Fig. 3: Treatment with GIR significantly improved cognitive control circuit function from pretreatment baseline to the 8-week post-treatment follow-up.

a, Treatment with GIR significantly improved cognitive control circuit function as evidenced by increased dACC activity from pretreatment baseline to the 8-week post-treatment follow-up, with a medium effect size (t(16) = 2.334, P = 0.033, d = 0.566, 95% CI 0.021−1.112). b, GIR-related improvements in cognitive control circuit dACC activity are shown for individual patients, indicated by individual data points and connected by faint lines with a bolded line for the sample mean. c, Treatment with GIR significantly improved cognitive control circuit function, as further evidenced by increased connectivity of the dACC with the left dLPFC, with a medium effect size (t(16) = 2.753, P = 0.014, d = 0.668, 95% CI 0.001−1.337). d, GIR-related improvements in cognitive control circuit dACC–left dLPFC connectivity are shown for individual patients, indicated by individual data points and connected by faint lines with a bolded line for the sample mean. Data are presented as mean values ± s.e.m. Analyses were conducted using general linear models with two-sided alpha values, n = 17 participants. The primary circuit outcome measures were modeled as a repeated measures factor to account for correlations among the measures and control for multiple comparisons by estimating effect within a unified model framework, and no correction for multiple comparisons across secondary outcome measures was applied. Replicates are not applicable as we are not reporting on laboratory tests. There was no control group.