Clonus is explained from increased reflex gain and enlarged tissue viscoelasticity.

Upper motor neuron diseases (UMND), such as stroke and spinal cord injury (SCI), are assumed to produce alterations in muscle tissue in association with neural damage. Distinguishing between these two factors is of clinical importance in choosing appropriate therapy. We studied the effect of changes in the gain of the Ia reflex pathway and tissue viscoelasticity on the emergence, frequency, and persistence of ankle clonus: a clinically significant, involuntary oscillatory movement disorder. Monte Carlo simulations were performed to explain our experimental observations in patients with stroke (n = 3) and SCI (n = 4) using a nonlinear antagonistic muscle model of the human ankle joint. Ia reflex gain was varied by changing motor unit pool threshold and gain, and passive tissue viscosity and elasticity were varied by changing optimal muscle length. Tissue viscoelasticity appeared to have a strong effect on the emergence and persistence of clonus. Observed frequencies of ankle movement, prior to and after the experimental intervention of a sudden damper, was predicted by the model. The simulations revealed that reflex gains were largest in patients with the largest tissue viscoelasticity. We conclude that ankle clonus in stroke and SCI is the result of a combination of, and suggests a relation between, (i) a decrease in threshold and an increase in gain of the motor unit pool and (ii) a decrease in optimal muscle length.

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