• Lynsey D Duffell, Geoffrey L Brown, and Mehdi M Mirbagheri.
• Department of Physical Medicine and Rehabilitation, Northwestern University, 345 E Superior Street, Chicago, USA. l.duffell@ucl.ac.uk.
• J Neuroeng Rehabil. 2015 Mar 20; 12: 29.

BackgroundThe objective of this study was to investigate whether an anti-spasticity medication can facilitate the effects of robotic locomotor treadmill training (LTT) to improve gait function in people with incomplete spinal cord injury (SCI).MethodsIndividuals with chronic incomplete SCI were recruited and carried out a 4 week intervention of either locomotor treadmill training (LTT) alone (n = 26) or LTT combined with Tizanidine (TizLTT), an anti-spasticity medication (n = 22). Gait function was evaluated using clinical outcome measures of gait, speed and endurance. To better understand the underlying mechanisms of the therapeutic effects, maximal strength, active range of motion (AROM) and peak velocity (Vp) of ankle dorsi- and planter-flexor muscles were also measured. Differences were assessed using two-way mixed design analysis of variance. The number of subjects that achieved the minimal important difference (MID) for clinical scores was also measured for each group, and the results of those that did attain the MID were compared with those that did not.ResultsBoth LTT and TizLTT resulted in significant improvements in walking speed and dorsiflexion maximum strength, with no significant differences between them, using group-averaging analysis. However, using the MID analysis, a higher proportion of subjects in the TizLTT group achieved the MID for walking speed (40%) compared with LTT alone (13%). Those that achieved the MID for walking speed were significantly higher functioning at baseline than those that did not in the TizLTT group, and the change in walking speed was associated with the change in dorsiflexion peak velocity (R(2) = 0.40; P < 0.05).ConclusionTizanidine appears to facilitate the effects of LTT on gait function in individuals with chronic SCI that are higher functioning at baseline. We speculate that this may be due to restoration of inhibitory mechanisms by Tizanidine, resulting in greater stretch in the planterflexor muscles during the LTT.

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