Transcranial Direct Current Stimulation in Obsessive Compulsive Symptoms: A Personalised Approach

Background: Transcranial-direct-current-stimulation (tDCS) is a non-invasive form of neurostimulation with potential for development as a self-administered intervention. It has been shown to be promising as a safe and effective treatment for obsessive compulsive disorder (OCD) in a recently published paper1. Our aim is to investigate if specific neurocognitive markers of inhibition and flexibility, implicated in the mechanism of effect of tDCS, represent viable predictive biomarkers for personalising the choice of stimulation target and thereby optimising clinical outcomes. Methods: FEATSOCS was a randomised, double-blind, sham-controlled, cross-over, multicentre study. Twenty adults with DSM-5-defined OCD took part: each received three courses of clinic-based tDCS (SMA-supplementary motor area, L-OFC-left orbitofrontal cortex and Sham), randomly allocated and delivered in counterbalanced order. Each course comprised four 20-minute 2 mA stimulations, delivered over two consecutive days, separated by a ‘washout’ period of at least four weeks. Patient representatives with lived experience of OCD were actively involved at all stages. In this project, we focused on the neurocognitive data collected via the CANTAB-Battery2 and in particular on motor-impulsivity (stop signal reaction time - SSRT) and cognitive inflexibility (stage-8 and stage-9 of the Intra/Extra-Dimensional-Set-Shifting-Task – assessing extra dimensional set shifting and reversal learning). Neurocognitive assessments were conducted before and after stimulation. We used a paired samples T-test to compare the baseline scores and the post-stimulation scores on the CANTAB tasks for each treatment group. Results: By stimulating the OFC, we obtained a reduction in cognitive inflexibility on stage-8 and stage-9 of the Intra/Extra-Dimensional-Set-Shifting-Task (effect sizes of d=0.24 and d=0.18, respectively), but we see a worsening of motor impulsivity (stop signal reaction time - SSRT) with a negative effect size of d=-0-25. By stimulating the SMA, on the other hand, we see a less clear effect on cognitive inflexibility (effect size of d=0.16 on stage 8 and d=-0.22 on stage 9), but a numerically significant improvement in motor impulsivity (SSRT - effect size of d=0.37). These results are not statistically significant, but considering the sample of this feasibility study, these numerically significant figures are important signals of effect. Stimulating with Sham did not have numerically significant and clear signals of effect on any of these neurocognitive tasks. Conclusions, These preliminary results could lead to the use of the latent phenotypes of cognitive inflexibility and motor impulsivity as markers to drive and deliver tDCS in a personalised approach3. Cognitive inflexibility has been shown to be a challenge in clinical practice and currently there are no effective treatment for this transdiagnostic latent phenotype. tDCS could constitute an effective and feasible option to treat cognitive inflexibility and the OFC could be targeted if aiming at improving this endophenotype. For example, the OFC could be the target in patients with OCD and OCPD/ASD comorbidity. On the other hand, motor impulsivity is a frequent endophenotype that we find in patients with OCD and SMA could be stimulated to reduce impulsivity (e.g., patients with OCD and ADHD). These results should be corroborated by a larger trial, possibly adopting a home-based approach.