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Motor cortex rTMS restores defective intracortical inhibition in chronic neuropathic pain

From the Departments of Physiology (J.P.L., X.D., I.M.-L.) and Neurosurgery (Y.K., J.P.N.), Hôpital Henri Mondor, Assistance Publique–Hôpitaux de Paris, INSERM U 421, IM3-Faculté de Médecine de Créteil, Créteil, France.

Address correspondence and reprint requests to Dr. Jean-Pascal Lefaucheur, Service Physiologie, Explorations Fonctionnelles, Hôpital Henri Mondor, 51 avenue de Lattre de Tassigny, 94010 Créteil cedex, France; e-mail: jean-pascal.lefaucheur{at}hmn.ap-hop-paris.fr

Objective: To assess cortical excitability changes in patients with chronic neuropathic pain at baseline and after repetitive transcranial magnetic stimulation (rTMS) of the motor cortex.

Methods: In 22 patients with unilateral hand pain of various neurologic origins and 22 age-matched healthy controls, we studied the following parameters of cortical excitability: motor threshold at rest, motor evoked potential amplitude ratio at two intensities, cortical silent period (CSP), and intracortical inhibition (ICI) and intracortical facilitation. We compared these parameters between healthy subjects and patients at baseline. We also studied excitability changes in the motor cortex corresponding to the painful hand of patients after active or sham rTMS of this cortical region at 1 or 10 Hz.

Results: At baseline, CSP was shortened for the both hemispheres of patients vs healthy subjects, in correlation with pain score, while ICI was reduced only for the motor cortex corresponding to the painful hand. Regarding rTMS effects, the single significant change was ICI increase in the motor cortex corresponding to the painful hand, after active 10-Hz rTMS, in correlation with pain relief.

Conclusion: Chronic neuropathic pain was associated with motor cortex disinhibition, suggesting impaired GABAergic neurotransmission related to some aspects of pain or to underlying sensory or motor disturbances. The analgesic effects produced by motor cortex stimulation could result, at least partly, from the restoration of defective intracortical inhibitory processes.

Supported by the Institut UPSA de la Douleur.

Disclosure: The authors report no conflicts of interest.

Received November 23, 2005. Accepted in final form July 7, 2006.

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