Abstract
This study introduced new MRI techniques such as neurite orientation dispersion and density imaging (NODDI); NODDI applies a three-compartment tissue model to multishell DWI data that allows the examination of both the intra- and extracellular properties of white matter tissue. This, in turn, enables us to distinguish the two key aspects of axonal pathology—the packing density of axons in the white matter and the spatial organization of axons (orientation dispersion (OD)). NODDI is used to detect possible abnormalities of posttraumatic encephalomalacia fluid-attenuated inversion recovery (FLAIR) hyperintense lesions in neurite density and dispersion. Methods. 26 epilepsy patients associated with FLAIR hyperintensity around the trauma encephalomalacia region were in the epilepsy group. 18 posttraumatic patients with a FLAIR hyperintense encephalomalacia region were in the nonepilepsy group. Neurite density and dispersion affection in FLAIR hyperintense lesions around encephalomalacia were measured by NODDI using intracellular volume fraction (ICVF), and we compare these findings with conventional diffusion MRI parameters, namely, fractional anisotropy (FA) and apparent diffusion coefficient (ADC). Differences were compared between the epilepsy and nonepilepsy groups, as well as in the FLAIR hyperintense part and in the FLAIR hypointense part to try to find neurite density and dispersion differences in these parts. Results. ICVF of FLAIR hyperintense lesions in the epilepsy group was significantly higher than that in the nonepilepsy group (P < 0.001). ICVF reveals more information of FLAIR(+) and FLAIR(-) parts of encephalomalacia than OD and FA and ADC. Conclusion. The FLAIR hyperintense part around encephalomalacia in the epilepsy group showed higher ICVF, indicating that this part may have more neurite density and dispersion and may be contributing to epilepsy. NODDI indicated high neurite density with the intensity of myelin in the FLAIR hyperintense lesion. Therefore, NODDI likely shows that neurite density may be a more sensitive marker of pathology than FA.
Highlights
Posttraumatic epilepsy is a recurrent and chronic brain dysfunction syndrome secondary to traumatic injury of the brain
Epilepsy is caused by brain injury; it was diagnosed based on International League Against Epilepsy (ILAE) (2017)
These diffusion parameters (ICVF, OD, fractional anisotropy (FA), and apparent diffusion coefficient (ADC) values) are the mean values within the drawn regions of interest (ROIs): (1) A two-sample t-test was performed to compare intracellular volume fraction (ICVF) values in the fluid-attenuated inversion recovery (FLAIR) hyperintense part of the epilepsy and nonepilepsy groups and to compare the OD, FA, and ADC values
Summary
Posttraumatic epilepsy is a recurrent and chronic brain dysfunction syndrome secondary to traumatic injury of the brain. Posttraumatic epilepsy has recurrent seizures after one week of the TBI; it is one of the most serious complications of brain trauma and is characterized by repeated epileptic seizures caused by abnormal discharge of neurons [1, 2]. As there are no nerve cells in encephalomalacia, the lesion itself does not cause epilepsy. The scars (composed of glial cell hyperplasia, crossing fiber bundles, and differentthickness fiber bundles) surrounding the encephalomalacia may affect the normal electrophysiological activity of neurons and cause hyperplastic glial dysfunction, which in turn may contribute to abnormal discharge leading to seizures [1, 2]. MRI can be used to study the volume, signal intensity, and adjacent structural changes of encephalomalacia. Structural MRI studies have shown encephalomalacia after brain contusion, but glial cell hyperplasia and crossing fiber
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