Disease relevance of Stress Disorders, Post-Traumatic

• The effect of stress doses of hydrocortisone during septic shock on posttraumatic stress disorder in survivors [1].
• The results of this preliminary study therefore suggest that a hypersensitivity of the HPA axis to endogenous CRH stimulation may occur in PTSD [2].
• BACKGROUND: Brain imaging research in posttraumatic stress disorder has been largely performed on patients with chronic disease, often heavily medicated, with current or past alcohol and substance abuse [3].
• Rather than blunting, four PTSD patients (36%) and only 10% of the control and MDD subjects had high TSH responses (13-24 microU/ml), which may be linked to high noradrenergic activity, since subclinical hypothyroidism seemed unlikely [4].
• RESULTS: Using questionnaires, 59% fulfilled criteria for PTSD on the Post-traumatic Diagnostic Scale and 44% on the Impact of Events Scale, whereas using structured interview (Clinician-Administered PTSD Scale) only 3% were 'cases'.This discrepancy may arise from confusions between effects of PTSD and traumatic brain injury [5].

Psychiatry related information on Stress Disorders, Post-Traumatic

• However, the lifetime prevalence of major depressive disorder, posttraumatic stress disorder, and substance use disorders was overrepresented compared to the general female population [6].
• The frequencies of current psychiatric disorders were as follows: panic disorder, 8.0% (95% CI, 4.6% to 12.7%), major depressive disorder, 4.5% (95% CI, 2.1% to 8.4%), post-traumatic stress disorder, 4.0% (95% CI, 1.7% to 7.7%), and generalized anxiety disorder, 3.5% (95% CI, 1.4% to 7.1%) [7].
• Participants were assessed for trauma severity, severity of PTSD and depressive symptoms, and DST cortisol response [8].
• CONCLUSIONS: Combat exposure predicted symptoms of PTSD but not nonspecific measures of psychopathology [9].
• RESULTS: Of the 11 survivors, four were diagnosed with PTSD (all of whom also had concurrent major depressive disorder), one with major depressive disorder, and two with adjustment disorder [10].

High impact information on Stress Disorders, Post-Traumatic

• Curiously, inhibitors of the acetylcholine-hydrolysing enzyme acetylcholinesterase may induce psychopathologies that are reminiscent of PTSD [11].
• An intent-to-treat analysis (n = 168) confirmed significant differences between treatment and control groups for nightmares, sleep, and PTSD (all P<.02) with moderate effect sizes for treatment (mean Cohen d = 0.60) and small effect sizes for controls (mean Cohen d = 0.14) [12].
• Efficacy and safety of sertraline treatment of posttraumatic stress disorder: a randomized controlled trial [13].
• OBJECTIVE: To determine if treatment with sertraline hydrochloride effectively diminishes symptoms of PTSD of moderate to marked severity [13].
• A twin registry study of the relationship between posttraumatic stress disorder and nicotine dependence in men [14].

Chemical compound and disease context of Stress Disorders, Post-Traumatic

• Cortisol and catecholamines in posttraumatic stress disorder: an epidemiologic community study [15].
• RESULTS: Combat veterans with PTSD suppressed cortisol to a greater extent than did combat veterans without PTSD and normal controls in response to both doses of dexamethasone [16].
• CONCLUSION: These findings are consistent with our previous hypothesis of enhanced norepinephrine release in the brain with yohimbine in patients with PTSD [17].
• Posttraumatic stress disorder and the incidence of nicotine, alcohol, and other drug disorders in persons who have experienced trauma [18].
• These results only partially support previous positive reports of phenelzine treatment of PTSD [19].
• The preferential effect of cortisol administration on working memory in PTSD may be related to the superimposition of PTSD and age, as cortisol had impairing effects on this task in a previously studied, younger cohort [20].
• Offspring with parental PTSD displayed lower mean cortisol levels, reflected by the circadian mesor and reduced cortisol amplitude, compared with offspring without parental PTSD and children of nonexposed parents [21].
• Low cortisol levels in PTSD are only found under certain conditions [22].
• The self-reported acute effects of pesticides and of pyridostigmine bromide during deployment were associated with lower ACTH levels, controlling for BMI and PTSD [23].
• DEX-induced increase in lipopolysaccharide-stimulated interleukin-10 was less pronounced in traumatized veterans with and without PTSD compared to healthy controls [24].

Biological context of Stress Disorders, Post-Traumatic

• OBJECTIVE: The purpose of this study was to explore the relationship between combat-related posttraumatic stress disorder (PTSD) and specific augmentation versus reduction patterns for the N100 and P200 components of auditory event-related potentials evoked by tones of increasing intensity [25].
• Cyclic AMP signal transduction in posttraumatic stress disorder [26].
• Circadian rhythm of salivary cortisol in Holocaust survivors with and without PTSD [27].
• Given previous findings of abnormal dopamine (DA) function in PTSD, and given the putative effect of dopamine neurotransmission in shaping the responses to stress in animals, this study examined the association of the dopamine transporter (DAT) SLC6A3 3' variable number tandem repeat (VNTR) polymorphism with PTSD [28].
• In this study, PTSD patients (n = 11) and asymptomatic controls (n = 11) were compared on measures of basal sympathoadrenal function, including plasma norepinephrine and epinephrine as well as heart rate and blood pressure [29].

Anatomical context of Stress Disorders, Post-Traumatic

• However, only veterans with PTSD showed a decrease in lymphocyte glucocorticoid receptor number following dexamethasone administration [16].
• BACKGROUND: This study was designed to assess both central and peripheral aspects of thyroid function in combat-related posttraumatic stress disorder (PTSD), with the particular purpose of finding a mechanistic explanation for an imbalance between serum levels of free thyroxine (T4) and total T4 previously observed in pilot work [30].
• OBJECTIVE: Despite evidence of hyperresponsive peripheral and central nervous system (CNS) noradrenergic activity in posttraumatic stress disorder (PTSD), direct measures of CNS norepinephrine in PTSD have been lacking [31].
• The goals of this study were 1) to determine the relationship between hippocampal atrophy and posttraumatic stress disorder in the absence of alcohol abuse, and 2) to test if loss of N-acetylaspartate (a neuron marker) in the hippocampus of posttraumatic stress disorder occurs separate from atrophy [32].
• MHPG and cortisol were not correlated in the sample as a whole, but were correlated among individuals who did not subsequently develop PTSD (p = .04) CONCLUSIONS: The results suggest that different neuroendocrine systems may mediate different components of the response to traumatic stress [33].

Gene context of Stress Disorders, Post-Traumatic

• Our hormone data show further evidence for a corticotropin-releasing hormone (CRH) overdrive and enhanced negative glucocorticoid feedback in PTSD patients [34].
• CONCLUSIONS: The results suggest that PTSD is associated with increased IL-6 signaling [35].
• The authors investigated the associations between APOE allele status, memory function, and posttraumatic stress disorder (PTSD) symptom severity in PTSD subjects [36].
• Startle plasticity is measured by inhibition of startle by sensory stimuli, i.e., prepulse inhibition (PPI), and is disrupted in patients with panic or posttraumatic stress disorders in which CRF neurotransmission may be overactive [37].
• We hypothesize that excessive CRF1 activation combined with reduced CRF2 signaling may contribute to information processing deficits seen in panic and posttraumatic stress disorder patients and support CRF1-specific pharmacotherapy [37].
• The low-expression variant of the 5-HTTLPR polymorphism increased risk of posthurricane PTSD and major depression but only under the conditions of high hurricane exposure and low social support after adjustment for sex, ancestry (as determined by Bayesian clustering of genotypes), and age [38].

Analytical, diagnostic and therapeutic context of Stress Disorders, Post-Traumatic

• METHOD: Lumbar punctures for collection of CSF were performed in Vietnam combat veterans with PTSD (N = 11) and comparison subjects (N = 17) [39].
• Next, using a within-subject, crossover design, the authors sampled CSF for 6 hours through an indwelling subarachnoid catheter in PTSD patients before, during, and after exposure to a 60-minute traumatic or neutral videotape stimulus [40].
• Stress-induced enhancement of fear learning: an animal model of posttraumatic stress disorder [41].
• Dosing strategies for the SSRIs sertraline and paroxetine are provided, and an algorithm for PTSD pharmacotherapy is discussed [42].
• An open-label, 12-week clinical and sleep EEG study of nefazodone in chronic combat-related posttraumatic stress disorder [43].

Chemical compound and disease context of Stress Disorders, Post-Traumatic

• Guanfacine had no effect on PTSD symptoms, subjective sleep quality, or general mood disturbances [44].

References