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| Title: | 以磁振照影探討睡眠脆弱特質之神經生理基礎
The neurophysiological basis of stress-related sleep vulnerability : a fMRI study |
| Authors: | 陳怜均
Chen, Ling-Chun |
| Contributors: | 楊建銘
陳怜均
Chen, Ling-Chun |
| Keywords: | 睡眠脆弱特質
過度激發
磁振照影
EEG腦波頻譜分析
Stress-related sleep vulnerability
Hyperarousal
fMRI
EEG power spectrum analysis |
| Date: | 2018 |
| Issue Date: | 2018-07-23 16:51:23 (UTC+8) |
| Abstract: | 研究目的 Spielman (1986) 將失眠依病程時間軸區分成前置因子、促發因子與維持因子，而目前研究支持睡眠脆弱特質為一個重要的失眠前置因子，此特質較高者，較易在壓力下產生自主神經系統過度激發的現象，並出現短暫性失眠。但過去並未探討此特質之中樞神經生理機制，藉由多方了解此因子的神經生理機制，可幫助釐清失眠病程之前置因子的神經生理機制。因此，本研究以fMRI在靜息態及睡眠起始點前、後五分鐘進行測量，分析可反應各區神經元自發活動高低的低頻振幅值 (amplitude of low frequency fluctuations, ALFF)，及與認知、記憶及情緒相關腦區的功能性連結，並以EEG在睡眠起始點前、後五分鐘進行測量，分析其相對功率值，以此作為中樞神經系統激發程度指標，藉以探討睡眠脆弱特質之中樞神經生理相關機制。此研究假設高睡眠脆弱特質者在壓力下會出現較長的入睡耗時、較高的高頻腦波，且與過度激發相關腦區的ALFF值會較高，同時與認知、記憶及情緒相關腦區的功能性連結變化會與失眠者相似。
研究方法 本研究以福特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 (high FIRST; HF) 18位及低睡眠脆弱特質組 (low FIRST; LF) 10位。在正式實驗前一晚會要求受試者進行2至3小時的睡眠剝奪，並於實驗當天不得補眠，於實驗當晚進行fMRI及EEG量測，在靜息態量測後，請受試者在磁振照影儀中嘗試入睡。結果分析部分，在功能性連結部份以杏仁核 (Amygdala) 、預設模式網絡 (Default Mode Network)、額頂葉網絡 (Frontoparietal Network) 及海馬迴 (Hippocampus) 為主，EEG部份，則以腦波頻譜分析為主，用以比較高、低頻腦波之相對功率。
研究結果 在EEG部分，以2 (組別) x2 (時間) 之混合設計二因子變異數分析比較兩組在睡眠起始點前、後五分鐘的腦波功率值是否有差異。結果顯示低睡眠脆弱特質組的入睡時距顯著高於高睡眠脆弱特質組，在睡後的低頻腦波，包括Delta及Theta波都顯著比睡前高，而睡後的高頻腦波，包括Alpha及Beta波都顯著比睡前低。相較於低睡眠脆弱特質組，高睡眠脆弱特質組在睡後的Theta波顯著較高。另外在fMRI的結果中，不管在靜息態或是睡眠起始點前、後五分鐘，於腦區的活化程度及各腦區間的功能性連結則無顯著差異。
結論 本研究探討睡眠脆弱特質之中樞神經生理相關機制，結果並不支持研究假設，在高頻腦波 (Alpha及Beta波) 以及fMRI的結果上無顯著差異，反而在EEG分析發現高睡眠脆弱特質者，在入睡歷程中有較高的Theta波及較短的入睡時距。綜合過去文獻及此研究結果可推論，睡眠脆弱特質相關的過度激發可能來自於自主神經系統過度活躍，並非中樞神經系統，而中樞神經系統的過度活躍可能是在失眠慢性化過程中逐漸發展而成。
關鍵字：睡眠脆弱特質、過度激發、磁振照影、EEG腦波頻譜分析
Introduction: According to the 3P model proposed by Spielman (1986), the contributing factors for the development of chronic insomnia can be categorized into three categories: predisposing factors, precipitating factors, and perpetuating factors. Previous research indicates that stress-related sleep vulnerability is an important predisposing factor and have shown that individuals with high stress-related sleep vulnerability (HF) demonstrated hyperarousal of the autonomic nervous system as seen in patients with chronic insomnia. However, it is not clear whether they also have hyperaroused central nervous system as chronic insomnia patients do. Therefore, this study aims to examine the association between the stress-related sleep vulnerability and neurophysiological arousal by conducting fMRI and EEG recordings simultaneously with the following measures: (1) fMRI of the resting state, (2) fMRI during the first five minutes before and after the onset of sleep, (3) the amplitude of low frequency fluctuations (ALFF) in fMRI, (4) the functional connectivity of fMRI in cognitive-, memory-, and emotion-related regions, and (5) EEG during the five minutes before and after the onset of sleep. It is hypothesized that HF would have a longer sleep onset latency under the stress from sleeping in a MRI scanner, greater high-frequency EEG activity, and greater ALFF in arousal-related regions. We further predicted that HF will show a pattern in functional connectivity in cognitive-, memory-, and mood-related brain regions similar to chronic insomnia patients.
Method: Ten healthy individuals scoring low (LF) and eighteen healthy individuals scoring high (HF) on the Ford Insomnia Response to Stress Test (FIRST) were chosen as subjects for the study. On the night before the experiment, the subjects were asked to deprive themselves of 2 to 3 hours of sleep, and on the day of the experiment, they were not allowed to take a nap. After the resting state recording was taken, the fMRI and EEG recording was conducted simultaneously while the participants were trying to fall asleep in an MRI scanner. For the MRI data, the functional connectivities based on Amygdala, Default Mode Network, Frontoparial Network, and Hippocampus networks were analyzed; whereas for the EEG data, spectrum analysis is used to compare the relative power of different frequency bands.
Result: For the EEG data, 2 (group) x2 (time) two-way ANOVAs with mixed design, were performed to compare the power of the two groups for different frequency bands. Low frequency EEG activities, including Delta and Theta waves, were significantly higher after sleep onset than before sleep onset, whereas high frequency EEG activity, including Alpha and Beta waves, are significantly lower after sleep onset than before sleep onset regardless of the groups. HF had significantly higher theta waves than LF after sleep onset, but there was no significant difference in the high frequency EEG activity between the two groups. The fMRI revealed no significant difference in the degree of activation in the brain regions and functional connectivities in resting state, before sleep onset, or after sleep onset. In addition, LF, unexpectedly, exhibited significantly higher sleep onset latency than HF did.
Conclusion: This study compared the neurophysiological activation of the central nervous system between individuals with high and low stress-related sleep vulnerability. The results do not support our hypotheses, as there was no significant difference in high frequency EEG activity (alpha and beta wave), ALFF, or functional connectivity between HF and LF. In contrast, HF group was shown to have higher theta power and a shorter sleep onset latency. Based on the findings from previous studies and the results of the present study, it suggests that the stress-related sleep vulnerability may be more associated with hyper-activation of the autonomic nervous system rather than the central nervous system. The hyperarousal of the central nervous system as a feature of patients with chronic insomnia may be developed as the insomnia becoming more chronic in course.
Keyword: stress-related sleep vulnerability, hyperarousal, fMRI, EEG power spectrum analysis |
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| Description: | 碩士
國立政治大學
心理學系
103752006 |
| Source URI: | http://thesis.lib.nccu.edu.tw/record/#G0103752006 |
| Data Type: | thesis |
| DOI: | 10.6814/THE.NCCU.PSY.008.2018.C01 |
| Appears in Collections: | [心理學系] 學位論文
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