单一连续应激对大鼠行为学和海马Bcl-2、Bax表达的影响

目的 检测单一连续应激(single prolonged stress,SPS)对大鼠行为学和海马神经细胞Bax、Bcl-2表达的影响.方法 将Wistar大鼠分为对照组和应激组.应激组给予SPS应激,采用旷场实验、拒俘反应实验、Morries水迷宫实验等观察大鼠情感行为改变,采用化学发光法测定血清皮质醇浓度,应用免疫组织化学方法检测海马神经元Bcl-2、Bax的表达.结果 对照组水迷宫实验逃避潜伏期为5.632s±1.065s,应激组为20.762s±3.236s(t=9.932,P＜0.01);对照组血清皮质醇浓度为1.25 μg/dl ±0.12μg/dl,应激组为0.58μg/dl±0.09μg/dl(t=7.340,P＜0.01).应激组海马Bcl-2、Bax表达升高,Bcl-2/Bax上调.结论 SPS应激能使大鼠表现出创伤后应激障碍行为,使海马神经细胞Bcl-2/Bax上凋,这可能与创伤后应激障碍发病机制有关.     

创伤后应激障碍大鼠海马中脑源性生长因子的表达变化

目的研究创伤后应激障碍(PTSD)大鼠血浆、海马CA_1区和齿状回神经元内脑源性生长因子(BDNF)的变化。方法用单一连续刺激(SPS)方法刺激大鼠产生PTSD模型,另进行强迫游泳(FS)刺激作为对照,ELISA检测不同时间(正常、刺激后2 h、12 h、1 d、7 d以及7 d后再次给予强迫游泳后2 h)大鼠血浆BDNF;取SPS后2 h、7 d、SPS+再次游泳后2 h和FS+再次游泳后2 h鼠脑组织,正常脑组织为对照,免疫组织化学技术观察大鼠海马神经元内BDNF的表达,以及采用荧光实时定量PCR法检测大鼠海马神经元内的BDNF-mRNA相对表达。结果大鼠经SPS刺激后2 h时血浆BDNF明显高于正常,7 d时与正常大鼠无明显差异,SPS+再游泳-2 h时明显高于各时间段及FS+再游泳后2 h;大鼠海马CA1区、齿状回内BDNF的表达以及海马内BDNF-mRNA相对表达也出现相似的改变。结论 PTSD大鼠血浆中BDNF浓度变化与海马内BDNF表达相关,BDNF的改变影响PTSD大鼠对创伤刺激的恐惧记忆形成、巩固和再摄取。     

创伤后应激障碍大鼠海马组织5-HT1受体mRNA的表达

目的探讨创伤后应激障碍(posttraumatic stress disorder,PTSD)大鼠海马组织中5-羟色胺受体1mRNA的表达。方法随机将雄性Wistar大鼠分为对照组和PTSD组,采用改良的单一连续应激(SPS&S)方法刺激大鼠建立PTSD大鼠模型,Morris水迷宫实验检测大鼠记忆功能,化学发光法检测大鼠血清皮质醇浓度。建模后1d、4d、7d、14d分离海马组织,RT-PCR方法检测5-羟色胺受体1的变化。结果 (1)对照组水迷宫实验逃避潜伏期为(5.632±1.065)s,模型组为(20.762±3.236)s(t=9.932,P<0.01);(2)对照组血清皮质醇浓度为(1.25±0.12)μg/dl,模型组为(0.58±0.09)μg/dl(t=7.340,P<0.01);(3)应激后1d、4d、7d、14d海马5-HT1A受体mRNA表达相对水平分别为0.846±0.067、0.510±0.052、1.007±0.137、1.109±0.106,与对照组1.223±0.152相比较,1d、4d、7d表达低于对照组(P<0.05);5-羟色胺1受体其他亚型未见表达。结论 PTSD大鼠海马中5-HT1A受体mRNA表达降低。     

创伤后应激障碍大鼠海马组织5-HT1受体mRNA的表达

目的探讨创伤后应激障碍(Posttraumatic Stress Disorder,PTSD)大鼠海马组织中5-羟色胺受体1mRNA的表达。方法随机将雄性wistar大鼠分为对照组和PTSD组,采用SPS(single-prolonged stress)方法刺激大鼠建立PTSD大鼠模型,Morris水迷宫实验检测大鼠记忆功能,化学发光法检测大鼠血清皮质醇浓度。SPS刺激后1d、4d、7d、14d分离海马组织,RT-PCR方法检测5-羟色胺受体1的变化。结果 (1)对照组水迷宫实验逃避潜伏期为(5.632±1.065)s,模型组为(20.762±3.236)s(t=9.932,P0.01);(2)对照组血清皮质醇浓度为(1.25±0.12)μg/dl,模型组为(0.58±0.09)μg/dl(t=7.340,P0.01);(3)SPS刺激后1d、4d、7d、14d海马5-HT1A受体mRNA表达相对水平分别为0.846±0.067、0.510±0.052、1.007±0.137、1.109±0.106,与对照组相1.223±0.152比较,1d、4d、7d表达低于对照组(P0.05);5-羟色胺1受体其他亚型未见表达。结论 PTSD大鼠海马中5-HT1A受体mRNA表达降低。     

捕食应激致大鼠海马钙/钙调素依赖性蛋白激酶途径调控紊乱

目的　探讨创伤后应激障碍 (PTSD)样行为异常的神经生物学机制。方法　将 16 0只Wistar大鼠随机分为捕食应激组和对照组 (每组各 80只 )。采用流式细胞仪、荧光标记术和免疫印迹法 ,检测捕食应激后 4 8h内大鼠海马细胞内游离Ca2 + 浓度与钙调素 (CaM )相对活性平均通道荧光 ,以及海马组织总CaM、Ca2 + /CaM依赖性蛋白激酶IIα (CaMKⅡα)与IV(CaMKⅣ )的表达变化。结果实验后即刻捕食应激大鼠海马细胞内游离Ca2 + 浓度明显增高 [应激组 (2 81± 70 )nmol/L ,对照组(2 0 7± 5 1)nmol/L ,P <0 0 1],12h增至顶峰 [应激组 (332± 84 )nmol/L ,对照组 (2 2 0± 5 4 )nmol/L ,P <0 0 1],2 4h仍明显增高 [应激组 (2 73± 6 7)nmol/L ,对照组 (2 0 0± 4 8)nmol/L ,P <0 0 1];实验后即刻游离CaM平均通道荧光则同步降低 (应激组 2 2± 0 5 ,对照组 3 4± 0 8,P <0 0 1;2 4h应激组2 7± 0 7,对照组 3 3± 0 8,P <0 0 5 ) ;而海马总CaM于实验后第 2 4h、CaMKⅡα和CaMKⅣ于实验后第 12h内表达明显增高 (P <0 0 1)。结论　捕食应激后早期海马细胞Ca2 + CaM及其依赖性蛋白激酶途径调控紊乱 ,在严重心理应激所致实验大鼠PTSD样行为异常中可能有意义。     

成人创伤后应激障碍海马体积研究的Meta分析

目的 综合评价成人创伤后应激障碍(Posttraumatic stress disorder,PTSD)的左、右侧海马体积.方法 利用Meta分析方法对国内外公开发表的关于成人PTSD左、右侧海马体积的研究文献进行综合定量分析.结果 共收集到符合纳入标准的文献23篇,累计病例共337例,累计对照共389名.PTSD组与健康对照组左侧海马体积分析显示,总体效应检验有统计学意义(Z=4.77,P<0.01),95%CI横线位于无效竖线左侧.提示PTSD的左侧海马体积减小;PTSD组与健康对照组右侧海马体积比较分析显示,总体效应检验有统计学意义(Z=5.01,P<0.01),95%CI横线位于无效竖线左侧,提示PTSD的右侧海马体积减小.漏斗图分布呈倒漏斗形,近似对称,Begg检验证实发表无偏倚.结论 成人PTSD患者左、右侧海马体积均减小.     

重症监护病房患者配偶创伤后应激障碍海马体积的研究

目的:探索重症监护病房(ICU)患者配偶中患创伤后应激障碍(PTSD)者双侧海马体积变化。方法:采用3.0 T磁共振检查(MRI)对20例ICU患者之配偶中患有PTSD者(PTSD组)及20例未患有PTSD者(对照组)进行全脑3D T1扫描;使用FreeSurfer获取并分析双侧海马体积变化,同时分析PTSD组双侧海马体积与PTSD诊断量表(CAPS)得分的相关性。结果:与对照组比较,PTSD组的双侧海马体积均显著缩小,差异具有统计学意义(P均0.01),但左侧海马体积减小比例大于右侧(左侧15%,右侧11%)。同时PTSD组的左右侧海马均与CAPS得分呈负相关(P均0.05)。结论:ICU患者配偶中患有PTSD者其海马体积存在缩小并存在偏侧性,需要给予及时有效的关心和干预。     

捕食应激对大鼠行为及空间学习记忆的影响

目的建立较理想的创伤后应激障碍(PTSD)动物实验模型.方法将42只雄性Wistar大鼠随机分为单纯捕食应激组(单纯组,n=15)、加强捕食应激组(加强组,n=15)和对照组(n=12).单纯组鼠仅与猫无生理伤害性接触10min(即单纯捕食应激);加强组鼠则在与猫接触后1周被再次被置于实验环境中5min(即加强捕食应激).结果在1个月的观察时间内,加强捕食应激可致实验动物旷场活动性明显减少[(10.2±2.4)分,P＜0.05],拒俘反应性明显增强[(2.67±0.51)分,P＜0.01].实验后第3天,加强组鼠Morris水迷宫训练潜伏期明显延长[(58.6±11.7)s,P＜0.01];空间觅向能力测试时在水迷宫的四个象限中无目的漫游.结论加强捕食应激成功诱发了实验动物较长时间的活动习性改变、警觉水平过高、惊恐行为、环境适应能力下降、躲藏逃避反应等多种行为异常,以及短暂空间学习和记忆能力障碍,可基本满足PTSD的主要临床表现.     

慢性应激对大鼠学习记忆功能和海马神经细胞粘附分子表达的影响

目的观察慢性应激对大鼠学习记忆功能和海马神经细胞粘附分子（NCAM）表达的影响,探讨海马NCAM表达在慢性应激影响学习记忆机制的作用。方法20只SD大鼠随机被分为对照组（10只）和慢性应激组（10只）,后者以束缚浸水应激方式连续应激21天,三周后行水迷宫实验,并用免疫组化法测定大鼠的脑海马区NCAM的表达。结果应激组在水迷宫测试中寻找水中隐藏平台的潜伏期为（7．1±8．9）秒,对照组为（12．3±4．2）秒,差异有统计学意义;穿越平台次数：应激组为（8．4±1．1）次,对照组为（12．5±1．9）次,差异有统计学意义。应激组海马CA3区NCAM的表达：25．2％±3．6％,对照组为37．9％±5．1％,差异有统计学意义。结论慢性应激对大鼠的学习记忆功能有抑制作用。其机制可能与应激抑制海马CA3区NCAM表达有关。     

创伤后应激障碍的睡眠障碍

尽管睡眠障碍在精神疾病中非常常见，但他常常被当作精神疾病的二级症状，认为对其主要精神疾病的治疗才是缓解睡眠苦恼的最可行办法。事实上，比如创伤后应激障碍(PTSD)的噩梦并不随总症状评分的下降而减少，有时可持续很长时间，而采用针对睡眠紊乱的治疗方案后，超过50％患者的创伤后应激症状可得到有效缓解。现论述PTSD对睡眠的影响，并讨论睡眠紊乱的治疗问题。     

Posttraumatic stress disorder

The authors review posttraumatic stress disorder in terms of clinical features, historical development and phenomenology, and relationship to other psychiatric disorders. Treatment modalities are detailed.     

Posttraumatic stress disorder and blindness

Four cases of posttraumatic stress disorder in blind patients are described. They demonstrate the importance of visual imagery in the processing of traumatic events and highlight the disruption of selective attention in this disorder.     

Posttraumatic stress disorder and bipolar mood disorder

Bipolar disorder (BD) is not only an endogenous condition. Severe negative life events have been shown to influence the development of the first episode and lifetime course of BD. Posttraumatic stress disorder (PTSD) is a severe and incapacitating mental condition that affect a significant proportion of the general population at some time in their lives. The concomitant presence of BD and PTSD has been shown to be more frequent than previously suggested and psychotic patients with trauma histories have a tendency to present more severe symptoms and are more proned to present substance use disorders. Trauma-related intrusive memories and nightmares of PTSD have been associated with mood changes. Also, kindling and behavioral sensitization have been proposed to explain the etiology and course of both disorders. Pharmacological approaches for this comorbidity are still based on empirical or not controlled approaches. In this article, we critically review the current literature regarding this co morbid condition, and highlight some aspects related to epidemiology, etiology, course and pharmacological treatment of both disorders. Overall, our review emphasizes the importance of systematically evaluate trauma histories in patients with BD.     

Posttraumatic stress disorder among Croatian veterans: a causal model

The present study investigates the etiological roles of premilitary risk factors, military entry conditions, war zone experiences, dissociative reactions to war zone experiences and homecoming reception in the development of chronic posttraumatic stress disorder (PTSD) among Croatian veterans. A total of 150 Croatian war veterans with the diagnosis of chronic combat-related PTSD, who sought treatment at Psychiatric Clinic, Osijek, Croatia, in the period 1993-1998, and who provided complete data, were selected as the sample for the present study from the treatment-seeking group of the ex-soldier population. Structural equation modeling is used to develop an etiological model concerning the relationships of premilitary risk factors, military entry conditions, war zone experiences, dissociative reactions, and homecoming reception with current symptoms of PTSD. An etiological model with satisfactory fit and parsimony was developed. In terms of the magnitude of variables' total contributions to the development of PTSD, war zone experiences are the most influential contributor which is followed by dissociative reactions, homecoming reception, military entry conditions and premilitary risk factors. Statistical significant direct effects to the development of PTSD were found for dissociative reactions and low family postwar support. The etiology of combat-related PTSD among Croatian veterans remains largely unexplained. Partial explanations are omission of other etiological factors, retrospective nature of the data and small study sample. The results are the source of questions for further research.     

Posttraumatic stress disorder and major depressive disorder: investigating the role of overlapping symptoms in diagnostic comorbidity

Studies of posttraumatic stress disorder (PTSD) have found high levels of comorbid major depressive disorder (MDD). One reason suggested for the comorbidity is the symptom overlap (contaminated symptoms) between the disorders. The present study investigated the contribution of contaminated symptoms (anhedonia, concentration, and sleep problems) to the comorbidity of PTSD and MDD. PTSD symptoms were subdivided into two groups: the contaminated symptoms and the 14 unique symptoms. It was speculated that if the contaminated symptoms are responsible for the comorbidity, then they will show less specificity than the unique symptoms, will be less highly correlated with a PTSD symptom total count, and be more frequently endorsed in PTSD patients with than without MDD. These hypotheses were tested in a sample (N = 1300) of psychiatric outpatients, 260 of whom had lifetime PTSD. None of the hypotheses were supported, thereby suggesting that the comorbidity between PTSD and MDD is not an artifact of symptom overlap.     

Posttraumatic stress disorder and psychiatric co-morbidity following stroke: the role of alexithymia

More research is needed to further our understanding of posttraumatic stress disorder symptoms (PTSD) and psychiatric co-morbidity following stroke, especially the trajectories of such symptoms over time. Previous studies suggest that exposure to a traumatic experience such as stroke is not sufficient to explain the etiology of PTSD. Alexithymia may be involved, but its relationships with PTSD and psychiatric co-morbidity following stroke remains unclear. This study aims to address these knowledge gaps. While in hospital, stroke patients (n = 90) completed questionnaires assessing PTSD symptoms, psychiatric co-morbidity, alexithymia and physical disability. PTSD symptoms and psychiatric co-morbidity were re-assessed approximately 3 months post-stroke (n = 78). The severity of post-stroke PTSD did not change significantly over time, while psychiatric co-morbidity reduced significantly. Alexithymia, in particular difficulty in identifying feelings, was associated with severity of post-stroke PTSD and psychiatric co-morbidity at baseline, but after adjusting for these, there was no significance 3 months post-stroke. We suggest that patients' difficulty in identifying feelings had a role to play in influencing relatively short-term rather than long-term PTSD and co-morbid psychiatric symptoms. Alternatively, PTSD could be interpreted as driving the alexithymic characteristics.