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.

Friday, October 25, 2013

C-reactive protein and cognition are unrelated to leukoaraiosis

My doctor just threw off a comment to me that I had had some earlier infarcts, so I'm assuming it was some white matter hyperintensities, obviously not important since I didn't get to see a picture of them or any explanation of what to do about them. My doctor told me nothing and as far as I could tell knew nothing, did nothing and should have never been paid for his non-efforts. So even though I have leukoaraiosis I think my cognition is still damn good, better than my doctors.
http://scholar.google.com/scholar_url?hl=en&q=http://downloads.hindawi.com/journals/tswj/aip/121679.pdf&sa=X&scisig=AAGBfm1sH0XbW4TGUMjDn5PEQgJ5eR3ILA&oi=scholaralrt
Introduction
Inflammation has been increasingly recognized as component in cerebrovascular (1) and neurodegenerative diseases (2, 3). In addition, biological aging of the brain is partly attributable to aging of the cerebrovascular circulation and the effects of vascular changes on the brain (4). Inflammation has been linked to the pathogenesis of cardiovascular disease, obesity and insulin resistance, which are so related to cognitive impairment (5). The hypothesis that inflammation is related to cognitive impairment, although new, is consistent (2). Therefore, few studies evaluated that circulating inflammatory proteins are associated with increased risk of dementia (6), cognitive impairment (7) and cerebral white matter lesions (WML), common referred to leukoaraiosis (8-10).
CRP, composed of five 23 kDa subunits, is a hepatically derived pentraxin that has important role in the human immune system (11). That protein is a sensitive nonspecific marker of systemic low-grade inflammation (5) and increased serum concentrations of CRP have been associated with impaired cognition, stroke and depression (2, 6, 8).

Beyond pro-inflammatory response, that causes neuronal damage directly, increased concentrations of CRP acting as cardiovascular risk factor - approved predictor by Food and Drug Administration - or causing brain atherosclerosis can result in cerebral macro or microangiopathies. Both lesions can disrupt the integrity of frontal-subcortical circuits and are responsible for the development of cognitive impairment, dementia or depressive disorders (12). There are some evidences that elevated serum CRP levels may be a useful biomarker to identify individuals at an increased risk for cognitive impairment (7).

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