A new window in multiple sclerosis pathology: non-conventional quantitative magnetic resonance imaging outcomes.
Recent findings suggest that neuronal pathology occurs early in the course of multiple sclerosis and seems to be responsible for accumulation of disability. Nonetheless, the nervous system has an intrinsic potential for repair and compensation in the neuronal component. Disease-modifying drugs such as glatiramer acetate interfere with, and down-regulate, inflammatory pathology and slow neurodegeneration. Moreover, certain regulatory cytokines and neurotrophic factors have the capacity to promote neuronal and axonal repair. Given the importance of neuronal injury in multiple sclerosis and the potential of certain treatments for neuronal repair, it is important to possess adequate and sensitive tools to visualise the pathology in the neuronal compartment. The most promising tools to measure neuronal and axonal damage in multiple sclerosis, as well as neuroprotection and repair, are whole brain volume change for quantification of general brain atrophy, and T1 hypointensity (black holes) and magnetisation transfer ratio for measuring evolution of lesion damage. Other promising techniques, such as diffusion tensor imaging-based fibre tracking and magnetic resonance spectroscopy may allow detailed analyses, but these are still in the experimental stage and are not available for routine clinical practice. Further paraclinical measurements such as optical coherence tomography for the evaluation of the anterior visual pathway may have potential as objective surrogate markers for neurodegeneration in multiple sclerosis.
Zipp
Frauke
F
University Medicine Mainz, Johannes Gutenberg University Mainz, Department of Neurology, Mainz, Germany. zipp@uni-mainz.de
D001369:Axons / Q000473:pathology / Q000502:physiology; D001921:Brain / Q000473:pathology / Q000503:physiopathology; D006801:Humans; D008279:Magnetic Resonance Imaging / Q000379:methods*; D009103:Multiple Sclerosis / Q000473:pathology* / Q000503:physiopathology; D009474:Neurons / Q000473:pathology / Q000502:physiology