OBJECTIVE: To characterize gait characteristics of adults with traumatic brain injury (TBI) and lower limb muscle hypertonia, distinguishing gait adaptations inherent to TBI motor impairment from those of healthy subjects walking at slower speed. METHODS: Temporospatial and kinematic data of 31 patients with TBI (41 ± 30 months post-injury) walking at self-selected speed (free speed) were compared with 31 healthy subjects walking at free and very slow speeds using an optoelectronic motion analysis system. RESULTS: All step parameters differed (p < 0.05) between more affected (MA) and less affected (LA) sides in TBI except foot angle and toe clearance. Significant differences existed between TBI and controls in most parameters regardless of speed. These differences frequently involved the LA side. In TBI, most temporospatial parameters significantly correlated with stride velocity, whereas the averaged lower limb Ashworth score on the MA side (2.1 ± 0.4) showed few significant correlations. CONCLUSIONS: Gait deviations in subjects with TBI and lower limb muscle hypertonia cannot be solely explained by slower walking. The preponderance of changes involving the LA side particularly suggests prevalent use of compensatory walking strategies. Temporospatial gait parameters are not closely related to static measures of muscle hypertonia after TBI.
OBJECTIVE: To characterize gait characteristics of adults with traumatic brain injury (TBI) and lower limb muscle hypertonia, distinguishing gait adaptations inherent to TBI motor impairment from those of healthy subjects walking at slower speed. METHODS: Temporospatial and kinematic data of 31 patients with TBI (41 ± 30 months post-injury) walking at self-selected speed (free speed) were compared with 31 healthy subjects walking at free and very slow speeds using an optoelectronic motion analysis system. RESULTS: All step parameters differed (p < 0.05) between more affected (MA) and less affected (LA) sides in TBI except foot angle and toe clearance. Significant differences existed between TBI and controls in most parameters regardless of speed. These differences frequently involved the LA side. In TBI, most temporospatial parameters significantly correlated with stride velocity, whereas the averaged lower limb Ashworth score on the MA side (2.1 ± 0.4) showed few significant correlations. CONCLUSIONS: Gait deviations in subjects with TBI and lower limb muscle hypertonia cannot be solely explained by slower walking. The preponderance of changes involving the LA side particularly suggests prevalent use of compensatory walking strategies. Temporospatial gait parameters are not closely related to static measures of muscle hypertonia after TBI.