Preliminary evidence on the neural correlates of timing deficit in post-traumatic stress disorder.
Ontology highlight
ABSTRACT:
SUBMITTER: Vicario CM
PROVIDER: S-EPMC8794066 | biostudies-literature |
REPOSITORIES: biostudies-literature
Similar Datasets
Project description:BackgroundPost-traumatic stress disorder (PTSD) can occur after life-threatening events, including illness, but correlates of PTSD after stroke or transient ischemic attack (TIA) have not been well described.MethodsWe measured the prevalence of stroke-induced PTSD with the PTSD Checklist Specific for stroke (PCL-S) in adults who had a stroke or TIA within 5 years. A PCL-S score of 50 or more indicated likely PTSD. We tested for potential predictors of stroke-associated PTSD, including demographics, stroke history, disability, medical comorbidities, depression, and emotional support and then examined the association between poststroke PTSD and measures of physical and mental health.ResultsOf 535 participants, 95 (18%) had a PCL-S score of 50 or more; the mean score was 35.4 ± 13.7 (range 17-80 of 85). In logistic regression analysis, low income (odds ratio [OR] 1.98, 95% confidence interval [CI] 1.01-3.61), recurrent stroke or TIA (OR 1.86, 1.10-3.16), more disability (OR 1.79, 1.43-2.23), and increased comorbidities (OR 1.90, 1.05-3.45) were independently associated with PTSD. Older age (OR .93, .90-.95), marriage or partnership (OR .52, .28-.98), and having emotional support (OR .25, .11-.54) were protective against developing PTSD. Participants with likely PTSD had worse physical and mental health.ConclusionsIn this racially and ethnically diverse cohort of stroke and TIA survivors, stroke-induced PTSD was associated with younger age, recurrent strokes, greater disability, and comorbidities. PTSD was associated with a substantially increased physical, mental, and quality of life burden in this already vulnerable population. Having social support was protective, suggesting a potential target for intervention.
| S-EPMC3992186 | biostudies-literature
Project description:BackgroundSelf-stigma refers to the internalisation of negative societal views and stereotypes. Self-stigma has been well-characterised in the context of mental disorders such as schizophrenia but has received little attention in relation to post-traumatic stress disorder (PTSD).ObjectiveThis work aimed to determine the prevalence of self-stigma in a sample of adults with PTSD and to establish factors associated with the internalisation of stigma in this population.MethodParticipants were 194 adults (mean age 46.07 (SD = 12.39); 64.4% female; 96.6% white Caucasian; residing in the UK), who self-reported a diagnosis of PTSD and currently screened positive for the disorder according to the PTSD Checklist for DSM-5 (PCL-5). Structured interviews and validated self-report questionnaires were used to ascertain clinical and sociodemographic information for analysis.ResultsThe prevalence of self-stigma measured by the Internalized Stigma of Mental Illness Scale (ISMIS) was 41.2% (95% CI 34.24-48.22). There was no evidence of an association between self-stigma and gender (β = -2.975 (95% CI -7.046-1.097) p = .151), age (β = 0.007 (95% CI -0.152-0.165) p = .953), sexual trauma (β = 0.904 (95% CI -3.668-5.476) p = .697), military trauma (β = -0.571 (95% CI -4.027-7.287) p = .571). Self-stigma was associated with lower income and higher levels of anxiety (β = 5.722 (95% CI 2.922-8.522) p = <.001), depression (β = 6.937 (95% CI 4.287-9.588) p = <.000), and traumatic stress symptoms (β = 3.880 (95% CI 1.401-6.359) p = .002).ConclusionsThe results indicate that self-stigma may be a significant issue among people with a diagnosis of PTSD. Further work is needed to understand the long-term impact and to develop interventions to address the internalisation of stigma in this population.HighlightsThe prevalence of self-stigma among a sample of participants with PTSD was 41.2%.There was no evidence of an association between self-stigma and gender, age or sexual / military trauma.Self-stigma was associated with lower income and higher levels of anxiety, depression, and traumatic stress symptoms.
| S-EPMC9310800 | biostudies-literature
Project description:Therapeutic alliance and perceived social support are important predictors of treatment response for post-traumatic stress disorder (PTSD). Intranasal oxytocin administration may enhance treatment response by increasing sensitivity for social reward and thereby therapeutic alliance and perceived social support. As a first step to investigate this therapeutical potential, we investigated whether intranasal oxytocin enhances neural sensitivity to social reward in PTSD patients. Male and female police officers with (n = 35) and without PTSD (n = 37) were included in a double-blind, randomized, placebo-controlled cross-over fMRI study. After intranasal oxytocin (40 IU) and placebo administration, a social incentive delay task was conducted to investigate neural responses during social reward and punishment anticipation and feedback. Under placebo, PTSD patients showed reduced left anterior insula (AI) responses to social rewards (i.e. happy faces) compared with controls. Oxytocin administration increased left AI responses during social reward in PTSD patients, such that PTSD patients no longer differed from controls under placebo. Furthermore, in PTSD patients, oxytocin increased responses to social reward in the right putamen. By normalizing abberant insula responses and increasing putamen responses to social reward, oxytocin administration may enhance sensitivity for social support and therapeutic alliance in PTSD patients. Future studies are needed to investigate clinical effects of oxytocin.
| S-EPMC5390752 | biostudies-literature
Project description:While diagnosis of PTSD is based on behavioral symptom clusters that are most directly associated with brain function, epigenetic studies of PTSD in humans to date have been limited to peripheral tissues. Animal models of PTSD have been key for understanding the epigenetic alterations in the brain most directly relevant to endophenotypes of PTSD, in particular those pertaining to fear memory and stress response. This chapter provides an overview of neuroepigenetic studies based on animal models of PTSD, with an emphasis on the effect of stress on fear memory. Where relevant, we also describe human-based studies with relevance to neuroepigenetic insights gleaned from animal work and suggest promising directions for future studies of PTSD neuroepigenetics in living humans that combine peripheral epigenetic measures with measures of central nervous system activity, structure and function.
| S-EPMC6474244 | biostudies-literature
Project description:Six hundred and one patients, who sustained injuries in militant activities, admitted during a 7 month period to a zonal referral hospital were studied. The majority, 54.6% from the Armed Forces and 38.8% from the para-military forces, were in the age group of 22-53 years. There were 40 (6.7%) civilian casualties. These were in the age group of 20-45 years. A large number (75.7%) of the casualties manifested with post-traumatic stress symptoms. 24.3% of them were rated as post-traumatic stress disorder. Six months follow-up revealed persistence of post-traumatic stress disorder in 17.1% of the cases. By one year, 42.1% who responded to the follow-up letters had persistence of post-traumatic stress disorder in 4.95%. Early recognition of this psychic trauma and preventive strategies are discussed.
| S-EPMC5530272 | biostudies-other
Project description:Previous research in post-traumatic stress disorder (PTSD) has identified disrupted ventromedial prefrontal cortex (vmPFC) function in those with v. without PTSD. It is unclear whether this brain region is uniformly affected in all individuals with PTSD, or whether vmPFC dysfunction is related to individual differences in discrete features of this heterogeneous disorder.In a sample of 51 male veterans of Operation Enduring Freedom/Operation Iraqi Freedom, we collected functional magnetic resonance imaging data during a novel threat anticipation task with crossed factors of threat condition and temporal unpredictability. Voxelwise regression analyses related anticipatory brain activation to individual differences in overall PTSD symptom severity, as well as individual differences in discrete symptom subscales (re-experiencing, emotional numbing/avoidance, and hyperarousal).The vmPFC showed greater anticipatory responses for safety relative to threat, driven primarily by deactivation during threat anticipation. During unpredictable threat anticipation, increased PTSD symptoms were associated with relatively greater activation for threat v.However, simultaneous regression on individual symptom subscales demonstrated that this effect was driven specifically by individual differences in hyperarousal symptoms. Furthermore, this analysis revealed an additional, anatomically distinct region of the vmPFC in which re-experiencing symptoms were associated with greater activation during threat anticipation.Increased anticipatory responses to unpredictable threat in distinct vmPFC subregions were uniquely associated with elevated hyperarousal and re-experiencing symptoms in combat veterans. These results underscore the disruptive impact of uncertainty for veterans, and suggest that investigating individual differences in discrete aspects of PTSD may advance our understanding of underlying neurobiological mechanisms.
| S-EPMC4900910 | biostudies-other
Project description:The identification of biomarkers for post-traumatic stress disorder (PTSD) and resilience/recovery is critical for advancing knowledge about pathophysiology and treatment in trauma-exposed persons. This study examined a series of glucocorticoid-related biomarkers prior to and in response to psychotherapy. Fifty-two male and female veterans with PTSD were randomized 2 : 1 to receive either prolonged exposure (PE) therapy or a weekly minimal attention (MA) intervention for 12 consecutive weeks. Psychological and biological assessments were obtained prior to and following treatment and after a 12-week naturalistic follow-up. Response was defined dichotomously as no longer meeting criteria for PTSD at post-treatment based on the Clinician Administered PTSD Scale for DSM-IV (CAPS). Clinical improvement on the CAPS was apparent for both PE and MA, with no significant difference according to treatment condition. Biomarkers predictive of treatment gains included the BCLI polymorphism of the glucocorticoid receptor gene. Additional predictors of treatment response were higher bedtime salivary cortisol and 24 h urinary cortisol excretion. Pre-treatment plasma dehydroepiandrosterone/cortisol ratio and neuropetide Y (NPY) levels were predictors of reductions in PTSD symptoms, and, for NPY only, of other secondary outcomes as well, including anxiety and depression ratings. Glucocorticoid sensitivity changed in association with symptom change, reflecting clinical state. It is possible to distinguish prognostic and state biomarkers of PTSD using a longitudinal approach in the context of treatment. Identified markers may also be relevant to understanding mechanisms of action of symptom reduction.
| S-EPMC4142020 | biostudies-literature
Project description:Impulsive behaviours are common symptoms of attention-deficit hyperactivity disorder (ADHD). Although previous studies have suggested functional models of impulsive behaviour, a full explanation of impulsivity in ADHD remains elusive. To investigate the detailed mechanisms behind impulsive behaviour in ADHD, we applied an economic intertemporal choice task involving gains and losses to adults with ADHD and healthy controls and measured brain activity by functional magnetic resonance imaging. In the intertemporal choice of future gains, we observed no behavioural or neural difference between the two groups. In the intertemporal choice of future losses, adults with ADHD exhibited higher discount rates than the control participants. Furthermore, a comparison of brain activity representing the sensitivity of future loss in the two groups revealed significantly lower activity in the striatum and higher activity in the amygdala in adults with ADHD than in controls. Our preliminary findings suggest that an altered size sensitivity to future loss is involved in apparent impulsive choice behaviour in adults with ADHD and shed light on the multifaceted impulsivity underlying ADHD.
| S-EPMC5928218 | biostudies-literature
Project description: Not available
| S-EPMC5263061 | biostudies-literature
Project description:In this paper, a first in a Series of two, we look at the evidence for an association of post-traumatic stress disorder with incident cardiovascular disease risk and the mechanisms that might cause this association, as well as the prevalence of post-traumatic stress disorder due to cardiovascular disease events and its associated prognostic risk. We discuss research done after the publication of previous relevant systematic reviews, and survey currently funded research from the two most active funders in the field: the National Institutes of Health and the US Veterans Administration. We conclude that post-traumatic stress disorder is a risk factor for incident cardiovascular disease, and a common psychiatric consequence of cardiovascular disease events that might worsen the prognosis of the cardiovascular disease. There are many candidate mechanisms for the link between post-traumatic stress disorder and cardiovascular disease, and several ongoing studies could soon point to the most important behavioural and physiological mechanisms to target in early phase intervention development. Similarly, targets are emerging for individual and environmental interventions that might offset the risk of post-traumatic stress disorder after cardiovascular disease events.
| S-EPMC5499153 | biostudies-literature