Author + information
- 1Basic Medical College, Beijing University of Chinese Medicine, Beijing, China
- 2School of Traditional Chinese Medicine, Capital Medical University, Beijing, China
- 3Beijing Key Lab of TCM Collateral Disease Theory Research, Beijing, China
- 4School of Life Sciences, Beijing University of Chinese Medicine, Beijing, China
Stroke is one of the leading causes of disability throughout the world. The microstructural changes of white matter after stroke are complex. Currently, the evaluation of altered microstructures caused by stroke mainly derives from regional histological measurements which do not allow dynamic assessment of these changes in vivo. In our study, diffusion tensor imaging (DTI) was used to noninvasively monitor the temporal profiles of white matter injury, involving neuronal necrosis, axonal disconnection and myelin degradation.
Rat model of ischemic stroke was induced by middle cerebral artery occlusion (MCAO). T2-weighted (T2WI) and DTI were performed in all rats on the 3rd, 7th, 14th and 30th days. T2WI was used to evaluate the evolutional changes of cerebral infarct volume after ischemic stroke. Fractional anisotropy (FA) map, apparent diffusion coefficient (ADC) map and three eigenvector (λ1, λ2, λ3) maps were reconstructed from DTI original file. For quantitative assessment, FA, ADC, axial diffusivity, and radial diffusivity values were analyzed in ROIs drawn on white matter, including corpus callosum, external capsule and internal capsule. Fiber tractography was conducted using diffusion toolkit to determine the orientation and integrity of fiber systems. Moreover, at last time point, hematoxylin-eosin (HE) staining was performed to evaluate pathological changes.
The cerebral infraction volume was gradually reduced from 3 to 30 days in stroke rats. The statistical results of fiber reconstruction showed that the mean fiber length was markedly decreased at all time points after ischemic stroke. The decrease in FA, which is consistent with axonal injury, myelin injury or both in white matter fibers, was found in corpus callosum on the 3rd day in stroke group. The internal and external capsule were damaged at all stage of ischemic stroke evidenced by the decreased FA on the 3rd, 7th, 14th and 30th days. In addition, all parameters derived from DTI indicated that the external capsule injury was the most serious in white matter. FA was decreased while accompanied by an increase in ADC, axial diffusivity, radial diffusivity on the 3rd day in external capsule. The increased ADC on the 30th day in external capsule indicated the tissue liquefaction necrosis in the chronic phase of ischemic stroke. HE provided evidence that most cells were arranged disorderly, with pyknotic or severely shrunken nuclei in ischemic region after stroke.
The evolution of white matter injury in stroke rats could be characterized by longitudinal multi-parametric DTI study. Corpus callosum was damaged in early stage while internal and external capsule were damaged at all stage of ischemic stroke. The external capsule injury was the most serious in white matter during ischemic stroke.