Do catatonia and ME/CFS have pathophysiological similarities?

By the way Karl, in correspondence, highlighted that he fully supported the decision to fund GWAS. I won't be able to do it justice but when you don't know the cause of a disease then you can use techniques like GWAS to find clues --- I sort of think of it as scoring everything and then interpreting the results to see the clues which turn up.

I liked Hanson's recent [aptamer-based proteomics] paper* but I wonder if there's something in the 4 million odd (?) proteins we are missing. Again your trying to test for everything and seeing what turns up.

I'm hoping there will be Horizon Europe funding available - perhaps something for Karl to consider; UK participates in the (EU) Horizon Europe program.

*https://www.mdpi.com/2227-7382/9/1/6

 

Actually the situation is completely different. With a genetic study if you pick up a signal you can be pretty sure that it is linked to cause, even if through an indirect route, because genes must have come first. For metabolites it is highly likely that any finding is picking up downstream effects.Also gene data are black and white. Either a gene allele is present or not. For metabolites a lot may depend on conditions of sampling, the test quality and so on. When you are trawling huge numbers of measurements GWAS looks a realistic option. To my mind metabolomics does not, unless you have a clear lead, which we don't.

 

I occasionally get something similar but instead of noticing the tinnitus aspect I get a sudden slight colour shift that disappears. Mind you I have tinnitus all the time and it does change in pitch and intensity from time to time anyway so maybe I just wouldn't notice.

I've often wondered of it's migraine related.

 

I hear what you are saying but Karl Morten has some very interesting preliminary data. He needs funding to replicate and then figure out what the unknown items he highlighted are. He measured 30,000 - what if one of the VIP ones really is key. What if his phenylalanine finding is a key and he can detect other items in that pathway that leads to and understanding of pathology. What if one of the findings could lead to treatment. We will never know. At least not in the near term.

I agree with you about metabolomics in general, that if you are measuring 1000 metabolites in 20 patients and 20 controls, then the results are pretty much meaningless. I also understand that good reference standards in metabolomics is still in it's infancy, whereas GWAS is established.

Regarding GWAS, I do agree it's worthwhile but I think it too has a big chance to be underwhelming. Too many studies find variants that are very common and that make not much sense. I am a member for Nebula Genomics health update reports based on my WGS. Every week I get a report on two new GWAS studies and how they are relevant to me or not. Most of it looks like garbage to me.

Here is one hypothetical example where GWAS can provide an answer for ME. Many think MBL levels are relevant in ME. Say the GWAS finds MBL2 has some relevance in ME. What does that mean? We are more susceptible to infections? Doesn't lead us to figuring out the disease, understanding pathology, or lead to treatment. What then? Back to square one?

But there is a chance GWAS will find something important. Just like there is a chance Karl Morten and his 30,000 metabolites, or Raman Spectrocopy might find something important. BOTH are worthwhile fishing projects.

Otherwise we are left to speculate in threads like these and be told there is no evidence for the speculation.

EDIT. I guess what I'm trying to say is that Glutamate or Glutamate clearance seems relevant to Catatonia and other neurological diseases. Karl Morten found Glutamate and Glutamine to be relevant in one study. He has no funding to replicate and extend the work. So in this thread all we can do is speculate if Catatonia could have some relevence to severe or very severe ME because we have no good quality biological data to discuss.

 

Love the RantML (markup language )

 

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 or mature enough yet. The GC/MS and LC/MS setups and protocols between labs are quite different. The community is working to make results more comparable and reproducible but honestly it will take additional years of work.

 

I'd much rather it wasn't catatonia, though I had it dismissed as that and called a classic sign of hysteria.

I had wondered if it was like cataplexy as it also happens suddenly if I laugh or get excited but when I asked about that I was told disgustedly that I did not have cataplexy.

I wish the fact that ME has all sorts of odd neurological symptoms, and, of course, all the other things had not been lost to simple "fatigue"

 

That sounds like an incompetent opinion. A frozen state that looks superficially like catatonia occurs in people who are deliberately faking signs - I am not sure what you call them, maybe hypochondriacs or manipulative personality disorders. Maybe it can occur in people who get classified as hysteria - I have no experience. But it is nothing like catatonia as such, as seen chiefly in schizophrenia. Catatonic subjects have grossly abnormal thought patterns as indicated by their behaviour. They are in another world. People who get called hysterical tend to appear rational.

 

Catatonia and ME/CFS don't look anything alike but it certainly caught my attention that there are apparent responders to lorazepam and aripiprazole in our community. Both these drugs are used for catatonia (especially the former) even in cases where catatonia is due to an identifiable neurological cause such as autoimmune encephalitis. Even severe ME/CFS looks quite different from the motor manifestations of catatonia, though, so I presume no one has tried a high dose IV lorazepam challenge which has dramatic results in many cases if you've ever seen catatonic patients rise from the dead, so to speak.