Spasticity of the ankle reduces quality of life by impeding walking and other activities of daily living. Robot-driven continuous passive movement (CPM) is a strategy for lower limb spasticity management but effects on spasticity, walking ability and spinal cord excitability (SCE) are unknown. The objectives of this experiment were to evaluate (1) acute changes in SCE induced by 30 min of CPM at the ankle joint, in individuals without neurological impairment and those with lower limb spasticity; and, (2) the effects of 6 weeks of CPM training on SCE, spasticity and walking ability in those with lower limb spasticity. SCE was assessed using soleus Hoffmann (H-) reflexes, collected prior to and immediately after CPM for acute assessments, whereas a multiple baseline repeated measures design assessed changes following 18 CPM sessions. Spasticity and walking ability were assessed using the Modified Ashworth Scale, the 10 m Walk test, and the Timed Up and Go test. Twenty-one neurologically intact and nine participants with spasticity (various neurological conditions) were recruited. In the neurologically intact group, CPM caused bi-directional modulation of H-reflexes creating ‘facilitation’ and ‘suppression’ groups. In contrast, amongst participants with spasticity, acute CPM facilitated H-reflexes. After CPM training, H-reflex excitability on both the more-affected and less-affected sides was reduced; on the more affected side H@Thres, H@50 and H@100 all significantly decreased following CPM training by 96.5 ± 7.7%, 90.9 ± 9.2%, and 62.9 ± 21.1%, respectively. After training there were modest improvements in walking and clinical measures of spasticity for some participants. We conclude that CPM of the ankle can significantly alter SCE. The use of CPM in those with spasticity can provide a temporary period of improved walking, but efficacy of treatment remains unknown.

Spinal cord excitability, as assessed by modulation of Hoffmann (H-) reflexes, is reduced with fatiguing isometric contractions. Furthermore, spinal cord excitability is reduced during non-fatiguing arm and leg cycling. Presynaptic inhibition of Ia terminals is believed to contribute to this suppression of spinal cord excitability. Electrical stimulation to cutaneous nerves reduces Ia presynaptic inhibition, which facilitates spinal cord excitability, and this facilitation is present during arm cycling. Although it has been suggested that reducing presynaptic inhibition may prolong fatiguing contractions, it is unknown whether sensory stimulation can alter the effects of fatiguing exercise on performance or spinal cord excitability. Thus, the aim of this experiment was to determine if sensory stimulation can interfere with fatigue-related suppression of spinal cord excitability, and alter fatigue rates during cycling sprints. Thirteen participants randomly performed three experimental sessions that included: unloaded cycling with sensory stimulation (CONTROL + STIM), sprints with sensory stimulation (SPRINT + STIM) and sprints without stimulation (SPRINT). Seven participants also performed a fourth session (CONTROL), which consisted of unloaded cycling. During SPRINT and SPRINT + STIM, participants performed seven, 10 s cycling sprints interleaved with 3 min rest. For CONTROL and CONTROL + STIM, participants performed unloaded cycling for ~30 min. During SPRINT + STIM and CONTROL + STIM, participants received patterned sensory stimulation to nerves of the right foot. H-reflexes and M-waves of the right soleus were evoked by stimulation of the tibial nerve at multiple time points throughout exercise. Sensory stimulation facilitated soleus H-reflexes during unloaded cycling, whereas sprints suppressed soleus H-reflexes. While receiving sensory stimulation, there was less suppression of soleus H-reflexes and slowed reduction in average power output, compared to sprints without stimulation. These results demonstrate that sensory stimulation can substantially mitigate the fatiguing effects of sprints.