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, February 14, 2017

Association of exhaled carbon monoxide with stroke incidence and subclinical vascular brain injury

You'll have to ask your doctor about all these benefits vs. this negative article.

Carbon Monoxide Releasing Molecule-A1 (CORM-A1) Improves Neurogenesis: Increase of Neuronal Differentiation Yield by Preventing Cell Death

Carbon monoxide may actually protect the brain from damage after subarachnoid hemorrhage

Deadly carbon monoxide prevents miscarriage

we found that inhaled low dose carbon monoxide was anti-inflammatory. It reduced the amount of cell death (apoptosis), and increased levels of the anti-apoptotic molecule BAG-1, in the placenta and additionally increased the level of vascular endothelial growth factor (VEGF), which is associated with angiogenesis and blood vessel repair." 

 

 


The negative article here:

Association of exhaled carbon monoxide with stroke incidence and subclinical vascular brain injury

Stroke, 02/12/2016
The authors related exhaled carbon monoxide (CO) to magnetic resonance imaging measures of subclinical cerebrovascular disease cross–sectionally and to incident stroke/transient ischemic attack prospectively in the Framingham Offspring study. In this large, community–based sample of individuals without clinical stroke/transient ischemic attack at baseline, higher exhaled CO was associated with a greater burden of subclinical cerebrovascular disease cross–sectionally and with increased risk of stroke/transient ischemic attack prospectively. Further investigation is necessary to explore the biological mechanisms linking elevated CO with stroke.

Methods

  • The authors measured exhaled CO in 3313 participants (age 59±10 years; 53% women), and brain magnetic resonance imaging was available in 1982 individuals (age 58±10 years; 54% women).
  • Participants were analyzed according to tertiles of exhaled CO concentration.

Results

  • In age- and sex-adjusted models, the highest tertile of exhaled CO was associated with lower total cerebral brain volumes, higher white-matter hyperintensity volumes, and greater prevalence of silent cerebral infarcts (P<0.05 for all).
  • The results for total cerebral brain volume and white-matter hyperintensity volume were consistent after removing smokers from the sample, and the association with white-matter hyperintensity volume persisted after multivariable adjustment (P=0.04).
  • In prospective analyses (mean follow-up 12.9 years), higher exhaled CO was associated with 67% (second tertile) and 97% (top tertile) increased incidence of stroke/transient ischemic attack relative to the first tertile that served as referent (P<0.01 for both).
  • These results were consistent in nonsmokers and were partially attenuated upon adjustment for vascular risk factors.
Go to PubMed Go to Abstract Print Article Summary Cat 2 CME Report

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