难治性强迫症与非难治性强迫症临床特征比较

目的 比较难治性强迫症与非难治性强迫症的临床特征之间的差异.方法 分别用YBOCS量表评估51例难治性强迫症和59例非难治性强迫症患者的强迫症状,并比较两组临床症状特征的差异.结果 难治性强迫症组中的强迫思维分(11.18±3.07)、强迫行为分(7.35±4.92)及强迫总分(18.53±6.09)均显著性高于非难治性强迫症组(8.12±4.01,4.59±4.67,12.63±5.67;P＜0.05).难治性强迫症与非难治性强迫症两组中有无伴发其他精神症状(x2=0.016,P=0.899)、有无阳性家族史(x2=0.053,P=0.818)、发病年龄(20.29±8.72,20.56±8.00; t=0.113,P=0.911)及病程(7.56±3.23,8.56±3.52;t=0.486,P=0.629)无明显差异(P＞0.05).结论 难治性强迫症的临床症状严重程度(特别是强迫思维)显著性高于非难治性强迫症.     

成人与儿童强迫症的临床特征对照分析

目的：为了解儿童强迫症与成人强迫症临床现象的差异，旨在探讨儿童强迫症的临床特征。方法：本组强迫症病人共107例，按年龄分为儿童组和成人组，采用自行设计的调查收集资料，并进行回顾性对照分析。结果：两组在强迫性穷思竭虑，强迫意向，强迫情绪，强迫性仪式动作及单纯强迫行为出现频率上有显著差异。儿童组伴随焦虑、抑郁症状者较成人组发生率低，而伴随一过性精神病性症状，抽动障碍者较成人组发生率高。儿童组自知力丧失，且缺乏反强迫意识者较多见。结论：儿童强迫症的强迫症状不典型，易误诊。     

１８例带强迫症状的精神分裂症的临床分析

强迫症状包括强迫观念、强迫情绪和强迫动作。强迫症状可见于神经症、精神分裂症、癫痫等疾病。为了了解强迫症状与精神分裂症的关系，作对２０００年８月－２００２年３月在我院门诊求治的１８例带强迫症状的精神分裂症患的症状、治疗情况及愈后作了观察、比较。     

再谈强迫症和抑郁症的治疗问题

自从今年4月上海精神医学（第19卷第2期）刊出我的一篇“有关强迫症的几个问题”以后,有好几位病家拿了杂志复印件来找我咨询。我认为这几个病例很值得临床医生参考,所以介绍如下：     

强迫症患者的症状群分型及其临床特征

强迫症是异质性的障碍,有研究试图划分临床亚型来降低异质性,如早发性强迫症~([1])、强迫症伴自知力不全~([2]),还有依据症状群划分亚型~([3]).源于耶鲁-布朗强迫症状检查提纲(Y-BOCS-SC)的症状群分型得到广泛研究,并且结果较为一致~([3]).     

强迫症的家庭特征

本文综述了家庭因素在强迫症起病与发展中的作用。     

血管性抑郁症的临床特征及治疗

本介绍血管性抑郁症的概况、临床特征及治疗原则,强调临床医生应重视这组特殊抑郁症。     

强迫症的研究进展

本介绍了近几年强迫症的流行学，病因，发病机制，临床和治疗方面的进展。     

儿童精神分裂症强迫症状的临床特征研究

目的　了解儿童精神分裂症强迫症状的临床特征。方法　采用自编的调查表 ,对 110例住院精神分裂症患者 (年龄≤ 15岁 )的病案资料进行分析。根据有无强迫症状 ,分为两组 ,即研究组 (有强迫症状 )和对照组 (无强迫症状 )。结果　 (1)强迫症状的发生率为 2 2 .73% (2 5 / 110 ) ;(2 )强迫观念主要见于 13～ 15岁儿童 ,强迫动作主要见于 8～ 12岁儿童 ;(3)研究组和对照组在住院天数、住院次数以及疗效方面差异均有显著性 (P <0 .0 1或P <0 .0 5 )。结论　强迫症状可能出现于儿童精神分裂症的各个时期 ,表明它是精神分裂症的一个组成部分 ,并且与精神分裂症的预后有关     

强迫障碍的临床表现和同病研究

目的：研究强迫障碍的现象学和病程。方法：对同时符合ＣＣＭＤ－２Ｒ及ＤＳＭ－Ⅲ强迫障碍诊断标准的患者进行动态ＡＤＩＳ－Ｐ,简明精神病评定量表（ＢＰＲＳ）,汉密尔顿焦虑量表（ＨＡＭＡ）,同的阳性精神障碍家族史,起病早,就诊迟,Ｂｅａｒ分别中Ⅱ型（污染／检查型）最多,同经高。治疗上均用氯丙咪嗪或ＳＳＲＩｓ联用或不联用其它精神药物。似以药物加心理治疗效果较好。结论：强迫障碍的现象学表现较为复杂,应引起重视     

Sleep in obsessive compulsive disorder

Several lines of evidence suggest that brain serotonergic systems may be disturbed in obsessive compulsive disorder (OCD). The serotonergic system strongly affects sleep and characteristic abnormalities of sleep are documented in depression. This study, therefore, aimed to investigate sleep structure of OCD patients in order to evaluate whether similar changes as in depression are present. Up to now, this issue has been addressed only in few studies with small numbers of patients. Sleep patterns of 62 unmedicated patients with primary OCD and 62 age- and sex-matched healthy controls were investigated by polysomnography. Additionally, the impact of tryptophan depletion on sleep was studied in a subgroup of 12 OCD patients and 12 controls. The OCD patients exhibited moderate, but significant disturbances of sleep continuity measures but no abnormalities of slow wave sleep or REM sleep, except a significant elevation of 1st REM density. Tryptophan depletion induced a worsening of sleep continuity, but no changes of REM sleep or slow wave sleep. Assuming that changes of sleep architecture indicate underlying neurobiological abnormalities, this study indicates that neurobiological disturbances are different in primary OCD as compared with primary depression.     

Neurobiology of obsessive compulsive disorder.

In this brief review of two of the neurobiologic aspects of OCD, two simplistic models have been suggested. Although these models reflect different perspectives, they may not be independent. For instance, the striatum, which is a focus for the neuroanatomic model, receives a dense serotonergic projection from the dorsal raphé. Similarly, as mentioned previously, combining PET studies and drug treatment demonstrates that the increased metabolic activity seen in the orbital cortex appears to normalize with serotonin uptake inhibitor treatment. Insights into the neurobiology of this syndrome will require combining perspectives as well as developing additional approaches. In addition, the search for neurobiologic abnormalities must be guided by a continuing regard for phenomenology. There is no reason, a priori, to assume that this syndrome subsumes only one disorder. The careful dissection of subgroups--whether based on symptom type, character style, or comorbid diagnoses--will be increasingly vital for understanding the results of neuropharmacologic and functional imaging studies.     

The epidemiology of obsessive compulsive disorder

The literature on the epidemiology and genetics of obsessive compulsive disorder (OCD) is reviewed. The application of recently developed diagnostic criteria, psychometric testing, and biologic markers to epidemiologic studies of OCD should provide important new data for increasing our understanding of the pathogenesis of the disorder. Identification of diagnostic subgroups will be important in reliably evaluating treatment response to current and new therapeutic agents. Directions for potential research in these areas are discussed.     

Treatment duration of obsessive compulsive disorder

The first breakthrough in the treatment of obsessive-compulsive disorder (OCD) came in 1967, when Fernandez and Lopez-Ibor reported on the efficacy of clomipramine (CMI) in the treatment of 16 patients with OCD (Fernandez and Lopez-Ibor, 1967). However, controlled studies with CMI were not published until 1980 (Montgomery, 1980; Thoren et al, 1980), and only in the last 5 years have large well-controlled studies been published (Clomipramine Collaborative Study, 1991). Several studies demonstrated that among the tricyclics (TCA), only CMI is effective in OCD, while effective antidepressants with a noradrenergic profile, such as desipramine (DMI), appear to be totally ineffective (Zohar and Insel, 1987; Goodman et al, 1990; Leonard et al, 1989). This selective response to TCA with a serotonergic profile led to the formulation of the serotonergic hypothesis of OCD and to the development and use of other serotonergic agents in the treatment of this disorder. Several drugs, possessing a serotonergic profile are currently being studied worldwide, among them CMI, fluoxetine, fluvoxamine, sertraline, paroxetine and citalopram. Currently, as the knowledge regarding the pharmacological approach to OCD is only beginning to accumulate, very little is known regarding treatment duration in OCD. In this review we shall attempt to examine the existing data regarding treatment duration in OCD.     

Tricyclic response in obsessive compulsive disorder

Therapeutic responses to the tricyclic antidepressant clomipramine have been demonstrated in five double blind studies of patients with obsessive compulsive disorder. Biological alterations in patients with obsessive compulsive disorder resemble those of depressed patients for the dexamethasone suppression test, for some measures of sleep physiology, and in similar neuroendocrine responses to clonidine. Clomipramine's antiobsessional effect does not require high baseline depression ratings or biological abnormalities similar to those seen in depressives. Preliminary results suggest that in contrast to depressives, patients with obsessive compulsive disorder may respond to clomipramine but not to the tricyclic antidepressant desipramine.     

Social adjustment in obsessive compulsive disorder

The Social Adjustment Scale-Self Report was administered to 32 subjects with Obsessive Compulsive Disorder and age-sex matched controls. The patients had global impairment, especially during leisure, which correlated with severity of the disorder. The improvement of this impairment with therapy is highlighted. It is stressed that social adjustment in Obsessive Compulsive Disorder subjects should be considered during their therapy.