Journal article 278 views 24 downloads
Meningeal inflammation and cortical demyelination in acute multiple sclerosis / Ryan J. Bevan; Rhian Evans; Lauren Griffiths; Lewis M. Watkins; Mark Rees; Roberta Magliozzi; Ingrid Allen; Gavin McDonnell; Rachel Kee; Michelle Naughton; Denise C. Fitzgerald; Richard Reynolds; James W. Neal; Owain Howell
Annals of Neurology
PDF | Accepted ManuscriptDownload (1.47MB)
Cortical grey matter (GM) pathology, involving demyelination and neurodegeneration, associated with meningeal inflammation, could be important in determining disability progression in multiple sclerosis (MS). However, we need to know more about how cortical demyelination, neurodegeneration and menin...
|Published in:||Annals of Neurology|
Check full text
No Tags, Be the first to tag this record!
Cortical grey matter (GM) pathology, involving demyelination and neurodegeneration, associated with meningeal inflammation, could be important in determining disability progression in multiple sclerosis (MS). However, we need to know more about how cortical demyelination, neurodegeneration and meningeal inflammation contribute to pathology in early stages of MS to better predict long-term outcome. Tissue blocks from short disease duration MS (n=12, median disease duration 2 years), progressive MS (n=21, disease duration 25 years), non-diseased controls (n=11) and other neurological inflammatory disease controls (n=6), were quantitatively analysed by immunohistochemistry, immunofluorescence and in situ hybridisation.Cortical GM demyelination was extensive in some cases of acute MS (range 1– 48% of total cortical GM) and subpial lesions were the most common type (62%). The numbers of activated (CD68+) microglia/ macrophages were increased in cases with subpial lesions and the density of neurons was significantly reduced in acute MS normal appearing and lesion GM, compared to controls (p<0.005). Significant meningeal inflammation and lymphoid-like structures were seen in 4 of 12 acute MS cases. The extent of meningeal inflammation correlated with microglial/ macrophage activation (p<0.05), but not the area of cortical demyelination, reflecting the finding that lymphoid-like structures were seen adjacent to GM lesions as well as areas of partially demyelinated/remyelinated, cortical GM. Our findings demonstrate that cortical demyelination, neuronal loss and meningeal inflammation are notable pathological hallmarks of acute MS and support the need to identify early biomarkers of this pathology to better predict outcome.
B-cells; follicles; pathology
Swansea University Medical School