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, May 31, 2016

Neural Substrates of Motor Recovery in Severely Impaired Stroke Patients With Hand Paralysis

Do these fucking idiots not even comprehend that there has to be different interventions for dead brain vs. damaged brain. They talk but never tell us anything useful. They excluded primary motor cortex damage, cherry picking at its' worst.
http://nnr.sagepub.com/content/30/4/328.full

  1. Michelle L. Harris-Love, PhD1,2
  2. Evan Chan, MS2
  3. Alexander W. Dromerick, MD1,2,3
  4. Leonardo G. Cohen, MD4
  1. 1Georgetown University Medical Center, Washington, DC, USA
  2. 2MedStar National Rehabilitation Hospital, Washington, DC, USA
  3. 3District of Columbia VA Medical Center, Washington, DC, USA
  4. 4Human Cortical Physiology and Neurorehabilitation Section, NINDS, NIH, Bethesda, MD, USA
  1. Michelle L. Harris-Love, PhD, 102 Irving Street NW, Room 1058, Washington, DC 20010, USA. Email: Mh672@georgetown.edu

Abstract

In well-recovered stroke patients with preserved hand movement, motor dysfunction relates to interhemispheric and intracortical inhibition in affected hand muscles. In less fully recovered patients unable to move their hand, the neural substrates of recovered arm movements, crucial for performance of daily living tasks, are not well understood. Here, we evaluated interhemispheric and intracortical inhibition in paretic arm muscles of patients with no recovery of hand movement (n = 16, upper extremity Fugl-Meyer Assessment = 27.0 ± 8.6). We recorded silent periods (contralateral and ipsilateral) induced by transcranial magnetic stimulation during voluntary isometric contraction of the paretic biceps and triceps brachii muscles (correlates of intracortical and interhemispheric inhibition, respectively) and investigated links between the silent periods and motor recovery, an issue that has not been previously explored. We report that interhemispheric inhibition, stronger in the paretic triceps than biceps brachii muscles, significantly correlated with the magnitude of residual impairment (lower Fugl-Meyer scores). In contrast, intracortical inhibition in the paretic biceps brachii, but not in the triceps, correlated positively with motor recovery (Fugl-Meyer scores) and negatively with spasticity (lower Modified Ashworth scores). Our results suggest that interhemispheric inhibition and intracortical inhibition of paretic upper arm muscles relate to motor recovery in different ways. While interhemispheric inhibition may contribute to poorer recovery, muscle-specific intracortical inhibition may relate to successful motor recovery and lesser spasticity.


Introduction


Over the past nearly 2 decades, there has been a great deal of investigation into mechanisms of impairment and recovery of hand movement after human stroke.(But no protocols) This work has demonstrated that limitations in recovery of functional hand movements poststroke are often linked to abnormalities in intracortical and interhemispheric inhibition. These findings have provided insight into the mechanisms of behavioral rehabilitation approaches, such as constraint-induced movement therapy,1-5 and have informed the development of cortical stimulation paradigms to improve hand recovery.6-9

Previous studies have used transcranial magnetic stimulation (TMS) to investigate intracortical inhibition of primary motor cortex (M1) hand representations in well-recovered stroke patients with at least partial recovery of hand function. Paired-pulse measurements of short-interval intracortical inhibition (SICI),10 associated with GABAA-mediated intracortical inhibition,11 have shown abnormally decreased levels of intracortical inhibition targeting the paretic hand.1,2,12-15 In contrast, intracortical inhibition reflected by the contralateral silent period (cSP), associated with GABAB receptor–mediated inhibition,11 is reported to be abnormally increased in the paretic hand1,15-19 and to decrease with recovery.16 Thus, it appears that SICI, reflecting GABAA-mediated intracortical inhibition, is abnormally decreased while cSP, reflecting GABAB receptor–mediated inhibition, is abnormally increased in the paretic hand post-stroke.

In addition to intracortical inhibition, interhemispheric inhibition between M1 hand representations in stroke patients with hand recovery has also been widely studied, and like intracortical inhibition, it has been studied using both paired-pulse and silent period TMS techniques. Paired-pulse measurements have shown that interhemispheric inhibition targeting the affected hemisphere (ie, paretic hand) is stronger than that targeting the unaffected hemisphere20-22 and abnormally persistent during paretic finger movement preparation,23,24 particularly in those with poorer hand recovery. Ipsilateral silent period measurements have provided further support for the notion that interhemispheric inhibition targeting the paretic hand is stronger than that targeting the nonparetic hand15,25 and that measured in controls.26

Mechanisms of upper arm motor recovery in stroke patients unable to use their hands, however, are not well understood. To examine interhemispheric and intracortical inhibition in paretic elbow flexors and extensors, we evaluated silent periods during voluntary isometric contractions of paretic arm biceps (flexor) or triceps (extensor) brachii and measured the correlation between these measures and clinical and behavioral tests of motor ability, reaching performance, and spasticity. Recognizing that specific electrophysiological measurements, such as silent periods, reflect only a portion of the larger processes of intracortical and interhemispheric inhibition, we emphasize that when we refer to intracortical and interhemispheric inhibition we are referring only to that reflected by the contralateral and ipsilateral silent periods, respectively.

Given that many patients have particular difficulty deactivating elbow flexors, we postulated that inhibition targeting an elbow flexor muscle (biceps brachii) would be less than that targeting an elbow extensor (triceps brachii) and that biceps inhibition would correlate negatively with motor impairment. We report that interhemispheric inhibition and intracortical inhibition of these paretic upper arm muscles relate to paretic arm motor recovery differently in this population. 

More at link.

No comments:

Post a Comment