A cognitive model of insomnia.

A number of paradoxes are apparent in the assessment and treatment of psychophysiological insomnia and sleep state misperception. Three of these paradoxes exist as discrepancies between polysomnographic (PSG) measures and the subjective impressions regarding sleep quality and quantity. The remaining incongruity exists largely within the objective domain. In the case of subjective-objective discrepancies, patients with insomnia: (1) frequently identify themselves as having been awake when awakened from PSG defined sleep; (2) tend to overestimate sleep latency and underestimate total sleep time as compared with PSG measures; (3) appear to derive more benefit from pharmacotherapy that can be explained by objective gains. The remaining paradox pertains to the observation that hypnotic medications, by and large, do not normalize sleep architecture or produce a more 'sleep-like' EEG. In this paper, we review possible explanations for these various paradoxes, introduce a new perspective and suggest possible research avenues. The model introduced is based on the observation that beta and/or gamma activity (which have been found to be associated with cognitive processes) is enhanced in insomnia at or around sleep onset. We propose that this kind of high frequency EEG activity may interfere with the normal establishment of sleep onset-related mesograde amnesia. As a result, the patient with insomnia maintains a level of information and/or memory processing that blurs the phenomenological distinction between sleep and wakefulness and influences retrospective judgments about sleep initiation and duration.

Psychophysiological insomnia: the behavioural model and a neurocognitive perspective.

Summary: Insomnia is a condition which affects millions of individuals, giving rise to emotional distress, daytime fatigue, and loss of productivity. Despite its prevalence, it has received scant clinical attention. An adequate evaluation of persistent insomnia requires detailed historical information as well as medical, psychological and psychiatric assessment. Use of a classification system for sleep disorders and familiarity with major diagnostic groups will facilitate the clinician's evaluation and treatment. Thorough assessment also requires attention to the unique aspects of presentation and specific set of etiologies which are associated with particular age groups.

An American Academy of Sleep Medicine Review

Daytime symptoms in primary insomnia: a prospective analysis using ecological momentary assessment.

Many patients suffering from the majority of anxiety disorders complain about their sleep by reporting difficulties in initiating and maintaining it. Polysomnographic studies have shown that, in comparison to normal subjects, the sleep of patients with panic disorder is characterized by longer sleep latency, increased time awake and reduced sleep efficiency. Sleep architecture is normal and there are no significant changes in REM sleep measures. Nocturnal panic attacks are non-REM-related events and occur without an obvious trigger in 18-45% of panic disorder patients. Regarding generalized anxiety disorder, the patients complain of 'trouble sleeping' in 60-70%, while polysomnography has shown increased sleep latency and decreased sleep continuity measures. The findings in REM sleep and sleep architecture generally do not show any aberration to exist. In patients with obsessive-compulsive disorder (OCD) and post-traumatic stress disorder (PTSD), results from the sleep laboratory do not seem to support the subjective complaints of poor sleep. The early reports of shortened REM latency in OCD could not be replicated by recent studies. A dysregulation of the REM sleep control system has been reported for patients with PTSD. Finally, no significant differences were found in all sleep parameters between social phobia patients and controls.

Sleep disturbance in anxiety disorders.

Objective: In the absence of clear distinctions in alertness between patients with primary insomnia and normal subjects, the goal of this study was to identify psychometric and electrophysiological measures that would distinguish these two groups. Method: The daytime alertness of 20 primary insomnia patients and 20 normal subjects was investigated through their scores on a 26-item hyperarousal scale and measurement ofauditory evoked potentials and alpha and nonalpha band EEG activity. Statisticalanalysis ofthe data included correlation of the hyperarousal scores and the electrophysiological measures. Results: The hyperarousal scores showed clearly higher daytime alertness in the insomnia patients compared with the normal subjects. In addition, during wakefulness, the insomnia patients showed greater amplitudes ofP1N1, a durable, intrinsic, late (cortical) component ofthe auditory evoked potential, as well as greater EEG activity across the frequency spectrum. The hyperarousal scores correlated positively with the amplitude of P1N1 at each of three sound intensities. Conclusigns: To the authors’ knowledge, this is the first study to offer evidence that patients with primary insomnia have objectively definable features during wakefulness that clearly distinguish them from normal subjects. The measurement of hyperarousal might be used to refine descriptions of insomnia populations in experimental studies. (Am J Psychiatry 1993; 150:1529-1534)

Margaret Paine

Papers

Daytime alertness in patients with primary insomnia.