The lesion in multiple sclerosis: clinical, pathological, and magnetic resonance imaging considerations.
Despite the cause of multiple sclerosis remaining elusive, recent studies of the disease using magnetic resonance imaging (MRI) and detailed pathological analysis have provided new insights into the events involved in the evolution of the lesion in multiple sclerosis. Most evidence points to disruption of the blood-brain barrier as the initial event in development of the lesion in multiple sclerosis. It is thought that antigen specific T cells enter the nervous system, recognise antigen, and begin a cytokine cascade that mediates disruption of the blood-brain barrier seen on contrast enhanced MRI. Subsequently, the inflammatory response is amplified and the effector stage leading to myelin damage is initiated. The mechanism(s) causing myelin damage is uncertain. MRI and pathological studies now indicate that damage to the axon may occur earlier in lesion development than generally thought. Although T2 weighted MRI techniques lack pathological specificity, considerable attention is now focused on studying newer techniques that should provide greater insight into lesion development. These include studies of hypointensities on T1 weighted images, proton spectroscopy, magnetisation transfer imaging, and diffusion imaging. Hopefully, these new techniques will provide a better understanding of events involved in the multiple sclerosis lesion as well as an improved understanding of the relation between disease as measured on MRI and that seen clinically.
McFarland
H F
HF
Neuroimmunology Branch, National Institutes of Health, National Institute of Neurological disorders and Stroke, Bethesda, MD 20892, USA.
D001284:Atrophy / Q000150:complications / Q000473:pathology; D001812:Blood-Brain Barrier / Q000502:physiology; D001921:Brain / Q000473:pathology*; D018450:Disease Progression; D006801:Humans; D008279:Magnetic Resonance Imaging; D009103:Multiple Sclerosis / Q000150:complications / Q000473:pathology*; D013116:Spinal Cord / Q000473:pathology