Cause of hypopneas?

rooster wrote:The pause that refreshes and the pause that don't.

Sorry Pepsi. Sorry Mrs. Smith.

Rooster's message works ... simple and to the point.

I have been following this forum for the last seven years and I consider that City above has posed a very vital question which remained unasnwered during the present discussion. He writes as follows:

Snoredog wrote:
Remember as you fall deeper into sleep you relax more, the more you relax and reach those deeper stages of sleep the more pressure is needed to keep those apneas under control.


Here's a question for you Snoredog (or anybody else out there). If, as you say, you relax more as you reach deeper sleep (and therefore, muscle activity is lower), why do most OSA patients experience less apnea events during slow-wave sleep (stages 3 and 4) compared to stages 1 and 2?


Now would the experts here clarify as to why do most OSA patients experience less apnea events during stages 3 and 4 compared to 1 and 2.

Snore dog and all other friends, we are all looking for your expert guidance.
and comments.

In the above commendable comments by split city and snore dogs, one question also remained unaswered. Snore dog suggested, that in order to open up air passages, the pressure may be increased gradually. (If I understood the matter properly being a layman). However, I am using bipap auto at a pressure of 7:11. So, would I be right to assume, that the opening of the airway on account of narrowing down of the airway passage will be taken care of by the machine itself by increasing the pressure.

Please do reply to this post as also another just sent on this subject. Thanks.

Birdwood wrote:I have been following this forum for the last seven years and I consider that City above has posed a very vital question which remained unasnwered during the present discussion. He writes as follows:

Snoredog wrote:
Remember as you fall deeper into sleep you relax more, the more you relax and reach those deeper stages of sleep the more pressure is needed to keep those apneas under control.


Here's a question for you Snoredog (or anybody else out there). If, as you say, you relax more as you reach deeper sleep (and therefore, muscle activity is lower), why do most OSA patients experience less apnea events during slow-wave sleep (stages 3 and 4) compared to stages 1 and 2?


Now would the experts here clarify as to why do most OSA patients experience less apnea events during stages 3 and 4 compared to 1 and 2.

Snore dog and all other friends, we are all looking for your expert guidance.
and comments.

Well I'm no expert and Snoredog can speak for himself ... and then some

But I thought that stage 3 and 4 were the deeper stages of sleep ... never mind

I guess the apneas themselves keep people from reaching stages 3 and 4. As I recall mine occured mostly in stage 3 but I have to go back and look at my PSG.

DreamStalker wrote:

Birdwood wrote:I have been following this forum for the last seven years and I consider that City above has posed a very vital question which remained unasnwered during the present discussion. He writes as follows:

Snoredog wrote:
Remember as you fall deeper into sleep you relax more, the more you relax and reach those deeper stages of sleep the more pressure is needed to keep those apneas under control.


Here's a question for you Snoredog (or anybody else out there). If, as you say, you relax more as you reach deeper sleep (and therefore, muscle activity is lower), why do most OSA patients experience less apnea events during slow-wave sleep (stages 3 and 4) compared to stages 1 and 2?


Now would the experts here clarify as to why do most OSA patients experience less apnea events during stages 3 and 4 compared to 1 and 2.

Snore dog and all other friends, we are all looking for your expert guidance.
and comments.

I guess the apneas themselves keep people from reaching stages 3 and 4

Once certainly might predict that. However, lots of OSA patients eventually do "crash through the barrier" and make it through to stages 3 and 4...and then kinda just pass go (collecting $200) and entering REM. This is kinda like landing on the "go directly to jail. Do not pass go. Do not collect $200" square as they have even more severe apnea events, leading to an arousal.

Birdwood wrote:I have been following this forum for the last seven years and I consider that City above has posed a very vital question which remained unasnwered during the present discussion. He writes as follows:

Snoredog wrote:
Remember as you fall deeper into sleep you relax more, the more you relax and reach those deeper stages of sleep the more pressure is needed to keep those apneas under control.


Here's a question for you Snoredog (or anybody else out there). If, as you say, you relax more as you reach deeper sleep (and therefore, muscle activity is lower), why do most OSA patients experience less apnea events during slow-wave sleep (stages 3 and 4) compared to stages 1 and 2?


Now would the experts here clarify as to why do most OSA patients experience less apnea events during stages 3 and 4 compared to 1 and 2.

Snore dog and all other friends, we are all looking for your expert guidance.
and comments.

Hey I'm no expert, but I'd be willing to wager that you and he are of the same, as he likes to argue with himself over his own theories. But on the shrinking neck theory, we discussed that years and years ago, even thought you could wear a orthopedic neck brace to bed and stretch that neck tissue back out, but then the cervical vertebra didn't want to cooperate with that theory either

You would think if a person fell asleep like many do during a MRI scan that they could "capture" the state of those airway tissues and either confirm or exclude sc's theory quite easily.

I've slept through more than 9 different high res MRI's, fell asleep every time, they finally resorted to sticking my head in that cage so I wouldn't move from a hypnic jerk or apnea event recovery. That bong on the MRI puts me right to sleep.

It is like the medical establishment is "afraid" of finding the root cause of OSA, doing so would mean a lot of people looking for work.

Here is an example cervical MRI scan, you can clearly see not only the lesion to the spinal cord, but to the left the tongue, the Uvula, everything is clearly seen on the MRI, and applying different weighting algorithm you can have a 3 dimensional view of what is happening. While the film is shown vertical, the patient is actually horizontal when the scan is taken, all you have to do is hook up a portable PSG equipment in the Radiology department and you would have invaluable information on this disorder. How hard is that?

Snoredog wrote:

Birdwood wrote:I have been following this forum for the last seven years and I consider that City above has posed a very vital question which remained unasnwered during the present discussion. He writes as follows:

Snoredog wrote:
Remember as you fall deeper into sleep you relax more, the more you relax and reach those deeper stages of sleep the more pressure is needed to keep those apneas under control.


Here's a question for you Snoredog (or anybody else out there). If, as you say, you relax more as you reach deeper sleep (and therefore, muscle activity is lower), why do most OSA patients experience less apnea events during slow-wave sleep (stages 3 and 4) compared to stages 1 and 2?


Now would the experts here clarify as to why do most OSA patients experience less apnea events during stages 3 and 4 compared to 1 and 2.

Snore dog and all other friends, we are all looking for your expert guidance.
and comments.

Hey I'm no expert, but I'd be willing to wager that you and he are of the same, as he likes to argue with himself over his own theories. But on the shrinking neck theory, we discussed that years and years ago, even thought you could wear a orthopedic neck brace to bed and stretch that neck tissue back out, but then the cervical vertebra didn't want to cooperate with that theory either

You would think if a person fell asleep like many do during a MRI scan that they could "capture" the state of those airway tissues and either confirm or exclude sc's theory quite easily.

I've slept through more than 9 different high res MRI's, fell asleep every time, they finally resorted to sticking my head in that cage so I wouldn't move from a hypnic jerk or apnea event recovery. That bong on the MRI puts me right to sleep.

It is like the medical establishment is "afraid" of finding the root cause of OSA, doing so would mean a lot of people looking for work.

Here is an example cervical MRI scan, you can clearly see not only the lesion to the spinal cord, but to the left the tongue, the Uvula, everything is clearly seen on the MRI, and applying different weighting algorithm you can have a 3 dimensional view of what is happening. While the film is shown vertical, the patient is actually horizontal when the scan is taken, all you have to do is hook up a portable PSG equipment in the Radiology department and you would have invaluable information on this disorder. How hard is that?

Snoredog. There have been a couple of studies which have imaged the airway in OSA patients during sleep. However, generally subjects were asked to sleep deprive themselves for 24 hours the night before or they were on high doses of sedatives. Certainly not the native sleep state.

While you may have fell asleep easily during an MRI imaging session, this is certainly not the case for everyone. Furthermore, providing one picture of the tongue flopping back in yourself certainly does not prove your theory or disprove mine.

I'll ask you this question again as you didn't answer it previously. If you think that the airway collapse is the result of the tongue flopping back, why or how can the airway collapse when someone is sleeping on their stomach or even when on their side? How does the flaccid tongue flop backwards against gravity?

Anyways, you actually ignored the posters question (a question that I actually asked you). Why does the airway seem to be protected during stages 3 and 4 sleep, despite this period of sleep being deeper and muscles are more relaxed? Why doesn't the tongue flop back then if it's relaxed?

Perhaps you better have a chat with Richard Schwab. He's the expect in the field in relation to upper airway imaging. Richard is a nice chap and is easy to talk to. Perhaps you could spin a few of your theories his way.

Or even better still, perhaps you could set up your own research lab and test some of your theories yourself.

split_city wrote:

Snoredog wrote:

Birdwood wrote:I have been following this forum for the last seven years and I consider that City above has posed a very vital question which remained unasnwered during the present discussion. He writes as follows:

Snoredog wrote:
Remember as you fall deeper into sleep you relax more, the more you relax and reach those deeper stages of sleep the more pressure is needed to keep those apneas under control.


Here's a question for you Snoredog (or anybody else out there). If, as you say, you relax more as you reach deeper sleep (and therefore, muscle activity is lower), why do most OSA patients experience less apnea events during slow-wave sleep (stages 3 and 4) compared to stages 1 and 2?


Now would the experts here clarify as to why do most OSA patients experience less apnea events during stages 3 and 4 compared to 1 and 2.

Snore dog and all other friends, we are all looking for your expert guidance.
and comments.

Hey I'm no expert, but I'd be willing to wager that you and he are of the same, as he likes to argue with himself over his own theories. But on the shrinking neck theory, we discussed that years and years ago, even thought you could wear a orthopedic neck brace to bed and stretch that neck tissue back out, but then the cervical vertebra didn't want to cooperate with that theory either

You would think if a person fell asleep like many do during a MRI scan that they could "capture" the state of those airway tissues and either confirm or exclude sc's theory quite easily.

I've slept through more than 9 different high res MRI's, fell asleep every time, they finally resorted to sticking my head in that cage so I wouldn't move from a hypnic jerk or apnea event recovery. That bong on the MRI puts me right to sleep.

It is like the medical establishment is "afraid" of finding the root cause of OSA, doing so would mean a lot of people looking for work.

Here is an example cervical MRI scan, you can clearly see not only the lesion to the spinal cord, but to the left the tongue, the Uvula, everything is clearly seen on the MRI, and applying different weighting algorithm you can have a 3 dimensional view of what is happening. While the film is shown vertical, the patient is actually horizontal when the scan is taken, all you have to do is hook up a portable PSG equipment in the Radiology department and you would have invaluable information on this disorder. How hard is that?

Snoredog. There have been a couple of studies which have imaged the airway in OSA patients during sleep. However, generally subjects were asked to sleep deprive themselves for 24 hours the night before or they were on high doses of sedatives. Certainly not the native sleep state.

While you may have fell asleep easily during an MRI imaging session, this is certainly not the case for everyone. Furthermore, providing one picture of the tongue flopping back in yourself certainly does not prove your theory or disprove mine.

I'll ask you this question again as you didn't answer it previously. If you think that the airway collapse is the result of the tongue flopping back, why or how can the airway collapse when someone is sleeping on their stomach or even when on their side? How does the flaccid tongue flop backwards against gravity?

Anyways, you actually ignored the posters question (a question that I actually asked you). Why does the airway seem to be protected during stages 3 and 4 sleep, despite this period of sleep being deeper and muscles are more relaxed? Why doesn't the tongue flop back then if it's relaxed?

Perhaps you better have a chat with Richard Schwab. He's the expect in the field in relation to upper airway imaging. Richard is a nice chap and is easy to talk to. Perhaps you could spin a few of your theories his way.

Or even better still, perhaps you could set up your own research lab and test some of your theories yourself.

Hey those aren't my MRI's or cartoons, here's one from that company found in your own homeland, here is what they say it is caused by:

http://www.resmed.com/en-uk/patients/ab ... 40x380.swf

Watch what the tongue does during their own demonstration. I suspect the patient in that cartoon (looks like Fred Flintstone to me, but that is only a guess, it could very well be Barney). But I'm still trying to figure out the beer belly connection and reinvention of the wheel.

Snoredog wrote:

split_city wrote:

Snoredog wrote:

Birdwood wrote:I have been following this forum for the last seven years and I consider that City above has posed a very vital question which remained unasnwered during the present discussion. He writes as follows:

Snoredog wrote:
Remember as you fall deeper into sleep you relax more, the more you relax and reach those deeper stages of sleep the more pressure is needed to keep those apneas under control.


Here's a question for you Snoredog (or anybody else out there). If, as you say, you relax more as you reach deeper sleep (and therefore, muscle activity is lower), why do most OSA patients experience less apnea events during slow-wave sleep (stages 3 and 4) compared to stages 1 and 2?


Now would the experts here clarify as to why do most OSA patients experience less apnea events during stages 3 and 4 compared to 1 and 2.

Snore dog and all other friends, we are all looking for your expert guidance.
and comments.

Hey I'm no expert, but I'd be willing to wager that you and he are of the same, as he likes to argue with himself over his own theories. But on the shrinking neck theory, we discussed that years and years ago, even thought you could wear a orthopedic neck brace to bed and stretch that neck tissue back out, but then the cervical vertebra didn't want to cooperate with that theory either

You would think if a person fell asleep like many do during a MRI scan that they could "capture" the state of those airway tissues and either confirm or exclude sc's theory quite easily.

I've slept through more than 9 different high res MRI's, fell asleep every time, they finally resorted to sticking my head in that cage so I wouldn't move from a hypnic jerk or apnea event recovery. That bong on the MRI puts me right to sleep.

It is like the medical establishment is "afraid" of finding the root cause of OSA, doing so would mean a lot of people looking for work.

Here is an example cervical MRI scan, you can clearly see not only the lesion to the spinal cord, but to the left the tongue, the Uvula, everything is clearly seen on the MRI, and applying different weighting algorithm you can have a 3 dimensional view of what is happening. While the film is shown vertical, the patient is actually horizontal when the scan is taken, all you have to do is hook up a portable PSG equipment in the Radiology department and you would have invaluable information on this disorder. How hard is that?

Snoredog. There have been a couple of studies which have imaged the airway in OSA patients during sleep. However, generally subjects were asked to sleep deprive themselves for 24 hours the night before or they were on high doses of sedatives. Certainly not the native sleep state.

While you may have fell asleep easily during an MRI imaging session, this is certainly not the case for everyone. Furthermore, providing one picture of the tongue flopping back in yourself certainly does not prove your theory or disprove mine.

I'll ask you this question again as you didn't answer it previously. If you think that the airway collapse is the result of the tongue flopping back, why or how can the airway collapse when someone is sleeping on their stomach or even when on their side? How does the flaccid tongue flop backwards against gravity?

Anyways, you actually ignored the posters question (a question that I actually asked you). Why does the airway seem to be protected during stages 3 and 4 sleep, despite this period of sleep being deeper and muscles are more relaxed? Why doesn't the tongue flop back then if it's relaxed?

Perhaps you better have a chat with Richard Schwab. He's the expect in the field in relation to upper airway imaging. Richard is a nice chap and is easy to talk to. Perhaps you could spin a few of your theories his way.

Or even better still, perhaps you could set up your own research lab and test some of your theories yourself.

Hey those aren't my MRI's or cartoons, here's one from that company found in your own homeland, here is what they say it is caused by:

http://www.resmed.com/en-uk/patients/ab ... 40x380.swf

Watch what the tongue does during their own demonstration. I suspect the patient in that cartoon (looks like Fred Flintstone to me, but that is only a guess, it could very well be Barney). But I'm still trying to figure out the beer belly connection and reinvention of the wheel.

I'm not denying that the tongue flopping back isn't a cause of OSA. But I'm also not naive to suggest that it's the only cause.

Ok, here's another question for you which definately supports the view that the tongue flopping back isn't the only cause of OSA. I have stated this many times before. Upper airway size and collapsibility are lung volume dependent. Increasing lung volume decreases airway collapsibility and vice versa. This finding even happens when you are awake when your tongue is active. How does this finding support your view about the floppy tongue?

Search for Heinzer in pubmed. He conducted two studies in 2005 and 2006 looking at the effect of lung volume on RDI and CPAP requirements. He showed that RDI decreased during sleep when lung volume was increased and also showed that the therapeutic CPAP (to prevent flow limitation) decreased when lung volume was increased. Patients were sleeping on their back in these studies. Have a read through these papers if you can get the full text. It might open up your mind.

Anyways, are you actually going to attempt to answer the other questions I asked?

_________________

CPAPopedia Keywords Contained In This Post (Click For Definition): CPAP, RDI

there have been studies done on onychocryptosis, but is that also a cause?

split_city said: "Increasing lung volume decreases airway collapsibility and vice versa." Can you recommend a way to increase lung volume? Although my lung function studies were on the low end of normal my breath capacity has diminished over the past 18 months. I become short of breath when I walk up stairs and hills. Because of chronic pain from old foot fractures I cannot walk vigorously or for long distances. I've asked several health professionals for help but have not been given any useful advice. I enjoy swimming and can swim an hour (slowly) but this has not improved my breathing.

Snoredog wrote:there have been studies done on onychocryptosis, but is that also a cause?

So is that your only reply?

Why are you trying to dodge the questions I asked?

I provided evidence which suggest other causes for airway collapse. If you believe that the tongue flopping back is the cause of OSA, you should be easily able to disprove (with evidence) the points I raised.

You can admit that you don't know the answers

Auricula wrote:split_city said: "Increasing lung volume decreases airway collapsibility and vice versa." Can you recommend a way to increase lung volume? Although my lung function studies were on the low end of normal my breath capacity has diminished over the past 18 months. I become short of breath when I walk up stairs and hills. Because of chronic pain from old foot fractures I cannot walk vigorously or for long distances. I've asked several health professionals for help but have not been given any useful advice. I enjoy swimming and can swim an hour (slowly) but this has not improved my breathing.

Which lung volume is at the low end of capacity? Total lung capacity? Lung volume at the end of expiration? Do you know what sort of lung disease you have? COPD? Asthma?

I'm not a respiratory physician so I can't suggest ways to improve your breathing. However, in terms of increasing lung volume: sleep standing! Just joking. Lung volume is higher when you are standing but obviously it might be a bit too difficult to sleep while standing. Sleeping with your back raised can help some people in terms of their OSA or sleeping on your side. However, there was a study I quoted a few weeks ago showing that only about 55% of patients (in their group) had worse OSA on their back i.e. apnea events were no different in ~45% of patients between the supine position and all other positions.

CPAP helps keep the airway open by several mechanisms but probably the two most important are 1) positive airway 'pushes' (splints) the airway open and 2) increases lung volume. The Heinzer papers definately prove the beneficial effects of increased lung volume on airway patency. Lung volume was increased by an iron lung in the Heinzer papers. The iron lung is just a large box in which you lie in. Your head and neck is outside the chamber. A vacuum/blower is attached to the chamber and lung volume can be increased by turning the blower on (compresses the chest and abdomen) or decreased by turning the vacuum on (sucks chest and abdomen out). So, if you can't handle CPAP, you can always sleep in an iron lung!

split_city wrote:

DreamStalker wrote:

Birdwood wrote:I have been following this forum for the last seven years and I consider that City above has posed a very vital question which remained unasnwered during the present discussion. He writes as follows:

Snoredog wrote:
Remember as you fall deeper into sleep you relax more, the more you relax and reach those deeper stages of sleep the more pressure is needed to keep those apneas under control.


Here's a question for you Snoredog (or anybody else out there). If, as you say, you relax more as you reach deeper sleep (and therefore, muscle activity is lower), why do most OSA patients experience less apnea events during slow-wave sleep (stages 3 and 4) compared to stages 1 and 2?


Now would the experts here clarify as to why do most OSA patients experience less apnea events during stages 3 and 4 compared to 1 and 2.

Snore dog and all other friends, we are all looking for your expert guidance.
and comments.

I guess the apneas themselves keep people from reaching stages 3 and 4

Once certainly might predict that. However, lots of OSA patients eventually do "crash through the barrier" and make it through to stages 3 and 4...and then kinda just pass go (collecting $200) and entering REM. This is kinda like landing on the "go directly to jail. Do not pass go. Do not collect $200" square as they have even more severe apnea events, leading to an arousal.

Ok, I just checked my PSG report ... I never went into stage 4 ... I went straight to REM from stage 4.

My arousal index was 78 in REM and 105 in NREM.

DreamStalker wrote:

split_city wrote:

DreamStalker wrote:

Birdwood wrote:I have been following this forum for the last seven years and I consider that City above has posed a very vital question which remained unasnwered during the present discussion. He writes as follows:

Snoredog wrote:
Remember as you fall deeper into sleep you relax more, the more you relax and reach those deeper stages of sleep the more pressure is needed to keep those apneas under control.


Here's a question for you Snoredog (or anybody else out there). If, as you say, you relax more as you reach deeper sleep (and therefore, muscle activity is lower), why do most OSA patients experience less apnea events during slow-wave sleep (stages 3 and 4) compared to stages 1 and 2?


Now would the experts here clarify as to why do most OSA patients experience less apnea events during stages 3 and 4 compared to 1 and 2.

Snore dog and all other friends, we are all looking for your expert guidance.
and comments.

I guess the apneas themselves keep people from reaching stages 3 and 4

Once certainly might predict that. However, lots of OSA patients eventually do "crash through the barrier" and make it through to stages 3 and 4...and then kinda just pass go (collecting $200) and entering REM. This is kinda like landing on the "go directly to jail. Do not pass go. Do not collect $200" square as they have even more severe apnea events, leading to an arousal.

Ok, I just checked my PSG report ... I never went into stage 4 ... I went straight to REM from stage 4.

My arousal index was 78 in REM and 105 in NREM.

Did you mean you just went from stage 3 into REM?

I'm not really looking at the arousal index but more your AHI in REM and NREM. More importantky, it would be interesting to see what your AHI was in each sleep stage i.e. stage 1, 2, 3 and REM