Targeting interhemispheric inhibition with neuromodulation to enhance stroke rehabilitation

 In my case there is no interhemispheric inhibition since it is dead brain over there. So what is your dead brain rehab protocol? There must be millions of us out there and I've never seen any research on that problem.

Targeting interhemispheric inhibition with neuromodulation to enhance stroke rehabilitation

 L.J. Boddington, J.N.J. Reynolds * Brain Health Research Centre and Brain Research NZ Centre of Research Excellence, Department of Anatomy, University of Otago, New Zealand article info Article history: Received 26 February 2016 Received in revised form 10 December 2016 Accepted 10 January 2017 Available online xxx Keywords: Interhemispheric inhibition Stroke Rehabilitation Neuromodulation Transcranial magnetic stimulation Electrical stimulation  

abstract  

Background/Objectives:  

Interhemispheric inhibition in the brain plays a dynamic role in the production of voluntary unimanual actions. In stroke, the interhemispheric imbalance model predicts the presence of asymmetry in interhemispheric inhibition, with excessive inhibition from the contralesional hemisphere limiting maximal recovery. Stimulation methods to reduce this asymmetry in the brain may be promising as a stroke therapy, however determining how to best measure and modulate interhemispheric inhibition and who is likely to benefit, remain important questions.  

 

Methods:  

 

This review addresses current understanding of interhemispheric inhibition in the healthy and stroke lesioned brain. We present a review of studies that have measured interhemispheric inhibition using different paradigms in the clinic, as well as results from recent animal studies investigating stimulation methods to target abnormal inhibition after stroke.  

 

Main findings/Discussion:  

 

The degree to which asymmetric interhemispheric inhibition impacts on stroke recovery is controversial, and we consider sources of variation between studies which may contribute to this debate. We suggest that interhemispheric inhibition is not static following stroke in terms of the movement phase in which it is aberrantly engaged. Instead it may be dynamically increased onto perilesional areas during early movement, thus impairing motor initiation. Hence, its effect on stroke recovery may differ between studies depending on the technique and movement phase of eliciting the measurement. Finally, we propose how modulating excitability in the brain through more specific targeting of neural elements underlying interhemispheric inhibition via stimulation type, location and intensity may raise the ceiling of recovery following stroke and enhance functional return.