心跳變異率(心跳間距上的變化)受交感與副交感神經系統影響,可作為自主神經系統激發程度的指 標。本研究在睡前五分鐘及早晨喚醒後五分鐘收集心電圖的資料進行分析,分別分析三組在不同情境 中的(1) R-R interval(RRI):心電圖中R峰之平均間隔時間,表心跳速率,此值越小代表心跳越快;(2) 正規化低頻譜功率(LF(nu):反映交感神經與副交感神經之共同狀態;(3)正規化高頻譜功率(HF(nu):反
RRI (msec) 890.86±80.58 877.98±103.50 897.82±108.84 .17 LF(nu) 28.54±16.51 31.31±14.95 36.53±22.72 .75 HF(nu) 50.37±18.06 53.53±15.88 48.75±20.59 .29
LF/HF 0.64±0.49 0.72±0.60 1.09±1.30 1.13
早晨
RRI(msec) 884.64±87.33 832.34±85.87 811.18±91.30 2.82+ LF(nu) 38.17±15.35 41.68±16.02 46.95±17.24 1.15 HF(nu) 38.96±11.79 37.76±17.82 32.58±19.03 .65
LF/HF 1.16±0.93 1.68±1.55 2.34±2.01 2.21
註: .09 < + < .05。
在壓力情境中,如表十七所示,發現三組在睡前五分鐘的LF/HF有顯著差異,F(2, 43) = 3.26, p
= .048,經事後比較發現IN組的LF/HF有大於LV組的傾向,但僅達臨界顯著水準(p = .088),但其餘兩兩 比較皆未發現顯著的差異。其餘睡前五分鐘的RRI(F(2, 43) = 1.15, p = .325)、LF(nu)(F(2, 43) = 2.47, p
= .097)、HF(nu)(F(2, 43) = 1.67, p = .200)皆未發現三組有顯著不同。而在早晨喚醒後五分鐘的指標中,
RRI的組間差異達顯著水準,F(2, 43) = 11.56, p<.001,經事後比較發現IN組的RRI (M = 884.64)大於HV 組(M = 761.17, p< .001),以及LV組(M = 793.93, p = .005),但HV組與LV組之間並無差異(p = .668),顯 示IN組的心跳速率慢於HV與LV組,但後兩者無異。其餘早晨喚醒後五分鐘的LF(nu)(F(2, 43) = 2.05, p = 141)、HF(nu)(F(2, 43) = 1.72, p = 192)以及LF/HF(F(2, 43) = 2.02, p = 145)並未發現三組有顯著差異。
表十七、壓力情境下之各自主神經系統指標之平均數±標準差以及單因子變異數分析結果
RRI(msec) 890.86±80.58 850.30±80.58 886.75±80.86 1.15 - LF(nu) 28.54±16.51 33.83±14.69 41.90±18.47 2.47 -
RRI(msec) 884.64±87.33 761.17±68.77 793.93±62.98 11.56***
IN>HV,
表十八、各自主神經系統指標之平均數±標準差與二因子變異數分析之結果
(Bonnet & Arand, 1997; Edinger & Means, 2005; Nicassio et al., 1985);而高睡眠脆弱特質者在一般狀 況下的激發程度與低脆弱特質者並無異,但其主觀認知激發的向度則易受壓力的激發而趨近於失眠患
研究結果並沒有看到過去研究一致發現失眠者的N350較低的現象(Yang & Lo, 2007; Bastien et al.,
基礎情境(B) 壓力情境(S) F 值 事後
2008;Hairston et al., 2010),原因之一可能因為本研究的失眠患者的年齡相對較高的緣故,需進一步 研究驗證。
在自主神經系統的激發程度部分,本研究以心跳速率以及變異率來加以測量,結果顯示高低睡眠 脆弱特質之兩組在這些指標上在睡前並無顯著差異,在壓力操弄後僅提高了早晨起床後的心跳速率,
並降低了副交感神經系統的活動,但對於睡前的自主神經系統的狀態並沒有顯著的影響。而失眠組也 僅在壓力情境下自主神經系統活動有較高的現象,並沒有呈現過去研究發現整體自主神經系統較高的 激發現象(Bonnet & Arand, 1997)。
綜合而言,本研究的結果顯示,高睡眠脆弱性的個體在一般狀況下主觀的激發程度與低脆弱特質 者無太大差異,然而在面對壓力時主觀的認知激發可能會有較接近失眠者的活化程度,這樣的反應也 可能造成剛入睡時對於外界訊息較快的反應性;然而,當進入較深層的睡眠時,高脆弱特質組反而會 比失眠組及低脆弱特質組有較高的抑制作用,這個抑制作用可能是保護高脆弱特質組不致變成慢性失 眠的機制。而在自主神經系統的激發程度方面,研究結果顯示高低脆弱特質組在睡眠並無太大差異,
也沒有呈現對於壓力有不同的反應性,僅在慢性失眠組有較明顯的差異。因此,本研究結果傾向指出 認知層面的激發狀態與中樞神經系統的反應性可能是失眠的前置因子,然而在失眠尚未慢性化之前,
中樞神經系統會有補償的抑制作用,仍然讓脆弱性高的個體能進入深層的睡眠。但倘若在較長期的壓 力狀態下,有可能會造成此補償機制失去作用,此時面對壓力便可能同時造成神經認知歷程及自主神 經系統的過度活化,形成慢性失眠。
本研究結果雖然增進了對於過度激發在失眠病理發展機制的角色的了解,但研究當中可能的問題 仍然可能對其結果的推論有所限制。首先,本研究當中三組的年齡有所差異,失眠組的受試者的年齡 顯著高於其他兩組,所以研究結果的差異有可能部分來自年齡的差異,結果的推論必須考量到年齡可 能造成的影響,但高低睡眠脆弱特質兩組的年齡則相當,結果不受年齡的影響。其次,本研究在失眠 組的主觀激發、中樞神經系統及自主神經系統的測量結果,相較於過去發表的文獻,與非失眠組比較 所得到的差異都相對來得小,可能原因之一是上述的年齡差異,但失眠組的年齡較高,或許應該預期 有更顯著的差異;此外,失眠組在睡眠參數上雖品質偏向較差,但統計結果也與其他兩組沒有顯著差 異,因此可能本研究的失眠個案屬較輕微者,有可能因為本研究的程序複雜,又需在夜間聽聲音,因 此失眠較嚴重者多半不願參與,而有選擇偏誤;過去研究也曾呈現失眠者在睡眠實驗室反而睡得較好 的矛盾現象,也可能解釋本研究沒有見到的預期差異。這些都是未來研究可以繼續澄清及需特別注意 的現象。
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