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, August 7, 2012

A Perfusion fMRI Study of the Neural Correlates of Sustained-Attention and Working-Memory Deficits in Chronic Traumatic Brain Injury

We need something like this for strokes  to be able to tell whether the capillaries have properly opened up - pericytes. And to assure that there is enough blood flow for neurogenesis.
http://nnr.sagepub.com/content/26/7/870.abstract?etoc

Abstract

Background. Given that traumatic brain injury (TBI) results in chronic alteration of baseline cerebral perfusion, a perfusion functional MRI (fMRI) method that dissociates resting- and task-related cerebral blood flow (CBF) changes can be useful in noninvasively investigating the neural correlates of cognitive dysfunction and recovery in TBI. Objective. The authors used continuous arterial spin-labeled (ASL) perfusion fMRI to characterize CBF at rest and during sustained-attention and working-memory tasks. Methods. A total of 18 to 21 individuals with moderate to severe TBI and 14 to 18 demographically matched healthy controls completed 3 continuous 6-minute perfusion fMRI scans (resting, visual sustained attention, and 2-back working memory). Results. For both tasks, TBI participants showed worse behavioral performance than controls. Voxelwise neuroimaging analysis of the 2-back task found that group differences in task-induced CBF changes were localized to bilateral superior occipital cortices and the left superior temporal cortex. Whereas controls deactivated these areas during task performance, TBI participants tended to activate these same areas. These regions were among those found to be disproportionately hypoperfused at rest after TBI. For both tasks, the control and TBI groups showed different patterns of correlation between performance and task-related CBF changes. Conclusions. ASL perfusion fMRI demonstrated differences between individuals with TBI and healthy controls in resting perfusion and in task-evoked CBF changes as well as different patterns of performance-activation correlation. These results are consistent with the notion that sensory/attentional modulation deficits contribute to higher cognitive dysfunction in TBI.

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