Gait coordination is generated by neuronal inter-connections between central pattern generators in the spinal cord governed by cortical areas. Malfunction of central vestibular processing areas generates vestibular symptoms in the absence of an identifiable peripheral vestibular system lesion. Walking in the dark enforces a coordinated afference primarily from the vestibular and somatosensory systems. We hypothesized that patients with aberrant central vestibular processing would demonstrate unique gait characteristics, and have impaired gait coordination compared with those patients with abnormal peripheral vestibular function and healthy controls. One-hundred and eighteen subjects were recruited. Peripheral vestibular function was determined based on laboratory and clinical examinations. Patients with abnormal central vestibular processing had normal peripheral vestibular function. Subjects were instructed to walk at a comfortable pace during three visual conditions; eyes open, eyes open and closed intermittently, and eyes closed. Both patient groups showed a similar spatiotemporal gait pattern, significantly different from the pattern of the healthy controls. However, only the central vestibular patient group had an abnormal coordination of gait as measured by the phase coordination index (PCI). There were no significant interactions between the groups and walking conditions. Peripheral vestibular deficits impair gait though our data suggest that it is the central processing of such peripheral vestibular information that has a greater influence. This impairment may be related to a neural un-coupling between the brain and central pattern generator of the spinal cord based on the abnormal PCI, which seems to be a good indicator of the integrity of this linkage.
Keywords: Gait coordination; Gait rhythmicity; Migraine; Sensory integration; Sensory reweighting; Vestibular.