32. : Baseline peri-infarct N-acetylaspartic acid concentration correlates with subsequent white matter atrophy after ischaemic stroke

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Longitudinal changes in cerebral volume have been described in ischaemic stroke and may correlate with long-term outcome. We tested the hypothesis that baseline peri-infarct concentration of the neuronal metabolite N-acetylaspartic acid (NAA) correlates with subsequent cerebral volume change after stroke. Patients with supratentorial ischaemic stroke underwent 3 Tesla MRI within 1 week and at 1 and 3 months from onset. Structural imaging involved a T1-weighted axial magnetization prepared rapid gradient echo (1 mm slices, repetition time 1.9 s, echo time 2.82 ms). NAA estimation was performed at baseline using single-voxel spectroscopy (3 × 3 × 3 cm voxels, echo time 30 ms) with the voxel placed in the peri-infarct region determined by visual assessment of the diffusion-weighted image. Quantitative spectroscopic analysis was performed in LCmodel. Cerebral volume change was determined between the 1 and 3 month scans due to the effects of oedema on baseline scans. Grey and white matter volume, normalised for head size, were determined using SIENAX (part of FSL). The result was validated using Freesurfer. Fifteen patients were included in the analysis. Mean age was 69 years (interwquartile range [IQR] 62–78). Median baseline National Institutes of Health Stroke Scale score was 10 (IQR 5–14). Mean peri-infarct NAA concentration was 6.2 mM (IQR 5.1–7.6) versus 7.0 mM (IQR 6.0–8.0) in the contralateral hemisphere (p < 0.05, paired t-test). Age was inversely correlated with baseline grey matter volume (r = −0.84, p < 0.001) but not with white matter volume. Lower concentrations of baseline peri-infarct NAA were significantly associated with white matter volume loss between 1 and 3 months (r = 0.69, p < 0.005) but not with grey matter volume change. There was a similar trend using Freesurfer (r = 0.51, p = 0.06) which was driven by changes in the stroke hemisphere (r = 0.69, p = 0.007). Estimation of peri-infarct NAA may predict subsequent white matter atrophy. Correlation with clinical endpoints is required.

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