RESUMO
Intravoxel Incoherent Motion (IVIM) imaging provides non-invasive perfusion measurements, eliminating the need for contrast agents. This work explores the feasibility of IVIM imaging in whole brain perfusion studies, where an isotropic 1 mm voxel is widely accepted as a standard. This study follows the validity of a time-limited, precise, segmentation-ready whole-brain IVIM protocol suitable for clinical reality. To assess the influence of SNR on the estimation of S0, f, D*, and D IVIM parameters, a series of measurements and simulations were performed in MATLAB for the following three estimation techniques: segmented grid search, segmented curve fitting, and one-step curve fitting, utilizing known "ground truth" and noised data. Scanner-specific SNR was estimated based on a healthy subject IVIM MRI study in a 3T scanner. Measurements were conducted for 25.6 × 25.6 × 14.4 cm FOV with a 256 × 256 in-plane resolution and 72 slices, resulting in 1 × 1 × 2 mm voxel size. Simulations were performed for 36 SNR levels around the measured SNR value. For a single voxel grid, the search algorithm mean relative error S0, f^, D^*, and D^ of at the expected SNR level were 5.00%, 81.91%, 76.31%, and 18.34%, respectively. Analysis has shown that high-resolution IVIM imaging is possible, although there is significant variation in both accuracy and precision, depending on SNR and the chosen estimation method.
RESUMO
Premature birth or complications during labor can cause temporary disruption of cerebral blood flow, often followed by long-term disturbances in brain development called hypoxic-ischemic (HI) encephalopathy. Diffuse damage to the white matter is the most frequently detected pathology in this condition. We hypothesized that oligodendrocyte progenitor cell (OPC) differentiation disturbed by mild neonatal asphyxia may affect the viability, maturation, and physiological functioning of oligodendrocytes. To address this issue, we studied the effect of temporal HI in the in vivo model in P7 rats with magnetic resonance imaging (MRI), microscopy techniques and biochemical analyses. Moreover, we recreated the injury in vitro performing the procedure of oxygen-glucose deprivation on rat neonatal OPCs to determine its effect on cell viability, proliferation, and differentiation. In the in vivo model, MRI evaluation revealed changes in the volume of different brain regions, as well as changes in the directional diffusivity of water in brain tissue that may suggest pathological changes to myelinated neuronal fibers. Hypomyelination was observed in the cortex, striatum, and CA3 region of the hippocampus. Severe changes to myelin ultrastructure were observed, including delamination of myelin sheets. Interestingly, shortly after the injury, an increase in oligodendrocyte proliferation was observed, followed by an overproduction of myelin proteins 4 weeks after HI. Results verified with the in vitro model indicate, that in the first days after damage, OPCs do not show reduced viability, intensively proliferate, and overexpress myelin proteins and oligodendrocyte-specific transcription factors. In conclusion, despite the increase in oligodendrocyte proliferation and myelin protein expression after HI, the production of functional myelin sheaths in brain tissue is impaired. Presented study provides a detailed description of oligodendrocyte pathophysiology developed in an effect of HI injury, resulting in an altered CNS myelination. The described models may serve as useful tools for searching and testing effective of effective myelination-supporting therapies for HI injuries.