“The fact that atrophied lesion volume was the only measure that was predictive of conversion to progressive multiple sclerosis, and brain atrophy was not, is a major novel finding of this study.”

Inflammation and neurodegeneration


According to Zivadinov, atrophied brain lesion volume is predictive of disease progression primarily because it reflects both inflammatory and neurodegenerative pathological processes, which together result in the disappearance of brain lesions into cerebrospinal fluid.

In their previous work, Zivadinov and his colleagues established an MRI marker, which measures brain lesions that have been replaced by cerebrospinal fluid. Lesions are signs of damage to the brain from physical trauma, a stroke, normal aging or chronic disease. It is the disintegration of these lesions into cerebrospinal fluid that the UB team has proven is the main indicator of disease progression in MS.

“This study showed that atrophied brain lesion volume represents a robust marker for predicting conversion from relapsing-remitting to secondary-progressive stages of MS,” Zivadinov said.

The routine use of atrophied brain lesion volume as a marker for disease progression in MS depends on the completion of retrospective and prospective studies, some of which the UB team is already performing, on a large scale in clinical settings.

“Atrophied lesion volume can be measured with a pair of simple MRI scans,” said Zivadinov. “What has not been done yet is to test how visual or qualitative assessment compares to quantitative assessment performed in this study and previous studies we conducted.”

He added that a better understanding is needed of the pathophysiological differences between those lesions that disappear compared to those that do not. To begin to address this, advanced nonconventional MRI and positron emission tomography studies are beginning now at UB.

Co-authors are: Niels Bergsland, PhD, research assistant professor of neurology in the Jacobs School and BNAC; Michael G. Dwyer, III, PhD, assistant professor of neurology and bioinformatics; Channa Kolb, MD and Alexis A. Lizarraga, MD, both assistant professors of neurology in the Jacobs School; Deepa P. Ramasamy, MD, clinical trial neuroimager, BNAC; Dejan Jakimovski, MD, PhD candidate at UB; Bianca Weinstock-Guttman, MD, professor of neurology in the Jacobs School; Jesper Hagemeier, research scientist at BNAC and Antonia Valentina Genovese of the University of Pavia.

Kolb, Lizarraga and Weinstock-Guttman are also physicians with UBMD Neurology.

The research on atrophied brain lesion volume received no external funding but was supported in part by BNAC and the Center for Biomedical Imaging at the Clinical and Translational Science Institute at UB.

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