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Media type:
E-Article
Title:
Olfactory Pathology in Central Nervous System Demyelinating Diseases
Contributor:
DeLuca, Gabriele C.;
Joseph, Albert;
George, Jithin;
Yates, Richard L.;
Hamard, Marie;
Hofer, Monika;
Esiri, Margaret M.
imprint:
Wiley, 2015
Published in:Brain Pathology
Language:
English
DOI:
10.1111/bpa.12209
ISSN:
1015-6305;
1750-3639
Origination:
Footnote:
Description:
<jats:title>Abstract</jats:title><jats:p>Olfactory dysfunction is common in multiple sclerosis (<jats:styled-content style="fixed-case">MS</jats:styled-content>). Olfactory bulb and tract pathology in <jats:styled-content style="fixed-case">MS</jats:styled-content> and other demyelinating diseases remain unexplored. A human autopsy cohort of pathologically confirmed cases encompassing the spectrum of demyelinating disease (<jats:styled-content style="fixed-case">MS</jats:styled-content>; n = 17), neuromyelitis optica [(<jats:styled-content style="fixed-case">NMO</jats:styled-content>); n = 3] and acute disseminated encephalomyelitis [(<jats:styled-content style="fixed-case">ADEM</jats:styled-content>); n = 7] was compared to neuroinflammatory [herpes simplex virus encephalitis (<jats:styled-content style="fixed-case">HSE</jats:styled-content>); n = 3], neurodegenerative [<jats:styled-content style="fixed-case">A</jats:styled-content>lzheimer's disease (<jats:styled-content style="fixed-case">AD</jats:styled-content>); n = 4] and non‐neurologic (n = 8) controls. For each case, olfactory bulbs and/or tracts were stained for myelin, axons and inflammation. Inferior frontal cortex and hippocampus were stained for myelin in a subset of <jats:styled-content style="fixed-case">MS</jats:styled-content> and <jats:styled-content style="fixed-case">ADEM</jats:styled-content> cases. Olfactory bulb/tract demyelination was frequent in all demyelinating diseases [<jats:styled-content style="fixed-case">MS</jats:styled-content> 12/17 (70.6%); <jats:styled-content style="fixed-case">ADEM</jats:styled-content> 3/7 (42.9%); <jats:styled-content style="fixed-case">NMO</jats:styled-content> 2/3 (66.7%)] but was absent in <jats:styled-content style="fixed-case">HSE</jats:styled-content>, <jats:styled-content style="fixed-case">AD</jats:styled-content> and non‐neurologic controls. Inflammation was greater in the demyelinating diseases compared to non‐neurologic controls. Olfactory bulb/tract axonal loss was most severe in <jats:styled-content style="fixed-case">MS</jats:styled-content> where it correlated significantly with the extent of demyelination (<jats:italic>r</jats:italic> = 0.610, <jats:italic>P</jats:italic> = 0.009) and parenchymal inflammation (<jats:italic>r</jats:italic> = 0.681, <jats:italic>P</jats:italic> = 0.003). The extent of olfactory bulb/tract demyelination correlated with that found in the adjacent inferior frontal cortex but not hippocampus. We provide unequivocal evidence that olfactory bulb/tract demyelination is frequent, can occur early and is highly inflammatory, and is specific to demyelinating disease.</jats:p>