No abstract

No abstract

No abstract

Acute stress disorder (ASD) is a precursor of chronic posttraumatic stress disorder (PTSD). Twenty-four participants with ASD following civilian trauma were given 5 sessions of either cognitive-behavioral therapy (CBT) or supportive counseling (SC) within 2 weeks of their trauma. Fewer participants in CBT (8%) than in SC (83%) met criteria for PTSD at posttreatment. There were also fewer cases of PTSD in the CBT condition (17%) than in the SC condition (67%) 6 months posttrauma. There were greater statistically and clinically significant reductions in intrusive, avoidance, and depressive symptomatology among the CBT participants than among the SC participants. This study represents the 1st demonstration of successful treatment of ASD with CBT and its efficacy in preventing chronic PTSD.

Despite advances in the treatment of bipolar disorder, a significant proportion of patients experience disabling symptoms between episodes, and relapse rates are high. These circumstances suggest that there is a critical need to achieve a mechanistic understanding of triggers of relapse and to target them with specific, empirically derived treatments. Sleep disturbances are among the most prominent correlates of mood episodes and inadequate recovery, yet sleep has been minimally studied in ways that integrate mechanistic understanding and treatment. In this article, the author seeks to define the limits of current knowledge and to specify preliminary clinical implications. Sleep disturbance is important because it impairs quality of life, contributes to relapse, and has adverse consequences for affective functioning. While sleep disturbance and circadian dysregulation are critical pathophysiological elements in bipolar disorder, many questions about the mechanisms that underpin the association remain. The author presents a model that recognizes a role for genetic vulnerability and suggests that there is a bidirectional relationship between daytime affect regulation and nighttime sleep such that an escalating vicious circle of disturbance in affect regulation during the day interferes with nighttime sleep/circadian functioning, and the effects of sleep deprivation contribute to difficulty in affect regulation the following day.

Insomnia is a significant problem among euthymic patients with bipolar disorder. Components of cognitive behavior therapy for insomnia, especially stimulus control and cognitive therapy, may be a helpful adjunct to treatment for patients with bipolar disorder.

Insomnia disorder affects a large proportion of the population on a situational, recurrent or chronic basis and is among the most common complaints in medical practice. The disorder is predominantly characterized by dissatisfaction with sleep duration or quality and difficulties initiating or maintaining sleep, along with substantial distress and impairments of daytime functioning. It can present as the chief complaint or, more often, co-occurs with other medical or psychiatric disorders, such as pain and depression. Persistent insomnia has been linked with adverse long-term health outcomes, including diminished quality of life and physical and psychological morbidity. Despite its high prevalence and burden, the aetiology and pathophysiology of insomnia is poorly understood. In the past decade, important changes in classification and diagnostic paradigms have instigated a move from a purely symptom-based conceptualization to the recognition of insomnia as a disorder in its own right. These changes have been paralleled by key advances in therapy, with generic pharmacological and psychological interventions being increasingly replaced by approaches that have sleep-specific and insomnia-specific therapeutic targets. Psychological and pharmacological therapies effectively reduce the time it takes to fall asleep and the time spent awake after sleep onset, and produce a modest increase in total sleep time; these are outcomes that correlate with improvements in daytime functioning. Despite this progress, several challenges remain, including the need to improve our knowledge of the mechanisms that underlie insomnia and to develop more cost-effective, efficient and accessible therapies.

Insomnia is prevalent, causing severe distress and impairment. This review focuses on illuminating the puzzling finding that many insomnia patients misperceive their sleep. They overestimate their sleep onset latency (SOL) and underestimate their total sleep time (TST), relative to objective measures. This tendency is ubiquitous (although not universal). Resolving this puzzle has clinical, theoretical, and public health importance. There are implications for assessment, definition, and treatment. Moreover, solving the puzzle creates an opportunity for "real world" applications of theories from clinical, perceptual, and social psychology as well as neuroscience. Herein we evaluate thirteen possible resolutions to the puzzle. Specifically, we consider the possible contribution, to misperception, of: (1) features inherent to the context of sleep (e.g., darkness); (2) the definition of sleep onset which may lack sensitivity for insomnia patients; (3) insomnia being an exaggerated sleep complaint; (4) psychological distress causing magnification; (5) a deficit in time estimation ability; (6) sleep being misperceived as wake; (7) worry and selective attention toward sleep-related threats; (8) a memory bias influenced by current symptoms and emotions, a confirmation bias/belief bias or a recall bias linked to the intensity/recency of symptoms; (9) heightened physiological arousal; (10) elevated cortical arousal; (11) the presence of brief awakenings; (12) a fault in neuronal circuitry; and (13) there being two insomnia subtypes (one with and one without misperception). The best supported resolutions were misperception of sleep as wake, worry, and brief awakenings. A deficit in time estimation ability was not supported. We conclude by proposing several integrative solutions.