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Introduction: The neurocognitive perspective on insomnia posits that conditioned hyperarousal is reflected by increased high frequency EEG activity resulting in impairment of information processing, and, as such, interfering with normal sleep onset and - maintenance processes. The presence of cortical hyperarousal can be evaluated in different ways going from the analysis of the electroencephalogram (EEG) during wake as well as sleep time, specific event-related potentials (ERPs) and even the analysis of the Cyclic Alternating Pattern (CAP) which is thought to reflect the stability of sleep. The aim of this study was to evaluate the presence of cortical hyperarousal at different time points (during wake versus sleep) and levels, using the above techniques. Method: 17 insomnia patients diagnosed according to DSM-IV criteria with polysomnographically verified sleep disruptions and 12 good sleepers were included in this study. A wake EEG and an ERP paradigm were performed. After standard sleep scoring, FFT and CAP analysis were performed. Delta (1-3.5 Hz), theta (4-7.5 Hz), alpha (8-12 Hz), beta1 (SMR: 12-15 Hz), beta2 (15-17.5 Hz), beta3 (18-25 Hz), and high beta (25.5-30 Hz) were the outcome variables for the FFT analysis. Furthermore, N100 and P200 mean amplitudes at Fz and Cz were analyzed as a measure of respectively general arousability and inhibition of information processing. Finally, CAP time and CAP rate were used as a measure of sleep stability. Results: Indications of cortical arousal in the EEG were only present during the sleep onset period, reflected by a stable alpha EEG level and slower increase of delta power. In addition, decreased P200 amplitudes, but no significant differences in N100 amplitudes were observed in the evening. Finally, increased CAP time and CAP rate were found in insomnia patients compared to good sleepers. Conclusion: These results suggest that our group of insomnia patients was not characterized by cortical hyperarousal, rather a deficit in de-arousal was observed. Indeed, decreased P200 amplitudes in combination with a lack of increased N100 suggests an impairment of inhibitory processing rather than increased arousal. The phenomenon of impaired de-arousal continues during sleep onset, as a delay in delta EEG activity in combination with the absence of a decrease in alpha EEG activity and a normal level of beta activity was observed. Finally, no significant difference in the sleep EEG was observed.