Early detection of secondary damage in ipsilateral thalamus after acute infarction at unilateral corona radiata by diffusion tensor imaging and magnetic resonance spectroscopy

Twelve patients with unilateral corona radiata infarction underwent MR imaging including DTI and MRS at one week (W1), four weeks (W4), and twelve weeks (W12) after onset of stroke. Twelve age-matched controls were imaged. Mean diffusivity (MD), fractional anisotropy (FA), N-acetylaspartate (NAA), choline(Cho), and creatine(Cr) were measured in thalami.T1-weighted fluid attenuation inversion recovery (FLAIR), T2-weighted, and T2-FLAIR imaging showed an infarct at unilateral corona radiate but no other lesion in each patient brain. In patients, MD was significantly increased at W12, compared to W1 and W4 (all P< 0.05). NAA was significantly decreased at W4 compared to W1, and at W12 compared to W4 (all P< 0.05) in the ipsilateral thalamus. There was no significant change in FA, Cho, or Cr in the ipsilateral thalamus from W1 to W12. Spearman's rank correlation analysis revealed a significant negative correlation between MD and the peak area of NAA, Cho, and Cr at W1, W4, and W12 and a significant positive correlation of FA with NAA at W1.These findings indicate that DTI and MRS can detect the early changes indicating secondary damage in the ipsilateral thalamus after unilateral corona radiata infarction. MRS may reveal the progressive course of damage in the ipsilateral thalamus over time.Secondary damage in the ipsilateral thalamus separate from the primary infarcted area has been demonstrated by a number of studies [1-9]. In rats with distal middle cerebral artery occlusion (MCAO), secondary neuronal degeneration and gliosis in non-ischemic ipsilateral thalamus were observed at 1 week after ischemic injury of the thalamocortical pathway [5]. In addition, in patients with unilateral middle cerebral artery (MCA) infarcts, 47% showed hyperintensity within the ipsilateral thalamus 1-12 months after stroke on T2-weighted images. Post-mortem examination in one patient demonstrated neuronal loss and gliosis at this thalamic hyperintensity four months after stroke [6]. Alth