Recovery from vestibular dysfunction following Traumatic Brain Injury: A prospective behavioural and neuro-imaging study

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Traumatic Brain Injury (TBI) is the commonest cause of chronic disability in young adults. We found that 86% of acute TBI patients have problems with their balance. The problem of imbalance is important for this young working age group since previous studies have shown that following a mild TBI, at 6 months, 66% of TBI patients with balance problems will still be unemployed versus only 25% of those without balance dysfunction. A key step in treating TBI imbalance is to understand the underlying pathophysiology, however previous studies could not identify a clear-cut cause in 25% of TBI patients with chronic imbalance.Our acute TBI data show that most patients have a type of imbalance that is typical for patients with a loss of function of the inner ear balance organ - the vestibular organ. When we tested acute TBI patients with normal inner ear function we still found the same type of vestibular gait impairment, implying that the problem lay with the brain's processing of the vestibular organ's signals. Whilst screening acute TBI patients we also observed that acute TBI patients appeared to lose the perception of vertigo (the sensation of bodily self-motion) despite overt vestibular activation (vestibular nystagmus, nausea and vomiting). This again implies a failure by the brain to adequately process the inner ear vestibular signals. Taken together, TBI impairs the brain processing of vestibular signals with a major impact upon balance function. But what is the mechanism underlying this impairment of vestibular processing?Our previous work (Nigmatullina 2015) showed that vertigo perception is mediated by a cerebral cortical network. Congruent with this notion and using a test to quantify the vestibular perception of self-motion, we found that focal cortical damage from stroke did not affect vestibular perception of self-motion (Kaski 2015). In contrast, in our pilot data, we quantitatively show that acute TBI does indeed impair this vestibular perception of self-motion (which we call 'Vestibular Agnosia').We thus hypothesise that TBI causes a disruption of a cerebral cortical network that processes vestibular signals important for perceiving our sense of bodily motion. We additionally hypothesise that impairment of this vestibular cortical network will also compromise balance, particularly in the dark, since excessive sway (normally indicated by vestibular signals of head motion) will not be detected, leading to falls.Hence in our study we propose to:(i) prospectively assess if our vestibular perceptual test (of vestibular agnosia) predicts functional outcome;(ii) test our hypothesis that vestibular agnosia is a marker of brain network dysfunction; (iii) develop models linking pathophysiology and symptoms and hence enable us to explain why the persistence of symptoms post-TBI correlates poorly with TBI severity.The output of this study will thus enable us to:(i): predict which patients will be at risk of imbalance and falls post-TBI; (ii) objectively monitor the improvement in brain network dysfunction and hence provide an objective indicator of response to treatment;(iii) provide a clinical framework to progress the research and treatment of TBI including sports concussion.