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.

Saturday, November 30, 2013

Plasticity beyond peri-infarct cortex: Spinal up regulation of structural plasticity, neurotrophins, and inflammatory cytokines during recovery from cortical stroke

I'm sure your wonderful up-to-date doctor can explain all this and how it is already incorporated into your 100% recovery protocol. You don't have a 100% recovery protocol? Why not? Is your doctor not any good?

Plasticity beyond peri-infarct cortex: Spinal up regulation of structural plasticity, neurotrophins, and inflammatory cytokines during recovery from cortical stroke

  • a Centre for Neuroscience, University of Alberta, Edmonton, Alberta, Canada T6G 2R3
  • b Faculty of Rehabilitative Medicine, University of Alberta, Edmonton, Alberta, Canada T6G 2R3
  • c Department of Psychiatry, University of Alberta, Edmonton, Alberta, Canada T6G 2R3
  • d Neurochemical Research Unit, University of Alberta, Edmonton, Alberta, Canada T6G 2R3

Highlights

Cortical stroke induces heightened expression of GAP-43 in the spinal cord
Plasticity in the spinal cord after cortical stroke has a finite temporal window
TNF-α, IL-6, and NT-3 protein levels in spinal cord correlate with GAP-43 levels
BDNF increases transiently in spinal cord prior to heightened GAP-43 expression

Abstract

Stroke induces pathophysiological and adaptive processes in regions proximal and distal to the infarct. Recent studies suggest that plasticity at the level of the spinal cord may contribute to sensorimotor recovery after cortical stroke. Here, we compare the time course of heightened structural plasticity in the spinal cord against the temporal profile of cortical plasticity and spontaneous behavioural recovery. To examine the relation between trophic and inflammatory effectors and spinal structural plasticity, spinal expression of brain derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) were measured. Growth-associated protein 43 (GAP-43), measured at 3, 7, 14, or 28 days after photothrombotic stroke of the forelimb sensorimotor cortex (FL-SMC) to provide an index of periods of heightened structural plasticity, varied as a function of lesion size and time after stroke in the cortical hemispheres and the spinal cord. Notably, GAP-43 levels in the cervical spinal cord were significantly increased after FL-SMC lesion, but the temporal window of elevated structural plasticity was more finite in spinal cord relative to ipsilesional cortical expression (returning to baseline levels by 28 post-stroke). Peak GAP-43 expression in spinal cord occurred during periods of accelerated spontaneous recovery, as measured on the Montoya Staircase reaching task, and returned to baseline as recovery plateaued. Interestingly, spinal GAP-43 levels were significantly correlated with spinal levels of the inflammatory cytokines TNF-α and IL-6 as well as the neurotrophin NT-3, while a transient increase in BDNF levels preceded elevated GAP-43 expression. These data identify a significant but time-limited window of heightened structural plasticity in the spinal cord following stroke that correlates with spontaneous recovery and the spinal expression of inflammatory cytokines and neurotrophic factors.

Abbreviations

  • IC, ipsilesional cortex;
  • CC, contralesional cortex;
  • CSC, cervical spinal cord;
  • LSC, lumbar spinal cord;
  • FL-SMC, forelimb sensorimotor cortex;
  • GAP-43, growth associated protein-43;
  • TNF-α, tumor necrosis factor - alpha;
  • IL-6, interleukin 6;
  • BDNF, brain derived neurotrophic factor;
  • NT-3, neurotrophin-3

Keywords

  • Ischemia;
  • Sensorimotor cortex;
  • Plasticity;
  • Spinal cord;
  • Inflammation;
  • Neurotrophins;
  • GAP-43;
  • TNF-alpha;
  • IL-6;
  • BDNF;
  • NT-3

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