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, October 25, 2016

Magnetic resonance imaging of local and remote vascular remodelling after experimental stroke

From this we should be able to get an objective damage diagnosis which we can then go to the stroke protocol database for solutions to recover from such damage. This is so fucking easy to setup that even a stroke addled person like me knows what needs to be done. And if my minions in the ASA, NSA and WSO would just do my bidding this could be fixed in  no time.
http://jcb.sagepub.com/content/early/2016/10/18/0271678X16674737.abstract?&
  1. Pavel Yanev1
  2. Peter R Seevinck1
  3. Umesh S Rudrapatna1
  4. Mark JRJ Bouts1
  5. Annette van der Toorn1
  6. Karen Gertz2,3
  7. Golo Kronenberg2,4
  8. Matthias Endres2,3,4,5,6
  9. Geralda A van Tilborg1
  10. Rick M Dijkhuizen1⇑
  1. 1Biomedical MR Imaging and Spectroscopy Group, University Medical Center Utrecht, Utrecht, The Netherlands
  2. 2Department of Neurology, Charité – Universitaetsmedizin Berlin, Berlin, Germany
  3. 3Center for Stroke Research Berlin, Charité – Universitaetsmedizin Berlin, Berlin, Germany
  4. 4German Center for Cardiovascular Research (DZHK), Universitaetsmedizin Berlin, Berlin, Germany
  5. 5German Center for Neurodegenerative Diseases (DZNE), Universitaetsmedizin Berlin, Berlin, Germany
  6. 6Berlin Institute of Health (BIH), Berlin, Germany
  1. Rick M Dijkhuizen, Center for Image Sciences, University Medical Center Utrecht, Heidelberglaan 100, 3584 CX Utrecht, The Netherlands. Email: r.m.dijkhuizen@umcutrecht.nl

Abstract

The pattern of vascular remodelling in relation to recovery after stroke remains largely unclear. We used steady-state contrast-enhanced magnetic resonance imaging to assess the development of cerebral blood volume and microvascular density in perilesional and exofocal areas from (sub)acutely to chronically after transient stroke in rats. Microvascular density was verified histologically after infusion with Evans Blue dye. At day 1, microvascular cerebral blood volume and microvascular density were reduced in and around the ischemic lesion (intralesional borderzone: microvascular cerebral blood volume = 72 ± 8%; microvascular density = 76 ± 8%) (P < 0.05), while total cerebral blood volume remained relatively unchanged. Perilesional microvascular cerebral blood volume and microvascular density subsequently normalized (day 7) and remained relatively stable (day 70). In remote ipsilateral areas in the thalamus and substantia nigra – not part of the ischemic lesion – microvascular density gradually increased between days 1 and 70 (thalamic ventral posterior nucleus: microvascular density = 119 ± 9%; substantia nigra: microvascular density = 122 ± 8% (P < 0.05)), which was confirmed histologically. Our data indicate that initial microvascular collapse, with maintained collateral flow in larger vessels, is followed by dynamic revascularization in perilesional tissue. Furthermore, progressive neovascularization in non-ischemic connected areas may offset secondary neuronal degeneration and/or contribute to non-neuronal tissue remodelling. The complex spatiotemporal pattern of vascular remodelling, involving regions outside the lesion territory, may be a critical endogenous process to promote post-stroke brain reorganization.
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