Search results

Yeah I don’t know what they are talking about. https://www.genome.gov/FAQ/Rare-Diseases So 200,000 in US is less than 0.06% of population.

Yep, I think they mentioned this under Limitations of Study:

Absolutely, genetic and genomic technologies are much more reproducible because they are mature technologies and the scientific community and vendors spent many years, since 2000 or so, developing this field. Metabolomics has high lab to lab reproducibility issues and isn’t really standardized...

Love the RantML (markup language :nerd:)

Catatonia supposedly originates from disturbances in GABA, glutamate, and dopamine signaling. I know, it’s not really precise but just stating it doesn’t only involve glutamate.

Exactly, and over a million people supposedly got encephalitis lethargica after the Spanish flu in 1918 (an H1N1 type virus), with Parkinson’s like symptoms, psychosis, catatonia, etc. I don’t think we can say for certain that there are definitely no possibly helpful pathophysiological...

Newsweek has long gone down the drain when it comes to political news reporting, so forgive me but this article is relevant. They mention LC ME/CFS relationship too and feature NINDS. Newsweek Magazine: COVID-19 Could Increase Dementia, Other Brain Disorders for Decades to Come

I didn’t even know they prescribed antidepressants for these conditions... thought they used NSAIDS.

GABAergic modulation with classical benzodiazepines prevent stress-induced neuro-immune dysregulation and behavioral alterations. Ramirez et al. Brain Behav Immun (2016)

Read Whitney’s description here of how much Ativan helps his ME symptoms:

Yes totally, maybe too when a person deteriorates to severe or very severe ME the pathophysiology takes on new aspects, and lorazepam might only benefit here.

I thought Whitney and others reported that lorazepam not only helps with strength but multiple other ME symptoms, like noise and sound sensitivity, ability to talk again, etc? It was posited by Davis that efficacy of lorazepam might also involve its other mechanism of action at the...

I read that clorazepam (Klonopin) has no affinity for the TSPO/PBR receptor. Have severe patients reported the same significant temporary improvement from clorazepam as for lorazepam? That would help answer one of the questions I wrote in the OP.

Lorazepam also is an agonist of the TSPO/PBR receptor on mitochondria, which has immunomodulatory and other effects, though much we don’t know about this receptor.

Sorry if I’m not clear, I’m not meaning if symptoms are shared between the two syndromes, but if there might be some underlying pathophysiological similarities, particularly as ME becomes more severe. Catatonia is believed to involve disturbances in GABA, glutamate, and dopamine signalling...

Well it’s a clinical syndrome just like ME/CFS. Your description above fits for ME/CFS too, we don’t know what the underlying condition(s) or illness are, and there could be multiple. Just like with ME, biological abnormalities have been found in catatonia.

A friend of mine on PR mentioned this to me, so all credit goes to him (you know who you are!). I had no idea of the theory that catatonia and ME/CFS might share pathophysiological features. Catatonia is not always caused by psychiatric disorders, there are neurobiological and immune causes...

Given that there is anecdotal evidence of lorazepam (Ativan) causing rapid temporary improvement of ME symptoms, even in very severe cases, I’ve wondered why ME researchers aren’t looking more closely at researching selective translocator protein (TSPO) agonists. TSPO is also known as the...

Hopefully this study will get published soon. They did a talk at a conference last year. I believe it does replicate some of what Nakatomi et al. found and I believe they used a 2nd gen radiotracer [11C]DPA-713 (Nakatomi used a 1st gen)...