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Methods to Quantify Pharmacologically Induced Alterations in Motor Function in Human Incomplete SCI
Published on: April 18, 2011
Reduction of lower limb spasticity after the suppression of intravesical noxious stimulus documented by gait analysis
S Ribault1,2,3,4, C Oberle1,2,3, H Ardaillon1,2,3
1Service de Médecine Physique et Réadaptation, Hôpital Henry-Gabrielle, Hospices Civils de Lyon, Saint-Genis-Laval, France.
Context:
Spasticity is characterized by muscle hypertonia due to a velocity-dependent increase in tonic stretch reflexes, mostly related to hyperactive spinal reflexes. After spinal cord injury, the impact of noxious stimuli on autonomic dysreflexia is well documented. It is admitted in clinical practice that sublesional noxious stimuli can also increase spasticity. However, this has never been reported in the literature. In this single case study, we describe the impact of a noxious stimulus (bladder stone) on the spasticity of lower limbs in a male with spinal cord injury, using quantitative gait analysis before and after stone removal.
Findings:
: Clinical evaluation was performed on the subject before and after bladder lithiasis removal, by two physiotherapists using ASIA score and the Modified Ashworth scale. Quantitative gait analyses were compared before and 3 months after lithiasis resection.Regarding gait kinematics, there was a reduction of the right knee recurvatum, and of the successive increases of flexion (double bump) of flexion in the swing phase. In the stance phase, the right ankle maximum dorsiflexion increased. In the swing phase, the double bump of ankle dorsiflexion disappeared. Surface electromyography showed a reduction of the triceps surae hypertonia, especially in the right gastrocnemius muscle at the swing.
Conclusion:
We propose that lithiasis created a noxious stimulus regarding the S2, S3 and S4 metamers with a diffusion of the spinal reflex to the metamers S1, S2, S3 and S4. This highlights a potential causal link between an intravesical noxious stimulus and an increase in the subject's spasticity, through a disinhibited spinal nociceptive reflex.
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