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.

Saturday, February 15, 2014

Predicting Future Brain Tissue Loss From White Matter Connectivity Disruption in Ischemic Stroke

This is something that is desperately needed, although once we know the damage in the white matter, I know of no stroke protocols that will alleviate the problem. So ask your doctor what they will do once this is identified.
http://stroke.ahajournals.org/content/early/2014/02/12/STROKEAHA.113.003645.abstract
  1. Costantino Iadecola, MD
+ Author Affiliations
  1. From the Department of Radiology (A.K., A.R.), Brain and Mind Research Institute (A.K., H.K., B.B.N., A.R., C.I.), and Department of Neurology (H.K., B.B.N., C.I.), Weill Cornell Medical College, New York, NY.
  1. Correspondence to Amy Kuceyeski, PhD, Department of Radiology, Weill Cornell Medical College, 515 E 71st St, New York, NY 10065. E-mail amk2012@med.cornell.edu

Abstract

Background and Purpose—The Network Modification (NeMo) Tool uses a library of brain connectivity maps from normal subjects to quantify the amount of structural connectivity loss caused by focal brain lesions. We hypothesized that the Network Modification Tool could predict remote brain tissue loss caused by poststroke loss of connectivity.
Methods—Baseline and follow-up MRIs (10.7±7.5 months apart) from 26 patients with acute ischemic stroke (age, 74.6±14.1 years, initial National Institutes of Health Stroke Scale, 3.1±3.1) were collected. Lesion masks derived from diffusion-weighted images were superimposed on the Network Modification Tool’s connectivity maps, and regional structural connectivity losses were estimated via the Change in Connectivity (ChaCo) score (ie, the percentage of tracks connecting to a given region that pass through the lesion mask). ChaCo scores were correlated with subsequent atrophy.
Results—Stroke lesions’ size and location varied, but they were more frequent in the left hemisphere. ChaCo scores, generally higher in regions near stroke lesions, reflected this lateralization and heterogeneity. ChaCo scores were highest in the postcentral and precentral gyri, insula, middle cingulate, thalami, putamen, caudate nuclei, and pallidum. Moderate, significant partial correlations were found between baseline ChaCo scores and measures of subsequent tissue loss (r=0.43, P=4.6×10–9; r=0.61, P=1.4×10–18), correcting for the time between scans.
Conclusions—ChaCo scores varied, but the most affected regions included those with sensorimotor, perception, learning, and memory functions. Correlations between baseline ChaCo and subsequent tissue loss suggest that the Network Modification Tool could be used to identify regions most susceptible to remote degeneration from acute infarcts.

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