Pathophysiology of sleep disturbances/unrefreshing sleep in pwME?

Back on topic, I've tested baclofen, clonidine and agomelatine (discussed in different thread) these past months.

Agomelatine makes me fall asleep, baclofen and clonidine make me sleep deeper (objectively measured with sleep as Android and polar verity sense).

I prefer baclofen over clonidine due to clonidine giving me side effects like dry mouth (and as I don't know whether it interferes with agomelatine's suggested secondary effect of DA and NE disinhibition in the PFC via 5-HT2C antagonism).

I take agomelatine daily, the others as needed - once a week more or less. Yesterday, for instance, I had PEM and really wanted to sleep well, so I took 25 mg of baclofen, had an awesome sleep and I woke up feeling much much better.

I feel much better than before trying to "optimize" my sleep. Not only more rested in the mornings but also overall less fatigued. Would be interesting to see if nightly baclofen, clonidine or gabapentinoids would over time lose effect and whether a sustained physical improvement could be reached through this. Currently I'm happy enough with my nightly agomelatine though.

I'm more and more convinced that ME/CFS is to a larger-than-expected extent a sleeping disorder. Hope we'll figure out more on the pathophysiology of this.
 
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Utsikt said:
How would that be an indication that ME/CFS is a sleeping disorder?
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Ah, just by proxy of these medications affecting sleep architecture in a specific/different fashion compared to hypnotics like Z drugs, antihistamines and such. The latter had never improved the restfulness of my sleep, besides sleeping longer.

Baclofen and gabapentinoids being able to increase deep sleep (while clonidine potentially decreasing microarousals) and agomelatine, affecting the circadian rhythm, did have a positive effect.

To me, this points to something being out of balance in my sleeping architecture (for whatever reason) that can be targeted through specific medication, while other sleep medication does not move the right knobs.

"To a larger-than-expected extent a sleeping disorder" sounds confusing, now that I read it again. I am rather emphasizing the larger than expected part of the phrase. In my perception, the unrefreshing sleep has been seen as a symptom but not as much more. My N=1 tests (and the RCT on agomelatine and pwME) make me believe its more than just a common symptom, but that it might play a central role in the pathophysiology of ME. Whether I would call it a full blown sleep disorder like narcolepsy - No, not at this point.

I would like to see studies focussing more on modulation of sleep architecture in pwME.
 
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rapidboson said:
FWIW baclofen and sodium oxybate are used in narcolepsy - and seem to improve my quality of sleep and restfulness to an extent as well.

Some S4ME posts regarding orexin antagonists and orexin in PASC
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just stumbled on this, https://www.takeda.com/newsroom/new...esults-phase-3-oveporexton-narcolepsy-type-1/

but not something i know much about, do you know much about this study? i’m only interested because I got some type of inability to move when waking up after suvorexant
 
Sounds interesting. Does anybody know whether orexin/hypocretin levels have been measured in pwME?
This drug increases wakefulness as an agonist of the OX-2R. Seems to have worked well in Phase 3 and anecdotally it seems to be a game changer in type 1 narcolepsy. And similar drugs for type 2 narcolepsy.

Just saw an thread here on a recent review, will check it out.
 
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