Dissociative Symptomatology in Posttraumatic Stress Disorder and Disorders of Extreme Stress

In this final session, the patient reviews the skills learned in the treatment program and looks at his or her overall progress. The patient is encouraged to very deliberately keep practicing the skills learned in therapy over the next several months (or as long as necessary), and, if they run into problems, they are advised to call the therapist for a booster session. There may be times in the future when it feels as though the posttraumatic stress disorder (PTSD) symptoms are coming back or seem to be worsening. This might happen at times of stress or maybe during times of change. Moving, getting a new job, getting married, having babies, children moving out, and children getting married are all generally happy times, but they can be stressful. The patient’s body has learned to react to extreme stress with PTSD symptoms, and he or she may notice some of these symptoms in the future. It does not mean that they are relapsing, but does mean that they need to pay attention.

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Transcriptomic Organization of Human Posttraumatic Stress Disorder

10.1101/2020.01.27.921403 ◽

2020 ◽

Cited By ~ 1

Author(s):

Matthew J. Girgenti ◽

Jiawei Wang ◽

Dingjue Ji ◽

Dianne Cruz ◽

Murray B. Stein ◽

...

Keyword(s):

Posttraumatic Stress Disorder ◽

Posttraumatic Stress ◽

Stress Disorder ◽

Extensive Study ◽

Network Analyses ◽

Extreme Stress ◽

Significant Gene ◽

Significant Divergence ◽

Differential Gene ◽

Molecular Substrates

ABSTRACTPosttraumatic stress disorder (PTSD) affects approximately 8% of the general population, with higher rates in extreme stress groups, including combat veterans or victims of sexual assault. Despite extensive study of the neurobiological correlates of PTSD, little is known about its molecular substrates. Here differential gene expression and network analyses of 4 prefrontal cortex (PFC) postmortem subregions of male and female PTSD subjects demonstrates extensive remodeling of the transcriptomic landscape. The data revealed a highly connected down-regulated set of interneuron transcripts in the most significant gene network associated with PTSD and integration of this data with genotype data from the largest PTSD GWAS identified the interneuron synaptic gene ELFN1 as conferring significant genetic liability for PTSD. We also identified marked sexual dimorphism in the transcriptomic signatures that could contribute to the higher rates of PTSD in women. Comparison with a matched major depressive disorder (MDD) cohort revealed significant divergence between the molecular profiles of subjects with PTSD and depression despite their high comorbidity. Our analysis provides convergent systems-level evidence of genomic networks within the PFC that contribute to the pathophysiology of PTSD in humans.

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The Neuroendocrinology of Posttraumatic Stress Disorder: New Directions

CNS Spectrums ◽

10.1017/s1092852900008841 ◽

2003 ◽

Vol 8 (9) ◽

pp. 651-667 ◽

Cited By ~ 99

Author(s):

Ann M. Rasmusson ◽

Meena Vythilingam ◽

Charles A. Morgan

Keyword(s):

Posttraumatic Stress Disorder ◽

Posttraumatic Stress ◽

Hpa Axis ◽

Stress Disorder ◽

Psychiatric Symptoms ◽

Population Characteristics ◽

Therapeutic Interventions ◽

Extreme Stress ◽

Complex Interactions ◽

The Brain

ABSTRACTStudies of the hypothalamic-pituitary-adrenal (HPA ) axis in persons with posttraumatic stress disorder (PTSD) have produced variable findings. This review focuses on the factors likely to have affected the outcome of these studies, including population characteristics and experimental design. Also discussed is a possible role for the adrenal neurosteroid dehydroepiandrosterone (DHEA) as a mediator of HPA axis adaptation to extreme stress and the psychiatric symptoms associated with PTSD. The antiglucocorticoid properties of DHEA may contribute to an upregulation of HPA axis responses as well as mitigate possible deleterious effects of high cortisol levels on the brain in some PTSD subpopulations. The neuromodulatory effects of DHEA and its metabolite DHEAS at γ-arninobutyric acid and N-methyl-D-aspartate receptors in the brain may contribute to psychiatric symptoms associated with PTSD. The possible importance of other neurohormone systems in modulating HPA axis and symptom responses to traumatic stress is also discussed. Understanding the complex interactions of these stress-responsive neurosteroid and peptide systems may help explain the variability in patterns of HPA axis adaptation, brain changes, and psychiatric symptoms observed in PTSD and lead to better targeting of preventive and therapeutic interventions.

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The Role of Serotonin in Posttraumatic Stress Disorder: Neurobiology and Pharmacotherapy

CNS Spectrums ◽

10.1017/s1092852900007318 ◽

1998 ◽

Vol 3 (S2) ◽

pp. 42-51 ◽

Cited By ~ 12

Author(s):

Kathryn M. Connor ◽

Jonathan R.T. Davidson

Keyword(s):

Posttraumatic Stress Disorder ◽

Posttraumatic Stress ◽

Stress Disorder ◽

Open Label ◽

Model Studies ◽

Extreme Stress ◽

Clinical Investigations ◽

Paroxetine Binding ◽

Neuroimaging Data

AbstractMuch attention has been given to the role of catecholamine dysfunction in posttraumatic stress disorder (PTSD), and only recently have researchers begun to focus on serotonin (5-HT) in PTSD. Serotonin appears to be a factor in responses followin extreme stress, such as those that precede PTSD. In this review, the authors provide a brief overview of the concept of PTSD and specific issues of clinical concern. The role 5-HT in the neurobiology of PTSD is explored in a review of animal model studies and of clinical investigations of paroxetine binding, pharmacologic challenges, and neuroimaging. Data on the use of 5-HT in PTSD treatment are provided in a review of both open-label and controlled studies of serotonergically active drugs.

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