Myelocortical multiple sclerosis: a subgroup of multiple sclerosis patients with spinal cord and cortical demyelination
ECTRIMS Online Library. Hendrickson M. Oct 4, 2013; 34294
Disclosure(s): This work was supported by NIH grant 35058. Megan Hendrickson, Ansi Chang, Sverre Mork and Susan Staugaitis have nothing to disclose. Robert Fox has received personal consulting fees from Allozyne, Avanir, Biogen Idec, Novartis, Questcor, Teva, and Xenoport. Bruce Trapp has served as a consultant for TEVA, Serono, Biogen Idec, Novartis and has received grant support from Biogen Idec.Elizabeth Fisher has received research support from Biogen Idec and NeuroRx and consulting fees from Biogen Idec, Genzyme and Novartis.
Megan Hendrickson
Megan Hendrickson
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Background: Multiple sclerosis (MS) is characterized by diverse clinical course and varying patterns of disease progression. It affects millions of people worldwide and therefore there is a significant interest in understanding the underlying pathologic processes that are responsible for the disability in MS patients. Abnormal magnetic resonance imaging (MRI) signals in cerebral white matter (WM) are detected in MS patients, and are often observed macroscopically in postmortem brain. MRI facilitates early diagnosis as well as observation of disease progression. WM lesions (WML) are considered the pathological hallmark of MS. Gray matter (GM) demyelination also occurs in MS brains and can exceed WM demyelination. GM demyelination is only detected by immunohistochemical analysis. The extent of GM demyelination independent of WML has not been studied.
Goal: The goal is to determine the extent of GM demyelination in MS patients with few cerebral WML.
Methods: From a collection of 97 postmortem MS cases, we identified 13 cases (referred to as myelocortical MS) displaying an unusually low number of macroscopic WML upon gross examination of 1cm thick coronal brain slices, despite postmortem MRI that was predictive of extensive cerebral WML burden. All brains had premortem MRI indicative of MS pathology, bilateral hemispheric WM abnormalities on postmortem MRI and confirmed pathological diagnosis of MS. For comparison we used 10 classical MS brains that contained significant macroscopic cerebral WML. Immunohistochemistry for proteolipid protein and MHC Class II from five neocortical regions, hippocampus, thalamus and four levels of spinal cord (SC) was performed.
Results: The extent of subpial demyelination was similar between the two groups for all cortical regions examined. Only myelocortical MS cases demonstrated significantly more demyelination in GM than WM of hippocampus (p=0.001). The total demyelinated area in the SC was similar between the two groups, which was likely to have contributed to the severe disability in these MS patients (mean EDSS 7.5). We compared the areas of cerebral WML of one hemisphere and found the total lesion area to be statistically greater in classical MS cases (p=0.006). Postmortem MRI-pathology correlations of the WM from the other hemisphere correlated MRI changes with breakdown of the blood-brain-barrier, microglial activation but little primary demyelination.
Conclusion: Myelocortical MS patients have a low WML load and significant SC and GM demyelination.
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