Publications [#326840] of Guillermo Sapiro

Papers Published

1. Gunalan, K; Chaturvedi, A; Howell, B; Duchin, Y; Lempka, SF; Patriat, R; Sapiro, G; Harel, N; McIntyre, CC, Creating and parameterizing patient-specific deep brain stimulation pathway-activation models using the hyperdirect pathway as an example., PloS one, vol. 12 no. 4 (January, 2017), pp. e0176132 [doi]
   (last updated on 2024/04/15)

   Abstract:
   

   Background

   Deep brain stimulation (DBS) is an established clinical therapy and computational models have played an important role in advancing the technology. Patient-specific DBS models are now common tools in both academic and industrial research, as well as clinical software systems. However, the exact methodology for creating patient-specific DBS models can vary substantially and important technical details are often missing from published reports.

   Objective

   Provide a detailed description of the assembly workflow and parameterization of a patient-specific DBS pathway-activation model (PAM) and predict the response of the hyperdirect pathway to clinical stimulation.

   Methods

   Integration of multiple software tools (e.g. COMSOL, MATLAB, FSL, NEURON, Python) enables the creation and visualization of a DBS PAM. An example DBS PAM was developed using 7T magnetic resonance imaging data from a single unilaterally implanted patient with Parkinson's disease (PD). This detailed description implements our best computational practices and most elaborate parameterization steps, as defined from over a decade of technical evolution.

   Results

   Pathway recruitment curves and strength-duration relationships highlight the non-linear response of axons to changes in the DBS parameter settings.

   Conclusion

   Parameterization of patient-specific DBS models can be highly detailed and constrained, thereby providing confidence in the simulation predictions, but at the expense of time demanding technical implementation steps. DBS PAMs represent new tools for investigating possible correlations between brain pathway activation patterns and clinical symptom modulation.