创伤暴露后吸烟行为变化与创伤后应激障碍的相关性研究

目的 了解创伤暴露后吸烟情况的变化与创伤暴露、创伤后应激障碍(PTSD)之间的关系.方法 在汶川地震6个月后,采用目前美国PTSD流行病学调查和诊断工具,按整群分层抽样原则对1125名参加汶川抗震救灾现场救援军人在抗震救灾前后吸烟情况的变化及PTSD的患病情况进行调查.PTSD诊断分别采用Davidson创伤量表(DTS)和DSM-Ⅳ标准确定.结果 实查1 056人,共检出PTSD患者69例,患病率为6.53%.本调查发现:(1)创伤暴露未对吸烟产生不利影响.创伤暴露后总的吸烟人数仅增加5例,吸烟量由创伤暴露前的(9.43±6.13)支/天减少到创伤暴露后的(8.04±6.05)支/天(t=6.595,P=0.000).(2)PTSD对吸烟有显著影响.PTSD与非PTSD相比会增加创伤暴露后初始吸烟的危险性(31.3%vs12.9%,X2=4.394,P=0.036).虽然PTSD组创伤暴露前、后总的吸烟量无明显改变(t=1.802,P=0.077),但创伤暴露后自诉吸烟量增多者PTSD组显著高于非FTSD组(X2=17.127,P=0.000).(3)多元Iogistic回归分析表明,服役满意度低(OR=2.574,P:0.000)、创伤暴露后患PTSD(OR=2.529,P=0.001)、创伤暴露前为烟草依赖者(OR=1.334,P=0.002)、军龄长(OR=1.334,P=0.002)是地震现场救援军人创伤暴露后吸烟行为增加的显著危险因素.结论 创伤暴露对吸烟无明显影响,而患PTSD会增加吸烟的危险.     

创伤后应激障碍综合征及其与海马-垂体-肾上腺轴的关系

介绍创伤后应激障碍综合征（PTSD）的基本特点及其与海马-垂体-肾上腺轴之间的关系。对PTSD患者的研究表明，海马内的皮质酮受体MR、GR是HPA轴调节的作用位点，它们在应激后引起的基因变化可能是PTSD发生的原因。通过对PTSD的动物模型——SPS模型的研究发现，海马和杏仁核的突触可塑性及杏仁核MAPK磷酸化水平的降低可能是造成PTSD患者出现众多精神症状的原因。     

地震现场救援军人吸烟与创伤后应激障碍的相关性

目的:了解吸烟与创伤暴露、创伤后应激障碍(PTSD)之间的关系.方法:共1 125名地震现场救援军人在四川汶川地震6个月后纳入调查.调查工具包括一般人口学资料、Davidson创伤量表(DTS)及烟草依赖情况调查表.结果:实查1 056人,共检出PTSD患者69例,PTSD患病率6.53%.调查发现:①PTSD组吸烟率...     

创伤后应激障碍中创伤记忆的研究进展

创伤后应激障碍(PTSD)是强烈精神创伤后发生的临床综合征。PTSD创伤记忆有其复杂性。本文对PTSD中创伤记忆的特点、创伤记忆重建以及认知神经科学的临床、动物实验研究现状进行综述。     

颅脑损伤患者术后创伤后成长与创伤后应激障碍的相关性

目的观察颅脑损伤患者术后创伤后成长水平及创伤后应激障碍(PTSD)情况,分析创伤后成长水平与PTSD的关系。方法选取2017-02—2019-02郑州市第九人民医院手术治疗的63例颅脑损伤患者,所有患者术后1个月接受创伤后成长评定量表(PTGI)评估,依据评估结果分为高水平组与低水平组,调查2组一般资料并评估患者术后PTSD评分,分析颅脑损伤患者术后PTSD与创伤后成长水平较低的关系。结果63例颅脑损伤患者经外科手术治疗后,创伤后成长低水平患者43例(68.25%)。不同创伤后成长水平的颅脑损伤患者年龄、性别、婚姻、职业、家庭月收入、发病原因、疾病类型、居住环境情况比较差异无统计学意义(P>0.05);低水平患者受教育年限(<12 a)、PTSD评分高于高水平患者,差异有统计学意义(P<0.05)。相关性分析显示,颅脑损伤患者术后创伤后成长与PTSD间呈负相关(r<0,P<0.05)。经单项Logistic回归分析,建立多元回归模型,在在校正各基线资料带来的影响后,结果显示受教育年限(<12 a)、PTSD可能是颅脑损伤患者术后创伤后成长水平低下的影响因素(OR>1,P<0.05)。结论颅脑损伤患者术后创伤后应激水平偏低,可能与PTSD有关,未来可考虑通过颅脑损伤术后早期评估患者是否伴有PTSD指导干预,可能对提高患者创伤后成长水平有积极意义。     

矿难后急性重性创伤后应激障碍症状激发和创伤有关短期记忆提取的功能性磁共振成像研究

目的 探讨急性重性创伤后应激障碍(post traumatic stress disorder,PTSD)患者的脑功能及执行记忆功能时的脑反应.方法 采用功能磁共振成像技术,对经历矿难的10例急性重性PTSD患者(PTSD组)和7例非PTSD对照(非PTSD组)执行症状激发任务,并首次采用1项创伤有关的短期记忆提取任务...     

矿难后急性重性创伤后应激障碍症状激发和创伤有关短期记忆提取的功能性磁共振成像研究

目的 探讨急性重性创伤后应激障碍(post traumatic stress disorder,PTSD)患者的脑功能及执行记忆功能时的脑反应.方法 采用功能磁共振成像技术,对经历矿难的10例急性重性PTSD患者(PTSD组)和7例非PTSD对照(非PTSD组)执行症状激发任务,并首次采用1项创伤有关的短期记忆提取任务进行记忆功能的测定.结果 症状激发试验中,PTSD组负性图片相比中性图片,左侧后扣带回、双侧尾状核和右侧丘脑等脑区激活增强,右侧扣带回和双侧额中回激活下降;PTSD组相比非PTSD组,右侧前扣带回、左侧额下回、双侧额中回及双侧颞中回等脑区激活下降,左侧海马旁回激活增高.短期记忆提取任务中,PTSD组负性图片相比中性图片,右侧后扣带回和双侧海马存在明显激活;PTSD组相比非PTSD组,右侧额下回、右侧额中回、左侧枕中回等脑区激活下降.记忆提取任务相比症状激发任务,PTSD组右侧海马旁回激活下降.结论 急性重性PTSD患者在急性期已存在部分脑区激活的下降以及记忆功能的减退.     

创伤后应激障碍的中枢神经系统机制

创伤后应激障碍（PTSD）所表现的各种精神症状，是与中枢神经系统（CNS）对应激信息的记忆密切相关的，本文就创伤后CNS的突触可塑性、CNS内神经递质的变化、PTSD的神经解剖学基础及改变、丘脑-垂体-肾上腺轴功能和PTSD治疗等方面对PTSD发生的中枢神经机制进行阐述。     

34例汶川地震灾区籍大学生创伤后应激障碍症状叙事疗法的疗效研究

目的 了解汶川地震2年后灾区籍大学生心理状况,观察叙事疗法对创伤后应激障碍（PTSD）患者症状的疗效.方法 采用方便取样.以四川某学院460例5·12地震灾区学生为研究对象,用创伤后应激障碍（PTSD）症状清单平民版（PTSD Checklist-Cicilian version, PCL-C）（分B、C、D三组症候群）,进行自填式调查.使用抑郁自评量表（SDS）、焦虑自评量表（SAS）对灾区籍大学生进行测评,采用叙事疗法对其中34例重度PTSD患者进行了治疗.结果 地震后2年灾区籍大学生PTSD患病率为7.39%,女性（4.78%）高于男性（2.61%）,叙事治疗前后除SDS总分外,其余各项差异显著（P＜0.05）.结论 叙事疗法对地震后灾区籍大学生PTSD治疗有效,在以后的叙事心理干预中应注意关注PTSD患者的抑郁症状.     

PTSD相关睡眠障碍的概述

创伤后应激障碍（PTSD）是突发威胁性或灾难性事件所致的延迟出现且长期存在的一组精神障碍，以再度体验创伤、回避行为和警觉性增高等为表现。创伤应激后常出现睡眠障碍，尤其那些发展为PTSD者。睡眠障碍是PTSD标志性症状之一，以梦魇和失眠最常见，不仅出现早，严重影响生活质量、健康和well—being，且预示PTSD的发生、程度和转归（Maher等，CNSDrugs，2006）。本文简述了PTSD相关睡眠障碍，现报道于后。     

Single prolonged stress: toward an animal model of posttraumatic stress disorder

Although selective serotonin reuptake inhibitors (SSRIs) are reported to be effective in decreasing posttraumatic stress disorder (PTSD) symptoms, a subgroup of PTSD patients remain chronically symptomatic and maintain conditioned fear responses to traumatic stimuli. In this context, the establishment of an appropriate animal model of PTSD is necessary to promote better understanding of the mechanisms of the disorder and to facilitate the development of more effective therapeutic alternatives to SSRIs. Although no single widely accepted animal model of PTSD has been established to date, the single prolonged stress (SPS) animal model has been partially validated as a model for PTSD. SPS rats mimic the pathophysiological abnormalities and behavioral characteristics of PTSD, such as enhanced anxiety‐like behavior and glucocorticoid negative feedback, and they exhibit the expected therapeutic response to paroxetine on enhanced fear memory. In addition, SPS rats exhibit enhanced freezing in response to contextual fear conditioning, and impaired extinction of fear memory, which is alleviated by D ‐cycloserine. The enhanced consolidation and impaired extinction of fear memory found in SPS rats suggests that this model has additional value because recent studies of PTSD indicate that memory abnormalities are a central feature. In this study, we summarize the behavioral and pathophysiological PTSD‐like symptoms in SPS, focusing on memory abnormalities, and evaluate the validity of SPS as an animal model of PTSD. Depression and Anxiety, 2009. © 2009 Wiley‐Liss, Inc.     

Mechanisms of Sex Differences in Fear and Posttraumatic Stress Disorder

Following sexual maturity, females disproportionately have higher rates of posttraumatic stress disorder (PTSD) and experience greater symptom severity and chronicity as compared with males. This observation has led many to examine sex differences in PTSD risk factors. Though relatively few, these studies reveal that the root causes of PTSD sex differences are complex, and partly represent interactions between sex-specific nonbiological and biological risk factors, which differentially shape PTSD vulnerability. Moreover, these studies suggest that sex-specific PTSD vulnerability is partly regulated by sex differences in fear systems. Fear, which represents a highly conserved adaptive response to threatening environmental stimuli, becomes pathological in trauma- and stress-based psychiatric syndromes, such as PTSD. Over the last 30 years, considerable progress has been made in understanding normal and pathological molecular and behavioral fear processes in humans and animal models. Thus, fear mechanisms represent a tractable PTSD biomarker in the study of sex differences in fear. In this review, we discuss studies that examine nonbiological and biological sex differences that contribute to normal and pathological fear behaviors in humans and animal models. This, we hope, will shed greater light on the potential mechanisms that contribute to increased PTSD vulnerability in females.     

Traumatic stress: effects on the brain

Brain areas implicated in the stress response include the amygdala, hippocampus, and prefrontal cortex. Traumatic stress can be associated with lasting changes in these brain areas. Traumatic stress is associated with increased cortisol and norepinephrine responses to subsequent stressors. Antidepressants have effects on the hippocampus that counteract the effects of stress. Findings from animal studies have been extended to patients with post-traumatic stress disorder (PTSD) showing smaller hippocampal and anterior cingulate volumes, increased amygdala function, and decreased medial prefrontal/anterior cingulate function. In addition, patients with PTSD show increased cortisol and norepinephrine responses to stress. Treatments that are efficacious for PTSD show a promotion of neurogenesis in animal studies, as well as promotion of memory and increased hippocampal volume in PTSD.     

Long-term behavioural alterations in female rats after a single intense footshock followed by situational reminders

Post-traumatic stress disorder (PTSD) affects a vulnerable sub-population of individuals exposed to a traumatic event. This psychopathology induces long-lasting hypothalamo-pituitary-adrenal (HPA) axis hypoactivity, hyperarousal and avoidance of trauma-like situation. PTSD also manifests a high co-morbidity with anxiety disorders. The aim of the present study was to characterise long-term biobehavioural alterations in female rats in an animal model of PTSD consisting in an intense footshock (2 mA, 10s) followed by three weekly situational reminders. This procedure induced several long-term alterations: increased anxiety behaviour, reduced time spent in an 'aversive-like' context, altered social behaviour and blunted corticosterone response to stress. These results demonstrate that exposure to an intense footshock associated with repeated situational reminders elicited long-term disturbances which lasted more than 1 month after the footshock administration. Our findings suggest that this paradigm could provide a useful animal model of PTSD.     

Memory and prefrontal functions in earthquake survivors: differences between current and past post-traumatic stress disorder patients

Objective: Many studies reported deficits in cognitive functions in post‐traumatic stress disorder (PTSD). Most were, however, conducted on man‐made trauma survivors. The high comorbidity of alcohol use and depression with PTSD in these studies further complicated the interpretation of their results. We compared prefrontal lobe functions and memory in three earthquake survivor groups: current PTSD, past PTSD and no PTSD. We hypothesized that prefrontal performances of the current and past PTSD groups would be worse than that of control group. Method: Survivors of the 1999 earthquakes in Turkey were evaluated for current and lifetime PTSD. Memory and prefrontal functions were assessed by a neuropsychological test battery. Results: Current PTSD patients performed worse on attention, verbal memory, verbal fluency, and psychomotor speed. Past PTSD group was similar to the controls on most cognitive measures, except for their vulnerability to proactive interference and low performance in verbal fluency for animal names. Conclusion: Our findings indicate that the prefrontal organization and monitorization of verbally processed information are defective in earthquake‐related PTSD patients, more so in the current PTSD group.     

Genetic predisposition and the development of posttraumatic stress disorder in an animal model.

BACKGROUND: Exposure to extremely stressful events can lead to Posttraumatic stress disorder (PTSD). Due to the complexity of PTSD, animal models have been designed and advanced to address the role of psychosocial stressors in the etiology; however, the apparent role of genetics in susceptibility to PTSD-like behaviors in animals remains unexplored. METHODS: An animal model of congenital learned helpless (cLH) behavior has been used to study the effects of genetic disposition as a risk factor for the development of PTSD-like behaviors. Animals were monitored for changes in pain tolerance, spatial memory and hypothalamic-pituitary-adrenal functioning after re-exposure to intermittent stress in the presence and absence of situational cues. RESULTS: Exposure to stress resulted in an increase in pain tolerance in the cLH animals. In the spatial memory test 80% of the cLH animals manifested a decrease in performance after exposure to stress. These animals also had a blunted poststress corticosterone response. CONCLUSIONS: The genetic learned helpless animal model exhibited physiologic symptoms of analgesia, cognitive deficits and hyporesponsivity of the hypothalamic-pituitary-adrenal axis similar to those observed in human subjects with PTSD. It is proposed that the cLH model may be a valuable tool for exploring the role of genetic predisposition in the etiology of PTSD.     

Neuroimaging and neurocircuitry in post-traumatic stress disorder: What is currently known?

Neurobiologic, psychologic, and social factors interact jointly to create and perpetuate the symptoms of posttraumatic stress disorder (PTSD). The fear conditioning paradigm in animal research helped researchers gather preclinical evidence for the possible contribution of several brain areas to PTSD symptoms. In the past 10 years, highly sophisticated neuroimaging techniques made it possible for researchers to look at the brain of patients with PTSD and draw conclusions about the neurocircuitry underlying PTSD symptoms. In this article, the author will review the evidence from neuroimaging studies for the involvement of the following brain areas in PTSD neurocircuitry: the amygdala, the anterior cingulate cortex and subcallosal gyrus, the inferior frontal gyrus, the posterior cingulate cortex, and the hippocampus. Neuroimaging studies have shown these areas as altered in structure or function in patients with PTSD. The author also presents the normal functions that these areas subserve and, whenever possible based on the evidence, infer how their dysfunction may contribute importantly to the symptomatology of PTSD.