Anisotropic conductivity modeling for tDCS in Parkinson's disease using multidimensional diffusion MRI
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Updated: Nov 6, 2026

Diffusion Tensor Magnetic Resonance Imaging in the Analysis of Neurodegenerative Diseases
Published on: July 28, 2013
Santiago Osorio Jurado1,2, Mikael Skorpil3, Per Svenningsson4
1Department of Biomedical Engineering, The City College of New York, City University of New York, New York, NY, United States.
Introduction:
Predictions of the electric field (E-field) induced by transcranial direct current stimulation (tDCS) depend on how brain conductivity is modeled. White matter anisotropy is conventionally estimated from single-shell diffusion tensor imaging (DTI). Multidimensional diffusion MRI (MD-dMRI), specifically q-space trajectory imaging (QTI), instead gives a mean tensor expected to carry less kurtosis bias. Our primary question was whether replacing the conventional single-shell tensor with this mean tensor would change the predicted E-field.
Methods:
We built, to our knowledge, the first MD-dMRI tDCS conductivity model and compared it against DTI and isotropic models in 29 participants (12 with Parkinson's disease and 17 controls) across four montages, with the same mesh, electrodes, and solver.
Results:
The two anisotropic models differed mainly in tensor orientation (18-25 degrees across the white matter), with E-field magnitudes differing by 6.6% or less. E-fields were not significantly different between patients and controls in any region or montage (which was an exploratory, underpowered comparison). Whole-brain E-field correlated with MR elastography stiffness (partial r = 0.58) but attenuated to non-significance once cerebrospinal fluid (CSF) morphology was accounted for (r = 0.06 to 0.09).
Discussion:
With no ground-truth E-field or conductivity available, the study establishes the feasibility of the MD-dMRI model and characterizes E-field sensitivity rather than improved dosimetry accuracy. The choice of diffusion tensor is second order for the predicted E-field, which is primarily influenced by individual anatomy. For Parkinson's disease, modeling efforts should focus on CSF- and atrophy-aware head models and dose normalization, rather than a more complex diffusion tensor.

