Why doesn't APAP respond to apneas?

Snoredog wrote: SWS: see Bev's latest Encore report, notice how the little chairs change when an event is detected, notice her AHI even went down further to .8 (Bev you can stop trying to lower your AHI now )

I absolutely agree that the pressure chairs occur in response to incessant little flow variations from Bev. But look at that left-most chair. It's not chair shaped. It's actually shaped like the Empire State Building, and King Kong is sitting on top of it----waiting to devastate that sleep architecture by angrily hurling RDI sleep disturbances across that nocturnal landscape.

One of the potential problems that SAG wanted to look for on Bev's PSG discs was the presence of alpha wave intrusions. He just may spot other interesting clues relevant to Bev's sleep architecture as well. Also, ozij may know something about Lexapro's possible long-term effects. I haven't completely dismissed Lexapro's potential role in this sustained sleep architecture mess either. Not by a long shot.

...By the way, I'm right back to thinking Bev's BiPAP AutoSV really needed to have its EPAP set at 14 cm:

Stephen E. Brown, MD, DABSM wrote:In another patient, undertitration occurred as the technologist adjusted the EEP for apneas and hypopneas, but did not adequately increase the pressure for residual RERAs.

That's exactly what I think may be happening in Bev's case with the autoSV's EPAP set too low. The end result is that IPAP peak uncomfortably throttles up and down near IPAP max for extended periods as we see on the SV charts.

I think she probably has a narrow airway that simply needs more constant dilation via EPAP at 14 cm. That constant EPAP dilation may keep the IPAP peak activity from running into an apparent vicious cycle of: 1) very rapid airway inflation (via a huge EPAP/IPAP peak gap), 2) a counterproductive (pressure-variation) stimulus/response reaction from Bev, followed by 3) an even more aggressive and counterproductive IPAP peak "countering response" from the BiPAP autoSV. That third step conceivably brings Bev back to (neurologically reactive) step two in that incessantly repeating vicious cycle.

She conceivably needs EPAP's constant airway dilation right up there at the same 14 cm that yielded satisfactory results in the lab and at home on APAP. Then SV can take a more refined approach at straightening out those flow-amplitude variations with a bit more finesse and hopefully greater comfort.

...it's a much greater likelihood that most of the "chairs" (although, to me, they look more like "bidets") are "normal" phenomenon (as noted somewhere by RG), a result of event searches ("trolling"). Their frequency correlates closer to that vs any phenomenon in sleep.

The result on straight 14 cmH2O should shed some light on this.

SAG

SAG, the discs are in!

I picked up the disc this morning. She said that both PSGs ar on one CD..

Last night I set my APAP on CPAP 14. Guess what? "M" vacation. No details this morning. Page 1 indicates an AHI of 2.. Is that accurate when there are no details?

Bev, I wonder how you feel, and what's with you aerophagia - after all, the numbers are rarely the whole story.

I don't know about the long term effects of Lexapro, but here's what I do know:

Those medications chage the brain's response to the chemical is uses for transmitting information (aka the "neurotransmitters"). They make the nerve cells less responive, or, on the hand, keep the transmition chemicals hanging around longer than they would otherwise. And then the brain tries to handle that changed chemistry.

Bev it not the first to report "brain zaps" during the weaning off process, and she had 4 weeks of them. I have every reason in the world assume that her sleep was affected during this time for at least as long as she was feeling the "brain zap".

http://www.benzo.org.uk/ashtonad.htm
ANTIDEPRESSANT WITHDRAWAL EFFECTS
Professor C Heather Ashton

PSYCHOLOGICAL SYMPTOMS:
agitation, crying spells, irritability,
overactivity, aggression, depersonalisation,
memory problems, confusion, lowered mood.


PHYSICAL SYMPTOMS:

GASTROINTESTINAL:
abdominal pain, diarrhoea, anxiety,
nausea, vomiting.

INFLUENZA-LIKE:
fatigue, headache, muscle pain,
weakness, sweating, chills,
palpitations.

SLEEP DISTURBANCE:
insomnia, vivid dreams, nightmares.

SENSORY DISTURBANCES:
dizziness, light-headedness, vertigo,
pins and needles, electric shock sensations.

MOTOR DISORDERS:
tremor, loss of balance, muscle stiffness,
abnormal movements.

O.

HI Bev, I sure wish I had a better understand about all the info this thread is telling me ? Now I take both Cymbalta and Lexapro and am having good results with my cpap now that I have a new mask. I am glad I am a mouth breather if it keeps me from having to tape up my face as much as I read that so many of you do. A full face mask seems better than having to do that. I have been trying to understand this thread but I am pretty lost by it. But it is comforting to know that if I needed help so many people would be there for info. This has been interesting to read. I am going to get my results an see if I can figure this out. Bev I sure hope all this make sense to you an is helping you with your sleep or lack there of. Blessings,Melinda

Ozij,
I weaned off of Lexapro to see if I would feel better without it. Now the Dr. at Sheltering Arms wants me to try Cymbalta for the myofascial pain I've had since my injury. Given what I've learned about Lexapro and knowing that Cymbalta is similar, I am reluctant to start and have not started taking it. He thinks, less pain, sleep better, heal faster. I'm not sure that it is that simple. I want to get my sleep straightened out before I introduced another variable. Clearly, I had sleep irregularities long before my injury. If Cymbalta doesn't work, he wants to try Lyrica. It's too easy for them to spend 5 minutes with me and write a prescription. All of the Drs freely admit that they don't know what is causing the pain or the sleep disturbances, but they are willing to put my body through a series of drugs. I'd rather take my chances with changes in air pressures than drugs.

I feel the same today , as usual and the aerophagia is the same.

Melinda,
Don't worry, I don't understand it all, either, but you are right about knowing you can come to a place where people are willing to help. I'm glad you are doing well.

Bev

OutaSync wrote:If Cymbalta doesn't work, he wants to try Lyrica.

I'm currently taking 50mg of Lyrica twice a day to keep my facial pain in check. I have trigeminal neuralgia, though. When I first start up Lyrica for the cold months, I sleep considerably longer the first couple or few days. Then, while continuing Lyrica my own night time sleep actually seems more restorative.

Google "Lyrica" and "sleep architecture" and you'll see that Lyrica can actually help sleep architecture. I'm very seriously considering taking Lyrica year round for that reason. That was my neurologist's original suggestion. However, I am admittedly very heavily biased against unnecessary use of pharmaceuticals. As expensive as Lyrica is, I'm starting to think it's well justified.

Lyrica is also great for the likes of fibromyalgia----which causes the alpha wave intrusions SAG wants to look for in your data. On that basis alone, I'm not surprised that Lyrica can improve sleep architecture in some cases. Again, Lyrica sure seems to improve mine... probably by mitigating some pain. I don't have fibromyalgia, but I wouldn't be surprised if I consistently suffered pain-related alpha wave intrusions when not using Lyrica.



[note to self: get away from the cold months because of trigeminal neuralgia; move with wife to the Caribbean since rested gal spends so darn much time there anyway. ]

Interesting. A month ago my neurologist wrote a prescription for Lyrica, When I asked waht it would do, he told me that it "would help my muscles relax". I didn't think that was a good explanation, so I waited until I had the appt with my other Dr., last Thursday. He thought I could try Cymbalta first and gave me some samples. So far I haven't taken either. Would I have the problem with brain zaps getting off Lyrica? I don't want to go through that again. The Dr. had never heard of brain zaps.

Bev

OutaSync wrote: Would I have the problem with brain zaps getting off Lyrica? I don't want to go through that again. The Dr. had never heard of brain zaps.

Well, Lyrica is not an SSRI. However, it's a "taper off slowly" drug for people with seizure disorders:

rxlist.com wrote:Withdrawal of Antiepileptic Drugs (AEDs)

As with all AEDs, LYRICA should be withdrawn gradually to minimize the potential of increased seizure frequency in patients with seizure disorders. If LYRICA is discontinued this should be done gradually over a minimum of 1 week.

Pharmaceutical manufacturer's FAQ page: http://www.lyrica.com/content/main_common_questions.jsp

Only downside for me is that when my trigeminal neuralgia pain gets extremely bad, Lyrica doesn't do a darn thing for it. It sure helps with the "background pain" though. I have "atypical trigeminal neuralgia" because of that background pain that tends to stay around for weeks or months---separate from the inordinately intense and highly typical TN pain flareups. Lyrica's great for that "background pain" as well as other types of nerve pain conditions. I think Lyrica even works adequately at preventing the highly typical TN pain flareups in some patients.

I take Lyrca for my Fibro too. I have gone off it before an had a hard time but I was on several other meds that I went off all of them together. Not a good plan I was very loopy. But it was from depression mostly not the Lyrca,as well as stopping the drugs together. I now know it was not the Lycra that was the problem,as I have been taken it for several months now with no problems. Bev it may really do well to stop your pain,my docs say you need to keep your levels even for it to work right. Just a thought from my experiences which is about what we do in here . Exchange our cpap trials and if we are so lucky sometimes our success story too. Blessings,Melinda

-SWS wrote: <snip>

...By the way, I'm right back to thinking Bev's BiPAP AutoSV really needed to have its EPAP set at 14 cm:

Stephen E. Brown, MD, DABSM wrote:In another patient, undertitration occurred as the technologist adjusted the EEP for apneas and hypopneas, but did not adequately increase the pressure for residual RERAs.

That's exactly what I think may be happening in Bev's case with the autoSV's EPAP set too low. The end result is that IPAP peak uncomfortably throttles up and down near IPAP max for extended periods as we see on the SV charts.

I think she probably has a narrow airway that simply needs more constant dilation via EPAP at 14 cm. That constant EPAP dilation may keep the IPAP peak activity from running into an apparent vicious cycle of: 1) very rapid airway inflation (via a huge EPAP/IPAP peak gap), 2) a counterproductive (pressure-variation) stimulus/response reaction from Bev, followed by 3) an even more aggressive and counterproductive IPAP peak "countering response" from the BiPAP autoSV. That third step conceivably brings Bev back to (neurologically reactive) step two in that incessantly repeating vicious cycle.

She conceivably needs EPAP's constant airway dilation right up there at the same 14 cm that yielded satisfactory results in the lab and at home on APAP. Then SV can take a more refined approach at straightening out those flow-amplitude variations with a bit more finesse and hopefully greater comfort.

I must admit I was convinced that 14 would be proven far too high but inlight of the 'bouncing around' at IpapMax, it seems quite probable that 14 could make an improvement.

On my own machine I capped it at 20 CMs for IpapMax but a couple of nights back ran IpapMax to 24 to see if the SV would push me higher. The data showed exactly the usual pattern - IpapCurr maxing out at 19/20 Cms - I have been wondering what Bev's charts would show if IpapMax had been set higher - am now thinking she may also max out around 19-20 but it does seem that PS han't helped Bev with her quality of sleep.

Normal IpapMax = 20 http://www.internetage.ws/cpapdata/dsm- ... 0oct08.pdf

Testing IpapMax = 24 http://www.internetage.ws/cpapdata/dsm- ... 1oct08.pdf



DSM

PS still battling large leaks - something happened to the machine after I did the experiments - new hose hasn't improved them - possibly the H/H to machine coupling is failing as I can now and then feel air escaping around it.

dsm wrote:still battling large leaks - something happened to the machine after I did the experiments - new hose hasn't improved them - possibly the H/H to machine coupling is failing as I can now and then feel air escaping around it.

Can you somehow generate some inert or even pleasant smelling smoke? Smoke is a great way to locate both vacuum and pressure leaks.

on edit: I think you probably found the large leak:

possibly the H/H to machine coupling is failing as I can now and then feel air escaping around it.

Well, I think in order to predict if those drugs are going to improve sleep architecture, you would have to figure out what sleep architecture you're trying to improve and/or if you have something that that the selected drug would actually address (like depression, CFS, FBM, or chronic pain)(although you could argue that the treatment algorithm for chronic pain is analgesics)(but pregabalin data showed increased SWS and decreased awakenings in normals)(hold that thought).

Bev's sleep architecture during split study:



and titration night:



showed a goodly amount of SWS, so one would wonder if working on that would offer any opportunity.

However, there are tons of awakenings (you should really only have about 2-5, and you're in the high 20's) so that might be something to work on. Unfortunately, since those NPSG are severely tainted by incomplete treatment of SDB and the Lexapro, I don't think you can necessarily use them to determine treatment course. But I'm guessing the influence of pain is still there in substantial force, so attacking that could give some bang for the buck.

Using a dual RI (duloxetine)? I think the question there would be how much you gain vs how much you lose (reduction of awakenings, if that's the current problem vs side effects like somnolence or fatigue).

However, if sleep has now become normalized (and we're back to the need for another NPSG and probably MSLT), then now we fall into the category of Non-Restorative Sleep (sleep architecture is great, but it doesn't help) and then the N. path (or CFS, or FBM, or Idiopathic Hypersomnolence) needs to be strolled.

BTW, it doesn't make any difference what the physician thinks about insurance covering additional testing, it's what the insurance people think about insurance covering additional testing. At some point, they'll need to be called.

So, in summary, got me.

SAG

SAG wrote:But I'm guessing the influence of pain is still there in substantial force, so attacking that could give some bang for the buck.

The effects of pain on restorative sleep has been the biggest stumper for me over the years. Interestingly my primary physician, a wonderfully sharp internist who doesn't specialize in sleep, had been guessing that for years. I didn't think that was the case, however, since my body always readily turned off chronic pain---with the exception of trigeminal neuralgia's chronic "background" pain. I would even guess that my body's tendency to turn off chronic pain signals is why I suffered from the "silent" version of acid reflux disease. There was quite a bit of esophageal damage there, and I had no clue.

Right around the time that SAG, I, and several others were exploring K1 and K2, cryptic ASV learn circuit, etc. I was having a heck of a time with both chronic and acute trigeminal pain because of an abscessed tooth. Despite that, I still managed to sleep with the help of ambien. Honestly felt like hell by day, regarding energy and cognition, despite frequently managing to sleep through each night. The tooth needed to be extracted. As a temporary measure to help with the pain, the dentist alleviated pressure by draining the abscess and also administering Vicodin for pain. The next morning was the first time in many weeks that I woke up feeling refreshed.

I was absolutely astonished that pain and pain alone could allow me to consistently sleep the entire night, while so obviously destroying my sleep architecture----so obvious only by a retrospective comparison of sleep and especially daytime cognitive/EDS symptoms.

A quick comment about analgesics and pain. Before trigeminal neuralgia I had never given the topics of chronic and acute pain much thought. Analgesics are clearly the first course of action for pain treatment. However, they tend to work most effectively for chronic pain versus acute pain, and when the nerve itself and neurologic pain-signal handling are both in perfect working order. However, when disordered nerve or pain signal processing is central to the pain itself, analgesics tend to be ineffective. In Bev's case she suffers myofascial pain related to injury---possibly nerve injury. Based on medications recommended by Bev's doctors, I am guessing analgesics are going to be about as ineffective for her as they are for me.

Regardless, I know first hand that pain is my own sleep architecture's worst enemy. My apnea is well controlled by PAP treatment. My hunch is that there are a lot of people out there besides myself who would never suspect that pain can render sleep utterly non-restorative---despite still being able to sleep the entire night. What a royal pain in the...... sleep architecture.

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I still think Bev is a neurologically sensitive sleeper. Aside from investigating pain, I think she may stand to gain better sleep by continuing her various PAP modality and even presure experiments. Being able to do that reminds me of trying out different chairs or mattresses to see which one "feels" better. I personally suspect that's important for any neurologically sensitive sleeper.

And I still haven't dismissed the notion that autoSV set up correctly may be the best choice for Bev----if, indeed, there's some outstanding "wobbly" respiratory controller activity that may yield more restorative sleep when properly counteracted/stabilized with much more refined increments of automatic PS. The majority of all combined modality and pressure experiments are still ahead for Bev.