Deans' stroke musings: Primary Motor Cortex Excitability During Recovery AfterStroke: Implications for Neuromodulation

Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Tuesday, July 23, 2019

Primary Motor Cortex Excitability During Recovery AfterStroke: Implications for Neuromodulation

Hopefully your doctor did something with this from 4 years ago.

Primary Motor Cortex Excitability During Recovery AfterStroke: Implications for Neuromodulation

Abstract

Background: Non-invasive brain stimulation techniques may be useful adjuvants to promote recoveryafter stroke. They are typically used to facilitate ipsilesional cortical excitability directly, or indirectly bysuppressing contralesional cortical excitability and reducing interhemispheric inhibition from the con-tralesional to ipsilesional hemisphere. However, most of the evidence for this approach comes fromstudies of patients at the chronic stage of recovery.
Hypothesis: We hypothesized that corticomotor excitability and interhemispheric inhibition wouldinitially be asymmetric, with greater interhemispheric inhibition from contralesional to ipsilesional M1.We also hypothesized that balancing of corticomotor excitability and interhemispheric inhibition wouldbe associated with greater improvements in paretic upper-limb impairment and function. We conducted a retrospective analysis of longitudinal data collected from 46 patients during ﬁrst six months after stroke. Transcranial magnetic stimulation was used to measure rest motor threshold, stimulus-response curves, and ipsilateral silent periods from the extensor carpiradialismuscles of both upper limbs. Analyses of variance and linear regression modeling were used to evaluatethe effect of time on corticomotor excitability and interhemispheric inhibition in both hemispheres, andassociations between these effects and improvements in paretic upper-limb impairment and function.
Results:All participants had subcortical damage and only two had motor cortex involvement. As ex-pected, ipsilesional corticomotor excitability was initially suppressed and increased over time, and thisincrease was associated with improved upper-limb impairment and function. However, interhemisphericinhibition was symmetrical and stable over time, and there was no evidence for a decrease in con-tralesional corticomotor excitability.
Conclusions:Neuromodulation interventions applied during spontaneous recovery may be more beneﬁcial if they facilitate ipsilesional corticomotor excitability directly.2015 Elsevier Inc. All rights reserved.