Abstract

BackgroundSpasticity is prevalent following Traumatic Brain Injury. ‘Focal’ muscle spasticity has been defined as spasticity affecting a localised muscle group, but it's impact on gait kinetics remains unclear. The aim of this study was to investigate the relationship between focal muscle spasticity and gait kinetics following Traumatic Brain Injury. MethodsNinety-three participants attending physiotherapy for mobility limitations following Traumatic Brain Injury were invited to participate in the study. Participants underwent clinical gait analysis and were grouped depending on the presence or absence of focal muscle spasticity. Kinetic data was obtained for each sub-group, and participants were compared to healthy controls. FindingsHip extensor power generation at initial contact, hip flexor power generation at terminal stance, and knee extensor power absorption at terminal stance were all significantly increased, and ankle power generation was significantly reduced at push-off when comparing Traumatic Brain Injury to healthy control populations. There were only two significant differences between participants with and without focal muscle spasticity, hip extensor power generation at initial contact was increased (1.53 vs 1.03 W/kg, P < .05) for those with focal hamstring spasticity, and knee extensor power absorption in early stance was reduced (−0.28 vs −0.64 W/kg, P < .05) for those with focal rectus femoris spasticity. However, these results should be interpreted with caution as the sub-group of participants with focal hamstring and rectus femoris spasticity was small. InterpretationFocal muscle spasticity had little association with abnormal gait kinetics in this cohort of independently ambulant people with Traumatic Brain Injury.

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