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Abstract
We observed a marked prolongation of the transcranially evoked silent period during
continuous intrathecal administration of high doses of the gamma-aminobutyric acid
(GABA)B receptor agonist baclofen in a patient with generalized dystonia. Size of
motor evoked potentials and central conduction time remained unchanged during intrathecal
baclofen administration. The selective prolongation of the silent period during high-dose
continuous intrathecal baclofen therapy supports the notion that GABA(B)-ergic intracortical
interneurons play a part in the generation of the transcranially evoked silent period.