Ohara Keiichiro, Inoue Yoshiaki, Sumi Yuka, Morikawa Miki, Matsuda Shigeru, Okamoto Ken, Tanaka Hiroshi
Department of Emergency and Critical Care Medicine Juntendo University Urayasu Hospital Urayasu City Chiba Japan.
Acute Med Surg. 2014 Dec 11;2(3):163-168. doi: 10.1002/ams2.97. eCollection 2015 Jul.
Peripheral vertigo has been reported to result from oxidative stress or autonomic nervous dysfunction. Recently, heart rate variability has been used to evaluate autonomic nervous activity. Parasympathetic nervous dysfunction is associated with peripheral vertigo; however, the relationships between vertigo, oxidative stress, and autonomic nervous activity have not been investigated. The aim of this study was to elucidate the changes in oxidative stress and autonomic nervous activity in vertigo patients compared with healthy volunteers.
Oxidative stress was assessed by evaluating biological antioxidant potential and reactive oxygen metabolites, and heart rate variability was measured to evaluate autonomic nervous activity. Thirty-four patients who complained of peripheral vertigo and were treated in our emergency department between January and August 2011 were enrolled in study 1. Oxidative stress and heart rate variability were measured and compared with those of healthy volunteers ( = 23). In study 2, oxidative stress in 18 vertigo patients and heart rate variability in 41 vertigo patients were measured between January and August 2012 before and after conventional treatment of vertigo to evaluate the effect of the treatment on oxidative stress and autonomic nervous activity.
Reactive oxygen metabolites were higher in vertigo patients than in healthy volunteers. Parasympathetic nervous activity was lower and the sympathetic/parasympathetic nervous activity ratio (autonomic nervous activity ratio) was higher in vertigo patients than in healthy volunteers. After treatment of vertigo, reactive oxygen metabolites decreased significantly and the autonomic nervous activity ratio became similar to that observed in healthy volunteers.
Bedside monitoring of oxidative stress and heart rate variability may be useful for the diagnosis of vertigo and evaluation of the effect of treatment.
据报道,外周性眩晕是由氧化应激或自主神经功能障碍引起的。最近,心率变异性已被用于评估自主神经活动。副交感神经功能障碍与外周性眩晕有关;然而,眩晕、氧化应激和自主神经活动之间的关系尚未得到研究。本研究的目的是阐明眩晕患者与健康志愿者相比氧化应激和自主神经活动的变化。
通过评估生物抗氧化潜能和活性氧代谢产物来评估氧化应激,并测量心率变异性以评估自主神经活动。2011年1月至8月期间在我们急诊科就诊的34例主诉外周性眩晕的患者纳入研究1。测量氧化应激和心率变异性,并与健康志愿者(n = 23)进行比较。在研究2中,于2012年1月至8月期间对18例眩晕患者在眩晕常规治疗前后测量氧化应激,对41例眩晕患者测量心率变异性,以评估治疗对氧化应激和自主神经活动的影响。
眩晕患者的活性氧代谢产物高于健康志愿者。眩晕患者的副交感神经活动较低,交感/副交感神经活动比值(自主神经活动比值)高于健康志愿者。眩晕治疗后,活性氧代谢产物显著降低,自主神经活动比值变得与健康志愿者相似。
床边监测氧化应激和心率变异性可能有助于眩晕的诊断和治疗效果评估。