Who develops acute stress disorder after accidental injuries?

BACKGROUND: Acute stress disorder (ASD) is still a much discussed diagnosis, and research on predictors of ASD is sparse. The aim of this study was to assess the prevalence of ASD in a random sample of accident victims and to investigate the associations between different independent variables and ASD symptomatology with the objective to find a regression model best explaining the variance in ASD symptom level. METHODS: We collected a randomized sample of hospitalized accident victims (n = 323). ASD was assessed using the Peritraumatic Dissociative Experiences Questionnaire and the Clinician-Administered Posttraumatic Stress Disorder Scale. Correlations and multiple regression analyses were computed with four groups of variables. This yielded the variables entered into a final multiple regression analysis. RESULTS: Thirteen patients (4.0%) met all criteria for a diagnosis of ASD. Thirty-two patients (9.9%) met the criteria for a diagnosis of subsyndromal ASD. Thirty-eight percent of the variance in ASD symptom level was explained with a regression model including stay at the intensive care unit, preexisting psychiatric disorder, sense of coherence, sense of death threat, appraisal of accident severity, preventability of the accident by others, pain and appraisal of coping ability regarding physical recovery. CONCLUSIONS: This study furthers the discussion about the requirements for the ASD diagnosis. It also points to the importance of not only assessing objective accident-related variables in the aftermath of an accident but also of giving more consideration to the subjective experience and appraisal of the accident in the prevention of ASD.     

Chronic pain and posttraumatic stress disorder: mutual maintenance?

Common sequelae following a traumatic event include chronic pain and posttraumatic stress disorder (PTSD). Over the last decade, the literature relating to PTSD has become progressively more sophisticated, resulting in well-supported theories and treatments for sufferers. Equivalent research relating to chronic pain has more recently gathered momentum. However, to date there has been minimal attention devoted to the concurrence of the two disorders, even though high comorbidity has been noted. This review begins by briefly summarizing the literature relating to the two disorders in terms of symptoms, prevalence and comorbidity. It explicates the major psychological theories of chronic pain and PTSD and reviews the evidence relating what factors maintain the disorders. A number of pathways by which chronic pain and PTSD may be mutually maintaining are highlighted. We conclude that chronic pain and PTSD are mutually maintaining conditions and that there are several pathways by which both disorders may be involved in the escalation of symptoms and distress following trauma. Treatment implications are considered, as are issues for future research.     

Fibromyalgia: a stress disorder? Piecing the biopsychosocial puzzle together

Fibromyalgia (FM) is a controversial syndrome, characterised by persistent widespread pain, abnormal pain sensitivity and additional symptoms such as fatigue and sleep disturbance. The syndrome largely overlaps with other functional somatic disorders, particularly chronic fatigue syndrome (CFS). Although the exact aetiology and pathogenesis of FM are still unknown, it has been suggested that stress may play a key role in the syndrome. This article first reviews the function of the stress response system, placing special emphasis on the relationships between adverse life experiences, stress regulation and pain-processing mechanisms, and summarising the evidence for a possible aetiopathogenetic role of stress in FM. Finally, an integrative biopsychosocial model that conceptualizes FM as a stress disorder is proposed, and the clinical and research implications of the model are discussed.     

Posttraumatic stress disorder and traumatic brain injury: can they co-exist?

The possibility that posttraumatic stress disorder (PTSD) can develop following traumatic brain injury (TBI) has been the subject of considerable debate. The traditional view has held that impaired consciousness that occurs with TBI precludes encoding of the traumatic experience, and this prevents subsequent reexperiencing symptoms. This paper critically reviews available, empirical studies on PTSD in TBI populations and suggests that these two conditions can co-exist. The various mechanisms that may mediate PTSD following TBI are discussed, and special attention is given to issues that recognize the distinctive features of PTSD following TBI. These processes include implicit processing, biologically mediated fear conditioning, and reconstruction of trauma memories. Finally implications for assessment, treatment, and forensic investigation of PTSD in TBI populations are, addressed. This review concludes that TBI populations provide a useful means by which the role of traumatic memories (and impaired memories) in posttraumatic adjustment can be studied.     

Is posttraumatic stress disorder associated with specific deficits in episodic memory?

People with PTSD often report difficulties remembering day to day information unrelated to their traumatic episode. In addition, structural and functional imaging techniques have identified abnormalities in the brains of people with PTSD in regions known to be important for memory functioning. Nevertheless, studies investigating cognitive functioning in people with PTSD have reported widely varying results. The aim of this review is to investigate studies reporting performance on tests of episodic memory. Specifically, papers were examined in relation to the hypothesised memory functions of the frontal lobes, the hippocampus and the amygdala. It is concluded that while there is reasonable evidence of frontal lobe involvement, memory deficits caused by hippocampal involvement have been more difficult to detect. There are no published studies looking at the involvement of the amygdala although preliminary evidence suggests that people with PTSD do have memory deficits resulting from dysfunction of this structure. Reasons for the inconclusiveness of the results are discussed.     

Can we predict intensive care relatives at risk for posttraumatic stress disorder?

Aims:

To identify the relatives of the intensive care unit (ICU) patients at risk for developing symptoms of posttraumatic stress disorders.

Setting:

A multidisciplinary hospital ICU.

Design:

Prospective single center observational study.

Material and Methods:

Relatives of patients admitted in the ICU (May06-Nov06) who consented to answer the questionnaire participated in the study. Anxiety was assessed by using the Hospital Anxiety and Depression Scale (HAD) and vulnerability to posttraumatic disorder (PTSD) by using the Impact of Event Scale Revised (IES-R) which was administered on the fifth day of admission and at two months following discharge or death.

Results:

During admission, 48% of the relatives had a HAD score >11 and 72% showed IES-R score >26. There was no association of HAD with gender, patient outcome, working status, age of the patient, or mode of payment of the bills. There was significant association of IES-R >26 with trauma admission, HAD score >11 and mode of payment with the relatives of insured being more stressed as compared to those who settled their bills personally. A total of 35% relatives showed symptoms of posttraumatic stress reaction consistent with a high risk of PTSD after two months. Death in the hospital resulted in elevated HAD and IES-R score during admission and at the two month follow-up. Persistence of stress symptoms was more in school drop outs, working relatives, parents and those with initial anxiety score >11.

Conclusions:

HAD score greater than 11 was the only factor at admission which could statistically predict a higher PTSD score on follow-up. Adequate counseling of this group of relatives may prevent lasting psychological sequelae of an ICU admission in the relatives of critically ill.     

Do all psychological treatments really work the same in posttraumatic stress disorder?

A recent meta-analysis by Benish, Imel, and Wampold (2008, Clinical Psychology Review, 28, 746–758) concluded that all bona fide treatments are equally effective in posttraumatic stress disorder (PTSD). In contrast, seven other meta-analyses or systematic reviews concluded that there is good evidence that trauma-focused psychological treatments (trauma-focused cognitive behavior therapy and eye movement desensitization and reprocessing) are effective in PTSD; but that treatments that do not focus on the patients' trauma memories or their meanings are either less effective or not yet sufficiently studied. International treatment guidelines therefore recommend trauma-focused psychological treatments as first-line treatments for PTSD. We examine possible reasons for the discrepant conclusions and argue that (1) the selection procedure of the available evidence used in Benish et al.'s (2008)meta-analysis introduces bias, and (2) the analysis and conclusions fail to take into account the need to demonstrate that treatments for PTSD are more effective than natural recovery. Furthermore, significant increases in effect sizes of trauma-focused cognitive behavior therapies over the past two decades contradict the conclusion that content of treatment does not matter. To advance understanding of the optimal treatment for PTSD, we recommend further research into the active mechanisms of therapeutic change, including treatment elements commonly considered to be non-specific. We also recommend transparency in reporting exclusions in meta-analyses and suggest that bona fide treatments should be defined on empirical and theoretical grounds rather than by judgments of the investigators' intent.     

Disorders of extreme stress following war-zone military trauma: associated features of posttraumatic stress disorder or comorbid but distinct syndromes?

Disorders of extreme stress not otherwise specified (DESNOS) and posttraumatic stress disorder (PTSD) were found to be comorbid but distinct among military veterans seeking inpatient PTSD treatment: 31% qualified for both conditions, 29% were diagnosed PTSD only, 26% were classified DESNOS only, and 13% met criteria for neither. PTSD diagnosis was associated with elevated levels of war-zone trauma exposure and witnessing atrocities and with impairment on the Mississippi Scale for Combat-Related PTSD and the Penn Inventory. DESNOS classification (but not PTSD) was associated with (a) early childhood trauma and participation in war-zone atrocities, (b) extreme levels of intrusive trauma reexperiencing, (c) impaired characterological functioning (object relations), and (d) use of intensive psychiatric services. PTSD and DESNOS may be comorbid but distinct posttraumatic syndromes and, as such, warrant careful clinical and scientific investigation.     

Are the neural substrates of memory the final common pathway in posttraumatic stress disorder (PTSD)?

A model for the posttraumatic stress disorder (PTSD) as a disorder of memory is presented drawing both on psychological and neurobiological data. Evidence on intrusive memories and deficits in declarative memory function in PTSD-patients is reviewed in relation to three brain areas that are involved in memory functioning and the stress response: the hippocampus, amygdala, and the prefrontal cortex. Neurobiological studies have shown that the noradrenergic stress-system is involved in enhanced encoding of emotional memories, sensitization, and fear conditioning, by way of its effects on the amygdala. Chronic stress also affects the hippocampus, a brain area involved in declarative memories, suggesting that hippocampal dysfunction may partly account for the deficits in declarative memory in PTSD-patients. Deficits in the medial prefrontal cortex, a structure that normally inhibits the amygdala, may further enhance the effects of the amygdala, thereby increasing the frequency and intensity of the traumatic memories. Thus, by way of its influence on these brain structures, exposure to severe stress may simultaneously result in strong emotional reactions and in difficulties to recall the emotional event. This model is also relevant for understanding the distinction between declarative and non-declarative memory-functions in processing trauma-related information in PTSD. Implications of our model are reviewed.     

Posttraumatic stress disorder and depression among new mothers at 8?months later of the 2008 Sichuan earthquake in China

On May 12, 2008, a magnitude 8.0 earthquake struck China's southwestern Sichuan province. Recent studies have identified mental health problems among the survivors, but little is known about the impact of the Sichuan earthquake on the mental health of new mothers in the area. The main objective was to assess the impact of the Sichuan earthquake on the posttraumatic stress disorders (PTSD) and depression of new mothers. A total of 317 new mothers were interviewed in the hospital from January 2009 to March 2009. Symptoms of PTSD were measured using the impact of event scale-revised, and symptoms of postpartum depression were measured using the Center for Epidemiologic Studies Depression scale. The prevalence rates of PTSD and postpartum depression were 19.9% and 29.0%, respectively. Women with high earthquake exposure had higher risks of PTSD (odds ratio (OR), 5.91; 95% confidence interval (CI), 1.75–19.97; P < 0.001) and postpartum depression (OR, 7.28; 95% CI, 2.51–21.08; P < 0.001) than women without earthquake experience. In addition, women with low monthly family income and farm workers had a higher risk of having PTSD; women who were unemployed or with lower monthly family income and poor sleep had a higher risk of having depression. Earthquake experience increased the risks of having PTSD and depression among new mothers at 8 months later of the earthquake.     

Major depressive disorder with anger: a bipolar spectrum disorder?

BACKGROUND: Depression with anger may be more common in bipolar disorders. The aim of the study was to assess whether major depressive disorder (MDD) with anger could be included in the bipolar spectrum, by comparing it to MDD without anger and to bipolar II disorder. METHODS: Consecutive outpatients (281 bipolar II disorder and 202 MDD) presenting for major depressive episode (MDE) treatment were interviewed with the DSM-IV structured clinical interview. Clinical variables used to support the inclusion of MDD with anger in the bipolar spectrum were age of onset, many MDE recurrences, atypical features of depression, depressive mixed state (an MDE plus some concurrent hypomanic symptoms), and bipolar family history. RESULTS: Frequency of MDE with anger was 50.5% [61.2% in bipolar II, and 35.6% in MDD (z = 5.5, p = 0.0000, 95% CI 16.8-43.3%)]. Logistic regression of MDE with anger (dependent variable) versus bipolar variables showed that MDE with anger was significantly associated with all bipolar variables, apart from recurrences. MDD with anger, compared with MDD without anger, had significantly lower age of onset, more marked depressive mixed state, a bipolar family history with more cases, but comparable atypical features and Global Assessment of Functioning scores. MDD with anger, compared with bipolar II disorder, had significantly higher age of onset, less atypical features, and a bipolar family history with less cases. CONCLUSIONS: MDE with anger was common in outpatients (more in bipolar II disorder). MDD with anger may be midway between MDD without anger and bipolar II disorder, and might be included into the bipolar spectrum. However, MDD with anger does not appear to be associated with the often reported negative response to monotherapy with antidepressants.     

Is bipolar II disorder misdiagnosed as major depressive disorder in children?

OBJECTIVES: To estimate the lifetime prevalence of bipolar II disorder in children and adolescents presenting with DSM-IV major depressive disorder (MDD). METHODS: Sixty-one consecutive subjects aged < or =18 years attending the outpatient services of the Child and Adolescent Psychiatric (CAP) services of the National Institute of Mental Health and Neurosciences (NIMHANS), Bangalore, India with a diagnosis of MDD were evaluated using the Missouri Assessment of Genetics Interview for children (MAGIC). Two psychiatrists, one of whom was a child psychiatrist diagnosed hypomania by consensus. RESULTS: Twelve children had a past episode of hypomania (20%), which was hitherto undiagnosed clinically. LIMITATIONS: We recruited subjects from a psychiatric hospital, thus limiting the generalizability of the finding. Sample size was relatively small and assessments were cross-sectional. CONCLUSIONS:: Our study shows that bipolar II disorder is often misdiagnosed as MDD in children. The study also highlights that the chance of diagnosing bipolarity is enhanced by using semi-structured interview in routine clinical practice.