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Introduction: Post-traumatic stress disorder (PTSD) is a psychiatric disorder triggered by exposure to a life-threatening or sexually violent traumatic event, and is characterized by symptoms involving intrusive re-experiencing, persistent avoidance of associated stimuli, emotional and cognitive disturbances, and hyperarousal for long periods after the trauma has occurred. These debilitating symptoms induce occupational and social impairments that contribute to a significant clinical burden for PTSD patients, and substantial socioeconomic costs, reaching approximately $20,000 dollars per individual with PTSD each year in the US. Despite increased translational research focus in the field of PTSD, the development of novel, effective pharmacotherapies for its treatment remains an important unmet clinical need. Observations: In this review, we summarize the evidence implicating dysfunctional activity of the amygdala in the pathophysiology of PTSD. We identify the transient receptor potential canonical (TRPC) ion channels as promising drug targets given their distribution in the amygdala, and evidence from animal studies demonstrating their role in fear response modulation. We discuss the evidence-based pharmacotherapy and psychotherapy treatment approaches for PTSD. Discussion: In view of the prevalence and economic burden associated with PTSD, further investigation is warranted into novel treatment approaches based on our knowledge of the involvement of brain circuitry and the role of the amygdala in PTSD, as well as the potential added value of combined pharmacotherapy and psychotherapy to better manage PTSD symptoms. [ABSTRACT FROM AUTHOR]

Chronic posttraumatic stress disorder (PTSD) may occur secondary to combat, terrorism, civilian assaults including physical and sexual abuse, or other traumatic experiences. This month's special report includes a series of [...]

Byline: Mark B. Hamner, MD Posttraumatic stress disorder (PTSD) is an anxiety disorder that occurs after severe psychological stress, eg, assault, combat, natural disasters, terrorism, or other stressors. The stressor [...]

The alpha-2 adrenergic receptor antagonist, yohimbine, can facilitate fear extinction in animals and humans. One potential mechanism is increased noradrenergic activity and associated arousal in the presence of conditioned stimuli. Accordingly, yohimbine might augment prolonged exposure (PE) therapy for posttraumatic stress disorder (PTSD), where heightened exposure-oriented arousal is a theorized driver and empirical predictor of treatment success. A double-blind placebo-controlled randomized trial (NCT 01031979) piloted yohimbine augmentation in 26 males with combat-related PTSD. Participants were given one-time dose of yohimbine or placebo prior to the first imaginal exposure. Subsequently, both arms completed standard PE. The primary outcome was trauma-cued heart-rate reactivity a week after the drug/exposure visit, a highly specified, objective measure sensitive to incremental change. Secondary outcomes included arousal during the drug/exposure visit and slope of distress, PTSD, and depression over the course of PE. Consistent with hypothesis, yohimbine led to higher objective and subjective arousal during the drug/exposure visit and to lower trauma-cued heart-rate reactivity one-week later. One dose of yohimbine also led to greater between-session habituation and more rapid improvement on depression, but not PTSD, over the course of care. Results of this controlled pilot indicate support for continued investigation of yohimbine-augmented exposure therapy for PTSD. [ABSTRACT FROM AUTHOR]

Objective: This was a 12-week randomized, placebo-controlled trial to assess the efficacy of quetiapine monotherapy in the treatment of posttraumatic stress disorder (PTSD).Method: Eighty patients were randomly assigned to treatment with either quetiapine or placebo. The primary outcome measure was the Clinician-Administered PTSD Scale (CAPS). Secondary efficacy measures included the CAPS subscales, the Davidson Trauma Scale, the Positive and Negative Syndrome Scale (PANSS), the Clinical Global Impressions (CGI) scales for severity of Illness and improvement, the Hamilton Depression Rating Scale (HAM-D), and the Hamilton Anxiety Rating Scale (HAM-A). Safety measurements included adverse events, vital signs, the Abnormal Involuntary Movement Scale, the Barnes Akathisia Scale, the Simpson-Angus Scale, and the Arizona Sexual Experiences Scale.Results: After a 1-week placebo run-in, quetiapine was started at a daily dosage of 25 mg and increased to a maximum of 800 mg; the average was 258 mg (range, 50-800 mg). Reductions in CAPS total, re-experiencing, and hyperarousal scores were significantly greater for the quetiapine group than for the placebo group. Greater improvements were also observed for quetiapine in scores on the Davidson Trauma Scale, CGI severity and improvement ratings, PANSS positive symptom and general psychopathology subscales, HAM-A, and HAM-D than for placebo. Adverse events were generally mild and expected based on prior studies of quetiapine in this and other patient population. There were no differences in safety measures between groups.Conclusion: Quetiapine monotherapy was efficacious in the treatment of PTSD. These findings suggest quetiapine as a single agent is effective in treating military PTSD. [ABSTRACT FROM AUTHOR]

BACKGROUND: Case reports and open trials have reported beneficial effects of divalproex in the treatment of posttraumatic stress disorder (PTSD). The objective of this study was to conduct a placebo-controlled study of the efficacy and tolerability of divalproex in chronic PTSD patients. METHODS: Patients were randomized to receive placebo or divalproex. The primary outcome measure was the Clinician Administered PTSD Scale (CAPS). RESULTS: Of 29 patients randomized, 16 received divalproex and 13 placebo. There were no significant differences between groups in mean change from baseline to end point (last observation carried forward) on the CAPS total score or subscales except for a significant decrease in avoidance/numbing scores with placebo. The only significant difference in secondary outcomes was a greater improvement in Clinical Global Impression Scale-Severity favoring placebo. CONCLUSIONS: Divalproex was not superior to placebo in this study. This could be due to lack of efficacy of divalproex in this population, inadequate sample size to detect differences, or other factors. Further study of divalproex is needed to better clarify the role of this agent in PTSD. [ABSTRACT FROM AUTHOR]

We compared the efficacy of telepsychiatry and same-room treatment of combat-related post-traumatic stress disorder (PTSD) using cognitive behavioural therapy in 14 weekly, 90-min treatment sessions. Of 97 patients referred for study participation, 38 were randomized (17 into telepsychiatry, 21 into same-room), and approximately 25 (the number differed by instrument) had at least one post-baseline assessment. Measures of clinical and process outcomes were examined. No group differences were found on clinical outcomes at three-month follow-up. Satisfaction with treatment ratings was similar in both groups, with 'strong satisfaction' indicated by veterans in both modalities. Attendance and drop-out were similar in the two groups. The same-room group reported more comfort in talking with their therapist at post-treatment and had better treatment adherence. The results provide preliminary support for the use of telepsychiatry in the treatment of PTSD to improve access to care. [ABSTRACT FROM AUTHOR]

This article investigated subtypes of symptom patterns among male combat veterans diagnosed with posttraumatic stress disorder (PTSD) through a cluster analysis of their Minnesota Multiphasic Personality Inventory-2 (MMPI-2; Butcher, Graham, Ben-Porath, Tellegen, Dahlstrom, & Kaemmer, 2001 ) clinical and validity scales. Participants were 126 veterans seeking outpatient treatment for combat-related PTSD at a Veterans Affairs Medical Center. Two well-fitting MMPI-2 cluster solutions (a four-cluster solution and a three-cluster solution) were evaluated with several statistical methods. A four-cluster solution was determined to best fit the data. Follow-up analyses demonstrated between-cluster differences on MMPI-2 "fake bad" scales and content scales, the Beck Depression Inventory (BDI; Beck, Ward, Mendelson, Mock, & Erbaugh, 1961 ), Dissociative Experiences Scale (DES; Bernstein & Putnam, 1986), Mississippi Combat PTSD scale (M-PTSD; Keane, Caddall, & Taylor, 1988), and Clinician-Administered PTSD Scale (CAPS-l; Blake et al., 1990). Clusters also were different in disability-seeking status, employment status, and income. Implications for research and clinical practice using the MMPI-2 with combat veterans presenting with PTSD are briefly addressed. [ABSTRACT FROM AUTHOR]

We tested the hypothesis that race may influence clinical presentation and symptomatology in combat veterans with posttraumatic stress disorder (PTSD). African-American and Caucasian veterans were administered the Psychotic Screen Module of the Structured Clinical Interview for DSM, Minnesota Multiphasic Personality Inventory-2 (MMPI-2), and other psychometric measures at a Veterans Affairs outpatient PTSD clinic. Subjects were consecutive referrals who were not matched for level of combat trauma or preexisting trauma; however, there were no group differences in other relevant demographic or diagnostic variables. Significant racial differences, with modest effect sizes, were found on clinician ratings of psychotic symptoms, MMPI-2 scale 6 (“paranoia”), and a measure of dissociation. No significant differences were found for the MMPI-2 scale 8 (“schizophrenia”), or on measures that might suggest comorbid depression or anxiety. African-Americans with PTSD endorsed more items suggesting positive symptoms of psychosis, without higher rates of primary psychosis, depression, or anxiety than Caucasians. Depression and Anxiety 16:157–161, 2002. © 2002 Wiley-Liss, Inc. [ABSTRACT FROM AUTHOR]

Focuses on the differentiation of depression and post-traumatic stress disorder (PTSD) symptoms in combat veterans. Outcome of the combination of questionnaire items from forms of psychopathology such as depression and PTSD; Factor analyses of combat PTSD and Beck depression inventory item sets.

Procaine, a local anesthetic, selectively activates the anterior limbic region of the brain, including the anterior cingulate, and may produce powerful emotional and other behavioral responses (including psychotic symptoms) in humans. In a pilot study, we administered intravenous procaine and placebo (saline) to nine combat veterans with PTSD at a dose of procaine known to produce significant behavioral responses in healthy subjects (1·38 mg/kg). All but one PTSD patient had mild to moderate, subjective responses to procaine that were statistically elevated on a procaine symptom rating scale (p <0·01) compared with saline. Symptoms that occurred only during the procaine infusion included anxiety or euphoria, auditory and visual hallucinations or illusions, and certain physical symptoms such as paresthesias. Two of the nine patients had specific PTSD reexperiencing symptoms. However, all patients tolerated the procedure well and, in eight of the patients, symptoms resolved within 5–10 min of procaine administration. One patient had possible dissociative symptoms up to 1 h after procaine that resolved without a recurrence. No patient had a persistent exacerbation of PTSD symptoms. This pilot study suggests that procaine may be a feasible pharmacologic probe to test anterior limbic function in PTSD. Copyright © 1999 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

Many symptoms of PTSD represent conditioned responses to stimuli associated with a traumatic experiences. In this review, we propose that the anterior cingulate—a brain region that appears to be involved in fear-conditioning—is dysfunctional in PTSD, thus facilitating exaggerated emotional and behavioral responses (hyperarousal) to conditioned stimuli. Preclinical studies suggest that the anterior cingulate may serve a critical gating function in modulating conditioned fear responses. As such, this region would be a key component of a neural circuit involved in the pathophysiology of PTSD. An amygdala-locus coeruleus-anterior cingulate circuit may be consistent with evidence for chronic noradrenergic activation documented in PTSD patients. According to this model, efferent noradrenergic projections from the locus coeruleus may dampen anterior cingulate function. This in turn would allow myriad external or internally driven stimuli to produce the exaggerated emotional and behavioral responses characteristic of PTSD. If confirmed in future research, cingulate dysfunction would have important theoretical and treatment implications. Depression and Anxiety 9:1–14, 1999. Published 1999 Wiley-Liss, Inc. [ABSTRACT FROM AUTHOR]

Psychotic symptoms and psychotic disorder diagnoses have occasionally been reported in association with chronic posttraumatic stress disorder (PTSD). Although psychotic features may be related to core PTSD symptoms, i.e., part of the reexperiencing phenomena, it is possible that they are secondary to certain comorbid disorders which are also prevalent in this patient population, e.g. major depression or substance abuse. In a prospective study, combat associated PTSD patients (n = 25) were administered clinical ratings, including the Structured Clinical Interview for DSM-III-R with psychotic screen (SCID-P), Clinician Administered PTSD Scale (CAPS) and the Impact of Events Scale (IES). Thirty-six percent (n = 9) endorsed psychotic symptoms with associated comorbidity including: major depressive episode, bipolar disorder, alcohol or polysubstance abuse panic disorder, and phobias. All but one of the patients with psychotic features also met criteria for major depressive episode. None had a primary psychotic disorder diagnosis. There were no significant differences in total CAPS scores between patients with or without psychotic features (82.6 +/-0 17.6 versus 75.3 +/- 22.4, p ns), nor for the different symptom cluster subscales. There were also no differences in the IES scores between groups (34.8 +/- 10 versus 32.6 +/- 10 p ns). This suggests that these psychotic features may not necessarily reflect severity of PTSD symptoms. PTSD may share a common diathesis with mood disorders including psychotic depression. Further study is needed of these phenomena. [ABSTRACT FROM AUTHOR]

This section introduces articles in the issue's special section about the pathology, treatment and cases of posttraumatic stress disorder (PTSD). Among the topics covered are psychopharmacological therapy for cognitive deficits associated with traumatic brain injury, pharmacotherapy, prediction model for PTSD, and violence and suicidal behavior among PTSD patients.

Abstract: Although posttraumatic stress disorder (PTSD) is relatively common in community epidemiologic surveys (5–6% for men, 10–12% for women), and psychiatric patients with PTSD are known to have poor functioning and high levels of psychiatric comorbidity, there are no studies that address PTSD prevalence, functioning, and burden in primary care settings. This article reports on (1) the prevalence of PTSD using Diagnostic and Statistical Manual of Mental Disorders-Fourth Edition diagnostic criteria in Veterans Affairs (VA) primary care settings, (2) associated sociodemographic characteristics and comorbidities, (3) functional status related to PTSD, (4) the extent to which PTSD was recognized by providers and (5) health services use patterns (including specialty mental health) of PTSD patients. Patients were randomly selected from those who had an outpatient visit in FY 1999 at one of four VA hospitals; 888 patients consented (74.1% of 1198 contacted); 746 patients (84.0% of consenting patients; 62.3% of contacted patients) were reached for telephone diagnostic interviews. Diagnostic interviews with the Clinician Administered PTSD Scale yielded estimates of current PTSD prevalence of 11.5%. At statistically significant levels, PTSD was positively associated with a variety of comorbid psychiatric disorders, war zone service, age &#60;65 years, not working, less formal education and decreased functioning. Of patients diagnosed with PTSD by study procedures, 12-month medical record review indicated that providers identified only 46.5% and only 47.7% had used mental health specialty services. PTSD-positive [PTSD(+)] patients who used mental health care in the past 12 months were more apt to be identified as having PTSD than nonmental health service users (78.0% vs. 17.8%). Although PTSD(+) patients had more medical record diagnoses than PTSD-negative [PTSD(−)] patients (6.28 vs. 4.95), their use of primary care, urgent care and inpatient care was not different from PTSD(−) patients. [Copyright &y& Elsevier]