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.

Thursday, April 14, 2016

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

This is so godammed obvious, you look at the dead areas of the brain. Did the dead area formerly control hand function? If so then recovery is unlikely to happen easily. My motor control area for the hand seems to be dead and likewise the premotor cortex is mostly dead. My hand recovery is almost non-existent. It requires moving and finding neurons somewhere else to take over that functionality. It has  never been identified how to do that.
http://nnr.sagepub.com/content/30/4/328?etoc
  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.

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