Insomnia disorder and endogenous neurophysiological dynamics

Insomnia symptoms are the most common medical complaints, affecting up to a third of the general population. Insomnia symptoms include sleep problems (initiating or maintaining sleep) as well their repercussions on wake-time functioning. Insomnia Disorder can be diagnosed when insomnia symptoms are recurrent (>3 times a week), persistent (> 3 months), cannot be attributed to sleep-disrupting circumstances, and impair daytime functioning. Insomnia Disorder affects approximately 10% of the population and tends to persist over months or years. Insomnia Disorder severely reduces the quality of life and carries an increased risk of severe, long-lasting health problems, including cardiovascular and mood disorders. Given its high prevalence, persistence and impact on health, it is highly important to study the pathophysiology of Insomnia Disorder during wakefulness and sleep. Overall, the study of the endogenous EEG dynamics in Insomnia Disorder revealed that hyperarousal of the central nervous system occurs not only during sleep but also during wakefulness. During wakefulness, Insomnia Disorder is characterized by stronger cortical oscillations in a broad beta band and by increased cortical sensitivity to cardiac activity. Furthermore, people with more severe insomnia complaints show stronger Long-Range Temporal Correlations of the amplitude fluctuations of cortical oscillations; which is consistent with a weaker inhibitory bias in the cortical balance between excitation and inhibition. During sleep, the shallow and more fragmented sleep that characterizes Insomnia Disorder may particularly involve N2 instability. Resolving the causal relationship between sleep fragmentation and excitation/inhibition balance is the next key-step in the understanding of the pathophysiology of Insomnia Disorder.