Sandra Bense

Psychiatric comorbidity in different organic vertigo syndromes

ObjectiveA 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.Methods68 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.ResultsPatients 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).ConclusionAs 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.

Sensory system interactions during simultaneous vestibular and visual stimulation in PET

The patterns of regional cerebral blood flow (rCBF) increases and decreases in PET were compared for unimodal vestibular, unimodal visual, and for simultaneous vestibular and visual stimulation. Thirteen healthy volunteers were exposed to a) caloric vestibular stimulation, b) small‐field visual motion stimulation in roll, c) simultaneous caloric vestibular and visual pattern stimulation. Unimodal vestibular stimulation led to activations of vestibular cortex areas, in particular the parieto‐insular vestibular cortex (PIVC), and concurrent deactivations of visual cortical areas [Brodmann area (BA) 17–19]. Unimodal visual motion stimulation led to activations of the striate visual cortex and the motion‐sensitive area in the middle temporal/middle occipital gyri (BA 19/37) with concurrent deactivations in the PIVC. Simultaneous bimodal stimulation resulted in activations of the cortical representation of both sensory modalities. In the latter condition activations and deactivations were significantly smaller compared to unimodal stimulation. The findings are consistent with the concept of an inhibitory reciprocal vestibulo‐visual interaction in all three stimulus conditions. Hum. Brain Mapping 16:92–103, 2002.

Interaction of somatoform and vestibular disorders

Background: The high coincidence of organic vestibular and somatoform vertigo syndromes has appeared to support pathogenic models showing a strong linkage between them. It was hypothesised that a persisting vestibular dysfunction causes the development of anxiety disorders. Objective: To determine the relation between vestibular deficits and somatoform vertigo disorders in an interdisciplinary prospective study. Methods: Participants were divided into eight diagnostic groups: healthy volunteers (n = 26) and patients with benign paroxysmal positioning vertigo (BPPV, n = 11), vestibular neuritis (n = 11), Menière’s disease (n = 7), vestibular migraine (n = 15), anxiety (n = 23), depression (n = 12), or somatoform disorders (n = 22). Neuro-otological diagnostic procedures included electro-oculography with rotatory and caloric testing, orthoptic examination with measurements of subjective visual vertical (SVV) and ocular torsion, and a neurological examination. Psychosomatic diagnostic procedures comprised interviews and psychometric instruments. Results: Patients with BPPV (35.3%) and with vestibular neuritis (52.2%) had pathological test values on caloric irrigation (p<0.001). Otolith dysfunction with pathological tilts of SVV and ocular torsion was found only in patients with vestibular neuritis (p<0.001). Patients with Menière’s disease, vestibular migraine, and psychiatric disorders showed normal parameters for vestibular testing but pathological values for psychometric measures. There was no correlation between pathological neurological and pathological psychometric parameters. Conclusions: High anxiety scores are not a result of vestibular deficits or dysfunction. Patients with Menière’s disease and vestibular migraine but not vestibular deficits showed the highest psychiatric comorbidity. Thus the course of vertigo syndromes and the possibility of a pre-existing psychopathological personality should be considered pathogenic factors in any linkage between organic and psychometric vertigo syndromes.

Visual-Vestibular and Visuovisual Cortical Interaction

Abstract: PET and fMRI studies have revealed that excitation of the vestibular system by caloric or galvanic stimulation not only activates the parietoinsular vestibular cortex but also bilaterally deactivates the occipital visual cortex. Likewise, visual motion stimulation not only activates the visual cortex but also deactivates the parietoinsular vestibular cortex. These findings are functionally consistent with the hypothesis of an inhibitory reciprocal visual‐vestibular interaction for spatial orientation and motion perception. Transcallosal visuovisual interaction between the two hemispheres was found by using half‐field visual motion stimulation: activation of motion‐sensitive areas hMT/V5 and deactivations of the primary visual cortex contralateral to the stimulated hemisphere. The functional significance of these inter‐ and intra‐sensory interactions could be that they (A) allow a shift of the sensorial weight between two incongruent sensory inputs and (B) ensure a correspondence of the two hemispheres during evaluation of contradictory motion stimulation of the right and left hemifields. In terms of mathematical modeling, these findings may reflect the concepts of a sensory conflict mechanism or a mismatch between expected and actual sensory input.

Metabolic changes in vestibular and visual cortices in acute vestibular neuritis

Five right‐handed patients with a right‐sided vestibular neuritis were examined twice with fluorodeoxyglucose positron emission tomography while lying supine with eyes closed: once during the acute stage (mean, 6.6 days) and then 3 months later when central vestibular compensation had occurred. Regional cerebral glucose metabolism (rCGM) was significantly increased (p < 0.001 uncorrected) during the acute stage in multisensory vestibular cortical and subcortical areas (parietoinsular vestibular cortex in the posterior insula, posterolateral thalamus, anterior cingulate gyrus [Brodmann area 32/24], pontomesencephalic brainstem, hippocampus). Simultaneously, there was a significant rCGM decrease in the visual (Brodmann area 17 to 19) and somatosensory cortex areas in the postcentral gyrus as well as in parts of the auditory cortex (transverse temporal gyrus). Fluorodeoxyglucose positron emission tomography thus allows imaging of the cortical activation pattern that is induced by unilateral peripheral vestibular loss. It was possible to demonstrate that the central vestibular system including the vestibular cortex exhibits a visual‐vestibular activation–deactivation pattern during the acute stage of vestibular neuritis similar to that in healthy volunteers during unilateral labyrinthine stimulation. Contrary to experimental vestibular stimulation, the activation of the vestibular cortex was not bilateral but was unilateral and contralateral to the right‐sided labyrinthine failure. Ann Neurol 2004

Hemifield visual motion stimulation: an example of interhemispheric crosstalk.

Coherent motion stimulation of the right or left visual hemifield was performed in nine healthy volunteers in order to investigate interhemispheric visuo-visual interaction by means of functional magnetic resonance imaging. The vertical edge of the motion pattern field was located 8° distant from the fixation point to avoid stimulating the vertical meridian, which is represented retinotopically in both hemispheres. Bilateral activation was significant in the middle occipital gyrus (motion-sensitive middle temporal/middle superior temporal areas; BA 19/37). A negative signal change was found in the primary visual cortex including the lingual and fusiform gyri (BA 18/17) and the occipital white matter containing the optic radiation contralateral to the stimulated hemisphere. These data are most compatible with an interhemispheric transfer of visual motion information, most likely through the corpus callosum. Transcallosal transfer of visual motion information, evident as increases (BA 19/37) and decreases (BA 18/17) of the fMRI signals, may be functionally significant for the processing of motion perception.

Neural correlates of hemispheric dominance and ipsilaterality within the vestibularsystem

Earlier functional imaging studies on the processing of vestibular information mainly focused on cortical activations due to stimulation of the horizontal semicircular canals in right-handers. Two factors were found to determine its processing in the temporo-parietal cortex: a dominance of the non-dominant hemisphere and an ipsilaterality of the neural pathways. In an investigation of the role of these factors in the vestibular otoliths, we used vestibular evoked myogenic potentials (VEMPs) in a fMRI study of monaural saccular-otolith stimulation. Our aim was to (1) analyze the hemispheric dominance for saccular-otolith information in healthy left-handers, (2) determine if there is a predominance of the ipsilateral saccular-otolith projection, and (3) evaluate the impact of both factors on the temporo-parieto-insular activation pattern. A block design with three stimulation and rest conditions was applied: (1) 102 dB-VEMP stimulation; (2) 65 dB-control-acoustic stimulation, (3) 102 dB-white-noise-control stimulation. After subtraction of acoustic side effects, bilateral activations were found in the posterior insula, the superior/middle/transverse temporal gyri, and the inferior parietal lobule. The distribution of the saccular-otolith activations was influenced by the two factors but with topographic disparity: whereas the inferior parts of the temporo-parietal cortex were mainly influenced by the ipsilaterality of the pathways, the upper parts reflected the dominance of the non-dominant hemisphere. This is in contrast to the processing of acoustic stimulation, which showed a predominance of the contralateral pathways. Our study proves the importance of the hemispheric preponderance also in left-handers, which is of relevance in the superior parts of the insula gyrus V, the inferior parietal lobule, and the superior temporal gyri.

Brainstem and cerebellar fMRI-activation during horizontal and vertical optokinetic stimulation.

Animal studies have shown that not only cortical, but also brainstem and cerebellar areas are involved in the initiation and generation of optokinetic nystagmus (OKN), e.g., cortico-(pretecto)pontine-olivo-cerebellar pathways. The aim of this fMRI study was to identify and differentiate brainstem and cerebellar areas involved in horizontal and vertical OKN (h/vOKN) in humans. In a group of nine healthy volunteers, hOKN and vOKN were statistically compared with a stationary control condition. There were common activated regions for hOKN and vOKN directions located in the transition zone between the posterior thalamus and the mesencephalon bilaterally covering the pretectal nucleus complex, which is known to be a major structure within the afferent branch of the optokinetic system. Furthermore, during hOKN, activation occurred bilaterally in the mediodorsal and dorsolateral ponto-medullary brainstem, which could be best attributed to the reticular formation, especially the paramedian pontine reticular formation (PPRF). For vOKN, additional activated areas in the dorsal mesencephalic brainstem could be best localized to the ocular motor nuclei and the rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF). For both OKN directions, the cerebellar activation was localized in the oculomotor vermis (declive VI, folium and tuber VIIA/B, in part pyramis VIIIA), and the flocculus bilaterally as well as widespread in the cerebellar hemispheres. In conclusion, fMRI allowed first attributions of neuronal substrates in the cerebellum and brainstem to hOKN and vOKN in humans. Consistent with the animal data, the dorsal ponto-medullary routes were involved bilaterally for hOKN, whereas the rostral mesencephalic routes were involved for vOKN.

18F-fluorodeoxyglucose hypometabolism in cerebellar tonsil and flocculus in downbeat nystagmus.

A patient with downbeat nystagmus was examined by 18F-fluorodeoxyglucose-positron emission tomography once while off and twice while on successful treatment with 4-aminopyridine. All positron emission tomography scans of the patient showed a reduced cerebral glucose metabolism bilaterally in the region of the cerebellar tonsil and flocculus/paraflocculus when compared with a normal database of the whole brain. An additional region-of-interest analysis revealed that 4-aminopyridine treatment lessened the hypometabolism. This finding supports the hypothesis that the cerebellar tonsil and (para-) flocculus play a crucial role in downbeat nystagmus. The hypometabolism might reflect reduced inhibition or even disinhibition of the circuits to the vestibular nuclei, thus causing downbeat nystagmus. The reduced hypometabolism during treatment probably indicates an improvement of the cerebellar inhibition.

Rollvection versus linearvection: Comparison of brain activations in PET

We conducted a PET study to directly compare the differential effects of visual motion stimulation that induced either rollvection about the line of sight or forward linearvection along this axis in the same subjects. The main question was, whether the areas that respond to vection are identical or separate and distinct for rollvection and linearvection. Eleven healthy volunteers were exposed to large‐field (100° × 60°) visual motion stimulation consisting of (1) dots accelerating from a focus of expansion to the edge of the screen (forward linearvection) and (2) dots rotating counterclockwise in the frontal plane (clockwise rollvection). These two stimuli, which induced apparent self‐motion in all subjects, were compared to each other and to a stationary visual pattern. Linearvection and rollvection led to bilateral activations of visual areas including medial parieto‐occipital (PO), occipito‐temporal (MT/V5), and ventral occipital (fusiform gyri) cortical areas, as well as superior parietal sites. Activations in the polar visual cortex around the calcarine sulcus (BA 17, BA 18) were larger and more significant during linearvection. Temporo‐parietal sites displayed higher activity levels during rollvection. Differential activation of PO or MT/V5 was not found. Both stimuli led to simultaneous deactivations of retroinsular regions (more pronounced during linearvection); this is compatible with an inhibitory interaction between the visual and the vestibular systems for motion perception. Hum. Brain Mapp. 21:143–153, 2004.