Contralateral Activation of the Vestibular Cortex in Acute Vestibular Neuritis (FDG-PET Study)

Earlier positron-emission tomography (PET) water activation studies during caloric vestibular stimulation in healthy volunteers showed bilateral increases of the regional cerebral blood flow in several multisensory vestibular areas, e.g., the parieto-insular vestibular cortex in the posterior insula, adjacent temporo-parietal areas such as superior temporal gyrus (BA22) and inferior parietal lobule (BA 40), posterolateral thalamus, and anterior cingulate gyrus. This bilateral activation pattern was modulated by two factors: A) a dominance of the non-dominant hemisphere, B) a predominant projection to the hemisphere ipsilateral to the stimulation. The aim of this fluorodeoxyglucose (FDG)-PET study was to determine how an acute peripheral vestibular loss right or left caused by vestibular neuritis (VN) influences this cerebral activation pattern. FDG-PET was performed in 16 right-handed patients (11 VN left; 5 VN right) twice: A) in the acute phase of VN at day 6.5 mean after symptom onset and B) after clinical recovery due to central compensation 3 months later. For PET scanning, patients were placed supine with the eyes closed without any stimulation. Subtraction analysis (A vs. B; B vs. A) was done with the SPM99b software (p ≤ 0.001). In the acute phase patients with vestibular neuritis right and left showed increased rCGM in the posterior insular region contralateral to the affected ear. Further rCGM increases were localized in the paramedian ponto-mesencephalic brainstem merging into the hippocampus and the thalamus. Within the cerebellum rCGM increases were found in the ipsilateral dentate nucleus and simple lobule as well as the contralateral tonsil. The asymmetry of multisensory vestibular cortex activation could be explained by assuming that the more dominant ipsilateral ascending projections to the insular cortex are depressed by the lack of the tonic endorgan input due to vestibular neuritis. Alternatively or additionally, the tonus imbalance at the vestibular nuclei level (with a higher resting discharge rate of the unaffected vestibular nuclei complex) could mimic a contralateral vestibular excitation.