We studied the effects of low-frequency transcranial magnetic stimulation (TMS) on motor cortex excitability in humans. TMS at 0.1 Hz for 1 hour did not change cortical excitability. Stimulation at 0.9 Hz for 15 minutes (810 pulses), similar to the parameters used to induce long-term depression (LTD) in cortical slice preparations and in vivo animal studies, led to a mean decrease in motor evoked potential (MEP) amplitude of 19.5%. The decrease in cortical excitability lasted for at least 15 minutes after the end of the 0.9 Hz stimulation. The mechanism underlying this decrease in excitability may be similar to LTD. TMS-induced reduction of cortical excitability has potential clinical applications in diseases such as epilepsy and myoclonus. Spread of excitation, which may be a warning sign for seizures, occurred in one subject and was not accompanied by increased MEP amplitude, suggesting that spread of excitation and amplitude changes are different phenomena and also indicating the need for adequate monitoring even with stimulations at low frequencies.

We studied the effects of a loading dose of phenytoin on motor cortex excitability in five healthy volunteers. Phenytoin elevated motor thresholds to transcranial magnetic stimulation (TMS) in all subjects, but had no effects on motor-evoked potential amplitudes, silent period durations, and intracortical excitability tested by paired TMS during rest and voluntary muscle activation. These results are consistent with the hypothesis that blockade of voltage-gated sodium channels decreases membrane excitability and elevates the threshold to TMS, but will not reduce intracortical excitability.

Postexercise facilitation of motor evoked potentials (MEPs) elicited to transcranial magnetic stimulation occurs after brief, nonfatiguing muscle activation. This phenomenon may be related to post-tetanic potentiation or long-term potentiation (LTP) observed in animal studies. Phenytoin reduces post-tetanic potentiation but does not block LTP. We studied the effects of phenytoin on postexercise MEP facilitation and its decay over time. Phenytoin did not result in either significant change in postexercise MEP facilitation nor significant change in the decay of facilitation. We conclude that postexercise MEP facilitation is unlikely to be secondary to post-tetanic potentiation.

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