T121. Effect of electroconvulsive therapy and repetitive transcranial magnetic stimulation on corticol excitability in patients with major depression

Abstract

Repetitive transcranial magnetic stimulation (rTMS) can enhance or depress cortical excitability depending on stimulation frequency and intensity. These features of rTMS may be related to its antidepressant action that has been recently demonstrated. Changes in cortical excitability may also play an important role in the mechanisms of action of other antidepressant treatments, electroconvulsive therapy (ECT) in particular. Twenty-two patients with MD were randomized to receive either ECT + rTMS or ECT + sham rTMS in a double blind design. ECT was given twice weekly and 12 rTMS was applied throughout 3 weeks. rTMS was administered to the right prefrontal cortex with a circular coil. 900 stimuli in each session were delivered at a rate of 1 Hz and at an intensity of 110% of the resting motor threshold (rMT). Severity of depression was assessed by the Hamilton Depression Rating Scale (HDRS). The rMT and the size of motor evoked potential (MEP) were assessed before and after ECT. The MEP/M-wave area ratio was then calculated by dividing the MEP area by the maximal M-wave area obtained after electrical stimulation of the median nerve. For assessment of changes in the intra-cortical inhibition (ICI) and intra-cortical facilitation (ICF), the standard paired-pulse TMS paradigm was used at baseline and after the last ECT. The inter-hemispheric (IHR) ratio was calculated as Rt/Lt for each MEP parameter. 19 out of the 22 patients showed a marked clinical improvement treatments. The left aMT was significantly decreased following 6 ECTs. This was associated with significant change of the rMT inter-hemispheric ratio towards a relative decrease of the left hemisphere rMT indicating enhancement of the excitability in the left hemisphere. Only those patients who improved following ECT or ECT + TMS, had a significant increase of the MEP/M-wave area ratio in the left hemisphere but not in the right hemisphere. Each ECT caused an increase of MEP size in the left hemisphere. The cumulative effect of ECT on the left hemisphere MEP size was significant after 3 ECTs. Paired-pulse TMS paradigm revealed a significant reduction of the intracortical inhibition only in the left hemisphere in patients who clinically improved ECT causes a relative decrease of motor thresholds to TMS in the left hemisphere. The antidepressant effect of ECT is associated with an increase of the MEP size and reduction of the intracortical inhibition in the left hemisphere. These findings suggest that enhancement of left hemispheric excitability may be related to therapeutic effect of ECT. Similar results were obtained in patients who improved in response to antidepressant medication or rTMS. Taken together, this may suggest that an increase of left hemispheric excitability is shared by different antidepressant treatments and might be related to their therapeutic effect. rTMS as applied in our study does not seem to have an additive effect on cortical excitability and does not enhance the therapeutic effect of ECT.