艾司西酞普兰治疗儿童少年抑郁障碍临床研究

目的观察艾司西酞普兰治疗儿童少年抑郁障碍的临床疗效及安全性。方法对43例儿童少年抑郁障碍患者应用非固定剂量的艾司西酞普兰进行治疗,观察4w。于治疗前及治疗1w、2w、3w、4w末采用汉密顿抑郁量表评定疗效,副反应量表评定不良反应。结果人组患者于治疗第1w末起,汉密顿抑郁量表总分较治疗前有显著下降（P〈0．01）,并随着治疗时间的延续呈持续性下降;减分率〉25％,有效率达21．4％,且均随着治疗时间的延续呈持续性升高;治疗4w末有效率达81．0％。不良反应多为消化系统症状,症状轻微,多在治疗初期出现,随着治疗时间的延续逐渐缓解或消失。结论艾司西酞普兰治疗儿童少年抑郁障碍安全有效。     

西酞普兰治疗冠心病伴惊恐障碍的疗效观察

文献报道,在冠心病人群中,惊恐障碍的共病发生率为6.5%~53%[1],严重地影响病人的生活质量。西酞普兰和帕罗西汀同属于选择性5-羟色胺再摄取抑制剂(SSRI)类的药物,而帕罗西汀是第一个经美国食品与药物管理局(FDA)批准用于治疗惊恐障碍的SSRI。目前有学者报道西酞普兰治疗惊恐障碍有效,而且疗效与帕罗西汀相当[2]。为了探讨西酞普兰治疗冠心病伴惊恐障碍的疗效,我们将西酞普兰与帕罗西汀治疗冠心病伴惊恐障碍患者的疗效进行比较。1资料与方法1.1病例选择2004年6月至2007年8月在洛阳市4家三级甲等医院心血管内科或心理科住院部就诊的冠心…     

艾司西酞普兰治疗难治性抑郁症的临床研究

目的:观察艾司西酞普兰治疗难治性抑郁症的临床效果。方法:选取我院2015年3月~2017年9月收治的难治性抑郁症患者120例为研究对象,根据治疗方式的不同分为对照组和观察组各60例。对照组采用常规治疗,观察组在对照组基础上采用艾司西酞普兰治疗。比较两组患者临床疗效及用药安全性。结果:治疗前,两组患者HAMD、HAMA及SDSS评分比较无显著性差异(P0.05);治疗后,观察组HAMD、HAMA及SDSS评分均低于对照组(P0.05);观察组治疗总有效率明显高于对照组,不良反应发生率低于对照组(P0.05)。结论:艾司西酞普兰治疗难治性抑郁症效果显著,具有较高的安全性及可行性。     

艾司西酞普兰治疗广泛性焦虑的疗效

目的:探讨艾司西酞普兰治疗广泛性焦虑症患者的疗效及不良反应.方法:将84例广泛性焦虑症患者随机分为艾司西酞普兰组和西酞普兰组,疗程6周,并用汉密顿焦虑量表(HAMA)、临床疗效总评量表、药物不良反应评定量表对患者治疗前后进行评估.结果:在治疗的第2、4、6周末两组的HAMA分值差异有显著性(P＜0.05).在治疗6周末时,艾司西酞普兰组显效率为78.6%,有效率为90.4%,西酞普兰组分别为73.8%、85.7%,两组差异有显著性(P＜0.05).在不良反应方面,艾司西酞普兰低于西酞普兰组,两组差异有显著性(P＜0.05).结论:艾司西酞普兰治疗广泛性焦虑症安全有效.     

音乐治疗联合艾司西酞普兰治疗首发抑郁障碍临床疗效评价

目的:对音乐治疗联合艾司西酞普兰治疗首发抑郁障碍进行临床疗效评价。方法:将71例首发抑郁障碍患者随机分为联合组(36例)和药物组(35例)。药物组给予艾司西酞普兰常规药物治疗,联合组采用音乐治疗联合艾司西酞普兰治疗,均治疗8周。治疗8周末使用临床疗效总评量表(CGI)评价总体疗效;分别于基线时、治疗4周末、治疗8周末使用汉密尔顿抑郁量表(HAMD)-17量表评价临床疗效,使用席汉残疾量表(SDS)评估患者的社会功能。使用副反应量表(TESS)记录治疗全过程发生的药物不良反应。结果:治疗8周末根据CGI-GI评定结果,药物组有效率71.43%,联合组有效率91.67%,高于药物组(P0.05)。治疗前,2组的HAMD评分、SDS评分差异无统计学意义(P0.05);治疗4周末、治疗8周末,2组的HAMD、SDS评分均低于同组较治疗前(均P0.01),且联合组均低于药物组(P0.01或0.05)。2组均未发生严重不良事件。结论:音乐治疗联合艾司西酞普兰治疗抑郁障碍安全性高,在有效性方面优于单用艾司西酞普兰治疗,对患者社会功能恢复有积极作用。     

艾司西酞普兰治疗帕金森病抑郁40例分析

目的观察艾司西酞普兰治疗帕金森病抑郁的临床疗效。方法将80例患者随机分为艾司西酞普兰组、氟西汀组,分别采用汉密尔顿抑郁量表(HAMD)在治疗前和治疗后1、2、4、6、8周末评定,简易智能状态检查表(MMSE)、帕金森统一评分量表(UPDRS)于治疗前后评定并比较。结果艾司西酞普兰组、氟西汀组治疗后HAMD评分较治疗前有改善(P<0.05),两组抗抑郁疗效相似;HAMD评分于1周即明显改善,2周后与氟西汀组相似;8周其MMSE评分与氟西汀组相似,与治疗前无差异;8周其UPDRS评分优于氟西汀组。结论艾司西酞普兰治疗帕金森病抑郁与氟西汀相似,改善PD患者生活质量更明显,起效更快。     

基因检测指导下艾司西酞普兰治疗复发性抑郁障碍的疗效

目的:探讨基因检测指导下艾司西酞普兰治疗复发性抑郁障碍的临床效果。方法:选取2018年5月～2020年1月收治的200例复发性抑郁障碍患者为研究对象,采用随机数字表法分为对照组与观察组,各100例。对照组行单纯艾司西酞普兰治疗,观察组行基因检测指导下艾司西酞普兰治疗。比较两组心理状况及并发症发生情况。结果:两组治疗后焦虑自评量表、抑郁自评量表评分均较治疗前降低,且观察组焦虑自评量表、抑郁自评量表评分低于对照组,差异有统计学意义(P0.05);观察组并发症总发生率(4.00%)低于对照组(12.00%),差异有统计学意义(P0.05)。结论:对复发性抑郁障碍患者采用基因检测指导下艾司西酞普兰治疗可有效改善患者心理状况,且未见明显并发症增加,安全性高。     

艾司西酞普兰治疗老年期抑郁障碍疗效观察

艾司西酞普兰是一种新型抗抑郁剂,治疗非老年期情感障碍相关报道较多,但对老年期抑郁障碍的疗效及安全性尚少见报道.为了解艾司西酞普兰治疗老年期抑郁障碍的临床疗效及安全性,我们进行了临床观察,现将结果报告如下.     

Interpretation of Ambiguous Interoceptive Stimuli in Panic Disorder and Nonclinical Panic

Cognitive bias in the misinterpretation of ambiguous interoceptive stimuli has been demonstrated in panic disorder. This study investigated whether this cognitive bias also occurs in people with nonclinical panic who are at risk of developing panic disorder. The responses of 25 people with nonclinical panic were compared to those of 20 people with panic disorder and 69 nonpanic controls on a measure of interpretive bias, the Brief Body Sensations Interpretation Questionnaire. There was evidence for interpretive cognitive bias for ambiguous interoceptive stimuli among the nonclinical panickers which did not differ from that of the people with panic disorder, but which differed from the nonpanic controls. High anxiety sensitivity predicted interpretive bias toward both interoceptive and external stimuli. Results therefore suggest that interpretive cognitive bias for ambiguous interoceptive stimuli may be a risk factor for the development of panic disorder.     

Panic Disorder and Emergency Services Utilization

OBJECTIVES: The characteristics of patients with panic disorder in emergency department (ED) patient populations are unknown. This study compares demographic information and emergency care use among patients identified as having a high likelihood of having panic disorder with that of patients who tested negative on the screening test for panic disorder. METHODS: Prospective cross-sectional study of a convenience sample of patients presenting to an urban ED. Patients were excluded if they were aged 18 years or younger, were unstable, or could not speak English or Spanish. Of 968 patients, 813 agreed to participate. Over a period of 23 days, patients were administered a Diagnostic and Statistical Manual (DSM)-IV screening questionnaire (PRIME-MD) for panic disorder along with a survey assessing their use of medical services during the prior year. RESULTS: One hundred patients (12.3%) met PRIME-MD criteria for having a high likelihood of panic disorder. Patients with Medicare were 2.84 times more likely to have a positive result on the screening test than those without insurance. Patients who had four to seven ED visits or eight or more ED visits in one year were 2.63 and 3.10 times more likely to screen positive on the PRIME-MD, respectively, compared with those who had one to three visits. Patients who activated 911 two to ten times or 11 or more times in one year were 2.02 and 4.99 times more likely to screen positive for panic disorder, respectively, compared with those who had never activated 911. CONCLUSIONS: Patients who screen positive for panic disorder use emergency medical services and ED services more frequently. In addition, the overall prevalence of screening positive for panic disorder in an ED is higher than previously reported.     

米氮平与丁螺环酮治疗惊恐障碍的对照研究

目的比较米氮平与丁螺环酮治疗惊恐障碍的疗效及安全性。方法将86例惊恐障碍患者随机分为观察组和对照组各43例,观察组予以米氮平30～60 mg/d,对照组予以丁螺环酮15～30 mg/d。两组疗程均为8周。疗效评定采用Hamilton焦虑量表(HAMA),安全性评价采用副反应量表(TESS)、实验室检查及体检。结果观察组有效率为90.7%,对照组有效率为83.7%(χ²=1.17,P>0.05);治疗1、2周末,观察组HAMA评分均低于对照组(分别为t=2.94,P<0.01;t=2.49,P<0.05),但治疗4、8周末,两组HAMA评分均无显著性差异(P>0.05)。两组不良反应程度均较轻微。结论米氮平治疗惊恐障碍起效快,疗效与丁螺环酮相仿。     

A Test of Core Assumptions of the Catastrophic Misinterpretation Model of Panic Disorder

The catastrophic misinterpretation model of panic disorder proposes that spontaneous panic attacks are the result of misinterpretation of harmless autonomic arousal as precursors to physical (e.g. heart attack) or psychological (e.g. insanity) emergency. Mixed research findings to date have provided equivocal support. A modified form of the Body Sensations Interpretation Questionnaire was used to investigate core assumptions of the model amongst 38 people with panic disorder (PD), 20 with non-clinical panic, 21 with social anxiety disorder, and 34 non-anxious controls. The PD group gave more harm-related interpretations of ambiguous internal stimuli than all other groups only when anxiety-related responses (e.g. “I'm going to panic”) were scored as harm, however there was no evidence that anxiety-related interpretations were masking perceived catastrophic physical or psychological outcomes. Despite this, people with PD rated harm and anxiety outcomes as more negative than non-anxious controls. Results failed to unequivocally support core assumptions of the model.     

探究团体正念认知疗法对惊恐障碍的疗效

目的:探究团体正念认知疗法对惊恐障碍(PD)患者的疗效。方法:PD患者120例,按单双号分为研究组(60例,完成56例)和对照组(60例,完成53例),2组均接受药物治疗,研究组同时接受团体正念认知疗法。在治疗前、治疗12周及治疗6月后分别对2组进行PD严重程度量表(PDSS)、状态-特质焦虑问卷(STAI-Form Y)、五因素正念量表(FFMQ)评估和心跳知觉的心理追踪范式测试。结果:PDSS、STAI-Form Y中的S-AI因子、FFMQ中的有觉知地行动和不判断因子评分和心跳知觉水平在组间效应、时间效应及组别×时间交互作用差异有统计学意义(P<0.05);STAI-Form Y中的T-AI因子、FFMQ中的观察、描述、不反应因子评分在组间效应和时间效应作用差异有统计学意义(P<0.05)。结论:团体正念认知疗法能有效缓解PD患者的焦虑症状,提高患者的正念水平,降低患者的心跳知觉水平。     

惊恐障碍临床路径表的构建

目的构建适用于惊恐障碍患者的临床路径表。方法成立临床路径小组,在文献回顾、病历回顾的基础上,构建临床路径初步框架,结合专家意见及临床实际调查,以循证医学为基础制定惊恐障碍临床路径表。结果确定临床路径表的框架、诊疗计划项目、常规医嘱项目、非医嘱项目和标准住院时间,最终设计出以标准住院时间为21d的惊恐障碍临床路径表。结论通过循证的方法构建的惊恐障碍临床路径表,能指导惊恐障碍患者的诊疗和护理。     

Gender Differences in Patients with Panic Disorder: Evaluating Cognitive Mediation of Phobic Avoidance

Epidemiologic reports have consistently found that females are at greater risk for the development of panic disorder, in particular, when it is accompanied by agoraphobia. Although gender appears to be a well-established risk factor for the development of phobic avoidance, the mechanisms that account for this increased risk have yet to be delineated. Often, gender differences in phobic avoidance are speculated to arise from differences in courage (e.g., men are expected to be brave and endure fear-provoking situations). Our study evaluated this popular but unsubstantiated theory and advanced another hypothesis: Differences in panic- and arousal-related cognitions may account for gender differences in phobic avoidance. Male (n = 27) and female (n = 61) patients meeting DSM-IV criteria for panic disorder with or without agoraphobia were evaluated. Data did not support gender differences in courage; nor were these indices related to phobic avoidance. In contrast, there were significant gender differences in several cognitive domains. Moreover, anxiety sensitivity and panic-related appraisals mediated gender differences in phobic avoidance.     

Cognitive Bias in Panic Disorder: A Process Dissociation Approach to Automaticity

We applied a variant of Jacoby's (1991) process dissociation procedure to parse the relative contributions of automatic and controlled processes to word-stem completion performance involving threatening, positive, and neutral material in patients with panic disorder and healthy control participants. Contrary to prediction, processing of threatening (relative to nonthreatening) information in panic disorder was not disproportionately influenced by automatic processing. We found limited evidence, however, that panic patients exhibit a baseline bias for completing stems relevant to threat relative to nonthreat stems, perhaps indicating a proneness to engage in self-generated priming of threat material.     

Panic Disorder and Migraine: Comorbidity,Mechanisms, and Clinical Implications

A growing body of literature suggests that comorbid anxiety disorders are more common and more prognostically relevant among migraine sufferers than comorbid depression. Panic disorder (PD) appears to be more strongly associated with migraine than most other anxiety disorders. PD and migraine are both chronic diseases with episodic manifestations, involving significant functional impairment and shared symptoms during attacks, interictal anxiety concerning future attacks, and an absence of identifiable secondary pathology. A meta‐analysis of high‐quality epidemiologic study data from 1990 to 2012 indicates that the odds of PD are 3.76 times greater among individuals with migraine than those without. This association remains significant even after controlling for demographic variables and comorbid depression. Other less‐rigorous community and clinical studies confirm these findings. The highest rates of PD are found among migraine with aura patients and those presenting to specialty clinics. Presence of PD is associated with greater negative impact of migraine, including more frequent attacks, increased disability, and risk for chronification and medication overuse. The mechanisms underlying this common comorbidity are poorly understood, but both pathophysiological (eg, serotonergic dysfunction, hormonal influences, dysregulation of the hypothalamic–pituitary–adrenal axis) and psychological (eg, interoceptive conditioning, fear of pain, anxiety sensitivity, avoidance behavior) factors are implicated. Means of assessing comorbid PD among treatment‐seeking migraineurs are reviewed, including verbal screening for core PD symptoms, ruling out medical conditions with panic‐like features, and administering validated self‐report measures. Finally, evidence‐based strategies for both pharmacologic and behavioral management are outlined. The first‐line migraine prophylactics are not indicated for PD, and the selective serotonin re‐uptake inhibitors used to treat PD are not efficacious for migraine; thus, separate agents are often required to address each condition. Core components of behavioral treatments for PD are reviewed, and their integration into clinical headache practice is discussed.