Cortical demyelination and diffuse white matter injury in multiple sclerosis.

By A. Kutzelnigg, C. Lucchinetti, C. Stadelmann, Wolfgang Brück, H. Rauschka, M. Bergmann, M. Schmidbauer, Joseph E. Parisi, Hans Lassmann. Brain : a journal of neurology, 2005

1,850 citations recorded by the source corpus.

Subfields: Neurology, Pathology and Forensic Medicine, Rheumatology

View Paper: https://www.semanticscholar.org/paper/bdecc4c3b947050cd84647bc0846046e3b141ba5

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Citations in the corpus

Multiple Sclerosis Pathology. (2018, background): “They consist of perivascular inflammatory infiltrates, moderate brain edema, diffuse microglia activation, diffuse axonal injury, and astrocytic gliosis (Kutzelnigg et al. 2005).”
Remyelination is extensive in a subset of multiple sclerosis patients. (2006, background): “This may have been due to the fact that most lesions examined were in a stage of early active demyelination (Kutzelnigg et al., 2005).”
Understanding pathogenesis and therapy of multiple sclerosis via animal models: 70 years of merits and culprits in experimental autoimmune encephalomyelitis research. (2006, background): “In contrast, global diffuse white matter injury and extensive cortical demyelination are additional pathological hallmarks in patients with primary and secondary progressive multiple sclerosis (Kutzelnigg et al., 2005).”
The relation between inflammation and neurodegeneration in multiple sclerosis brains (2009, background): “Active lesions were classified on the basis of myelin degradation products within macrophages (Bruck et al., 1995; Kutzelnigg et al., 2005).”
Pathogenic Mechanisms Associated With Different Clinical Courses of Multiple Sclerosis (2019, background): “Cortical lesions, including the subpial lesions, may already arise in the early stages of MS, being present in brain biopsies or autopsies of patients with a disease duration of weeks to months (82), but the number and size increases with disease duration, thus being most extensive in patients with ”
The neurobiology of multiple sclerosis: genes, inflammation, and neurodegeneration. (2006, background): “Microglia activation and diffuse axonal injury are typically associated with active lesions in the cortex, but the classical perivascular lymphocytic infiltration characteristic of the white matter plaques is absent (Bo et al., 2003; Peterson et al., 2001; Kutzelnigg et al., 2005).”
Meningeal inflammation is widespread and linked to cortical pathology in multiple sclerosis. (2011, background): “, 2003a, b), precludes a role for perivascular inflammation and suggests that an immune response in the inflamed meninges might play a role in the pathogenesis of the underlying grey matter pathology (Peterson et al., 2001; Kutzelnigg et al., 2005; Magliozzi et al., 2007; Dal Bianco et al., 2008).”
An updated histological classification system for multiple sclerosis lesions (2016, background): “3a, d) are the initial phenotype of MS lesions; accordingly, they are most frequently found in MS patients with short disease duration and/or a relapsing remitting disease course; they are also detected in MS patients with secondary progressive disease, but decrease in frequency with disease duratio”