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.

Thursday, October 27, 2011

Leukoaraiosis is associated with arterial wall thickness: A quantitative analysis

Leukoaraiosis or periventricular white matter disease is a term for changes in the cerebral white matter that can be detected with high frequency by CT and MRI in aged individuals.
http://onlinelibrary.wiley.com/doi/10.1111/j.1440-1789.2011.01262.x/full

Keywords:

  • blood vessels;
  • leukoaraiosis;
  • stroke;
  • white matter changes

Leukoaraiosis refers to an age-related, abnormal appearance of the brain white matter on neuroimaging. The association between leukoaraiosis and cerebrovascular disease suggests that ischemia may be an important contributing factor; however, the pathogenesis of the condition remains controversial. We hypothesized that physical abnormalities of blood vessels might be culpable and compared the external and internal measurements of blood vessel walls between brains that demonstrated leukoaraiosis on imaging and normal control brains. Fourteen brains of individuals who had been diagnosed as having severe leukoaraiosis and five non-leukoaraiosis control brains were studied. Arterial cross-sections were evaluated by length measurements with an image analysis device. Arterial wall thickness and the ratio of the outer and inner diameters of the vessel were measured. We measured a total of 108 vessels in the leukoaraiosis group and 95 vessels in the control group. The vessel walls of the leukoaraiosis patients were an average of 5.5 µm thicker than the walls of control vessels of the same inside diameter (P = 0.0000, 95% CI 3.01–8.08) and an average of 2.3 µm thicker than walls of control vessels of the same outside diameter (P = 0.016, 95% CI 0.48–4.17). Our data provide evidence that leukoaraiosis is associated with vessel wall thickening in an additive fashion and indicate that structural vascular abnormalities are associated with leukoaraiosis.

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