Affiliations: Department of Otolaryngology, Osaka University School of Medicine, Osaka, Japan
Correspondence:
[*]
Corresponding author: Dr. A. Horii, Department of Otolaryngology, Osaka University School of Medicine, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan. Tel.: +81 6 6879 3951; Fax: +81 6 6879 3959; E-mail: ahorii@ent.med.osaka-u.ac.jp
Abstract: 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.
