AIM: Gait impairment in cervical spondylotic myelopathy (CSM) is characterised by a number of kinematic and kinetic abnormalities. Surface electromyography (EMG) can evaluate the contributions of individual muscles to a movement pattern and provide insight into the underlying impairments that characterise an abnormal gait. This study aimed to analyse EMG signals from major lower limb muscles in people with CSM and healthy controls during gait. METHODS: Sixteen people with radiologically confirmed CSM and 16 matched healthy controls participated in gait analysis. Surface EMG was recorded during walking from four lower limb muscles bilaterally. The timing of muscle activation, relative amplitudes of each burst of activity and baseline activation during gait, and the muscles' responses to lengthening as a measure of spasticity were compared using previously validated methods of EMG analysis. RESULTS: Compared to healthy controls, people with CSM had prolonged duration of activation of biceps femoris (12.5% longer) and tibialis anterior (12.4%), prolonged co-activation of rectus femoris and biceps femoris (5.14%), and impaired scaling of the amplitude of rectus femoris and biceps femoris. Muscle activation in response to lengthening was similar between groups. CONCLUSION: The results provide evidence for paresis as a contributory factor to gait impairment in CSM, indicated by impaired amplitude and the need for proximal co-activation to compensate for lack of distal power generation. Poor proprioception may have contributed to prolonged activation of tibialis anterior. Analysis of muscle responses to lengthening suggested that spasticity was not an important contributor. These findings have implications for the assessment and rehabilitation of gait impairment in CSM.
AIM: Gait impairment in cervical spondylotic myelopathy (CSM) is characterised by a number of kinematic and kinetic abnormalities. Surface electromyography (EMG) can evaluate the contributions of individual muscles to a movement pattern and provide insight into the underlying impairments that characterise an abnormal gait. This study aimed to analyse EMG signals from major lower limb muscles in people with CSM and healthy controls during gait. METHODS: Sixteen people with radiologically confirmed CSM and 16 matched healthy controls participated in gait analysis. Surface EMG was recorded during walking from four lower limb muscles bilaterally. The timing of muscle activation, relative amplitudes of each burst of activity and baseline activation during gait, and the muscles' responses to lengthening as a measure of spasticity were compared using previously validated methods of EMG analysis. RESULTS: Compared to healthy controls, people with CSM had prolonged duration of activation of biceps femoris (12.5% longer) and tibialis anterior (12.4%), prolonged co-activation of rectus femoris and biceps femoris (5.14%), and impaired scaling of the amplitude of rectus femoris and biceps femoris. Muscle activation in response to lengthening was similar between groups. CONCLUSION: The results provide evidence for paresis as a contributory factor to gait impairment in CSM, indicated by impaired amplitude and the need for proximal co-activation to compensate for lack of distal power generation. Poor proprioception may have contributed to prolonged activation of tibialis anterior. Analysis of muscle responses to lengthening suggested that spasticity was not an important contributor. These findings have implications for the assessment and rehabilitation of gait impairment in CSM.