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This Article Full Text Full Text (PDF) All Versions of this Article: 574/3/917    most recent jphysiol.2006.108563v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Irlbacher, K. Articles by Rothwell, J. C. Search for Related Content PubMed PubMed Citation Articles by Irlbacher, K. Articles by Rothwell, J. C. Related Collections Integrative

¹ Department of Neurology, Charité, Humboldt University of Berlin, 10117 Berlin, Germany
² Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, Queen Square, London, UK
³ Department of Psychiatry, Charité University Hospital/St Hedwig Hospital, 10559 Berlin, Germany

Fast ballistic flexion movements of the wrist are produced by a triphasic pattern of electromyographic (EMG) activity in flexor and extensor muscle. Whereas it is generally accepted that the primary motor cortex generates the first agonist burst (AG1), its contribution to the following antagonist burst (ANT) and second agonist burst (AG2) is unresolved. We applied single pulses of suprathreshold transcranial magnetic stimulation (TMS) at different times to the motor cortex ipsilateral to wrist flexion. This produced interhemispheric inhibition of the opposite motor cortex and a silent period in the ballistic EMG pattern that started about 30 ms after the stimulus and lasted for a further 30 ms. If the silence was timed to start within the first 30 ms of AG1, then timing of the subsequent ANT and AG2 bursts was delayed. However, if the silence began later, then the timing of the ANT burst was not changed. A similar effect on the onset latency of the AG2 was seen if the silence began in the first part of the ANT burst. The results are compatible with a model in which the triphasic pattern is not triggered as a single entity. Instead we suggest that each burst has its own trigger that occurs about 30–40 ms after the start of AG1 (or ANT). If AG1 (or ANT) is interrupted within this time period then this trigger, and hence later bursts, are delayed. If the interruption occurs after 30–40 ms it has no effect on the onset of later bursts since they have already been triggered.

(Received 28 February 2005; accepted after revision 30 March 2006; first published online 31 March 2006)
Corresponding author J. C. Rothwell: Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, University College London, London WC1N 3BG, UK. Email: j.rothwell{at}ion.ucl.ac.uk

Bernd-Ulrich Meyer died on 24 November 2001.