Early and phasic cortical metabolic changes in vestibular neuritis onset

Abstract

Functional brain activation studies described the presence of separate cortical areas responsible for central processing of peripheral vestibular information and reported their activation and interactions with other sensory modalities and the changes of this network associated to strategic peripheral or central vestibular lesions. It is already known that cortical changes induced by acute unilateral vestibular failure (UVF) are various and undergo variations over time, revealing different cortical involved areas at the onset and recovery from symptoms. The present study aimed at reporting the earliest change in cortical metabolic activity during a paradigmatic form of UVF such as vestibular neuritis (VN), that is, a purely peripheral lesion of the vestibular system, that offers the opportunity to study the cortical response to altered vestibular processing. This research reports [(18)F]fluorodeoxyglucose positron emission tomography brain scan data concerning the early cortical metabolic activity associated to symptoms onset in a group of eight patients suffering from VN. VN patients' cortical metabolic activity during the first two days from symptoms onset was compared to that recorded one month later and to a control healthy group. Beside the known cortical response in the sensorimotor network associated to vestibular deafferentation, we show for the first time the involvement of Entorhinal (BAs 28, 34) and Temporal (BA 38) cortices in early phases of symptomatology onset. We interpret these findings as the cortical counterparts of the attempt to reorient oneself in space counteracting the vertigo symptom (Bas 28, 34) and of the emotional response to the new pathologic condition (BA 38) respectively. These interpretations were further supported by changes in patients' subjective ratings in balance, anxiety, and depersonalization/derealization scores when tested at illness onset and one month later. The present findings contribute in expanding knowledge about early, fast-changing, and complex cortical responses to pathological vestibular unbalanced processing.

Figure 1. T1 MRI superimposition showing the cluster of voxels in the right parahippocampal gyrus (BAs 34 and 28) in which 18F-FDG uptake was significantly higher at PET0 (n = 8) as compared to PET1 (n = 8) (on the left sagittal and on the right coronal projections).

Coordinates and regional details are presented in Table 1.

Figure 2. T1 MRI superimposition showing the cluster of voxels in the superior temporal gyrus (BA 38) in which 18F-FDG uptake was significantly higher at PET0 (n = 8) as compared to PET1 (n = 8) (on the left sagittal and on the right coronal projections).

Coordinates and regional details are presented in Table 1.

Figure 3. Mean and standard deviations of patients scores in the questionnaires on Balance (Gomez-Alvarez and Jauregui-Renaud, 2011), Anxiety (Zung, 1971), and Depersonalization/Derealization scales (Dep/Der, Cox and Swinson, 2002) at PET0 and PET1.

Figure 4. Hystogram showing the values of the three tests scores and the metabolism in the cluster of voxels showing statistically significant hypometabolism at PET0 as compared to PET1 (A) and viceversa (B).

The mean of glucose metabolism values in the eight patients are expressed as percent of the values found in cerebellum.