The possible role of changes in presynaptic inhibition of muscle spindle primary afferent terminals in Parkinson's disease was investigated. The pathway from tibialis anterior Ia afferents to soleus Ia terminals was assessed in 20 patients with Parkinson's disease and in 17 age matched controls, both at rest and during maintenance of tonic plantar flexing torques about the ankle. At all torques less presynaptic inhibition was present in the patients with Parkinson's disease than in the controls. The difference was significant at rest (p < 0.03) and at 2 Nm (p < 0.05) but not at 5 Nm and 7 Nm torque. The amount of presynaptic inhibition did not change with torque in either group. The observed alteration in presynaptic inhibition in Parkinson's disease is likely to make only a small contribution to the rigidity and impaired movement control.
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