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Published on: April 14, 2014
Mapping white matter damage distribution in neuromyelitis optica spectrum disorders with a multimodal MRI approach
Laura Cacciaguerra1, Maria A Rocca2, Loredana Storelli3
1Neuroimaging Research Unit, Institute of Experimental Neurology, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy/Vita-Salute San Raffaele University, Milan, Italy.
Background:
The pathogenetic mechanisms sustaining neuroinflammatory disorders may originate from the cerebrospinal fluid.
Objective:
To evaluate white matter damage with diffusion tensor imaging and T1/T2-weighted ratio at progressive distances from the ventricular system in neuromyelitis optica spectrum disorders and multiple sclerosis.
Methods:
Fractional anisotropy, mean, axial, and radial diffusivity and T1/T2-weighted ratio maps were obtained from patients with seropositive neuromyelitis optica spectrum disorders, multiple sclerosis, and healthy controls (n = 20 each group). White matter damage was assessed as function of ventricular distance within progressive concentric bands.
Results:
Compared to healthy controls, neuromyelitis optica spectrum disorders patients had similar fractional anisotropy, radial and axial diffusivity, increased mean diffusivity (p = 0.009-0.013) and reduced T1/T2-weighted ratio (p = 0.024-0.037) in all bands. In multiple sclerosis, gradient of percentage lesion volume and intra-lesional mean and axial diffusivity were higher in periventricular bands. Compared to healthy controls, multiple sclerosis patients had reduced fractional anisotropy (p = 0.001-0.043) in periventricular bands, increased mean (p < 0.001), radial (p < 0.001-0.004), and axial diffusivity (p = 0.002-0.008) and preserved T1/T2-weighted ratio in all bands.
Conclusion:
White matter damage is higher at periventricular level in multiple sclerosis and diffuse in neuromyelitis optica spectrum disorders. Fractional anisotropy preservation, associated with increased mean diffusivity and reduced T1/T2-weighted ratio may reflect astrocyte damage.
