Purpose: To assess changes in intracellular diffusion as a mechanism for the reduction in water ADC that accompanies brain injury. Using NAA as a marker of neuronal cytoplasmic diffusion, NAA diffusion was measured before and after global ischemia (immediately postmortem) in the female Sprague-Dawley rat.
Methods: Diffusion-weighted PRESS spectra, with diffusion encoding in a single direction, were acquired from large voxels of rat brain gray matter in vivo and postischemia employing either pairs of pulsed half-sine-shaped gradients (in vivo and postischemia, bmax = 19 ms/μm2 ) or sinusoidal oscillating gradients (in vivo only) with frequencies of 99.2-250 Hz. A 2D randomly oriented cylinder (neurite) model gave estimates of longitudinal and transverse diffusivities (DL and DT , respectively). In this model, DL represents the "free" diffusivity of NAA, whereas DT reflects highly restricted diffusion. Using oscillating gradients, the frequency dependence of DT [DT (ω)] gave estimates of the cylinder (axon/dendrite) radius.
Results: A 10% decrease in DL,NAA followed global ischemia, dropping from 0.391 ± 0.012 μm2 /ms to 0.350 ± 0.009 μm2 /ms. Modeling DT,NAA (ω) provided an estimate of the neurite radius of 1.0 ± 0.6 μm.
Conclusion: Whereas the increase in apparent intraneuronal viscosity suggested by changes in DL,NAA may contribute to the overall reduction in water ADC associated with brain injury, it is not sufficient to be the sole explanation. Estimates of neurite radius based on DT (ω) were consistent with literature values.
Keywords: N-acetyl aspartate; intraneuronal viscosity; metabolite diffusion; stroke.
© 2022 International Society for Magnetic Resonance in Medicine.