Abstracts

Rationale: A novel approach is presented for implanting investigational responsive neurostimulation (RNS) therapy depth electrodes for maximally influencing the epileptic network of a double band heterotopia. White matter pathways are targeted for RNS therapy near ictal-related transient regions of hyperperperfusion. The biophysical properties of axons are used to propagate electrical current beyond the source of stimulation Methods: Scalp video-EEG monitoring and subtracted ictal SPECT co-registered to MRI (SISCOM) localized two active right posterior-inferior parietal epileptic sources for a subject with a previously identified double band heterotopia. Stereotactic guidance for two 4-contact 3.5mm center-center depth electrodes employed the subject's diffusion tensor imaging data set. Diffusion tensor tractography was generated (MRDiffusion) using seed regions of interest (ROI) taken from 3D electric fields (radius 3.75mm) predicted to activate the surrounding white matter (COMSOL Multiphysics). The two depth electrodes were implanted in an orthogonal orientation in the right posterior-inferior parietal region overlapping the seed ROI. Both electrode tips extended to the wall of the right lateral ventricle. SAS acquisition and analysis (AnalyzeR) were performed 5 months following implantation of the RNS system. Bipolar stimulation of the posterior two of four depth lead contacts was performed during peripheral intravenous administration of Tc99-HMPAO. The injection of radiotracer occurred during delivery of 12 high frequency stimuli (200Hz) at 0.5Hz (stimulation intensity=5mA, pulse width=160μsec, burst duration=100msec). A post-stimulation baseline SPECT was acquired 24 hours following the stimulation session. The data were normalized, subtracted and co-registered to the subject's 3D Fourier transform SPGR magnetic resonance neuroimaging dataset. Results: Transient hyper- and hypo-perfusion related changes associated with repetitive bipolar stimulation of white matter were seen in the visual cortices medially and bilaterally. In addition, a region of transient hyper-perfusion was seen in the ipsilateral basal frontal cortex. Behaviorally, repetitive bipolar stimulation of the subject's posterior-inferior parietal depth contacts was associated with bright elementary flashes of light in the left upper visual quadrant. No afterdischarges were recorded by electrocorticography during stimulation. Conclusions: SAS demonstrates propagation of RNS therapy beyond the electrode's generated electric field to distant epileptic tissue of a double band heterotopia. These data ostensibly represent the extent of cortical modulation for a given set of focal stimulation parameters delivered though a specific electrode contact shape, orientation and location in white matter. Presurgical planning can predict axonal pathways that direct the spread of RNS current to distant neural tissue. As a result, a greater extent of the epileptic circuit can be potentially modulated with a minimum number of electrodes.