have more bipolar relatives than unipolar patients, but unipolar patients had an observable morbid risk for bipolar disorder in their relatives. Ethnicity and age of onset did not appear to be related to transmissible factors in the prevalence of affective disorders in relatives, although age of onset was associated with morbid risk. Sex-linkage or genetic liability to affective disorder related to sex did not appear to be present. A spectrum of related disorders for this population was defined by those disorders which were more prevalent in relatives of affective disorder patients than in relatives of controls. Assortative mating was not found, but a modest degree of inbreeding appeared to be present. For purposes of testing liability-threshold models for genetic factors in the transmission of mood disorders, only the data on polarity seems suitable.