A retrospective study was conducted on 90 patients with episodic vertigo that could be related to migraine as the most probable pathomechanism. Since the majority of the patients did not fulfill the criteria of the International Headache Society (IHS) for basilar migraine, the diagnosis was substantiated by disease course, medical efficacy in treating (ergotamines) and preventing (metoprolol, flunarizine) attacks, ocular motor abnormalities in the symptom-free interval, and careful exclusion of the most relevant differential diagnoses, such as transient ischemic attacks, Menière's disease, and vestibular paroxysmia. The following clinical features were elaborated. The initial manifestation could occur at any time throughout life, with a peak in the fourth decade in men and a "plateau" between the third and fifth decades in women. The duration of rotational (78%) and/or to-and-fro vertigo (38%) could last from a few seconds to several hours or, less frequently, even days; duration of a few minutes or of several hours was most frequent. Monosymptomatic audiovestibular attacks (78%) occurred as vertigo associated with auditory symptoms in only 16%. Vertigo was not associated with headache in 32% of the patients. In the symptom-free interval 66% of the patients showed mild central ocular motor signs such as vertical (48%) and/or horizontal (22%) saccadic pursuit, gaze-evoked nystagmus (27%), moderate positional nystagmus (11%), and spontaneous nystagmus (11%). Combinations with other forms of migraine were found in 52%. Thus, migraine is a relevant differential diagnosis for episodic vertigo. According to the criteria of the IHS, only 7.8% of these patients would be diagnosed as having basilar migraine. However, to ensure that at least those presenting with monosymptomatic episodic vertigo (78% in our study) receive effective treatment, we propose the use of the more appropriate term "vestibular migraine."

The aim of this (15)O-labelled H(2)O bolus positron emission tomography (PET) study was to analyse the hemispheric dominance of the vestibular cortical system. Therefore, the differential effects of caloric vestibular stimulation (right or left ear irrigation with warm water at 44 degrees C) on cortical and subcortical activation were studied in 12 right-handed and 12 left-handed healthy volunteers. Caloric irrigation induces a direction-specific sensation of rotation and nystagmus. Significant regional cerebral blood flow increases were found in a network within both hemispheres, including the superior frontal gyrus/sulcus, the precentral gyrus and the inferior parietal lobule with the supramarginal gyrus. These areas correspond best to the cortical ocular motor centres, namely the prefrontal cortex, the frontal eye field and the parietal eye field, known to be involved in the processing of caloric nystagmus. Furthermore, distinct temporo-parietal activations could be separated in the posterior part of the insula with the adjacent superior temporal gyrus, the inferior parietal lobule and precuneus. These areas fit best to the human homologues of multisensory vestibular cortex areas identified in the monkey and correspond to the parieto-insular vestibular cortex (PIVC), the visual temporal sylvian area (VTS) and areas 7 and 6. Further cortical activations were seen in the anterior insula, the inferior frontal gyrus and anterior cingulum. The subcortical activation pattern in the putamen, thalamus and midbrain is consistent with the organization of efferent ocular motor pathways. Cortical and subcortical activation of the described areas was bilateral during monaural stimulation, but predominant in the hemisphere ipsilateral to the stimulated ear and exhibited a significant right hemispheric dominance for vestibular and ocular motor structures in right-handed volunteers. Similarly, a significant left hemispheric dominance was found in the 12 left-handed volunteers. Thus, this PET study showed for the first time that cortical and subcortical activation by vestibular caloric stimulation depends (i) on the handedness of the subjects and (ii) on the side of the stimulated ear. Maximum activation was therefore found when the non-dominant hemisphere was ipsilateral to the stimulated ear, i.e. in the right hemisphere of right-handed subjects during caloric irrigation of the right ear and in the left hemisphere of left-handed subjects during caloric irrigation of the left ear. The localization of handedness and vestibular dominance in opposite hemispheres might conceivably indicate that the vestibular system and its hemispheric dominance, which matures earlier during ontogenesis, determine right- or left-handedness.

Functional magnetic resonance imaging blood-oxygenation-level-dependent (BOLD) signal increases (activations) and BOLD signal decreases ("deactivations") were compared in six healthy volunteers during galvanic vestibular (mastoid) and galvanic cutaneous (neck) stimulation in order to differentiate vestibular from ocular motor and nociceptive functions. By calculating the contrast for vestibular activation minus cutaneous activation for the group, we found activations in the anterior parts of the insula, the paramedian and dorsolateral thalamus, the putamen, the inferior parietal lobule [Brodmann area (BA) 40], the precentral gyrus (frontal eye field, BA 6), the middle frontal gyrus (prefrontal cortex, BA 46/9), the middle temporal gyrus (BA 37), the superior temporal gyrus (BA 22), and the anterior cingulate gyrus (BA 32) as well as in both cerebellar hemispheres. These activations can be attributed to multisensory vestibular and ocular motor functions. Single-subject analysis in addition showed distinctly nonoverlapping activations in the posterior insula, which corresponds to the parieto-insular vestibular cortex in the monkey. During vestibular stimulation, there was also a significant signal decrease in the visual cortex (BA 18, 19), which spared BA 17. A different "deactivation" was found during cutaneous stimulation; it included upper parieto-occipital areas in the middle temporal and occipital gyri (BA 19/39/18). Under both stimulation conditions, there were signal decreases in the somatosensory cortex (BA 2/3/4). Stimulus-dependent, inhibitory vestibular-visual, and nociceptive-somatosensory interactions may be functionally significant for processing perception and sensorimotor control.

The vestibular system--a sensor of head accelerations--cannot detect self-motion at constant velocity and thus requires supplementary visual information. The perception of self-motion during constant velocity movement is completely dependent on visually induced vection. This can be linear vection or circular vection (CV). CV is induced by large-field visual motion stimulation during which the stationary subject perceives the moving surroundings as being stable and himself as being moved. To determine the unknown cortical visual-vestibular interaction during CV, we conducted a PET activation study on CV in 10 human volunteers. The PET images of cortical areas activated during visual motion stimulation without CV were compared with those with CV. Hitherto, CV was explained neurophysiologically by visual-vestibular convergence with activation of the vestibular nuclei, thalamic subnuclei and vestibular cortex. If CV were mediated by the vestibular cortex, one would expect that an adequate visual motion stimulus would activate both the visual and vestibular cortex. Contrary to this expectation, it was shown for the first time that visual motion stimulation with CV not only activates a medial parieto-occipital visual area bilaterally, separate from middle temporal/medial superior temporal areas, it also simultaneously deactivates the parieto-insular vestibular cortex. There was a positive correlation between the perceived intensity of CV and relative changes in regional CBF in parietal and occipital areas. These findings support a new functional interpretation: reciprocal inhibitory visual-vestibular interaction as a multisensory mechanism for self-motion perception. Inhibitory visual-vestibular interaction might protect visual perception of self-motion from potential vestibular mismatches caused by involuntary head accelerations during locomotion, and this would allow the dominant sensorial weight during self-motion perception to shift from one sensory modality to the other.

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