OBJECTIVE: To evaluate whether ulnar neuropathy could induce changes in spinal cord and motor cortex excitability and therefore predispose to development of focal dystonia. BACKGROUND: A high incidence of ulnar neuropathy has been observed in patients with musician's cramp. Polygraphic electromyograph recordings in patients with entrapment of the ulnar nerve at the elbow have demonstrated long-duration bursts of co-contraction in antagonistic muscles, similar to those observed in focal dystonia. METHODS: All control subjects and 12 patients with ulnar neuropathy underwent an electrophysiologic protocol consisting of polygraphic recordings of a repetitive tapping task of the fourth finger, assessment of reciprocal inhibition in forearm muscles, and investigation of motor cortex excitability after paired transcranial magnetic stimulation. RESULTS: Eleven of 12 patients with ulnar neuropathy showed a loss of alternation and of well-formed bursts in both flexor and extensor muscles. Evaluation of reciprocal inhibition in these patients revealed a reduction in the amount of inhibition in the disynaptic and presynaptic phases. None of the patients presented with a clinically evident dystonia of the upper limb. The study of intracortical excitability after paired shocks did not reveal any difference in the amount of intracortical inhibition and facilitation compared with the control group. CONCLUSIONS: A peripheral nerve injury can induce a rearrangement of reciprocal inhibition circuits at the spinal cord level. These changes might predispose to the development of a focal dystonia. However, it is likely that another, yet unknown, factor is required to alter the intracortical circuits and produce a clinically evident dystonia.
OBJECTIVE: To evaluate whether ulnar neuropathy could induce changes in spinal cord and motor cortex excitability and therefore predispose to development of focal dystonia. BACKGROUND: A high incidence of ulnar neuropathy has been observed in patients with musician's cramp. Polygraphic electromyograph recordings in patients with entrapment of the ulnar nerve at the elbow have demonstrated long-duration bursts of co-contraction in antagonistic muscles, similar to those observed in focal dystonia. METHODS: All control subjects and 12 patients with ulnar neuropathy underwent an electrophysiologic protocol consisting of polygraphic recordings of a repetitive tapping task of the fourth finger, assessment of reciprocal inhibition in forearm muscles, and investigation of motor cortex excitability after paired transcranial magnetic stimulation. RESULTS: Eleven of 12 patients with ulnar neuropathy showed a loss of alternation and of well-formed bursts in both flexor and extensor muscles. Evaluation of reciprocal inhibition in these patients revealed a reduction in the amount of inhibition in the disynaptic and presynaptic phases. None of the patients presented with a clinically evident dystonia of the upper limb. The study of intracortical excitability after paired shocks did not reveal any difference in the amount of intracortical inhibition and facilitation compared with the control group. CONCLUSIONS: A peripheral nerve injury can induce a rearrangement of reciprocal inhibition circuits at the spinal cord level. These changes might predispose to the development of a focal dystonia. However, it is likely that another, yet unknown, factor is required to alter the intracortical circuits and produce a clinically evident dystonia.
Authors: Jonathan F Prather; Paul Nardelli; Stan T Nakanishi; Kyla T Ross; T Richard Nichols; Martin J Pinter; Timothy C Cope Journal: J Physiol Date: 2011-07-25 Impact factor: 5.182