Biological and clinical framework for posttraumatic stress disorder

摘要: Three decades of posttraumatic stress disorder (PTSD) research have placed it well on the map. PTSD is a young that started being properly understood only from 1980 with incorporation in DSM-III, which was acknowledged exposure to traumatic events can lead long-term psychopathology. This chapter reviews history and nosology disorder, epidemiology, etiology, as clinical features. It lists diagnostic assessments provides an overview biological framework by addressing brain, neurohormonal, transmitter alterations. Exposure commonplace. The majority exposed subjects are resilient, this still rule rather than exception. reported prevalence twice common females compared males. A criterion expressed event, after symptom clusters based intrusions, avoidance, irritability. Gene–environmental studies needed, focus specific, distinct endophenotypes influences environmental factors (e.g., early-life experiences, abuse or neglect, disasters combat). often accompanied comorbid disorders, such depression other anxiety drug alcohol dependence. heterogeneous, sometimes complex features emotional dysregulation, attachment, dissociation. Several validated trauma available allow quantification symptomatology. The concepts sensitization fear conditioning failure inhibition. After decade hippocampus we seen shift amygdala new millennium. Given specific role prefrontal cortex (neuro)psychological functions patients (i.e., attention cognitive interference), interest will increase significantly. Increased multidisciplinary involvement, inclusion genetics, endocrinology, immunology, (neuro)psychology, psychopathology, essential find consistency between biological, emotional, dysfunction PTSD. A variety effective psychological pharmacological interventions be used treat PTSD. mechanisms therapy influencing neurobiological markers need further investigated. same goes for emerging therapies eye movement desensitization reprocessing, virtual reality exposure, internet therapy, neurofeedback. There no drugs PTSD, except treatment irritability depressive selective serotonin reuptake inhibitors. Other options, serotonergic agents, e.g., 5-HT1A antagonists, norepinephrine blockers, corticotropin-releasing factor glucocorticoid receptor prazosin α1-adrenergic blocker nightmares, use beta-blockers early New options d-cycloserine cortisol seem offer opportunities influence memory consolidation experiences timed relation exposure. For health economy important aware there economic burden associated treatments require scarce resources. They ultimately provide tools ascertain relative efficiency different plan availability these affected population. biggest challenge future evolution disorder.