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Brain, Vol. 125, No. 2, 404-420, February 1, 2002
© 2002 Oxford University Press

Inhibitory control of acquired motor programmes in the human brain

Friedhelm Hummel1, Frank Andres1, Eckart Altenmüller2, Johannes Dichgans1 and Christian Gerloff1

1 Eberhard-Karls University Tübingen, Cortical Physiology Research Group, Department of Neurology, Hoppe-Seyler-Str. 3, D-72076 Tübingen and 2 University of Music and Drama, Institute of Music Physiology and Performing Arts Medicine, Hannover, Germany

Correspondence to: Christian Gerloff, MD, Cortical Physiology Research Group, Department of Neurology, University of Tübingen, Medical School, Hoppe-Seyler-Str. 3, D-72076 Tübingen, Germany E-mail: christian.gerloff{at}uni-tuebingen.de

An important basis of skilled human behaviour is the appropriate retrieval of acquired and memorized motor programmes (‘motor memory traces’). Appropriate retrieval is warranted if motor programmes are only activated if necessary and are, probably more often, inhibited if required by the context of a given situation. It is unknown how this type of inhibition is accomplished in the brain. We studied context-dependent modulation of motor memory traces in 18 volunteers and six patients with focal dystonia. Cortical function was assessed with transcranial magnetic stimulation over the primary motor cortex (M1) and with task-related analysis of oscillatory EEG activity. An activation (ACT) and inhibition (INH) condition were compared. In both, visual cues were presented at 1/s. In ACT, subjects had to respond to these cues with individual finger movements as learned in a preceding training session. In INH, subjects had to observe the cues without retrieval of motor responses. During INH, inhibitory control of the motor memory trace was confirmed by significant amplitude reduction of motor evoked potentials (MEPs) compared with baseline. This was accompanied by a significant increase of 11–13 Hz oscillatory activity over the sensorimotor areas during INH. During active retrieval of the motor memory traces, the reverse was true (increased MEP amplitudes, decreased oscillatory 11–13 Hz activity). In a small sample of dystonic patients (n = 6), the increase of 11–13 Hz oscillatory activity during INH was consistently absent. The present data demonstrate for the first time cortical correlates of appropriate, context-dependent inhibition of motor memory traces. We propose that focal increases of oscillatory activity are instrumental for inhibitory control at the cortical level. This concept is supported by the preliminary observations in dystonic patients who are known to have deficits of inhibitory motor control and in whom these context-dependent focal increases of oscillatory activity were absent.


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