Repetitive transcranial magnetic stimulation (rTMS) is extensively used to study cognitive and motor function in humans and might be of value in the treatment of various disorders. For a better understanding of the effects of rTMS and its more efficient application it is crucial to identify the sites and neural circuits affected by rTMS. It is well known that low frequency rTMS applied to the motor cortex (M1) produces long-lasting depression of motor evoked potentials (MEPs) evoked over the same stimulation site (Speer et al., 2003). It is commonly assumed that this depression largely reflects changes in cortical circuits. However, Perez et al. (2005) demonstrated that rTMS affected not only the size of the MEP, but also that of the H-reflex. Therefore, the aim of the present study was to further elucidate the site of action of low frequency rTMS. To evaluate changes in the corticomotoneuronal transmission to the a-motoneurons, the soleus H-reflex was conditioned either by magnetic stimulation of the cervicomedullary junction (CMS-conditioning) or the motor cortex (M1-conditioning). The first detectable facilitation of the H-reflex (early facilitation) was determined after M1- and CMS-conditioning by testing interstimulus intervals (ISIs) from -9 to 0 ms (for instance “ISI -3 ms” indicated that the H-reflex was elicited 3 ms before the supraspinal stimulus). The amplitude of the short-latency facilitation was expressed as percentage of the unconditioned control H-reflex and compared before and after a 20 minute rTMS intervention with a stimulation intensity of 1.2 motor threshold and a frequency of 1 Hz.
The short-latency facilitation occurred around 3ms earlier with CMS- compared to M1-conditioning. After rTMS, the amplitudes of the short-latency facilitations induced by both M1-and CMS-conditioning decreased significantly (M1: minus 16.6 ± 3.6%; P = 0.0006; CMS: minus 5.86 ± 2.3%; P = 0.02).
This confirms that rTMS induces changes at a subcortical site. Since the short-latency facilitation of the H-reflex reflects activation of monosynaptic corticomotoneuronal projections, the most likely site is the synapses of the corticomotoneuronal neurones on the spinal motoneurones.
Perez et al. (2005). Exp Brain Res 162, 202-212.
Speer et al. (2003). Biol Psychiatry 54, 818-825.