Neurorecovery and Neuroplasticity: Neurostimulation to Improve Recovery After Brain Injury*

We aim to delineate the network dynamics of learning and to develop physiologically-inspired stimulation to enhance motor recovery. Our research particularly focuses on large scale recordings and frameworks for processing such as oscillatory dynamics and cross-area filtering. Our approach is also grounded in developing a deeper understanding of how activity in the motor network drives recovery over both short and longer timescales. During this session, I will review our past work highlighting the importance of low-frequency oscillatory dynamics for movement control and as a target for modulation. I will also present new work on the dysregulation of cortical and subcortical dynamics after injury and how low-frequency stimulation can improve coordination. Our work provides insight into how to design therapeutic stimulation that selectively targets population dynamics in the distributed motor network and to improve dexterity after brain injury

The presentation will provides a comprehensive summary of both invasive and noninvasive neuromodulation tools in post-stroke motor recovery including brief mechanism, major trials results and stage of translational chain.

Parvalbumin (PV) inhibitory interneurons may be important regulators of plasticity in the healthy and injured cortex. We used longitudinal two-photon calcium imaging to record the activity of individual PV cells in the healthy somatosensory cortex during experience-dependent plasticity (whisker trimming) and in the peri-infarct cortex after stroke. Whisker trimming leads to recruitment of PV cells responsive to the spared whisker in deprived cortical barrels, and there are long-lasting shifts in responsivity to the spared whisker in the spared barrel even after whisker regrowth. Furthermore, chemogenetic inhibition of PV cells during experience-dependent plasticity blocks whisker trimming-induced remapping. In the peri-infarct cortex, sensory-evoked responses to the principal whisker of the infarcted barrel are selectively impaired after stroke, similar to the effects observed in pyramidal cells. Together, these results suggest that proper functioning of PV cells is essential for adaptive plasticity in the healthy and injured cortex.

Post-stroke aphasia is common and causes substantial disability. Although speech-language therapy can help improve aphasia, recovery is often incomplete. Non-invasive brain stimulation methods provide a potential avenue for improving aphasia recovery, but effects in studies to date are rarely clinically significant. Understanding the brain basis of aphasia recovery is essential to improving brain stimulation treatments for aphasia. In this presentation, I will briefly review the approaches used to date in brain stimulation studies for aphasia. I will then provide an update on new research examining the brain basis of aphasia recovery, and will discuss new approaches to brain stimulation suggested by recent findings.