Characterizing high velocity angular vestibulo ocular reflex function in service members post blast exposure

Abstract

PURPOSE: Blasts are the most common mechanism of injury in modern warfare. Traumatic Brain Injury (TBI) and dizziness are common sequelae associated with blast exposure, however little is known about their underlying cause. Data suggest Service Members (SMs) with complaints of dizziness may have vestibular dysfunction. It has also been suggested that dizziness experienced during running may be related to pitch plane gaze instability. The purpose of this study was to prospectively assay the vestibular systems of blast-exposed SMs with TBI and assess their symptoms while running. METHODS: 24 SMs recovering from mild or moderate TBI sustained in Iraq or Afghanistan were prospectively assigned to one of two groups based on presence or absence of dizziness. Wireless monocular scleral search coil and rate sensor was used to characterize yaw and pitch plane angular vestibulo-ocular reflex (aVOR) gain. Visual analog scale (VAS) was used to monitor subject severity of vestibular symptoms during an exertional treadmill protocol. Each subject was assessed using standard vestibular function tests. RESULTS: The aVOR during yaw head impulses in the symptomatic group were lower for active impulses (Ga symptomatic = .794 ± .15, Ga asymptomatic = .867 ± .18) but not passive rotations (Ga symptomatic = .781 ± .14, Ga asymptomatic = .745 ± .18) (p= 0.0005). For pitch head rotations, aVOR gains were lower in the symptomatic group (active Ga = 0.915 ± .24, passive Ga = 0.878 ± .22) than the asymptomatic group (Ga = 1.03 ± .27, passive pitch Ga = 0.97 ± .23) (p= 0.004). VAS was worse for severity of vertigo, oscillopsia, motion intolerance, and dysequilibrium during and after treadmill testing relative to baseline (p ≤ 0.05). CONCLUSION: Our findings suggest highly variable injury profiles in blast-exposed SMs including deficient as well as elevated aVOR responses. Our data demonstrate that some symptomatic SMs have diminished capability to generate compensatory eye movement responses during high velocity, actively generated head movements, which are typically greater than those during passive head rotations. This may suggest disruption of the efference copy to the brainstem vestibular nuclei.