There is an ongoing debate about how best to conceptualize the unconscious. Early psychodynamic views employed theories influenced by physics to explain clinical material, while subsequent cognitivist views relied on computational models of the mind to explain laboratory data. More recently, advances in cognitive-affective neuroscience have provided new insights into the workings of unconscious cognition and affect. We briefly review some of this recent work and its clinical implications.

Posttraumatic stress disorder (PTSD) is a well-defined clinical syndrome that develops in individuals who have witnessed or been exposed to an event that involves a direct threat to life or physical and/or psychological integrity.

While numerous studies indicate that PTSD will develop in 15% to 25% of trauma victims, time-limited responses develop in a larger portion of victims during the first 48–72 hours (acute stress reaction) and to a lesser extent over the first 4 weeks (acute stress disorder). Many of those who suffer from acute posttraumatic symptoms eventually recover and overcome the consequences of the traumatic event. However, ∼30% to 50% of those with acute stress disorder will eventually develop PTSD. It is obvious that some individuals are vulnerable to the adverse effects of trauma while others have neurobiological and psychological resources that make them resilient to the long-term impact of traumatic exposure. The identification of risk factors and early predictors for PTSD is thus of major importance for identifying those at risk and for initiating therapeutic interventions aimed to reduce long-term morbidity and suffering.

Posttraumatic stress disorder (PTSD) has a discernible starting point and typical course, hence the particular appropriateness of longitudinal research in this disorder. This review outlines the salient findings of longitudinal studies published between 1988 and 2004. Studies have evaluated risk factors and risk indicators of PTSD, the disorder's trajectory, comorbid disorders and the predictive role of acute stress disorder. More recent studies used advanced data analytic methods to explore the sequence of causation that leads to chronic PTSD. Advantages and limitations of longitudinal methods are discussed.

Traumatic memories, and the mechanisms by which they operate, continue to occupy a central role in the scientific investigation of risk factors for the development of posttraumatic stress disorder (PTSD). However, empirically based studies are constrained by practical and ethical considerations and are limited to naturalistic models. Consequently, the paradigms most appropriate for the exploration of the relationship between traumatic memories and PTSD have been identified in conditions involving traumatic events where memories may be compromised. Indeed, traumatic brain injury, a condition that is commonly associated with memory impairment, has often been utilized as a naturally occurring model for the study of traumatic memory and its contribution to the development of PTSD. This article presents a critical review of these research efforts and discusses their theoretical and clinical implications.

Sleep disturbances, including nightmares and insomnia, are prominent following trauma and with posttraumatic stress disorder (PTSD) and likely contribute to the pathogenesis of the disorder. Findings from laboratory studies of PTSD have been inconsistent in terms of documenting objective impaired sleep maintenance but have been somewhat more consistent in indicating alterations of rapid eye movement (REM) sleep. Studies of the early aftermath of trauma can reduce the complexity associated with chronicity and comorbidity, and may have implications for early diagnosis and prevention. Multiple studies indicate that dream content is affected by recent threatening experiences. The development of PTSD is associated with a more replicative type of nightmare content. Sleep is reported to be generally disrupted following trauma especially among those developing PTSD. The limited number of studies that provide objective recorded indices during the early aftermath of trauma also provide a mixed picture regarding overall sleep maintenance. Recent data suggest that a more specific disruption of REM sleep may be associated with the development of PTSD and that this disruption is associated with an increased signal of sympathetic nervous system activation during REM sleep. Disrupted REM sleep and increased sympathetic/noradrenergic activity may have implications for understanding recent promising interventions for PTSD sleep disturbance that can be applied to early intervention.

A growing number of common traumatic events involve both physical and emotional injuries. In contrast to previously held beliefs, the rapidly growing body of literature shows quite convincingly that physical injury, over and above exposure to the traumatic event itself, increases rather than decreases the risk for posttraumatic stress disorder (PTSD). A pertinent question becomes how bodily injury contributes to the risk of developing PTSD. In this article, we review contemporary findings regarding the neurobiological and psychological mechanisms by which bodily injury may augment or independently contribute to chronic posttraumatic stress. In addition, we propose three theoretical pathways through which physical injury can increase the risk for PTSD. These pathways are: additive, unique, and recovery impeding. Finally, we highlight unresolved issues pertaining to each one of these pathways and propose directions for future research to address them.

Introduction: Attention-deficit/hyperactivity disorder (ADHD) is a serious neurobehavioral disorder of childhood onset that often persists into adolescence and adulthood. Functional impairments, underachievement, and difficult interpersonal relationships illustrate the need for effective treatment of ADHD through adulthood.

Method: This prospective, multisite, randomized, double-blind, placebo-controlled, parallel-group, dose-escalation study was conducted to assess the efficacy, safety, and duration of action of mixed amphetamine salts extended-release (MAS XR) in adults with ADHD, combined type. Adults ≥ 18 years of age were given placebo or MAS XR 20, 40, or 60 mg/day for 4 weeks. The main outcome measures were the ADHD Rating Scale and Conners' Adult ADHD Rating Scale Short Version Self-Report (CAARS-S-S).

Results: Two hundred fifty-five subjects were randomly assigned to treatment with MAS XR or placebo. MAS XR treatment was associated with statistically and clinically significant ADHD symptom reduction at endpoint; mean ADHD Rating Scale scores were 18.5 for the 20-mg group (P=.001), 18.4 for the 40-mg group (P<.001), and 18.5 for the 60-mg group (P<.001). Adults with severe symptoms (ADHD Rating Scale score ≥32 at baseline) had significantly greater symptom reduction with the highest MAS XR dose (60 mg/day), however, this dose-response relationship was determined by post-hoc analysis. The mean MAS XR effect size was 0.8. Statistically significant (P<.05) improvements in CAARS-S-S ADHD index scores occurred at 4- and 12-hours postdose for all MAS XR groups, indicating a 12-hour duration of effect. Symptoms improved within the first treatment week. Most adverse events reported were mild or moderate in intensity, arid the most commonly reported adverse events were consistent with the known profile of stimulant medications. Vital signs and electrocardiograms showed no clinically significant cardiovascular changes.

Conclusion: These results suggest that MAS XR is safe and effective in adults with ADHD and controlled ADHD symptoms for up to 12 hours.