Warren M. Grill

TL;DR: The hypothesis of stimulation-induced modulation of pathological network activity as a therapeutic mechanism of DBS is supported after apparently contradictory results showing suppression of activity in the stimulated nucleus, but increased inputs to projection nuclei.

TL;DR: Geometrically and electrically accurate models of mammalian motor nerve fibers are developed to gain insight into the biophysical mechanisms that underlie the changes in axonal excitability and regulate the recovery cycle.

TL;DR: Overcoming the biophysical and biological challenges will enable effective high-density neural interfaces for stimulation and recording and consider emerging opportunities to improve neural interfaces, including cellular-level silicon to neuron connections, optical stimulation, and approaches to control inflammation.

TL;DR: Synthesis of theoretical and empirical findings is used to provide guidance for the selection of stimulus parameters and the recommended charge density limit for DBS represents a liberal estimate for non-damaging stimulation.

TL;DR: Detailed computer-based models of CNS cells and axons were developed that accurately reproduced the dynamic firing properties of mammalian motoneurons including afterpotential shape, spike-frequency adaptation, and firing frequency as a function of stimulus amplitude to provide a biophysical basis for understanding frequency-dependent outputs during CNS stimulation and provide useful tools for selective stimulation of the CNS.