Pathophysiology of sleep disturbances/unrefreshing sleep in pwME?

jnmaciuch said:
Someone with ME/CFS may ill-advisedly get behind the wheel underestimating how tired they are, but I don’t know of a single story of someone with ME/CFS jumping in the car completely unaware that there might be some medical problem which makes this a potentially bad idea (unless they also had other comorbidities where this is common). My relatives with dementia, on the other hand, will insistently claim that they have absolutely no problems operating heavy machinery and that they just need to get to work for the job they retired from 20 years ago.
Click to expand...
Absurdly enough, reading this soon after looking at the latest CBT app turd from Stone and Carson, the ideologues call this having poor metacognition.

They actually point to the fact that we are aware of having cognitive problems not as evidence that we have both cognitive impairment and awareness of it, but rather that we have some fear-based distress about potentially having such impairment, when in their opinion we have perfectly normal cognitive performance. Basically, we simply underestimate what is a normal cognitive function, with bits of having unrealistic expectations, based on who knows what nonsense.

So there's no winning. It is definitely different from dementia, we are as fully aware of our cognitive problems as we can be, but where there is usually a fondness to throw vague labels, such as alexithymia, or whatever is fashionable these days, when we explain that we have difficulties explaining those deficits, they love to throw the opposite labels when we explain that we are aware of those deficits, simply because they don't believe in them. Or, actually, that they have different beliefs about them.

In a person with normal reasoning skills, not tainted with odd biases, this argument is actually very useful, and likely an important clue. But it will always be distorted to push what is clearly the generic concept that has lately become the main fashion: we are simply afraid. Afraid of standing, of moving, of experiencing things, of thinking, of talking, of whatever.
 
rvallee said:
Absurdly enough, reading this soon after looking at the latest CBT app turd from Stone and Carson, the ideologues call this having poor metacognition.

They actually point to the fact that we are aware of having cognitive problems not as evidence that we have both cognitive impairment and awareness of it, but rather that we have some fear-based distress about potentially having such impairment, when in their opinion we have perfectly normal cognitive performance. Basically, we simply underestimate what is a normal cognitive function, with bits of having unrealistic expectations, based on who knows what nonsense.

So there's no winning. It is definitely different from dementia, we are as fully aware of our cognitive problems as we can be, but where there is usually a fondness to throw vague labels, such as alexithymia, or whatever is fashionable these days, when we explain that we have difficulties explaining those deficits, they love to throw the opposite labels when we explain that we are aware of those deficits, simply because they don't believe in them. Or, actually, that they have different beliefs about them.

In a person with normal reasoning skills, not tainted with odd biases, this argument is actually very useful, and likely an important clue. But it will always be distorted to push what is clearly the generic concept that has lately become the main fashion: we are simply afraid. Afraid of standing, of moving, of experiencing things, of thinking, of talking, of whatever.
Click to expand...
That’s what my neuropsych said after my evaluation. Found out later that he considers LC to be psychosomatic. Wonder why he’s the only neuropsych at my health insurance..
 
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.
 
Last edited:
rapidboson said:
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.
Click to expand...
Of course going from bad sleep to a bit better sleep will make you feel better overall. How would that be an indication that ME/CFS is a sleeping disorder?
 
Utsikt said:
How would that be an indication that ME/CFS is a sleeping disorder?
Click to expand...

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.
 
Last edited:
You must log in or register to reply here.
Back
Top Bottom