
Contributions
Abstract: P792
Type: Poster Sessions
Abstract Category: Pathology and pathogenesis of MS - MRI and PET
Background: Previous studies in multiple sclerosis (MS) suggest that phase contrast is useful for staging and characterizing white matter (WM) lesions. The presence of susceptibility hypointense rims or nodular appearance has been related to activated microglia and/or to an expanding/developing lesion pattern. Some data, however, also suggest that phase contrast can disappear with extreme tissue destruction.
Objective: To characterize, in early MS, using the restricted fraction (FR), an index of axonal density obtained through the Composite Hindered and Restricted Model of Diffusion (CHARMED), microstructural integrity underlying different WM lesion patterns seen on magnitude and phase images at 7T.
Methods: Eighteen early MS subjects (mean disease duration 1.5 years) underwent acquisition of a) 7T T2*weighted scans (0.33x0.33x1.0 mm) yielding magnitude and phase images for WM lesion segmentation; b) 3T 3D T1weighted scans for image co-registration; c) CHARMED diffusion sequence (300mT/m maximum gradient strength) for FR maps. WM lesions were classified as: 1) present on both magnitude and phase, which were subdivided based on phase aspect in a) nodular hypointense, b) hypointense peripheral rim; 2) visible only on magnitude; 3) visible only on phase (nodular hypointensity). FR in each lesion subtype was compared to homologous normal-appearing contralateral WM using paired t-test or Wilcoxon signed rank test based on normality.
Results: Only 241 of 495 magnitude lesions (48.6%) were seen on phase images. Five WM lesions appeared only on phase. Based on the phase appearance, 223 lesions were classified as nodular hypointense and 18 with a hypointense rim at the periphery. WM lesions visible either only on magnitude or present on magnitude but having a nodular phase pattern were characterized by lower FR compared to the contralateral homologous region (0.24±0.06 vs. 0.30±0.07, p=0.01 and 0.23±0.07 vs. 0.33±0.1, p< 0.0005). The same comparison in FR metrics in lesions observed only in phase and in lesions with phase rim demonstrated no significant difference.
Conclusion: The combined use of magnitude and phase contrast could be helpful for characterizing WM MS lesions: its detection only on phase could reflect mild tissue damage, while only on magnitude could represent severe tissue destruction. In the latter, assessment of microstructural integrity with advanced multi-shell diffusion might represent a complementary tool for lesion characterization.
Disclosure: This study was supported by the National Institute of Health (NIH R01NS07832201 A1); C.A Treaba: nothing to disclose. S.De Santis: nothing to disclose.T. Granberg was supported by Stockholm City Council and Karolinska Institutet (ALF grant 20150166) and the Swedish Society for Medical Research. E. Herranz has received research supported by the NMSS fellowship FG150705459. R. Ouelette: nothing to disclose. V. Barletta: nothing to disclose. A. Mehndiratta: nothing to disclose. J. Sloane: nothing to disclose. N.Toschi: nothing to disclose. C. Mainero received research support from EMD Merck Serono and speaker honoraria from Biogen.
Abstract: P792
Type: Poster Sessions
Abstract Category: Pathology and pathogenesis of MS - MRI and PET
Background: Previous studies in multiple sclerosis (MS) suggest that phase contrast is useful for staging and characterizing white matter (WM) lesions. The presence of susceptibility hypointense rims or nodular appearance has been related to activated microglia and/or to an expanding/developing lesion pattern. Some data, however, also suggest that phase contrast can disappear with extreme tissue destruction.
Objective: To characterize, in early MS, using the restricted fraction (FR), an index of axonal density obtained through the Composite Hindered and Restricted Model of Diffusion (CHARMED), microstructural integrity underlying different WM lesion patterns seen on magnitude and phase images at 7T.
Methods: Eighteen early MS subjects (mean disease duration 1.5 years) underwent acquisition of a) 7T T2*weighted scans (0.33x0.33x1.0 mm) yielding magnitude and phase images for WM lesion segmentation; b) 3T 3D T1weighted scans for image co-registration; c) CHARMED diffusion sequence (300mT/m maximum gradient strength) for FR maps. WM lesions were classified as: 1) present on both magnitude and phase, which were subdivided based on phase aspect in a) nodular hypointense, b) hypointense peripheral rim; 2) visible only on magnitude; 3) visible only on phase (nodular hypointensity). FR in each lesion subtype was compared to homologous normal-appearing contralateral WM using paired t-test or Wilcoxon signed rank test based on normality.
Results: Only 241 of 495 magnitude lesions (48.6%) were seen on phase images. Five WM lesions appeared only on phase. Based on the phase appearance, 223 lesions were classified as nodular hypointense and 18 with a hypointense rim at the periphery. WM lesions visible either only on magnitude or present on magnitude but having a nodular phase pattern were characterized by lower FR compared to the contralateral homologous region (0.24±0.06 vs. 0.30±0.07, p=0.01 and 0.23±0.07 vs. 0.33±0.1, p< 0.0005). The same comparison in FR metrics in lesions observed only in phase and in lesions with phase rim demonstrated no significant difference.
Conclusion: The combined use of magnitude and phase contrast could be helpful for characterizing WM MS lesions: its detection only on phase could reflect mild tissue damage, while only on magnitude could represent severe tissue destruction. In the latter, assessment of microstructural integrity with advanced multi-shell diffusion might represent a complementary tool for lesion characterization.
Disclosure: This study was supported by the National Institute of Health (NIH R01NS07832201 A1); C.A Treaba: nothing to disclose. S.De Santis: nothing to disclose.T. Granberg was supported by Stockholm City Council and Karolinska Institutet (ALF grant 20150166) and the Swedish Society for Medical Research. E. Herranz has received research supported by the NMSS fellowship FG150705459. R. Ouelette: nothing to disclose. V. Barletta: nothing to disclose. A. Mehndiratta: nothing to disclose. J. Sloane: nothing to disclose. N.Toschi: nothing to disclose. C. Mainero received research support from EMD Merck Serono and speaker honoraria from Biogen.