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Brain, Vol. 125, No. 6, 1402-1413, June 2002
© 2002 Guarantors of Brain

Cortical excitability changes induced by deafferentation of the contralateral hemisphere

Konrad J. Werhahn1, Jennifer Mortensen1, Alain Kaelin-Lang2, Babak Boroojerdi3 and Leonardo G. Cohen1

1 Human Cortical Physiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA, 2 Department of Neurology, University Hospital Inselspital, Bern, Switzerland and 3 Department of Neurology, Aachen Technical University, Germany

Correspondence to: Dr K. J. Werhahn or Dr L. G. Cohen, Human Cortical Physiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Building 10, Room 5N2226, 10 Center Drive, MSC-1430, Bethesda, MD 20892-1428, USA E-mail: werhahnk{at}ninds.nih.gov or cohenL{at}ninds.nih.gov

Short-term deprivation of sensory input by ischaemic nerve block (INB) leads to functional reorganization in the deafferented motor cortex. Here, we show that INB also elicits functional changes in homotopic regions of the cortex contralateral to the deafferented one. We measured motor evoked potential (MEP) amplitudes elicited by transcranial magnetic stimulation (TMS) in small hand and biceps brachii muscles before, during and after INB of the right hand. INB increased excitability of the cortical representation of (i) the intact hand and (ii) body parts proximal to the deafferented hand (upper arm), in the absence of excitability changes in other body part representations such as thorax or leg muscles. This effect persisted throughout the entire period of deafferentation and returned to baseline values afterward. Motor responses to brainstem electrical stimulation remained unchanged during INB, indicating that the effect is probably of cortical origin. Lorazepam, a GABAA receptor agonist, blocked this increased excitability. Interhemispheric inhibition between hand muscles decreased during INB. After chronic deafferentation in amputees, MEP amplitudes and motor output curves in small hand muscles were depressed and motor thresholds were elevated compared with aged-matched controls. These results indicate that acute hand deafferentation can elicit a focal increase in excitability in the hand motor representation contralateral to the deafferented cortex that is influenced by transcallosal interactions and GABAergic transmission, and is balanced in the setting of chronic deafferentation.


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