What is post-traumatic stress disorder?

Although post-traumatic stress disorder (PTSD) and traumatic brain injury (TBI) are categorized as separate and discrete disorders, the boundary between them is sometimes indistinct. Their separation is based on the assumption that PTSD results primarily from psychological stress, while TBI is the consequence of an identifiable injury to the brain. This distinction is based on an antiquated polarity between mind and brain, and the separation of the two disorders often becomes arbitrary in day-to-day psychiatric practice and research.     

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.     

Comorbidities in posttraumatic stress disorder: rule or exception?

Posttraumatic stress disorder (PTSD) commonly occurs in conjunction with other psychiatric disorders. The present article reviews PTSD and its comorbidities such as anxiety disorders, substance abuse, mood disorders, suicide attempts, dissociative disorder and somatoform disorder.     

The weaker sex? Gender and post-traumatic stress disorder

We discuss the gender-specific differences for traumatic events and Post-Traumatic Stress Disorder (PTSD) as found in the epidemiological literature. Recent research literature consistently reports three interesting findings: 1) men experience traumatic events more often, 2) women and men differ in the type of traumatic experiences they experience, and 3) women more often develop PTSD after the experience of a traumatic event. In the second part of the present article we provide some explanations for these differences. The reported higher vulnerability of women for PTSD could be due to the methodology used, the higher prevalence of childhood sexual abuse and rape in women, the different coping styles of women and men, or the more limited socio-economic resources of women.     

Does acute stress disorder predict post-traumatic stress disorder in traffic accident victims? Analysis of a self-report inventory

The objective of this study was to account for acute stress disorder (ASD) and post-traumatic stress disorder (PTSD) morbidity in a self-report survey of traffic accident victims and to evaluate the relationship between ASD and PTSD in this sample, and furthermore, to find both a model of independent variables accounting for variance in ASD and PTSD symptom level. Ninety patients, treated at an emergency ward after traffic accidents, participated in this longitudinal self-report survey. ASD was assessed using the Acute Stress Disorder Scale (ASDS) and PTSD was assessed at 6-8 months follow-up using the Posttraumatic Diagnostic Scale (PDS). Twenty-five patients (28%) met the cutoff scores for ASDS. Fifteen patients (17%) fulfilled criteria for PTSD according to the PDS. ASD was only able to predict 50% of patients who later developed high levels of PTSD symptomatology. A model of three variables explained 35% of the variance in ASD symptom level. Two variables explained 40% of the variance in PTSD symptom level. In both regression models, dissatisfaction with social support was associated with a higher symptom level. The results from this study reflect already voiced problems with the ASD diagnosis. The lack of precision in predicting who will develop PTSD is pronounced in this study. The acute traumatic symptom level explains a large part of the variance in PTSD symptom level. However, other variables also seem to play an important role.     

Is overactivity the core feature of hypomania in bipolar II disorder?

BACKGROUND: Recent studies found that overactivity (increased goal-directed activities) may be as important as mood change (elevated and/or irritable mood) for the diagnosis of mania/hypomania (on family history and psychometric grounds), questioning DSM-IV-TR criteria always requiring mood change and listing overactivity among the other symptoms. The aim of the study was to find out if overactivity was at least as important as mood change for the diagnosis of hypomania. SAMPLING AND METHODS: A consecutive sample of 137 bipolar II disorder (BP-II) and 76 major depressive disorder remitted outpatients were interviewed with the Structured Clinical Interview for DSM-IV by a senior clinical and research psychiatrist in a private practice. Patients were asked if they had had hypomanic symptoms and episodes, and which were the most common hypomanic symptoms during the various episodes. The study aim had not been planned when variables were collected for different study goals. RESULTS: Overactivity was the most common hypomanic symptom in BP-II, more common than elevated mood, and had the strongest association with BP-II among all the hypomanic symptoms (overactivity odds ratio = 15.4, elevated mood odds ratio = 12.6). Three factors were found: an 'elevated mood' factor including elevated mood and increased self-esteem; a 'mental activation' factor including racing/crowded thoughts, and a 'behavioral activation' factor including overactivity. There was no relationship between overactivity and mood change. Irritable mood was not associated with overactivity and elevated mood. BP-II was present in 21.6%of patients without a history of overactivity, and in 81.0% of patients with a history of overactivity. BP-II was present in 25.0% of patients without elevated mood, and in 63.3% of patients with elevated mood. As a predictor of BP-II, overactivity had a sensitivity of 90.5%, a specificity of 61.8%, and a positive predictive value of 81.0% (elevated mood: 72.2, 82.8, and 88.3%, respectively). Five or more hypomanic symptoms had the most balanced combination of sensitivity (82.4%) and specificity (85.5%) for BP-II, and a positive predictive value of 91.1%. Overactivity was present in 89.5% of patients with a history of > or = 5 hypomanic symptoms, while elevated mood was present in 76.6%. CONCLUSIONS: Theresults seem to support the view that overactivity may be a core feature of hypomania, suggesting the upgrading of overactivity to a stem criterion for hypomania.     

Stress-induced increases in avoidance responding: an animal model of post-traumatic stress disorder behavior?

One prominent symptom of post-traumatic stress disorder (PTSD) is avoidance of stimuli reminiscent of the traumatic event. We attempted to study this aspect of PTSD in two experiments. Groups of rats received forty 3-s tailshocks, or served as home cage controls (HCC). Twenty-four hours later, all subjects received a 4-h session of leverpress escape/avoidance conditioning. In Experiment 1, shock periods in the absence of a response were 1 s; in Experiment 2 they were 30 s. No group differences were observed in Experiment 1. In Experiment 2, previously shocked animals made more avoidance responses and had a higher percent avoidance during the fourth hour of the session than controls. Further, previously shocked animals had a higher efficiency ratio (the percent of responses that were avoidances). No group differences were observed in leverpresses during the safety period (an index of anxiety) in either study. Results are discussed in terms of the effects of stress on avoidance behavior as a potential model for this important feature of PTSD.     

Does comorbid anxiety or depression affect clinical outcomes in patients with post-traumatic stress disorder and alcohol use disorders?

Post-traumatic stress disorder (PTSD) is commonly comorbid with other psychiatric disorders, including substance use disorders. In spite of this, pharmacologic treatment trials for PTSD often exclude individuals with significant psychiatric comorbidity. This study is a post hoc analysis of a 12-week double-blind placebo-controlled trial investigating sertraline in the treatment of patients with comorbid PTSD and an alcohol use disorder. Individuals with additional anxiety and affective disorders were included. Patients (N = 93) were stratified into four groups depending on presence or absence of additional anxiety or depressive disorders and evaluated for the effects of comorbidity on PTSD symptoms, depressive symptoms, and drinking behaviors. We hypothesized that additional comorbidity would be associated with poorer outcomes. Patients in all four subgroups showed marked and clinically significant improvement in alcohol drinking behaviors over the course of the study. For the entire sample, over the course of the 12 weeks, mean drinks per drinking day fell from 13.0 +/- 8.4 (SD) to 3.0 +/- 5.0 (SD); t = 10.2, df = 92, P <.000. There were, however, no significant differences among groups. Patients in all four groups showed moderate improvement in Hamilton Depression Rating Scale (HAMD) scores and Clinician-Administered PTSD scale (CAPS) scores at endpoint. For the entire sample, mean CAPS scores fell from 59.3 +/- 19.4 (SD) to 40.8 +/- 26.0, t = 8.9, df = 92, P <.000. Mean HAMD scores fell from 17. 9 +/- 6.7 (SD) at baseline to 11.8 +/- 9.4 (SD) at endpoint; t = 6.7, df = 92, P <.000. There were, however, no significant differences among groups for change in HAM-D or CAPS scores. Hence, contrary to our hypothesis, having additional anxiety or mood disorder comorbidity did not decrease treatment response in individuals with comorbid PTSD and an alcohol use disorder.     

Sensitivity to carbon dioxide in drug-naïve subjects with post-traumatic stress disorder

Post-traumatic stress disorder (PTSD) is currently classified as an anxiety disorder in DSM-IV, and as a neurosis or stress-related disorder in ICD-10. It shares many features with depression. Sensitivity to carbon dioxide (CO2), a classic provocation agent in the proto-typical anxiety disorder, panic disorder, has not been tested in PTSD. Twenty rigorously ascertained drug-na?ve subjects with PTSD inhaled a single vital capacity inhalation of 35% CO2; before and after the inhalation they completed measures of PTSD and panic anxiety, and were rated for the presence of a panic attack. These results were retrospectively compared with those of 39 healthy volunteers and 17 patients with panic disorder previously studied by the same research group. PTSD symptoms were not exacerbated by CO2. Two out of twenty PTSD subjects panicked. PTSD subjects' responses were indistinguishable from those of healthy volunteers, and differed from those of subjects with panic disorder. The lack of sensitivity to carbon dioxide in PTSD subjects in the present study adds to the literature on the differences between PTSD and other anxiety disorders, and to that on the specificity of the CO2 challenge in panic disorder.     

Is the borderline personality disorder a complex post-traumatic stress disorder? - The state of research

Regarding the high prevalence of traumatic experiences in patients with borderline personality disorders (BPD), we review the available literature focussing on the hypothesis that BPD is a subtype of trauma associated disorders. The criteria of BPD, of complex post-traumatic stress disorders (PTSD), and of disorders of extreme stress not otherwise specified (DESNOS) substantially overlap. Research of the long-term course of BPD and PTSD, trauma research, and research of vulnerability in both disorders yielded converging results. Neuropsychological deficits in BPD and PTSD as well as psychoendocrinological and neuroimaging studies in BPD und PTSD also revealed common features. A pathogenetic specificity of individual etiologic factors does not appear to exist, however the assumption of a diathesis-stress model with traumatisation as a necessary but etiologically insufficient condition seems justified. Further research will have to prove BPD as a complex and early-onset post-traumatic stress disorder after multiple and/or chronic (type II) traumatic experiences during childhood and/or youth. Definitive conclusions require further research efforts.     

Fatigue in Parkinson's disease: Motor or non-motor symptom?

Fatigue is one of the most disabling symptoms in patients with Parkinson's disease (PD), with a significant impact on patients' quality of life. Clinical studies using ad hoc questionnaires showed that in PD fatigue is associated with non-motor as well motor symptoms. Neurophysiological observations suggest that motor mechanisms play a role in the pathophysiology of fatigue but there is no clear correlation between fatigue measured with clinical instruments and fatigue assessed with neurophysiological tests. Neuroimaging studies show that fatigue is associated with an involvement of non-dopaminergic or extrastriatal dopaminergic pathways. It is conceivable that both motor and non-motor mechanisms underlie the pathophysiology of fatigue.     

How to prevent post-traumatic stress disorder before traumatization occurs?]

OBJECTIVE: To provide an update on methods of preventing the onset of posttraumatic stress disorder (PTSD) before trauma occurs. METHOD: Survey and analysis of the literature (mainly articles) found in the Medline, Psychinfo, and Pilot databases. RESULTS: Most research focuses on identifying risk factors and reinforcing individual resistance as the prime means of preventing PTSD. The severity of the trauma is by far the most serious risk factor. To reinforce resistance and prevent the onset of PTSD, the army has favoured psychoeducational approaches. However, the literature survey has found no pretrauma prevention program for other high-risk occupations. CONCLUSION: The usefulness of identified risk factors for the primary prevention of PTSD is limited, since with the exception of the trauma itself, they play a minor role on the onset of severe-trauma PTSD. Psychoeducational approaches aimed at reinforcing the resistance of individuals at risk are promising, but their potential has to be further explored in individuals in high-risk trades. Finally, it has been suggested that other avenues of research in the primary prevention (pretrauma) of PTSD be explored. These include the identification of possible protection factors, the influence of genetic make-up and of biological variables, the cumulative effects of exposure to stressors, and the presence of chronic stressors.     

Chemokines in bipolar disorder: Trait or state?

Recent evidence has suggested that inflammatory and immune mechanisms may play a role in the pathophysiology of bipolar disorder (BD). Only a few studies have assessed the profile of chemokines, a family of chemotactic cytokines related to the recruitment of leukocytes, in BD. The objective of our study was to evaluate the plasma levels of chemokines in BD patients in different mood states in comparison with healthy controls. Seventy BD type I patients (35 in euthymia and 35 in mania), and 50 healthy controls matched by age, gender, and education level were enrolled in this study. All subjects were assessed by the Mini-International Neuropsychiatry Interview and the patients by the Young Mania Rating Scale and the Hamilton Depression Rating Scale. The plasma levels of CCL2, CCL3, CCL11, CCL24, CXCL8, and CXCL10 were measured by enzyme-linked immunosorbent assay. BD patients presented higher plasma levels of CCL11 (1.69-fold increase; p < 0.001), CCL24 (1.40-fold increase; p = 0.02), CXCL10 (1.45-fold increase; p < 0.001) and decreased plasma levels of CXCL8 (8.68-fold decrease p < 0.001). Logistic regression stressed the main effect of increased plasma levels of CXCL10 (OR = 1.009, 95 % CI = 1.000–1.018, p = 0.042) and CCL11 (OR = 1.002, 95 % CI = 1.001–1.003, p = 0.003) and decreased plasma levels of CXCL8 (OR = 0.995, 95 % CI = 0.990–0.999, p = 0.013) to BD. This study reinforces the view that BD is associated with an immune dysfunction.     

Is developmental timing of trauma exposure associated with depressive and post-traumatic stress disorder symptoms in adulthood?

BackgroundTrauma exposure is a known risk factor for psychopathology. However, the impact of the developmental timing of exposure remains unclear. This study examined the effect of age at first trauma exposure on levels of adult depressive and posttraumatic stress disorder (PTSD) symptoms.MethodsLifetime trauma exposure (including age at first exposure and frequency), current psychiatric symptoms, and sociodemographic information were collected during interviews with adults participating in a study at a public urban hospital in Atlanta, GA. Multiple linear regression models assessed the association between timing of first trauma exposure, classified as early childhood (ages 0–5), middle childhood (ages 6–10), adolescence (ages 11–18), and adulthood (ages 19+), on adult psychopathology in 2892 individuals.ResultsParticipants exposed to trauma (i.e., child maltreatment, other interpersonal violence, non-interpersonal violence, and other events) at any age had higher depressive and PTSD symptoms compared to their unexposed peers. However, participants first exposed to child maltreatment during early childhood had depression and PTSD symptoms that were about twice as high as those exposed during later developmental stages. This association was detected even after controlling for sociodemographic characteristics, exposure to other trauma types, and frequency of exposure. Participants first exposed during middle childhood to other interpersonal violence also had depressive symptoms scores that were about twice as high as those first exposed during adulthood.ConclusionsTrauma exposure at different ages may differentially impact depressive and PTSD symptoms in adulthood. More detailed examination of timing of trauma exposure is warranted to aid in identifying sensitive periods in development.