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Theta Priming of 1-Hz rTMS in Healthy Volunteers: Effects on Motor Inhibition

Tallabs, Felipe A.; Hammond-Tooke, Graeme D.

Journal of Clinical Neurophysiology: February 2013 - Volume 30 - Issue 1 - p 79–85
doi: 10.1097/WNP.0b013e31827ed0e3
Original Research

Summary: Originally derived from animal experiments, the concept of priming in repetitive transcranial magnetic stimulation (rTMS) experiments refers to a pretreatment or preprotocol stimulation that enhances the effect of the protocol. This means that previous stimulation or bout of activity predisposes the synapse for a second stimulation protocol to produce an enhanced depression. The purpose of this study was to investigate the use of theta priming with 1-Hz rTMS to the motor cortex to induce corticospinal inhibition. The main question was whether there was any benefit in using theta priming instead of simply a longer period of 1-Hz rTMS. To address this, the authors compared 1-Hz rTMS with and without theta priming, using a protocol in which the total period of stimulation was the same. Eleven healthy volunteers were given rTMS to the right primary motor cortex in three separate sessions, in which the participant received one of the three protocols: (1) 1-Hz rTMS for 10 minutes, (2) 5 minutes of 6-Hz theta burst priming followed by 5 minutes of 1-Hz rTMS, or (3) 10 minutes of 1-Hz sham rTMS using a placebo coil. There was a significant effect of active 1-Hz rTMS alone on both resting motor evoked potential and active motor evoked potential amplitude, P < 0.05: both were significantly decrease after 1-Hz rTMS compared with sham. Resting motor evoked potential amplitude was unchanged compared with sham rTMS after the priming protocol, P = 0.001; 1-Hz rTMS with and without theta priming significantly reduced right unimanual reaction time compared with sham. While theta priming abolished or interfered with the inhibitory effect of 1-Hz rTMS on corticospinal excitability, the effect on ipsilateral reaction times was unaffected. The negative effect of priming can be interpreted as a functional interference of the priming preprotocol with the 1 Hz protocol.

Neurology Unit, Dunedin School of Medicine, Dunedin Hospital, University of Otago, Dunedin, New Zealand.

Address correspondence and reprint requests to Felipe A. Tallabs, BSc, Jose Revueltas 2748,Col Alta Vista sur, Lomas, Monterrey 64740, Mexico; e-mail:

This research was possible because of a Monterrey Foundation for Applied Science and Technology (MFAST, Mexico) Grant to F. A. Tallabs, grant number: 5002-MF-4.

Copyright © 2013 American Clinical Neurophysiology Society