Insomnia disorder is associated with 24-hour cortical hyperarousal

Cortical hyperarousal has been proposed as a primary underlying mechanism for insomnia disorder. However, most evidence comes from nighttime sleep and whether patients with insomnia disorder have cortical hyperarousal through the 24-h sleep/wake cycle is not resolved.

We included 49 patients with insomnia disorder and 49 age-and sex-matched normal sleepers. All participants underwent an over-night polysomnography followed by a Multiple Sleep Latency Test during daytime. Nighttime and daytime delta, theta, alpha, sigma and beta relative power at central electroencephalogram derivations during wakefulness and non-rapid eye movement (NREM) sleep were calculated. Insomnia disorder was defined based on the International Classification of Sleep Disorders Third Edition criteria. Insomnia with objective short sleep duration was defined as patients with insomnia who slept <7 h based on nighttime polysomnography recording.

Compared to normal sleepers, patients with insomnia disorder had significantly higher nighttime (P = 0.040) and daytime (P = 0.021) relative electroencephalogram power in beta during NREM sleep and marginally significantly lower relative electroencephalogram power in theta (P = 0.060) during nighttime wakefulness. Furthermore, linear trend association was observed across normal sleepers, and patients with insomnia who slept ≥7 h and insomnia who slept <7 h in relative electroencephalogram power in beta during nighttime and daytime NREM sleep, and relative electroencephalogram power in theta during nighttime wakefulness (all P for trend <0.05).

Increased high-frequency electroencephalogram power during nighttime and daytime sleep suggests that insomnia is a disorder of 24-h cortical hyperarousal. Decreasing both nighttime and daytime cortical arousal levels should be our therapeutic target for insomnia.