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?
http://stroke.ahajournals.org/content/45/Suppl_1/ATP73.short
  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

Abstract

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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