Anxiety and physical impairment in patients with central vestibular disorders.

BACKGROUND: There is increasing evidence for close interrelations between vestibular and emotional brain networks. A study in patients with bilateral peripheral vestibulopathy (BVP) showed relatively low vertigo-related anxiety (VRA), despite high physical impairment. The current working hypothesis proposes the integrity of the peripheral vestibular system as a prerequisite for development of VRA. Here we contribute by evaluating VRA and vestibular-related handicap in central vestibular disorders. METHODS: Of 6396 patients presenting in a tertiary vertigo centre, 306 were identified with four clear central vestibular disorders: pure cerebellar ocular motor disorder (COD; 61), cerebellar ataxia (CA; 63), atypical parkinsonian syndromes (APS; 28), vestibular migraine (VM; 154). Their results of the Vertigo Handicap Questionnaire (VHQ), with its subscales for anxiety and handicapped activity, were compared to those of 65 BVP patients. Postural instability was measured on a force-plate. Multivariate linear regression was used to adjust for patient demographics. RESULTS: Patients with chronic central vestibular disorders (COD, CA, APS) had relatively low VRA levels comparable to those in BVP, independent of increased handicapped activity or postural instability. Only VM patients showed significantly higher VRA, although their activity impairment and postural instability were lowest. No significant differences within chronic central vestibular disorders were found for VRA and subjective activity impairment. CONCLUSIONS: Subjective and objective vestibular-related impairment are not necessarily correlated with vestibular-related anxiety in central vestibular disorders. Our findings rather support the hypothesis that, in addition to an intact peripheral, an intact central vestibular system could also serve as a prerequisite to develop specific VRA.

Acetyl-DL-leucine in cerebellar ataxia ([18F]-FDG-PET study): how does a cerebellar disorder influence cortical sensorimotor networks?

OBJECTIVE: The aim of the study was to deepen our insights into central compensatory processes of brain networks in patients with cerebellar ataxia (CA) before and with treatment with acetyl-DL-leucine (AL) by means of resting-state [18F]-FDG-PET brain imaging. METHODS: Retrospective analyses of [18F]-FDG-PET data in 22 patients with CA (with vestibular and ocular motor disturbances) of different etiologies who were scanned before (PET A) and on AL treatment (PET B). Group subtraction analyses, e.g., for responders and non-responders, comparisons with healthy controls and correlation analyses of regional cerebral glucose metabolism (rCGM) with symptom duration, ataxia (SARA) and quality of life (QoL) scores were calculated. RESULTS: Prior to treatment rCGM was consistently downregulated at the cerebellar level and increased in multisensory cortical areas, e.g., somatosensory, primary and secondary visual (including V5, precuneus), secondary vestibular (temporal gyrus, anterior insula), and premotor/supplementary motor areas. With AL (PET B vs. A) cerebellar hypometabolism was deepened and sensorimotor hypermetabolism increased only in responders with clinical benefit, but not for the non-responders and the whole CA group. A positive correlation of ataxia improvement with rCGM was found in visual and vestibular cortices, a negative correlation in cerebellar and brainstem areas. QoL showed a positive correlation with rCGM in the cerebellum and symptom duration in premotor and somatosensory areas. CONCLUSIONS: Central compensatory processes in CA mainly involve multisensory visual, vestibular, and somatosensory networks as well as premotor/primary motor areas at the cortical level. The enhanced divergence of cortical sensorimotor up- and cerebellar downregulation with AL in responders could reflect amplification of inhibitory cerebellar mechanisms.

Vestibular syndromes after COVID-19 vaccination: A prospective cohort study.

BACKGROUND AND PURPOSE: Dizziness and vertigo are common symptoms after COVID-19-vaccination. We aimed to prospectively evaluate objective central or peripheral vestibular function in patients with dizziness, vertigo, and postural symptoms that started or worsened after COVID-19-vaccination. METHODS: Of 4137 patients who presented between January 2021 and April 2022 at the German Center for Vertigo and Balance Disorders, Ludwig Maximilian University of Munich, we identified 72 patients (mean age = 47 years) with enduring vestibular symptoms following COVID-19 vaccination. All underwent medical history-taking, and neurological and neuro-otological workup with bithermal caloric test, video head-impulse test, orthoptics, and audiometry. Diagnoses were based on international criteria. The distribution of diagnoses was compared to a cohort of 39,964 patients seen before the COVID-19 pandemic. RESULTS: Symptom onset was within the first 4 weeks postvaccination. The most prevalent diagnoses were somatoform vestibular disorders (34.7%), vestibular migraine (19.4%), and overlap syndromes of both (18.1%). These disorders were significantly overrepresented compared to the prepandemic control cohort. Thirty-six percent of patients with somatoform complaints reported a positive history of depressive or anxiety disorders. Nine patients presented with benign paroxysmal positional vertigo, three with acute unilateral vestibulopathy, and seven with different entities (vestibular paroxysmia, Ménière disease, polyneuropathy, ocular muscular paresis). Causally related central vestibular deficits were lacking. Novel peripheral vestibular deficits were found in four patients. CONCLUSIONS: Newly induced persistent vestibular deficits following COVID-19 vaccination were rare. The predominant causes of prolonged vestibular complaints were somatoform vestibular disorders and vestibular migraine, possibly triggered or aggravated by stress-related circumstances due to the COVID-19 pandemic or vaccination. An increase of other central or peripheral vestibular syndromes after COVID-19 vaccination was not observed.

Vestibular paroxysmia: clinical characteristics and long-term course.

In 2016, the Bárány Society defined new diagnostic criteria for the neurovascular compression syndrome of the eighth nerve, called "vestibular paroxysmia" (VP), differentiating between definite (dVP) and probable (pVP) forms. The aim of this study was (1) to describe clinical symptoms and laboratory findings in a well-diagnosed large patient cohort according to those criteria, and (2) to evaluate the long-term course over years in dVP. We identified 146 patients (73 dVP, 73 pVP) from our tertiary dizziness center registry. Data of structured history-taking, clinical neurological, neuro-ophthalmological/-otological examinations as well as MRI imaging were extracted for analyses. Overall, attack frequency ranged between 5 and 30 attacks per day; spinning vertigo was the most frequent type. In two-thirds of patients, attacks occurred spontaneously; in one-quarter, they were triggered by head movements. The majority (approximately 70%) reported no accompanying symptoms; in those with symptoms, mild unilateral cochlear symptoms prevailed. One-third of patients initially showed hyperventilation-induced nystagmus without specific direction, and a deviation of the subjective visual vertical between 3° and 6°. Complete loss of peripheral vestibular function was never evident. dVP and pVP significantly differed concerning the vertigo type, e.g., spinning vertigo was more frequent in dVP. Fortunately, three-quarters of dVP patients remained attack-free during follow-up (mean 4.8 years, standardized questionnaire), more than half of them even without any medication. Patients with ongoing attacks showed significantly higher attack frequency at baseline, but reported persistent frequency reduction. Overall, the long-term prognosis of VP appears favorable, not necessarily requiring ongoing treatment.

Chronic vestibular syndromes in the elderly: Presbyvestibulopathy-an isolated clinical entity?

BACKGROUND AND PURPOSE: Recently, the Classification Committee of the Bárány Society defined the new syndrome of "presbyvestibulopathy" for elderly patients with chronic vestibular symptoms due to a mild bilateral peripheral vestibular hypofunction. However, control of stance and gait requires multiple functioning systems, for example, the somatosensory, visual, auditory, musculoskeletal, and cardio- and cerebrovascular systems. The aim of this cross-sectional database-driven study was to evaluate the frequency and characteristics of presbyvestibulopathy and additional gait-relevant comorbidities. METHODS: In total, 707 patients aged ≥60 years with chronic vertigo/dizziness were admitted to our tertiary hospital and received detailed neurological, neuro-orthoptic, and laboratory audiovestibular examination. Medical history, comorbidities, functional impairment, and quality of life (Dizziness Handicap Inventory [DHI], European Quality of Life Scale, Vestibular Activities and Participation) were compared between presbyvestibulopathy and bilateral vestibulopathy in a matched-paired study. RESULTS: In 95.5% of patients, complaints were better accounted for by another vestibular, neurological, cardiac, or psychiatric disease, and 32 patients (4.5%) met the diagnostic criteria for presbyvestibulopathy. Of these 32 patients, the majority showed further relevant comorbidities in other sensorimotor systems. Only one patient of 707 had "isolated" presbyvestibulopathy (0.14%). The mean total DHI scores indicated lower moderate impairment in presbyvestibulopathy than in bilateral vestibulopathy (40.6 vs. 49.0), which was confirmed by significant differences in the matched-paired analysis (p < 0.001). CONCLUSIONS: Isolated presbyvestibulopathy is a very rare entity. It is regularly accompanied by other multisensory dysfunctions. These results indicate a potential role of mild vestibular hypofunction as a cofactor in multifactorial impairment. Thus, patients should be treated in an interdisciplinary setting with an awareness of diverse comorbidities.

White matter volume loss drives cortical reshaping after thalamic infarcts.

OBJECTIVE: The integration of somatosensory, ocular motor and vestibular signals is necessary for self-location in space and goal-directed action. We aimed to detect remote changes in the cerebral cortex after thalamic infarcts to reveal the thalamo-cortical connections necessary for multisensory processing and ocular motor control. METHODS: Thirteen patients with unilateral ischemic thalamic infarcts presenting with vestibular, somatosensory, and ocular motor symptoms were examined longitudinally in the acute phase and after six months. Voxel- and surface-based morphometry were used to detect changes in vestibular and multisensory cortical areas and known hubs of central ocular motor processing. The results were compared with functional connectivity data in 50 healthy volunteers. RESULTS: Patients with paramedian infarcts showed impaired saccades and vestibular perception, i.e., tilts of the subjective visual vertical (SVV). The most common complaint in these patients was double vision or vertigo / dizziness. Posterolateral thalamic infarcts led to tilts of the SVV and somatosensory deficits without vertigo. Tilts of the SVV were higher in paramedian compared to posterolateral infarcts (median 11.2° vs 3.8°). Vestibular and ocular motor symptoms recovered within six months. Somatosensory deficits persisted. Structural longitudinal imaging showed significant volume reduction in subcortical structures connected to the infarcted thalamic nuclei (vestibular nuclei region, dentate nucleus region, trigeminal root entry zone, medial lemniscus, superior colliculi). Volume loss was evident in connections to the frontal, parietal and cingulate lobes. Changes were larger in the ipsilesional hemisphere but were also detected in homotopical regions contralesionally. The white matter volume reduction led to deformation of the cortical projection zones of the infarcted nuclei. CONCLUSIONS: White matter volume loss after thalamic infarcts reflects sensory input from the brainstem as well the cortical projections of the main affected nuclei for sensory and ocular motor processing. Changes in the cortical geometry seem not to reflect gray matter atrophy but rather reshaping of the cortical surface due to the underlying white matter atrophy.

Reorganization of sensory networks after subcortical vestibular infarcts: A longitudinal symptom-related voxel-based morphometry study.

BACKGROUND AND PURPOSE: We aimed to delineate common principles of reorganization after infarcts of the subcortical vestibular circuitry related to the clinical symptomatology. Our hypothesis was that the recovery of specific symptoms is associated with changes in distinct regions within the core vestibular, somatosensory, and visual cortical and subcortical networks. METHODS: We used voxel- and surface-based morphometry to investigate structural reorganization of subcortical and cortical brain areas in 42 patients with a unilateral, subcortical infarct with vestibular and ocular motor deficits in the acute phase. The patients received structural neuroimaging and clinical monitoring twice (acute phase and after 6 months) to detect within-subject changes over time. RESULTS: In patients with vestibular signs such as tilts of the subjective visual vertical (SVV) and ocular torsion in the acute phase, significant volumetric increases in the superficial white matter around the parieto-opercular (retro-)insular vestibular cortex (PIVC) were found at follow-up. In patients with SVV tilts, spontaneous nystagmus, and rotatory vertigo in the acute phase, gray matter volume decreases were located in the cerebellum and the visual cortex bilaterally at follow-up. Patients with saccade pathology demonstrated volumetric decreases in cerebellar, thalamic, and cortical centers for ocular motor control. CONCLUSIONS: The findings support the role of the PIVC as the key hub for vestibular processing and reorganization. The volumetric decreases represent the reciprocal interaction of the vestibular, visual, and ocular motor systems during self-location and egomotion detection. A modulation in vestibular and ocular motor as well as visual networks was induced independently of the vestibular lesion site.

Intravenous Delayed Gadolinium-Enhanced MR Imaging of the Endolymphatic Space: A Methodological Comparative Study.

In-vivo non-invasive verification of endolymphatic hydrops (ELH) by means of intravenous delayed gadolinium (Gd) enhanced magnetic resonance imaging of the inner ear (iMRI) is rapidly developing into a standard clinical tool to investigate peripheral vestibulo-cochlear syndromes. In this context, methodological comparative studies providing standardization and comparability between labs seem even more important, but so far very few are available. One hundred eight participants [75 patients with Meniere's disease (MD; 55.2 ± 14.9 years) and 33 vestibular healthy controls (HC; 46.4 ± 15.6 years)] were examined. The aim was to understand (i) how variations in acquisition protocols influence endolymphatic space (ELS) MR-signals; (ii) how ELS quantification methods correlate to each other or clinical data; and finally, (iii) how ELS extent influences MR-signals. Diagnostics included neuro-otological assessment, video-oculography during caloric stimulation, head-impulse test, audiometry, and iMRI. Data analysis provided semi-quantitative (SQ) visual grading and automatic algorithmic quantitative segmentation of ELS area [2D, mm2] and volume [3D, mm3] using deep learning-based segmentation and volumetric local thresholding. Within the range of 0.1-0.2 mmol/kg Gd dosage and a 4 h ± 30 min time delay, SQ grading and 2D- or 3D-quantifications were independent of signal intensity (SI) and signal-to-noise ratio (SNR; FWE corrected, p < 0.05). The ELS quantification methods used were highly reproducible across raters or thresholds and correlated strongly (0.3-0.8). However, 3D-quantifications showed the least variability. Asymmetry indices and normalized ELH proved the most useful for predicting quantitative clinical data. ELH size influenced SI (cochlear basal turn p < 0.001), but not SNR. SI could not predict the presence of ELH. In conclusion, (1) Gd dosage of 0.1-0.2 mmol/kg after 4 h ± 30 min time delay suffices for ELS quantification. (2) A consensus is needed on a clinical SQ grading classification including a standardized level of evaluation reconstructed to anatomical fixpoints. (3) 3D-quantification methods of the ELS are best suited for correlations with clinical variables and should include both ears and ELS values reported relative or normalized to size. (4) The presence of ELH increases signal intensity in the basal cochlear turn weakly, but cannot predict the presence of ELH.

Structural reorganization of the cerebral cortex after vestibulo-cerebellar stroke.

OBJECTIVE: Structural reorganization following cerebellar infarcts is not yet known. This study aimed to demonstrate structural volumetric changes over time in the cortical vestibular and multisensory areas (i.e., brain plasticity) after acute cerebellar infarcts with vestibular and ocular motor symptoms. Additionally, we evaluated whether structural reorganization in the patients topographically correlates with cerebello-cortical connectivity that can be observed in healthy participants. METHODS: We obtained high-resolution structural imaging in seven patients with midline cerebellar infarcts at two time points. These data were compared to structural imaging of a group of healthy age-matched controls using voxel-based morphometry (2×2 ANOVA approach). The maximum overlap of the infarcts was used as a seed region for a separate resting-state functional connectivity analysis in healthy volunteers. RESULTS: Volumetric changes were detected in the multisensory cortical vestibular areas around the parieto-opercular and (retro-) insular cortex. Furthermore, structural reorganization was evident in parts of the frontal, temporal, parietal, limbic, and occipital lobes and reflected functional connections between the main infarct regions in the cerebellum and the cerebral cortex in healthy individuals. CONCLUSIONS: This study demonstrates structural reorganization in the parieto-opercular insular vestibular cortex after acute vestibulo-cerebellar infarcts. Additionally, the widely distributed structural reorganization after midline cerebellar infarcts provides additional in vivo evidence for the multifaceted contribution of cerebellar processing to cortical functions that extend beyond vestibular or ocular motor function.

Global multisensory reorganization after vestibular brain stem stroke.

OBJECTIVE: Patients with acute central vestibular syndrome suffer from vertigo, spontaneous nystagmus, postural instability with lateral falls, and tilts of visual vertical. Usually, these symptoms compensate within months. The mechanisms of compensation in vestibular infarcts are yet unclear. This study focused on structural changes in gray and white matter volume that accompany clinical compensation. METHODS: We studied patients with acute unilateral brain stem infarcts prospectively over 6 months. Structural changes were compared between the acute phase and follow-up with a group of healthy controls using voxel-based morphometry. RESULTS: Restitution of vestibular function following brain stem infarcts was accompanied by downstream structural changes in multisensory cortical areas. The changes depended on the location of the infarct along the vestibular pathways in patients with pathological tilts of the SVV and on the quality of the vestibular percept (rotatory vs graviceptive) in patients with pontomedullary infarcts. Patients with pontomedullary infarcts with vertigo or spontaneous nystagmus showed volumetric increases in vestibular parietal opercular multisensory and (retro-) insular areas with right-sided preference. Compensation of graviceptive deficits was accompanied by adaptive changes in multiple multisensory vestibular areas in both hemispheres in lower brain stem infarcts and by additional changes in the motor system in upper brain stem infarcts. INTERPRETATION: This study demonstrates multisensory neuroplasticity in both hemispheres along with the clinical compensation of vestibular deficits following unilateral brain stem infarcts. The data further solidify the concept of a right-hemispheric specialization for core vestibular processing. The identification of cortical structures involved in central compensation could serve as a platform to launch novel rehabilitative treatments such as transcranial stimulations.

Primary or secondary chronic functional dizziness: does it make a difference? A DizzyReg study in 356 patients.

In 2017, the term "persistent postural-perceptual dizziness" (PPPD) was coined by the Bárány Society, which provided explicit criteria for diagnosis of functional vertigo and dizziness disorders. PPPD can originate secondarily after an organic disorder (s-PPPD) or primarily on its own, in the absence of somatic triggers (p-PPPD). The aim of this database-driven study in 356 patients from a tertiary vertigo center was to describe typical demographic and clinical features in p-PPPD and s-PPPD patients. Patients underwent detailed vestibular testing with neurological and neuro-orthoptic examinations, video-oculography during water caloric stimulation, video head-impulse test, assessment of the subjective visual vertical, and static posturography. All patients answered standardized questionnaires (Dizziness Handicap Inventory, DHI; Vestibular Activities and Participation, VAP; and Euro-Qol-5D-3L). One hundred and ninety-five patients (55%) were categorized as p-PPPD and 162 (45%) as s-PPPD, with female gender slightly predominating (♀:♂ = 56%:44%), particularly in the s-PPPD subgroup (64%). The most common somatic triggers for s-PPPD were benign paroxysmal positional vertigo (27%), and vestibular migraine (24%). Overall, p-PPPD patients were younger than s-PPPD patients (44 vs. 48 years) and showed a bimodal age distribution with an additional early peak in young adults (about 30 years of age) beside a common peak at the age of 50-55. The most sensitive diagnostic tool was posturography, revealing a phobic sway pattern in 50% of cases. s-PPPD patients showed higher handicap and functional impairment in DHI (47 vs. 42) and VAP (9.7 vs. 8.9). There was no difference between both groups in EQ-5D-3L. In p-PPPD, anxiety (20% vs. 10%) and depressive disorders (25% vs. 9%) were more frequent. This retrospective study in a large cohort showed relevant differences between p- and s-PPPD patients in terms of demographic and clinical features, thereby underlining the need for careful syndrome subdivision for further prospective studies.

Direct comparison of activation maps during galvanic vestibular stimulation: A hybrid H2[15 O] PET-BOLD MRI activation study.

Previous unimodal PET and fMRI studies in humans revealed a reproducible vestibular brain activation pattern, but with variations in its weighting and expansiveness. Hybrid studies minimizing methodological variations at baseline conditions are rare and still lacking for task-based designs. Thus, we applied for the first time hybrid 3T PET-MRI scanning (Siemens mMR) in healthy volunteers using galvanic vestibular stimulation (GVS) in healthy volunteers in order to directly compare H215O-PET and BOLD MRI responses. List mode PET acquisition started with the injection of 750 MBq H215O simultaneously to MRI EPI sequences. Group-level statistical parametric maps were generated for GVS vs. rest contrasts of PET, MR-onset (event-related), and MR-block. All contrasts showed a similar bilateral vestibular activation pattern with remarkable proximity of activation foci. Both BOLD contrasts gave more bilateral wide-spread activation clusters than PET; no area showed contradictory signal responses. PET still confirmed the right-hemispheric lateralization of the vestibular system, whereas BOLD-onset revealed only a tendency. The reciprocal inhibitory visual-vestibular interaction concept was confirmed by PET signal decreases in primary and secondary visual cortices, and BOLD-block decreases in secondary visual areas. In conclusion, MRI activation maps contained a mixture of CBF measured using H215O-PET and additional non-CBF effects, and the activation-deactivation pattern of the BOLD-block appears to be more similar to the H215O-PET than the BOLD-onset.

Coronary artery calcification score in migraine patients.

Epidemiological studies have shown an increased risk of cardiovascular events in migraineurs. The pathophysiological mechanisms of this observation remain largely unknown. Recent genetic and epidemiologic studies suggest, that atherosclerosis might be the overlapping pathophysiological mechanism in migraine and coronary heart disease. The aim of the present study was to evaluate if the increased cardiovascular risk in migraineurs is attributed to an increased coronary artery calcification. For this the coronary artery calcium score was assessed by computed tomography of the heart in 1.437 patients of which 337 were migraineurs. All patients had a similar cardiovascular risk profile, so that the risk for coronary calcifications could be considered similar between migraineurs and non-migraineurs. The results showed no significant differences in the amount of coronary calcifications in patients with or without migraine. This suggests that a more pronounced coronary artery calcification, as a surrogate marker of coronary atherosclerosis, does not underlie the increased cardiovascular risk in migraineurs. A distinct common pathophysiological mechanism in migraine and coronary heart disease such as endothelial dysfunction or vasospasm should be discussed instead. However, it has to be considered, that the coronary artery calcification score does not indicate the total risk of atherosclerotic changes in the coronary arteries.

Neurologists' Assessment of Mental Comorbidity in Patients With Vertigo and Dizziness in Routine Clinical Care-Comparison With a Structured Clinical Interview.

Background: Mental health comorbidities are frequent in patients with vertigo and dizziness. The current study was conducted in a specialized interdisciplinary university center for vertigo and dizziness. Clinical routines consist of a structured work-up in which neuro-otological and neurological tests are performed to first detect possible organic vestibular deficits. In addition, psychiatric disorders and comorbidities are considered. The study aimed to evaluate neurologists' awareness of psychiatric next to somatic disorders within patients' first examination in terms of diagnostic congruence between neurologists' diagnoses and structured clinical assessment of mental disorders. Methods: The study involved 392 patients. Diagnostic evaluation included (a) structured history-taking (including psychosocial anamnesis), neurological, and neuro-otological diagnostics conducted by neurologists and (b) a structured clinical interview for mental disorders (SCID-I) conducted by psychologists and final-year medical or psychology students. Cohen's Kappa was calculated to determine agreement rates regarding depression and anxiety disorders; additionally, sensitivity and specificity were evaluated. Results: Neurologists' assessments led to at least one psychiatric diagnosis among the main diagnoses in 40 (10.2 %) patients, whereas the structured clinical interview led to at least one DSM-IV psychiatric diagnosis in 174 (44.4%) of the patients. Agreement was low (κ < 0.2); sensitivity was low (15%) but specificity was high (98%). Conclusions: Agreement between the diagnosis of neurologists and structured clinical interviews for psychiatric disorders is low. Since psychiatric disorders are frequent in vertigo and dizziness and tend to take a chronic course, improving early recognition and implementing appropriate care concepts is vital.

Multicenter data banking in management of dizzy patients: first results from the DizzyNet registry project.

PURPOSE: Comprehensive phenotypical data across countries is needed to understand the determinants, prognosis and consequences of vestibular disease. The registry is a data repository for the members of the European DizzyNet. We report results from a pilot study using data from Turkey and Germany. METHODS: The pilot study included a convenience sample of patients aged 18 or above referred to Ege University Medical School Hospital, Dokuz Eylül University Hospital, Izmir, Turkey, and the German Center for German Center for Vertigo and Balance Disorders, University on Munich, Germany, with symptoms of vertigo or dizziness. Health-related quality of life was assessed with the EQ5-D and the Dizziness Handicap Inventory (DHI). To obtain comparable groups we matched data from the two countries for age, sex and diagnosis by propensity score. RESULTS: We included 80 adult patients, 40 from each country (60% female, mean age 54.1, SD 12.4). Matching was successful. Vestibular migraine (34%) was the most frequent diagnosis, followed by benign paroxysmal positional vertigo (29%) and Menière's disease (12%). Clinical signs and symptoms were comparable in both countries. Patients from Turkey were more likely to report headaches (65 vs. 32%) and to show gait unsteadiness (51 vs. 5%). Patients from Germany reported significantly higher quality of life and lower values of the DHI score. CONCLUSIONS: Sharing data facilitates research, enhances translation from basic science into clinical applications, and increases transparency. The DizzyNet registry is a first step to data sharing in vestibular research across Europe.

Course and predictors of DSM-5 somatic symptom disorder in patients with vertigo and dizziness symptoms - A longitudinal study.

BACKGROUND: Somatic symptom disorder (SSD) is a diagnosis that was newly included in DSM-5. Currently, data on the course of SSD are largely lacking. The present study aimed to evaluate the natural course of SSD in a one-year follow-up study in patients with vertigo and dizziness (VD) symptoms. METHODS: We investigated n=239 outpatients presenting in a tertiary care neurological setting over a one-year period. Patients had a medical examination at baseline and completed self-report questionnaires, which were re-assessed after 12months. DSM-5 SSD was assigned retrospectively. We evaluated the prevalence of SSD at baseline and 12-month follow-up and investigated predictors of the persistence of SSD during the study period. RESULTS: The prevalence rate of SSD was 36% at baseline and 62% at 12-months follow-up. The persistence rate of SSD was 82% and the incidence rate was high, leading to a markedly increased prevalence rate at follow-up. Risk factors for persistent SSD were a self-concept of bodily weakness (OR: 1.52, 95% CI: 1.30-1.78) and an increase of depression during the study period (OR: 1.11, 95% CI: 1.02-1.22). Further, the diagnosis of an anxiety disorder (OR: 7.52, 95% CI: 1.17-48.23) or both anxiety and depressive disorder (OR: 23.14, 95% CI: 2.14-249.91) at baseline were significant predictors. CONCLUSIONS: Our findings point out that SSD is highly prevalent in patients with VD symptoms, the incidence of the disorder widely outweighs its remission. Potential predictors of a persistence of SSD are discussed and can be chosen as a focus in therapy.