Psychophysiological insomnia: the behavioural model and a neurocognitive perspective

Abstract

SUMMARY 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.

The Pathophysiology of Insomnia

“…21 Conditioned arousal is the repeated association of sleep-related cues with wakefulness and/or arousal, which, over time, results in an arousal response when a sleep-related stimulus is presented. 97 Th e neurocognitive model focuses specifi cally on cortical arousal as the mechanism underlying chronic insomnia, as indexed by high-frequency EEG activity ( b and g , 16-50 Hz).…”

“…98 , 99 High-frequency EEG enhances sensory and information processing, which may contribute to the subjective-objective discrepancy that oft en characterizes insomnia. 21 Evidence is mixed regarding insomnia-control diff erences in high-frequency EEG activity during wakefulness. 72 , 100 However, highfrequency waking EEG activity signifi cantly correlates with high-frequency EEG activity during NREM 100 and with self-reported hyperarousal symptoms.…”

When Thinking Impairs Sleep: Trait, Daytime and Nighttime Repetitive Thinking in Insomnia

“…One potential modifiable risk factor for insomnia is repetitive thinking (Borkovec, 1982;Perlis, Giles, Mendelson, Bootzin, & Wyatt, 1997;Morin, 1993). Repetitive thinking, originally studied in the context of anxiety and depression (for reviews, see Nolen-Hoeksema, Wisco, & Lyubomirsky, 2008;Watkins, 2008), is defined as "the process of thinking attentively, repetitively, or frequently about oneself and one's world" (Segerstrom, Stanton, Alden, & Shortridge, 2003, p. 909).…”

Repercussões imunológicas dos distúrbios do sono: o eixo hipotálamo-pituitária-adrenal como fator modulador

“…Therefore, the hyperactivity exacerbates vigilance and impacts negatively on sleep, thus forming a vicious circle in which difficulty to sleep becomes the stressful factor itself. 47 This hypothesis has been confirmed by the positive correlation between elevated levels of cortisol, increased activity of the sympathetic system and time of waking in chronic insomniacs. 48 However, there has always been a question of whether insomnia leads to increased HPA activity, or increased activity of the HPA axis is a risk factor for the development of stress-induced insomnia.…”