Tweet Storms

https://twitter.com/jenbrea/status/918494611214966785

Not easily on Twitter. ME originally described a disease that a small % of patients developed following a non-polio enteroviral infection.

Mine was triggered by Coxsackie B4 so in that sense, I have classic ME. I also have the muscle fatigability Ramsay describes.

ME in that narrower, historical sense has lost much of its meaning over time because of poor definitions and descriptions of the disease.

But ME and CFS – these names have no inherent meanings. What matters is the underlying biology and whether the definitions map to them.

There are a a cluster of symptoms [defined many different ways] that can be triggered usually by an infection but not always.

Let's just say that we say for the sake of argument that the core feature these symptoms have in come is PEM

And let's say that we knew for certain it was caused by an acquired defect in the pyruvate dehydrogenase enyzme.

And that that defect could be triggered in a very small number of people who were exposed to pesticides, or got Coxsackie B4, or got mono.

Do we define the disease by the trigger or the defect? It's actually an complex question to answer.

Coxsackie B4 can cause multiple different diseases but most people who get it don't even have symptoms.

If enteroviral antiviral treatment cured the disease, we'd really want to know if it was the cause + treat people by eradicating the virus.

If the virus is gone but what is left is an autoimmune disease that can be arrived at via many different paths

Then maybe the initial trigger matters much less and the disease is defined by an autoantibody panel

And a seemingly heterogenous group of patients actually has a common cure.

And even if that weren't true, we'd want to have a common set of public health messaging re: PEM and pacing.

The answer isn't likely to be that stark, which is why I find "ME is not CFS" so unhelpful.

Much more clear is to say "Ramsay's definition is not Fukuda."

I do think that there will be some treatments that are broadly effective for most or all patients with PEM

And that there will also be treatments depending on your specific trigger

It may be in the future that we prevent T1D by treating patients early with Coxsackie B4 antivirals http://www.pnas.org/content/104/12/5115.full …

Same may be for ME triggered by Coxsackie B4.

well - many patients probably have ANS dysfunction