William M. Spees1,
2, Dmitriy A. Yablonskiy1, 3, G. Larry Bretthorst1,
Alexander L. Sukstankii1, Jeffrey J. Neil, 14, Joseph
J.H. Ackerman, 15
1Department
of Radiology, Washington University, St. Louis, MO, United States; 2Hope
Center for Neurological Disorders, Washington University, St. Louis, MO,
United States; 3Department of Physics, Washington University, St.
Louis, MO, United States; 4Department of Pediatric Neurology,
Washington University, St. Louis, MO, United States; 5Department
of Chemistry, Washington University in St. Louis, St. Louis, MO, United
States
The source of the post-ischemic drop in the apparent diffusion coefficient of water in brain remains in question. In the current work, the diffusion properties of the intraneuronal metabolite N-acetylaspartate are characterized according to a biophysical model in rat brain pre- and post-ischemia at 37 &[deg]C. Based on the model, which accounts for local, microscopic diffusion anisotropy and diffusion kurtosis, a ~19% increase in intraneuronal cytoplasmic viscosity post-ischemia and evidence (via the increase in the kurtosis term) for beading of neurites are observed. Neither occurrence appears of sufficient magnitude to account principally for the decrease in water diffusion with stroke.