Horii Arata, Uno Atsuhiko, Kitahara Tadashi, Mitani Kenji, Masumura Chisako, Kizawa Kaoru, Kubo Takeshi
Department of Otolaryngology, Osaka University School of Medicine, Suita, Osaka, Japan.
J Vestib Res. 2007;17(1):1-8.
A prospective, open-label clinical trial was conducted for two aims: first, to evaluate the role of fluvoxamine, one of selective serotonin reuptake inhibitors, in the treatment of dizziness for the first time and to investigate its effective mechanisms. Second, to test the hypothesis that dizziness in patients without abnormal neuro-otologic findings would be induced by psychiatric disorders rather than by unnoticed neuro-otologic diseases. Nineteen patients with neuro-otologic diseases (Group I) and 22 patients in whom standard vestibular tests revealed no abnormal findings (Group II) were treated by fluvoxamine (200 mg/day) for eight weeks. Subjective handicaps due to dizziness using a questionnaire, anxiety and depressive symptoms measured with the Hospital Anxiety and Depression Scale (HADS), and stress hormones (vasopressin and cortisol) were examined before and 8 weeks after treatment. Overall, fluvoxamine decreased subjective handicaps of both Groups I and II. Fluvoxamine decreased HADS of only patients whose subjective handicaps were reduced (=responders) in both groups, suggesting that fluvoxamine was effective for dizziness via psychiatric action rather than a recovery of vestibular function through serotonergic activation. In non-responders of Group II, pre-treatment HADS was higher than in Group I non-responders and it was not decreased by the treatment, suggesting that dizziness of Group II non-responders was due to severe psychiatric disorders rather than unnoticed neuro-otologic diseases. Anxiety and depression components of HADS showed a good correlation at both pre- and post-treatment periods. No post-therapeutic decrease was observed in either vasopressin or cortisol even in responders, suggesting that dizziness was not the sole cause of stress in chronic dizziness patients. In conclusion, patients with or without physical neuro-otologic deficits who report chronic dizziness accompanied by anxiety and depression (as measured by HADS) showed improvements across a full range of subjective handicaps and psychological distress, while patients with physical neuro-otologic defects and minimal anxiety or depression did not benefit. The main causes of dizziness in patients without physical neuro-otologic findings were psychiatric disorders.
开展了一项前瞻性、开放标签的临床试验,旨在实现两个目标:其一,首次评估选择性5-羟色胺再摄取抑制剂之一的氟伏沙明在治疗头晕方面的作用,并探究其作用机制。其二,验证以下假设:神经耳科学检查无异常的患者出现头晕是由精神障碍引起,而非未被发现的神经耳科疾病所致。19例患有神经耳科疾病的患者(第一组)和22例标准前庭测试未发现异常的患者(第二组)接受了为期8周的氟伏沙明(200毫克/天)治疗。使用问卷评估头晕导致的主观障碍,采用医院焦虑抑郁量表(HADS)测量焦虑和抑郁症状,并在治疗前和治疗8周后检测应激激素(血管加压素和皮质醇)。总体而言,氟伏沙明减轻了第一组和第二组的主观障碍。氟伏沙明仅使两组中主观障碍减轻的患者(即有反应者)的HADS得分降低,这表明氟伏沙明对头晕的疗效是通过精神作用,而非通过5-羟色胺能激活来恢复前庭功能。在第二组无反应者中,治疗前的HADS得分高于第一组无反应者,且治疗后未降低,这表明第二组无反应者的头晕是由严重精神障碍引起,而非未被发现的神经耳科疾病所致。HADS的焦虑和抑郁分量表在治疗前和治疗后均显示出良好的相关性。即使在有反应者中,治疗后血管加压素或皮质醇也未出现下降,这表明头晕并非慢性头晕患者应激的唯一原因。总之,报告伴有焦虑和抑郁(通过HADS测量)的慢性头晕的患者,无论有无身体神经耳科缺陷,在主观障碍和心理困扰方面均有改善,而有身体神经耳科缺陷且焦虑或抑郁程度较轻的患者则未受益。无身体神经耳科异常表现的患者头晕的主要原因是精神障碍。