PSYCHOPHYSIOLOGICAL INSOMNIA - THE BEHAVIORAL-MODEL AND A NEUROCOGNITIVE PERSPECTIVE

A number of paradoxes are apparent in the assessment and treatment of psychophysiological insomnia and sleep state misperception. Three of t hese paradoxes exist as discrepancies between polysomnographic (PSG) m easures and the subjective impressions regarding sleep quality and qua ntity. The remaining incongruity exists largely within the objective d omain. In the case of subjective-objective discrepancies, patients wit h insomnia: (1) frequently identify themselves as having been awake wh en awakened from PSG defined sleep; (2) tend to overestimate sleep lat ency and underestimate total sleep time as compared with PSG measures; (3) appear to derive more benefit from pharmacotherapy that can be ex plained by objective gains. The remaining paradox pertains to the obse rvation that hypnotic medications, by and large, do not normalize slee p architecture or produce a more 'sleep-like' EEG. In this paper, we r eview possible explanations for these various paradoxes, introduce a n ew perspective and suggest possible research avenues. The model introd uced is based on the observation that beta and/or gamma activity (whic h have been found to be associated with cognitive processes) is enhanc ed in insomnia at or around sleep onset. We propose that this kind of high frequency EEG activity may interfere with the normal establishmen t of sleep onset-related mesograde amnesia. As a result, the patient w ith insomnia maintains a level of information and/or memory processing that blurs the phenomenological distinction between sleep and wakeful ness and influences retrospective judgments about sleep initiation and duration.