Deans' stroke musings

Changing stroke rehab and research worldwide now.Time is Brain!Just think of all the trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 493 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:

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's quite disgusting that this information is not available from every stroke association and doctors group.
My back ground story is here:

Thursday, February 20, 2014

Peri Infarct N-Acetylaspartic Acid Predicts White Matter Atrophy After Ischemic Stroke

Finally someone thinking about objectively measuring white matter damage. What does your doctor think of that?
  1. Stephen M Davis1
+ Author Affiliations
  1. 1Melbourne Brain Cntr, Univ of Melbourne, Parkville, Australia
  2. 2Priority Rsch Cntr for Translational Neuroscience and Mental Health, Univ of Newcastle, Newcastle, Australia
  3. 3Univ of Melbourne, Parkville, Australia
  4. 4Dept of Radiology, Univ of Melbourne, Parkville, Australia


Objective: Cerebral volume changes post stroke have recently been described and may correlate with clinical outcome. We aimed to determine whether peri infarct measurement of the neuronal marker N-Acetylaspartic acid (NAA) on Magnetic Resonance Spectroscopy (MRS) predicts progressive cerebral volume change after stroke.
Methods: 11 patients (7 male) with supratentorial ischemic stroke underwent serial MRI within 1 week of onset, and at 1 and 3 months. Imaging was performed on a 3T Siemens Trio scanner. Structural imaging utilized a T1-weighted axial MPRAGE acquisition (1mm slices, TR1.9sec, TE2.82msec). NAA estimation was performed at the baseline scan using single voxel MRS (TE30msec, 3x3x3cm voxels). The voxel was placed in the peri infarct region as determined by assessment of the diffusion weighted image. Quantitative MRS analysis was performed using LCmodel using water referencing. Brain tissue volume, normalized for subject head size, was estimated with SIENAX, part of FSL. Due to anticipated effects of edema on initial cerebral volume, changes in grey, white and total brain volume were assessed as percentage change between the 1 and 3 month scans.
Results: Mean age was 71yr (IQR 62-79yr). Median baseline NIHSS was 11 (IQR 6-14). Mean baseline grey, white and total brain volume were 713ml (IQR 683-749), 731mL (IQR 721-747) and 1444mL (IQR 1384-1503) respectively. There was a significant correlation between age and baseline grey matter volume (r2=0.73, p=0.001) and total brain volume (r2=0.74, p=0.001). Mean peri infarct NAA concentration was 6.2mM (SD 1.3) compared with 7.0mM (SD 1.2) in the contralateral hemisphere (p=0.09, paired t-test). Mean percentage grey, white and total brain volume changes were 1.2% (IQR -1.8-4.1), 0.4% (IQR -2.2-3.7) and 0.8% (IRQ -1.0-2.6) respectively. There was a significant correlation between baseline NAA in the peri infarct region and change in white matter volume between the 1 and 3 month time points (r2=0.26, p=0.008).
Conclusions: Estimation of the neuronal marker NAA using MRS may signify varying degrees of neuronal damage after stroke which may correlate with the severity of axonal degeneration and subsequent white matter volume changes. Further validation and correlation with clinical outcomes is required.

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