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.