Medical Student University of Pittsburgh Pittsburgh, Pennsylvania, United States
Disclosure(s):
Jonathan Ho: No financial relationships to disclose
Introduction: Stroke patients often experience motor deficits in the limbs and do not reach satisfactory recovery. Deep brain stimulation (DBS) can target intrinsic pathways that project to vital cortical areas. One structure of interest is the ventro-oralis posterior (VOP)/ventro-intermedium (VIM) of the motor thalamus. The VOP/VIM is a thalamic relay with outgoing excitatory connectivity to the primary motor cortex (M1) and could be a potential target for DBS to facilitate motor function after stroke. We hypothesized that VOP/VIM stimulation may increase the excitability of M1 and strengthen corticospinal motor output and control.
Methods: Five non-human primates (NHP) were implanted with DBS electrodes into the ventral lateral motor thalamus, the internal capsule (IC), and intracortical microelectrode arrays over M1. This setup was replicated in six patients undergoing implantation of DBS electrodes targeting the VOP/VIM for essential tremor with the addition of a macroarray placed over M1. Intraoperatively, direct cortical stimulation (DCS) was paired with VOP/VIM stimulation. When patients returned for DBS programming, they were asked to modulate their force along a trace and the error of deviation was measured with and without DBS.
Results: In the NHPs, a significantly increased amplitude of evoked potentials (EP) and single unit spike counts recorded in M1 with VOP/VIM stimulation was observed. IC stimulation with VOP/VIM stimulation increased the amplitude of motor evoked potentials (MEP) and kinematics of hand muscles. In the intraoperative human studies, when VOP/VIM was stimulated, similar amplification in M1 EPs and MEPs recorded in upper extremity muscles were observed. During the force modulation tasks, a reduction in deviation error was observed when DBS stimulation was on.
Conclusion : This study documented that direct electrical stimulation of the motor thalamus strengthens motor output, both in NHPs and humans. These outcomes support DBS of the motor thalamus as a potential therapeutic approach to treat post-stroke motor deficits.
