高唤醒对创伤后应激障碍形成发展的影响及其神经机制

高唤醒是创伤后应激障碍(PTSD)的主要症状之一, 对创伤后应激障碍的形成与发展起核心作用。急性应激期产生的高唤醒可以预测其后PTSD的回避与麻木、再体验等症状的形成, 在创伤后早期, 降低唤醒程度可以减轻PTSD相关的症状表现。下丘脑-垂体-肾上腺轴异常变化会导致去甲肾上腺素(NE)、促肾上腺皮质激素释放因子(CRF)过度释放, 同时皮质醇(酮)水平下降, 这二者是高唤醒产生与维持的主要原因。另外, 5-羟色胺(5-HT)系统的高度激活也影响了高唤醒的形成。食欲素神经肽与NE、CRF与5-HT系统有密切的神经联系, 可能参与高唤醒的调节, 是近年来研究的一个热点。     

PTSD与PTG的关系：来自教师群体的追踪研究证据

采用追踪研究的方式,在汶川地震后一年和一年半两个时间点,对极重灾区的116名中小学教师进行问卷调查,通过建立交叉滞后模型,探讨其创伤后应激障碍（PTSD）和创伤后成长（PTG）在时间进程中的相互关系。结果显示：（1）震后一年和一年半的教师,其PTSD水平较低,PTG水平中等,两者具有一定稳定性;（2）在同一个时间点上,PTSD和PTG的相关不显著;（3）震后一年的PTG能显著负向预测震后一年半的PTSD,而震后一年的PTSD不能显著预测震后一年半的PTG。成长对于长期的创伤后负性应激降低有积极作用,可采用积极的视角来进行心理重建。     

Beyond monoamines: glutamatergic function in mood disorders

The monoamine theory has implicated abnormalities in serotonin and norepinephrine in the pathophysiology of major depression and bipolar illness and contributed greatly to our understanding of mood disorders and their treatment. Nevertheless, some limitations of this model still exist that require researchers and clinicians to seek further explanation and develop novel interventions that reach beyond the confines of the monoaminergic systems. Recent studies have provided strong evidence that glutamate and other amino acid neurotransmitters are involved in the pathophysiology and treatment of mood disorders. Studies employing in vivo magnetic resonance spectroscopy have revealed altered cortical glutamate levels in depressed subjects. Consistent with a model of excessive glutamate-induced excitation in mood disorders, several antiglutamatergic agents, such as riluzole and lamotrigine, have demonstrated potential antidepressant efficacy. Glial cell abnormalities commonly associated with mood disorders may at least partly account for the impairment in glutamate action since glial cells play a primary role in synaptic glutamate removal. A hypothetical model of altered glutamatergic function in mood disorders is proposed in conjunction with potential antidepressant mechanisms of antiglutamatergic agents. Further studies elucidating the role of the glutamatergic system in the pathophysiology of mood and anxiety disorders and studies exploring the efficacy and mechanism of action of antiglutamatergic agents in these disorders, are likely to provide new targets for the development of novel antidepressant agents.     

Role of stress, corticotrophin releasing factor (CRF) and amygdala plasticity in chronic anxiety

Stress initiates a series of neuronal responses that prepare an organism to adapt to new environmental challenges. However, chronic stress may lead to maladaptive responses that can result in psychiatric syndromes such as anxiety and depressive disorders. Corticotropin-releasing factor (CRF) has been identified as a key neuropeptide responsible for initiating many of the endocrine, autonomic and behavioral responses to stress. The amygdala expresses high concentrations of CRF receptors and is itself a major extrahypothalamic source of CRF containing neurons. Within the amygdala, the basolateral nucleus (BLA) has an important role in regulating anxiety and affective responses. During periods of stress, CRF is released into the amygdala and local CRF receptor activation has been postulated as a substrate for stress-induced alterations in affective behavior. Previous studies have suggested that synaptic plasticity in the BLA contributes to mechanisms underlying long-term changes in the regulation of affective behaviors. Several studies have shown that acute glutamate receptor-mediated activation, by either GABA-mediated disinhibition or CRF-mediated excitation, induces long-term synaptic plasticity and increases the excitability of BLA neurons. This review summarizes some of the data supporting the hypotheses that stress induced plasticity within the amygdala may be a critical step in the pathophysiology of the development of chronic anxiety states. It is further proposed that such a change in the limbic neural circuitry is involved in the transition from normal vigilance responses to pathological anxiety, leading to syndromes such as panic and post-traumatic stress disorders.     

术后乳腺癌患者体象对创伤后应激障碍和创伤后成长的影响：反刍的中介作用

为探讨乳腺癌患者反刍这一认知情绪调节方式在体象和创伤后应激障碍（PTSD）、创伤后成长（PTG）之间的中介作用,采用体象量表（BIS）、认知情绪调节问卷中文版（CERQ-C）、创伤后应激障碍量表（PSS）和创伤后成长问卷（PTGI）对150名乳腺癌术后患者进行研究。结果发现：（1）乳腺癌患者的体象可以正向预测PTSD和PTG;（2）乳腺癌患者的反刍在体象和PTSD的闯入性症状、回避性症状中起中介作用,在体象与PTG中的中介作用不显著。结果表明,体象既可以正向预测乳腺癌患者的PTSD和PTG,也可以通过反刍的中介作用影响PTSD。     

MMPI configural interpretation as applied to posttraumatic stress disorder in Vietnam veterans

This study investigated the systems of Minnesota Multiphasic Personality Inventory (MMPI) configural interpretation of Skinner and Jackson (1978) and Kunce (1979) with Vietnam veterans with posttraumatic stress disorder (PTSD). MMPI profiles of four groups differing in combat exposure were compared on four MMPI configural variables from Kunce (1979) and Skinner and Jackson (1978). The four groups were (a) PTSD sufferers, (b) Vietnam combat veterans without PTSD, (c) Vietnam noncombat veterans, and (d) Vietnam era veterans. All groups were further divided into hospitalized versus nonhospitalized subgroups. Dependent variables were Skinner and Jackson's (a) sociopathic modal profile, (b) neurotic profile, (c) psychotic profile, and (d) Kunce's emotional expression (enthusiastic-reserved) dimension. Results indicated that hospitalized PTSD subjects had significantly higher scores on Skinner and Jackson's neurotic profile; both hospitalized and nonhospitalized PTSD subjects had higher scores on the psychotic profile and were more "reserved" on Kunce's emotional expression dimension. Results were interpreted in terms of configural MMPI interpretation systems and the adjustment of Vietnam veterans with PTSD. PTSD was viewed as exhibiting cognitive, somatic, and affective features.     

青少年的自我同情对创伤后应激障碍与创伤后成长的影响:感恩的中介作用

采用自我同情量表、感恩问卷、创伤后应激障碍症状核查表和创伤后成长问卷对雅安地震4.5年后的499名中学生进行调查,以考察自我同情对创伤后应激障碍(PTSD)和创伤后成长(PTG)的影响,并检验感恩在其间的中介作用。结果发现,积极自我同情可以直接负向预测PTSD、正向预测PTG,消极自我同情可以直接正向预测PTSD;积极自我同情可以通过感恩负向预测PTSD、正向预测PTG,消极自我同情可以通过感恩正向预测PTSD、负向预测PTG。研究显示,积极的自我同情可以缓解青少年的PTSD、促进PTG的发展,而消极自我同情会加重青少年的PTSD;感恩在自我同情与PTSD和PTG之间发挥了显著的中介作用。     

MMPI Configural Interpretation as Applied to Posttraumatic Stress Disorder in Vietnam Veterans

This study investigated the systems of Minnesota Multiphasic Personality Inventory (MMPI) configural interpretation of Skinner and Jackson (1978) and Kunce (1979) with Vietnam veterans with posttraumatic stress disorder (PTSD). MMPI profiles of four groups differing in combat exposure were compared on four MMPI configural variables from Kunce (1979) and Skinner and Jackson (1978). The four groups were (a) PTSD sufferers, (b) Vietnam combat veterans without PTSD, (c) Vietnam noncombat veterans, and (d) Vietnam era veterans. All groups were further divided into hospitalized versus nonhospitalized subgroups. Dependent variables were Skinner and Jackson's (a) sociopathic modal profile, (b) neurotic profile, (c) psychotic profile, and (d) Kunce's emotional expression (enthusiastic-reserved) dimension. Results indicated that hospitalized PTSD subjects had significantly higher scores on Skinner and Jackson's neurotic profile; both hospitalized and nonhospitalized PTSD subjects had higher scores on the psychotic profile and were more "reserved" on Kunce's emotional expression dimension. Results were interpreted in terms of configural MMPI interpretation systems and the adjustment of Vietnam veterans with PTSD. PTSD was viewed as exhibiting cognitive, somatic, and affective features.     

The neuroendocrinology of posttraumatic stress disorder: new directions

Studies of the hypothalamic-pituitary-adrenal (HPA) axis in persons with posttraumatic stress disorder (PTSD) have produced variable findings. This review focuses on the factors likely to have affected the outcome of these studies, including population characteristics and experimental design. Also discussed is a possible role for the adrenal neurosteroid dehydroepiandrosterone (DHEA) as a mediator of HPA axis adaptation to extreme stress and the psychiatric symptoms associated with PTSD. The antiglucocorticoid properties of DHEA may contribute to an upregulation of HPA axis responses as well as mitigate possible deleterious effects of high cortisol levels on the brain in some PTSD subpopulations. The neuromodulatory effects of DHEA and its metabolite DHEAS at gamma-aminobutyric acid and N-methyl-D-aspartate receptors in the brain may contribute to psychiatric symptoms associated with PTSD. The possible importance of other neurohormone systems in modulating HPA axis and symptom responses to traumatic stress is also discussed. Understanding the complex interactions of these stress-responsive neurosteroid and peptide systems may help explain the variability in patterns of HPA axis adaptation, brain changes, and psychiatric symptoms observed in PTSD and lead to better targeting of preventive and therapeutic interventions.     

Symptoms Among Partners,Family, and Friends of Individuals with Posttraumatic Stress Disorder: Associations with Social Support Behaviors,Gender, and Relationship Status

Social support represents an important recovery factor for individuals with posttraumatic stress disorder (PTSD). Nevertheless, partners, family, and friends who take on the role of caregiver for individuals with PTSD might face multiple difficulties. For example, they are at risk for developing anxiety and depressive symptoms, which could negatively affect their ability to offer support. This study examined the associations between the difficulties of individuals with PTSD (i.e., symptoms and level of functioning), their caregivers’ (partners, family, and friends) anxiety and depressive symptoms, and social support behaviors according to 2 variables: relationship status and gender. Sixty-five individuals with PTSD and either their partner, family member, or friend filled out questionnaires and participated in a trauma-oriented discussion. Social support behaviors were coded. Results revealed no associations between the difficulties of individuals with PTSD and their caregivers’ symptoms. However, caregivers’ depressive symptoms were negatively associated with the quality of some of their social support behaviors. Moreover, relationship status and gender were significant moderators, indicating stronger negative associations between anxiety and depressive symptoms and some social support behaviors of men and caregiving partners. Male caregivers could have difficulties offering appropriate support and responding to traditional masculine roles (e.g., being strong and self-reliant) when they report symptoms themselves. Partners are particularly involved in the everyday life of individuals with PTSD. Thus, they could have difficulties keeping an optimal emotional distance to offer support when they report symptoms themselves. Future directions as well as clinical implications are discussed.     

Trauma-Related Negative Cognitions Mediate the Relationship Between Avoidant Personality Beliefs and Impeded Response to Psychotherapy for PTSD

There is strong research evidence for the association of personality pathology and posttraumatic stress disorder (PTSD), as well as trauma-related negative cognitions (TRNC) and PTSD symptoms. However, the relationship between personality pathology and TRNC in the context of PTSD is mostly unknown. In the present study, we aimed to examine whether avoidant and borderline personality beliefs (PB, indicator of personality pathology) could predict therapy outcome in PTSD, and whether the relationship between PB and therapy outcome could be mediated by TRNC. Sixty patients with PTSD were assessed for PB, TRNC and PTSD symptoms at baseline, and for PTSD symptoms at the termination of Prolonged Exposure Therapy. Baseline avoidant PB predicted significant variance in PTSD symptoms at termination over and above baseline PTSD symptoms (16% reduction in treatment effect per SD on avoidant PB). Moreover, TRNC at baseline fully mediated the relationships between baseline avoidant PB and PTSD symptoms at termination. This is the first study to show that avoidant PB predicts treatment response in PTSD, and that patients with avoidant beliefs are more vulnerable to have TRNC, which are associated with impeded therapy response. Our results highlight the importance of targeting both dysfunctional PB and TRNC in PTSD interventions.     

Feigning combat-related posttraumatic stress disorder on the personality assessment inventory

This study examined whether individuals who were instructed on the Diagnostic and Statistical Manual of Mental Disorders (4th ed. [DSM-IV]; American Psychiatric Association, 1994) criteria for posttraumatic stress disorder (PTSD) could feign PTSD on the Personality Assessment Inventory (PAI; Morey, 1991). The study also investigated whether PAI indexes of symptom exaggeration, the Negative Impression Management (NIM) scale and the Malingering index, could identify individuals feigning PTSD. The diagnostic rule for PTSD (Morey, 1991, 1996) was applied to the profiles of a group of 23 veterans with combat-related PTSD and 23 male undergraduates instructed to malinger PTSD. Seventy percent of the student malingerers produced profiles that received diagnostic consideration for PTSD. The NIM cutting score (> or = 8) was highly effective in detecting simulation of PTSD but resulted in the misclassification of a large number of true PTSD cases. There were no significant differences in the overall efficiency of the test with various validity criteria. We discuss the implications of these findings for the use of the PAI in the diagnosis of combat-related PTSD.     

睡眠问题在创伤后应激障碍各症状间的独特作用：基于交叉滞后网络分析模型

借助交叉滞后网络的分析方法, 探讨睡眠问题在创伤后应激障碍(PTSD)的症状系统中与其他症状的格兰杰因果关系。以经历舟曲泥石流的1460名儿童青少年为研究对象, 在灾后3, 15和27个月对其PTSD症状进行测量。交叉滞后网络分析结果显示：3到15个月时的睡眠问题的发出预期影响最高; 而15到27个月时与他人疏离和线索引发生理反应的发出预期影响最高。结果表明了睡眠问题对PTSD症状影响的时间特异性, 并为儿童青少年的PTSD干预方案和诊断模式提供了启示。     

The Biological Findings in Post-Traumatic Stress Disorder: A Review1

In this paper the authors review the literature on biological and treatment studies of post-traumatic stress disorder (PTSD) and present current unifying hypotheses regarding the pathophysiology. The psychophysiological studies stress overarousal, while endocrine studies suggest a decreased Cortisol production in denial and low symptom states with increases in highly symptomatic states. Suggestive evidence is provided that PTSD is associated with permanent changes in brain mechanisms involving the locus coeruleus, amygdala, and the hypothalamo-pituitary-adrenal axis. Drug treatments are promising but not fully satisfactory as yet. Directions for further research are provided.     

Measures of prefrontal system dysfunction in posttraumatic stress disorder

Clinical observations have suggested that individuals who have suffered traumatic stressful events exhibit disruption in abilities mediated by frontal brain systems. Therefore, this study employed tasks sensitive to frontal lobe dysfunction, including delayed response (DR), delayed alternation (DA), object alternation (OA), delayed matching-to-sample (DMTS), and delayed nonmatching-to-sample (DNMTS), with participants having posttraumatic stress disorder (PTSD). Compared to controls, the PTSD participants were unimpaired on DA and DMTS, but they showed deficits on DR, OA, and DNMTS tasks. This pattern of results suggests disruption of functioning in selective prefrontal brain systems. Results are discussed in the context of the neuropsychological features of PTSD, as well as possible neuropathological and etiological underpinnings of this disorder.     

Physiological arousal and attention in veterans with posttraumatic stress disorder

Psychophysiological reactivity has been well documented in WWII, Korean Conflict, and Vietnam veterans with posttraumatic stress disorder (PTSD). In addition, these individuals have demonstrated cognitive impairments within the domains of attention, concentration, new learning, and memory. However, there has been no research examining the impact of physiological arousal on attention in individuals with PTSD. This study documents the level of physiological arousal and associated disruption of attentional abilities in 28 Persian Gulf War veterans (18 without PTSD or other psychopathology and 10 with PTSD). This population represents a group of combat trauma victims who experienced a relatively acute onset of PTSD, thus providing a unique opportunity to compare prior psychophysiological and cognitive results with a group of veterans who manifested a recent onset of PTSD. Results indicated relatively comparable psychophysiological reactivity and arousal between Persian Gulf War veterans with PTSD and Persian Gulf War veterans without PTSD. Furthermore, attentional processes of veterans with PTSD were not more disrupted than in comparison soldiers. Results suggest that the intensity and chronicity of the disorder may impact physiological arousal and disruption of cognitive functioning. Following Persian Gulf War veterans with PTSD over time may reveal that psychophysiological arousal becomes more pronounced with chronicity, perhaps as memory networks become strengthened and/or neuroendocrine systems become increasingly disrupted.     

Fluoxetine inhibits corticotropin-releasing factor (CRF)-induced behavioural responses in rats

Corticotropin-releasing factor (CRF) is a potent neuromodulator of stress-related behaviour but the neural mechanisms underlying these effects are not clear. Studies were designed to test the hypothesis that CRF-induced behavioural arousal involves interactions with brainstem serotonergic systems. To examine interactions between CRF and serotonergic systems in the regulation of behaviour, CRF (1 microg, intracerebroventricular (i.c.v.)) or vehicle was infused in the presence or absence of the selective serotonin re-uptake inhibitor fluoxetine (0, 0.1, 1 or 10 mg/kg, intravenous (i.v.)). Fluoxetine was used at these doses because it is known to decrease serotonin cell firing rates while increasing extracellular serotonin concentrations in select forebrain regions. We then measured behavioural, neurochemical and endocrine responses. CRF increased locomotion and spontaneous non-ambulatory motor activity (SNAMA) in the home cages. Fluoxetine decreased tissue 5-hydroxyindoleacetic acid concentrations, a measure of serotonin metabolism, in specific limbic brain regions of CRF-treated rats (nucleus accumbens shell region, entorhinal cortex, central nucleus of the amygdala). Furthermore, fluoxetine inhibited CRF-induced SNAMA. CRF and fluoxetine independently increased plasma corticosterone concentrations, but the responses had distinct temporal profiles. Overall, these data are consistent with the hypothesis that CRF-induced facilitation of behavioural activity is dependent on brainstem serotonergic systems. Therefore, fluoxetine may attenuate or alleviate some behavioural responses to stress by interfering with CRF-induced responses.     

Social capital and PTSD among PLWHA in China: the mediating role of resilience and internalized stigma

Post-traumatic Stress Disorder (PTSD) is frequent among people living with HIV/AIDS (PLWHA). Few studies have investigated social-psychological predictors of PTSD in China. This study aimed to examine relationships between social capital, stigma, resilience and PTSD among PLWHA in China, and to provide effective suggestions for PTSD intervention. A cross-sectional study of 520 PLWHA was conducted from November 2015 to January 2016. Survey data were collected using anonymous self-reported questionnaire. Multivariable analyses were used to examine related factors of PTSD, and causal mediation analyses were conducted to assess whether stigma and resilience were mediators. Results indicated that higher risk of PTSD was independent associated with stronger stigma, decreasing social capital and lower resilience. There was an indirect relationship of social capital on PTSD mediated through resilience and HIV-related stigma. Therefore, PTSD intervention programs should not only pay attention to the role of social capital on PTSD, but also attach importance to stigma and resilience on PTSD symptoms.     

Conceptual and perceptual priming and dissociation in chronic posttraumatic stress disorder

Cognitive models of posttraumatic stress disorder (PTSD) assert that memory processes play a significant role in PTSD (see e.g., Ehlers & Clark, 2000). Intrusive reexperiencing in PTSD has been linked to perceptual processing of trauma-related material with a corresponding hypothesized lack of conceptual processing. In an experimental study that included clinical participants with and without PTSD (N = 50), perceptual priming and conceptual priming for trauma-related, general threat, and neutral words were investigated in a population with chronic trauma-induced complaints as a result of the Troubles in Northern Ireland. The study used a new version of the word-stem completion task (Michael, Ehlers, & Halligan, 2005) and a word-cue association task. It also assessed the role of dissociation in threat processing. Further evidence of enhanced perceptual priming in PTSD for trauma stimuli was found, along with evidence of lack of conceptual priming for such stimuli. Furthermore, this pattern of priming for trauma-related words was associated with PTSD severity, and state dissociation and PTSD group made significant contributions to predicting perceptual priming for trauma words. The findings shed light on the importance of state dissociation in trauma-related information processing and posttraumatic symptoms.     

Enhanced priming for trauma-related words predicts posttraumatic stress disorder

There is preliminary evidence that enhanced priming for trauma-related cues plays a role in posttraumatic stress disorder (PTSD). A prospective study of 119 motor vehicle accident survivors investigated whether priming for trauma-related stimuli predicts PTSD. Participants completed a modified word-stem completion test comprising accident-related, traffic-related, general threat, and neutral words at 2 weeks post-trauma. Priming for accident-related words predicted PTSD at 6 months follow-up, even when initial symptom levels of PTSD and depression and priming for other words were controlled. The results are in line with the hypothesis that enhanced priming for traumatic material contributes to the development of chronic PTSD.