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題名 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
作者 陳怜均
Chen, Ling-Chun
貢獻者 楊建銘
陳怜均
Chen, Ling-Chun
關鍵詞 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
日期 2018
上傳時間 23-Jul-2018 16:51:23 (UTC+8)
摘要 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
參考文獻 林一真(民89)。貝克焦慮量表(BAI)中文版。台北:中國行為
科學社。
林詩淳 (民97)。慢性失眠者與情境性失眠高危險族群之壓力因應與
失眠的關係。國立政治大學心理所碩士論文,未出版,台北
市。
車先蕙、盧孟良、陳錫中、張尚文、李宇宙(民95)。中文版貝克
焦慮量表之信效度。台灣醫學,10(4),447-454。
陳心怡 (民89)。貝克憂鬱量表第二版 (BDI-II) 中文版。 台北: 中國
行為科學社。
American Psychiatric Association, A. P. (2013). Diagnostic and
Statistical Manual of Mental Disorder, 4th edn. Washinton,
DC: American Psychiatriy Association.
Agnew, H. W., Webb, W. B., & Williams, R. L. (1966).
Psychophysiology, 2, 263-266.
Altena, E., Van Der Werf, Y. D., Sanz-Arigita, E. J., Voorn, T. A.,
Rombouts, S. A., Kuijer, J. P. (2008). Prefrontal
hypoactivation and recovery in insomnia. Sleep, 31(9),
1271–1276.
Borkovec, T. D. (1982). Insomnia. Journal of Consulting and
Clinical Psychology, 50, 880-895.
Buckner, R. L., Andrew-Hanna, J. R., & Schacter, D. L. (2005).
The brain’s default network : anatomy, function, and
relevance to disease. Annals of the New York Academy of
Sciences, 1124, 1-38.
Buysse, D. J., Reynolds, C. F., Monk, T. H., Berman, S. R., &
Kupfer, D. J. (1989). Pittsburgh Sleep Quality Index: A new
instrument for psychiatric practice and research. Psychiatry
Research, 28, 193-213.
Chen, I. Y., Jarrin, D. C., Ivers, H., & Morin, C. M. (2017)
Investigating psychological and physiological responses to
the trier social stress test in young adault with insomnia.
Sleep medicine, 40, 11-22.
Drake, C. L., Cheng, P., Almeida, D. M., & Roth, T.(2017).
Familial risk for insomnia is associated with abnormal
cortisol response to stress. Sleep, 40.
Drake, C. L., Jefferson, C., Roehrs, T., & Roth, T.(2006). Stress-
related sleep disturbance and polysomnographic response
to caffeine. Sleep Medicine, 7(7), 567–572.
Drake, C. L., Roehrs, T., & Roth, T.(2003). Insomnia Causes,
Consequences, and Therapeutics: An Overview. Depression
and Anxiety, 18, 163–176.
Drake, C., Richardson, G., Roehrs, T., Scofield, H., & Roth, T.,
(2004).Vulnerability to Stress-related Sleep Disturbance and
Hyperarousal. Sleep, 27, 285-291.
Drake, C. L., Scofield, H., & Roth, T. (2008). Vulnerability to
insomnia: the role offamilial aggregation. Sleep Medicine,
9(3), 297-302.
Drummond, S. P., Walker, M., Almklov, E., Campos, M.,
Anderson, D. E., & Straus, L. D. (2013) Neural correlates of
working memory performance in primary insomnia. Sleep,
36(9), 1307–16.
Edinger, J. D., Carney, C. E., & Wohlgemuth, W. K. (2008).
Pretherapy cognitivedispositions and treatment outcome in
cognitive behavior therapy for insomnia.insomnia. Behavior
Therapy, 39(4), 406-416.
Finelli, L. A., Baumann, H., Borbely, A. A., & Achermann, P.
(2000). Dual electroencephalogram markers of human sleep
homeostasis: correlation between theta activity in waking
and slow-wave activity in sleep. Neuroscience, 101(3),
523-529.
Fernandez-Mendoza, J., Vela-Bueno, A., Vgontzas, A. N.,
Ramos-Platon, M. J., Olavarrieta-Bernardino, S., Bixler, E. O.,
et al. (2010). Cognitive-emotional hyperarousal as a
premorbid characteristic of individuals vulnerable to
insomnia. Psychosomatic Medicine, 72(4), 397-403.
Hauri, P. J. (1983). A cluster analysis of insomnia. Sleep, 6(4),
326-338.
Hauri, P. J., Olmstead, E. M. (1989). Reverse first night effect in
insomnia. Sleep, 12(2), 97-105.
Hwang, Z., Liang, P., Jia, X., Zhan, S., Li, N., Ding, Y., Lu, J.,
Wang, Y., & Li, K. (2012). Abnormal amygdala connectivity in
patients with primary insomnia: Evidence from resting state
fMRI. European Journal of Radiology, 81, 1288– 1295.
Jarrin, D. C., Chen, I. Y., Ivers, H., & Morin, C. M.,(2014) The role
of vulnerability in stress-related insomnia, social support and
coping styles on incidence and persistence of insomnia.
European Sleep Research Society, 23, 681–688.
Kao, C. C., Huang, C. J., Wang, M. Y., & Tsai, P. S. (2008).
Insomnia: Prevalence and its impact on excessive daytime
sleepiness and psychological well-being in the adult
Taiwanese population. Quality of Life Research, 17(8),
1073-1080.
Kalmbach, D., Pillai, V., Arnedt, T., & Drake, C. (2016).
Identifying at-risk individuals for insomnia using the Ford
Insomnia Response to Stress Test. Sleep, 39(2), 449-456.
Lundh, L., & Broman, J. (2000). Insomnia as an interaction
between sleep-interfering and sleep-interpreting processes.
Journal of Psychosomatic Research, 49, 299-310.
Lin, Y. H., Jen, C. H., & Yang, C. M. (2015). Information
processing during sleep and stress-related sleep
vulnerability. Psychiatry and clinical neurosciences, 69,
84-92.
Li, Wang, Zhang, Dou, Liu, Tong, Lei, Wang, Xu, Shi, & Zhang.
(2014). Functional connectivity changes between parietal
and prefrontal cortices in primary insomnia patients:
evidence from resting-state fMRI. European Journal of
Medical Research, 19:32. http://www.eurjmedres.com/
content/19/1/32
Larson-Prior, L. J., Zempel, J. M., Nolan, T. S., Prior, F. W.,
Snyder, A. Z., & Raichle, M. E. (2009). Cortical network
functional connectivity in the descent to sleep. Proceedings
of the National Academy of Sciences of the United States of
America, 106, 4489–4494.
Morin, Belanger, LeBlanc, Ivers, Savard, Espie, Merette,
Baillargeon, & Gregoire. (2009). The Natural History of
Insomnia : A Population-Based 3-year Longitudinal Study.
Archives of Internal Medicine, 169(5), 447-453.
Nofzinger, E. A., Buysse, D. J., Germain, A., Price, J. C.,
Miewald, J. M., & Kupfer, D. J. (2004) Functional
neuroimaging evidence for hyperarousal in insomnia. The
American Journal of Psychiatry, 161(11), 2126–2128.
Noh, H. J., Joo, E. Y., Kim, S. T., Yoon, S. M., Koo, D. L., & Kim,
D. (2012) The relationship between hippocampal volume and
cognition in patients with chronic primary insom- nia. Journal
Clinical Neurology, 8(2), 130–138.
Neckelmann, D., Mykletun, A., & Dahl, A. A. (2007). Chronic
insomnia as a risk factor for developing anxiety and
depression. Sleep, 30(7), 873-880.
Nofzinger, E. A., Nissen, C., Germain, A., Moul, D., Hall, M.,
Price, J. C., Miewald, J. M., & Buysse, D. J. (2006) Regional
cerebral metabolic correlates of WASO during NREM sleep in
insomnia. Journal of Clinical Sleep Medicine, 2(3), 316–322.
Ohayon, M. M. (2002) Epidemiology of insomnia: what we know
and what we still need to learn. Sleep Medicine Reviews,
6(2), 97-111.
O’Byrne, J. N., Berman rosa, M., Gouin, J. P., & Dang-Vu, T. T.
(2014). Neuroimaging findings in primary insomnia.
Pathologie Biologie, 62, 262–269.
Perlis, M. L., Giles, D. E., Mendelson, W. B., Bootzin, R. R., &
Wyatt, J. K. (1997). Psychophysiological insomnia: the
behavioural model and a neurocognitive perspective. Journal
of Sleep Research, 6(3), 179-188.
Perlis, M. L., Kehr, E. L., Smith, M. T., Andrews, P. J., Orff, H., &
Giles, D. E. (2001). Temporal and stagewise distribution of
high frequency EEG activity in patients with primary and
secondary insomnia and in good sleeper controls. Journal of
Sleep Research, 10(2), 93-104.
Spielman, A. J. (1986). Assessment of insomnia. Clinical
Psychology Review, 6, 11-25.
Saper, C. B., Chou, T. C. & Scammell, T. E. (2001) The sleep
switch: hypothalamic control of sleep and wakefulness.
Trends Neurosci. 24, 726-731.
Smith, M. T., Perlis, M. L., Chengazi, V. U., Soeffing, J., &
McCann, U. (2005). NREM sleep cerebral blood flow before
and after behavior therapy for chronic primary insomnia:
Preliminary single photon emission computed tomography
(SPECT) data [3]. Sleep Medicine, 6(1), 93-94.
Sheehan, D. V., Lecrubier, Y., Sheehan, K. H., Amorim, P.,
Janavs, J., Weiller, E., & Dunbar, G. C. (1998). The Mini
International Neuropsychiatric Interview (M.I.N.I.): the
development and validation of a structured diagnostic
psychiatric interview for DSM-IV and ICD-10. Journal of
Clinical Psychiatry, 59 Suppl 20, 22-33;quiz 34-57.
Sharpley, A. L., Solomon, R. A., & Cowen, P. J. (1988).
Evaluation of first night effect using ambulatory monitoring
and automatic sleep stage analysis. Sleep, 11(3), 273-276.
Saper, C. B., Scammell, E. T., & Lu, J. (2005). Hypothalamic
regulation of sleep and circadian rhythms. Nature, 437,
1257-1263.
Spielman, A. J., Saskin, P., & Thorpy, M. J. (1987) Treatment of
chronic insomnia by restriction of time in bed. Sleep, 10,
45-56.
Sämann, P. G., Wehrle, R., Hoehn, D., Spoormaker, V. I., Peters,
H., Tully, C., Holsboer, F., & Czisch, M. (2011). Development
of the brain`s default mode network from wakefulness to
slow wave sleep. Cerebral Cortex, 21(9), 2082-2093.
Turcotte, I., & Bastien, C. H. (2009). Is quality of sleep related
to the N1 and P2 ERPs in chronic psychophysiological
insomnia sufferers? International Journal of
Psychophysiology, 72, 314-322.
Toussaint, M., Luthringer, Remy., Schaltenbrand, Nicolas.,
Carelli, G., Lainey, E., Jacqmin, A., Muzet, A., & Mcher, J.
(1995). Sleep, 18(6), 463-469.
Thomsen, D. K., Mehlsen, M. Y., Christensen, S., & Zachariae,
R. (2003). Rumination-relationship with negative mood and
sleep quality. Personality and Individual Differences, 34,
1293-1301.
Von Economo, C. (1930). Sleep as a problem of localization.
The Journal of Nervous and Mental Disease, 71, 249-259.
Vgontzas, A. N., Tsigos, C., Bixler, E. O., et al. (1998). Chronic
insomnia and activity of the stress system: a preliminary
study. Journal of Psychosom Research, 45(1), 21–31.
Winkelman, J. W., Benson, K. L., Buxton, O. M., Lyoo, I. K., Yoon,
S., & O’Connor, S. (2010). Lack of hippocampal volume
differences in primary insomnia and good sleeper controls:
an MRI volumetric study at 3 Tesla. Sleep Medicine, 11(6),
576–582.
Winkelman, J. W., Plante, D. T., Schoerning, L., Benson, K.,
Buxton, O. M., & O’Connor, S. P. (2013). Increased rostral
anterior cingulate cortex volume in chronic primary insomnia.
Sleep, 36(7), 991–998.
Yang, C. M., Hung, C. Y., & Lee, H. C. (2014). Stress-Related
Sleep Vulnerability and Maladaptive Sleep Beliefs Predict
Insomnia at Long-Term Follow-Up. Journal of Clinical Sleep
Medicine, 10(9), 997-1001.
Yang, C. M., Lin, S. C., & Cheng, C. P. (2013). Transient
Insomnia Versus ChronicInsomnia: A Comparison oStudy of
Sleep-Related Psychological/ Behavioral Characteristics.
Journal of Clinical Psychology. 69(10), 1094-1107.
Zoccola, M., Dickerson, S., & Lam, S. (2009). Rumination
Predicts Longer Sleep Onset Latency After an Acute
Psychosocial Stressor. Psychosomatic Medicine, 71, 771-775.
描述 碩士
國立政治大學
心理學系
103752006
資料來源 http://thesis.lib.nccu.edu.tw/record/#G0103752006
資料類型 thesis
dc.contributor.advisor 楊建銘zh_TW
dc.contributor.author (Authors) 陳怜均zh_TW
dc.contributor.author (Authors) Chen, Ling-Chunen_US
dc.creator (作者) 陳怜均zh_TW
dc.creator (作者) Chen, Ling-Chunen_US
dc.date (日期) 2018en_US
dc.date.accessioned 23-Jul-2018 16:51:23 (UTC+8)-
dc.date.available 23-Jul-2018 16:51:23 (UTC+8)-
dc.date.issued (上傳時間) 23-Jul-2018 16:51:23 (UTC+8)-
dc.identifier (Other Identifiers) G0103752006en_US
dc.identifier.uri (URI) http://nccur.lib.nccu.edu.tw/handle/140.119/118808-
dc.description (描述) 碩士zh_TW
dc.description (描述) 國立政治大學zh_TW
dc.description (描述) 心理學系zh_TW
dc.description (描述) 103752006zh_TW
dc.description.abstract (摘要) 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
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dc.description.abstract (摘要) 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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dc.description.tableofcontents 中文摘要……………… IV
英文摘要…………………………… VI
第一章、前言………………………………………01
第二章、文獻探討…………………………… 04
第一節、失眠的定義與流行病學研究………………………………04
第二節、失眠之相關病程理論……………………………………………04
第三節、失眠之過度激發理論………………………………………………08
第四節、壓力下睡眠脆弱性特質與失眠之相關研究…………………………14
第五節、神經生理測量與睡眠之相關研究……………………………………………18
第六節、研究問題與假設………………………………………23
第三章、 研究方法…………………………………………27
第一節、研究對象及研究程序 ……………………………27
第二節、研究設計及流程………………………………………27
第三節、研究工具 …………………………………………………30
(一) MINI國際神經精神科晤談表台灣版………………30
(二) 貝克憂鬱量表第二版中文版………………………………30
(三) 貝克焦慮量表中文版……………………………………………31
(四) 失眠嚴重度量表 (ISI)………………………………………31
(五) 福特壓力下失眠反應量表 (FIRST)………………32
(六) 功能性磁振照影……………………………32
(七) 磁振照影相容之腦波記錄儀器………………………33
第四節、資料分析……………………………33
第四章、 研究結果……………………………36
第一節、受試者之人口統計學及量表資料………………………………36
第二節、睡眠起始點前、後五分鐘的腦波頻譜分析…………………38
第三節、fMRI資料……………………45
第五章、討論………………………………50
第一節、 睡眠起始點前、後五分鐘的腦波頻譜分析…………………50
第二節、 fMRI資料………………54
第三節、 結論、研究限制及未來研究建議……………57
參考文獻………………61
附錄一、 FIRST量表……………………69
附錄二、 睡眠嚴重度量表……………70
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dc.format.extent 2203313 bytes-
dc.format.mimetype application/pdf-
dc.source.uri (資料來源) http://thesis.lib.nccu.edu.tw/record/#G0103752006en_US
dc.subject (關鍵詞) 睡眠脆弱特質zh_TW
dc.subject (關鍵詞) 過度激發zh_TW
dc.subject (關鍵詞) 磁振照影zh_TW
dc.subject (關鍵詞) EEG腦波頻譜分析zh_TW
dc.subject (關鍵詞) Stress-related sleep vulnerabilityen_US
dc.subject (關鍵詞) Hyperarousalen_US
dc.subject (關鍵詞) fMRIen_US
dc.subject (關鍵詞) EEG power spectrum analysisen_US
dc.title (題名) 以磁振照影探討睡眠脆弱特質之神經生理基礎zh_TW
dc.title (題名) The neurophysiological basis of stress-related sleep vulnerability : a fMRI studyen_US
dc.type (資料類型) thesisen_US
dc.relation.reference (參考文獻) 林一真(民89)。貝克焦慮量表(BAI)中文版。台北:中國行為
科學社。
林詩淳 (民97)。慢性失眠者與情境性失眠高危險族群之壓力因應與
失眠的關係。國立政治大學心理所碩士論文,未出版,台北
市。
車先蕙、盧孟良、陳錫中、張尚文、李宇宙(民95)。中文版貝克
焦慮量表之信效度。台灣醫學,10(4),447-454。
陳心怡 (民89)。貝克憂鬱量表第二版 (BDI-II) 中文版。 台北: 中國
行為科學社。
American Psychiatric Association, A. P. (2013). Diagnostic and
Statistical Manual of Mental Disorder, 4th edn. Washinton,
DC: American Psychiatriy Association.
Agnew, H. W., Webb, W. B., & Williams, R. L. (1966).
Psychophysiology, 2, 263-266.
Altena, E., Van Der Werf, Y. D., Sanz-Arigita, E. J., Voorn, T. A.,
Rombouts, S. A., Kuijer, J. P. (2008). Prefrontal
hypoactivation and recovery in insomnia. Sleep, 31(9),
1271–1276.
Borkovec, T. D. (1982). Insomnia. Journal of Consulting and
Clinical Psychology, 50, 880-895.
Buckner, R. L., Andrew-Hanna, J. R., & Schacter, D. L. (2005).
The brain’s default network : anatomy, function, and
relevance to disease. Annals of the New York Academy of
Sciences, 1124, 1-38.
Buysse, D. J., Reynolds, C. F., Monk, T. H., Berman, S. R., &
Kupfer, D. J. (1989). Pittsburgh Sleep Quality Index: A new
instrument for psychiatric practice and research. Psychiatry
Research, 28, 193-213.
Chen, I. Y., Jarrin, D. C., Ivers, H., & Morin, C. M. (2017)
Investigating psychological and physiological responses to
the trier social stress test in young adault with insomnia.
Sleep medicine, 40, 11-22.
Drake, C. L., Cheng, P., Almeida, D. M., & Roth, T.(2017).
Familial risk for insomnia is associated with abnormal
cortisol response to stress. Sleep, 40.
Drake, C. L., Jefferson, C., Roehrs, T., & Roth, T.(2006). Stress-
related sleep disturbance and polysomnographic response
to caffeine. Sleep Medicine, 7(7), 567–572.
Drake, C. L., Roehrs, T., & Roth, T.(2003). Insomnia Causes,
Consequences, and Therapeutics: An Overview. Depression
and Anxiety, 18, 163–176.
Drake, C., Richardson, G., Roehrs, T., Scofield, H., & Roth, T.,
(2004).Vulnerability to Stress-related Sleep Disturbance and
Hyperarousal. Sleep, 27, 285-291.
Drake, C. L., Scofield, H., & Roth, T. (2008). Vulnerability to
insomnia: the role offamilial aggregation. Sleep Medicine,
9(3), 297-302.
Drummond, S. P., Walker, M., Almklov, E., Campos, M.,
Anderson, D. E., & Straus, L. D. (2013) Neural correlates of
working memory performance in primary insomnia. Sleep,
36(9), 1307–16.
Edinger, J. D., Carney, C. E., & Wohlgemuth, W. K. (2008).
Pretherapy cognitivedispositions and treatment outcome in
cognitive behavior therapy for insomnia.insomnia. Behavior
Therapy, 39(4), 406-416.
Finelli, L. A., Baumann, H., Borbely, A. A., & Achermann, P.
(2000). Dual electroencephalogram markers of human sleep
homeostasis: correlation between theta activity in waking
and slow-wave activity in sleep. Neuroscience, 101(3),
523-529.
Fernandez-Mendoza, J., Vela-Bueno, A., Vgontzas, A. N.,
Ramos-Platon, M. J., Olavarrieta-Bernardino, S., Bixler, E. O.,
et al. (2010). Cognitive-emotional hyperarousal as a
premorbid characteristic of individuals vulnerable to
insomnia. Psychosomatic Medicine, 72(4), 397-403.
Hauri, P. J. (1983). A cluster analysis of insomnia. Sleep, 6(4),
326-338.
Hauri, P. J., Olmstead, E. M. (1989). Reverse first night effect in
insomnia. Sleep, 12(2), 97-105.
Hwang, Z., Liang, P., Jia, X., Zhan, S., Li, N., Ding, Y., Lu, J.,
Wang, Y., & Li, K. (2012). Abnormal amygdala connectivity in
patients with primary insomnia: Evidence from resting state
fMRI. European Journal of Radiology, 81, 1288– 1295.
Jarrin, D. C., Chen, I. Y., Ivers, H., & Morin, C. M.,(2014) The role
of vulnerability in stress-related insomnia, social support and
coping styles on incidence and persistence of insomnia.
European Sleep Research Society, 23, 681–688.
Kao, C. C., Huang, C. J., Wang, M. Y., & Tsai, P. S. (2008).
Insomnia: Prevalence and its impact on excessive daytime
sleepiness and psychological well-being in the adult
Taiwanese population. Quality of Life Research, 17(8),
1073-1080.
Kalmbach, D., Pillai, V., Arnedt, T., & Drake, C. (2016).
Identifying at-risk individuals for insomnia using the Ford
Insomnia Response to Stress Test. Sleep, 39(2), 449-456.
Lundh, L., & Broman, J. (2000). Insomnia as an interaction
between sleep-interfering and sleep-interpreting processes.
Journal of Psychosomatic Research, 49, 299-310.
Lin, Y. H., Jen, C. H., & Yang, C. M. (2015). Information
processing during sleep and stress-related sleep
vulnerability. Psychiatry and clinical neurosciences, 69,
84-92.
Li, Wang, Zhang, Dou, Liu, Tong, Lei, Wang, Xu, Shi, & Zhang.
(2014). Functional connectivity changes between parietal
and prefrontal cortices in primary insomnia patients:
evidence from resting-state fMRI. European Journal of
Medical Research, 19:32. http://www.eurjmedres.com/
content/19/1/32
Larson-Prior, L. J., Zempel, J. M., Nolan, T. S., Prior, F. W.,
Snyder, A. Z., & Raichle, M. E. (2009). Cortical network
functional connectivity in the descent to sleep. Proceedings
of the National Academy of Sciences of the United States of
America, 106, 4489–4494.
Morin, Belanger, LeBlanc, Ivers, Savard, Espie, Merette,
Baillargeon, & Gregoire. (2009). The Natural History of
Insomnia : A Population-Based 3-year Longitudinal Study.
Archives of Internal Medicine, 169(5), 447-453.
Nofzinger, E. A., Buysse, D. J., Germain, A., Price, J. C.,
Miewald, J. M., & Kupfer, D. J. (2004) Functional
neuroimaging evidence for hyperarousal in insomnia. The
American Journal of Psychiatry, 161(11), 2126–2128.
Noh, H. J., Joo, E. Y., Kim, S. T., Yoon, S. M., Koo, D. L., & Kim,
D. (2012) The relationship between hippocampal volume and
cognition in patients with chronic primary insom- nia. Journal
Clinical Neurology, 8(2), 130–138.
Neckelmann, D., Mykletun, A., & Dahl, A. A. (2007). Chronic
insomnia as a risk factor for developing anxiety and
depression. Sleep, 30(7), 873-880.
Nofzinger, E. A., Nissen, C., Germain, A., Moul, D., Hall, M.,
Price, J. C., Miewald, J. M., & Buysse, D. J. (2006) Regional
cerebral metabolic correlates of WASO during NREM sleep in
insomnia. Journal of Clinical Sleep Medicine, 2(3), 316–322.
Ohayon, M. M. (2002) Epidemiology of insomnia: what we know
and what we still need to learn. Sleep Medicine Reviews,
6(2), 97-111.
O’Byrne, J. N., Berman rosa, M., Gouin, J. P., & Dang-Vu, T. T.
(2014). Neuroimaging findings in primary insomnia.
Pathologie Biologie, 62, 262–269.
Perlis, M. L., Giles, D. E., Mendelson, W. B., Bootzin, R. R., &
Wyatt, J. K. (1997). Psychophysiological insomnia: the
behavioural model and a neurocognitive perspective. Journal
of Sleep Research, 6(3), 179-188.
Perlis, M. L., Kehr, E. L., Smith, M. T., Andrews, P. J., Orff, H., &
Giles, D. E. (2001). Temporal and stagewise distribution of
high frequency EEG activity in patients with primary and
secondary insomnia and in good sleeper controls. Journal of
Sleep Research, 10(2), 93-104.
Spielman, A. J. (1986). Assessment of insomnia. Clinical
Psychology Review, 6, 11-25.
Saper, C. B., Chou, T. C. & Scammell, T. E. (2001) The sleep
switch: hypothalamic control of sleep and wakefulness.
Trends Neurosci. 24, 726-731.
Smith, M. T., Perlis, M. L., Chengazi, V. U., Soeffing, J., &
McCann, U. (2005). NREM sleep cerebral blood flow before
and after behavior therapy for chronic primary insomnia:
Preliminary single photon emission computed tomography
(SPECT) data [3]. Sleep Medicine, 6(1), 93-94.
Sheehan, D. V., Lecrubier, Y., Sheehan, K. H., Amorim, P.,
Janavs, J., Weiller, E., & Dunbar, G. C. (1998). The Mini
International Neuropsychiatric Interview (M.I.N.I.): the
development and validation of a structured diagnostic
psychiatric interview for DSM-IV and ICD-10. Journal of
Clinical Psychiatry, 59 Suppl 20, 22-33;quiz 34-57.
Sharpley, A. L., Solomon, R. A., & Cowen, P. J. (1988).
Evaluation of first night effect using ambulatory monitoring
and automatic sleep stage analysis. Sleep, 11(3), 273-276.
Saper, C. B., Scammell, E. T., & Lu, J. (2005). Hypothalamic
regulation of sleep and circadian rhythms. Nature, 437,
1257-1263.
Spielman, A. J., Saskin, P., & Thorpy, M. J. (1987) Treatment of
chronic insomnia by restriction of time in bed. Sleep, 10,
45-56.
Sämann, P. G., Wehrle, R., Hoehn, D., Spoormaker, V. I., Peters,
H., Tully, C., Holsboer, F., & Czisch, M. (2011). Development
of the brain`s default mode network from wakefulness to
slow wave sleep. Cerebral Cortex, 21(9), 2082-2093.
Turcotte, I., & Bastien, C. H. (2009). Is quality of sleep related
to the N1 and P2 ERPs in chronic psychophysiological
insomnia sufferers? International Journal of
Psychophysiology, 72, 314-322.
Toussaint, M., Luthringer, Remy., Schaltenbrand, Nicolas.,
Carelli, G., Lainey, E., Jacqmin, A., Muzet, A., & Mcher, J.
(1995). Sleep, 18(6), 463-469.
Thomsen, D. K., Mehlsen, M. Y., Christensen, S., & Zachariae,
R. (2003). Rumination-relationship with negative mood and
sleep quality. Personality and Individual Differences, 34,
1293-1301.
Von Economo, C. (1930). Sleep as a problem of localization.
The Journal of Nervous and Mental Disease, 71, 249-259.
Vgontzas, A. N., Tsigos, C., Bixler, E. O., et al. (1998). Chronic
insomnia and activity of the stress system: a preliminary
study. Journal of Psychosom Research, 45(1), 21–31.
Winkelman, J. W., Benson, K. L., Buxton, O. M., Lyoo, I. K., Yoon,
S., & O’Connor, S. (2010). Lack of hippocampal volume
differences in primary insomnia and good sleeper controls:
an MRI volumetric study at 3 Tesla. Sleep Medicine, 11(6),
576–582.
Winkelman, J. W., Plante, D. T., Schoerning, L., Benson, K.,
Buxton, O. M., & O’Connor, S. P. (2013). Increased rostral
anterior cingulate cortex volume in chronic primary insomnia.
Sleep, 36(7), 991–998.
Yang, C. M., Hung, C. Y., & Lee, H. C. (2014). Stress-Related
Sleep Vulnerability and Maladaptive Sleep Beliefs Predict
Insomnia at Long-Term Follow-Up. Journal of Clinical Sleep
Medicine, 10(9), 997-1001.
Yang, C. M., Lin, S. C., & Cheng, C. P. (2013). Transient
Insomnia Versus ChronicInsomnia: A Comparison oStudy of
Sleep-Related Psychological/ Behavioral Characteristics.
Journal of Clinical Psychology. 69(10), 1094-1107.
Zoccola, M., Dickerson, S., & Lam, S. (2009). Rumination
Predicts Longer Sleep Onset Latency After an Acute
Psychosocial Stressor. Psychosomatic Medicine, 71, 771-775.
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dc.identifier.doi (DOI) 10.6814/THE.NCCU.PSY.008.2018.C01-