Speaking of low arousal thresholds... (layman needs help)

In researching known factors and/or remedies for a low arousal threshold... I came across the following two studies:

http://www.ncbi.nlm.nih.gov/pubmed/21269278

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2732198/

I pretty much understand the one related to eszopiclone (lunesta), but the study on trazodone is a bit more difficult for me to grasp.

Am I to discern that under the right circumstances and with the right patients BOTH are effective in raising said threshold?

Anyone care to elaborate or translate it for the pea brained among us? i.e., me?!?!?!

And by anyone, I mean you -SWS. Ha.

Thanks,

Z

I don't know about the other meds...but I can share what I have found.
I have really bad arthritis in my cervical spine and lower back and pelvis. Low arousal index secondary to pain when I move.
Simply put...every time I turn over in bed or move it hurts like the devil and it wakes me up.
Figured this out pretty early in my therapy. Great reports but felt like crap from waking up 30 plus times a night. Doesn't take a rocket scientist to figure out that those awakenings sure mess with sleep cycle and thus how I might feel.

Spent some time talking to the doctor (both sleep and PCP) about this problem so we elected to try various meds to help me "sleep through the pain" which effectively raises the arousal threshold. Different meds go about it differently but end result is I don't wake up a gazillion times each night and I feel better.

I tried everything I could outside of meds to reduce the pain without marked success. So I opted for the drug route.
My normal pain pill for daytime use is Ultram...works pretty good but it wires me up something fierce if I take it near bedtime so we have tried various other meds for bedtime use. Ambien actually did a decent job of raising that arousal threshold. Hydrocodone worked by masking the pain. Amitryptiline (very low dose) works but I am unsure why...it is used for treatment of pain in low doses but not sure what the mechanics are...reduce pain or simply raise arousal threshold with being more sleepy.

So I suppose that one has to decide what is perhaps causing the low arousal threshold and then work on doing what needs to be done to raise the arousal threshold.

For me...I rotate the meds. I don't like the idea of becoming dependent on the controlled drugs so I don't take them regularly. My doctor wants me on the Amitryptiline regularly though so that is my main drug I suppose. At 20 mg it leaves minimal morning hangover if I take it early enough in the evening.

Thanks P. I have a feeling my chronic pain/stiffness from my racing accident might be the primary cause of my fragmentation. Helps to have some idea of what has worked for others... obviously depending on the source and level of the pain...

Z

FWIW...on the nights where my pain really wants to give me fits and I do remember several awakenings and tossing and turning I almost always see more centrals. I am pretty confident that they are likely post arousal centrals. Sometimes up to 3 or 4 within an hour. Reports look really ugly but I since I usually see them after a "bad" restless night (usually because I did something stupid to make the back issues worse) I just shrug my shoulders and move on.
Sunday night I had one huge cluster of centrals and obstructives and I know for a fact I was awake for about an hour because I was horribly nauseated. I posted that report in the Aloha issues thread as leak number example. It just happened to fit the example I was looking for.

I also will sometimes see a little group of centrals pretty much within first 30 minutes or so of going to bed. I am pretty certain those are sleep onset "centrals". No history of "centrals" in my sleep study either but I see them now and since I can usually explain them away except for maybe a rare single one, I just don't see the need to worry about them.

If I was really pro active I would wear the pulse ox to see if I had any desats with those "higher" central nights but I never know when I am going to have a night with 3 centrals an hour or even an overall AHI of less than 0.5 (I had 23 of those in April). Just isn't worth the effort at this point in my therapy. Remember...I am the first to admit I am lazy and if something isn't extremely pressing concern to me and I don't know that I could do anything about it anyway....I am apt to not bother. Just me though. Another YMMV sticker for cpap therapy.

Am I saying your all "centrals" are for sure post arousal? Heck no. But some of them might be.
If you have issues with pain and sleep...that needs to be addressed no matter what the sleep reports show..centrals or not.
Remember, anything that messes with our sleep is unwanted and even without sleep apnea diagnosis if it messes with sleep it needs to be worked on.

Zzzzzzzzzzz... wrote: And by anyone, I mean you -SWS. Ha.

Thanks,

Z

Ha! Okay, sir, I'll look at those two studies tomorrow...

Pugsy wrote: Remember, anything that messes with our sleep is unwanted and even without sleep apnea diagnosis if it messes with sleep it needs to be worked on.

True words, those are.

delete

-SWS wrote:

Zzzzzzzzzzz... wrote: And by anyone, I mean you -SWS. Ha.

Thanks,

Z

Ha! Okay, sir, I'll look at those two studies tomorrow...

Pugsy wrote: Remember, anything that messes with our sleep is unwanted and even without sleep apnea diagnosis if it messes with sleep it needs to be worked on.

True words, those are.

No, thank YOU, sir.

PS: Oddly enough, my AHI continues to drop. I swear it knows I've been talking about it! 4.5 last night. Down from 5.1 the night before. Still mainly central, but I'm encouraged. I'm also doubtful that I have CSA. If I have ANYTHING at this point, it's confusion. . Will definitely be discussing this prior to my Bipap/ASV titration. However, I'm doubting it will have much of an effect if my CA's are post arousal.

Zzzzzzzzzzz... wrote: If I have ANYTHING at this point, it's confusion. .

Well, at least you're in good company, as your doctor seems at least as confused as you are.

Zzzzzzzzzzz... wrote:In researching known factors and/or remedies for a low arousal threshold... I came across the following two studies:

http://www.ncbi.nlm.nih.gov/pubmed/21269278

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2732198/

I pretty much understand the one related to eszopiclone (lunesta), but the study on trazodone is a bit more difficult for me to grasp.

Am I to discern that under the right circumstances and with the right patients BOTH are effective in raising said threshold?

The trazadone study aimed its sights on simulating and studying two different arousal mechanisms: a) CO2-based arousals (arousal thresholds measured using end-tidal CO2 tension and EEG), and b) effort-based arousals (arousal thresholds measured using an esophageal pressure balloon and EEG). These two arousal mechanisms are suspected to occur across the obstructive SDB population.

Trazadone raised the arousal threshold in the CO2 part of the study; however, trazadone did not alter the arousal threshold when esophageal pressure swings were induced via CPAP decrements (simulating effort-based arousals). The mixed results suggest that trazadone might help SDB patients who are susceptible to arousals associated with transient CO2 elevation.

By contrast to the above trazadone study, the eszopiclone study claims to have raised the effort-based arousal threshold. The eszopiclone study also goes on to measure lower AHI. Recall the trazadone methodology did not measure nightly AHI.

SleepingUgly wrote:

Zzzzzzzzzzz... wrote: If I have ANYTHING at this point, it's confusion. .

Well, at least you're in good company, as your doctor seems at least as confused as you are.

SU, the trazadone study might have relevance to your Provent struggles. I'll post about it in your Provent thread since it's off-topic here.

-SWS wrote:

Zzzzzzzzzzz... wrote:In researching known factors and/or remedies for a low arousal threshold... I came across the following two studies:

http://www.ncbi.nlm.nih.gov/pubmed/21269278

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2732198/

I pretty much understand the one related to eszopiclone (lunesta), but the study on trazodone is a bit more difficult for me to grasp.

Am I to discern that under the right circumstances and with the right patients BOTH are effective in raising said threshold?

The trazadone study aimed its sights on simulating and studying two different arousal mechanisms: a) CO2-based arousals (arousal thresholds measured using end-tidal CO2 tension and EEG), and b) effort-based arousals (arousal thresholds measured using an esophageal pressure balloon and EEG). These two arousal mechanisms are suspected to occur across the obstructive SDB population.

Trazadone raised the arousal threshold in the CO2 part of the study; however, trazadone did not alter the arousal threshold when esophageal pressure swings were induced via CPAP decrements (simulating effort-based arousals). The mixed results suggest that trazadone might help SDB patients who are susceptible to arousals associated with transient CO2 elevation.

By contrast to the above trazadone study, the eszopiclone study claims to have raised the effort-based arousal threshold. The eszopiclone study also goes on to measure lower AHI. Recall the trazadone methodology did not measure nightly AHI.

Yeah, that's what I thought. Ha. But in all seriousness, thanks for the recap. If anything, it seems as though Lunesta would have the better chance at raising my arousal threshold. Only problem is not really wanting to try Lunesta long term to see if it helps over that period. Better to try and find the root of the problem and solve for it rather than cover it up somehow...

Zzzzzzzzzzz... wrote: If anything, it seems as though Lunesta would have the better chance at raising my arousal threshold.

Dunno for sure. The Lunesta methodology did not try to study CO2-based arousal threshold. The sole arousal mechanism studied in that Lunesta link was breathing effort itself----and indirectly measured via catheter pressure swings.

And neither study aimed for yet other arousal mechanisms and their respective sleep-disturbance thresholds: pain, noise, etc.

True enough. As a matter of course, I was prescribed trazodone FOR sleep and pain management about a year ago (prior to xpap rx) and even on the lowest dose, I couldn't tolerate it after a couple of weeks. Though at the onset, it DID seem to help a bit. Daytime symptoms appeared and I wasn't willing to endure the "drugged feeling" everyday. Regardless of dosage or at what time I took it. Hell, maybe the answer is ADVIL.

Z

Zzzzzzzzzzz... wrote:In researching known factors and/or remedies for a low arousal threshold... I came across the following two studies:

http://www.ncbi.nlm.nih.gov/pubmed/21269278

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2732198/

Thanks for very intersting papers. I have just started Trazadone (along with CPAP) and so far my sleep quality greatly improved.

yrnkrn wrote:

Zzzzzzzzzzz... wrote:In researching known factors and/or remedies for a low arousal threshold... I came across the following two studies:

http://www.ncbi.nlm.nih.gov/pubmed/21269278

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2732198/

Thanks for very intersting papers. I have just started Trazadone (along with CPAP) and so far my sleep quality greatly improved.

Very good. In hindsight, seeing how I wasn't on xpap back then, I'm wondering if my daytime symptoms on Trazadone were merely due to not getting restorative sleep. I'm going to look into this and might try the
Traz again... though at a lower dosage. 150mg might have been WAY too much. Thanks for posting your positive feedback.

Z