The mirrored burden and accountable handovers in cancer survivorship: co‑designing a post‑treatment transition standard.

Transcranial magnetic stimulation (TMS) is an FDA‐approved treatment for major depressive disorder; however, clinical response rates remain modest and variable, ranging from 40% to 60% across trials and naturalistic studies (Carpenter et al. ; Cirillo et al. ; Conelea et al. ; George et al. ; O'Reardon et al. ). Multiple factors potentially contribute to this variability, including target selection, stimulation protocol parameters, and patient characteristics (Caulfield and Brown ; Cerins et al. ; Fox et al. ; Hutton et al. ). Among these, stimulation intensity represents a readily modifiable parameter that has received limited systematic investigation despite its potential influence on treatment outcomes. Current clinical practice uses resting motor threshold (rMT), a visible indicator of neuronal activation, as a proxy for determining stimulation intensity at non‐motor brain targets. Following rMT determination at the primary motor cortex (M1), a fixed percentage, conventionally 120% of rMT, is applied to the left dorsolateral prefrontal cortex (DLPFC) for depression treatment (Addicott et al. ; Rossi et al. ; Rothwell et al. ). This approach assumes that distance from coil‐to‐cortex and excitability requirements for M1 activation translate to the DLPFC in a fixed ratio for each patient. Computational modeling of TMS‐induced electric‐Fields (E‐Fields) has emerged as a tool to estimate the actual cortical stimulation delivered to brain targets, accounting for individual anatomical differences in skull geometry, brain morphology, and tissue conductivity (Dannhauer et al. ; Quinn et al. ; Van Hoornweder et al. ). Offline approaches using finite element method (FEM) modeling have demonstrated substantial interindividual variability in required intensities when targeting equivalent E‐Field strengths (Dannhauer et al. ; Van Hoornweder et al. ; Caulfield et al. ). Two notable studies sought to determine the exact translation between M1 and DLPFC as measured by induced E‐Field. Nahas and colleagues reported that subjects required, on average, 114% of rMT to compensate for differences in coil‐to‐cortex distance at the DLPFC, while Caulfield and colleagues found a mean of 134% rMT was needed for equivalent E‐Field strength at the DLPFC relative to M1. Both substantially varied from the 120% convention for many individuals (Caulfield et al. ; Nahas et al. ). These findings suggest that fixed‐percentage dosing may inadequately account for individual anatomical variation and could over or under‐stimulate, and in turn, yield suboptimal outcomes.