神经症与正常人的社会心理因素、个性和躯体症状的对照研究

目的为了探索神经症患者与正常人在社会心理因素、个性和躯体症状方面的差异。方法采用社会心理问题问卷、艾森克个性问卷（ＥＰＱ）和躯体症状定式检查表对神经症和正常人进行评定。结果神经症患者的遗传因素和社会心理因素明显高于正常人（Ｐ＜００５）；神经症的艾森克Ｐ、Ｎ分明显高于正常人（Ｐ＜００５）；男性Ｅ分较正常人低（Ｐ＜００５），Ｌ分两组比较无明显差异（Ｐ＞００５）。神经症的情绪不稳和内倾性格明显高于正常人（Ｐ＜００５）。神经症的躯体症状明显多于正常人（Ｐ＜００５）。结论个性缺陷在神经症的发病中起了重要作用     

情感性精神障碍遗传学家系调查

目的评价情感性精神障碍的遗传效应。方法对符合国际疾病分类第１０版和中国精神疾病分类方案与诊断标准第２版修订本中情感性精神障碍诊断的１０２个先证者家系登门调查。结果共调查先证者一、二级亲属４８９８人。１０２个先证者家系精神障碍的阳性率为５８．８％，其中情感性精神障碍同病率为８５．０％，遗传率加权平均值为１０６．３％±２．４％，高发家系为１５０．７％±１４．８％。结论遗传因素在情感性精神障碍病因中具有十分重要地位，遗传方式可能是具有显性主基因的多基因遗传     

酒精依赖的遗传方式探讨

目的 :探讨酒精依赖患者的遗传方式。　方法 :应用医学遗传的数学方法 ,对 63例酒精依赖的索引病例进行分析。　结果 :在连续两代出现酒精依赖患者的 3 5个家系 ,共有患者所生子女 161人 ,其中发病 67例 ,实际值与理论值 ( 161× 5 0 % )差异有显著性 ( P<0 .0 5 )。对索引病例父母正常的 2 8个家系进行了分析 ,其校正分离率为 0 .2 5 ,符合常染色体隐性遗传的分离率 1/ 4。7例其父为酒精依赖患者 ,同胞中的男性均为酒精依赖患者。未见父亲专门将致病基因传递女儿的规律 ,在父母正常的男性患者中 ,无明显交叉遗传现象。　结论 :酒精依赖与遗传有关 ,遗传方式符合常染色体隐性遗传和 Y连锁显性遗传。     

癔症与正常人社会心理因素及个性和躯体症状对照研究

目的探索癔症患者与正常人在社会心理应激因素、个性和躯体症状方面的差异。方法采用社会心理问题问卷、艾森克个性问卷（ＥＰＱ）和躯体症状定式检查表对癔症和正常人进行评定。结果癔症患者社会心理应激因素明显高于正常人（Ｐ＜００５）；Ｐ、Ｅ、Ｎ、Ｌ分高于正常人（Ｐ＜００５）；癔症个性以外向居多，且多数为情绪不稳，与正常组对照有显著性差异（Ｐ＜００５）；癔症的躯体症状明显高于正常组（Ｐ＜００５）。结论在临床上正确引导患者认识自己的个性缺陷，并采用相应的心理疏导和特殊治疗方法，对于癔症的防治具有实际意义。     

内科住院患者情感性精神障碍的研究

目的了解综合医疗机构患者中情感性精神障碍的患病率。方法对综合医院内科４１７例住院患者进行调查，并以中国精神疾病分类与诊断标准第２版修订本和国际疾病分类第１０版诊断标准进行诊断。结果亚临床抑郁性障碍和焦虑性障碍的患病率分别为２３．７％和３４．８％，重性抑郁症、心境恶劣、惊恐障碍和躯体形式障碍的患病率分别为３．６％、２．４％、１．２％和１．０％；内科医师对情感性精神障碍的识别率仅为１０．５％。结论在综合医疗机构患者中情感性精神障碍的患病率较高，应重视对其研究，并提高综合科医师的识别和处理能力     

酒精所致精神障碍住院患者妻子的心理健康状况调查

采用９０项症状清单（ＳＣＬ－９０）对３８例酒精所致精神障碍住院患者正好了的心理健康状况进行了测评；并对其中慢性酒中毒和酒依赖患者妻子的心理健康状况进行比较。结果发现，酒精所致精神障碍鹗２正好了的躯体化、人际关系、抑郁、焦虑、敌对和偏执６个因子均分显著高于国内常模（Ｐ〈０．０１～０．０５）；慢必不朽事毒患者正好了在人际关系、抑郁、敌对３项因子均分高于酒依赖患者妻子（Ｐ〈０．０１～０．０５）。提示由于     

精神分裂症语音和音乐刺激时的闭眼眼球活动

目的 探索精神分裂症患者在语音和音乐刺激时闭眼眼球活动的特征。方法 对７０例精神分裂症，３４例情感性精神障碍和３３例正常对照者进行语音和音乐刺激，观察其闭眼眼球活动（ＣＥＭＳ）的变化。结果 精神分裂症组中，ｒ波次数的平均秩和与怀古性精神障碍相似，但高于正常对照组（Ｐ〈０．０１）；ｓ波则分别低于后二者（Ｐ〈０．０５￣０．０１）；此外，每次语音刺激前和刺激时的ｒ波次数均无显著性差异。ＣＥＭＳ值与ＢＰＲ     

92例酒精依赖患者的遗传学研究

目的　探讨酒精依赖患者的遗传方式。方法　应用医学遗传的数学方法对 92例酒精依赖患者的家系进行分析。结果　一、二级亲属总患病率为 9 16 % ,一级亲属患病率为 18 87% ,明显高于二级亲属患病率 4 19%。在连续两代出现酒精依赖患者有 5 2个家系 ,共有患者子女 170人 ,其中发病 6 9例 ,实际值与理论值 (170× 5 0 % )有显著性差异 (P <0 0 5 )。对索取病例父母正常的 4 1个家系进行计算分析 ,其校正分离率为 0 2 5 ,符合常染色体隐性遗传的分离率 1/ 4。 10例其父为酒精依赖患者 ,同胞中的男性均为酒精依赖患者。在父母正常的男性患者中 ,无明显的交叉遗传现象。结论　酒精依赖与遗传有关 ,遗传方式符合常染色体隐性遗传和Y连锁显性遗传     

情感性精神障碍治疗前后血清甲状腺激素水平的对照观察

目的了解血清甲状腺激素水平与情感性精神障碍的关系。方法对２６例住院的情感性精神障碍患者做了治疗前后血清三碘甲状腺原氨酸（Ｔ３）、甲状腺素（Ｔ４）、Ｔ３树脂摄取比值（ＲＵＲ）和游离甲状腺素指数（ＦＴ４Ｉ）的对照观察，其中躁狂发作１９例，抑郁发作７例。同时以３０名健康人作为对照组。治疗前后应用Ｂｅｃｈ－Ｒａｆａｅｌｓｅｎ躁狂量表（ＢＲＭＳ）和汉密尔顿抑郁量表（ＨＡＭＤ）评定躁狂和抑郁症状的严重程度。结果患者组治疗前后的Ｔ４（１４２±４０和１３１±３７ｍｍｏｌ／Ｌ）、ＦＴ４Ｉ（１０．６±３．４和１０．５±３．７ｍｍｏｌ／Ｌ）明显高于对照组（１１１±２２，８．３±２．４ｍｍｏｌ／Ｌ）。治疗前７例躁狂发作患者的Ｔ３（１．０９±０．１６ｍｍｏｌ／Ｌ）低于正常组（２．０±０．５ｍｍｏｌ／Ｌ）；抑郁发作的Ｔ４（１７９±３１ｍｍｏｌ／Ｌ）、ＦＴ４Ｉ（１２．５±４．５ｍｍｏｌ／Ｌ）治疗前高于正常水平，治疗后均恢复到正常范围，ＢＲＭＳ和ＨＡＭＤ评分也随之明显下降。结论提示某些情感性精神障碍患者的甲状腺激素改变与症状的消长有关，甲状腺素异常是继发于情绪障碍，这种类型可能是情感性精神障碍的具有某种生物学异常的一个亚型。     

双相情感性精神障碍与精神分裂症脑CT扫描比较

为了比较双相情感性精神障碍、精神分裂症病人脑结构的变化，收集符合国际疾病分类第１０版和中国精神疾病分类方案与诊断标准第２版修订本的双相情感性精神障碍病人２７例，以及精神分裂症病人２５例，应用脑ＣＴ定量分析脑室、脑沟。结果显示，双相情感性精神障碍和精神分裂症病人前角指数、第三脑室最大宽度、乳突间比值和脑萎缩差异均无显著性（Ｐ＞０．０５）。提示精神分裂症和双相情感性精神障碍这些所谓的功能性疾病可能和非特异性脑室、脑沟结构异常相关。     

Mode of inheritance in families of patients with lithium-responsive affective disorders

A better understanding of the role of genetic factors in affective disorders is likely to result from investigating more homogeneous populations. To achieve this goal, we have systematically studied patients who are excellent responders to long-term lithium treatment and their relatives. In the families of 71 such probands, we have analyzed the mode of inheritance by comparing the observed morbidity risks with the risks expected under different genetic models. The results demonstrate major-gene effects in the transmission of primary affective disorders; the polygenic model with sex-specific thresholds could be rejected. Discrimination between the autosomal and X-chromosome models was not possible, but the autosomal recessive model predicts more realistic, gender-specific frequencies of affective disorders in the general population. These results suggest that autosomal recessive inheritance deserves serious consideration in molecular genetic investigations.     

Novel animal models of affective disorders

Is there an appropriate animal model for human affective disorders? The traditional difficulties in accepting animal models for psychopathology stem from the argument that there is no evidence for concluding that what occurs in the brain of the animal is equivalent to what occurs in the brain of a human. However, if one models any or some core aspects of affective disorder, this model can become an invaluable tool in the analysis of the multitude of causes, genetic, environmental, or pharmacological, that can bring about symptoms homologous to those of patients with affective disorders. Animal models can also allow the study of the mechanisms of specific behaviors, their pathophysiology, and can aid in developing and predicting therapeutic responses to pharmacologic agents. Although animals exhibit complex and varied social and emotional behaviors for which well-validated and standardized measures exist, an understanding that a precise replica of human affective disorders cannot be expected in a single animal model is crucial. Instead, a good animal model of a human disorder should fulfill as many of the four main criteria as possible: (1) strong behavioral similarities, (2) common cause, (3) similar pathophysiology, and (4) common treatment. An animal model fulfilling any or most of these criteria can be used to elucidate the mechanisms of the specific aspect of the model that is homologous to the human disorder. A wide range of animal models of affective disorders, primarily depression, has been developed to date. They include models in which "depressive behavior" is the result of genetic selection or manipulation, environmental stressors during development or in adulthood, or pharmacologic treatments. The assessment of these animal models is based either on behavioral tests measuring traits that are homologous to symptoms of the human disorder they model, or behavioral tests responsive to appropriate pharmacologic treatments. The goal of this review is to focus on relatively recent developments of selected models, to aid in understanding their strengths and weaknesses, and to help those choosing the difficult task of developing novel animal models of affective disorders. The ideal animal model of affective disorders of the future would be an endogenous, genetic model that reiterates the essential, core aspects of the human disease and responds to the standard regimens of therapy. Because complex diseases have been approached from the genetic startpoint by using rodent models, a genetic model of affective disorder would open up possibilities for genetic analysis of polygenic traits that seem to underlie these disorders.     

重症肌无力的遗传学调查

对５９７９４４人进行重症肌无力（ＭＧ）流行病学调查，确诊ＭＧ６０例，ＭＧ患病率为１０／１０万。遗传学调查５５个家系，共有一级亲属３７４人，同胞患者２人，一级亲属患病率０．５３％，Ｐ＜０．００１；遗传度为５８％。提示ＭＧ与遗传有关，不符合单基因遗传模式，可能为多基因遗传。     

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.     

Genetic models of the transmission of affective disorders

Multiple threshold models of inheritance of liability to semi-continuous traits are applied to data on affective and related disorders in relatives of 70 patients with bipolar or unipolar affective disorder, relatives of 75 normal controls, and population prevalence data. Unipolar and bipolar affective disorders and related affective disturbances are represented in the model at different thresholds on a single continuum of genetic-environmental liability. Neither a multifactorial inheritance or single major locus inheritance can be ruled out as a mode of transmission. The heritability of affective disorders appears to be greater than 0·.     

高发精神分裂症的遗传方式探讨

目的 探讨高发精神分裂症的遗传方式。方法 采用分离分析和多基因阈值理论分析方法对56例高发家系进行探讨。结果 高发精神分裂症的遗传方式既不符合常染色体单基因显性和隐性遗传，也不符合连锁遗传，而符合一个显性主基因的多基因遗传。结论 精神分裂症是一种多基因遗传疾病。     

Multiple sclerosis and affective disorder. Family history, sex, and HLA-DR antigens

To investigate a possible genetic cause underlying the clinical association between multiple sclerosis (MS) and affective disorder, we studied 56 patients with MS for psychiatric and genetic (family history, sex, and HLA-DR) characteristics. The 2:1 ratio of females to males expected for patients with MS was observed in this sample (40:16), but the excess of females occurred entirely among the 31 MS patients with major affective disorder (27 females and four males). Bipolar probands with MS had significantly more relatives with affective disorder or MS than did unipolar probands with MS. The HLA-DR antigen frequencies in patients with MS categorized by type and family history of affective disorder suggest that it may be possible to validate such clustering of patients. We concluded that sex and other genetic factors are related to the affective symptoms in MS and emphasize the importance of psychiatric evaluation of these patients.     

Inhibition of the regenerative growth of central noradrenergic neurons by intracerebrally administered anti-NGF serum

Serial coronal or sagittal sections were stained for myelin and examined in 6 inbred, 4 hybrid, and 2 outbred mouse strains. Absent corpus callosum was seen only in BALB/cJ as reported by Wimer, but a wide range of the size of corpus callosum was also noted. The action of a major gene was not evident in backcross or F2 generations; polygenic and perhaps epistatic inheritance was indicated. In A/J, and to a lesser extent A/HeJ and BALB/cJ, the columns of fornix frequently collided with the anterior commissure and either passed around it to make a normal termination or deflected dorsally to make an abnormal termination in lateral septum. In some BALB/cJ brains the anterior commissure instead was displaced and passed behind or through the columns of fornix. Backcross and F2 data suggested inheritance was polygenic and that genetic variation affected the spatio-temporal coordination of ontogeny of the two tracts. Finally, unusual longitudinal bundles were detected in the septal region of BALB/cJ. Results of crosses were consistent with the hypothesis that a single, incompletely dominant gene was acting, but further study of both the anatomy and heredity of the defect was deemed necessary.     

Familial association of schizotypal traits with psychotic and affective disorders

The criteria for schizotypal personality disorder were developed on the basis of traits observed in biologic relatives of schizophrenic and borderline schizophrenic probands from the Danish adoption studies. In this review, the relationship between schizotypal personality disorder and the schizophrenic spectrum, affective disorders, and psychotic disorders is explored. A dimension of psychosis may overlap with the schizophrenia spectrum to yield chronic schizophrenia, with the affective disorders spectrum to yield psychotic affective disorder, or by itself lead to other psychotic disorders. Schizotypal personality disorder in this model is posited to represent schizophrenia spectrum disorder that does not overlap with psychosis, whereas nonpsychotic affective disorders represent the affective disorders that do not overlap with psychosis. Delusional disorder represents another psychotic disorder that is not specifically related to either schizophrenia or the affective disorders. Evidence suggests that the schizotypal personality disorder criteria, particularly those emphasizing the negative symptoms or deficit-like symptoms of this disorder, specifically identify a unique relationship to the schizophrenia spectrum.     

Comorbid bipolar disorder and panic disorder in families with a high prevalence of bipolar disorder.

OBJECTIVE: Panic attacks are a common complication of affective disorder, although the etiologic relationship of panic and affective symptoms has not been determined. Evidence from a family study suggests that panic attacks and panic disorder may be related genetically to bipolar disorder. This study used diagnostic data from the NIMH Bipolar Disorder Genetics Initiative to assess in a separate, larger family set the familiality of panic combined with bipolar disorder. METHOD: First-degree relatives (N=966) of probands with bipolar I disorder (N=192) and schizoaffective disorder, bipolar type, (N=11) were included in the study. All subjects were interviewed directly and were assigned best-estimate diagnoses for major affective and other psychiatric disorders. The risk of a family member being diagnosed with panic disorder if the proband with bipolar disorder had panic attacks or panic disorder was calculated with logistic regression analysis with generalized estimating equations that controlled for sex and affective disorder subdiagnosis. RESULTS: More than 90% of the probands and first-degree relatives with panic disorder also had an affective disorder diagnosis. Panic disorder was present in 17% of the relatives with recurrent major affective disorder and in 3% of the relatives without recurrent major affective disorder. Risk of panic disorder in relatives with bipolar disorder was increased significantly if the proband had panic attacks or panic disorder. CONCLUSIONS: Risk for panic disorder with familial bipolar disorder appears to be inherited. Inherited risk for panic disorder with bipolar disorder may indicate a shared genetic etiology for both disorders in some families. The patterns of bipolar disorder and panic disorder comorbidity observed in families imply a complex genetic etiology, which may be elucidated by using endophenotypes.