What does this research mean for the field?

Cognitive Behavioral Therapy for Insomnia (CBT-I) reduces cortical hyperarousal in patients with Chronic Insomnia Disorder, as indicated by an increase in the delta/beta ratio during non-REM sleep. Novelty: ClaimNovelty.NOVEL_FINDING. Consensus alignment: ConsensusAlignment.SUPPORTS_CONSENSUS.

What question did this study set out to answer?

The study aims to assess the effects of Cognitive-Behavioral Therapy for Insomnia on EEG indicators of sleep-related hyperarousal.

February 16, 2026Open Access

The effectiveness of Cognitive behavioral therapy for insomnia on sleep EEG hyperarousal: a multicentric polysomnographic study

Key Points

The study aims to assess the effects of Cognitive-Behavioral Therapy for Insomnia on EEG indicators of sleep-related hyperarousal.
Conducted a multicentric study with 98 participants diagnosed with Insomnia Disorder.
Administered a 6-8 week CBT-I program followed by assessments using polysomnography and sleep diaries.
Analyzed changes in sleep parameters and cortical hyperarousal using the delta/beta ratio from quantitative EEG.
CBT-I significantly increased the delta/beta ratio, indicating reduced cortical hyperarousal (baseline: 13.4 ± 4.9, end: 14.6 ± 5.9; p = 0.002).
Measured improvements in insomnia severity and sleep parameters were noted in both self-reports and polysomnography, with smaller effects observed in PSG.
Participants with insomnia and short sleep duration showed greater improvements in the delta/beta ratio compared to those with normal sleep duration (p = 0.014).

Abstract

Chronic Insomnia Disorder (ID) is characterized by hyperarousal, a key pathophysiological feature. While Cognitive-Behavioral Therapy for Insomnia (CBT-I) is the first-line treatment, its physiological effects on sleep-related hyperarousal remain underexplored. This study assessed the impact of CBT-I on cortical hyperarousal using quantitative EEG (qEEG) during non-REM (NREM) sleep, with the delta/beta ratio as the primary outcome. Secondary aims included evaluating changes in sleep stability and exploring phenotypic differences in treatment response. Ninety-eight ID patients across five centers completed a 6-8-week CBT-I program. Pre-and post-treatment assessments included polysomnography (PSG), sleep diaries, and Insomnia Severity Index (ISI). Cortical hyperarousal was indexed by the NREM delta/beta ratio; sleep stability (Sstab) was derived from a transition probability matrix. Patients were categorized as insomnia with short (ISSD) or normal sleep duration (INSD) based on PSG-derived total sleep time (median TST = 347.3 min). CBT-I significantly improved ISI and sleep parameters (sleep onset latency, wake after sleep onset, time in bed, sleep efficiency) in both self-reported and PSG, with smaller effects in the latter. qEEG analyses revealed a significant increase in the delta/beta ratio post-CBT-I (baseline:13.4 ± 4.9, end-of-treatment:14.6 ± 5.9; p = 0.002), indicating reduced cortical hyperarousal, with no center effects. Sstab improved significantly (p = 0.005), though it was not correlated with delta/beta changes. ISSD showed greater delta/beta improvements than INSD (p = 0.014), suggesting phenotypic differences. CBT-I reduces cortical hyperarousal in ID, as reflected by increased delta/beta ratio. The dissociation from sleep stability suggests distinct mechanisms. These findings support qEEG biomarkers as valuable tools for understanding the neurophysiological mechanisms of insomnia treatment and guiding precision medicine approaches.

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