F137. Effects of repetitive transcranial magnetic stimulation on short-latency afferent inhibition: A study in treatment-resistant depression.

Introduction Short-latency afferent inhibition (SAI) is a phenomenon in which transcranial magnetic stimulation (TMS) induced motor evoked potentials (MEPs) are decreased in amplitude due to preceding electrical stimulation of the peripheral nerve, such as the median nerve at the wrist. If the nerve is stimulated around 21 ms before giving the TMS pulse to the cortical representation area of a muscle innervated by the same nerve, the resulting MEP amplitude is smaller than without electrical stimulation. On the contrary, if the nerve is stimulated 30 ms before giving the TMS pulse, there is no effect in MEP amplitude in healthy humans. In some movement disorders, such as in writer’s cramp, the 30 ms stimulation may, however, result in facilitation of the MEP amplitude. SAI is thought to reflect the sensorimotor interaction and cholinergic activity of the cerebral cortex and is likely mediated by the GABA A receptor subtype bearing the α 1-subunit. In this study, we evaluated the effects of repetitive TMS (rTMS) therapy on SAI in treatment-resistant depression (TRD). Methods Two patient groups received either active (12 patients) or sham (12 patients) rTMS daily for 27 days. During treatment, excitatory 10 Hz stimulation was applied on the left and inhibitory 1 Hz on the right dorsolateral prefrontal cortex. Before and after the treatment, SAI was measured from right abductor pollicis brevis muscle by using time-intervals of 21 ms and 30 ms between the electric stimulation of the right median nerve at the wrist and TMS of the left motor cortex. Furthermore, baseline MEPs were recorded before and after the treatment. Results Before the treatment, the 21 ms SAI was inhibitory ( p  = 0.001) whereas the 30 ms SAI was facilitatory ( p  = 0.023) in TRD patients. After treatment in the active group, the baseline MEPs decreased in amplitude ( p  = 0.030), the 21 ms SAI MEPs stayed the same ( p  = 0.299) and the 30 ms SAI MEPs decreased ( p  = 0.047) compared to pre-treatment amplitudes. In the sham group, treatment did not induce any changes ( p  ⩾ 0.188). Conclusion rTMS treatment modulates the sensorimotor interaction of TRD patients. [ABSTRACT FROM AUTHOR]