研究目的 失眠的過度激發假說是目前最廣為接受的失眠病因之一，失眠者通常可觀察到具有身心過度激發的狀態，其中認知神經過度激發假說更由中樞神經的角度探討失眠者的過度激發現象，且已有許多證據支持此觀點。然而過度激發因素在失眠病程上的影響仍不明確，不論在前置因子或是持續因子的層面，激發因素皆經常被提及與討論。本研究以未失眠但具有高睡眠脆弱特質之族群作為研究對象，企圖模擬失眠者在失眠初發之前的狀態，另加入睡前及早晨的自主神經系統與主觀激發狀態之測量，比較其與低睡眠脆弱特質組在有無壓力誘發狀態下，兩組的睡眠中訊息處理程度、睡前及早晨的自主神經系統激發程度與主觀激發狀態，藉以了解（1）壓力是否會引發個體進入較高的主、客觀激發狀態；(2)睡眠脆弱特質在不同的激發程度下，是否會對於個體的睡前、睡眠中及早晨的激發程度造成影響，以初步推論激發狀態因素在失眠病程中所扮演之角色。 方法 以壓力下失眠反應量表（Ford Insomnia Response to Stress Test, FIRST）區分出高睡眠脆弱特質組（HV）13位（6男、7女）、低睡眠脆弱特質組（LV）14位（6男、8女），年齡為19-32歲之健康成人。每位受試者均需在睡眠實驗室進行3個夜晚之夜間睡眠記錄，包含第一晚的PSG測量以排除個案有其他睡眠疾患，並讓受試者習慣實驗環境；第二晚及第三晚則交互平衡操弄基礎情境或壓力情境，在壓力情境下，受試者被告知將進行即席演講，需在睡前抽出演講題目，並於隔天早晨喚醒後10分鐘內發表一篇內容充實、呼應主題之演說，隨後測量心跳變異率（heart rate variability，HRV）、平均心跳間距（r-r interval，RRI）、主觀身心激發狀態（Pre sleep arousal scale，PSAS）等主客觀激發程度，入睡後進行整夜的ERP（事件相關電位[Event-related potential，ERP]）測量，誘發ERPs之實驗流程以oddball典範為主，並於早晨起床後再次進行HRV、RRI及PSAS之測量。 結果 以2（組別）x 2（情境）之混和設計二因子變異數分析比較各組在不同情境下的主客觀激發程度指標是否有所不同。結果顯示壓力確實能引發受試者進入較高的主客觀激發狀態，包含睡前及早晨有較快的平均心跳速率、較高的主觀身心激發程度，而在NREM睡眠中可發現HV在有壓力的情境下，對外界的訊息處理程度顯著較LV組增加，包含較快的N1與較慢的N350出現，但HV在壓力下亦有較快的P2與較強的P900，顯示對外界訊息的抑制功能上升，且隨著睡眠更深，進入慢波睡眠時，P2及P900亦顯著較LV強，表現出更多的抑制外界訊息能力。 結論 本研究探討睡眠脆弱特質在不同激發狀態下對於睡眠的影響，結果顯示壓力能引發個體較高的激發狀態，然而在未失眠族群中，高睡眠脆弱特質對於認知激發狀態下的睡眠中訊息處理程度雖有提高，但可發現高睡眠脆弱特質組亦有較高的抑制外界訊息能力，而不致於使得激發狀態過度影響其睡眠，此結果部分支持失眠的認知神經過度激發假說，過度激發因素可能在持續因子的部分影響性較大，造成個體產生對睡眠的抱怨。另一方面，本研究結果亦彰顯失眠的高危險群的及早介入預防之重要性。 / Introduction: Conditioned hyperarousal has been theorized to be a major etiological factor in chronic insomnia patients. It has been suggested that insomniacs showed more arousal than non-insomniacs in many psychological and physiological measures, including enhanced information processing during sleep as measured by NREM ERPs. However, the role of hyperarousal on the course of development of insomnia remained unclear, it has been considered as a predisposing trait and/or perpetuating factor in the cause of insomnia. The present study compared arousal levels around sleep onset, during sleep and in the morning between non-insomniac individuals with low and high vulnerability to stress-related sleep disturbance, as high vulnerable individuals were proposed to be predisposed to chronic insomnia. The objectives of the study are therefore to investigate: 1) the effect of an acute stressor on arousal level prior, after, and during sleep, and 2) the differences in stress reactivity between individual with high and low vulnerability to stress-related sleep disturbances. Method: Fourteen healthy individuals scoring low (LV) and thirteen healthy individuals scoring high (HV) on the Ford Insomnia Response to Stress Test (FIRST) were studied. All subjects had to sleep in the lab for three nights: a screening/ adaptation night, then a baseline night and a stress night. The sequences of the later two nights were counterbalanced across subjects. During the stress night, subjects were informed that they would be required to give a speech immediately after waking up. Heart rate variability (HRV), r-r interval (RRI) of EKG and subjective arousal level (Pre sleep arousal scale, [PSAS]) was accessed before lights off and in the morning. Then sleep ERP was recorded during the night. An odd-ball paradigm was conducted to evoke ERPs throughout the night. Result: Mixed two-way ANOVAs were used to compare the differences between vulnerabilities and conditions. Both HV ans LV showed higher subjective arousal level and smaller RRI under the stress condition than the baseline condition. During NREM sleep, HV showed increased information processing under stress condition than LV as shown by faster N1, slower N350. Also, HV showed increased inhibition under stress condition than LV, with faster P2 and higher P900. Stronger P2 and P900 were also observed in HV when reached slow-wave sleep stage, comparing to LV. Conclusion: Both groups showed more arousal under stress condition than baseline condition, indicating an acute stress can lead to a higher arousal level. Moreover, high vulnerable individuals showed increased information processing during NREM sleep than low vulnerable individuals, but also showed more inhibition to prevent sleep from being disturbed by external stimulus. The results suggest that increased information processing in reacting to stress may be a predisposing trait for sleep disturbances. However, sleep may be protected by a compensatory inhibitory process in those who have not developed a long-term insomnia.