Brain cells

sneyz said:
Thought I'd bump this closer to the top of the pile now that the eMSN connection has surfaced:

Thread on "Three cases with chronic obsessive compulsive disorder report gains in wellbeing and function following rituximab treatment, 2024, Gallwitz et al"

Thread on "Rituximab for psychosis (double-blind RCT protocol)"

Comment by the second team on the works of the first team ("Three cases with chronic obsessive compulsive disorder report gains in wellbeing and function following rituximab treatment, 2024, Gallwitz et al")

Sorry if that's already been brought to attention elsewhere. There are some very honest comments in the thread on the quality of the scientific reasoning in the second paper. The data points might suddenly have become very interesting though.
Click to expand...
Ritux doesn’t work for ME/CFS as far as we know.
 
ScoutB said:
Even after years of this, I am always a little surprised by the range of symptoms my vyvanse dose reduces (which then return when it wears off). Flu-y symptoms, muscle aches, cognitive problems I have with fine motor skills and shakiness. I guess maybe this isn't too surprising because stimulants can reduce feelings/symptoms of sickness in other contexts too (e.g. the stimulant decongestant Pseudoephedrine can make people feel less flu-y when they have the flu). I wish we understood how this was happening though!
Click to expand...
I'm not on any stimulant but I do feel like whenever I'm stimulated I get less symptoms and feel like I'm able to do more without getting PEM. Now whether that's due to dopamine, adrenaline, cortisol or other neurotransmitters I do not know.

I think @Hutan has also mentioned this a few times in the past.

It's not really sustainable long-term as it usually does lead to an extended crash if I push it too much for too long. But it makes me feel better and able to do more than I otherwise could. Basically if I have very little stimulation and only try to rest I just start feeling worse and worse. So I need to balance stimulation and rest.

Edit: to clarify: with stimulated I generally mean things like excitement/novelty and other forms of mild stress/activation.
 
Last edited:
Bethea said:
With migraine, the breakthrough was made when they took blood from the external jugular vein during a migraine attack and found high levels of CGRP. Interestingly this doesn't show up if you take blood from the body. I wonder if it would be worth doing this for pwME/CFS during PEM to see if anything showed up.

The researchers then infused CGRP into migraine patients and healthy controls and found it triggered an attack in the migraine patients but the healthy controls only had a mild headache.
Click to expand...
This is super interesting to me. My mom has had severe migraines for most of her life. Tried all the treatments and nothing worked. Until CGRP inhibitors.. she hasn't had a single episode since. Another disease that's been woefully underfunded. But on a more positive note it shows what can happen once targeted research happens and a drug gets developed that directly targets the disease-specific biology.

It would be so interesting if we would find any abnormal blood or brain measurement during PEM. There has to be something significant going on in the brain.
 
Last edited:
What's kind of interesting is that on the other hand benzos also reduce my symptoms, allow me to do slightly more without getting PEM and helps me get into "recovery mode" after overexertion.

So that's an interesting juxtaposition between excitatory and inhibatory drugs..

Benzos might also tie into glutamate which I've seen mentioned a few times. As glutamate and GABA basically try to balance neuronal activity. I know many people get the wired but tired feeling. Could that involve excessive glutamate / neuronal activity? Benzos do help me calm the wired feeling in moments like that.
 
Last edited:
My attempt at tying all of the above together, also including @hotblack's post. Might be all bogus and way too simplistic, please let me know ;)

I could see many similarities with migraine attacks and PEM. Apparantly in migraine the current view is that there's a certain threshold which when crossed triggers a migraine attack. What might also be similar is external and internal stimuli being the thing this threshold is about.
Now what seems different is that the threshold seems more way variable in migraine compared to PEM. Most ME/CFS patients roughly know what exertion will trigger PEM, while with migraine it seems more unpredictable.

So the way I would think about it then is that most types of exertion are generally correlated with internal and external stimuli. When pwME exert too much, it crosses our threshold for stimuli which then triggers PEM. Now of course I have no idea what pathways are involved. It also seems to further increase our sensitivity to stimuli (lowered threshold), which might be part of a loop prolonging the state.

Now back to dopamine: one could argue that stimulants (and their impact on dopamine) allows the brain to better handle all these stimuli through sensory gating or another mechanism. As far as I know people with ADHD see this benefit. When I'm stimulated I'm less sensitive to sound for example, while when not-stimulated or in PEM I'm way more sensitive to sound.

The link with GABA would be that due to its neural inhibitory effect it dampens the overwhelming effect of incoming stimuli.

Bottom line: might migraine be a helpful model for how PEM could work as a neurological issue?
And could an overload of internal and external stimuli be what triggers PEM?
 
Last edited:
Bethea said:
The researchers then infused CGRP into migraine patients and healthy controls and found it triggered an attack in the migraine patients but the healthy controls only had a mild headache.
Click to expand...
Whenever I suggest that researchers try something similar (something that might make PWME temporarily worse) to identify reliable factors, it gets shot down because "researchers aren't allowed to do anything that might cause even temporary harm". I think it would be very helpful to learn that Interleukin-whichever reliably makes symptoms worse in 87% of PWME, or whatever. I'm guessing that the migraine study used levels that were normally encountered in humans, which seems to be the case in ME, since no one has found dramatically elevated levels of anything.
 
You must log in or register to reply here.
Back
Top Bottom