CompSA, Hypoventilation, PLMs, Bradycardia and Hypotension?

blizzardboy · Post by **blizzardboy** » Sun May 23, 2010 12:48 am

-SWS wrote:The All World Informatics dispensary forgot Alpha Wave Intrusions (AWI) again...

Thank you for the clarification, and I thought I had hit the nail on the head (must have confused AWI and AI/AwI)! I will edit my post to correct. Cheers,

Muffy · Post by **Muffy** » Sun May 23, 2010 4:11 am

kteague wrote:At the risk of confirming what may have previously been only suspected - I'm as lost as a ball in high weeds?

And in reading your question, kathy, I am either not understanding it or not allowing myself to understand it.

IIWY, I would go back and get my sleep study to find out exactly what was happening EEG-wise with your movements. For instance, if the frequency of your movements are every couple of seconds or so, then they can't be PLMs because they're too fast. If they occur at sleep onset, you could be looking at hypnagogic foot tremor. If you're looking at REM, it could be REM behavior disorder.

Muffy

Muffy · Post by **Muffy** » Sun May 23, 2010 4:15 am

blizzardboy wrote:If, as it would seem, that my arousals are associated with alpha-polluted delta waves then presumably I will see an improvement in respiration stability (as recorded in my DLs) once the source of intrusions is quelled/squashed/terminated e.g. if fluoxetine is my problem and I wean off and withdraw then I should see an improvement in my DLs with the need for an other PSG. Sound reasoning?

No. Even alpha-delta sleep is respiratory-stable.

Muffy

Muffy · Post by **Muffy** » Sun May 23, 2010 4:18 am

blizzardboy wrote:Last night I attempted to further increase the baseline ventilation provided to me by the ASV by lowering EEP to 9.0 and increasing PS to 5->10 (yes, I realise these are big shifts from EEP=9.6 and PS=4->9) Interesting to see four 5-minute-ish periods of relatively stable respiration during the night: http://users.adam.com.au/sixsome/ASV/0510/052210/. That means I had a total of 20 minutes of stable-ish respiration for the night - you beauty!

I thought your new sleep physician said to go to low-level CPAP and stop dial wingin'.

Muffy

Muffy · Post by **Muffy** » Sun May 23, 2010 4:35 am

blizzardboy wrote:So can we safely say that I suffer from OSA (and not CompSA) in parallel with a deep-sleep-disruption "...problem"

Interpreting that literally, not yet. I didn't see a single obstructive apnea. It may more likely be that the underlying SDB identity (if present) is UARS.

And the deep sleep is not "disrupted", it's "infected".

OK, I'm off to celebrate Memorial Day. In small towns up here, in order to get enough stuff to put together a parade, communities band together and pool resources. Unfortunately, it also results in celebrating the actual holiday on a day that is assigned similarly to the way they assign time zones in Australia.

Dart board.

Hmmm.

Holiday wingin'.

Muffy

blizzardboy · Post by **blizzardboy** » Sun May 23, 2010 6:06 am

Muffy wrote:No. Even alpha-delta sleep is respiratory-stable.

Thanks for that Muffy. So some other reason than AWI for my "chaotic" breathing then, right?

Muffy wrote:I thought your new sleep physician said to go to low-level CPAP and stop dial wingin'.

IIRC, he suggested that CPAP could be a viable option. Anyhow, I don't think I have much else to try as far as "dial wingin'" goes! Certainly no obvious quick CPAP fixes to date as far as I can see. Considering I have been on one form or another of CPAP since October last year (bar 4 weeks around my PSGs), simply splinting my airway open is obviously not the only fix that I require for my sleep architecture and sleep breathing issues. So, as I think you infer, maybe I should stick to fixed CPAP to help keep my airway open for now and accept that my unstable breathing and compromised sleep architecture are probably due to other causes.

Muffy wrote:Interpreting that literally, not yet. I didn't see a single obstructive apnea. It may more likely be that the underlying SDB identity (if present) is UARS.

No OSA, well there you go! UARS+(deep sleep alpha infection)+(healthy centrals) would be a considerably different diagnosis than CompSA. How on earth did I get diagnosed with CompSA?

Muffy wrote:And the deep sleep is not "disrupted", it's "infected".

So what then is the downside of the "infection" of delta wave sleep by alpha waves in terms of sleep architecture?

All the best for Memorial Day. Cheers,

blizzardboy · Post by **blizzardboy** » Sun May 23, 2010 4:17 pm

Interesting (for me at least ) to note in last night's data http://users.adam.com.au/sixsome/ASV/0510/052310/ (fixed CPAP@10) that the Adapt SV assigned no apneas and very few hypopnoeas during the most unstable period of my breathing (3a), but there some events reported each side of this period. Maybe this shows that the characteristic period of the chaotic events is well under 10 seconds? Was my RR really hitting 40 bpms or is this an artifact? Cheers,

jnk · Post by **jnk** » Sun May 23, 2010 5:57 pm

Interesting overview of pharmacological treatments for FM, and a mention of effect on NREM alpha-delta, under heading "Tricyclic antidepressants and Selective serotonin reuptake inhibitors," on page 4 of 10 (or, page 29) of this pdf, "Treatment Options for Fibromyalgia" in the 2008 The Pain Practitioner:

http://www.aapainmanage.org/currents/im ... pfibro.pdf

ps-Only 85 replies to number one!!!!!

Muffy · Post by **Muffy** » Sun May 23, 2010 6:29 pm

blizzardboy wrote:Was my RR really hitting 40 bpms or is this an artifact?

Well, "IMHO", the actual number is academic. The important part is identifying chaotic breathing when it occurs (not that using these trend numbers is necessarily the Gospel either).

Muffy

Muffy · Post by **Muffy** » Sun May 23, 2010 6:32 pm

jnk wrote:Only 85 replies to number one!!!!!

Wow! I can't believe it may actually make it!

Muffy

Muse-Inc · Post by **Muse-Inc** » Sun May 23, 2010 6:34 pm

Gotta hand it to y'all, this has been a most informative thread. Thanks for all the great info!

Muffy · Post by **Muffy** » Sun May 23, 2010 6:35 pm

Muffy wrote:
jnk wrote:Only 85 replies to number one!!!!!
Wow! I can't believe it may actually make it!

I mean, I didn't think we'd even make 600, let alone 700.

Muffy

Muffy · Post by **Muffy** » Sun May 23, 2010 6:41 pm

blizzardboy wrote:
Muffy wrote:And the deep sleep is not "disrupted", it's "infected".
So what then is the downside of the "infection" of delta wave sleep by alpha waves in terms of sleep architecture?

Nothing. You can't tell it's there, SWS just goes merrily chugging along (the sleep stage, not the person).

Muffy

SleepingUgly · Post by **SleepingUgly** » Sun May 23, 2010 6:47 pm

"alpha-delta NREM sleep disruptions" vs. alpha intrusions--what's the difference?

jnk · Post by **jnk** » Sun May 23, 2010 7:04 pm

SleepingUgly wrote:"alpha-delta NREM sleep disruptions" vs. alpha intrusions--what's the difference?

The persistence of alpha activity during sleep (the α-EEG anomaly or alpha-delta anomaly) and its superimposition on delta waves, was initially described in patients with psychiatric illness and subsequently in patients with fibromyalgia. Many subsequent reports have found a similar association of the α-EEG anomaly with fibromyalgia and with chronic "non-organic pain." The study of the α-EEG anomaly in the sleep of patients with chronic pain suggests that the anomaly represents an "intrusion" into normal sleep, i.e. that the anomaly acts as an indicator of a more vigilant state during sleep with resulting daytime symptoms of non-restorative sleep.

The α-EEG anomaly is not always associated with pain, and painful conditions are not always associated with the anomaly. Rains and Penzien, examining the sleep records of over 1000 patients referred to a sleep disorders clinic, reported that the α-EEG anomaly occurred at a similar rate in patients with chronic pain, other medical/sleep disorders, and in psychiatric patients and that 60% of patients with the anomaly did not report pain. The authors concluded that the α-EEG anomaly may reflect a non-specific response to a variety of noxious stimuli. Why some patients would show such a response to noxious stimuli when it is absent in others exposed to the same stimuli is unclear, but we postulate that psychological factors could play a role.--http://www.bpsmedicine.com/content/1/1/20

CompSA, Hypoventilation, PLMs, Bradycardia and Hypotension?

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