Preclinical and clinical studies suggest that supplementation with omega-3 fatty acids after trauma might reduce subsequent posttraumatic stress disorder (PTSD). To date, we have shown in an open trial that PTSD symptoms in critically injured patients can be reduced by taking omega-3 fatty acids, hypothesized to stimulate hippocampal neurogenesis. The primary aim of the present randomized controlled trial is to examine the efficacy of omega-3 fatty acid supplementation in the secondary prevention of PTSD following accidental injury, as compared with placebo. This paper describes the rationale and protocol of this trial.
The Tachikawa Project for Prevention of Posttraumatic Stress Disorder with Polyunsaturated Fatty Acid (TPOP) is a double-blinded, parallel group, randomized controlled trial to assess whether omega-3 fatty acid supplementation can prevent PTSD symptoms among accident-injured patients consecutively admitted to an intensive care unit. We plan to recruit accident-injured patients and follow them prospectively for 12 weeks. Enrolled patients will be randomized to either the omega-3 fatty acid supplement group (1,470 mg docosahexaenoic acid and 147 mg eicosapentaenoic acid daily) or placebo group. Primary outcome is score on the Clinician-Administered PTSD Scale (CAPS). We will need to randomize 140 injured patients to have 90% power to detect a 10-point difference in mean CAPS scores with omega-3 fatty acid supplementation compared with placebo. Secondary measures are diagnosis of PTSD and major depressive disorder, depressive symptoms, physiologic response in the experiment using script-driven imagery and acoustic stimulation, serum brain-derived neurotrophic factor, health-related quality of life, resilience, and aggression. Analyses will be by intent to treat. The trial was initiated on December 13 2008, with 104 subjects randomized by November 30 2012.
This study promises to be the first trial to provide a novel prevention strategy for PTSD among traumatized people.
ClinicalTrials.gov Identifier NCT00671099
Fish oil; Omega-3 fatty acid; Docosahexaenoic acid; Eicosapentaenoic acid; Posttraumatic stress disorder; Accidental injury; Prevention
Posttraumatic stress disorder (PTSD) is associated with long-term changes in neurobiology. Brain areas involved in the stress response include the medial prefrontal cortex, hippocampus, and amygdala. Neurohormonal systems that act on the brain areas to modulate PTSD symptoms and memory include glucocorticoids and norepinephrine. Dysfunction of these brain areas is responsible for the symptoms of PTSD. Brain imaging studies show that PTSD patients have increased amygdala reactivity during fear acquisition. Other studies show smaller hippocampal volume. A failure of medial prefrontal/anterior cingulate activation with re-experiencing of the trauma is hypothesized to represent a neural correlate of the failure of extinction seen in PTSD. The brain has the capacity for plasticity in the aftermath of traumatic stress. Antidepressant treatments and changes in environment can reverse the effects of stress on hippocampal neurogenesis, and humans with PTSD showed increased hippocampal volume with both paroxetine and phenytoin.
PET; depression; cortisol; glucocorticoids; stress; PTSD
Among trauma patients relatively high prevalence rates of posttraumatic stress disorder (PTSD) have been found. To identify opportunities for prevention and early treatment, predictors and course of PTSD need to be investigated. Long-term follow-up studies of injury patients may help gain more insight into the course of PTSD and subgroups at risk for PTSD. The aim of our long-term prospective cohort study was to assess the prevalence rate and predictors, including pre-hospital trauma care (assistance of physician staffed Emergency Medical Services (EMS) at the scene of the accident), of probable PTSD in a sample of major trauma patients at one and two years after injury. The second aim was to assess the long-term course of probable PTSD following injury.
A prospective cohort study was conducted of 332 major trauma patients with an Injury Severity Score (ISS) of 16 or higher. We used data from the hospital trauma registry and self-assessment surveys that included the Impact of Event Scale (IES) to measure probable PTSD symptoms. An IES-score of 35 or higher was used as indication for the presence of probable PTSD.
One year after injury measurements of 226 major trauma patients were obtained (response rate 68%). Of these patients 23% had an IES-score of 35 or higher, indicating probable PTSD. At two years after trauma the prevalence rate of probable PTSD was 20%. Female gender and co-morbid disease were strong predictors of probable PTSD one year following injury, whereas minor to moderate head injury and injury of the extremities (AIS less than 3) were strong predictors of this disorder at two year follow-up. Of the patients with probable PTSD at one year follow-up 79% had persistent PTSD symptoms a year later.
Up to two years after injury probable PTSD is highly prevalent in a population of patients with major trauma. The majority of patients suffered from prolonged effects of PTSD, underlining the importance of prevention, early detection, and treatment of injury-related PTSD.
Major trauma; Posttraumatic stress disorder; Follow-up study
On March 11, 2011, a magnitude 9.0 earthquake, the most powerful ever recorded in Japan, and a massive tsunami struck off the coast of the Sanriku region. A Disaster Medical Assistance Team, a mobile medical team with specialized training that is deployed during the acute phase of a disaster, was dispatched to areas with large-scale destruction and multiple injured and sick casualties. Previous studies have reported critical incident stress (i.e. posttraumatic stress disorder symptoms and depressive symptoms) among rescue workers as well as the need for screening and prevention for posttraumatic stress disorder. So far we have shown in an open trial that posttraumatic stress disorder symptoms in critically injured patients can be reduced by taking omega-3 fatty acids intended to stimulate hippocampal neurogenesis.
This study is designed to determine the effectiveness of attenuating posttraumatic distress with omega-3 polyunsaturated fatty acids among Disaster Medical Assistance Team members after the Great East Japan Earthquake, and is named the APOP randomized controlled trial which is currently ongoing. First, we will provide psycho-education on posttraumatic distress, which is common in responders to the Disaster Medical Assistance Team members deployed to the disaster area. Second, observational research will be conducted to evaluate critical incident stress following the completion of medical activities. Third, team members who provide consent to participate in the intervention research will be randomly divided into a group given an omega-3 fatty acid supplement and a group not given the supplements. Outcome will be evaluated at 12 weeks after the supplements are shipped to the team members.
Measures that address critical incident stress in disaster responders are important, but there is no substantial evidence that links such measures with prevention of posttraumatic stress disorder. Thus, any confirmation through this study that the intake of omega-3 fatty acid supplements serves as a simple preventative measure for critical incident stress will be of great significance.
UMIN Clinical Trials Registry, UMIN000005367
Mild traumatic brain injury (mTBI, cerebral concussion) is a risk factor for the development of psychiatric illness such as posttraumatic stress disorder (PTSD). We sought to evaluate how omega-3 fatty acids during brain maturation can influence challenges incurred during adulthood (transitioning to unhealthy diet and mTBI) and predispose the brain to a PTSD-like pathobiology. Rats exposed to diets enriched or deficient in omega-3 fatty acids (n-3) during their brain maturation period, were transitioned to a western diet (WD) when becoming adult and then subjected to mTBI. TBI resulted in an increase in anxiety-like behavior and its molecular counterpart NPY1R, a hallmark of PTSD, but these effects were more pronounced in the animals exposed to n-3 deficient diet and switched to WD. The n-3 deficiency followed by WD disrupted BDNF signaling and the activation of elements of BDNF signaling pathway (TrkB, CaMKII, Akt and CREB) in frontal cortex. TBI worsened these effects and more prominently in combination with the n-3 deficiency condition. Moreover, the n-3 deficiency primed the immune system to the challenges imposed by the WD and brain trauma as evidenced by results showing that the WD or mTBI affected brain IL1β levels and peripheral Th17 and Treg subsets only in animals previously conditioned to the n-3 deficient diet. These results provide novel evidence for the capacity of maladaptive dietary habits to lower the threshold for neurological disorders in response to challenges.
The coexistence of traumatic brain injury (TBI) and posttraumatic stress disorder (PTSD) remains a controversial issue in the literature. To address this controversy, we focused primarily on the civilian-related literature of TBI and PTSD. Some investigators have argued that individuals who had been rendered unconscious or suffered amnesia due to a TBI are unable to develop PTSD because they would be unable to consciously experience the symptoms of fear, helplessness, and horror associated with the development of PTSD. Other investigators have reported that individuals who sustain TBI, regardless of its severity, can develop PTSD even in the context of prolonged unconsciousness. A careful review of the methodologies employed in these studies reveals that investigators who relied on clinical interviews of TBI patients to diagnose PTSD found little or no evidence of PTSD. In contrast, investigators who relied on PTSD questionnaires to diagnose PTSD found considerable evidence of PTSD. Further analysis revealed that many of the TBI patients who were initially diagnosed with PTSD according to self-report questionnaires did not meet the diagnostic criteria for PTSD upon completion of a clinical interview. In particular, patients with severe TBI were often misdiagnosed with PTSD. A number of investigators found that many of the severe TBI patients failed to follow the questionnaire instructions and erroneously endorsed PTSD symptoms because of their cognitive difficulties. Because PTSD questionnaires are not designed to discriminate between PTSD and TBI symptoms or determine whether a patient's responses are accurate or exaggerated, studies that rely on self-report questionnaires to evaluate PTSD in TBI patients are at risk of misdiagnosing PTSD. Further research should evaluate the degree to which misdiagnosis of PTSD occurs in individuals who have sustained mild TBI.
Posttraumatic stress disorder; Traumatic brain injury
Exposure to traumatic events that produce extreme fear and horror is all too common in both military and civilian populations, but not all individuals develop posttraumatic stress disorder (PTSD) as a result of the exposure. What mediates risk and resilience in the development of PTSD and other stress-related psychopathology is of paramount importance to our further understanding of trauma-related psychopathology as well as the development of new treatment approaches. Biological factors, such as genotype and neurobiology, interact with environmental factors, such as childhood background and trauma load, to affect vulnerability and resilience in the aftermath of trauma exposure. One of the core symptoms of PTSD is the inability to control fear, which has led some investigators and clinicians to conceptualize PTSD as a disorder of fear or, more importantly, its inhibition. This review focuses on translational methods that have been used to examine fear conditioning and inhibition of fear in PTSD and summarizes genetic and neurobiological factors related to fear inhibition. The authors also discuss different pharmacological approaches that enhance fear inhibition and may improve treatment outcomes for patients with PTSD.
A central problem in posttraumatic stress disorder (PTSD) is a reduced capacity to suppress fear under safe conditions. Previously, we have shown that combat-related PTSD patients have impaired inhibition of fear-potentiated startle. Given the high comorbidity between PTSD and depression, our goal was to see whether this impairment is specific to PTSD, or a nonspecific symptom associated with both disorders.
Fear-potentiated startle (FPS) was assessed in 106 trauma-exposed individuals divided into four groups: a) No diagnosis control, b) PTSD only, c) major depression (MDD) only, and d) comorbid PTSD and MDD. We used a novel conditional discrimination procedure, in which one set of shapes (the danger signal) was paired with aversive airblasts to the throat, and different shapes (the safety signal) were presented without airblasts. The paradigm also included fear inhibition transfer test.
Subjects with comorbid MDD and PTSD had higher FPS to the safety signal and to the transfer test compared to controls and MDD only subjects. In contrast to the control and MDD groups, the PTSD and comorbid PTSD and MDD groups did not show fear inhibition to safety cues.
These results suggest that impaired fear inhibition may be a specific biomarker of PTSD symptoms.
PTSD; Depression; Hyper-arousal Symptoms; Physiology; Fear-Potentiated Startle
Severe traumatic stressors such as war, rape, or life-threatening accidents can result in a debilitating psychopathological development conceptualised as Posttraumatic Stress Disorder (PTSD). Pathological memory formation during an alarm response may set the precondition for PTSD to occur. If true, a lack of memory formation by extended unconsciousness in the course of the traumatic experience should preclude PTSD.
46 patients from a neurological rehabilitation clinic were examined by means of questionnaires and structured clinical interviews. All patients had suffered a TBI due to an accident, but varied with respect to falling unconscious during the traumatic event.
27% of the sub-sample who were not unconscious for an extended period but only 3% (1 of 31 patients) who were unconscious for more than 12 hours as a result of the accident were diagnosed as having current PTSD (P < .02). Furthermore, intrusive memories proved to be far more frequent in patients who had not been unconscious. This was also the case for other re-experiencing symptoms and for psychological distress and physiological reactivity to reminders of the traumatic event.
TBI and PTSD are not mutually exclusive. However, victims of accidents are unlikely to develop a PTSD if the impact to the head had resulted in an extended period of unconsciousness.
Studies in animals showed that stress is associated with changes in hippocampal function and structure, an effect mediated through decreased neurogenesis, increased glucocorticoids, and/or decreased brain derived neurotrophic factor. Antidepressants and some anticonvulsants block the effects of stress and/or promote neurogenesis in animal studies. Patients with posttraumatic stress disorder (PTSD) have been shown to have smaller hippocampal volume on magnetic resonance imaging and deficits in hippocampal-based memory. Symptom activation is associated with decreased anterior cingulate and medial prefrontal function, which is proposed as the neural correlate of a failure of extinction seen in these patients. Treatment with antidepressants and phenytoin reverse hippocampal volume reduction and memory deficits in PTSD patients, suggesting that these agents may promote neurogenesis in humans.
One of the central problems in posttraumatic stress disorder (PTSD) is the inability to suppress fear even under safe conditions. The neural underpinnings of fear is a clinically relevant issue that is poorly understood. This study assessed fear potentiation and fear inhibition using fear-potentiated startle in a conditional discrimination procedure (AX+/BX-). We hypothesized that patients with PTSD would show normal fear potentiation and impaired fear inhibition. 28 healthy volunteers and 27 PTSD patients (14 with low current symptoms, 13 with high current symptoms) were presented with one set of colored lights (AX trials) paired with aversive air blasts to the throat, and a different series of lights (BX trials) presented without air blasts. We then presented A and B together (AB trials) to see whether B would inhibit fear potentiation to A. All groups showed robust fear potentiation in that they had significantly greater startle magnitude on AX trials compared to noise alone trials. However, the high symptom PTSD group did not show fear inhibition: these subjects had significantly greater fear potentiation on the AB trials than both the controls and the low symptom PTSD patients.
Acoustic Startle Response; Classical Conditioning; Fear-Potentiated Startle; Electromyography; PTSD; Human
Animal studies have shown that stress is associated with damage to the hippocampus, inhibition of neurogenesis, and deficits in hippocampal-based memory dysfunction. Studies in patients with posttraumatic stress disorder (PTSD) found deficits in hippocampal-based declarative verbal memory and smaller hippocampal volume, as measured with magnetic resonance imaging (MRI). Recent preclinical evidence has shown that selective serotonin reuptake inhibitors promote neurogenesis and reverse the effects of stress on hippocampal atrophy. This study assessed the effects of long-term treatment with paroxetine on hippocampal volume and declarative memory performance in PTSD.
Declarative memory was assessed with the Wechsler Memory Scale–Revised and Selective Reminding Test before and after 9–12 months of treatment with paroxetine in PTSD. Hippocampal volume was measured with MRI. Of the 28 patients who started the protocol, 23 completed the full course of treatment and neuropsychological testing. Twenty patients were able to complete MRI imaging.
Patients with PTSD showed a significant improvement in PTSD symptoms with treatment. Treatment resulted in significant improvements in verbal declarative memory and a 4.6% increase in mean hippocampal volume.
These findings suggest that long-term treatment with paroxetine is associated with improvement of verbal declarative memory deficits and an increase in hippocampal volume in PTSD.
Posttraumatic stress disorder; memory; hippocampus; stress; paroxetine; selective serotonin reuptake inhibitors
Posttraumatic stress disorder (PTSD) has only relatively recently been introduced into the diagnostic classification of mental disorders. Building on advances in the treatment of other anxiety disorders, a range of effective psychological treatments for PTSD has been developed. The most effective of these treatments focus on the patient’s memory for the traumatic event and its meaning. This paper briefly reviews the currently available evidence for these treatments. It then illustrates the process of developing effective psychological treatments by discussing how a combination of phenomenological, experimental and treatment development studies and theoretical considerations was used to develop a trauma-focused cognitive-behavioral treatment, Cognitive Therapy (CT) for PTSD. This treatment program builds on Ehlers and Clark’s (2000) model of PTSD, which specifies two core cognitive abnormalities in PTSD. First, people with chronic PTSD show idiosyncratic personal meanings (appraisals) of the trauma and/or its sequelae that lead to a sense of serious current threat. Second, the nature of the trauma memory explains the occurrence of reexperiencing symptoms. It is further proposed that the idiosyncratic appraisals motivate a series of dysfunctional behaviors (such as safety-seeking behaviors) and cognitive strategies (such as thought suppression and rumination) that are intended to reduce the sense of current threat, but maintain the problem by preventing change in the appraisals and trauma memory, and/or lead to increases in symptoms. CT addresses the cognitive abnormalities and maintaining behaviors in an individualized, but focused, way. Four randomized controlled trials and two dissemination studies showed that CT for PTSD is acceptable and effective.
Posttraumatic stress disorder; trauma; cognitive behavior therapy; cognitive therapy; randomized controlled trial; clinical trial
Neuroimaging research on the neurobiology of chronic PTSD (posttraumatic stress disorder) has revealed structural and functional alterations primarily affecting areas of the medial temporal lobe (hippocampus, amygdala, and parahippocampal gyrus) and the frontal cortex known to be associated with the disorder. Using functional magnetic resonance imaging (fMRI), the present study studied the functional neuroanatomy of traumatic and non-traumatic emotional memory in two surgical patients who had sustained severe accident trauma. While patient 1 had developed acute PTSD following the traumatic event, patient 2 (control) did not. When confronted with traumatic (relative to negatively valenced non-traumatic) memory, the PTSD patient exhibited evidence for increased neural activity in the right and the left superior temporal lobe, the amygdala, the left angular gyrus, and the medial frontal gyrus, while the non-PTSD patient exposed to identical conditions showed increased activations in frontal and parietal regions. Both patients exhibited identical activation patterns when recalling non-traumatic memories relative to neutral memories. It is concluded that the pronounced activation patterns in the PTSD patient may be considered specific for acute PTSD, involved with the emotional arousal and the vivid visual recollections typical for the acute phase of the disorder.
The past few years have seen an increase in the clinical awareness of post-traumatic stress disorder (PTSD), one of the most disabling and least understood behavioral disorders. Although the biological bases of PTSD are poorly understood, fatty-acid amide hydrolase (FAAH) activity has been linked with arousability and aversive-memories extinction, that is, two key features of PTSD. In this study, we investigated the association between the FAAH genetic polymorphisms and PTSD development and maintenance. We assessed PTSD frequency in a group of male Vietnam war veterans who suffered combat-related penetrating traumatic brain injury, that is, a relatively homogeneous population regarding the nature of the events that led to PTSD. We showed that rs2295633, a single-nucleotide polymorphism of FAAH, was significantly associated with PTSD diagnosis in subjects without lesions in the ventromedial prefrontal cortex. Moreover, the presence of the C allele was associated with more severe re-experiencing of trauma and more negative reported childhood experiences. In conclusion, our data suggest that FAAH has an important role in PTSD through modulation of aversive memories and point to both a novel therapeutic target and a possible risk marker for this condition.
endocannabinoids; post-traumatic stress disorder; single-nucleotide polymorphisms
Injured trauma victims are at risk of developing Posttraumatic Stress Disorder (PTSD) and other post-trauma psychopathology. So far, interventions using cognitive behavioral techniques (CBT) have proven most efficacious in treating early PTSD in highly symptomatic individuals. No early intervention for the prevention of PTSD for all victims has yet proven effective. In the acute psychosocial care for trauma victims, there is a clear need for easily applicable, accessible, cost-efficient early interventions.
To describe the design of a randomized controlled trial (RCT) evaluating the effectiveness of a brief Internet-based early intervention that incorporates CBT techniques with the aim of reducing acute psychological distress and preventing long-term PTSD symptoms in injured trauma victims.
In a two armed RCT, 300 injured trauma victims from two Level-1 trauma centers in Amsterdam, the Netherlands, will be assigned to an intervention or a control group. Inclusion criteria are: being 18 years of age or older, having experienced a traumatic event according to the diagnostic criteria of the DSM-IV and understanding the Dutch language. The intervention group will be given access to the intervention's website (www.traumatips.nl), and are specifically requested to login within the first month postinjury. The primary clinical study outcome is PTSD symptom severity. Secondary outcomes include symptoms of depression and anxiety, quality of life, and social support. In addition, a cost-effectiveness analysis of the intervention will be performed. Data are collected at one week post-injury, prior to first login (baseline), and at 1, 3, 6 and 12 months. Analyses will be on an intention-to-treat basis.
The results will provide more insight into the effects of preventive interventions in general, and Internet-based early interventions specifically, on acute stress reactions and PTSD, in an injured population, during the acute phase after trauma. We will discuss possible strengths and limitations.
injury; trauma; early intervention; prevention; Internet; e-Mental Health; PTSD; cognitive behavioral therapy (CBT)
Women with posttraumatic stress disorder (PTSD) report poor health, but associations with health care utilization are understudied.
To determine associations between medical/surgical utilization and PTSD in female Veterans Affairs (VA) patients.
Prospective comparison of utilization rates between women screening positive or negative for PTSD on a mailed survey.
Women receiving care at an urban VA medical center between October 1996 and January 2000.
Survey responses, including a validated screen for PTSD (PCL-C), and VA utilization data through September 2002.
Two thousand five hundred and seventy-eight (2,578) women (78% of those eligible) completed the PCL-C; 858 (33%) of them screened positive for PTSD (PTSD+). In unadjusted models, PTSD+ women had higher rates of medical/surgical hospitalizations and surgical inpatient procedures. Among women ages 35 to 49, mean days hospitalized/100 patients/year was 43.4 (95% CI 26 to 61) for PTSD+ women versus 17.0 (16 to 18) for PTSD negative (PTSD–) women. More PTSD+ women underwent surgical procedures (P<.001). Mean annual outpatient visits were significantly higher among PTSD+ women, including: emergency department (ED) (1.1 [1.0 to 1.2] vs 0.6 [0.5 to 0.6]), primary care (3.2 [3.0 to 3.4] vs 2.2 [2.1 to 2.3]), medical/surgical subspecialists (2.1 [1.9 to 2.3] vs 1.5 [1.4 to 1.6]), ancillary services (4.1 [3.7 to 4.5] vs 2.4 [2.2 to 2.6]), and diagnostic tests (5.6 [5.1 to 6.1] vs 3.7 [3.4 to 4.0]). In multivariate models adjusted for demographics, smoking, service access, and medical comorbidities, PTSD+ women had greater likelihood of medical/surgical hospitalization (OR=1.37 [1.04 to 1.79]) and of being among the top quartile of patients for visits to the ED, primary care, ancillary services, and diagnostic testing.
Female veterans who screen PTSD+ receive more VA medical/surgical services. Appropriateness of that care deserves further study.
mental health; survey research; utilization; veterans; women's health
Network orientation is conceptualized as an individual’s attitudes and expectations regarding the usefulness of support networks in coping with stress. The present research examined the potential for network orientation to explicate the well documented association between posttraumatic stress disorder (PTSD) and attenuated social support. Data collected from survivors of serious motor vehicle trauma (N = 458) were used to test the hypothesis that severity of PTSD would hold a significant indirect relationship with social support through negative network orientation. Childhood victimization and elapsed time from the accident were examined as potential moderators of this indirect relationship. Consistent with hypotheses, path analyses demonstrated a significant indirect relationship between PTSD and social support through negative network orientation. Specifically, this indirect effect was the result of a direct association between PTSD severity and negative network orientation and an inverse association between negative network orientation and social support. This pattern of relationships was invariant across mode of PTSD assessment (interview vs. self-report). No moderation effects were noted. These data suggest that network orientation may be an important factor in understanding interface of interpersonal processes and posttrauma pathology.
PTSD; social support; network orientation; motor vehicle accidents; MVA
Sleep facilitates the consolidation of fear extinction memory. Nightmares and insomnia are hallmark symptoms of posttraumatic stress disorder (PTSD), possibly interfering with fear extinction and compromising recovery. A perpetual circle may develop when sleep disturbances increase the risk for PTSD and vice versa. To date, therapeutic options for alleviating sleep disturbances in PTSD are limited.
We conducted three studies to examine the relationship between sleep and posttraumatic symptoms: (1) a prospective longitudinal cohort study examining the impact of pre-deployment insomnia symptoms and nightmares on the development of PTSD; (2) a cross-sectional study examining subjective sleep measures, polysomnography, endocrinological parameters, and memory in veterans with PTSD, veterans without PTSD, and healthy controls (HCs); (3) a randomized controlled trial (RCT) (n=14) comparing the effect of prazosin and placebo on sleep disturbances in veterans with PTSD. In addition to these studies, we systematically reviewed the literature on treatment options for sleep disturbances in PTSD.
Pre-deployment nightmares predicted PTSD symptoms at 6 months post-deployment; however, insomnia symptoms did not. Furthermore, in patients with PTSD, a correlation between the apnea index and PTSD severity was observed, while obstructive sleep apnea syndrome was not more prevalent. We observed a significant increase in awakenings during sleep in patients with PTSD, which were positively correlated with adrenocorticotropic hormone (ACTH) levels, negatively correlated with growth hormone (GH) secretion, and the subjective perception of sleep depth. Also, heart rate was significantly increased in PTSD patients. Interestingly, plasma levels of GH during the night were decreased in PTSD. Furthermore, GH secretion and awakenings were independent predictors for delayed recall, which was lower in PTSD. In our RCT, prazosin was not associated with improvement of any subjective and objective sleep parameters. Only a few RCTs have been published. They show promising results for atypical antipsychotics and prazosin, the latter especially on nightmare reduction.
Disturbed sleep due to nightmares increases the risk for PTSD. PTSD in turn leads to increased sleep fragmentation, decreased GH secretion, and frequent nightmares, which may again compromise fear extinction, synaptic plasticity, and recovery. This suggests that disturbed sleep is a precipitating and perpetuating factor in PTSD symptomatology, creating a perpetual circle. This dissertation suggests that activity of the hypothalamic–pituitary–adrenal axis and the sympathetic nervous system (SNS) is involved in disturbed sleep in patients with PTSD.
PTSD; sleep; nightmares; polysomnography; cortisol; growth hormone; memory; noradrenalin
Posttraumatic stress disorder (PTSD) is associated with decreased activity in the
dorsolateral prefrontal cortex (DLPFC), the brain region that regulates working memory and
preparation and selection of fear responses. We investigated gene expression profiles in DLPFC
Brodmann area (BA) 46 of postmortem patients with (n=6) and without PTSD (n=6) using human
mitochondria-focused cDNA microarrays. Our study revealed PTSD-specific expression fingerprints
of 800 informative mitochondria-focused genes across all of these 12 BA46 samples, and 119
(±>1.25, p<0.05) and 42 (±>1.60,
p<0.05) dysregulated genes between the PTSD and control samples.
Quantitative RT-PCR validated the microarray results. These fingerprints can essentially
distinguish the PTSD DLPFC BA46 brains from controls. Of the 119 dysregulated genes
(±≥125%, p<0.05), the highest percentages were
associated with mitochondrial dysfunction (4.8%, p=6.61x10-6),
oxidative phosphorylation (3.8%, p=9.04x10-4), cell
survival-apoptosis (25.2%, p<0.05) and neurological diseases (23.5%,
p<0.05). Fifty (50) dysregulated genes were present in the molecular
networks that are known to be involved in neuronal function-survival and contain 7 targets for
neuropsychiatric drugs. Thirty (30) of the dysregulated genes are associated with a number of
neuropsychiatric disorders. Our results indicate mitochondrial dysfunction in the PTSD DLPFC
BA46 and provide the expression fingerprints that may ultimately serve as biomarkers for PTSD
diagnosis and the drugs and molecular targets that may prove useful for development of remedies
for prevention and treatment of PTSD.
PTSD; Brain dorsolateral prefrontal cortex BA46; Gene expression pattern; Biomarker; Mitochondria; Canonical pathways; Molecular networks; Neuropsychiatric drug targets
Although there is increasing evidence that panic attacks are common in posttraumatic stress disorder (PTSD), little is known if posttraumatic panic is comparable to panic attacks observed in panic disorder (PD).
This study examined the cognitive responses to panic attacks in participants with PD and PTSD.
Participants with PD (n=22) and PTSD (n=18) were assessed on the Anxiety Disorder Interview Schedule for DSM-IV and subsequently administered the Agoraphobic Cognitions Questionnaire and a measure of fears related to trauma memories.
Although participants did not differ in terms of catastrophic appraisals about somatic sensations, PTSD participants were more likely to experience fears about trauma memories and being harmed by trauma again during their panic attacks than PD participants.
These findings suggest that although PTSD participants fear somatic outcomes during panic attacks, their panic attacks are distinguished by a marked fear of trauma memories.
Panic attack; posttraumatic stress disorder; panic disorder; trauma memories
This five year long-term follow-up study estimated the prevalence of Posttraumatic Stress Disorder (PTSD) and other mental health problems in traffic accident victims. 70 patients were invited for a personal interview to assess mental disorders (DIA-X), depression (BDI), mental distress (SCL-90-R), and psychosocial (SDS) and physical impairments at least five years after their first admission to a university hospital (Department of Traumatology). Prevalence of PTSD was 10%, and another 14.2% of the patients also had a partial PTSD. Other mental disorders had a lower prevalence (7.2%). Patients with PTSD did not differ in sociodemographic characteristics from patients without PTSD. PTSD patients were more depressed and showed more general psychological distress. Furthermore, PTSD was associated with impairments in job, social interaction, and leisure activities. Persistent medical and mental problems correlated highly with PTSD. Implications for secondary prevention of persistent mental health problems of traffic accident patients are discussed in their connection with PTSD.
Posttraumatic Stress Disorder; partial Posttraumatic Stress Disorder; traffic accident; epidemiology; comorbidity; psychosocial impairment; physical impairment
Poor social support in the aftermath of a traumatic event is a well-established risk factor for posttraumatic stress disorder (PTSD) among adult trauma survivors. Yet, a great deal about the relationship between social support and PTSD remains poorly understood. In this study, we analyzed data from 102 survivors of a serious motor vehicle accident (MVA) at 4 weeks (Time 1) and 16 weeks (Time 2) post-MVA. We assessed the role of perceived dyadic social support, positive dyadic interaction, and negative dyadic interaction in the development and maintenance of PTSD. In addition, we examined how these social support constructs work together with negative post-trauma cognitions to affect the maintenance of PTSD. Neither perceived social support nor the quality of social interaction (i.e., positive or negative) was associated with PTSD symptom severity at Time 1. However, among those with elevated PTSD symptom severity at Time 1, greater social support and positive social interaction and lower negative social interaction were each associated with reductions in PTSD symptom severity from Time 1 to Time 2. For social support and negative social interaction, this association ceased to be significant when jointly assessed with negative post-trauma cognitions, suggesting that perceived social support and negative dyadic interaction were associated with maintenance of PTSD symptom severity because of their association with negative post-trauma cognitions. These results provide support to models and treatments of PTSD that emphasize the role of negative post-trauma cognitions in maintenance of PTSD.
Individuals who experience a serious motor vehicle accident (MVA) are at increased risk for psychological problems, particularly Posttraumatic Stress Disorder (PTSD). In this article, we review the literature on PTSD among MVA survivors, with particular attention to available instruments to screen for and assess symptomatology of the disorder. Approaches to the treatment of PTSD in this population are reviewed, separated into interventions designed to prevent PTSD in unselected samples, treatment targeting individuals with Acute Stress Disorder that are designed to prevent subsequent development of PTSD, and therapy for individuals with chronic PTSD. Treatment process issues are discussed, in an effort to integrate empirical findings with clinical observations. The empirical literature suggests several approaches to treatment that have good potential outcomes, although continued work is needed to identify factors that predict treatment response, as well as augment individual-based treatment formats.
Trauma; Road traffic accidents; Cognitive Behavior Therapy; Supportive Psychotherapy; Acute Stress Disorder
More than 1.5 million persons in the United States sustain traumatic physical injuries each year. A significant proportion of traumatic injury survivors develop serious mental health problems such as posttraumatic stress disorder (PTSD), yet few obtain professional mental health care. According to the commonsense model of self-regulation (Leventhal, Diefenbach, & Leventhal, 1992), illness-related perceptions can influence coping responses including the use of professional treatment. Using the commonsense model as a guiding framework, we conducted semi-structured interviews with non-treatment seeking trauma injury survivors with PTSD (N = 23). Illness perceptions regarding the following key conceptual dimensions were examined: PTSD symptoms (identity), experienced or perceived consequences of PTSD symptoms, and beliefs about the causes, controllability, and course of PTSD symptoms. Results revealed that no respondents identified their symptoms as indicative of PTSD. Common illness perceptions included believing that symptoms would be short-lived, that symptoms were reflective of poor physical health or were a natural reaction to life in a violent community, and that symptoms were functionally adaptive. Respondents also reported exerting some limited control over symptoms by relying on religious forms of coping. None of the respondents perceived professional treatment as being able to completely control symptoms. Findings indicated that respondents’ conceptualizations of PTSD symptoms may have inhibited the recognition of symptoms as a serious mental health condition that warrants professional treatment.