Increases in the proportion of FA > 8 (P < 0001), distribution

Increases in the proportion of FA > .8 (P < .0001), distribution of FA (P < .0001), and distributions of longitudinal (P < .0001) and radial diffusivity (P < .0001) were observed. Histogram analysis showed increased peak frequency of FA (Fig 1C). Decreases in the distribution of MD (P < .0001) also occurred. Fiber tracking using fiber assignment by continuous tracking[9] was performed with termination criteria

set to FA < .15 and angle >60°. Tractography this website showed displacement and compression of the corticospinal tract by the enlarged Virchow–Robin spaces (Fig 1D). Fiber density index was calculated as the number of fiber paths passing through the ROI divided by the area of the ROI in pixels. Fiber density index was 14.6 (1157/8973) as compared to 8.8 (fibers/voxels = 746/6029) for the normal contralateral tract. We report a case with enlarged Virchow–Robin spaces adjacent to the corticospinal tract, which showed increased FA, decreased MD, and thinning and compression at tractography. Increased FA suggests augmented diffusion anisotropy and structural coherence, whereas decreased MD suggests diminished diffusion magnitude. These tensor abnormalities, however, did not

correlate with any clinical signs or symptoms. Zhu and colleagues[10] found Virchow–Robin spaces were ubiquitous in 1,818 elderly patients, SB203580 supplier of whom 32% had enlarged Virchow–Robin spaces. In a patient with enlarged Virchow–Robin spaces, Ugawa see more and colleagues[11] reported normal clinical findings and sensorimotor conduction. In 2 patients with enlarged Virchow–Robin spaces just below the Rolandic cortex, Mathias et al[12] described decreased white matter tract vectors on the side of the enlarged spaces. Given normal neuropsychological

evaluations, they postulated that these represented technical limitations of tractography. We instead hypothesize that the DTI changes are due to alterations in the extravascular extracellular space (EES). Increased FA may occur from increased myelination, increased axonal diameter, increased axonal density, and/or increased directionality.[13] The case patient had increased FA that was confirmed by increased peak frequency and increased skewness at histogram analysis, and by increased longitudinal and radial diffusivity. Mass effect by enlarged Virchow–Robin spaces decreases unrestricted water in the EES that has low anisotropy. This suggests compression or increased density of normal axons, as corroborated by the increased fiber density index. DTI in acute ischemia has correlated transient increases in FA with changes in the EES.[14] In vitro nerve research has also shown that decreased EES causes decreased MD.[15] Calculation of the EES fraction VE is possible using T1 perfusion imaging but beyond the scope of this study. The main limitation is the complicated oncological history. The case patient had two primary cancers and multiple brain metastases, but none near the corticospinal tracts or motor gyri.

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