Re: My experience with Provent
Posted: Wed May 09, 2012 4:33 pm
And perhaps mount them on a mouth guard like the CpapPro?
That's ridiculous of your supplier!. Chinstraps are sold all over the internet without a prescription. People who don't have apnea but snore are among those who buy them.neurotony wrote: I went to the medical supplier yesterday and they said I need a prescription so I'll likely have to wait until after my consultation in a week and a half to get one.
SleepingUgly wrote:After the initial few days on Provent, I went off for about 4 or 5 days to preserve my sleep, then went back on a few days ago. Going off of it at that point basically set me back to where I started. The first night back on I couldn't fall asleep with it. Since then I've slept a few hours with it but can't seem to sleep more than 3.5 or so hours before I have to take it off, for all the same reasons as last week (e.g., feel I can't breathe, dry mouth, too many awakenings to keep going, etc.). I hope that over the next few days I'll be able to stretch that time, as last week I logged more hours with it than this. I need to get to where I can sleep with it all night. Then the challenge will be figuring out if my mouth is open or closed during that time.
I'm in favor of a new thread, "Using Provent", for Provent users' ideas and experiences. Personally, I am going to stick with my sleep doctor's advice for selecting treatment, so I would not be much of a participant in the other thread.SleepingUgly wrote:I wish we had all active and prior successful users on one thread, as this is getting hard to follow, especially since I appear to no longer get email notifications when I've subscribed to threads... Maybe we could have one thread for people looking to get or give INSTRUMENTAL help in how to use Provent and another thread for people to critique whether anyone should even be bothering with Provent. At this point I don't know if I should posting for help in my thread or Pats' thread
or Neurotropy's thread (assuming he ever returns to us)...
What say those of you on Provent?
I don't post very often but I do subscribe to some threads and keep up with them as time allows. The notifications have stopped for me also. When I look at the subscriptions tabs I see my list of subscriptions, but at the top of the list it says I am subscribed to no threads???? I have not changed any settings. Sounds like something is wrong with the program.SleepingUgly wrote:
... especially since I appear to no longer get email notifications when I've subscribed to threads...
OK. I'm kind of waiting until the work week begins, with the hope that they'll fix the notifications issue first...pats wrote:I'm in favor of a new thread, "Using Provent", for Provent users' ideas and experiences. Personally, I am going to stick with my sleep doctor's advice for selecting treatment, so I would not be much of a participant in the other thread.
-SWS wrote: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.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/
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.
Do I have a low CO2-based arousal threshold?-SWS wrote: And while CO2 elevation stimulates the drive to breathe, it can conceivably introduce those CO2-based arousals discussed in the trazadone study. However, susceptible patients would likely need to have a low CO2-based arousal threshold for Provent's CO2 elevation to introduce this problem.
I don't know. I think it's difficult to know without measuring. Perhaps an even more germane question is: How does Provent affect your CO2 fluctuations relative to your threshold of CO2 arousal?"SleepingUgly wrote: Do I have a low CO2-based arousal threshold?
The authors are referring to the type of central instability that commences with arousal, and then results in post-arousal ventilatory overshoot---which can, in turn, result in central apneas. Z is a candidate for that scenario, given his post-arousal central apneas (so ping to Z). By contrast, SU, you never presented much central instability on your S9 reports.SleepingUgly wrote: I didn't know this:A low arousal threshold is believed to predispose to breathing instability during sleep.
They wrote the statement as if it's true for all! The other abstract similarly states:-SWS wrote:The authors are referring to the type of central instability that commences with arousal, and then results in post-arousal ventilatory overshoot---which can, in turn, result in central apneas. Z is a candidate for that scenario, given his post-arousal central apneas (so ping to Z). By contrast, SU, you never presented much central instability on your S9 reports.SleepingUgly wrote: I didn't know this:A low arousal threshold is believed to predispose to breathing instability during sleep.
Recent insights into sleep apnoea pathogenesis reveal that a low respiratory arousal threshold (awaken easily) is important for many patients. As most patients experience stable breathing periods mediated by upper-airway dilator muscle activation via accumulation of respiratory stimuli, premature awakening may prevent respiratory stimuli build up as well as the resulting stabilization of sleep and breathing.
Well, I don't think that statement was intended as a universalism. And here is what the authors used to clarify their abstract statement:SleepingUgly wrote:They wrote the statement as if it's true for all!-SWS wrote:The authors are referring to the type of central instability that commences with arousal, and then results in post-arousal ventilatory overshoot---which can, in turn, result in central apneas. Z is a candidate for that scenario, given his post-arousal central apneas (so ping to Z). By contrast, SU, you never presented much central instability on your S9 reports.SleepingUgly wrote: I didn't know this:A low arousal threshold is believed to predispose to breathing instability during sleep.
That ventilatory overshoot and undershoot I underlined are central phenomena frequently discussed in medical literature.Younes also demonstrated that the occurrence of an arousal at upper airway opening (the end of the apnoea) is associated with a greater ventilatory overshoot and a greater subsequent undershoot, which may promote further breathing instability. This observation suggests that arousals may contribute to sleep apnoea severity.
I could be wrong, but I don't think that's the same pathogenesis the first authors are discussing. Both pathogeneses have been frequently discussed in medical literature, and there is increasing conjecture about the interrelatedness of those two in at least a subset of patients. But I don't think the two are commonly discussed as being universally interrelated. Rather, frequent awakenings/arousals across the SDB population are associated with all four of these scenarios: a) central increases, b) obstructive increases, c) increases in both phenotypes, and d) increases in neither. I don't think scenario-b is the most common post-arousal sequelae across the SDB population.SleepingUgly wrote: The other abstract similarly states:Recent insights into sleep apnoea pathogenesis reveal that a low respiratory arousal threshold (awaken easily) is important for many patients. As most patients experience stable breathing periods mediated by upper-airway dilator muscle activation via accumulation of respiratory stimuli, premature awakening may prevent respiratory stimuli build up as well as the resulting stabilization of sleep and breathing.