本研究嘗試檢視原發性失眠 (Primary insomnia) 患者在接受完認知行為治療後，其生理激發系統與恆定系統相關生理指標的改變，並探討其主、客觀睡眠改善與生理指標變化之間的關聯，藉以瞭解不同的生理系統在影響原發性失眠患者其主、客觀睡眠改善程度上可能的重要性。本研究透過醫師轉介，共18名原發性失眠患者 (男5人，女13人，平均年齡37.4歲) 接受7週6次的失眠認知行為治療，在接受治療的前後，分別進行一個晚上的多頻道睡眠記錄檢查與主、客觀睡眠評估。再進一步分析高頻率腦波Beta波 (14~35Hz) ，用來反應其中樞神經系統的激發，低頻率腦波Delta波 (0.5~2.5Hz) 則用來反應個案的恆定系統；另外，透過心跳變異率分析得出的參數，包括低頻率 (Low frequency，簡稱LF) 功率與高頻率 (High frequency，簡稱HF) 功率，以LF/HF的比率值測量其交感神經系統的活動，而HF/ (LF+HF) 則是測量副交感神經系統的活動。研究結果顯示個案的失眠問題在主觀睡眠評估指標上有顯著改善，而客觀睡眠評估指標與睡眠結構於入睡時間與入睡後清醒時間有顯著降低，其餘則無顯著改善。而各項生理系統指標，僅後半夜階段二的腦波的Delta波有顯著上升，其餘均無顯著地改善，而LF/HF的下降與失眠嚴重度的下降有顯著地關聯。因此，本研究顯示原發性失眠患者接受認知行為治療前後，其交感神經系統的下降與失眠嚴重度之改善有明顯關聯，推論失眠認知行為治療對於原發性失眠患者的交感神經活動的改善，可能是使其失眠嚴重度改善的關鍵。 / The present study evaluated the changes in beta and delta ranges of electroencephalogram (EEG) power and heart rate variability (HRV) after cognitive behavioural therapy for insomnia (CBT-I) to understand the effect of CBT-I on arousal system and homeostatic system. The study also examined the correlations between change of sleep measurement and the physiological index to clarify underlying mechanisms of sleep improved by CBT-I. Eighteen primary insomnia patients (5 males, 13 female, mean age = 37.4) participated in this study. The participants were scheduled to come to the sleep laboratory for polysomnographic (PSG) recording twice, one prior to CBT-I and one following CBT-I. A course of 6-session CBT-I was conducted during a period of seven weeks. Subjects’ changes in subjective ratings of sleep quality and quantity and sleep parameters in PSG were calculated. Spectrum analyses were conducted for their EEG and electrocardiogram (EKG). Beta EEG activity (14~35 Hz) was used to indicate the central nervos system (CNS) arousal level and Delta EEG activity (0.5~2.5 Hz) for the intensity of homeostatic system. Low frequency power (LF) and high frequency power (HF) of the R-R interval were calculated for heart rate variability (HRV). LF/HF ratio was used as a index of sympathetic nervous system activity and the HF/ (LF+HF) ratio as a index of parasympathetic nervous system activity. The results show subjective sleep quality of subjects were significantly improved after CBT-I. PSG shows shortened sleep onset latency and decreased wake time after sleep onset, but not in the other measures. For EEG spectrum and HRV parameters, only Delta EEG activity in stage2 of the second half of the night was significantly improved. In addition, the decrease of LF/HF significantly correlated with the improvement of the insomnia severity index. Thus, the results suggests that sleep improvements by CBT-I may be associated with the reduction of sympathetic arousal.