Abstract
Vestibular neuritis (VN) is characterised by acute vertigo due to a sudden loss of unilateral vestibular function. A considerable proportion of VN patients proceed to develop chronic symptoms of dizziness, including visually induced dizziness, specifically during head turns. Here we investigated whether the development of such poor clinical outcomes following VN, is associated with abnormal visuo-vestibular cortical processing. Accordingly, we applied functional magnetic resonance imaging to assess brain responses of chronic VN patients and compared these to controls during both congruent (co-directional) and incongruent (opposite directions) visuo-vestibular stimulation (i.e. emulating situations that provoke symptoms in patients). We observed a focal significant difference in BOLD signal in the primary visual cortex V1 between patients and controls in the congruent condition (small volume corrected level of p < .05 FWE). Importantly, this reduced BOLD signal in V1 was negatively correlated with functional status measured with validated clinical questionnaires. Our findings suggest that central compensation and in turn clinical outcomes in VN are partly mediated by adaptive mechanisms associated with the early visual cortex.
Highlights
Acute vestibular neuritis (VN) is characterised by vertigo, nausea, postural instability and vestibular nystagmus (Dix and Hallpike, 1952; Strupp and Brandt, 2009)
The vestibular-ocular reflex (VOR) generates most of the slow phase eye movement required for image stabilization during head turns, with only minor contributions by the optokinetic system
The ability to deal with this head movement-induced visuo-vestibular mismatch may partly determine which VN patients proceed to develop chronic symptoms
Summary
Acute vestibular neuritis (VN) is characterised by vertigo, nausea, postural instability and vestibular nystagmus (Dix and Hallpike, 1952; Strupp and Brandt, 2009). During incongruent stimulation (i.e. the eye response is in opposite directions; an unfamiliar infrequent situation), there was a preferential activation of multisensory vestibular cortical areas including the posterior insular cortex, which may play a role in disambiguating visual and vestibular cues. Based on these results in healthy controls, and that during daily life VN patients must deal with mismatched visuo-vestibular signals during head movements, we postulate that the brain responses of chronic VN patients will differ to controls. We postulate that if a patient's clinical outcome is related to their degree of adaptation to lesion-induced mismatched visuo-vestibular signals, one would expect individual differences in BOLD signal response to correlate with symptom severity
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