Subpial Demyelination in the Cerebral Cortex of Multiple Sclerosis Patients
By Lars Bø, C. Vedeler, H. Nyland, B. Trapp, S. MØRk. Journal of Neuropathology and Experimental Neurology, 2003
765 citations recorded by the source corpus.
Subfields: Neurology, Pathology and Forensic Medicine, Rheumatology
View Paper: https://www.semanticscholar.org/paper/6bccc5620f3d223b2dfcf03bb7208cc451c07daa
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Citations in the corpus
- Meningeal inflammation is widespread and linked to cortical pathology in multiple sclerosis. (2011, background): “The primary inflammatory component of these lesions is the activated microglia (Kidd et al., 1999; Peterson et al., 2001; Gray et al., 2008), whose density is related spatially and quantitatively to the degree of lymphocyte infiltration of the meninges (Bo et al., 2003b; Dal Bianco et al., 2008).”
- The Immunopathology of Multiple Sclerosis: An Overview (2007, background): “Cortical lesions in progressive MS differ from white matter lesions in several fundamental aspects (12, 13, 47, 71).”
- Cytokines and Chemokines at the Crossroads of Neuroinflammation, Neurodegeneration, and Neuropathic Pain (2013, background): “Oligodendrocytes in brain tissue are especially vulnerable to demyelination as they are located immediately adjacent to the subarachnoid space, in the region known as the subpial space [161].”
- Meningeal B-cell follicles in secondary progressive multiple sclerosis associate with early onset of disease and severe cortical pathology. (2007, methodology): “Following a descriptive system used in previous studies (Peterson et al., 2001; Bö et al., 2003) GML were classified as type I (leucocortical), type II (intracortical) and type III (subpial) lesions.”
- Multiple Sclerosis Pathology. (2018, background): “Different types of cortical lesions are found in the MS brain, and their incidence is different between early relapsing and progressive MS (Kidd et al. 1999; Peterson et al. 2001; Bo et al. 2003).”
- Grey Matter Pathology in Multiple Sclerosis (2005, methodology): “(3): type I lesions extended across both white and grey matter (leukocortical lesions); type II lesions were located within the cortex and did not extend on the surface of the brain or to the subcortical white matter; type III lesions extended from the surface of the brain into the cortex, sparing t”