Literature DB >> 20633438

Physiology of repetitive transcranial magnetic stimulation of the human brain.

Janna Marie Hoogendam1, Geert M J Ramakers, Vincenzo Di Lazzaro.   

Abstract

During the last two decades, transcranial magnetic stimulation (TMS) has rapidly become a valuable method to investigate noninvasively the human brain. In addition, repetitive TMS (rTMS) is able to induce changes in brain activity that last after stimulation. Therefore, rTMS has therapeutic potential in patients with neurologic and psychiatric disorders. It is, however, unclear by which mechanism rTMS induces these lasting effects on the brain. The effects of rTMS are often described as LTD- or LTP-like, because the duration of these alterations seems to implicate changes in synaptic plasticity. In this review we therefore discuss, based on rTMS experiments and knowledge about synaptic plasticity, whether the physiologic basis of rTMS-effects relates to changes in synaptic plasticity. We present seven lines of evidence that strongly suggest a link between the aftereffects induced by rTMS and the induction of synaptic plasticity. It is, nevertheless, important to realize that at present it is impossible to demonstrate a direct link between rTMS on the one hand and synaptic plasticity on the other. Therefore, we provide suggestions for future, innovating research, aiming to investigate both the local effects of rTMS on the synapse and the effects of rTMS on other, more global levels of brain organization. Only in that way can the aftereffects of rTMS on the brain be completely understood. Copyright 2010 Elsevier Inc. All rights reserved.

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Year:  2009        PMID: 20633438     DOI: 10.1016/j.brs.2009.10.005

Source DB:  PubMed          Journal:  Brain Stimul        ISSN: 1876-4754            Impact factor:   8.955


  185 in total

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8.  Causal Contribution of Awake Post-encoding Processes to Episodic Memory Consolidation.

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9.  Differential intensity-dependent effects of magnetic stimulation on the longest neurites and shorter dendrites in neuroscreen-1 cells.

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