First adopted by DSM-III in 1980, this process revolutionized definitions of psychiatric disorders, most recently formalized in DSM-IV-TR. ![]() Robins and Guze proposed a procedure for validation of psychiatric diagnoses nearly 40 years ago (15). Because the etiology and pathogenesis of most psychiatric disorders remain largely unknown, diagnostic validity in psychiatry is largely limited to follow-up studies of illness course, response to treatment, and family studies (12). Most, e.g., coronary artery disease, cancer, and Parkinson’s disease, result from a mixture of etiologies and complex pathogenesis (12, 14). Few diseases have one necessary and sufficient cause or pathognomonic indicators. Traditional tests of the validity of these criteria entail demonstration of etiology, pathogenesis, illness course, including response to treatment, and familial patterns. Subsequent changes in the diagnostic criteria have provoked heated debate, largely surrounding definition of the traumatic event that anchors the symptoms.Įstablishing diagnostic criteria is an iterative process, beginning with a listing of clinical observations and revising these criteria as more empirical evidence is collected (12, 13). Although posttraumatic syndromes have been described for many centuries in various forms, PTSD is a relative newcomer in psychiatric diagnostic nomenclature with its debut in DSM-III in 1980. Questions about the very existence of PTSD persist (5, 7 – 11). If anything, it appears to be intensifying with the push toward DSM-V (2 – 8). The literature suggests the controversy has not cooled (2 – 6). More than two decades ago, a major commentary on posttraumatic stress disorder (PTSD) opened with a statement about “a long-standing debate” over validity of the diagnosis (p. Collaborations among trauma research biologists, epidemiologists, and nosologists to map the correspondence between the clinical and biological indicators of psychopathology are necessary to advance validation and further understanding of PTSD. In this process, diligent adherence to the criteria under examination is paramount to successful PTSD research, and changes in criteria are driven by empirical data rather than theory. The authors recommend that future research begin with existing diagnostic criteria, testing and further refining them in accordance with the classic Robins and Guze strategy for validation of psychiatric diagnoses. Research is now poised to answer questions about the relevance of traumatic events based on their relationship to symptomatic outcome. Of three categories of symptoms associated with PTSD-intrusive memories, avoidance and numbing, and hyperarousal-avoidance and numbing appear to be the most specific for identification of PTSD. On the other hand, the symptomatic description of PTSD is becoming more clear. It is still not established whether or not there are specific types of traumatic events and levels of exposure to them that are associated with a syndrome that is cohesive in clinical characteristics, biological correlates, familial patterns, and longitudinal diagnostic stability. Attempts to define the range of trauma exposure inherent in the diagnosis of PTSD have generated controversy, as reflected in successive revisions of the criterion from DSM-III onward. The diagnosis of PTSD thus inherently depends on two separate but confounded processes: exposure to trauma and development of a specific pattern of symptoms that appear following the trauma. ![]() Unlike most psychiatric diagnoses, posttraumatic stress disorder (PTSD) is defined in relation to a potentially etiologic event (the traumatic “stressor criterion”) that is fundamental to its conceptualization.
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