Cognitive behavior therapy for chronic subjective dizziness: longer-term gains and predictors of disability

Cognitive behavior therapy for chronic subjective dizziness: longer-term gains and predictors of disability

AM ER IC AN JOUR NA L OF OTOLARY NG OLOG Y –H EA D A N D N E CK ME D I CI N E AN D SUR G E RY 3 4 ( 2 0 13 ) 11 5–1 2 0 Available online at www.scien...

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AM ER IC AN JOUR NA L OF OTOLARY NG OLOG Y –H EA D A N D N E CK ME D I CI N E AN D SUR G E RY 3 4 ( 2 0 13 ) 11 5–1 2 0

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Cognitive behavior therapy for chronic subjective dizziness: longer-term gains and predictors of disability☆ Alison E.J. Mahoney, DPysch a,⁎, Sarah Edelman, PhD b , Phillip D. Cremer, PhD, FRACP c a Clinical Research Unit for Anxiety and Depression, University of New South Wales at St Vincent's Hospital, Darlinghurst, Sydney, New South Wales, Australia b Clinical Psychologist in Private Practice, Surry Hills, Sydney, New South Wales, 2010, Australia c Neurology Department, Royal North Shore Hospital, St. Leonards, Sydney, New South Wales, 2065, Australia

ARTI CLE I NFO

A BS TRACT

Article history:

Purpose: The study sought to evaluate the longer-term effects of a brief cognitive behavior

Received 10 June 2012

therapy (CBT) intervention for patients with chronic subjective dizziness (CSD). In addition, it sought to identify predictors of longer-term disability in this group. Materials and methods: Forty-four patients with CSD referred by a neuro-otological clinic were followed-up six months after completing a brief treatment program based on the CBT model of panic disorder. Patients completed the following measures: Dizziness Handicap Inventory, Depression, Anxiety and Stress Scales, Dizziness Symptoms Inventory, and the Safety Behaviours Inventory. Measures were completed at pre and post-treatment, as well as at one and six months post-treatment. Results: Treatment gains observed immediately after treatment were maintained at one and six months post-treatment. High levels of pre-treatment anxiety predicted higher levels of disability at six months post-treatment. Duration and severity of dizziness, and medical or psychiatric comorbidity did not predict disability at six month follow-up. Conclusions: A brief CBT intervention for patients with CSD produced improvements in physical symptoms, disability, and functional impairment which were sustained at one month and six months post intervention. Patients with high levels of anxiety prior to treatment had higher levels of disability at six months post-treatment. It is possible that more focused interventions that specifically target anxiety might produce further benefits for this cohort. © 2013 Elsevier Inc. All rights reserved.

1.

Introduction

Dizziness is a common and chronic symptom in the general community and has been associated with significant handicap [1]. Multiple studies have found a relationship between dizziness and psychiatric symptoms, particularly symptoms

associated with anxiety disorders [2–6]. For some, anxiety disorders are seen as the primary cause of the dizziness, while for others, neuro-otolgical conditions are thought to exacerbate pre-existing psychiatric disorders or trigger new ones [7,8]. Regardless of the etiology, dizziness that is perpetuated by anxiety has been frequently observed, and has been

☆ None of the authors have any conflict of interest, financial or otherwise in this work. The study was approved by St. Vincent's Hospital Human Ethics Committee (HREC: 08/SVH/61) and therefore conforms to the ethical standards specified in the 1964 Declaration of Helsinki. ⁎ Corresponding author. Clinical Research Unit for Anxiety and Depression, University of New South Wales at St Vincent's Hospital, Darlinghurst, Sydney, New South Wales, 2010, Australia. Tel.: + 61 2 8382 1407; fax: +61 2 8382 1402. E-mail address: [email protected] (A. E.J. Mahoney).

0196-0709/$ – see front matter © 2013 Elsevier Inc. All rights reserved. http://dx.doi.org/10.1016/j.amjoto.2012.09.013

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referred to as psychogenic dizziness [9], postural phobic vertigo [10], and chronic subjective dizziness (CSD) [11,12]. Possible psycho-physiological pathways have been speculated on [13,14]. Within this population treatments with selective serotonin reuptake inhibitors (SSRIs) produce benefits [15–19], however non-response and intolerance due to side-effects are in the order of 25 to 33% [17,19]. Vestibular rehabilitation (VR) has also been shown to reduce symptoms in many patients [20– 23]. In the last decade psychological treatment using cognitive behavior therapy (CBT) has also been reported. As CBT is an effective treatment for anxiety disorders [24], it has potential application in the treatment of anxiety-related dizziness. Two Swedish studies that evaluated CBT combined with VR in this patient cohort [25,26] found improvements in the treatment group relative to the waitlist control (including greater physical abilities and reduced disability) in the immediate post-therapy period. However the relative contribution of CBT versus VR was unclear, and follow-up data were not collected. Another study [27] evaluated an 8–12 session CBT intervention relative to a self-administered VR program. CBT was associated with greater reductions in anxiety, depression, and reported handicap in the post-therapy period. These improvements were not sustained at 12 month follow up [28]. In a recent study by Edelman, Mahoney, and Cremer [29], a threesession CBT intervention was shown to produce significant reductions in dizziness symptoms, disability, and functional impairment in the immediate post-therapy period, relative to waitlist control. There are some, albeit limited data available on longerterm outcomes of treatments for patients in this category. In trials of SSRIs, treatment gains have been reported to be maintained at two to three months post-treatment [22], 12 months post-treatment [17], and 16 to 36 months posttreatment [23]. Brandt and colleagues reported that over 70% of patients who had received a 2–3 session psychological intervention between six months and 5.5 years postintervention [30] and between five years and 15 years postintervention [31] had either resolution or substantial reduction in symptoms at follow-up. However, no immediate post-therapy data were collected and no control group had been used. The intervention had comprised an explanation of the underlying mechanisms contributing to symptoms, reassurance, encouragement to do regular physical activity, and to use repeated exposure to situations that provoked dizziness. While not specifically labeled as CBT, the description suggests many aspects in common with the CBT approach used by Edelman and colleagues [29]. The current study sought to determine the effects of a brief CBT intervention (see Edelman et al. [29]) on physical and psychological symptoms, disability, and functional impairment in patients with CSD, at one month and six months posttreatment. We hypothesized that improvements in symptoms, disability, and functional impairment made in the immediate post-treatment period would be maintained at one and six month follow-up. The study also sought to identify predictors of disability at six months post-treatment, as this information might lead to better understanding of the disorder and how

treatments might be improved. Previous studies have identified a variety of predictors. Brandt and colleagues [30,31] found that shorter duration of illness was associated with better longer-term outcomes, although some patients with the longest illness duration still made considerable improvements. Staab et al. [17] found that illness duration was not related to treatment response to SSRIs. However it was associated with degree of response, with shorter illness associated with higher likelihood of a very much improved status post-treatment. In addition, patients with central nervous system deficits had poorer post-treatment outcomes compared to those with coexisting peripheral vestibular conditions or migraine headaches, or those whose only diagnosis was a psychiatric disorder. The presence of major psychiatric disorders alone did not predict treatment response. Finally, studies that did not involve treatment, but which examined factors related to longer-term disability in patients with dizziness, have identified the presence of three or more chronic health problems, illness duration of more than one year, high anxiety levels and activity limitation due to illness [32], a history of fainting, vertigo, and avoidance of dizziness provoking situations [33] as significant predictors. Based on previous research we hypothesized that that duration of illness, co-morbid psychiatric and medical conditions, and the severity of pre-treatment symptoms of dizziness, anxiety, and avoidance would predict disability at six months post-treatment.

2.

Method

2.1.

Participants

Participants were 44 consecutive patients referred by a neurootological clinic for psychological assessment and treatment of medically unexplained dizziness, that is dizziness which persisted despite appropriate treatment or dizziness which was experienced beyond that expected given participants’ current diagnosis. Participants were predominantly (72.7%) female with mean age of 46.7 years (SD = 12.97). The diagnostic composition included Benign Paroxysmal Positional Vertigo (BPPV, 25.0%), presence of prior rotational vertigo episodes without definitive diagnosis (29.5%), migrainous vertigo (13.6%), Ménière's disease (4.5%), labyrinthitis (4.5%), and no history of vertigo or vestibular pathology (22.7%). Prior to referral for psychological assessment, participants with definitive vestibular pathology were treated appropriately (e.g., patients with BPPV were successfully treated with a canalith re-positioning maneuver) but continued to experience dizziness. The duration of dizziness in this sample ranged from one to 240 months (median = 8.5 months), with four participants reporting a previous period of dizziness (duration range 2–48 months). With respect to psychiatric diagnoses, 43.2% met criteria for generalized anxiety disorder, 36.4% for major depressive disorder, 38.6% for panic disorder, 6.8% reported dysthymia, and 2.3% reported social phobia. Nine participants (20.5%) did not meet criteria for any psychiatric disorder. Among patients

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who met criteria for a disorder, the number of diagnoses per patient ranged from one to four (M = 1.63, SD = .84).

2.2.

Measures

2.2.1.

Mini International Neuropsychiatric Interview (MINI)

The MINI [34] is a structured diagnostic interview for psychiatric diagnoses as described in the Diagnostic and Statistical Manual (DSM-IV) [35]. Reliability and validity have been demonstrated [36]. The anxiety and depression modules were administered shortly after recruitment.

2.2.2.

Dizziness Symptoms Inventory (DSI)

The DSI is a measure of the severity of dizziness and associated physical symptoms developed and used by Edelman, Mahoney, and Cremer [29]. Items on this inventory were based on symptoms described by Staab [12], as well as further symptoms that were frequently observed in these patients. In this study, internal consistency (α = .81) was good.

2.2.3.

Safety Behaviours Inventory (SBI)

This 18-item descriptive measure was developed by Edelman et al. [29] to assess the frequency of avoidance (e.g., driving, exercising, and socialising) and safety behaviors (e.g., take someone with me, walk close to the fence) related to dizziness. Current internal consistency was α = .90.

2.2.5.

Depression, Anxiety and Stress Scales-21 (DASS-21)

The DASS-21 [39] is a widely used and validated scale [40,41] consisting of three subscales that measure symptoms of depression, anxiety, and psychological stress. The Anxiety subscale was used in this study (α = .71).

2.3.

ist neuro-otological clinic and were randomized to immediate CBT treatment (n = 23) or to a waitlist treatment control group (n = 21). The waitlist treatment control group completed the CBT program four weeks after the immediate treatment group as part of an earlier randomized controlled trial (Edelman et al. [29]). The treatment protocol was identical for both groups. Treatment involved three weekly sessions and included psycho-education about dizziness, in-session behavioral experiments regarding the impact of attention on dizziness symptoms, exposure exercises aimed at reducing avoidance and safety behaviors, alternative strategies for responding to dizziness (e.g., attention refocussing and symptom ‘surfing’), and encouragement to resume normal lifestyle regardless of the presence of symptoms. All participants commenced and completed treatment. Participants completed selfreport measures at recruitment, and at pre- and post treatment. Follow-up data were collected one and six months after treatment. (For full details of procedures see Edelman et al.) [29].

Dizziness Handicap Inventory (DHI)

The DHI [37] is a widely used and validated measure [20,38] that assesses self-perceived disability associated with dizziness in three domains — functional, emotional, and physical. Internal consistency in this study was α = .89.

2.2.4.

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Procedure

The study was approved by St Vincent's Hospital Human Ethics Committee. Participants were recruited from a special-

3.

Results

3.1.

Preliminary analyses

3.1.1.

Combining treatment groups

Independent group t-tests and χ 2 tests were used to determine if treatment groups (1 = immediate therapy; 2 = waitlist therapy) were equivalent. The groups did not differ with respect to age, gender, duration of dizziness, or number of psychiatric disorders (ps > .05). However, groups differed with respect to treatment outcome measures (see Table 1 for means). Pre- and post-treatment DSI scores were equivalent across treatment groups (pre-treatment t42 = 1.61, p = .12 and post-treatment t42 = 1.51, p = .14). However, at both pre- and post-treatment, treatment group 1 reported greater scores on the DHI (pre-treatment t42 = 2.84, p = .007 and post-treatment t42 = 2.09, p = .043). SBI scores were also greater for treatment group 1 at pre-treatment and posttreatment (pre-treatment t42 = 2.52, p = .015 and post-treatment t42 = 2.82, p = .007). As such, treatment group was used as a covariate in analyses concerning follow-up data for outcome measures.

Table 1 – Outcome measures pre and post treatment, and 1 and 6 month follow up for treatment group 1 (n=23) and treatment group 2 (n=21). Outcome measure and treatment group DSI Treatment group Treatment group DHI Treatment group Treatment group SBI Treatment group Treatment group

Pre-treatment mean (SD)

Post-treatment mean (SD)

1-month follow-up mean (SD)

6-month follow-up mean (SD)

1 2

25.35 (12.16) 19.71 (10.92)

14.17 (8.57) 10.48 (7.56)

13.00 (9.84) 10.52 (7.14)

12.87 (8.60) 10.90 (9.00)

1 2

52.35 (20.34) 34.76 (20.73)

27.48 (19.82) 16.48 (14.41)

24.35 (21.16) 16.38 (11.84)

24.78 (20.21) 16.57 (14.96)

1 2

29.22 (14.62) 18.86 (12.38)

12.78 (9.51) 6.19 (5.13)

9.26 (7.72) 4.33 (3.26)

10.52 (10.18) 5.43 (5.7)

Note. DSI = Dizziness Symptom Inventory, DHI = Dizziness Handicap Inventory, SBI = Safety Behaviours Inventory.

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3.1.2.

Completion rates for follow-up data

Treatment group 1 and 2 did not differ in their completion rates for 1 month or 6 month follow-up questionnaires (ps > .05). For the combined group, 81.8% of participants completed the 1-month follow-up questionnaires, while 79.5% of participants completed the 6-month follow-up questionnaires. There were no differences between completers and non-completers with respect to outcome measures at pre and post-treatment, and 1 and 6 month follow-up (all ps > .05). Although completer and non-completers did not vary with respect to gender, duration of dizziness, or number of psychiatric diagnoses (all ps > .05), the participants who completed the 1 month follow-up questionnaire were significantly older than those who failed to complete (completer M = 49.11, SD = 12.16; non-completer M = 36.00, SD = 11.49, t41 = − 2.78, p = .008). Nevertheless, taken as a whole, these data suggest that the follow-up data are representative of the entire sample.

3.2.

Follow-up treatment outcomes

Pre- and post-treatment and follow-up scores for each treatment group are presented in Table 1. Three repeated measures one way ANOVAs (with treatment group as a covariate) were conducted to determine if treatment gains were sustained over time. For the DSI, significant differences were found for time (F3, 126 = 10.02, p < .001) with a nonsignificant time × treatment group interaction (F3, 126 = .68, p = .57). The same results were found for the DHI (time F3, 126 = 16.53, p < .001 and time × treatment group F3, 126 = 2.07, p = .11) and the SBI (time F3, 126 = 17.75, p < .001 and time × treatment group F3, 126 = 1.28, p = .29). Post-hoc Bonferroni-corrected pairwise comparisons were conducted to examine differences across time periods. For all outcome measures, there were significant differences between pre-treatment and all other time points (all ps < .01), whereas all other comparisons failed to reach significance (all ps > .05). Within treatment groups effect sizes (Cohen's d) were calculated from pre-treatment to 6 months post-treatment for the means given in Table 1 using the pooled standard deviation. For treatment group 1, effect sizes were 1.18, 1.36, and 1.51 for the DSI, DHI, and SBI respectively. For treatment group 2, effect sizes were .88, 1.01, and 1.39 for the DSI, DHI, and SBI respectively.

3.2.1.

Clinically significant change

According to recommended criteria [37,42], 73.9% participants in treatment group 1 achieved clinically significant change at

pre to post treatment, and 56.4% achieved it pre to 6 months post treatment. In treatment group 2, 66.7% participants achieved clinically significant change pre to post treatment and pre-treatment to 6 months post treatment.

3.3.

Predicting longer-term disability post-treatment

We examined whether longer-term disability post-treatment was associated with illness duration, the presence/absence of psychiatric and vestibular pathology, and pre-treatment symptoms of dizziness (DSI), anxiety (DASS-Anxiety), and avoidance (SBI). Pearson correlation coefficients were calculated between DHI scores at 6 months post-treatment and continuous predictor variables: pre-treatment DSI (r = .26, p = .091), DASSAnxiety (r = .49, p = .001), and SBI (r = .13, p = .40). Findings suggest that longer-term disability was related to pre-treatment anxiety, but not to the severity of pre-treatment dizziness symptoms or avoidance behaviors. Duration of illness was coded into a dummy variable by dividing at the median duration of illness (consistent with methodology used by Staab et al.) [17]. Other categorical predictor variables relating to psychiatric and medical conditions were also dummy coded (psychiatric disorder absent/ present; vestibular pathology absent/present). A hierarchical multiple linear regression was then conducted to examine if the aforementioned categorical variables in addition to pre-treatment anxiety predicted DHI at 6 months post-treatment. Treatment group was controlled for in Step 1 of the regression (see Table 2). Treatment group was not a significant predictor of longer-term disability at Step 1 (ΔR2 = .05, F1, 42 = 2.31, p = .14). At Step 2, a significant proportion of the variance in 6 months post-treatment disability scores was explained by the model (ΔR2 = .22, F4, 38 = 2.81, p = .04), however, only pre-treatment anxiety was a significant predictor. Other predictors failed to explain a significant proportion of variance in disability (all ps > .05).

4.

Discussion

The findings suggest that a brief CBT intervention confers substantial benefits for patients with anxiety-related dizziness. Consistent with our first hypothesis, improvements made immediately following treatment were maintained at one and six months post-treatment. Effect sizes from pretreatment to six months follow-up for reductions in dizziness symptoms, disability, and functional impairment were large

Table 2 – Summary of multiple linear regression predicting longer-term disability following treatment. Criterion DHI at 6 month follow-up DHI at 6 month follow-up

Predictors

ΔR2

B

SEB

Beta

Step 1: Treatment group Step 1: Treatment group Step 2: Pre-treatment anxiety Median symptom length Psychiatric condition present Vestibular pathology present

.05 .22*

8.21 4.54 2.05 4.87 4.11 1.26

5.40 5.27 .71 5.48 6.59 6.57

.23 .13 .46 .14 .09 .03

Note. DHI = Dizziness Handicap Inventory, * p < .05, ** p < .01.

t 1.52 .86 2.90** .89 .62 .19

Part r .23 .12 .40 .12 .09 .03

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(for both treatment groups). Moreover, the majority of participants maintained clinically significant improvements in disability at six months post treatment. Further improvements in outcomes did not occur during the follow-up period. This is consistent with Brandt et al. [30], who observed that improvements usually occurred days to weeks following treatment and gains were subsequently maintained. The reduction in physical symptoms and related disability observed in the current study was comparable to those reported for other treatments, including SSRIs [15–19] and vestibular rehabilitation [20–23], however they were achieved following a very brief and non-invasive treatment. The intervention used in the current study may have some advantages over those that combine CBT with VR [25,26] as the treatment duration is brief and effect sizes were substantial. However it is possible that a longer intervention might have yielded additional benefits, such as reductions in psychological distress. This was reported by Holmberg et al. [28] who evaluated an 8–12 session CBT intervention with this cohort. The authors report reduced anxiety, depression, and illness handicap associated with the intervention in the immediate post treatment period. These gains were lost at the 12 month follow-up. It is possible that the longer duration of illness among participants in that study (median 59 months versus 9 months in the current study) contributed to poorer longterm outcomes. In the current study treatment gains were maintained at six months post treatment. Nevertheless, a subgroup of patients (17.5%) who met criteria for clinically significant improvement at immediate post-treatment no longer did so six months later. It is not unusual for some relapse to occur following a psychological treatment, and this finding may suggest the need for further treatment sessions for this subgroup. Our second aim was to identify predictors of disability at six months post-treatment. Baseline anxiety scores were the single best predictor of longer-term disability. Other predictors identified by earlier studies, including illness duration, severity of baseline dizziness and avoidance, and the presence of psychiatric disorders and vestibular pathology, failed to predict longer-term disability in this study. The findings suggest that patients with greater comorbidity, illness duration, and functional impairment may still achieve sustained benefits following a brief CBT intervention. As patients with high levels of pre-treatment anxiety showed higher levels of disability at six months posttreatment, it is possible that interventions that target anxiety in a more focused way could further improve long-term treatment outcomes. It should be noted however that the correlational nature of this study precludes conclusions regarding causality, and further research is required to establish the exact relationship. Nevertheless, it is possible that augmenting or combining treatments such as CBT plus SSRIs to specifically address anxiety might lead to better longer-term outcomes. The present findings should be interpreted within the context of several limitations. Firstly, there was no control group comparison for each follow-up period, which presents the possibility that patients may have improved over time without treatment. While this is possible, the mean

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duration of illness (8.5 months) suggests that this is unlikely. Secondly, the Dizziness Symptoms Inventory and the Safety Behaviours Inventory are yet to be psychometrically evaluated. As stated in our earlier report [29] this was a significant limitation, although the other measures used in this study (Dizziness Handicap Inventory and Depression, Anxiety and Stress Scale) are well established and validated instruments. Thirdly, no reliability data were available for psychiatric and medical diagnoses. Finally, the sample size in the current study was comparatively modest, and further research with larger samples is needed to replicate and extend current findings. Further research may also help to identify optimal treatments, which might include combinations of CBT, SSRIs, VR, or identify how treatments can best be tailored to address specific presentations of individual patients.

REFERENCES

[1] Yardley L, Owen N, Nazareth I, et al. Prevalence and presentation of dizziness in a general practice community sample of working age people. Br J Gen Pract 1998;8:1131–5. [2] Asmundson GJ, Larsen DK, Stein MB. Panic disorder and vestibular disturbance: an overview of empirical findings and clinical implications. J Psychosom Res 1998;44:107–20. [3] Clark DB, Hirsch BE, Smith MG, et al. Panic in otolaryngology patients presenting with dizziness or hearing loss. Am J Psychiatry 1994;151:1223–5. [4] Eagger S, Luxon LM, Davies RA, et al. Psychiatric morbidity in patients with peripheral vestibular disorder: a clinical and neuro-otological study. J Neurol Neurosurg Psychiatry 1992;55:383–7. [5] Jacob RG, Furman JM, Durrant JD, et al. Panic, agoraphobia, and vestibular dysfunction. Am J Psychiatry 1996;153: 503–12. [6] Stein MB, Asmundson GJ, Ireland D, et al. Panic disorder in patients attending a clinic for vestibular disorders. Am J Psychiatry 1994;151:1697–700. [7] Furman JM, Jacob RG. A clinical taxonomy of dizziness and anxiety in the otoneurological setting. J Anxiety Disord 2001;15:9–26. [8] Staab JP, Ruckenstein MJ. Which comes first? Psychogenic dizziness versus otogenic anxiety. Laryngoscope 2003;113: 1714–8. [9] Simpson RB, Nedzelski JM, Barber HO, et al. Psychiatric diagnoses in patients with psychogenic dizziness or severe tinnitus. J Otolaryngol 1988;17:325–30. [10] Brandt T. Phobic postural vertigo. Neurology 1996;46:1515–9. [11] Odman M, Maire R. Chronic subjective dizziness. Acta Otolaryngol 2008;128:1085–8. [12] Staab JP. Chronic dizziness: the interface between psychiatry and neuro-otology. Curr Opin Neurol 2006;19:41–8. [13] Balaban CD. Neural substrates linking balances, control and anxiety. Physiol Behav 2002;77:469–75. [14] Yardley L, Redfern MS. Psychological factors influencing recovery from balance disorders. J Anxiety Disord 2001;15: 107–19. [15] Horii A, Uno A, Kitahara T, et al. Effects of fluoxamine on anxiety, depression, and subjective handicaps of chronic dizziness patients with or without neuro-otologic diseases. J Vestib Res 2007;17:1–8. [16] Simon NM, Parker SW, Wernick-Robinson M, et al. Fluoxetine for vestibular dysfunction and anxiety: a prospective pilot study. Psychosom 2005;46:334–9.

120

AM ER IC AN JOUR NA L OF OTOLARY NG OLOG Y –H EA D A N D N E CK ME D I CI NE AN D SUR G E RY 3 4 ( 2 0 13 ) 11 5–1 2 0

[17] Staab JP, Ruckenstain MJ, Solomon D, et al. Serotonin reuptake inhibitors for dizziness with psychiatric symptoms. Arch Otolaryngol Head Neck Surg 2002;128:554–60. [18] Staab JP, Ruckenstain MJ, Amerdam JD. A prospective trial of sertraline for chronic subjective dizziness. Laryngoscope 2004;114:1637–41. [19] Staab JP, Ruckenstein MJ. Chronic dizziness and anxiety: effect of course of illness on treatment outcome. Arch Otolaryngol Head Neck Surg 2005;131:675–9. [20] Badke M, Miedaner JA, Shea TA, et al. Effects of vestibular and balance rehabilitation on sensory organization and dizziness handicap. Ann Otol Rhinol Laryngol 2005;114:48–54. [21] Jacob RG, Whitney SL, Detweiler-Shostak G, et al. Vestibular rehabilitation for patients with agoraphobia and vestibular dysfunction: a pilot study. J Anxiety Disord 2001;15:131–46. [22] Meli A, Zimatore G, Badaracco C, et al. Effects of vestibular rehabilitation therapy on emotional aspects in chronic vestibular patients. J Psychosom Res 2007;63:185–90. [23] Pavlou M, Lingeswaran A, Davies RA, et al. Simulator based rehabilitation in refractory dizziness. J Neurol 2004;251: 983–95. [24] Butler AC, Chapman JE, Forman EM, et al. The empirical status of cognitive–behavioral therapy: a review of metaanalyses. Clin Psychol Rev 2006;26:17–31. [25] Andersson G, Asmundson GJ, Denev J, et al. A controlled trial of cognitive behaviour therapy with vestibular rehabilitation in the treatment of dizziness. Behav Res Ther 2006;44: 1265–73. [26] Johansson M, Akerlund D, Larson HC, et al. Randomised controlled trial of vestibular rehabilitation combined with cognitive behaviour therapy for dizziness in older people. Otolaryngol Head Neck Surg 2001;125:151–6. [27] Holmberg J, Karlberg M, Harlacher U, et al. Treatment of phobia postural vertigo: a controlled study of cognitive behavioural therapy and self-controlled desensitisation. J Neurol 2006;253:500–6. [28] Holmberg J, Karlberg M, Harlacher U, et al. One-year follow-up of cognitive behavioral therapy for phobic postural vertigo. J Neurol 2007;254:1189–92. [29] Edelman S, Mahoney AEJ, Cremer PD. Cognitive behaviour therapy for chronic subjective dizziness: a randomised controlled trial. Am J Otolaryngol [in press].

[30] Brandt T, Huppert D, Dieterich M. Phobic postural vertigo: a first follow-up. J Neurol 1994;241:191–5. [31] Huppert D, Strupp M, Rettinger N, et al. Phobic postural vertigo-a long-term follow-up (5 to 15 years) of 106 patients. J Neurol 2005;252:564–9. [32] Bailey KE, Sloane PD, Mitchell M, et al. Which primary care patients with dizziness will develop persistent impairment? Arch Fam Med 1993;2:847–52. [33] Nazareth I, Yardley L, Owen N, et al. Outcome of symptoms of dizziness in a general practice community sample. Fam Pract 1999;16:616–8. [34] Sheehan BV, Lecrubier Y, Sheehan KH, et al. The Mini International Neuropsychiatric Interview (MINI): the development and validation of structured diagnostic psychiatric interview for DSM-IV and ICD-10. J Clin Psychiatry 1998;59(Suppl. 20):22–33. [35] American Psychiatric Association. Diagnostic and statistical manual of mental disorders. . 4th ed.Washington (DC): American Psychiatric Association; 1994. [36] Lecrubier Y, Sheehan DV, Weiller E, et al. The Mini International Neuropsychiatric Interview (MINI). A short diagnostic structured interview: reliability and validity according to the CIDI. Eur Psychiatry 1997;12:224–31. [37] Jacobson GP, Newman CW. The development of the Dizziness Handicap Inventory. Arch Otolaryngol Head Neck Surg 1990;116:424–7. [38] Whitney SL, Wrisley DM, Brown KE, et al. Is perception of handicap related to functional performance in persons with vestibular dysfunction? Otolog Neurotol 2004;25: 139–43. [39] Lovibond SH, Lovibond PF. Manual for the depression anxiety stress scales. . 2nd ed.Sydney: Psychological Foundation of Australia; 1995. [40] Antony M, Bieling P, Cox BJ, et al. Psychometric properties of the 42-item and 21-item versions of the Depression Anxiety Stress Scales in clinical groups and a community sample. Psychol Assess 1998;10:176–81. [41] Gloster AT, Rhoades HM, Novy D, et al. Psychometric properties of the Depression Anxiety and Stress Scale-21 in older primary care patients. J Affect Disord 2008;110:248–59. [42] Treleaven J. Dizziness handicap inventory (DHI). Aust J Physiother 2006;52:67.