Mar 14, 2008 - Psychiatric comorbidity in different organic vertigo syndromes. JON 2697. Introduction. Nearly half of the patients presenting at specialized.
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J Neurol (2008) 255:420–428 DOI 10.1007/s00415-008-0697-x
Annegret Eckhardt-Henn Christoph Best Sandra Bense Peter Breuer Gudrun Diener Regine Tschan Marianne Dieterich
Received: 12 January 2007 Received in revised form: 10 July 2007 Accepted: 10 July 2007 Published online: 14 March 2008
PD Dr. med. A. Eckhardt-Henn (쾷) Dept. of Psychosomatic Medicine Klinikum Stuttgart – Bürgerhospital Tunzhoferstrasse 14–16 70191 Stuttgart, Germany Tel.: +49-711/253-2701 Fax: +49-711/253-2172 E-Mail: A.Eckhardt@klinikum-stuttgart.de C. Best · S. Bense · M. Dieterich Dept. of Neurology Johannes Gutenberg-University Mainz, Germany P. Breuer Dept. of Psychology Georg-August-University Göttingen, Germany G. Diener · R. Tschan · A. Eckhardt-Henn Dept. of Psychosomatic Medicine and Psychotherapy Johannes Gutenberg-University Mainz, Germany
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ORIGINAL COMMUNICATION
Psychiatric comorbidity in different organic vertigo syndromes
■ Abstract Objective A high degree of psychiatric disorders has repeatedly been described among patients with organic vertigo syndromes and attributed to vestibular dysfunction. Yet almost no investigations exist which differentiate between various organic vertigo syndromes with regard to psychiatric comorbidity. The following prospective, interdisciplinary study was carried out to explore whether patients with different organic vertigo syndromes exhibit different psychological comorbidities. Methods 68 patients with organic vertigo syndromes (benign paroxysmal positioning vertigo (BPPV) n = 20, vestibular neuritis (VN) n = 18, Menière’s disease (MD) n = 7, vestibular migraine (VM) n = 23) were compared with 30 healthy volunteers. All patients and control persons underwent structured neurological and neuro-otological testing. A structured diagnostic interview (-I) (SCID-I) and a battery of psychometric tests were used to evaluate comorbid psychiatric disorders. Results Patients
JON 2697
Introduction Nearly half of the patients presenting at specialized dizziness units show a high comorbidity with psychiatric disorders, above all with anxiety and depressive disorders [13]. In longitudinal studies, patients with
with VM and MD showed significantly higher prevalence of psychiatric comorbidity (MD = 57 %, VM = 65 %) especially with anxiety and depressive disorders, than patients with VN (22 %) and BPPV (15 %) compared to normal subjects (20 %). These elevated rates of comorbidities resulted in significantly elevated odds-ratios (OR) for the development of comorbid psychiatric disorders in general (for VM OR = 7.5, for MD OR = 5.3) and especially for anxiety disorders (for VM OR = 26.6, for MD OR = 38.7). Conclusion As a consequence, a structured psychological and psychometric testing and an interdisciplinary therapy should be proceeded in cases with complex and prolonged vertigo courses, especially in patients with VM and MD. Possible reasons of these unexpected results in VM and MD are discussed. ■ Key words vertigo · dizziness · psychiatric disorders · anxiety · depression
mixed organic and psychological symptoms are the ones most likely to remain symptomatic while also having the highest levels of handicap [15, 36]. About 70 % of dizziness patients may develop reactive psychiatric disorders, anxiety symptoms, directly after the onset of a vestibular disease; the symptoms are generally transient once the vestibular disease is resolved [3–5, 26, 36].
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Indeed, the lifetime prevalence of psychiatric disorders is heightened in classic migraine groups vs. people without migraine: depression in 23.9 % vs 10.3 % [6] anxiety disorders in 14.3–19.6 % vs 3.6 % [7]. Different explanations and suspected pathomechanisms of these findings in patients with common migraine were summarized by Silberstein and coworkers: 1) Migraine could be the cause of psychopathology, 2) psychopathological disorders could cause migraine, and 3) migraine and the psychiatric disorders associated with it could both share common genetic or environmental risk factors [8]. For patients with vestibular migraine (migrainous vertigo) to our knowledge no studies concerning psychiatric morbidity exist at the moment. Also MD patients with heightened psychological strain, which can negatively influence the course of illness, have been described. Subgroups of Menière patients were repeatedly reported to have a high comorbidity with anxiety and depressive disorders [8–10]. A subgroup of patients with MD report that (A) the attacks can be triggered or exacerbated by stress and distressing situations, and that (B) they feel subjectively heavily distressed by the attacks and their unpredictability.As a result, these patients develop frequently undetected, pronounced social and agoraphobic anxiety with avoidance behavior, which in turn can lead to strong impairment of daily activities [8–10]. In this subgroup in addition to Menière attacks patients suffer from additional somatoform dizziness that can be regarded as atypical anxiety attacks. Those attacks are falsely interpreted as organic by the patients and as well by the attending physician. In these cases the symptoms are attributed exclusively to the vestibular disorder or delayed vestibular compensation following a vestibular lesion and may lead to invasive unsuccessful treatment (e.g., gentamycin injections) [13]. Former studies described a triggering function of vestibular dysfunction for the development of psychiatric comorbidities in patients complaining of dizziness [2, 13–15]. In contrast, a recent systematic interdisciplinary study found no correlation between the presence or amount of acute or chronic vestibular dysfunction in vertigo syndromes such as benign paroxysmal positioning vertigo, vestibular neuritis, MD and vestibular migraine and pathologies on psychometric testing [6]. Not only patients with somatoform vertigo syndromes showed pathological values (anxiety, depression) but also patients with different types of organic vestibular diseases, especially the subgroup of patients with MD and VM [6]. Such a coexistence of pathological findings in psychometric scores and vestibular diseases has been described previously [3, 15]. These findings allow three possible interpretations: 1. The specific clinical symptoms lead to an increased risk of developing reactive psychiatric (somatoform) disorders (somatopsychic hypothesis).
2. The patients have “per se” and for unexplained reasons increased psychiatric comorbidity that leads to certain disorders in coping with the illness (e.g., reactive anxiety and depressive disorders). 3. In certain diseases such as migraine or Menière’s disease and anxiety or depressive disorders, common neurobiological and neuro-anatomical mechanisms play a pathogenetic role. While we have shown that the vestibular disorder itself apparently has no causal connection with the anxiety diseases and depressive disorders [3], this does not mean, however, that such connections might not exist on another (nonvestibular) level. Aim of this study was to follow the second hypothesis and analyze the question of whether there are different comorbid psychiatric disorders in patients with various organic vertigo syndromes and whether the quality of the vertigo syndrome or better the clinical phenomenology may influence the vulnerability for psychic distress and psychiatric disorders.
Methods In this prospective interdisciplinary study we recruited healthy subjects as a representative and age matched control sample through public announcements, while patients were recruited from our outpatient clinic for dizziness as well as from the wards of the Department of Neurology. Patients were included when the recurrent attack/presentation of the vestibular disorder leading to the diagnosis had occurred within the last 6 months prior to their presentation at our hospital. Patients with VN were included within seven days after the symptom onset. The aim was to include patients as early as possible after the symptom onset to minimize non-specific effects of a chronifying disease and to include patients in an acute and also patients in an active stage of the vestibular disorder. Due to the acuteness and symptom severity in vestibular neuritis, most of the patients were admitted via the emergency room, patients with BPPV, VM and MD in part were referred to our outpatient clinic because of their recurrent attacks. Furthermore, participants had to give written informed consent and were then examined at the Departments of Neurology and Psychosomatic Medicine and Psychotherapy. The study was approved by the local ethics committee according to the criteria of the declaration of Helsinki. ■ Exclusion criteria Other acute or chronic central vestibular or central ocular motor disorders with a pre-existing history of more than 6 months (e.g., due to infarctions, hemorrhages, multiple sclerosis), regular intake of benzodiazepines, barbiturates, or any other medication having an effect on the CNS within 8 days prior to study inclusion, inadequate knowledge of the German language, written or spoken, an ongoing psychotherapy, an acute psychotic disorder, acute disease of the CNS with cognitive impairment, and finally, an acute malignancy. Altogether, this prospective interdisciplinary study included 98 consecutive participants, 68 patients with organically caused vertigo disorders and 30 healthy control persons from February 2003 until February 2005. We differentiated the subgroups of patients with organic causes into (a) BPPV (n = 20), (b) VN (n = 18), (c) MD (n = 7) and (d) VM (n = 23). All participating patients and control persons
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underwent differentiated neurological, neuro-otological and psychiatric-psychosomatic testing.
use in research, because, while containing elements that increase reliability, several time sequences as beginning, progression, duration and number of attacks of the psychiatric disorders can be elevated [18].
■ Neurological and neuro-otological examinations All participants underwent a detailed diagnostic procedure consisting of clinical neurological and neuro-otological examinations including positioning maneuvers, stepping test, and neuro-orthoptic analysis (e.g., head-impulse test for the vestibulo-ocular reflex, examination with Frenzel’s glasses, head-shaking test). In addition, a series of neurophysiological investigations including fundus photography to detect tonic vestibular disorders such as ocular torsion, adjustments of the subjective visual vertical (SVV) to measure otolith dysfunction and an electro-oculography (EOG) including rotatory and caloric testing to measure semicircular canal function were performed. All patients and controls underwent the full program of clinical and neuro-physiological investigation. The neuro-physiological examinations were performed in the detailed manner as described elsewhere [16] to confirm the diagnosis based on the typical history and the clinical examination results for each disease entity. Distinction into the different diagnostic subgroups was performed as follows: (1) BPPV was diagnosed by the typical complaints of a positioning vertigo and a positive Dix-Hallpike head positioning test. Patients with complaints of positioning vertigo were not included when the Dix-Hallpike head positioning test was negative. Other causes were ruled out in all cases. (2) VN was diagnosed by three criteria: (A) the typical history, (B) the neurological signs (spontaneous nystagmus, ipsilateral body tilts, pathological head-impulse test) and (C) the neurophysiological findings such as ipsilateral tilts of SVV, ocular torsion, and ipsilateral caloric hyporesponsiveness. Again, all other causes were ruled out. (3) MD was diagnosed according to the diagnostic criteria of the American Academy of Otolaryngology [17]. (4) As there are no diagnostic guidelines for VM, these patients were diagnosed on the basis of the following criteria: (A) episodic vestibular symptoms, (B) positive history or positive family history of common migraine (according to the criteria of the International Headache Society), (C) migrainous symptoms during at least 2 attacks of vertigo, (D) migraine-precipitants before vertigo in more than 50 % of attacks (food triggers, sleep irregularities, hormonal changes) and (E) positive response to migraine medications in more than 50 % of the attacks. Furthermore, other causes for vertigo were ruled out. ■ Psychometric examinations The psychosomatic testing comprised 2 clinical interviews and a structured diagnostic interview (SCID-I) in all subjects. In addition, a psychometric test battery was used for measuring relevant psychosocial dimensions such as psychological strain (Symptom Check List 90; SCL-90R), anxiety and depression (Hospital Anxiety and Depression Scale; HADS), somatization (Screening for somatoform symptoms; SOMS) severity (Vertigo-Symptom Scale; VSS) and handicap (Vertigo Handicap Questionnaire;VHQ) caused by symptoms.In this study we focused on results of the Structural Clinical Interview (SCID-I) and the Symptom Check List 90 (SCL-90R) to determine the subjective impairment of patients due to somatic and psychiatric symptoms. The Structural Clinical Interview for DSM-IV Axis I (SCID-I) The SCID-I in its German version has been used since 1997 for patients with psychiatric disorders and is a very well known diagnostic instrument. The SCID is a semistructured interview for making the major DSM-IV Axis I diagnoses. The output of the SCID is a record of the presence or absence or sign of psychopathology of each of the disorders being considered, for current episodes and for lifetime occurrence. Thus, the SCID is a good choice as a diagnostic instrument for
Symptom-Check List 90 (SCL-90R) The SCL-90R is a standardized, self-reporting instrument that measures psychological strain on nine scales: somatization, obsessivecompulsive, interpersonal sensitivity, depression, anxiety, anger-hostility, phobic anxiety, paranoid ideation, and psychoticism. The Global Severity Index (GSI) provides information on the general degree of psychic impairment. We used the German version. Various studies have proven the validity of the scales [19]. ■ Statistical analysis Analysis of differences started with a one factorial multivariate analysis of variance (MANCOVA), which also generated univariate analysis of variance (ANOVA) followed by pair-wise post hoc tests (LSD). Age was than entered as a covariate to subtract the influence on the aim parameters. A Bonferroni correction for multiple testing had been entered in the design. Dependent variables include 10 psychometric (SCL-90 subscales) scores. To compare the relative incidence of psychiatric comorbidities, Chi-square tests were performed and to better characterize the differences between the groups additional Odds-Ratios were calculated. All computations were carried out using SPSS for Windows, version 12. Alpha error was set at 5 %.
Results The patients sample included 54 women and 44 men; average age of the entire group was 49 (± 14) years. Average age of the women was 47 (± 14) years and 51 (± 13) years for the men. For demographic data see Table 1. The healthy controls sample included 18 females and 12 males, average age of this group was 43 (± 17) years. As the mean age of the different diagnostic subgroups differed significantly (Table 1), age was entered as a covariate in a multivariate analysis design; thus the influence of age on analysis variables was subtracted before the analyses. Overall age had no significant influence on any of the parameters.
■ Results of neuro-otological testing The neuro-physiological examinations in all cases supported the diagnosis made on the basis of the patient’s history and the clinical examination. Pathological group mean values were found for the side difference on caloric testing in patients with BPPV, which was due to the fact that four patients had a secondary BPPV following a vestibular neuritis at least six months before the study inclusion. Furthermore, the patients with VN showed pathological group mean values for the side difference on caloric testing as well as pathological values for SVV and OT measurements, both as a sign of acute vestibular pathology. All other neuro-physiological measurements were within normal range.
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Table 1 Demographic data of participating patients and volunteers
N
Healthy controls BPPV Vestibular neuritis Menière’s disease Vestibular migraine Total
Fig.1 Top: Relative incidence (%) of all psychiatric comorbidities measured by the SCID-I within the different diagnostic subgroups (chi-square = 18.909, df = 4, p = 0.001). The hatched area gives a range of population based normal values. Bottom: Relative incidence (%) of the single psychiatric comorbidities measured by the SCID-I within the different diagnostic subgroups; A anxiety and phobic disorders as comorbidity (chi-square = 21.425, df = 4, p < 0.001), ICD 10: F40, F41; B depressive disorders as comorbidity (chi-square = 3.091, df = 4, p = 0.543), ICD 10: F32; C somatization disorders as comorbidity (chisquare = 7.244, df = 4, p = 0.124), ICD 10: F45; D all other psychiatric comorbidities (p = 0.340) (eating disorders, substance abuse, ICD 10: F10-F19)
%
30 20 18 7 23 98
Age (years)
30.6 20.4 18.4 7.1 23.5 100
Sex
Mean
SD
Range
Female
Male
43.43 54.25 53.83 61 43.09 48.72
16.57 12.55 10.68 11.49 8.73 14.02
22–76 24–71 36–70 42–73 29–61 22–76
18 9 11 3 13 54
12 11 7 4 10 44
All comorbidities
Relative Incidence (%)
80
60
40
20
0 HC
Relative Incidence (%)
80
BPPV
60
60
40
40
20
20
VM
Depressive disorders
0
0
b 80
Relative Incidence (%)
MD
80
Anxiety and phobic disorders
a
80
Somatization disorders
60
60
40
40
20
20
0
c
VN
Other psychiatric disorders
0 HC
■ Results of psycho-somatic examinations SCID results Using the standardized SCID interview we found significant differences between the diagnostic subgroups comprising elevated rates of psychiatric comorbidity in addition to the organic vestibular disorder for the patients with MD and VM (chi-square = 18.909, df = 4, p = 0.001; Fig. 1). The patients with VM had an overall rate of 65 % and the patients with MD a rate of 57 % for the existence of a manifest psychiatric comorbidity. In contrast to those very high rates of comorbid psychiatric disorders, patients with acute as well as with persistent vestibular deficits such as BPPV and VN (BPPV = 15 %,
BPPV
VN
MD
VM
d
HC
BPPV
VN
MD
VM
VN = 22 %) showed significantly lower percentages of psychiatric comorbid disorders in comparison to the patients with MD and VM. The results for the BPPV and VN patients were comparable to healthy controls (HC = 20 %) (see Fig. 1). In addition to the overall prevalence for psychiatric comorbidities, a significant group difference for anxiety and phobic disorders was discovered (chi-square = 21.425, df = 4, p < 0.001). Again, the patients with MD and VM showed the highest rates of comorbidity. Neither of the last three comorbidity subscales/entities (depressive disorders, somatization disorders and other disorders) revealed significant differences. Table 2 shows that these elevated rates of comorbidities resulted in significantly elevated odds ratios (OR)
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Table 2 Relative prevalences of psychiatric comorbidities and resulting ODDS ratios for the different patients in comparison to healthy controls
ODDS ratio and relative incidences for psychiatric comorbidity
HC (N = 30) BPPV (N = 20) VN (N = 18) MD (N = 7) VM (N = 23) Chi-square p
Any comorbidity
Anxiety
%
OR
%
20.0 15.0 22.2 57.1 65.2 18.909 0.001
– 0.706 1.143 5.333 7.500
3.3 – 16.7 10.0 3.222 10.0 22.2 8.286 11.1 57.1 38.667 28.6 47.8 26.580 26.1 21.425 3.091 0.000 0.543
OR
Depression
Somatization
Other
%
OR
%
OR
%
OR
– 0.556 0.625 2.000 1.765
0.0 0.0 5.6 0.0 13.0 7.244 0.124
– – – – –
10.0 0.0 0.0 0.0 8.7 4.519 0.340
– – – – 0.857
BPPV benign paroxysmal positioning vertigo; VN vestibular neuritis; MD Menière’s disease; VM vestibular migraine, HC healthy controls
for the development of comorbid psychiatric disorders in general for the patients with VM (OR of 7.5) and for the patients with MD (OR of 5.3). For the patients with BPPV and VN no elevated odds ratios were found (for BPPV: OR = 0.7, for VN: OR = 1.1). Analyzing the different subscales/entities of psychiatric comorbidity, especially the odds ratios for anxiety disorders and phobic disorders were elevated (Table 2) for the MD and VM groups.
SCL-90 results In addition to the manifest psychiatric disorders the patients were examined for psychological strain on different scales using the SCL-90-R. Significant group-differences (MANOVA: F = 2.537, df = 40;314, p < 0.001; Table 3) were found for the global severity index (GSI), anxiety, phobic anxiety, depression, somatization and psychotizism. The patients with MD and VM had the
highest scores on these scales (Fig. 2). Post hoc t-tests for specific subgroup comparisons are shown in Table 4. Patients with MD and VM had significant elevated scores for the GSI, anxiety, phobic anxiety, depression, somatization and psychotizism in comparison to the healthy controls. In addition, MD and VM patients were found to have elevated scores for the GSI, anxiety, phobic anxiety and somatization in comparison to the patients with BPPV. All other SCL-90R subscales did not reveal significant differences between the various diagnostic subgroups (Table 5). In conclusion, the recurrent organic vertigo syndromes without persisting objective vestibular deficits, MD and VM, showed a high level of psychological symptoms measured with both, the SCID-I and the SCL-90R. This indicates elevated rates and risk for manifest psychiatric disorders as well as for acute increased psychological strain.
Discussion Table 3 Multivariate analyses showing significant group differences and analyses of variance for the different subscales of the symptom checklist SCL-90 (showing significant differences for 6 of the 10 scales between the different diagnostic subgroups). For post-hoc-testing see Table 4 MANOVA/ANOVA (F-tests) F Multivariate SCL-90 – Somatization – Obsessive-compulsive – Interpersonal sensitivity – Depression – Anxiety – Hostility – Phobic anxiety – Paranoid ideation – Psychoticism – Global Severity Index (GSI)
df1
df2
P
2.537 40
314
0.000
89 89 89 89 89 89 89 89 89 89
0.000 0.069 0.166 0.002 0.000 0.223 0.000 0.061 0.045 0.000
14.033 2.261 1.661 4.468 9.766 1.454 10.053 2.343 2.545 7.628
4 4 4 4 4 4 4 4 4 4
In a recent study [3] we were unable to verify the hypothesis postulated by others that vestibular dysfunction per se has a pathological meaning for the development of somatoform/psychiatric disorders such as anxiety and depression [13–15]. The extent of pathological findings from the vestibular testing showed no correlation with the amount of psychological strain. In the current study we disclosed an unexpected distinct difference between patients with different types of vestibular vertigo syndromes such as VN and BPPV patients, on the one hand, and patients with MD and VM, on the other, comparing the various organic subgroups in terms of the psychopathological dimensions of anxiety and depression (SCID-I; SCL-90R). Further structured screening showed that these results were most readily attributable to different forms of psychiatric comorbidity in different vertigo syndromes (anxiety, phobic and depressive disorders). Patients with VM and patients
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0=low - 90 high
GSI
Anxiety
60
60
40
40
20
20 0
0
a
b Phobic Anxiety
0=low - 90 high
Fig.2 A Psychological strain measured by the Global Severity Index of the Symptom Check List 90, the differences between the diagnostic groups are significant (F = 7.880; df: 4.90; p < 0.001). B–F Psychological strain measured by different subscores of the Symptom Check List 90 with significant group differences for all shown psychometric scores: B anxiety (F = 10.099; df: 4.90; p < 0.001), C phobic anxiety (F = 10.023; df: 4.90 p < 0.001), D depression (F = 4.954, df: 4.90; p = 0.001), E somatization (F = 14.382; df: 4.90; p < 0.001) and F psychoticism (F = 2.752; df: 4.90; p = 0.033)
Depression
60
60
40
40
20
20
0
0
c
d
0=low - 90 high
Somatization
Psychotizism
60
60
40
40
20
20
0
0
e
HC
BPPV
VN
MD
f
VM
HC
BPPV
VN
MD
VM
Table 4 Post-hoc t-tests for comparison of the different diagnostic subgroups Post hoc tests for group differences SCL-90 scales
Group Differences HC-BPPV HC-VN HC-MD HC-VM BPPV-VN BPPV-MD BPPV-VM VN-MD VN-VM MD-VM
Somatization Obsessivecompulsive
Interpersonal Depression sensitivity
Anxiety
Hostility
Phobic anxiety
Paranoid ideation
Psychoticism Global Severity Index (GSI)
P 0.028 0.002 0.000 0.000 0.296 0.003 0.000 0.032 0.005 0.905
P 0.668 0.756 0.157 0.091 0.715 0.934 0.054 0.128 0.083 0.783
P 0.298 0.025 0.000 0.000 0.233 0.000 0.001 0.006 0.035 0.185
P 0.710 0.701 0.051 0.228 0.501 0.035 0.150 0.120 0.501 0.262
P 0.802 0.017 0.000 0.000 0.044 0.001 0.000 0.085 0.030 0.881
P 0.472 0.349 0.207 0.071 0.804 0.095 0.022 0.072 0.016 0.961
P 0.578 0.248 0.006 0.027 0.556 0.021 0.133 0.070 0.413 0.200
P 0.517 0.216 0.022 0.014 0.557 0.074 0.100 0.191 0.340 0.519
Table 5 Non-significant differences within the SCL-90 subscales
P 0.423 0.049 0.000 0.004 0.255 0.003 0.056 0.034 0.515 0.082
P 0.441 0.036 0.000 0.000 0.196 0.001 0.001 0.029 0.066 0.368
Diagnostic groups Controls N = 30 SCL-90 scales Obsessivecompulsive Interpersonal sensitivity Hostility Paranoid ideation
BPPV N = 20
VN N = 18
MD N=7
VM N = 23
Total N = 98
Mean
SD
Mean
SD
Mean
SD
Mean
SD
Mean
SD
Mean
SD
47.01
12.78
49.79
10.87
52.48
11.40
59.29
11.22
55.77
14.56
51.46
12.93
45.60 46.39
9.72 9.24
44.62 45.61
6.12 8.18
45.05 47.37
9.09 7.84
51.55 53.84
13.11 9.11
50.36 49.45
12.30 10.17
45.05 47.68
9.09 9.14
45.65
1.11
43.92
4.83
43.23
5.17
50.45
11.47
50.25
11.37
46.36
9.32
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with MD showed high comorbidity with anxiety and phobic disorders and depression. Among them, patients with VM suffered the most; 65 % showed manifest comorbid psychological disorders, as well as 57 % of patients with MD. In contrast, the comorbidity rates in patients with BPPV and VN were far less pronounced, corresponding roughly with the frequency of psychological and psychosomatic disorders in the general population [12]. High psychiatric comorbidity with anxiety and particularly with phobic disorders has previously been described in patients with VN [3, 15, 33], a finding which we could not verify. Likewise, a high rate of comorbidity for anxiety and depressive disorders has been reported in patients with classic migraine headaches [4–6, 22, 23] and studies on a few cases of patients with MD [9–11]. In the following for valuation and comparison we will refer to statistics from migraine without aura (i.e., headache without vertigo) or from other vertigo syndromes. Our results allow the comment on three different aspects referred to in the following questions: Can different forms of clinical symptom etiology of the organic vertigo syndromes be the cause of the increased risk of developing reactive psychiatric/somatoform disorders? Possible causes for these findings might be found in the different clinical symptom etiology of the four vertigo syndromes we investigated, BPPV,VN, MD and VM. The question to be addressed is whether or not the development of psychosomatic pathologies such as anxiety, phobic, and somatoform disorders depends on the patient’s ability to control or prevent the next vertigo attack. Comparing the four different entities of vestibular syndromes our results in conclusion suggest that the unpredictability and uncontrollable nature of VM and MD could induce a higher risk of exacerbation or acute development of a comorbid or reactive psychiatric disorder. The uncertainty of attacks seems to be as important as the relapsing character, since recurrent BPPV attacks alone do not induce a higher risk for the development of psychiatric disorders. The high amount of organic vestibular deficits in the acute phase of VN seems not to play a critical role, because the prevalence for psychiatric comorbidity was within normal range (22 %).
■ Psychiatric comorbidity per se? Patients with vestibular migraine Former investigations from 1973 to 1994 have described the personality structure of people suffering from common migraine as an obsessive, rigid, angry type [5]. In
later years, these concepts were abandoned because the studies gave too little consideration to the fact that organic disease can lead to reactive psychological disorders, which experts then wrongly interpreted as “migraine personalities” as well as a specific personality structure as formerly postulated could not be proved. This is also true for other diseases such as inflammatory bowel diseases or rheumatic disorders. In terms of individual features, some studies described an affective inhibition (alexithymic characteristics), increased irritability and interpersonal difficulties in patients with headache (migraine or tension-type headache) and an association between the chronification of symptoms with increased irritability [25]. More recent studies have investigated associations between common migraine and affective or anxiety disorders. There is repeated evidence of a high association between migraine and psychiatric disorders in clinical and community studies, most investigations examining comorbidity with depression. Migraine and depression anxiety disorders are strongly associated in the general population and in families with the strongest association for depression of “atypical subtype of migraine” and phobic anxiety syndromes [4, 5]. Numerous studies have even described two different time sequences of disorders, e.g., onset of anxiety disorders preceding onset of migraine, migraine preceding onset of major depression [4, 7]. Furthermore, in a longitudinal study a ‘bi-directional influence’ between migraine and depression has been shown with migraineurs having more than a three-fold risk of developing depression and patients with depression having a more than three-fold risk of developing migraine [7]. Similarly, an association between migraine, severe non-migrainous headache and panic-attacks was described by the same group in a subsequent study [7]. Based on our clinical experience and the psychometric outcomes of our study, we assume that patients with VM on the whole show greater anxiety, a higher psychiatric comorbidity and resulting irritability. They were considerably more heavily handicapped by the symptoms than patients with acute VN. Currently, we investigate in an ongoing prospective study if patients with acute vestibular disorders have a higher risk of developing comorbid or reactive psychiatric disorders during the further course of disease.
■ Patients with Menière’s disease Previous psychiatric history, age, sex, marital status, and education all seem to have an effect upon the onset and evolution of panic-phobic symptoms in patients with MD. This evolution is frequent in females of middle age, low level of education, long standing MD and large number of vertigo attacks [29]. A tendency toward a state of dysphoria and more striking somatizations as well as an
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elevated obsessionality score was also described in patients with MD [29]. Beside a worse quality of life in those patients, vertigo seems to have a greater influence on physical dimensions, tinnitus and hearing loss on psychological dimensions [30]. Furthermore, stress reaction seems to be an important factor associated with the triggering of symptoms. A tendency towards stresscausative behavioral characteristics in MD patients was discussed as important in the pathogenesis of an endolymphatic hydrops [9, 10]. Patients with or without active symptoms in the course of MD differ with regard to psychiatric comorbidity, as patients with active vestibular symptoms have an evidence of depression in 75 % compared to 35.5 % in the group without active symptoms [31]. These data fit the concept that frequent and unpredictive vertigo attacks increase the fear of further attacks and the feeling of being “at the mercy of the attacks”.
developing phobic avoidance behavior [14]. Similar hypotheses have been put forth by other authors [3, 36, 37]. These hypotheses in mind, one should take into consideration that vestibular dysfunction and vestibular deficits per se (e.g., VN or BPPV) do not lead to an increased risk for the development of anxiety or depressive disorders [3]. Neither the amount of the vestibular lesion nor the acuteness of occurrence were decisive factors for the development of anxiety disorders in our study. Thus, a “direct” influence of the vestibular system via a common pathway seems to be unlikely. Also the fact that patients with VM without significant persistent vestibular dysfunction presented with high psychological strain for anxiety and depression supports that view. At best a vestibular pathology could be an unspecific trigger for the further development of phobic and depressive disorders.
Do similar neuro-anatomical and neuro-physiological correlates exist in patients with migraine or MD and patients with anxiety disorders and depression? The vestibular system and the neural circuitry involved in anxiety have the following links in common: (a) the monoaminergic inputs to the vestibular system mediate the effects of anxiety on vestibular function, (b) the parabrachial nucleus network mediates emotional responses related to disordered vestibular function, (c) the widely distributed noradrenergic outflow from the locus coeruleus mediates the responsiveness of these symptoms to novel stimuli [2, 14, 32].Vestibular and visceral information as well as somatic nociceptive input converge in the parabrachial nucleus which has reciprocal connections to the central nucleus of the amygdala, and the infralimbic cortex and is under the control of higher cortical cognitive regions. Furthermore, close connections between the vestibular system and autonomic functions and respiration were described in animal studies many years ago and more recently were also observed in humans [33, 34]. Furman and co-workers [14] with respect to the monoaminergic pathways recently presented a model that postulates connections between migraine, dizziness, and anxiety. Based on neuro-anatomic and neurobiological findings, they proposed that “central vestibular activation can affect activity in monoaminergic pathways through direct connections from the vestibular nuclei to the dorsal raphe nucleus, nucleus raphe magnus, locus coeruleus, and lateral tegmental region. These changes in monoaminergic activity due to vestibular activation may both trigger migraine related symptoms and modulate activity in both pain-related and anxiety-related pathways.” These neuro-anatomical links could then lead to additive effects which influence the subjective perception of balance disorders and dizziness that could serve as an unconditioned stimulus for
Conclusions A number of papers have pointed out that patients with migraine without aura and comorbid anxiety and depressive disorders have increased risk of developing chronic vertigo disorders. According to our results, this must also be assumed for patients with vestibular migraine. It is the unpredictability and uncontrollability of the attacks that appear to be significant factors for the development of anticipation anxiety. In our experience, these patients often perceive panic-like anxiety during the attacks. Frequently the misdiagnosis of acute panic disorder is made and the vestibular migraine is overlooked as the underlying cause of the vertigo attacks. In various studies we were able to show that patients with organic vertigo syndromes and comorbid psychiatric disorders often develop somatoform dizziness syndromes as a consequence and altogether are greatly handicapped in their daily activities. Based on the findings presented here, we assume that patients with vestibular migraine and Menière’s disease have a distinctly increased risk of developing a somatoform dizziness syndrome and/or other reactive psychiatric disorders as a consequence of the organic disease compared to patients with vestibular neuritis and benign paroxysmal positioning vertigo. In addition to the damage for the patients, the health care system is saddled with increased costs due to chronification of the illness, the attending handicaps and frequent ongoing medical consultations. Differentiated interdisciplinary screening should therefore be administered to these high-risk patients early on. Particularly patients with vestibular migraine and Menière’s disease should always undergo diagnostic screening for psychiatric disorders. As a result from our findings we would recommend the use of the Vertigo Symptom Scale (VSS) and the Vertigo Handicap Questionnaire (VHQ) as clinical uncompli-
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cated and practicable screening tools. In case of pathological scores on these tools an interdisciplinary treatment and a referring to a psychologist/psychiatrist should be considered. The interesting hypotheses regarding possible neuro-anatomical and neuro-biological correlates in migraine patients and those with anxiety and depres-
sion disorders require further differentiated investigations. ■ Acknowledgments We wish to thank Anja Kühn for her help with the neuro-otological measurements. This work was supported by the Deutsche Forschungsgemeinschaft (EC 220/2-1) and Maifor University Clinic Mainz.
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