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.
No comments:
Post a Comment