Following vestibular neuritis (VN), long term prognosis is not dependent on the magnitude of the residual peripheral function as measured with either caloric or the video head-impulse test. Rather, recovery is determined by a combination of visuo-vestibular (visual dependence), psychological (anxiety) and vestibular perceptual factors. Our recent research in healthy individuals has also revealed a strong association between the degree of lateralisation of vestibulo-cortical processing and gating of vestibular signals, anxiety and visual dependence. In the context of several functional brain changes occurring in the interaction between visual, vestibular and emotional cortices, which underpin the aforementioned psycho-physiological features in patients with VN, we re-examined our previously published findings focusing on additional factors impacting long term clinical outcome and function. These included: (i) the role of concomitant neuro-otological dysfunction (i.e. migraine and benign paroxysmal positional vertigo (BPPV)) and (ii) the degree to which brain lateralisation of vestibulo-cortical processing influences gating of vestibular function in the acute stage. We found that migraine and BPPV interfere with symptomatic recovery following VN. That is, dizziness handicap at short-term recovery stage was significantly predicted by migraine (r = 0.523, n = 28, p = .002), BPPV (r = 0.658, n = 31, p < .001) and acute visual dependency (r = 0.504, n = 28, p = .003). Moreover, dizziness handicap in the long-term recovery stage continued to be predicted by migraine (r = 0.640, n = 22, p = .001), BPPV (r = 0.626, n = 24, p = .001) and acute visual dependency (r = 0.667, n = 22, p < .001). Furthermore, surrogate measures of vestibulo-cortical lateralisation were predictive of the amount of cortical suppression exerted over vestibular thresholds. That is, in right-sided VN patients, we observed a positive correlation between visual dependence and acute ipsilesional oculomotor thresholds (R2 0.497; p < .001), but not contralateral thresholds (R2 0.017: p > .05). In left-sided VN patients, we observed a negative correlation between visual dependence and ipsilesional oculomotor thresholds (R2 0.459; p < .001), but not for contralateral thresholds (R2 0.013; p > .05). To surmise, our findings illustrate that in VN, neuro-otological co-morbidities retard recovery, and that measures of the peripheral vestibular system are an aggregate of residual function and cortically mediated gating of vestibular input.