What about sleep homeostasis in insomnia? Comment on the European guideline for the diagnosis and treatment of insomnia

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The very recently published European guideline for the diagnosis and treatment of insomnia provides a comprehensive and thorough review of insomnia literature combined with concise and complete recommendations for caregivers in the field (Riemann et al., 2017). Nevertheless, we think that the authors may have omitted to mention the available evidence concerning relevant neurophysiological aspects of insomnia. Therefore, we were somewhat disappointed not to find any mention of a repeatedly suggested homeostatic dysfunction in insomnia in the ‘aetiology and pathophysiology’ section of the Introduction. Only very few lines were actually allotted to what can be described as neurological pathophysiology. With respect to objective findings in sleep electroencephalographs (EEGs) of insomnia patients, the authors refer mainly to reported power increases in faster frequency ranges, to greater cyclic alternating pattern (CAP) rate and sleep fragmentation by micro‐arousals (Riemann et al., 2017). As early as 2006, however, Pigeon and Perlis had already reviewed that there is sufficient evidence suggesting a dysfunction of sleep homeostasis in insomnia (Pigeon and Perlis, 2006). These authors summarized the lines of evidence for homeostatic dysfunction as follows: compared to controls, insomniacs show (a) lower increase or rebound of slow wave sleep (SWS) after sleep deprivation and reduced SWS pressure; (b) reduced delta sleep EEG power without reduced SWS duration; (c) longer SWS latencies; (d) normal or even decreased sleep propensity as measured by multiple sleep latency tests (MSLTs); (e) less (subjective) sleepiness than controls after sleep deprivation; and (f) differences of sleep stage proportion increases during recovery after total sleep deprivation. While also confirming the increased frontal power of faster EEG frequencies, we argued in a recent paper that findings of decreased slow oscillation (0.3–0.79 Hz) power proportions during SWS in insomnia patients—while SWS duration was preserved in comparison to healthy controls—could indeed also come as a support to the former evidence of homeostatic dysfunction in insomnia (Neu et al., 2015). Following these findings of lowered slow oscillation power in insomnia, a small pilot study has even reported an increase in slow oscillation power during SWS after external stimulation with slow oscillations (<0.75 Hz) by means of transcranial direct current (Saebipour et al., 2015). Conversely, these effects were related to enhanced sleep stabilization and also seemed to be associated with improvements of subjective sleep quality (Saebipour et al., 2015). However, whether this increase of slow oscillations during SWS can remain stable over time, or whether daytime fatigue could improve concomitantly, remains unknown at present. Nonetheless, given that the current range of efficient therapeutic strategies, especially for chronic forms of insomnia, is somewhat limited (gravitating mainly around cognitive and behavioural therapies), such physical treatments may, in turn, lead to an enlargement of available care options.
Finally, given that for more than a decade broad lines of evidence pinpoint a potential underlying homeostatic dysfunction (eventually related to reduced slow oscillation power during SWS) in insomnia, we think that citing these findings briefly, especially with respect to ‘physiopathology’, would have been worth mentioning.

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