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, December 20, 2014

BDNF Induced by Treadmill Training Contributes to the Suppression of Spasticity and Allodynia After Spinal Cord Injury via Upregulation of KCC2

How much of this would be useful for stroke survivors?  Is there a downside to doing this in humans even though it has only been tested in rats?
http://nnr.sagepub.com/content/early/2014/12/11/1545968314562110.abstract?&
  1. Syoichi Tashiro, MD1
  2. Munehisa Shinozaki, MD, PhD2
  3. Masahiko Mukaino, MD, PhD3
  4. François Renault-Mihara, PharmD, PhD2
  5. Yoshiaki Toyama, MD, PhD4
  6. Meigen Liu, MD, PhD1
  7. Masaya Nakamura, MD, PhD4
  8. Hideyuki Okano, MD, PhD2
  1. 1Department of Rehabilitation Medicine, Keio University School of Medicine, Tokyo, Japan
  2. 2Department of Physiology, Keio University School of Medicine, Tokyo, Japan
  3. 3Asahikawa Medical University, Hokkaido, Japan
  4. 4Department of Orthopaedic Surgery, Keio University School of Medicine, Tokyo, Japan
  1. Hideyuki Okano, Department of Physiology, Keio University School of Medicine, 35 Shinano-machi, Shinjuku-ku, Tokyo 160-8582, Japan. Email: hidokano@a2.keio.jp

Abstract

Background. Spasticity and allodynia are major sequelae that affect the quality of life and daily activities of spinal cord injury (SCI) patients. Although rehabilitation ameliorates spasticity and allodynia, the molecular mechanisms involved in these processes remain elusive. Objective. To investigate the molecular mechanisms by which rehabilitation ameliorates spasticity and allodynia after SCI in rats. Methods. The expression levels of brain-derived neurotrophic factor (BDNF) and potassium-chloride cotransporter-2 (KCC2), as well as the localization of KCC2, were examined in the lumbar enlargements of untrained and treadmill-trained thoracic SCI model rats. Spasticity and allodynia were determined via behavioral and electrophysiological analyses. The effects of BDNF on spasticity, allodynia, and KCC2 activation were determined by inhibition of BDNF signaling via intrathecal administration of TrkB-IgG. The effects of SCI and training on the expression levels of functional phospholipase C-γ in the lumbar enlargement were also examined. Results. Treadmill training after SCI upregulated endogenous BDNF expression and posttranslational modification of KCC2 in the lumbar enlargement significantly. There were also significant correlations between increased KCC2 expression and ameliorated spasticity and allodynia. Administration of TrkB-IgG abrogated the training-induced upregulation of KCC2 and beneficial effects on spasticity and allodynia. The expression level of functional phospholipase C-γ was reduced significantly after SCI, which may have contributed to the change in the function of BDNF, whereby it did not trigger short-term downregulation or induce long-term upregulation of KCC2 expression secondary to training. Conclusions. BDNF-mediated restoration of KCC2 expression underlies the suppression of spasticity and allodynia caused by rehabilitation.
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