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First published online on March 1, 2002.
 Copyright © 2002 by The Physiological Society
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Received May 31, 2001
Accepted after revision January 23, 2002

Modulation of human corticomotor excitability by somatosensory input

Alain Kaelin-Lang1, Andreas R. Luft2, Lumy Sawaki1, Aaron H. Burstein3, Young H. Sohn4, and Leonardo G. Cohen5*

1 Human Cortical Physiology Section, NINDS, National Institutes of Health, Bethesda, MD, USA
2 Department of Neurology, Johns Hopkins University, Baltimore, MD 21287, USA
3 Clinical Pharmacokinetics Research Laboratory, Clinical Center Pharmacy Department, National Institutes of Health, Bethesda, MD, USA
4 Human Motor Control Section, NINDS, National Institutes of Health, Bethesda, MD, USA
5 National Institutes of Health, Bldg.10, Room 5N234, 10 Center Drive, MSC 1430, Bethesda, MD 20892, USA

* To whom correspondence should be addressed. E-mail: cohenl{at}ninds.nih.gov.

In humans, somatosensory stimulation results in increased corticomotoneuronal excitability to the stimulated body parts. The purpose of this study was to investigate the underlying mechanisms. We recorded motor evoked potentials (MEPs) to transcranial magnetic stimulation (TMS) from abductor pollicis brevis (APB), first dorsal interosseous (FDI), and abductor digiti minimi (ADM) muscles. MEP amplitudes, recruitment curves (RC), intracortical inhibition (ICI), intracortical facilitation (ICF), resting (rMT) and active motor thresholds (aMT) were recorded before and after a 2-h period of ulnar nerve electrical stimulation at the wrist. Somatosensory input was monitored by recording somatosensory evoked potentials. To differentiate excitability changes at cortical vs. subcortical sites, we recorded supramaximal peripheral M-responses and MEPs to brainstem electrical stimulation (BES). In order to investigate the involvement of GABAergic mechanisms, we studied the influence of lorazepam (LZ) (a GABAA receptor agonist) relative to that of dextromethorphan (DM) (an NMDA receptor antagonist) and placebo in a double-blind design. We found that somatosensory stimulation increased MEP amplitudes to TMS only in the ADM, confirming a previous report. This effect was blocked by LZ but not by either DM or placebo and lasted between 8 and 20 min in the absence of (i) changes in MEPs elicited by BES, (ii) amplitudes of early somatosensory-evoked potentials or (iii) M-responses. We conclude that somatosensory stimulation elicited a focal increase in corticomotoneuronal excitability that outlasts the stimulation period and probably occurs at cortical sites. The antagonistic effect of LZ supports the hypothesis of GABAergic involvement as an operating mechanism.




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