Cheyne Stokes isn't always heart related

[sheepless]

I didn't reread this thread so sorry if I'm repeating myself.

your ca are spaced in a way that suggests the possibility that you may be holding your breath against the insult of plm. audio and/or video could help you determine if this is the case.

your pattern is different enough from my plm flow rate pattern that I'm not at all sure about it but if that's what's going on, getting your plm under control may resolve much of your ca without asv. and if the the ca are plm induced, asv probably won't resolve them anyway.

plm and asv don't play well together. pressure rapidly rises and falls against flow limitations and drops in minute ventilation and those fluctuations are about as disturbing as the plm. min and max pressure support for asv has to be at least 5 cmw apart which means plm breathing will raise ipap to at least 0 to 5 cmw above your epap. for me, asv's rapid pressure swings are wearing and the high pressure contributes to leaks and aerophagia. under these conditions, vauto is better because ps can be capped to avoid such high pressure. very high trigger with ti max 3.0 does the job on ca for me.

I went from apap to asv before vauto and I do alright with both but found asv to be problematic enough I wanted to try vauto. I switch back and forth between vauto and asv and each has pros and cons.

so again, just be aware that finding a way to minimize your plm may produce adequate results with your current machine and asv may or may not solve your ca problem if associated with plm. no harm other than expense in trying asv though.

btw, if I haven't mentioned it in a while, an inexpensive electrical/electronic nerve and muscle stimulator and ropinirole reduce my rls/plm by about 80% (a guesstimate).

[coldfeet7]

your ca are spaced in a way that suggests the possibility that you may be holding your breath against the insult of plm. audio and/or video could help you determine if this is the case.

Interesting idea...  

Have you used a motion and audio triggered camera that is reasonably priced and functions well in low light or infrared? Maybe there is an Android-based app that can do this?

plm and asv don't play well together. pressure rapidly rises and falls against flow limitations and drops in minute ventilation and those fluctuations are about as disturbing as the plm. min and max pressure support for asv has to be at least 5 cmw apart which means plm breathing will raise ipap to at least 0 to 5 cmw above your epap. for me, asv's rapid pressure swings are wearing and the high pressure contributes to leaks and aerophagia. under these conditions, vauto is better because ps can be capped to avoid such high pressure.

In my last polysomnograph, I noticed that the machine would come on with tremendous force to get me to breath. It was startling to get a BLAST of air. I figured you would have to get used to it.

very high trigger with ti max 3.0 does the job on ca for me.

I set my Trigger sensitivity to the most extreme sensitivity and I am crossing my fingers it is reducing CAs.

btw, if I haven't mentioned it in a while, an inexpensive electrical/electronic nerve and muscle stimulator and ropinirole reduce my rls/plm by about 80% (a guesstimate).

Tell me more about the nerve and muscle stimulator and how and when you use it.

My Dr. initially put me on Pramipexole (another DA), but in about three months I developed SEVERE augmentation. It was awful. That is when I we used gabapentin to wean from the pramipexole.

An in-law is being weaned off Ropinerole after his Dr let his dose get too high (according to the RLS expert he is seeing now). They are getting him off using Lyrica as a bridge, I guess.

[sheepless]

"Have you used a motion and audio triggered camera that is reasonably priced and functions well in low light or infrared? Maybe there is an Android-based app that can do this?"

I should but haven't used video because I've used 'sleep as android' to track sleep and record audio for years, my wife audio recorded my plm with her phone one night and I've learned to identify my respiratory response to plm in my flow rate. There are many discussions about camera's scattered around this site.

"In my last polysomnograph, I noticed that the machine would come on with tremendous force to get me to breath. It was startling to get a BLAST of air. I figured you would have to get used to it."

It took me a couple days to get used to the asv increasing pressure to trigger a breath as I was falling asleep but that's different than what I described relative to plm. initially playing with settings to self-titrate I reached 25 cmw at times. ps usually fluctuates rapidly so reaching such high pressure is usually brief and I'm unaware of it. it wasn't intolerable other than greater likelihood of leaks and aerophagia but it did/does leave me feeling worn out the next day.

"Tell me more about the nerve and muscle stimulator and how and when you use it."

TENS and EMS: transcutaneous electrical nerve stimulation / electronic muscle stimulation. I bought a unit advertising both capabilities a couple years ago for about $30 usd. you attach electrode pads to your skin. my unit has 24 different patterns of stimulation each having 20 levels of intensity. it's kind of awesome and useful for a variety of aches and pains.

I have observed that my rls seems to originate in the small of my back, laterally from hip to hip, from which the sensation travels down through the buttocks into the legs. my TENS/EMS unit is capable of driving 4 pads through 2 channels but I usually just use 2 pads and 1 channel. sometimes I put them on either side of the base of the spine, over the hip bones or somewhere on the butt. because it seems most effective I mostly use the pads at the upper part of the rear thighs, just below the butt.

when I can, I use it for 30 - 120 minutes when I start feeling rls coming on, usually in the mid to late afternoon. if rls is bad at bedtime, I'll wear it to bed with the timer set for 40 - 50 minutes. that lets me fall asleep for a while. sometimes I wake up when it stops, sometimes much later; either way, rls/plm is gone by then.

I'm not sure how to describe its effect. one hypothesis is that it triggers and maybe magnifies the same sensations as the rls (like scratching a poison ivy rash, it hurts so good!) such that it is less noticeable or gone when I stop. I'd like to think there's a more sophisticated and scientific explanation but I don't know what that would be.

I imagine placement of the pads and results might be different for others depending on what's causing the sensations and where they feel it. note that this is just my experience and that I stumbled upon it. no doctor suggested it and although I haven't really looked I've seen no authoritative sources on using TENS/EMS for rls/plm. but for me it's the best thing I've found so far.

"My Dr. initially put me on Pramipexole (another DA), but in about three months I developed SEVERE augmentation."

I'd love to hear more about your augmentation. I wonder about it but don't know how to know if it's been a problem for me. on the one hand, my waking rls has gotten much worse over the years but idk whether it's a 'natural' progression or aggravated by meds. on the other hand, I can see from my flow rate that my plm occurs through the night when I forget to take my full dose of ropinirole (because it only lasts about 6 hours I take it in 2 stages; when I remember to take the 2nd pill my plm, if present, abates around midnight). so it might be worsening my waking rls but helping my sleeping plm. does that sound like augmentation?

"An in-law is being weaned off Ropinerole after his Dr let his dose get too high (according to the RLS expert he is seeing now)."

what was his dosage? I have taken as much as 8mg but I didn't think it any better than the 4mg I settled on a long time ago.

[kappa]

Hi coldfeet. Glad you're trying to address your PLM. 100mg gabapentin seems like a very low dose - hopefully you can get some relief by titrating up (within whatever parameters your doctors have prescribed). For comparison I was put on 150mg pregabalin (titrating up in 25mg increments) which based on various statements is around 6 times stronger than gabapentin.

I think that pulse changes are a fairly good metric to try and optimize. Whether these are triggered by PLM or OAs or CAs (or some-other-arousal-cause) PCs are an easy to measure proxy for autonomic arousal that may work for some people (probably not all).

I wear an accelerometer on my ankle to directly measure leg movements and then have this loaded in to OSCAR (with a bunch of external scripts, etc to format and calculate PLMI). For example: 
   
You can see here jumps in pulse associated with brief leg movements, breathing changes and (one) CA associated with orientation/position changes.

[Sleeprider]

Thanks Kappa for posting the chart showing how PLM relates to the flow rate and other data. Really helps to understand what I might be looking at when I see this pattern. It would be great to see a thread on this topic with more details on rigging the accelerometer and data recording.

[SarcasticDave94]

Just addressing the aspect I'm familiar with, Central Apnea. This last OSCAR chart has 2 CA over the 6 hours plus. Not at all worth considering chasing the Centrals in this case, if this chart represents normal levels of CA to you. I'd focus on your PLM.

[coldfeet7]

"My Dr. initially put me on Pramipexole (another DA), but in about three months I developed SEVERE augmentation."

I'd love to hear more about your augmentation. I wonder about it but don't know how to know if it's been a problem for me. on the one hand, my waking rls has gotten much worse over the years but idk whether it's a 'natural' progression or aggravated by meds. on the other hand, I can see from my flow rate that my plm occurs through the night when I forget to take my full dose of ropinirole (because it only lasts about 6 hours I take it in 2 stages; when I remember to take the 2nd pill my plm, if present, abates around midnight). so it might be worsening my waking rls but helping my sleeping plm. does that sound like augmentation?

After a couple of months, I was up tp .375mg a night. Then one evening, my RLS becoming annoying. That night I got hardly any sleep. My legs were jerking, almost involuntarily. It was awful.  Desperate, I called the Dr and she said it sounded like augmentation and prescribed gabapentin so I could try to transition off pramipexole. The next couple of nights were bad, but less bad and finally I could fall asleep.

I feel SO SAD for people who are dealing with this with no relief. I can understand why it can be a source of major depression, coupled with the severe sleep loss.

I do feel like my RLS is a little more noticeable at times, ever sense that augmentation, but that might be my mind playing tricks on me.

My understanding is that augmentation makes the symptoms worse and so the Dr or patient increases their dosing. That cycle continues until you are taking TOO much med and then the only choice is to get you off of it.

For some people it takes a decade or more. For me, it took months and from what I have read, it is like that for some folks. I can only imagine that it would be much harder to wean off of it after a decade.

"An in-law is being weaned off Ropinerole after his Dr let his dose get too high (according to the RLS expert he is seeing now)."

what was his dosage? I have taken as much as 8mg but I didn't think it any better than the 4mg I settled on a long time ago.

His dosage was 4 x .5mg a time. So 2mg.

Mayo clinic's site said 4mg is the usual highest dose, so perhaps they allow higher in special cases? Maybe his at 2mg was too high because he was also taking Lyrica (perhaps they were trying to keep from getting the Ropinerole too high?).

From what I understand, eventually most who take a dopamine agonists will experience augmentation (worsening symptoms). Mine just exploded.

I have heard of a new treatment for RLS/PLM. Dipyridamole is showing promising results, but I am not sure about studies on long term use.

https://worldmedicinefoundation.com/heal...less-legs/

https://pubmed.ncbi.nlm.nih.gov/29680437/

[sheepless]

thanks for the feedback coldfeet7. I expect others have it worse but my rls feels pretty bad to me and it's certainly gotten worse over time. I can't say it exploded though, as in sudden, as it's been slow and incremental. my long serving doc retired; when I find a new one I'll ask about dipyridamole. I can't nap anymore because of rls. it drives me to distraction when I have it at bedtime. if it occured every night and didn't usually ease by midnight (with TENS/EMS & meds), I think I'd go stark raving mad.

the thing that kind of fascinates and puzzles me is that I've discovered that my waking rls flow rate pattern and my sleeping plm flow rate pattern (my respiratory response to rls and plm) are identical. my perception, otoh, is that rls movements are largely (not entirely) voluntary and chaotic while plm movements are involuntary and uniformly periodic. I'd expect the rls flow rate pattern to be chaotic but it's clearly periodic. intuitively that suggests the rls/plm flow rate pattern - my respiratory response to them - is not so much a function of movement per se but rather might be more a result of some underlying nervous system activity. just speculation though.

[coldfeet7]

Hi coldfeet. Glad you're trying to address your PLM. 100mg gabapentin seems like a very low dose - hopefully you can get some relief by titrating up (within whatever parameters your doctors have prescribed). For comparison I was put on 150mg pregabalin (titrating up in 25mg increments) which based on various statements is around 6 times stronger than gabapentin.

You are right. It is a low dose. Ridiculously low. I hear some take 1800mg (seems crazy high to me) and it takes quite a while for it to finally help. I had to stop taking it because when I get to 200-300mg, I start itching like crazy on my ankles and wrists. On another forum, I heard someone else say that is a reaction some have. I backed off and the itching subsided and waited two weeks. After starting again, the itching started back after two days on 200mg. So...

No pramipexole (or other dopamine agonist) and no gabapentin. Argghh... I am going to ask my Dr next week at my appointment about Dipyridamole, but I don't hold out hope. The most common side-effect is headache and they said it is worse for migraineurs and that is unfortunately me. I am going to look into TENS/EMS mentioned by sheepless.

I think that pulse changes are a fairly good metric to try and optimize. Whether these are triggered by PLM or OAs or CAs (or some-other-arousal-cause) PCs are an easy to measure proxy for autonomic arousal that may work for some people (probably not all).

That is very interesting. I have had many, many pulses changes. While I can greatly reduce the SpO2 drops with higher pressures, the frequent pulse changes remain.

I wear an accelerometer on my ankle to directly measure leg movements and then have this loaded in to OSCAR (with a bunch of external scripts, etc to format and calculate PLMI). For example: 

You can see here jumps in pulse associated with brief leg movements, breathing changes and (one) CA associated with orientation/position changes.

Did you start another thread about that on your setup for the accelerometer (as mentioned by sleeprider)?

[coldfeet7]

Just addressing the aspect I'm familiar with, Central Apnea. This last OSCAR chart has 2 CA over the 6 hours plus. Not at all worth considering chasing the Centrals in this case, if this chart represents normal levels of CA to you. I'd focus on your PLM.

I agree. The PLMs are the real issue and they are the 'sleepers' <grin> that don't appear in the AHI.
What I have found strange is that if I use 13/8 with a PS of 4 my CAs are in the minority, but OAs (3-4 to 1) then emerge and some are as long as 45-55 seconds (not good for your abdominal cavity and umbilical hernias). Pinch your nose, close your mouth and try to breath deeply. You can really feel the negative pressure in the abdomen. I feel like my taped mouth makes it worse since I can't get enough air to really snore (that is the only thing about mouth taping that really concerns me).
Before my VAUTO, my APAP settings were about 8-10 and an EPR of 2 or 3. In that protocol, I had 3 or 4 to 1 CAs over OAs, but I also had near hyponeas and rythmic breathing that I now realize was probably due to the pressure being too low. I shied away from higher pressures due to aerophagia.
If I try VAUTO at 10.4/8 with a PS of 2.4, my charts look again like the APAP days (CAs dominate). I can't seem to find the sweet spot.
But what has me down now is the aerophagia from my BiPAP settings. A 13/8 PS 4 is very uncomfortable. I know, lower the Inhalation pressure, but then I don't get that smooth SpO2 and much more regular flow rate.
A FFM is always an epic fail for me. No leaks show in OSCAR, but the CAs AND the OAs explode and my AHI climbs to 9 to 12 or even 20. I tried raising the pressure to 15/8 with a PS of 5 and it doesn't help. I get killed with my Airtouch F20. (I tried the soft cervical collar and didn't help and made things worse since I was so hot (they need to make ones with holes to allow it breath).
I have slogged through an APAP for a year and now a BiPAP for two months and I almost feeling like giving up. I know I can't because of the headaches, the stress of the O2 swings into the 80s, but I wish I could.