Background and aimAlthough Repetitive Transcranial Magnetic Stimulation (rTMS) is a promising new noninvasive brain stimulation therapy, its underlying mechanisms of action remain unknown. OCD patients exhibit impaired response control and attention shifting, which is linked to some brain areas such as anterior cingulate cortex and basal ganglia. OCD patients also display altered neurometabolic concentrations in cortical cortical-striatal-thalamic-cortical (CSTC). In this study, we aimed to elucidate efficacy of rTMS treatment in alleviating related symptoms and pregenual anterior cingulate cortex (pACC) neurometabolites. MethodsOCD patients were randomly divided into either drug (n = 23) or drug + rTMS (n = 29) groups, and those in the latter group subjected to 4-week rTMS treatment. All participants were visited twice, at baseline and follow-up after four weeks. During both visits, all patients were subjected to 1H-MRS, then Yale-Brown Obsessive Compulsive Scale (Y-BOCS) and the Global Assessment Function (GAF) used to assess severity of obsessive-compulsive symptoms. We also evaluated synchronous anxiety and depression by Beck Anxiety Inventory (BAI), Beck Depression Inventory (BDI), Hamilton Anxiety Scale (HAM-A) and Hamilton Depression Scale (HAM-D). ResultsAfter 4 weeks of treatment, patients in the Drug + rTMS group displayed significantly lower Y-BOCS (p = 0.038), BDI (p = 0.009), HAM-D (p = 0.013), HAM-A (p = 0.012) scores than their counterparts in the Drug group. Conversely, patients in the Drug + rTMS group had significantly higher tNAA concentrations (p = 0.030) than those in the Drug group. Notably, the Drug + rTMS group exhibited higher, but insignificant Glu (p = 0.055) and Glx (p = 0.068) concentrations compared to the Drug group. Partial correlation analysis revealed a significant negative correlation between post HAM-A scores and 4-week change of pACC glutamate levels in the Drug + rTMS group (r = −0.434, p = 0.02). ConclusionrTMS treatment is an efficacious treatment therapy for OCD, mainly by inducing changes in neurometabolites.
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