Anxiety Disorders and Phobias: A Cognitive Perspective

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Disturbed sleep in post-traumatic stress disorder: secondary symptom or core feature?

The hypothesis that rapid eye movement (REM) sleep disturbances are the hallmark of posttraumatic stress disorder (PTSD), proposed by Ross and colleagues in 1989, has stimulated a wealth of clinical, preclinical, and animal studies on the role of sleep in the pathophysiology of PTSD. The present review revisits this influential hypothesis in light of clinical and experimental findings that have since accumulated. Polysomnographic studies conducted in adults with PTSD have yielded mixed findings regarding REM sleep disturbances, and they generally suggest modest and nonspecific sleep disruptions. Prospective and treatment studies have provided more robust evidence for the relationship between sleep disturbances and psychiatric outcomes and symptoms. Experimental animal and human studies that have probed the relationship between REM sleep and fear responses, as well as studies focused more broadly on sleep-dependent affective and memory processes, also provide strong support for the hypothesis that sleep pl...

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Sleep Disturbances as the Hallmark of PTSD: Where Are We Now?

Sleep-specific mechanisms underlying posttraumatic stress disorder: Integrative review and neurobiological hypotheses

Subjective reports of sleep disturbance indicate that 70–91% of patients with post-traumatic stress disorder (PTSD) have difficulty falling or staying asleep. Nightmares are reported by 19–71% of patients, depending on the severity of their PTSD and their exposure to physical aggression. Objective measures of sleep disturbance are inconsistent, with some studies that used these measures indicating poor sleep and others finding no differences compared with non-PTSD controls. Future research in this area may benefit from examining measures of instability in the microstructure of sleep. Additionally, recent findings suggest that sleep disordered breathing (SDB) and sleep movement disorders are more common in patients with PTSD than in the general population and that these disorders may contribute to the brief awakenings, insomnia and daytime fatigue in patients with PTSD. Overall, sleep problems have an impact on the development and symptom severity of PTSD and on the quality of life and functioning of patients. In terms of treatments, SSRIs are commonly used to treat PTSD, and evidence suggests that they have a small but significant positive effect on sleep disruption. Studies of serotonin-potentiating non-SSRIs suggest that nefazodone and trazodone lead to significant reductions in insomnia and nightmares, whereas cyproheptadine may exacerbate sleep problems in patients with PTSD. Prazosin, a centrally acting α1-adrenoceptor antagonist, has led to large reductions in nightmares and insomnia in small studies of patients with PTSD. Augmentation of SSRIs with olanzapine, an atypical antipsychotic, may be effective for treatment-resistant nightmares and insomnia, although adverse effects can be significant. Additional medications, including zolpidem, buspirone, gabapentin and mirtazapine, have been found to improve sleep in patients with PTSD. Large randomised, placebo-controlled trials are needed to confirm the above findings. In contrast, evidence suggests that benzodiazepines, TCAs and MAOIs are not useful for the treatment of PTSD-related sleep disorders, and their adverse effect profiles make further studies unlikely. Cognitive behavioural interventions for sleep disruption in patients with PTSD include strategies targeting insomnia and imagery rehearsal therapy (IRT) for nightmares. One large randomised controlled trial of group IRT demonstrated significant reductions in nightmares and insomnia. Similarly, uncontrolled studies combining IRT and insomnia strategies have demonstrated good outcomes. Uncontrolled studies of continuous positive airway pressure for SDB in patients with PTSD show that this treatment led to significant decreases in nightmares, insomnia and PTSD symptoms. Controlled studies are needed to confirm these promising findings.

Sleep disturbances in patients with post-traumatic stress disorder: epidemiology, impact and approaches to management

Culture and Anxiety Disorders

Interferon for hepatitis C patients with psychiatric disorders [7] (multiple letters)

In this article we review the DSM-IV criteria for Panic Disorder (PD), provide a brief overview of the cognitive model of PD, discuss empirically supported treatment components, and review pivotal experiments examining cognitive behavioral therapy for PD. A case example is also included to illustrate the application of treatment components. Panic Disorder (PD) (with and without agoraphobia) is a debilitating condition with an estimated lifetime prevalence of 1.5% (American Psychiatric Association, 1994). Approximately twice as many women as men suffer from PD. Although PD typically first appears between late adolescence and early adulthood, it can also begin in childhood and in later life. While data on the course of PD are lacking, retrospective patient accounts indicate that PD appears to be a chronic condition that waxes and wanes in severity. Unfortunately, the chronicity of the disorder may be due, in part, to the lack of appropriate treatment. As defined in the DSM-IV (American Psychiatric Association, 1994), the essential feature of PD is the experience of recurrent, unexpected panic attacks. A panic attack is defined as a discrete period of intense fear or discomfort that develops abruptly and reaches a peak within 10 minutes and is accompanied by at least 4 of the following 13 somatic and cognitive symptoms: shortness of breath, dizziness, palpitations, trembling, sweating, feeling of choking, nausea/abdominal distress, depersonalization, paresthesias (numbness/tingling), flushes/chills, chest pain, fear of dying, fear of going crazy or doing something uncontrolled. To warrant the diagnosis of PD in accordance with the DSM-IV, the individual must experience at least two unexpected panic attacks followed by at least one month of concern about having another panic attack. The frequency of attacks varies widely and ranges from several attacks each day to only a handful attacks per year. Although community estimates suggest that approximately one-half of individuals who experience PD also develop agoraphobia, the prevalence of agoraphobia is much higher in clinical samples. In fact, the vast majority of PD patients seeking treatment present with agoraphobia. The DSM-IV defines agoraphobia as the experience of anxiety in situations in which escape might be difficult or where help may not be immediately available in the event of the occurrence of a panic attack. Common agoraphobic situations include airplanes, buses, trains, elevators, being alone, being in a crowd of people, and so forth. As a result of the anxiety experienced in these situations, individuals often develop phobic avoidance resulting in a constricted lifestyle. The severity of agoraphobia may range from relatively mild (e.g., travels unaccompanied when necessary but typically avoids traveling alone) to quite severe (e.g., unable to leave home alone). THE COGNITIVE MODEL OF PANIC DISORDER The cognitive model of PD proposes that panic attacks occur when individuals perceive certain somatic sensations as considerably more dangerous than they truly are, and interpret them to mean that they are about to experience sudden, imminent disaster (Clark, 1986). For example, individuals may develop a panic attack if they misinterpret heart palpitations as signaling an impending heart attack or jittery, shaky feelings as indicating that they will lose control or go crazy. Clark (1986) believes that these "catastrophic misinterpretations" may arise not only from fear but also from a variety of other emotions, such as anger or from other stimuli (e.g., caffeine, exercise). The vicious cycle culminating in a panic attack develops when a stimulus perceived as threatening creates feelings of apprehension. If the somatic sensations that accompany this state of apprehension are catastrophically misinterpreted, the individual experiences a further increase in apprehension, elevated somatic sensations, and so on, until a full-blown panic attack occurs. …

Empirically supported treatment for panic disorder: Research, theory, and application of cognitive behavioral therapy

http://psycnet.apa.org/books/12353/004.pdf

Simon A. Rego

Papers

Sleep disturbances in patients with post-traumatic stress disorder: epidemiology, impact and approaches to management

Culture and Anxiety Disorders

Interferon for hepatitis C patients with psychiatric disorders [7] (multiple letters)

Empirically supported treatment for panic disorder: Research, theory, and application of cognitive behavioral therapy

Behavioral theories of psychotherapy.