I know the terminology of MS and of neurology and more medical abbreviations than I care to. That’s why a recent paper struck me: It used an abbreviation — SELs — I’d never seen before and, quite frankly, I wasn’t very happy to read about them.
Black Holes: as Bad as They Sound
The paper, published in May in NeuroImage:Clinical, explained that SELs are slowly expanding lesions, which are closely associated with persisting black holes (PBHs), a term with which I am unfortunately, like many in the MS community, familiar. Persisting black holes are, in clinical terms, Tl-hypointense lesions, which are markers of axonal loss and neuronal destruction. (Axons are nerve fibers, the portion of the nerve cell that conducts electrical impulses away from the cell.) PBHs show themselves on magnetic resonance imaging (MRI) scans as dark spots — hence the daunting moniker “black holes.”
How SELs Are Different From Other MS Lesions
SELs differ from more standard MS lesions, which either (sometimes) heal themselves or scar over and remain static. SELs, as their name suggests, slowly expand in size and increase the damage they do to the axons beneath them. Not only do SELs expand; it appears from this research — which enrolled only people with relapsing-remitting MS — that they are at correlated with PBHs and may even develop into them. SELs are also highly predictive of increased disability levels as evaluated by the Expanded Disability Status Scale (EDSS). And greater SEL volumes are related to higher risk of confirmed disability progression.
Now That We Know About SELs, What Do We Do?
If that hat, as the kids say, is the bad news, what could possibly be the good news in this study? Well, I suppose the good news is that it’s always been this way. That researchers now know about it — and particularly that SELs are a factor early on in the disease — can be a trigger to treat the disease more aggressively, even in those early stages. When I was diagnosed in 2001, there were only three disease-modifying therapies for MS approved by the U.S. Food and Drug Administration (FDA). The aim of all of them was to reduce relapses and slow progression. Now, there are almost 8 times that many disease modifiers on the market, with more in the clinical trial pipeline. It is no longer good enough to slow progression toward disability. “No evidence of disease activity” (NEDA) is now the clinical goal by which our medical teams measure success. Identifying SELs early — by close observation of regular MRI scans — can trigger faster changes in prescription to more aggressive treatment. The hope would be that this new understanding that SELs are positively associated with PBHs will allow us to get ahead of the black holes before their massive gravity sucks us further and faster into the darkness of increased disability — what the medicos call “confirmed disease progression (CDP).” So now we all know a little more about slowly expanding lesions. I’m not sure I’m happy with what I know about them, but I’m happy that I know more about them — and very pleased to know that our MS neurology teams can do something positive with this information if it applies to us. Wishing you and your family the best of health. Cheers, Trevis
