研究背景與目的：2008年美國睡眠醫學會(American Academy of Sleep Medicine)對於失眠患者在助眠劑的臨床使用原則中(clinical guideline)，建議初次藥物治療的時間以2至4週較為適宜，後續是否繼續用藥則須專業醫師的重新評估，以降低身體對於藥物的依賴性及副作用的風險，但實際上許多失眠患者因擔心停用助眠劑就無法入眠，因此仍長期使用助眠劑。目前臨床上大都採用逐步減藥的方式協助患者降低助眠劑的使用，除了藥物因素會影響減藥成效之外，從心理因素來看，在過去研究指出自我效能會影響健康行為的改變，因此本研究將比較逐步減藥計畫加上提升減藥自我效能策略與單獨逐步減藥計畫對於原發性失眠患者在減藥上的成效。 研究方法：本研究的原發型失眠患者共48人(男17人，女31人，平均年齡46.8歲，平均使用助眠劑66.7個月)，被分為兩組進行10週的減藥介入計畫，一組為自我效能提升組(n=24)，受試者減藥前先接受為期兩週的提升減藥自我效能策略，再進行8週的逐步減藥計畫，另一組為單純減藥組(n=24)，受試者只進行8週的逐步減藥計畫。受試者每週均需填寫睡眠日誌、單題減藥自我效能量尺，以瞭解睡眠參數、減藥自我效能及助眠劑使用之情況。 研究結果：減藥成效方面，自我效能提升組在減少劑量的百分比顯著高於單純減藥組(自我效能提升組=78.62%；單純減藥組=64.10%)，且自我效能提升組在減藥前後劑量的改變也顯著高於單純減藥組(自我效能提升組=4.35顆/週；單純減藥組=3.22顆/週)，自我效能提升組在停藥人數的百分比上雖未顯著高於單純停藥組(自我效能提升組=29.2%；單純減藥組=16.7%)，但就整體結果來看均較為支持自我效能提升組在減藥的成效上是優於單純減藥組。減藥自我效能方面，在控制住第1週的減藥自我效能後，提升減藥自我效能策略造成的減藥自我效能改變量仍可以有效解釋21.9%的減藥百分比。 研究結論：自我效能提升組增加的提升減藥自我效能策略能有助於個案在執行逐步減藥計畫的成效，另外，提升減藥自我效能策略造成的減藥自我效能改變量是減藥百分比有效的預測因子。因此，減藥自我效能對於減藥成效來說，確實是一個可以著力的部分。 / Introduction：According to the 2008 clinical guidelines for insomnia by the American Academy of Sleep Medicine proposed, hypnotic use is recommended for short-term use for 2 to 4 weeks. However, many insomnia patients have difficulty to stop hypnotic use. In clinic practices, gradual tapering is usually applied in helping patients to reduce the hypnotic use. Previous studies have shown that self-efficacy of the patients are associated with medication tapering. The present study examine the effect of the institution of a self-efficacy enhancement strategy prior to gradual tapering plan on hypnotic tapering in patients with primary insomnia. Methods：Forty-eight patients with primary insomnia (17 men, 31 women；mean age of 46.8 years；mean duration of hypnotics use of 66.7 months) were assigned to two groups: a self-efficacy enhancement group and a tapering group. Patients in the self-efficacy enhancement group (n=24) underwent a two-week self-efficacy enhancement strategy prior to an eight-week gradual tapering plan. Patients in the tapering group (n=24) participated in the eight-week gradual tapering plan only. The main outcome measures were sleep parameters from sleep diary, a single-item tapering self-efficacy rating scale, number of pills taken per week, and percentage of dosage reduction. Results：The percentage of dosage reduction of patients in the self-efficacy enhancement group was significantly more than those in the tapering group (the self-efficacy enhancement group = 78.62%；the tapering group = 64.10%). The number of pills taken per week also showed significantly more reduction for patients in the self-efficacy enhancement group than those in the tapering group (the self-efficacy enhancement group = 4.35 pills per week；the tapering group = 3.22 pills per week). However, the percentage of drug-free patients at the end of the programs in the self-efficacy enhancement group was not significant different from those in the tapering group (the self-efficacy enhancement group = 29.2%；the tapering group = 16.7%). Overall, the effect of hypnotic tapering in the self-efficacy enhancement group was better than those in the tapering group. In addition, linear regression showed that the tapering self-efficacy data showed that, after controlling baseline tapering self-efficacy, the change of tapering self-efficacy following the first two weeks of self-efficacy enhancement strategy can explain the variation of percentage of dosage reduction up to 21.9%. Conclusions：The institution of self-efficacy enhancement strategy can increase the efficacy of gradual tapering plan for hypnotics. In addition, the level of tapering self-efficacy enhanced by the self-efficacy enhancement strategy is a good predictor for dosage reduction. This is a useful strategy that can be applied in clinical settings.

研究目的：失眠已是臨床上常見的健康抱怨之一，而近年來在探討原發性失眠的病因理論上，又以失眠患者的過度激發（hyperarousal）有較多的實徵研究支持。主要的理論之一為Perlis等人提出的「失眠神經認知模式」，該模式認為失眠患者的睡眠問題乃肇因於其在睡眠時內在的認知運作仍處於過度活躍狀態。後續相關研究透過腦波頻譜分析發現，原發性失眠患者不論在靠近入睡開始或NREM睡眠，都較一般正常睡眠者有增加的高頻腦波活動與減少的低頻腦波活動，顯示失眠患者確實有較高的生理激發狀態與較低的睡眠恆定趨力。而臨床上，失眠患者最常見的主觀抱怨為入睡困難，故本研究希望透過原發性失眠患者在睡眠中的腦波頻譜分析，以探討失眠患者在入睡歷程的生理激發狀態與睡眠恆定趨力的變化，並進一步探討失眠患者睡前主觀激發狀態感受與客觀生理激發測量之相關性。 研究方法：本研究的原發性失眠組共30人（男10人，女20人，平均年齡為36.7歲），正常睡眠者（控制組）共25人（男8人，女17人，平均年齡為34.8歲）。參與者需至睡眠實驗室進行一晚的多頻道睡眠檢查（PSG），以作為睡眠相關呼吸疾患與睡眠相關運動疾患之篩檢，並以入睡前5分鐘至入睡後15分鐘（共20分鐘）所記錄之腦電波（EEG）作為後續腦波頻譜分析之用。另外，參與者須在睡前填寫睡前激發量表（PSAS），以評估參與者在睡前的主觀激發狀態感受。 研究結果：在睡前主觀激發狀態評估中，原發性失眠患者不論在生理激發或認知激發主觀感受上，皆顯著高於一般正常睡眠者(F = 23.950，p < .001；F = 64.235，p < .001)。在PSG記錄的睡眠相關參數上，則顯示失眠患者有較多的入睡後醒來總時數(F = 5.510，p = .023)、較少的階段二睡眠時間與比例(F = 7.088，p = .010；F = 32.616，p < .001)、較少的REM睡眠比例(F = 4.810，p = .033)，以及較差的睡眠效率(F = 8.685，p = .005)。在入睡歷程的腦波頻譜分析上，結果顯示失眠患者在睡醒的過渡期有較高的Alpha波功率，在進到睡眠後則有較低的Delta波功率，並且在整個入睡歷程中則是有較高的Theta波功率與Beta波功率。進一步比較兩組在入睡歷程腦波頻譜波段的上升與下降速度，結果顯示失眠患者在入睡歷程中，不論是睡眠恆定趨力上升的速度或生理激發下降的速度，皆顯著較一般正常睡眠者慢。另外，主觀認知激發狀態感受與入睡後的Delta波呈現顯著正相關；而與Theta波的相關上，則主要在入睡過渡階段有顯著正相關；Alpha波則僅與入睡歷程最後階段有顯著負相關；在與Beta波相關上，則從入睡過渡階段到入睡後皆有顯著負相關。主觀生理激發狀態感受則僅有與入睡過渡階段的Theta波有顯著正相關。 結論：本研究發現原發性失眠患者在入睡歷程中，不論在睡眠恆定趨力的上升速度或生理激發的下降速度上，皆明顯較正常睡眠者慢，雖生理激發狀態仍會隨著時間而有所降低，但卻仍維持較一般正常睡眠者高；睡眠趨力雖亦會有所增加，卻較一般正常睡眠者難以發揮較佳的作用，而可能造成失眠患者在入睡歷程中需花費更長的時間才能入睡，且進入睡眠後，仍維持較高的生理激發狀態與睡眠趨力發揮較差，進而可能導致失眠患者較淺眠或難以維持睡眠等問題。 / Introduction：Insomnia is a common healthy complain. The neurocognitive perspective of hyperarousal model of insomnia, as proposed by Perlis(1997), hypothesized that the sleep difficulties in insomniacs may result from enhanced information processing around sleep onset and during sleep. Supporting evidences were primarily from the findings that insomnia patients have increased high frequency EEG activity and decreased low frequency EEG activity during sleep, indicating insomniacs in general have higher physical arousal and lower sleep homeostasis. This study further aims to explore arousal level and sleep homeostasis during the period of sleep onset by comparing the level and change of EEG spectrum in primary insomnia patients and normal control subjects during the process of sleep onset. Methods：30 patients with primary insomnia (10 men, 20women, mean age of 36.7years) and 25 normal sleepers (8 men, 17women, mean age of 34.8years) underwent one night of PSG recording in a sleep laboratory to screening sleep-related breathing disorders and sleep-related movement disorders. They also completed the Pre-sleep Arousal Scale (PSAS) before bedtime. EEG spectrum analyses were conducted for the EEG data collected during the 5 minutes prior to sleep onset and the 15 minutes after. Results：Subjective ratings of both pre-sleep cognitive and somatic arousal were significantly higher in insomnia group (F = 23.950, p < .001; F = 64.235, p < .001) than control group. More WASO (F = 5.510, p = .023), less time and percentage of stage 2 sleep (F = 7.088, p = .010; F = 32.616, p < .001), less percentage of REM sleep (F = 4.810, p = .033), and poor sleep efficiency (F = 8.685, p = .005) were showed in PSG. The EEG spectrum during sleep-onset period showed that insomniacs had higher alpha power in the sleep-wake transition, lower delta power after falling asleep, and higher theta and beta power during sleep-onset period. In terms of the slope of EEG specrtrum change during the period of sleep onset, insomniacs had slower change than normal sleepers in increasing of sleep homeostasis and decreasing of physical arousal. In addition, the correlations between PSAS score and EEG power, cognitive arousal and delta power after falling asleep and theta power in sleep-onset process showed significant positive correlation. Alpha power in the later part of sleep-onset period and beta power around sleep-wake trainsition, on the other hand, showed negative correlations with cognitive arousal. Physcial arousal only showed positive correlation to theta power in sleep-wake trainsition. Conclusions：Patients with primary insomnia showed significantly less and slower increase in sleep homeostatic drive as well as less and slower decrease in EEG arousal during sleep-onset period. Although EEG arousal did showed gradually decreased by time, it still maintianed higher than normal sleepers. Sleep homeostasis did also increase, but may be interfered by the hyperarousal. This may explain the complaints in insomnia patients of difficulty falling asleep, difficulty maintaining sleep, and light sleep.

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.