帕罗西汀联合奥氮平治疗躯体形式障碍的疗效观察

目的探讨帕罗西汀联合奥氮平对躯体形式障碍的疗效。方法将167例躯体形式障碍患者随机分为研究组和对照组,研究组即帕罗西汀联合奥氮平组,对照组为单用帕罗西汀组,治疗前后应用抑郁自评量表(SDS)和副反应量表(TESS)分别评定疗效及不良反应。结果治疗第2周末,研究组SDS评分较治疗前有显著性降低(P<0.05),而对照组无显著性变化。治疗第4周末及第8周末,两组SDS评分较治疗前均有显著性降低(P<0.05)。在第2周末及第4周末,研究组和对照组的治疗有效率有显著性差异(P<0.05)。两组均未出现严重不良反应。结论帕罗西汀联合奥氮平治疗躯体形式障碍较单用帕罗西汀,具有疗效好,起效快,不良反应少的优点。     

高频重复经颅磁刺激联合帕罗西汀治疗创伤后应激障碍的疗效

目的 观察高频重复经颅磁刺激（rTMS）对创伤后应激障碍（PTSD）的辅助疗效.方法 将60例创伤后应激障碍患者随机分为联合组及对照组,联合组采用帕罗西汀治疗,配合右侧前额叶背外侧部、10Hz高频rTMS.对照组采用帕罗西汀治疗及假性重复经颅磁刺激治疗.两组患者均治疗4周,并进行基线、治疗后创伤后应激障碍检查表（PCL）及汉密尔顿抑郁测评量表（HAMD）、汉密尔顿焦虑测评量表（HAMA）评定.结果 57例患者完成研究,两组患者治疗后PCL总分及重现、回避、警觉性增高因子分、HAMD、HAMA评分均较治疗前降低,差异有统计学意义（P＜0.05）;联合组治疗4周末PCL测评总分、重现、警觉性增高因子、HAMA治疗前后评分差均较对照组高,差异有统计学意义（P＜0.05）.结论 帕罗西汀能够改善PTSD的核心症状及抑郁、焦虑症状;在帕罗西汀治疗基础上,10 Hz重复经颅磁刺激能够增加对PTSD的重现、警觉性增高等核心症状及焦虑症状的疗效.     

心理行为干预联合帕罗西汀治疗惊恐障碍患者的临床疗效

目的:观察心理行为干预联合帕罗西汀对惊恐障碍的治疗效果。方法:60例住院惊恐障碍患者随机分为,研究组和对照组各30例。研究组给予心理行为干预联合帕罗西汀治疗,对照组单用帕罗西汀治疗。观察12周。采用汉密尔顿焦虑量表(HAMA)、临床疗效总评量表-病情严重程度(CGI-SI)在治疗前及治疗2、4、8和12周评定疗效;以治疗中出现的症状量表(TESS)评定不良反应。结果:两组治疗后HAMA及CGI-SI评分较治疗前均显著降低(P<0.05),两组比较,研究组下降更为明显(P<0.05)。结论:心理行为干预联合帕罗西汀治疗惊恐障碍效果优于单用帕罗西汀治疗。     

脑卒中后情感障碍的心理干预及帕罗西汀治疗的临床研究

目的 探讨脑卒中后情感障碍的发生率、脑卒中部位与情感障碍的关系,以及口服帕罗西汀合并早期心理干预对脑卒中后情感障碍患者日常生活能力和神经功能康复的影响.方法 采用抑郁自评量表(SDS)、焦虑自评量表(SAS)对181例脑卒中患者进行筛查,对脑卒中后同时出现抑郁和焦虑的54例患者随机分成治疗组和对照组,在接受脑血管病常规治疗的基础上,治疗组加用帕罗西汀和心理干预.采用斯堪的那维亚脑卒中量表(SSS)、Barthel指数(BI)、汉密尔顿抑郁量表(HAMD)、汉密尔顿焦虑量表(HAMA)分别于治疗前、治疗后2周、4周及6周末进行评测.结果 181例患者中发生情感障碍81例(44.75 %),其中66.67%(54例)同时出现抑郁和焦虑,情感障碍的发生与额叶、左侧大脑半球、基底节病灶有关(P<0.05～0.001);治疗后治疗组HAMD、HAMA、SSS评分减少和BI评分增加,与对照组比较差异有统计学意义(均P<0.01),治疗后2～6周显效率显著优于对照组(P<0.05～0.01).结论 脑卒中后抑郁/焦虑的发生与脑卒中部位相关;对脑卒中后抑郁/焦虑的患者应用帕罗西汀合并心理干预治疗能显著提高患者神经功能康复程度,促进生活能力的恢复.     

帕罗西汀联合度洛西汀对于抑郁伴躯体化障碍患者的临床效果

目的探讨帕罗西汀联合度洛西汀治疗抑郁伴躯体化障碍患者的疗效。方法采用症状自评量表(SCL-90)和Zung抑郁自评量表(SDS)筛选出抑郁伴躯体化障碍的患者30例,随机分为治疗组和对照组,每组各15例,分别给予口服帕罗西汀+度洛西汀和口服度洛西汀治疗,4周为一个疗程。在治疗前及治疗4周末测量患者的SCL-9和SDS评分。结果 (1)治疗前,两组的SCL-9和SDS评分无明显差异(P0.05);(2)治疗4周后,治疗组的SDS评分低于对照组,差异有统计学意义(P0.05);治疗组经过治疗后的SDS评分低于治疗前,差异有统计学意义(P0.05);(3)治疗4周后,治疗组的SCL-9评分低于对照组,差异有统计学意义(P0.05);两组在治疗4周后SCL-9评分均低于治疗前,差异有统计学意义(P0.05)。结论帕罗西汀联合度洛西汀可改善抑郁伴躯体化障碍,值得在临床推广应用。     

乌灵胶囊联合帕罗西汀治疗卒中后抑郁疗效观察

目的观察乌灵胶囊联合帕罗西汀治疗卒中后抑郁患者的疗效。方法将180例卒中后抑郁患者随机分为2组,实验组即乌灵胶囊联合帕罗西汀组92例,对照组即单用帕罗西汀组88例,疗程3个月。分别在治疗前和疗程结束后应用汉密尔顿抑郁量表(hamilton rating scale for depression,HAMD)评分来评估抑郁症状的改善情况,应用TESS不良反应量表(treatment emergent symptom scale,TESS)评估药物不良反应。结果实验组汉密尔顿抑郁量表评分较对照组明显降低,差异有统计学意义(P<0.05);2组TESS不良反应量表评分差异无统计学意义(P>0.05)。结论乌灵胶囊联合帕罗西汀治疗卒中后抑郁安全有效。     

阿立哌唑合并帕罗西汀治疗难治性抑郁症的研究

目的探讨阿立哌唑合并帕罗西汀对难治性抑郁症的疗效。方法将60例入组病例随机分为研究组与对照组各30例。研究组用阿立哌唑合并帕罗西汀,对照组仅用帕罗西汀,2周末视病情可酌情帕罗西汀加量至40mg/d,采用HAMD评定疗效,TESS量表评定不良反应,观察6周。结果2、4、6周末2组HAMD评分较治疗前相比差异均有显著性(P均<0.01);6周末HAMD评分2组间比较差异有统计学意义(P<0.05)。2组显进率经统计学分析差异有显著性(χ2=4.34,P<0.05),2组组间4周末TESS评分比较差异有显著性(P<0.01)、6周末TESS评分2组比较差异仍有显著性(P<0.05)。2组不良反应发生率比较差异也有显著性χ2=4.44,(P<0.05)。结论阿立哌唑合并帕罗西汀治疗难治性抑郁症缓解程度高,不良反应较少且轻。     

帕罗西汀治疗偏头痛疗效临床观察

目的探讨帕罗西汀治疗偏头痛的临床疗效。方法对32例偏头痛患者使用帕罗西汀治疗,治疗前及治疗6周后采用抑郁自评量表(SDS),焦虑自评量表(SAS)量表评定。结果经帕罗西汀治疗后,32例患者28例头痛明显改善,有效率87.5%;32例患者SDS、SAS治疗后评分均较治疗前显著降低(P0.01)。结论帕罗西汀治疗偏头痛是安全有效的。     

重复经颅磁刺激与帕罗西汀联合治疗对焦虑抑郁障碍患者的疗效及认知功能影响

目的研究重复经颅磁刺激联合帕罗西汀在焦虑抑郁障碍患者中的临床治疗效果及对患者认知功能的影响。方法选取2014年1月~2016年5月医院诊治的焦虑抑郁障碍患者90例,将患者随机分为对照组(45例)和观察组(45例)。对照组采用帕罗西汀治疗,观察组予以帕罗西汀联合重复经颅磁刺激治疗。采用汉密尔顿焦虑量表(HAMA)、汉密尔顿抑郁量表17项(HAMD-17)和临床疗效总评量表(CGI)总分变化评定疗效,采用事件相关电位(P300)及眼动测定患者认知功能。结果观察组治疗4周有效率为95.6%,显著高于对照组的80.0%(P0.05);两组治疗前HAMA量表评分、HAMD量表差异无统计学意义(P0.05),治疗后上述量表评分均逐渐地明显降低(P0.05);且观察组患者治疗后2周、4周HAMA量表、HAMD量表评分,显著低于对照组(P0.05);观察组治疗后P300的潜伏期,显著低于对照组(P0.05);观察组治疗后P300波幅及眼动测定NEF和RSS,显著高于对照组(P0.05)。结论焦虑抑郁障碍患者中采用重复经颅磁刺激联合帕罗西汀治疗比帕罗西汀单药治疗效果更理想,能更好地改善患者认知功能。     

尼莫地平联合帕罗西汀治疗脑卒中后抑郁临床观察

目的 探讨尼莫地平联合帕罗西汀治疗脑卒中后抑郁的疗效.方法 将2009-04-2011-09我科收治的脑卒中后抑郁患者94例随机分为2组,观察组与对照组各47例,观察组给予尼莫地平联合帕罗西汀治疗,对照组给予帕罗西汀治疗.结果 (1)治疗前,观察组与对照组的汉密尔顿抑郁量表(HAMD)评分、美国国立卫生院神经功能缺损(NIHSS)评分差异无统计学意义(P＞0.05);治疗后,观察组的HAMD评分、NIHSS评分显著低于对照组,2组比较差异有统计学意义(P＜0.05).(2)观察组的抗抑郁治疗效果显著优于对照组,2组比较差异有统计学意义(P＜0.05).(3)观察组的神经功能改善效果显著优于对照组,2组比较差异有统计学意义(P＜0.05).结论 尼莫地平联合帕罗西汀治疗脑卒中后抑郁患者具有抗抑郁效果好、神经功能改善效果佳等优点.     

Paroxetine in the treatment of chronic posttraumatic stress disorder: results of a placebo-controlled, flexible-dosage trial.

BACKGROUND: The objective of this double-blind, placebo-controlled study was to investigate the efficacy and safety of paroxetine in outpatients with posttraumatic stress disorder (PTSD). METHOD: Male and female outpatients 18 years and older who met DSM-IV criteria for PTSD and had baseline scores of 50 or greater on the Clinician Administered PTSD Scale (CAPS-2) were randomly assigned to treatment with paroxetine (20-50 mg/day) or placebo for 12 weeks. The primary efficacy variables were the change from baseline to the 12-week endpoint in the CAPS-2 total score and the proportion of responders on the Clinical Global Impressions-Global Improvement scale (CGI-1). Additional key outcome measures were the change from baseline in the reexperiencing, avoidance/ numbing, and hyperarousal scores of the CAPS-2 and in the total scores of the Treatment Outcome PTSD Scale and the patient-rated Davidson Trauma Scale and Sheehan Disability Scale (SDS). Depressive symptoms were assessed with the Montgomery-Asberg Depression Rating Scale. The proportion of patients achieving response and remission was also determined. RESULTS: 307 patients constituted the intent-to-treat population. At week 12, compared with the placebo group (N = 156), the paroxetine group (N = 151) showed significantly greater reduction of PTSD symptoms on both of the primary and all of the secondary outcome measures. Significantly greater improvement on the CAPS-2 total score was observed for paroxetine compared with placebo from week 4 (p < .05), and significantly greater proportions of paroxetine-treated patients achieved response (p < .001) and remission (p = .008) by week 12. The improvement in PTSD symptoms was similar in male and female patients. Functional improvement at the study endpoint was significantly greater (p < .05) in the paroxetine group in all 3 domains of the SDS (work, social life, family life). Treatment with paroxetine was well tolerated, with the frequency and type of adverse events recorded for the paroxetine group corresponding to the known safety profile of this medication. Conclusion: Paroxetine in doses of 20 to 50 mg once daily is effective as a treatment for chronic PTSD. Improvement is obtained for all 3 symptom clusters (reexperiencing, avoidance/numbing, hyperarousal) and is associated with significant reduction in disability after 12 weeks of treatment.     

Efficacy and safety of paroxetine treatment for chronic PTSD: a fixed-dose, placebo-controlled study.

OBJECTIVE: This study evaluated the efficacy and safety of paroxetine for the treatment of patients with chronic posttraumatic stress disorder (PTSD). METHOD: Outpatients with chronic PTSD according to DSM-IV criteria and a score of 50 or more on the Clinician-Administered PTSD Scale, part 2, were randomly assigned to take placebo (N=186), 20 mg/day of paroxetine (N=183), or 40 mg/day of paroxetine (N=182) for 12 weeks. Efficacy was assessed by examining the change in total score from baseline to endpoint on the Clinician-Administered PTSD Scale, part 2, and rates of response ("very much improved" or "much improved") for global improvement on the Clinical Global Impression scale. RESULTS: Paroxetine-treated patients in both dose groups demonstrated significantly greater improvement on primary outcome measures compared to placebo-treated patients in the intent-to-treat analysis. Moreover, paroxetine treatment resulted in statistically significant improvement compared to placebo on all three PTSD symptom clusters (reexperiencing, avoidance/numbing, and hyperarousal), social and occupational impairment, and comorbid depression. Paroxetine was effective for both men and women. Treatment response did not vary by trauma type, time since trauma, or severity of baseline PTSD or depressive symptoms. Both doses were well tolerated. CONCLUSIONS: Doses of 20 and 40 mg/day of paroxetine are effective and well tolerated in the treatment of adults with chronic PTSD.     

Posttraumatic stress disorder and identification in disaster workers

OBJECTIVE: Disaster workers who work with deceased victims are at increased risk of posttraumatic stress disorder (PTSD). Identification with the deceased has been proposed as one of the mechanisms in this stress-illness relationship. To examine this hypothesis, this study investigated three types of identification with the dead in a group of disaster workers: identification with the deceased as oneself, identification with the deceased as a friend, and identification with the deceased as a family member. METHOD: Fifty-four volunteer disaster workers who worked with the dead following an explosion on the USS Iowa naval ship were assessed 1, 4, and 13 months after the disaster. PTSD symptoms (measured with the DSMPTSD-IV scale), intrusive and avoidant disaster-related symptoms (measured with the Impact of Event Scale), somatization and general distress (measured with the SCL-90-R), and health care utilization were assessed. RESULTS: Disaster workers who reported identification with the deceased as a friend were more likely than those who did not to have PTSD, more intrusive and avoidant symptoms, and greater levels of other posttraumatic symptoms including somatization. Disaster workers who reported identification with the deceased as a family member had greater intrusive symptoms 1 month after the disaster than those who did not. There were no differences between those who did and did not identify with the deceased as self. Health care utilization was not associated with identification. CONCLUSIONS: Identification with the deceased is a risk factor for PTSD and posttraumatic symptoms in disaster workers exposed to the dead. Identification with the dead as a friend is specifically associated with higher risk for these workers.     

Long-term treatment with paroxetine increases verbal declarative memory and hippocampal volume in posttraumatic stress disorder.

BACKGROUND: Animal studies have shown that stress is associated with damage to the hippocampus, inhibition of neurogenesis, and deficits in hippocampal-based memory dysfunction. Studies in patients with posttraumatic stress disorder (PTSD) found deficits in hippocampal-based declarative verbal memory and smaller hippocampal volume, as measured with magnetic resonance imaging (MRI). Recent preclinical evidence has shown that selective serotonin reuptake inhibitors promote neurogenesis and reverse the effects of stress on hippocampal atrophy. This study assessed the effects of long-term treatment with paroxetine on hippocampal volume and declarative memory performance in PTSD. METHODS: Declarative memory was assessed with the Wechsler Memory Scale-Revised and Selective Reminding Test before and after 9-12 months of treatment with paroxetine in PTSD. Hippocampal volume was measured with MRI. Of the 28 patients who started the protocol, 23 completed the full course of treatment and neuropsychological testing. Twenty patients were able to complete MRI imaging. RESULTS: Patients with PTSD showed a significant improvement in PTSD symptoms with treatment. Treatment resulted in significant improvements in verbal declarative memory and a 4.6% increase in mean hippocampal volume. CONCLUSIONS: These findings suggest that long-term treatment with paroxetine is associated with improvement of verbal declarative memory deficits and an increase in hippocampal volume in PTSD.     

Noradrenergic vs serotonergic antidepressant with or without naltrexone for veterans with PTSD and comorbid alcohol dependence

The wars in Iraq and Afghanistan are associated with high rates of post-traumatic stress disorder (PTSD) and comorbid alcohol use disorders. The pharmacotherapy of these comorbid conditions has received relatively little study. The current study compared the serotonin uptake inhibitor, paroxetine, to the norepinephrine uptake inhibitor, desipramine. It also evaluated the adjunctive efficacy of the Food and Drug Administration (FDA)-approved alcoholism pharmacotherapy, naltrexone, relative to placebo. Four groups of predominately male veterans (n=88) meeting current diagnostic criteria for both alcohol dependence (AD) and PTSD were randomly assigned under double-blind conditions to one of four groups: paroxetine+naltrexone; paroxetine+placebo; desipramine+naltrexone; desipramine+placebo. Main outcome measures included standardized scales that assessed symptoms of PTSD and alcohol consumption. Paroxetine did not show statistical superiority to desipramine for the treatment of PTSD symptoms. However, desipramine was superior to paroxetine with respect to study retention and alcohol use outcomes. Naltrexone reduced alcohol craving relative to placebo, but it conferred no advantage on drinking use outcomes. Although the serotonin uptake inhibitors are the only FDA-approved medications for the treatment of PTSD, the current study suggests that norepinephrine uptake inhibitors may present clinical advantages when treating male veterans with PTSD and AD. However, naltrexone did not show evidence of efficacy in this population. This study was registered with ClinicalTrials.gov, registration number NCT00338962 and URL: http://clinicaltrials.gov/ct2/show/NCT00338962?term=desipramine+AND+alcohol+dependence+AND+depression&recr=Closed&rank=1.     

Association between change in sleep duration and posttraumatic stress symptoms in natural disaster victims: the mediating role of resilience

ObjectiveThis study investigated the association between changes in sleep duration after disaster and post-traumatic stress disorder (PTSD) symptoms and the mediating role of resilience on the association.MethodsData were collected from 2951 Korean adults who were victims of a natural disaster and did not have any mental or medical illnesses before the event. They completed a long-term survey on changes in life for disaster victims using computer-aided personal interviews. Changes in sleep duration before and one month after experiencing a disaster were assessed using a self-reported questionnaire. Resilience levels and PTSD symptoms were measured using the Brief Resilience Scale and the Impact of Event Scale – Revised, respectively, and more than 33 of the IES-R score items were defined as significant PTSD symptoms. Multivariate logistic regression was used to examine the associations between changes in sleep duration and PTSD symptoms. Additionally, mediating studies were conducted to identify the role of resilience on the association.ResultsCompared with participants without significant PTSD symptoms, those with PTSD symptoms were more likely to be older and female (group without significant PTSD symptom: mean age = 56.12 ± 18.70 years, female sex = 49.24%; group with significant PTSD symptoms: mean age = 60.88 ± 15.66 years, female sex = 59.52%). Compared with disaster victims without changes in sleep duration, those who had shorter sleep duration after disaster had a higher risk of significant PTSD symptoms (OR = 2.89, 95% Cl = 2.31–3.62, p < 0.001). In the mediating study, resilience level significantly mediated the relationship between reduced sleep duration and PTSD symptoms (direct effect: β = 0.208, 95% Cl = 0.166–0.250, p < 0.001; indirect effect: β = 0.007, 95% Cl = 0.002–0.011, p < 0.001; total effect: β = 0.215, 95% Cl = 0.173–0.257, p < 0.001).ConclusionThis study revealed that individuals with reduced sleep duration after disaster had a higher risk of PTSD symptoms, while those with increased sleep duration did not. In addition, mediating effects of resilience level on the relationship between reduced sleep duration and significant PTSD symptoms were observed.     

Amygdala Deep Brain Stimulation Is Superior to Paroxetine Treatment in a Rat Model of Posttraumatic Stress Disorder

BackgroundPosttraumatic stress disorder (PTSD) is a very debilitating disease refractory to current treatment with selective serotonin reuptake inhibitors (SSRIs) in up to 30 percent of patients, illustrating the need for new treatments of PTSD. Neuroimaging studies have shown increased activity of the amygdala of patients with PTSD.Objective/hypothesisTo investigate amygdala deep brain stimulation (DBS) as a possible novel treatment for PTSD and compare it to current treatment with a commonly used SSRI, paroxetine, in a rat PTSD model.MethodsA PTSD model was created by subjecting rats to inescapable foot shocks in the presence of a conspicuous ball. Response to treatment was measured as a decreased burying behavior when presented with the same ball 1 and 2 weeks after the shocks. Rats were treated with either daily intraperitoneal paroxetine injections or amygdala DBS via an electrode implanted 1 week prior to shocks. Generalized anxiety was assessed using an elevated plus maze.ResultsAnimals treated with amygdala DBS showed less ball burying at 2 weeks relative to the animals treated with paroxetine. The animals treated with paroxetine, however, had a lower general anxiety level compared to the DBS-treated group.ConclusionsIn this PTSD model, paroxetine was found to decrease the measured general anxiety level of rats that underwent the PTSD protocol, but did not counteract shock-induced hyper-vigilance toward the trauma-associated object (ball). Amygdala DBS, however, did decrease shock-induced hyper-vigilance as measured by a lower burying time, but had no effect on general anxiety assessed in the elevated plus maze. By attenuating amygdala function, DBS may act to treat the cause of PTSD, hyperactive amygdala function, and may be a promising novel alternative in cases of PTSD refractory to current pharmacological treatments.     

Posttraumatic stress disorder: a state-of-the-science review

This article reviews the state-of-the-art research in posttraumatic stress disorder (PTSD) from several perspectives: (1) Sex differences: PTSD is more frequent among women, who tend to have different types of precipitating traumas and higher rates of comorbid panic disorder and agoraphobia than do men. (2) Risk and resilience: The presence of Group C symptoms after exposure to a disaster or act of terrorism may predict the development of PTSD as well as comorbid diagnoses. (3) Impact of trauma in early life: Persistent increases in CRF concentration are associated with early life trauma and PTSD, and may be reversed with paroxetine treatment. (4) Imaging studies: Intriguing findings in treated and untreated depressed patients may serve as a paradigm of failed brain adaptation to chronic emotional stress and anxiety disorders. (5) Neural circuits and memory: Hippocampal volume appears to be selectively decreased and hippocampal function impaired among PTSD patients. (6) Cognitive behavioral approaches: Prolonged exposure therapy, a readily disseminated treatment modality, is effective in modifying the negative cognitions that are frequent among PTSD patients. In the future, it would be useful to assess the validity of the PTSD construct, elucidate genetic and experiential contributing factors (and their complex interrelationships), clarify the mechanisms of action for different treatments used in PTSD, discover ways to predict which treatments (or treatment combinations) will be successful for a given individual, develop an operational definition of remission in PTSD, and explore ways to disseminate effective evidence-based treatments for this condition.     

Association study of polymorphisms in the excitatory amino acid transporter 2 gene (SLC1A2) with schizophrenia

Background

This naturalistic open label follow-up study had three objectives: 1) To observe the course of illness in Panic Disorder patients receiving long-term versus intermediate-term paroxetine treatment 2) To compare the relapse rates and side-effect profile after long-term paroxetine treatment between patients with Panic Disorder and Panic Disorder with Agoraphobia. 3) To observe paroxetine's tolerability over a 24 month period.

Methods

143 patients with panic disorder (PD), with or without agoraphobia, successfully finished a short-term (ie 12 week) trial of paroxetine treatment. All patients then continued to receive paroxetine maintenance therapy for a total of 12 months. At the end of this period, 72 of the patients chose to discontinue paroxetine pharmacotherapy and agreed to be monitored throughout a one year discontinuation follow-up phase. The remaining 71 patients continued on paroxetine for an additional 12 months and then were monitored, as in the first group, for another year while medication-free. The primary limitation of our study is that the subgroups of patients receiving 12 versus 24 months of maintenance paroxetine therapy were selected according to individual patient preference and therefore were not assigned in a randomized manner.

Results

Only 21 of 143 patients (14%) relapsed during the one year medication discontinuation follow-up phase. There were no significant differences in relapse rates between the patients who received intermediate-term (up to 12 months) paroxetine and those who chose the long-term course (24 month paroxetine treatment). 43 patients (30.1%) reported sexual dysfunction. The patients exhibited an average weight gain of 5.06 kg. All patients who eventually relapsed demonstrated significantly greater weight increase (7.3 kg) during the treatment phase.

Conclusions

The extension of paroxetine maintenance treatment from 12 to 24 months did not seem to further decrease the risk of relapse after medication discontinuation. Twenty-four month paroxetine treatment is accompanied by sexual side effects and weight gain similar to those observed in twelve month treatment.     

Adolescent vulnerability to PTSD and effects of community‐based intervention: Longitudinal study among adolescent survivors of the Ehime Maru sea accident

The aim of the present study was to examine the psychological impact on adolescent survivors of a maritime disaster that resulted in the deaths of nine people, including four high school students, and the effects of psychiatric intervention for the survivors. Methods: Long‐term multidimensional intervention consisting of psychoeducation, hospital treatment, family support and day care, was provided for nine adolescent survivors. To evaluate these effects, the survivors were also assessed using self‐rating scales (Impact of Event Scale, General Health Questionnaire and Self‐rating Depression Scale) and psychiatric structured interviews (Clinician‐Administered Post‐Traumatic Stress Disorder [PTSD] Scale) at 2, 8, 14, 26, and 38 months after the accident. Results: Prevalence of PTSD among adolescent survivors was much higher than in adult survivors at the 2‐month examination (78% vs 12%, respectively). Although the observed prevalence remained high until the 14‐month examination, remarkable improvement occurred thereafter and none was diagnosed with PTSD at the 38‐month examination. Conclusion: Adolescents may have a specific vulnerability to PTSD and community‐based intervention is effective for adolescents with serious symptoms of PTSD.