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Journal of Vestibular Research 17 (2007) 1–8 Effects of fluvoxamine on anxiety,depression, and subjective handicaps ofchronic dizziness patients with or withoutneuro-otologic diseases Arata Horii∗, Atsuhiko Uno, Tadashi Kitahara, Kenji Mitani, Chisako Masumura, Kaoru Kizawa andTakeshi KuboDepartment of Otolaryngology, Osaka University School of Medicine, Osaka, Japan 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.
Keywords: SSRI, anxiety, depression, dizziness, stress 1. Introduction
In the treatment of dizzy patients, there are two ma- jor problems: first, treatment for patients without phys- ∗Corresponding author: Dr. A. Horii, Department of Otolaryngol- ical neuro-otologic findings, and second, therapy for ogy, Osaka University School of Medicine, 2-2 Yamadaoka, Suita,Osaka 565-0871, Japan. Tel.: +81 6 6879 3951; Fax: +81 6 6879 patients who do have neuro-otologic deficits but do not 3959; E-mail: ahorii@ent.med.osaka-u.ac.jp.
sufficiently respond to conventional medication with ISSN 0957-4271/07/$17.00  2007 – IOS Press and the authors. All rights reserved A. Horii et al. / Effects of fluvoxamine on anxiety, depression, and subjective handicaps of chronic dizziness patients anti-vertigo drugs. Regarding the first problem, we of Meniere’s disease) were excluded. This study was hypothesized that dizziness in patients with a negative approved by the local ethical committee of the Osaka neuro-otologic test would be mainly due to psychiatric University Hospital and performed in accordance with disorders. The second problem might be due to pro- dromal psychiatric disorders that would affect a neuro-otologic condition or to secondary psychiatric disor- 2.1. Diagnosis, medical treatment and measurement ders following a primary neuro-otologic condition that would cause or exacerbate physical symptoms. Thesebidirectional relationships between neuro-otologic dis- Otoneurologic examinations including smooth pur- eases and psychiatric disorders have previously been suit test, observation of nystagmus with infrared CCD proposed [5,9]. For these two problems, we hypothe- camera, caloric tests, posturography and pure-tone au- sized that appropriate treatments for psychiatric disor- diometry were performed. Neuroimaging such as CT ders would bring about a remission of dizziness.
or MRI/MRA of the brain and other examinations in- In this prospective study, we treated 41 consecutive cluding the glycerol test and electrocochleograms were dizzy patients with or without neuro-otologic diseases also performed if clinically indicated. Based on these using fluvoxamine, one of selective serotonin reuptake examinations and careful history taking, otoneurology inhibitors (SSRIs). We chose fluvoxamine because, to specialists diagnosed patients according to the guide- the best of our knowledge, there are no reports of the lines for the diagnosis of vertigo and dizziness estab- use of this drug in dizziness [3,10–12]. The outcome lished by the Japan Society for Equilibrium Research.
measures were: the Hospital Anxiety and Depression During the initial one week, patients were asked to Scale (HADS), a validated 14–item self-report of anxi- take 100 mg of fluvoxamine per os, per day. Then, dur- ety and depressive symptoms [17] and subjective hand- ing the following seven weeks, the dose was increased icaps due to dizziness, a validated 14–item self-report to 200 mg per day. Five mg of metoclopramide were of dizziness symptoms [3,7,8]. Plasma levels of vaso- also prescribed just in case nausea, an adverse effect pressin and cortisol were also measured as a hormon- of fluvoxamine, occurred. No other drug was used.
al stress marker [1]. All these parameters were mea- However, if a patient was already under treatment, they sured before and 8 weeks after treatment. Our work- were allowed to keep taking it. Anti-histamines, va- ing hypotheses are that patients without positive neuro- sodilators, diphenidol and diuretics such as isosorbide otologic findings would be mainly suffering from psy- chiatric disorders and thus having high HADS scores Subjective handicaps in daily life due to vertigo and and fluvoxamine would be effective on their subjective dizziness were assessed using a dizziness and unsteadi- handicaps due to dizziness. We also hypothesized that ness questionnaire as reported previously [3,7,8]. This fluvoxamine would be effective on subjective handi- questionnaire is a slightly modified version of the val- caps in neuro-otologic patients by acting on their pos- idated Jacobson’s Dizziness Handicap Inventory writ- sible comorbid psychiatric disorders. In both cases, a ten in Japanese [6]. The questionnaire consisted of 14 correlation between a recovery of subjective handicaps items and as the assessment, the answers to all the ques- tions were scored 1 to 5 on a scale in which severe hand-icap was scored 5, significant handicap 4, moderatehandicap 3, slight handicap 2, and no handicap 1. Thus, 2. Methods
full scores were 70 points. Table 1 shows the questionsof this inventory. Questions were classified into five Consecutive 60 patients with complaints of dizziness factors: disturbance of social activity (questions 1, 5, who visited the Department of Otolaryngology, Osaka 9), body motion precipitating dizziness (questions 2, University Hospital, were asked whether they agreed 6, 10), limitation of physical activity (questions 3, 7, to enter the study. Before entering the study, informed 11), emotional disturbance (questions, 4, 7, 10), and consent regarding the purpose of this study, possible trouble with interpersonal communications (questions effects and adverse effects of the drug was obtained from each patient. There were no patient selection Each patient was assessed for his/her depressive or criteria, however, patients whose symptoms were ex- anxious status using the Japanese version of the 14-item pected to disappear in a short time (i.e., patients with self-report symptoms of the Hospital Anxiety and De- benign paroxysmal positioning vertigo or acute stage pression Scale (HADS) [17]. While the HADS scores A. Horii et al. / Effects of fluvoxamine on anxiety, depression, and subjective handicaps of chronic dizziness patients The dizziness and unsteadiness questionnaire 1. Do you refrain from going out or traveling for work or amusement due to dizziness or unsteadiness? 2. Do you hate walking in dark places even around your home due to dizziness or unsteadiness? 3. Do you hate going downstairs due to dizziness or unsteadiness?4. Do you feel annoyed due to dizziness or unsteadiness?5. Do you feel that you are not able to do your work either at home or at an office due to dizziness or unsteadiness?6. Is the degree of dizziness or unsteadiness strengthened when you suddenly move your head (e.g. when looking back)?7. Do you hate walking through narrow spaces (e.g. narrow sidewalk) due to dizziness or unsteadiness?8. Do you feel that you have a physical handicap and are inferior to other persons due to dizziness or unsteadiness?9. Are you unable to concentrate on something due to dizziness or unsteadiness? 10. Do you think it is too much trouble to read books or newspaper due to dizziness or unsteadiness? Or do you have some trouble 11. Is the degree of dizziness or unsteadiness strengthened when you stand up from a chair?12. Do you feel anxiety about yourself when you are in the presence of others due to dizziness or unsteadiness?13. Do you refrain from meeting or going out with your family or friends due to dizziness or unsteadiness?14. Do you have difficulties in your daily life due to dizziness or unsteadiness? are not meant to offer strict diagnostic guidelines, they neuro-otologic findings nor vestibular diseases. Each have been shown to be of clinical value in indicating the patient anxiety or depression status. Although most the profiles of patients including age, sex, duration of of our patients were not assessed nor diagnosed by psy- dizziness, hearing levels (average for 1K, 2K, and 4K chiatrists, a previous study revealed that cut off point Hz of the worst hearing ear), canal paresis % (CP%), of > 12 (full scores, 42) predicted positive psychiatric and diseases. Group I included 14 patients with Me- disorders with 92% sensitivity while the specificity in niere’s disease, one with delayed endolymphatic hy- the screening of psychiatric disorders among ENT pa- drops, three with vestibular neuritis, and 12 with oth- tients was 90% [4]. Moreover, from a practical stand- point, the HADS may be more useful than psychiatric vestibular diseases included 10 patients who showed consultation to practicing otologists who must quickly unilateral caloric weakness more than 20% of CP% and judge the patients’ psychiatric status.
2 patients with head shake after-nystagmus. Hearing Before and 8 weeks after the start of fluvoxamine, levels and CP% were significantly worse in Group I we assessed HADS scores and subjective handicaps, than in Group II. No differences in other parameters and measured plasma levels of vasopressin and corti- were found between the two groups. Note that the sol. Plasma levels of vasopressin and cortisol were mean of duration of dizziness of both groups is relative- measured in the morning to control the pattern of their ly long (19.2 months for Group I and 21.2 months for Group II) indicating that most of patients had chronicdizziness.
Of the 60 patients who entered the study, 8 could not keep taking their medicine due to nausea and were Patients were divided into two groups: Group I thus removed from this study, and data could not be comprised patients with neuro-otologic diseases diag- retrieved in 11 patients for an unknown reason. There- nosed by the above mentioned vestibular tests, while fore, data from the remaining 41 patients (Group I, n = Group II included those with no abnormal physical 19; Group II, n = 22) were used to assess the effects A. Horii et al. / Effects of fluvoxamine on anxiety, depression, and subjective handicaps of chronic dizziness patients MD, Meniere’s disease; DEH, delayed endolymphatic hydrops; VN, vestibu-lar neuritis.
of fluvoxamine on various parameters. The 100 mgstarting dose of fluvoxamine was relatively high anddropout by unknown reason might be a result of thisdose-related nausea.
Pre-therapeutic differences in age, duration of the disease, hearing levels, caloric paresis, HADS scoresand subjective handicaps between Groups I and II weretested by the Mann-Whitney U-test. Differences insubjective handicaps, HADS scores, and stress hor-mone levels were tested 8 weeks after treatment andcompared to pre-treatment values using the Wilcoxon’ssigned-ranks test. The correlation coefficient between Pre-treatment vasopressin (A) and cortisol (B) levels in Group I (patients with neuro-otologic diseases) and Group II (patients anxious scores and depressive scores of HADS, their without physical neuro-otologic findings). Plasma vasopressin levels decline rates and subjective handicaps after 8 weeks of in both groups were higher than normal (0.3–3.5 pg/mL). Cortisol medication were calculated and tested using Fisher’s r levels in both groups were within normal range (4.0–18.3 µg/dL).
However, levels in Group I were significantly higher than those inGroup II.
3. Results
3.2. Effects of fluvoxamine on subjective handicaps, 3.1. Pre-medication Hospital Anxiety and Depression Scale (HADS) and stress hormones levels As shown in Fig. 2A, subjective handicaps were re- duced following treatment in Group I (p = 0.0208).
Of 30 patients with neuro-otologic diseases (Group I) Analysis of data from patients of this group with and 30 of Group II with no physical neuro-otologic reduced handicaps showed a significant decrease in findings, 21 and 22 showed high pre-medication HADSscores (> 12), respectively. The depressive scale in HADS scores after treatment as compared to pre- Group I and II was 7.5 ± 0.7 and 7.9 ± 0.9 (mean medication values (Fig. 2B, p = 0.0131). In patients of ± SE), respectively, while their anxious scale was 8.5 the same group with no recovery from subjective hand- ± 0.7 and 9.4 ± 0.6 (mean ± SE), respectively. No icaps, HADS scores were unchanged after treatment group differences were noted between both anxious (Fig. 2C). Pre-medication HADS tended to be low in and depressive scales. As shown in Fig. 1, plasma the latter subgroup compared to the former subgroup vasopressin levels in Group I and II were 5.9 ± 1.3, of Group I patients (11.8 ± 1.5 vs 18.1 ± 2.1, p = and 6.5 ± 1.8 pg/mL (mean ± SE), respectively, which 0.0693). The same observations were made for patients were higher than the normal (0.3–3.5 pg/mL). Cortisol of Group II (Fig. 3A, p = 0.0162; Fig. 3B, p = 0.0238; levels in Group I and II were 15.2 ± 1.1 and 10.3 ± 0.7 and Fig. 3C), though pre-treatment HADS scores of µg/dL (mean ± SE), respectively, which were within patients with no recovery from handicaps in Group II normal range (4.0–18.3 µg/dL), though significantly were significantly higher than those in Group I (21.5 ± higher in Group I than those in Group II (p = 0.0005).
3.3 vs 11.8 ± 1.5, p = 0.0252).
A. Horii et al. / Effects of fluvoxamine on anxiety, depression, and subjective handicaps of chronic dizziness patients Fig. 2. Pre- and post-treatment subjective handicaps in all Group I patients (A), HADS scores in responders (B) or non-responders (C). Subjectivehandicaps in Group I patients were reduced following the treatment (A). Post-medication HADS scores were decreased in responders (B) but notin non-responders (C).
Fig. 3. Pre- and post-treatment subjective handicaps in all Group II patients (A), HADS scores in responders (B) or non-responders (C). Subjectivehandicaps of Group II patients were reduced following fluvoxamine treatment (A). HADS scores were decreased following the treatment inresponders (B) but not in non-responders (C).
In addition, analysis of data only from responders of Group I and II showed that neither vasopressin (5.2± 1.0 → 7.8 ± 1.7 pg/mL) nor cortisol levels (12.5 ± 1.2 → 12.4 ± 1.1 µg/dL) were decreased after thetreatment.
As shown in Fig. 4A and 4B, anxious and depres- sive scales showed a high correlation in all patients atboth pre- and post-treatment periods (p < 0.0001, pre: r = 0.781; post: r = 0.757). Post/pre ratio of HADSscores and subjective handicaps showed a significantcorrelation (Fig. 5A, p = 0.0141, r = 0.388). When Fig. 4. Correlation between anxious and depressive scales before only patients with decreased HADS was analyzed, sub- (A) and after (B) fluvoxamine treatment in all patients. Anxious jective handicaps significantly reduced (Fig. 5B, p < and depressive scales showed a high correlation at both pre- and 0.0001). In turn, HADS was significantly decreased in patients whose handicap scores were reduced (Fig. 5C,p = 0.0015).
Of 30 patients with high pre-treatment HADS scores HADS scores decreased from 20.7 ± 6.7 to 15.9 (> 12), they decreased in 20 patients. Subjective hand- ± 7.6 (p = 0.0072) after treatment in a group of pa- icaps decreased from 55.1 ± 7.0 to 42.1 ± 16.0 (p = tients with high pre-treatment HADS scores (> 12).
0.0058) after treatment in a group of patients with high A. Horii et al. / Effects of fluvoxamine on anxiety, depression, and subjective handicaps of chronic dizziness patients Fig. 5. Correlation between post/pre ratio of HADS and subjective handicaps of all patients (A). Subjective handicap scores of patients withreduced HADS (B) and HADS scores of patients with reduced handicaps (C) of all patients at pre- and post-treatment. Post/pre ratio of HADSscores and subjective handicaps showed a significant correlation (A). Subjective handicaps were reduced in patients with reduced HADS (B) andin turn HADS decreased in responders (C).
pre-treatment handicap scores (> 43). Of 19 patients randomized study would be ideal, carefully designed with high pre-treatment handicap scores (> 43), they prospective studies are also valid. For instance, as dis- decreased in 13 patients. It is indicated that fluvox- cussed below in detail, fluvoxamine showed beneficial amine clearly had a beneficial effects on anxiety and effects only for limited patients, suggesting that this depression and its effects on dizziness were marked in was not a placebo effect. This study is a prospective patients even with severe subjective handicaps.
one to test the efficacy of fluvoxamine for the first timeand the number of patients was larger compared to theprevious studies [3,10–12]. This study would give fur- 4. Discussion
ther evidence for the use of SSRIs in the treatment ofchronic dizziness.
Staab and Ruckenstein classified otoneurologic- Regarding the use of HADS without consultation to psychiatric interactions into three types [9]: the oto- psychiatrist, a previous study revealed that cut off point genic group, in which physical neuro-otologic condi- of > 12 (full scores, 42) predicted positive psychiatric tions trigger a psychiatric dysfunction; the psychogenic disorders with 92% of sensitivity while the specificity group where psychiatric disorders produce dizziness; in the screening of psychiatric disorders among ENT and the interactive group characterized by the exacer- patients was 90% [4]. Moreover, from a practical stand- bation of prodromal psychiatric symptoms by neuro- point, the HADS may be more useful than psychiatric otologic conditions. In any of these groups, comor- consultation to practicing otologists who must quickly bid psychiatric disorders are thought to exacerbate the judge the patients’ psychiatric status.
dizziness of patients. The present study showed that70% (21/30) of Group I and 73% (22/30) of Group 4.1. Group I (patients with neuro-otologic diseases) II patients had high HADS scores (> 12), indicatingthat many patients with chronic dizziness had comorbid Seventy percent of Group I patients showed high psychiatric diseases whether they had neuro-otologic HADS scores, suggesting that many of neuro-otologic diseases or not. While this percentage seemed relative- patients had comorbid pasychiatric disorders that could ly high, this was consistent with previous reports [16].
be assigned to either the otogenic or interactive To date, no placebo controlled double blinded study has been conducted to examine the effects of SSRIs fective in Group I patients’ subjective handicaps due on chronic dizziness. Ideally, drug effects should be to dizziness (Fig. 2A). HADS scores in Group I pa- examined between a true and a negative (placebo) con- tients whose subjective handicaps were reduced (= re- trol drug. Because this study did not include a placebo sponders) decreased following fluvoxamine (Fig. 2B), control group, the observed effects of fluvoxamine on whereas fluvoxamine had no effects on HADS scores HADS and subjective handicaps might contain both a of non-responders of Group I (Fig. 2C). Moreover, pre- “true” drug effect plus “placebo” effects. Although a treatment HADS scores of non-responders in Group I A. Horii et al. / Effects of fluvoxamine on anxiety, depression, and subjective handicaps of chronic dizziness patients tended to be low compared to the responders. These having either anxiety or depression alone (see Results).
findings suggest that fluvoxamine was effective in Furthermore, anxious and depressive scales showed a controlling comorbid psychiatric disorders in neuro- high correlation at both pre- and post-treatment periods otologic patients leading to a recovery from subjective (Fig. 4A, 4B). These findings suggest that dizzy pa- handicaps in responders. If fluvoxamine contributes to tients are having both the anxiety and depression simul- recovery of vestibular function via serotonergic acti- taneously and that fluvoxamine was effective for both vation, it would be expected that the subjective handi- the psychiatric disorders in dizzy patients. There is one caps should be decreased irrespective of the pre-HADS.
more category of psychiatric disorders that could cause However, fluvoxamine was only effective for patients dizziness: undifferentiated somatoform disorders [13].
with high pre-HADS (Fig. 2B) but not for those with We could not rule out the possibility that some of pa- low pre-HADS (Fig. 2C). These observations did not tients with low-moderate HADS in Group II are suffer- support the hypothesis that fluvoxamine might help the recovery of the vestibular function through the activa-tion of serotonin-dependent neuronal pathways [11].
It is indicated that fluvoxamine is recommended forneuro-otologic patients with high pre-HADS (otogenic We measured plasma vasopressin and serum cortisol or interactive pattern) and that neuro-otologic patients as a marker of stress. Accordingly, plasma vasopressin with low pre-treatment HADS scores should be treated was higher in both Groups I and II than normal range by alternative kinds of drugs acting on the vestibular (Fig. 1A), suggesting that the stress level of dizzy pa- tients was higher than normal. Serum cortisol was with-in normal range, however, it was significantly higher 4.2. Group II (patients without physical in Group I than in Group II before treatment (Fig. 1B).
This was consistent with a recent study that reportedthat serum cortisol levels were higher in Meniere’s pa- Overall, fluvoxamine treatment was effective in pa- tients as a result of disease-induced stress rather than a tients’ subjective handicaps due to dizziness in Group II cause of Meniere’s disease per se [15]. Although there (Fig. 3A). In responders of this group, HADS scores has been a report of complex results for cortisol levels were also reduced (Fig. 3B), however, fluvoxamine in psychiatric disorders [14], we assume that the rela- had no effects on HADS scores in non-responders in tively high level of cortisol in Group I in our data may this group (Fig. 3C). In contrast to non-responders in be the result of neuro-otologic diseases including Me- Group I, pre-treatment HADS scores were significantly niere’s disease. Even in patients with post-medication higher than those in Group II (21.5 ± 3.3 vs 11.8 ± 1.5, reduced handicaps, neither vasopressin nor cortisol de- p = 0.0252). Moreover, no improvement of HADS creased (see Results). This suggests that the dizziness was observed even after fluvoxamine in non-responders is not the sole cause of stress in dizzy patients and that of Group II (Fig. 3C). These findings further suggest the level of stress hormones might not be a useful stress that fluvoxamine was effective in psychiatric disorders in this group leading to a recovery from their subjec-tive handicaps and that non-responders to fluvoxam- 4.5. Bidirectional relationship between ine in Group II were suffering from more severe psy- neuro-otologic diseases and psychiatric disorders chiatric disorders rather than very mild neuro-otologicconditions unnoticed by clinicians. Therefore, it is in- Based on prospective observations, Jacob and Fur- dicated that fluvoxamine should be used for dizzy pa- man [5] postulated that anxiety disorders could cause tients without physical neuro-otologic findings and that psychosomatic dizziness and conversely, vestibular more aggressive treatment for psychiatric disorders is dysfunction could also cause somatopsychic anxiety.
recommended for non-responders in this group.
Moreover, Staab and Ruckenstein examined the longi-tudinal relationships between physical neuro-otologic 4.3. Psychiatric disorders in dizzy patients: Anxiety illness and anxiety disorders and concluded that there is a bidirectional relationship between them [9]. Thisbidirectional relationship would form a “vicious cy- Anxious and depressive scales of all patients were al- cle” and lead to chronicity of the disease. Analysis most the same and it is not likely that dizzy patients are of data from all patients reveals a significant correla- A. Horii et al. / Effects of fluvoxamine on anxiety, depression, and subjective handicaps of chronic dizziness patients tion in the decrease of HADS scores and subjective References
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Acknowledgment
L. Yardley, J. Burgneay, I. Nazareth and L. Luxon, Neuro-otological and psychiatric abnormalities in a community sam- We thank Dr. T. Hosaka for his valuable suggestions ple of people with dizziness: a blind, controlled investigation, on the use of HADS and Dr. Kalubi Bukasa for his J Neurol Neurosurg Psychiatry 65 (1998), 679–684.
A.S. Zigmond and R.P. Snaith, The hospital anxiety and de- comments on the manuscript. This study was partly pression scale, Acta Psychiatr Scand 67 (1983), 361–370.
supported by a Research Grant for Intractable Disease(Vestibular Disorders) from the Ministry for Health andWelfare of Japan.

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