The aim of this meeting was to obtain a consensus on what constitutes good research practice in posttraumatic stress disorder (PTSD). Objectives were to review relevant parameters of trials, such as the patients recruited, the means of assessing PTSD at baseline, and the change in symptomatology in response to treatment, and to reach a consensus on the most appropriate parameters to use in future research. The bases for the discussion were the 1995 National Institute of Mental Health (NIMH) and the National Center for PTSD consensus on the assessment of PTSD, results of drug treatment trials, and information on the assessment scales used in PTSD research.

Posttraumatic stress disorder (PTSD) was associated in the past mainly with combatrelated events. This was reflected in the names given to the disorder, ie, “shell shock,” “soldier's heart,” “combat neurosis,” and “operational fatigue.” Only following the realization that PTSD can be related to all types of traumatic events, including noncombat associated events, were the terms “traumatic neurosis” and, later, “PTSD” coined. These new terms reflect the understanding that the condition need not necessarily be associated with war, but may also be related to events such as a severe automobile accident, violent personal assault (eg, rape, physical attack, robbery, or mugging), terrorist attack, natural or human-made disaster (such as a fire), witnessing serious injury or death due to any of the above, as well as to other situations, such as being kidnapped or being held hostage.

The tendency to interpret the symptoms of what we would consider now as PTSD, as a “normal response” to traumatic events was another factor that held up progress in the field. It is important to note that PTSD is a pathological response: The vast majority of individuals who are exposed to a traumatic event will later adapt and continue on with their lives. Only a small percent, which partially depends on the type of trauma and is partially associated with several risk factors, will develop a pathological fixation on the traumatic event, namely, PTSD.

It has been estimated that approximately one-third of the population will be exposed to a severe trauma (according to the definition of PTSD) during their lifetime.

This article reviews a series of studies conducted on Israeli war veterans that assessed the interrelationship of posttraumatic stress disorder (PTSD) and comorbid disorder, focusing on five issues in particular: (1) the frequency of comorbidity among veterans diagnosed with PTSD; (2) how this comorbidity can be accounted for; (3) whether PTSDs with and without comorbidity are different; (4) the validity of PTSD as a distinct diagnosis; and (5) the clinical implications of comorbidity of PTSD.

In 1980, the diagnosis of posttraumatic stress disorder (PTSD) was established to recognize that exposure to events such as rape, physical assault, torture, or combat can leave long-lasting psychological scars in persons who undergo these experiences. The intention of the diagnosis was to acknowledge that exposure to a traumatic event was a sufficient explanation for the occurrence of longterm psychological problems. Prior to this formulation, stressful events were thought to precipitate symptoms that would resolve over time. The symptoms manifested by persons following adverse events were characterized as transient adjustment reactions. Longerterm symptoms were considered to be a reflection of underlying neurosis, rather than stress exposure per se.

The diagnosis of PTSD provided a paradigm for acknowledging that exposure to devastating trauma can produce symptoms that can be quite severe and chronic in nature. Although many of the symptoms of PTSD were similar to those that occur in other anxiety or mood disorders, the hallmark of PTSD appeared to be a preoccupation with the traumatic event and a resultant set of behavioral changes that occurred because of attempts to avoid reminders of the event.

Contemporary neuroimaging methods have been used to gather initial data regarding the neural substrates of posttraumatic stress disorder (PTSD). Morphometric magnetic resonance imaging (MRI) studies have reliably shown reduced hippocampal volume in subjects with PTSD vs control cohorts. Functional imaging studies have implicated a network of brain regions in PTSD, comprising the amygdala, hippocampus, and anterior paralimbic territories (including anterior cingulate cortex), as well as Broca's area and visual cortex. Extant relevant neuroimaging data are reviewed, and a tentative heuristic neuroanatomical model of PTSD is provided. In conclusion, emerging strategies for advancement in this field are outlined.

Much 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.