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.

Monday, October 23, 2017

Hippocampal Deformations and Entorhinal Cortex Atrophy as an Anatomical Signature of Long-Term Cognitive Impairment: from the MCAO Rat Model to the Stroke Patient

Laziness, describe a problem but offer NO solution.
https://link.springer.com/article/10.1007/s12975-017-0576-9

  • C. Delattre
  • C. Bournonville
  • F. Auger
  • R. Lopes
  • C. Delmaire
  • H. Henon
  • A. M. Mendyk
  • S. Bombois
  • J. C. Devedjian
  • D. Leys
  • C. Cordonnier
  • R. Bordet
  • M. Bastide
  • C. Delattre
    • 1
  • C. Bournonville
    • 1
  • F. Auger
    • 1
  • R. Lopes
    • 1
  • C. Delmaire
    • 1
  • H. Henon
    • 1
  • A. M. Mendyk
    • 1
  • S. Bombois
    • 1
  • J. C. Devedjian
    • 1
  • D. Leys
    • 1
  • C. Cordonnier
    • 1
  • R. Bordet
  • M. Bastide
    • 1
    • 2
  1. 1.U1171 - Degenerative & Vascular Cognitive Disorders, Université Lille, INSERM, CHU LilleUniversité du Littoral Côte d’OpaleLilleFrance
  2. 2.U1171 - Degenerative & Vascular Cognitive Disorders, Faculté de MédecineUniversité Lille, INSERM, CHU LilleLille cedexFrance
Original Article

Abstract

Stroke patients have an elevated risk of developing long-term cognitive disorders or dementia. The latter is often associated with atrophy of the medial temporal lobe. However, it is not clear whether hippocampal and entorhinal cortex atrophy is the sole predictor of long-term post-stroke dementia. We hypothesized that hippocampal deformation (rather than atrophy) is a predictive marker of long-term post-stroke dementia on a rat model and tested this hypothesis in a prospective cohort of stroke patients.
Male Wistar rats were subjected to transient middle cerebral artery occlusion and assessed 6 months later. Ninety initially dementia-free patients having suffered a first-ever ischemic stroke were prospectively included in a clinical study. In the rat model, significant impairments in hippocampus-dependent memories were observed. MRI studies did not reveal significant atrophy of the hippocampus volume, but significant deformations were indeed observed—particularly on the ipsilateral side. There, the neuronal surface area was significantly lower in ischemic rats and was associated with a lower tissue density and a markedly thinner entorhinal cortex. At 6 months post-stroke, 49 of the 90 patients displayed cognitive impairment (males 55.10%). Shape analysis revealed marked deformations of their left hippocampus, a significantly lower entorhinal cortex surface area, and a wider rhinal sulcus but no hippocampal atrophy. Hence, hippocampal deformations and entorhinal cortex atrophy were associated with long-term impaired cognitive abilities in a stroke rat model and in stroke patients. When combined with existing biomarkers, these markers might constitute sensitive new tools for the early prediction of post-stroke dementia.

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