惊恐障碍临床路径的应用效果分析

目的评价临床路径应用于住院惊恐障碍患者的诊疗护理效果。方法依据随机数字表将62例惊恐障碍患者分为观察组30例和对照组32例。观察组采用临床路径管理模式进行诊疗护理,对照组采取常规诊疗护理。评价指标为平均住院时间、平均住院费用、治疗效果、患者满意度和医护人员满意度。结果两组痊愈率比较差异无统计学意义(P0.05),但观察组却提早1周时间达到了与对照组相似的结果;观察组的平均住院时间和住院总费用显著低于对照组(P0.05);观察组患者满意度优于对照组(P0.05);医务人员对路径的实施效果持肯定态度,对路径信息化完善程度及减少工作量方面不满意。结论临床路径可以应用于住院惊恐障碍患者。     

惊恐障碍发作间歇期循证护理干预

目的 探索惊恐障碍发作间歇期的最佳护理方案,提高治疗效果.方法 将符合惊恐障碍诊断标准的116例惊恐障碍患者分对照组与研究组.研究组以循证医学的方法确定护理问题,制定护理方案,对照组单纯药物治疗,在入组时和治疗2、4、8周末用汉密尔顿焦虑量表(HAMA)评定疗效,计数资料对照分析采用x2检验.结果 采用循证护理干预后HAMA评分研究组治疗2周末较治疗前有显著性下降;对照组治疗4周末较治疗前有显著性下降.结论 循证护理以证据为基础,理论结合实际,因人、因“证”施护,身心同治,护患与家属共同努力,帮助患者重建认知功能,提高应对能力,降低复发率.     

儿童惊恐障碍特征及临床干预

目的探讨儿童惊恐障碍发病的相关因素及特征和临床有效干预措施。方法对43例惊恐障碍患儿的一般资料及临床表现进行归类整理,对31例≥7a患儿采用艾森克儿童个性问卷及Achonbach儿童行为评定量表测查评定并与同年龄、同性别正常对照组进行比较分析。结果患儿多数具有惊恐、焦虑发作背景,人格内倾、内向行为居多,症状往往成组出现．突发突止,患儿对紧张性压力异常敏感,带有夸张的情感反应。结论儿童惊恐障碍是生物-社会-心理疾病．应以心理治疗为主．联合小剂量抗焦虑剂或抗抑郁剂治疗。     

惊恐障碍60例临床分析及护理对策

为了解惊恐障碍的诱发因素 ,临床表现 ,首诊医院等 ,以采取相应的对策。对 60例惊恐障碍病人作回顾性临床分析。结果显示家庭内压力更易使易罹者发生惊恐障碍 ;临床表现以心血管系及呼吸系症状较多见 ;75 %病人首次就诊于综合医院内科 ,以心内科为主。因此 ,重点在于精神卫生知识宣教 ,将精神卫生服务纳入综合医院十分重要。     

惊恐障碍临床特征及误诊分析

目的 :分析惊恐障碍的临床特征 ,探讨其误诊原因。方法 :回顾性分析惊恐障碍 78例在精神科确诊前的临床资料。结果 :全部多次误诊为躯体疾病 ,尤其易误诊为心血管疾病。误诊时间 1.5～ 5 6个月 ,平均 ( 9.6 5± 13.2 1)个月。结论 :惊恐障碍极易误诊 ,综合医院应提高临床医生对惊恐障碍的认识以减少误诊率。     

综合医院惊恐障碍的临床特点及对策

惊恐障碍过去国内也曾有报导 ,原因在于这类患者多认为自己是心血管疾病或其他急症 ,往往不到精神科就诊 ,而就诊于综合医院急诊科 ,此文收集了 34例惊恐障碍的患者 ,报告如下。1　对象和方法本组均为多次就医于我科的患者 ,经 SCL - 90测试及临床会谈 ,按 CCMD- - R标准诊断为惊恐障碍。其中男 10例 ,女2 4例 ,两组年龄无差异 ,以青中年居多 ,18～ 46岁。平均病程 :<1a有 2 5例 ,占 73.5 % ,其余 9例病程 1～ 5 a,占 2 6 .5 %。并发广场恐怖症状者 9例 ,占 2 6 .4% ,并发抑郁症状者 15例 ,占44 % ,并发疑病症状者 8例 ,占 2 3% ,同时…     

利培酮致惊恐障碍发作1例

1临床资料刘某,男,27岁,教师。因疑心、空闻人语、行为异常4a,加重1mo余入院。体格检查、神经系统及辅助检查均无异常。精神检查:意识清,定向力佳,有言语性幻听,思维松弛,有关系、被害妄想,注意力不集中,情感淡漠,意志活动减退,行为怪异,无自知力。依据《中国精神障碍分类与诊断标准》第3版(CCMD-3),诊断为精神分裂症。入院后给予利培酮联合氯氮平治疗,30d内利培酮由1mg.d-1渐增加剂量至4mg.d-1,氯氮平由50mg.d-1渐增加剂量至275mg.d-1,患者疑心、空闻人语、行为异常消失,自知力大部分恢复,但患者出现焦虑情绪,担心自己的病情还要复发,联…     

惊恐障碍、广泛性焦虑障碍病因学对比研究进展

惊恐障碍(PD)和广泛性焦虑障碍(GAD)是焦虑障碍的两种常见类型。既往研究发现PD和GAD具有相似的病因和发病机制,然而两者独特的临床特征可能存在不同的病理生理学改变,这些改变对两者之间的鉴别有重要的意义。本文通过对PD和GAD在心理学、血生化、遗传学、电生理及影像学方面的差异进行综述,为寻找鉴别PD和GAD的特异性标记提供参考。     

惊恐障碍16例误诊原因分析

惊恐障碍１６例误诊原因分析山东省济宁市精神病防治院［２７２１５１］王年生，李荣琴，于兴旺惊恐障碍比较常见，国外报道其终生患病率为１．５％［１］，然而，目前国内尚未引起足够的重视，不少病例被误诊。为引起重视，将１９９０年１月～１９９３年６月在我院就诊的...     

综合医院惊恐障碍误诊原因分析

惊恐障碍是一种急性焦虑障碍,以反复惊恐发作为特征,呈突然的强烈恐惧伴植物神经功能亢进。临床表现为一系列的躯体症状,患者往往就诊于综合医院的急诊科、心内科等,由于对本病缺乏认识,极易误诊。本文收集本院近3年确诊的惊恐障碍病例18例,先后一度误诊,为了解其误诊原因,提高     

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.     

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.     

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.     

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.     

艾司西酞普兰治疗惊恐障碍的临床研究

目的 探讨艾司西酞普兰治疗惊恐障碍的有效性及安全性.方法 40例惊恐障碍患者给予艾司西酞普兰治疗8周.于第2、4、8周末进行汉密尔顿焦虑量表(HAMA)、焦虑自评量表(SAS)及药物不良反应量表(TESS)评定.结果 因不良反应不能耐受1例患者脱落,艾司西酞普兰治疗惊恐障碍从第2周开始见效;不良反应在治疗期间缓解或减轻,患者耐受性较好.结论 艾司西酞普兰治疗惊恐障碍安全有效.     

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。     

Cerebrospinal Fluid Monoamine Metabolites and Neuropeptides in Patients with Panic Disorder

Concentrations of homovanillic acid (HVA), 5-hydroxyindoleacetic acid (5-HIAA), 3-methoxy-4-hydroxyphenylgycol (MHPG) as well as somatostatin (SRIF) and ß-endorphin (ß-END) were assayed in the cerebrospinal fluid (CSF) of 34 patients with panic disorder and of ten neurological controls. No aberrations of the monoaminergic or peptidergic variables measured were found in the nonpanic state of patients with panic disorder. A modest correlation (P = 0.04) between total anxiety scores and CSF MHPG was observed.     

不同性别惊恐障碍患者SCL-90评分比较

目的：了解惊恐障碍患SCL-90评分的性别差异。方法：对连续门诊的54例男性和46例女性惊恐障碍患的SCL-90评分进行比较．同时对照中国人男女SCL-90评分常模进行分析。结果：全部100例患SCL-90标准分均显高于常模组(P＜0．01)，惊恐障碍男女两组比较除精神病性项目外，也均有显性差异(P＜0．05)．恐怖因子男性组高于女性组。结论：惊恐障碍SCL-90评分存在显的性别差异．男女惊恐障碍可能为不同的亚型。     

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.