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1.
奥氮平合用氯米帕明治疗强迫症对照观察   总被引:1,自引:1,他引:0  
目的:观察奥氮平合用氯米帕明治疗强迫症的疗效与不良反应。方法:将43例强迫症患者随机分为两组,以奥氮平合用氯米帕明及单用氯米帕明治疗,以强迫症量表(Y-BOCS)和副反应量表(TESS)评定疗效与不良反应。结果:奥氮平合用氯米帕明组显效率高于单用组,8周末Y-BOCS评分低于单用组;合用组体重增加数高于单用组。结论:奥氮平合并氯米帕明治疗强迫症安全有效。  相似文献   

2.
目的了解国产奥氮平合并氯丙咪嗪治疗伴强迫症状的分裂症的疗效和副反应。方法对伴强迫症状的分裂症随机分为研究组和对照组,研究组用奥氮平合并氯丙咪嗪,对照组单用奥氮平,治疗周期均为8周。用PANSS、Y—BOCS评定疗效,TESS评定副反应。结果治疗8周末两组PANSS总分和各因子分与治疗前比较均明显下降(P〈0.01),且两组治疗2、4、8周末PANSS总分及其因子分的减分率差异无显著性(P〉0.05),但Y—BOCS总分和其因子分减分率研究组显著高于对照组(P〈0.01)。两组治疗后分裂症症状有效率、显效率、痊愈率比较差异无显著性(P〉0.05),但强迫症状有效率、显效率、痊愈率差异有显著性(P〈0.01)。研究组治疗后TESS总分较对照组高(P〈0.05)。结论奥氮平合并氯丙咪嗪治疗伴强迫症状的分裂症疗效肯定,副反应能够耐受,可作为治疗伴强迫症状分裂症的一个较好选择。  相似文献   

3.
目的探讨利培酮辅助治疗强迫症的临床疗效和安全性。方法对43例强迫症患者,在服用原抗抑郁药的基础上随机分为合用组和对照组,分别给予合用利培酮和安慰剂,共治疗12周。采用Yale—Brown强迫症量表(Y—BOCS)、Marks恐怖强迫量表(MSCPOR)和不良反应量表(TESS)评定疗效和不良反应。结果合用组Y—BOCS及MSCPOR评分治疗前后比较有显著性差异,对照组则无显著性差异;治疗后两组Y—BOCS及MSCPOR评分比较亦有显著差异。两组TESS评分相近。结论合用利培酮治疗强迫症有一定的辅助作用,不增加不良反应。  相似文献   

4.
目的:研究氟伏沙明联合奥氮平对难治性强迫症的疗效。方法:对难治性强迫症患者75例,随机分为两组,分别为氟伏沙明单用组和联合奥氮平治疗组,治疗8周。采用Yale-Brown强迫症量表(Y-BOCS)、汉密尔顿抑郁量表(HAMD)和治疗中出现的症状量表(TESS)评价疗效和不良反应。结果:氟伏沙明联合奥氮平治疗难治性强迫症的疗效显著,不良反应少。结论:两药联合应用治疗难治性强迫症的疗效显著,值得推广。  相似文献   

5.
目的:评价米氮平治疗强迫症的疗效和不良反应.方法:42例强迫症患者随机分为两组,分别予米氮平和安慰剂治疗,疗程8周.用强迫症量表(Y-B0CS)、Marks恐怖强迫量表(MSCPOR)、汉密尔顿抑郁量表(HAMD)评价其疗效,副反应量表(TESS)评价不良反应.结果:米氮平组显效率61.9%,明显优于安慰剂组,不良反应少而轻.结论:米氮平可作为一种安全而有效的抗强迫症药物.  相似文献   

6.
奥氮平对难治性抑郁症的辅助治疗作用   总被引:11,自引:2,他引:9  
目的了解抗抑郁药合并奥氮平治疗难治性抑郁症的疗效和安全性。方法32例符合CCMD-3抑郁症诊断标准且临床判断属于难治性患者,在原抗抑郁剂不变的基础上合并奥氮平治疗,疗程4周,分别在治疗前及治疗后进行汉密顿抑郁量表(HAMD)、汉密顿焦虑量表(HAMA)评定疗效,并用副反应量表(TESS)观察不良反应。结果治疗1周末时,HAMD减分率显示临床痊愈或显著有效率者6.3%(2例),进步率34.4%(11例);4周末时,总有效率75%,显著效率为53.1%(17例)。副反应较轻。结论对于抗抑郁药治疗反应不佳的难治性抑郁症合并奥氮平可提高疗效。  相似文献   

7.
目的探讨奥氮平治疗精神分裂症的疗效及不良反应。方法将213例精神分裂症患者随机分为研究组(奥氮平治疗)和对照组(氯丙嗪治疗),共治疗8周,治疗前后应用简明精神病评定量表(BPRS)、住院患者观察量表(NOSIE)和副反应量表(TESS)分别评定疗效及不良反应。结果在治疗后的第2周末、第8周末,研究组的BPRS各因子分及总分均低于对照组,差异具有显著性意义(P〈0.05)。在治疗后的第2周末、第8周末,研究组的NOSIE的社会功能、个人整洁、总积极因素因子分及病情总估计分均高于对照组,抑郁、迟缓及总消极因素因子分均低于对照组,差异均具有显著性意义(P〈0.05)。奥氮平组的不良反应少于氯丙嗪组。结论奥氮平可有效改善精神分裂症患者的精神病症状和社会功能。  相似文献   

8.
米氮平治疗强迫症对照研究   总被引:1,自引:0,他引:1  
目的:比较米氮平与氟西汀治疗强迫症的疗效和不良反应.方法:分别用米氮平和氟西汀治疗强迫症各27例,疗程8周.应用Yale-Brown强迫症量表(Y-BOCS)、汉密尔顿抑郁量表(HAMD)及汉密尔顿焦虑量表(HAMA)评定疗效.结果:治疗后米氮平组与氟西汀组Y-BOCS、HAMD、HAMA分值均显著下降,两组间疗效差异无显著性.米氮平组不良反应明显少于氟西汀组.结论:米氮平治疗强迫症疗效与氟西汀相仿,不良反应少,可在临床使用.  相似文献   

9.
奥氮平与氯氮平治疗精神分裂症对照研究   总被引:5,自引:3,他引:2  
以奥氮平与氯氮平治疗精神分裂症对照,报告如下。  相似文献   

10.
11.
BACKGROUND: One of the few combination approaches to the treatment of obsessive-compulsive disorder (OCD) with encouraging support is the addition of an antipsychotic to a serotonin reuptake inhibitor. METHODS: The study consisted of a 6-week, placebo-controlled addition of olanzapine 5-10 mg (6.1 +/- 2.1 mg, mean +/- SD) to fluoxetine in OCD subjects who were partial or nonresponders to an 8-week, open-label fluoxetine trial (40 mg in 43 subjects, 20 mg in 1 subject). RESULTS: Both the fluoxetine-plus-olanzapine (n = 22) and fluoxetine-plus-placebo (n = 22) groups improved significantly over 6 weeks [F(3,113) = 11.64, p <.0001] according to Yale-Brown Obsessive Compulsive Scale scores with repeated-measures analysis of variance; however, the treatment x time interaction was not significant for olanzapine versus placebo addition to fluoxetine. CONCLUSIONS: These findings indicate no additional advantage of adding olanzapine for 6 weeks in OCD patients who have not had a satisfactory response to fluoxetine for 8 weeks, compared with extending the monotherapy trial.  相似文献   

12.
目的:研究强迫型人格障碍(OCPD)在强迫障碍(OCD)中的共病情况,并研究OCD共病OCPD对OCD影响。方法:以69例门诊OCD患者为研究对象,采用DSM-Ⅳ轴Ⅱ障碍用临床定式检查(SCID-Ⅱ)研究强迫障碍患者的共病人格障碍(PD)情况,将研究对象分为2组:OCD共病OCPD组和OCD不共病OCPD组,对比研究2组间临床特征的不同。结果:79.7%强迫障碍患者合并有PD,C类中的OCPD和OCD共病率达43.5%。共病组较不共病组疾病严重程度更重,表现为发病年龄早、病程更长、强迫思维更严重。结论:OCPD和OCD关系密切,OCD共病OCPD是OCD严重程度的一个标志。  相似文献   

13.
目的:探讨奎硫平辅助治疗强迫症的临床疗效和安全性。方法:对48例强迫症患者,在服用原抗抑郁药的基础上随机分为奎硫平组和安慰剂组,分别给予合用奎硫平和安慰剂。疗程12周。采用Yale-Brown强迫症量表(Y-BOCS)和治疗中出现的症状量表(TESS)评定疗效和不良反应。结果:奎硫平组Y-BOCS评分治疗后有显著下降,安慰剂组则无差异;治疗后Y-BOCS评分以奎硫平组显著较低。两组TESS评分相仿。结论:抗抑郁药合用奎硫平治疗强迫症有一定辅助作用。  相似文献   

14.

概述

在双相障碍患者中强迫症状是常见的。因为双相障碍和强迫症的共病状态会令这两种障碍的临床治疗复杂化,所以确定这些共病的患者是很重要的。我们讨论了强迫症和双相障碍的共病,介绍了可能导致这种常见共病状态的发病机制,也讨论了该领域最新的研究进展,并提出一些管理这些患者的临床原则。

中文全文

本文全文中文版从2015年10月26日起在http://dx.doi.org/10.11919/j.issn.1002-0829.215009可供免费阅览下载 Previous studies have documented high rates of comorbidity of other psychiatric conditions among individuals with bipolar disorders (BD).[1] One study estimated that obsessive-compulsive disorders (OCD) accounted for 21% of all comorbidities in BD.[2] There is continuing debate about whether (a) these are two independent conditions that can co-occur or (b) OCD is a specific subtype of BD. Regardless of the interrelationship of the two conditions, the comorbid occurrence of these two types of symptoms can cause a clinical dilemma because selective serotonin reuptake inhibitors (SSRIs)-which are quite commonly used to treat OCD-increases the risk of precipitating manic symptoms.[3,4,5,6] The OCD symptoms that occur in individuals with BD often occur during the depressive episodes or during the intervals between episodes of depressive or manic symptoms.[7,8] This timing of OCD symptoms during BD is consistent with the cyclic nature of BD and suggests shared biological mechanisms between the two disorders. In support of this hypothesis, a study using Positron Emission Tomography (PET) found that in untreated persons with BD the serotonin-transporter binding potential in the insular and dorsal cingulate cortex was higher among BD patients with pathological obsessions and compulsions than among BD patients without such symptoms.[9] Moreover, a linkage study found that compared to OCD patients without comorbid BD, patients with comorbid OCD and BD were more likely to have a family history of mood disorders but less likely to have a family history of OCD.[10] However, another study found no significant difference in the rates of a positive family history of OCD between patients with OCD alone and those with comorbid OCD and BD.[11] Further support for the hypothesized common etiology comes from a preliminary molecular genetic study which found that hyperpolarization activated cyclic nucleotide-gated channel 4 (HCN4) is a common susceptible locus for both mood disorders and OCD, but further studies with larger sample sizes are needed to replicate this finding.[12] The presence of OCD in BD complicates the clinical presentation. Compared to patients with BD without comorbid OCD, those that have comorbid BD and OCD often have a more severe form of BD, have more prolonged episodes, are less adherent to medication, and are less responsive to medication. Recent studies about comorbid BD and OCD have reported the following: (a) Temporal relationship. Some studies suggest that OCD is an antecedent of BD,[10] but others report concurrent onset of OCD and BD.[13,14] (b) Course of disease. In 44% of patients with comorbid BD and OCD the episodes are cyclic.[15] The course of disease is more chronic among BD patients with OCD compared to those without comorbid OCD.[16,17] OCD is more commonly observed in patients with Type II BD, among whom the prevalence of OCD has been reported to be as high as 75%.[18] (c) Compulsive behaviors. The most commonly reported compulsions among patients with comorbid OCD and BD are compulsive sorting,[14,19,20,21] controlling or checking, [20] repeating behaviors,[13,22] excessive washing,[20] and counting.[19] Obsessive reassurance-seeking is also commonly reported in these patients.[23] In children and adolescents with BD, compulsive hoarding, impulsiveness,[24] and sorting[25] are more common. (d) Substance and alcohol abuse. A study found a higher prevalence of sedative, nicotine, alcohol, and caffeine use among individuals with comorbid OCD and BD compared to those with BD without OCD.[14] Similarly, compared to OCD patients without comorbid mood disorders, those with a comorbid mood disorder were more likely to have a substance abuse diagnosis (OR=3.18, 95%CI=1.81-5.58) or alcohol abuse diagnosis (OR=2.21, 95%CI=1.34-3.65).[11,13,26,27,28] (e) Suicidal behaviors. Compared to BD patients without OCD, a greater proportion of patients with both disorders had a lifetime history of suicidal ideation and suicide attempts.[2,11,13,29,30] The clinical management of comorbid OCD and BD requires first focusing on stabilizing the patient’s mood, which requires the combined use of multiple medications such as the use of lithium with anticonvulsants or atypical antipsychotic medications such as quetiapine;[31,32,33] adjunctive treatment with aripiprazole may be effective for the comorbid OCD symptoms.[4] In the case of OCD comorbid with type II BD, after full treatment of the mood symptoms with mood stabilizers the clinician can, while monitoring for potential drug interactions, cautiously try adjunctive treatment with antidepressants that are effective for both depressive symptoms and OCD symptoms and that have a low risk of inducing a full manic episode, including the selective serotonin reuptake inhibitors (SSRIs): fluoxetine, fluvoxamine, paroxetine, and sertraline.[32,35] In summary, BD comorbid with OCD may be etiologically distinct from either of the disorders. Clinicians should pay attention to its complex clinical manifestations and carefully consider the treatment principles outlined above.  相似文献   

15.
ABSTRACT– Six patients with Obsessive-Compulsive Disorder (DSM III) were treated in an open uncontrolled trial with Zimeldine, for 8 weeks. All six patients had cognitive deficits before treatment. Five patients improved on the clinical symptoms. Four of these showed pronounced amelioration of their cognitive deficits.  相似文献   

16.
We report a longitudinal study of 26 patients with medically intractable obsessive-compulsive disorder (OCD) who were treated with psychosurgery and had a comprehensive follow-up for a mean 10 years. Seventeen patients had combined orbitomedial and cingulate lesions, 6 cingulate lesions only and 3 orbitomedial lesions only. Eighteen patients were interviewed personally and lesions verified on magnetic resonance imaging scans in fourteen. On a 6-point global rating scale, 10 (38%) patients had obvious improvement, another 6 (23%) showed mild improvement of doubtful clinical value, and the remaining 10 showed either no change (n= 6; 23%) or were judged to be worse (n= 4; 15%). Both obsessive and compulsive symptoms improved, and this change was independent of the changes in anxiety and depression scores. No significant predictors of improvement were identified. Patients with cingulate lesions only fared worse. Eight patients who had a second operation did not show much improvement. A comparison of a subgroup of patients with 10 matched nonsurgical OCD controls supported the contention that the improvement in OCD was attributable to the psychosurgery. Important adverse effects in the stereotactic surgery group (n= 20) were epilepsy (1 patient) and personality change (2 patients). The psychosurgery group performed relatively poorly on the Wisconsin Card Sort Test but did not show any deterioration in Wechsler Intelligence and Memory scores.  相似文献   

17.
西酞普兰与氯米帕明治疗强迫症对照研究   总被引:4,自引:0,他引:4  
目的:比较西酞普兰与氯米帕明治疗强迫症的疗效和不良反应。方法:以西酞普兰和氯米帕明治疗强迫症各30例,疗程8周。应用Yale—Brown强迫症量表(Y—BOCS)、汉密尔顿抑郁量表(HAUD)及汉密尔顿焦虑量表(HAMA)评定疗效。结果:西酞普兰组与氯米帕明组治疗后Y-BOCS、HAMD、HAMA分值均显著下降,两组间差异无显著性。西酞普兰组不良反应明显少于氯米帕明组。结论:西酞普兰治疗强迫症疗效与氯米帕明相仿,不良反应较轻,值得推广。  相似文献   

18.
利培酮合并帕罗西汀治疗强迫症疗效分析   总被引:2,自引:3,他引:2  
目的:探讨利培酮合并帕罗西汀治疗强迫症的疗效。方法:40例强迫症患者随机分为利培酮合并帕罗西汀组和帕罗西汀组,治疗8周。采用强迫症量表(Y-BOCS)、汉密尔顿焦虑量表(HAMA)、汉密尔顿抑郁量表(HAMD)评定疗效。结果:治疗结束时两组Y-BOCs、HAMA、HAMD的评分均显著降低,更以合用利培酮组明显。结论:利培酮合并帕罗西汀治疗强迫症可以增加疗效。  相似文献   

19.
目的:比较难治性与非难治性强迫症患者生活质量差异。方法:采用汤旦林(TDL)生活质量量表评估51例难治性强迫症患者和59例非难治性强迫症患者的生活质量。结果:难治性强迫症的社会方面、尽职的能力、自我健康较非难治性强迫症差(t=2.230,P<0.05;t=2.328,P<0.05;t=2.177,P<0.05),而两组身体方面、心理方面及TDL量表总分差异均无统计学意义(t=0.937,P>0.05;t=0.917,P>0.05;t=1.649,P>0.05)。结论:难治性强迫症患者生活质量较非难治性强迫症差。  相似文献   

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