questions

[GuestJuly2]

split-city,

I think my own case indicates an unknown cause which contributes to both the OSAHS and abdominal obesity.

I am female with severe abdominal/stomach fat although my legs, thighs, buttocks, etc. have very little fat. Think of a ball with stick legs and no behind. My waist size is 40 inches. This pattern of deposition began long before puberty - sometime during early childhood.

I believe that I have had some form of sleep-disordered breathing also since childhood, but that the sleep-symptoms came BEFORE any significant weight gain. I was a very tired child, especially upon waking up in the morning after having had a full nights sleep.

On a tangent: A psychiatrist at a well regarded university discussed with me the possibility that this distribution of fat was the expression of a secret desire to become pregnant. (And I paid thousands of dollars for this "professional" medical treatment). This was years ago, but even then I told him that was ridiculous.

I was diagnosed finally at age 44 with OSAHS (moderate AHI of 17 in nonREM and severe AHI of 65 in REM - and what causes that difference?).

My question is this: Is there any info about the cause of the fat being deposited so specifically in the abdomin/stomach? Why am I so different from normal pear-shaped women? Is there anything that is even theorized to help shift anyone from the "apple" to the "pear" shape?

Thanks.

[GuestJuly2]

Sorry folks - I meant to post this to a another thread and will try to move it.

[StillAnotherGuest]

If I may take this from the other thread...

I am compliant on autoPAP with an AHI < 5, however my symptoms of fatigue and brain fog have shown little improvement after 6 months of treatment.

My diagnosis study showed few spontaneous arousals (SA), an index of < 4/hr. However the titration study *with PAP* showed an SA index of 30 during nonREM and 50 during REM. The AHI on PAP = 0.

Have you ever seen anything like this in the lab? If the PAP is causing the SA, then is it fruitless as far as expecting PAP treatment to improve the quality of my sleep? (very little SWS and REM and severe fragmentation).

How much REM did you have in the first sleep study?

Can you get the graphics from the two studies?

Were you on any medications at the time of either or both of the sleep studies?
SAG

[Guest]

If I may take this from the other thread..

ANY input is appreciated. Have posted numerous times on more than one forum and little feedback. TIA.

How much REM did you have in the first sleep study?

During the diagnosis study:
REM periods: 1
REM Latency: 5:33
REM Latency (less Wake time): 3:12
Time in REM: 11:04
REM Sleep Stage: 5.4%
Stage 3/4: 0% (actually 30 seconds of Stage 3)
AHI 17 in nonREM and 65 in REM, 85% obstructive hypopneas, only 1 central

I have seen a copy of the hypnogram, and it shows (for short periods) Stage 1, Stage 2, arousal, and then repeat.

During the titration:
AHI -0- at 4cm, however titrated to 7cm and was told that I hit SWS and REM.
Time in REM: 9.5 min
Number of SAs in REM: 8 for SA index of 50!
REM % Sleep Stage: 4.8%

My Oxygen levels are normal >95% throughout both studies.

Can you get the graphics from the two studies??

I can try but it will take some time. I have full report from 1st study but only summary report from titration study. Can you tell anything from what I have put so far?

Were you on any medications at the time of either or both of the sleep studies???

Yes. Lexpro which was is an antidepressant for both studies. Also known as Escitalopram. However I decreased the dosage after OSAHS diagnosis. Stopped completely after one month on autoPAP. I didn't notice any difference in symptoms. I practice sleep hygiene etc.

I have not been on any meds since mid-January, and started the Clonazepam last week. It's wonderful as I feel euphoric after taking it, but then I feel terrible and have anxiety when it wears off. I can see that it cannot be a long term solution for me.

MJ

[StillAnotherGuest]

Can you get the graphics from the two studies??

I can try but it will take some time. I have full report from 1st study but only summary report from titration study.

OK, get 'em both scanned and posted.

Can you tell anything from what I have put so far?

Without those reports, it's the tip of the iceberg. However...

Were you on any medications at the time of either or both of the sleep studies?

Yes. Lexpro which was is an antidepressant for both studies. Also known as Escitalopram.

I know Lexapro, it's a great drug to destroy your sleep architecture and generate a ton of spontaneous arousals.

It's also a REM suppressant. Which makes this

REM Latency: 5:33

otherwise known as a "SOREM", all the more interesting.

Because of the decreased time in REM, you have to be a little careful about about tossing around the high REM AHI density just yet. And sometimes hypopneas can be a little tricky. If you have 150 events (regardless of origin) in the diagnostic study, and 150 events in the treatment study, one would wonder if the events in the first study were really what you thought they were.

During the titration:
Time in REM: 9.5 min
Number of SAs in REM: 8 for SA index of 50!
REM % Sleep Stage: 4.8%

A highly fragmented REM can be another important clue, but again, the decreased time makes interpretation of this value difficult.

My Oxygen levels are normal >95% throughout both studies.

If you didn't have any desaturations, then arguably you didn't have any hypopneas, they were all RERAs, at most.

We'll also have to look at Sleep Efficiency, which looks like something on the order of 50% (Total Sleep Time of 3 hours 20 minutes based on REM%). You'd need another hour and a half just to get up to horrible.

Get the scans, there's probably a veritable treasure trove of additional information there.
SAG

[Guest]

SAG,

Ok understood and thank you for your response. It will take me several days to get the reports scanned in, but will do so. Please check back here sometimes.

Can you point me in any direction of possible conditions? Could it be early stage REM-BD? I understand that this is not medical advice and wouldn't be followed as such. It's just that I am trying to research any possibilities.

The Clonazepam seems to help a little.

[StillAnotherGuest]

It will take me several days to get the reports scanned in, but will do so. Please check back here sometimes.

OK, SAG is going to the beach for awhile anyway.

Can you point me in any direction of possible conditions?

No. The missing pieces are still missing.

Meanwhile, take this test, list all your answers.



SAG

[blarg]

(moderate AHI of 17 in nonREM and severe AHI of 65 in REM - and what causes that difference?).

My rudimentary understanding is that your throat muscles are more prone to relaxing during REM sleep. (Mine was 32 overall and 78 in REM)

Anyway, sorry to hear of your previous lack-luster experience with the medical industry. Please let us know how you get on in this complicated process of figuring out how to feel like a human being.

[Slinky]

Hey Sag! Enjoy the beach. Get a good dose of vitamin D but don't overdo those bad "rays"!

So where do we find the scoring on these HAS's??

[JulySky]

SAG,

Hope you enjoyed your day(s) at the beach.

Following are the complete report from the 1st sleep study (7pgs) and the summary report (2 pgs) from the titration study. It looks to me like I have difficulty maintaining Stage 1 & 2 sleep. BTW, my result on the HAS was 47, and note probably an increasing trend over the past few years.

Please note that I think that I did not have a "SOREM". The REM latency was 5:30 is five hours and 30 minutes and I should have identified the units.

Thanks again for your your input.





















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CPAPopedia Keywords Contained In This Post (Click For Definition): Titration

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CPAPopedia Keywords Contained In This Post (Click For Definition): Titration

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CPAPopedia Keywords Contained In This Post (Click For Definition): Titration

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CPAPopedia Keywords Contained In This Post (Click For Definition): Titration

[StillAnotherGuest]

Please note that I think that I did not have a "SOREM". The REM latency was 5:30 is five hours and 30 minutes...

No prob, that makes a heckuva lot more sense given the Lexapro thing.

my result on the HAS was 47

Score any 3's anywhere?

Assuming for the moment you do have some component of OSA and it has been corrected by pressure therapy, if your sleep quality is anything like what was seen in the studies, it is highly unlikely that the EDS and associated symptoms are going to improve. You need about 7.5 hours of actual sleep, done with an arousal index of <5, maybe 2-5 awakenings and no less than 85% efficiency (and 85% is really stretching it).

In your sleep studies, With 46.9% and 43.8% sleep efficiencies, you've scored beyond awful. Now, some of that, as well as the spontaneous arousals, could be attributed to the Lexapro. Since that's gone now, tho, and your symptoms have apparently changed little, there's at least one other issue underfoot.

While the definition of insomnia doesn't hinge on one or two sleep studies (it's usually something general like "difficulty initiating or maintaining sleep or experiencing nonrestorative sleep that results in clinically significant distress or impairment in functioning that lasts more than a month"), persistent sleep efficiencies <85% certainly raise strong suspicions about the ability to achieve and maintain sleep. And addressing insomnia will therefore give you the biggest bang for your buck.

OK, still more questions:

How you making out with your visits with the sleep physicians?

Those two sleep reports look like they're from two different software packages. Were they from two different laboratories?
If they weren't, were they scored by the same person?

Can you get the sleep architecture from the second study?

Why, if there's a perfectly good beach like 10 miles from where they live, do people have to drive 800 miles to find a different one?
SAG

[JulySky]

Hello SAG,

Thanks for working while at the water's edge.

Score any 3's anywhere?

Yes. I scored seven "3's". But, for example on #2 'I am slow to awaken mornings'.... what else would I score but a 3? I am toast everyday.

And addressing insomnia will therefore give you the biggest bang for your buck.

Ok, thank you, I will start looking into treatments for insomnia.

How you making out with your visits with the sleep physicians?

My sleep doc has been very good to me especially when compared to PCPs who mostly think that there is nothing wrong with me. However my sleep doc has referred me to another sleep doc for a second opinion. That appt is scheduled for next Monday 7/16.

Those two sleep reports look like they're from two different software packages. Were they from two different laboratories?
If they weren't, were they scored by the same person?

Well, you ARE a good detective. Yes, the studies were done at two different labs. Will skip the very long story. The initial scorers may have been different, but same certified sleep specialist who is said to review everything was the same person who signed off on both studies.

Can you get the sleep architecture from the second study?

Yes. They are mailing the complete report to me and I will post it as soon as I get it.

Why, if there's a perfectly good beach like 10 miles from where they live, do people have to drive 800 miles to find a different one?

Perhaps they know that you are there?

JulySky

[StillAnotherGuest]

Score any 3's anywhere?

Yes. I scored seven "3's". But, for example on #2 'I am slow to awaken mornings'.... what else would I score but a 3? I am toast everyday.

Where are the other 3's? In this test, some values carry more weight than others.

I will start looking into treatments for insomnia.

Try this State-of-the-Science blurb (Medscape is free):

Insomnia

And there's about a dozen different types of insomnia, so that story's just begun.

...my sleep doc has referred me to another sleep doc for a second opinion. That appt is scheduled for next Monday 7/16.

Getting a little ahead of the story, within the discipline of sleep medicine is a subspecialty called C.B.S.M. (Certified in Behavioral Sleep Medicine). This certification confirms an individual’s expertise in the application of behavioral and cognitive methods of prevention and treatment of insomnia. Utilizing Cognitive Behavioral Therapy (CBT) will be extremely important to the treatment approach to insomnia. You can ask your new sleep guy if he is certified in CBT, how well versed he is in it, or if he is, in fact, comfortable with it at all.

Here's a good summary of the type of approach one takes with CBT:

The ABC's of CBT

The initial scorers may have been different, but same certified sleep specialist who is said to review everything was the same person who signed off on both studies.

Even tho the "long report" has a lot of stuff, it's the actual raw data that should be looked at, even more so in your case. Put both studies side-by-side.

With the severely reduced REM (which makes it's analysis difficult, if not impossible) and a bunch of spontaneous arousals that could have been generated by the Lexapro, another PSG is certainly within the realm of possibilities. And for that matter, even taking a real critical look at the respiratory parameters to insure that there is an OSA/UARS component, and not something that was simply masked by a ton of spontaneous arousals and/or destroyed sleep architecture.
SAG

BTW, prior to the next PSG, I would avoid any activities involving "Karaoke", an entertainment activity that is loosely associated with music. It's very hard on the upper airway, especially for those who don't sing a lot.

Or can't.

"...Sweet Home, Alabama..."

[JulySky]

Hello SAG,

I hope you are still out there?

Where are the other 3's?

The 3's were scored on #s: 2, 6, 7, 12, 13, 23, & 24.

Put both studies side-by-side.

Yeah, I can see that the only improvement was that there was Stage 3 sleep with the PAP. But by most other parameters I am the same or worse.

it's usually something general like "difficulty initiating or maintaining sleep or experiencing nonrestorative sleep

Well, I have to again give you credit for finding answers! There is this in the doctor's report: "307.45-3 Disorder initiating and/or maintaining sleep". Although I don't think that I have difficulty falling asleep, it seems that my sleep is very strange, almost not asleep, but not awake, either. I may be awake, but I am not clearly aware that I am awake. Confusing.

Thanks for the links and info on C.B.S.M. Also, the doc's office did mail some documents to me, but not the report that I thought I had requested. I will try to get more info when I meet with the new doc on Monday.

I would avoid any activities involving "Karaoke"

I have learned to trust your advice.

Thanks.

[StillAnotherGuest]

I hope you are still out there?

Yeah, but sometimes the signal out here gets a little wea....

The 3's were scored on #s: 2, 6, 7, 12, 13, 23, & 24.

The Hyperarousal Scale was devised by Regestein et al as a tool to help evaluate Primary Insomnia (insomnia without a known cause). The insomnia group posted a mean score of 48.9, with the questions 4, 5, 14 and 16 frequently receiving the "Extreme" rating.

Say, speaking of #19 (smooth segue, huh?), how about caffeine intake (don't forget soda)?

Put both studies side-by-side.

Yeah, I can see that the only improvement was that there was Stage 3 sleep with the PAP. But by most other parameters I am the same or worse.

OK, when I refer to the "raw data", I'm talking about the sleep study itself, the 900 or so pages of data, the actual waveforms. Since you're going for a second opinion, then all aspects of the case should be reviewed, especially that. Being Mr. Skeptical, I would look very closely at the respiratory parameters. As noted before:

...sometimes hypopneas can be a little tricky. If you have 150 events (regardless of origin) in the diagnostic study, and 150 events in the treatment study, one would wonder if the events in the first study were really what you thought they were.

That means looking to see if there really were respiratory events in the first study, or if the breathing reductions were simply artifact from the surrounding sleep fragmentation. And if pressure therapy was adequate or even made a difference, like seeing if there was a change in the waveform such as improvement of "flow limitation" characteristics.

With no oxygen desaturations (oxygen drops of 4% or more), one could easily argue that there were no hypopneas at all, since many definitions of hypopnea require that. A simple flow reduction or limitation that occurs without an accompanying desaturation, and only an arousal, would then be a Respiratory Effort-Related Arousal (RERA). Now, these subtle flow restrictions can create severe sleep fragmentation, as well as a host of other issues, but RERAs should also be quite responsive to pressure therapy and at least some improvement would be expected (I wouldn't call 30 seconds of Stage 3 an improvement). If you end up with the identical sleep architecture and arousal index with treatment, then one must ask if the choice of therapy is indeed appropriate at all, and if they were even RERAs. The question that needs to be asked is, "Is there really a respiratory component, or is this entirely something else?" If it's "something else", then maybe a 180 degree change in approach is needed, namely, fix the sleep fragmentation and then assess the respiratory component.

Meanwhile, if you do choose to sing Karaoke, avoid all the stuff by AC/DC, especially "Thunderstruck."
SAG