28 replies to this topic

[zoolander]

Man I gotta tell you that the last year has been an eye opener for me. An eye opener because I am so particular about my health and do what I can to keep myself in tip top shape but recently had a bomb shell dropped on me. I'll get back to this.

I've lost count of the amount of times that I've read threads about people suffering from brain fog. There seems to be a new person reaching out for answers every other day about they can deal with their brain fog and general lack energy. Well if you are one of these people then ask yourself:

• do you snore
• choking or gasping for breath when you are asleep
• do you have an elevated arterial blood pressure?
• daytime sleepiness
• Morning headaches
• Memory or learning problems
• increased heart rate
• Feeling irritable
• Not being able to concentrate on your work
• Mood swings or personality changes; perhaps feeling depressed
• Dry throat when you wake up
• Frequent urination at night
• decreased libido

The first 2 in bold you may not notice and you may only notice when a family member or your partner points it out to you. Well if you have any of the above signs and symptoms there could be a chance that you have sleep apnea.

From wikipedia.....
Sleep apnea, sleep apnoea or sleep apnœa is a sleep disorder characterized by pauses in breathing during sleep. These episodes, called apneas (literally, "without breath"), each last long enough so one or more breaths are missed, and occur repeatedly throughout sleep. .......

There are three distinct forms of sleep apnea: Central, Obstructive and Complex (complex is a combination of central and obstructive) with 0.4%, 84% and 15% making up their respective percentages of cases^[1]. Breathing is interrupted by the lack of effort in central sleep apnea; in obstructive sleep apnea, breathing is interrupted by a physical block to airflow despite effort. In mixed sleep apnea, there is a transition from central to obstructive features during the events themselves. .....

Regardless of type, the individual with sleep apnea is rarely aware of having difficulty breathing, even upon awakening. Sleep apnea is recognized as a problem by others witnessing the individual during episodes or is suspected because of its effects on the body (sequelae). Symptoms may be present for years, even decades without identification, during which time the sufferer may become conditioned to the daytime sleepiness and fatigue associated with significant levels of sleep disturbance.

The last paragraph pretty much describes me. I have been a tosser and turner for years but do not snore. I can fall asleep quite easily but rarely wake up feeling refreshed. I toss and turn so much that my partner often sleeps in another bed. I can't stop the tossing and turning because I don't know that I am doing it. It's pretty much out of my control.

Anyhow.....I'm at the writing up stage of my Ph.D and am finding it hard to read and concentrate. I thought I was just being lazy but that's not the case. In trying to resolve problems related to my lack of focus I went to see a Neurologist/sleep specialist to get a prescription for modafinil. I thought that the modafinil will help me 1. get my focus back and 2. deal with the shiftwork. Well to cut a long story short a sleep study was conducted. A sleep study, or other wise known as polysomnography (PSG), is a test that is often done in a sleep center or sleep laboratory, which may be part of a hospital. You may stay overnight in the sleep center, although sleep studies are sometimes done in the home. I took my test at home. The study/test records:

• Brain activity
• Eye movement
• Muscle activity
• Breathing and heart rate
• How much air moves in and out of your lungs while you are sleeping
• The percentage of oxygen in your blood

A PSG is painless. You will go to sleep as usual. The results of your PSG will be analyzed by a sleep medicine specialist to see if you have sleep apnea, how severe it is, and what treatment may be recommended.


Anyhow.....I had my sleep study and it was the worst nights sleep of my life. I had all these electrodes attached to my body from head to tow, I was wearing a heart rate monitor, a respiratory bely, had tubes stuck up my nose and something attached to my finger tip to measure oxygen stauration.


from wiki again......The standard definition of any apneic event includes a minimum 10 second interval between breaths, with either a neurological arousal (3-second or greater shift in EEG frequency, measured at C3, C4, O1, or O2), or a blood oxygen desaturation of 3-4 percent or greater, or both arousal and desaturation.
.....
An "event" can be either an apnea, characterised by complete cessation of airflow for at least 10 seconds, or a hypopnea in which airflow decreases by 50 percent for 10 seconds or decreases by 30 percent if there is an associated decrease in the oxygen saturation or an arousal from sleep (American Academy of Sleep Medicine Task Force, 1999). To grade the severity of sleep apnea the number of events per hour is reported as the apnea-hypopnea index (AHI). An AHI of less than 5 is considered normal. An AHI of 5-15 is mild; 15-30 is moderate and more than 30 events per hour characterizes severe sleep apnea.

My result blew me away. They blew me away so much that I refused to believe them. I explained that the results are most likely just an artifact resulting from my bad nights sleep but the sleep technicial explained that the test was a technically acceptable test. I'm still in denial to be honest. The results are pretty conclusive.

I have severe sleep apnea.

My results:
Onset of sleep
= 4.5 minutes. Average is 15 minutes. It's understandible that I would fall asleep quickly considering that I'm not sleeping well

Respiratory events:(RDI/AHI)
Cylclical in phase hypopnoeas were observed during Non-REM (NREM) and REM sleep, in particular in the supine REM (supine REM AHI: 44.5/hr). These events were occasionally in association with leg movements, oxygen desturation and arousal

ECG:
Dominant sinus rhythm with an average heart rate of 50 bpm. No arrhythmias were present

Conclusion:
Average Respiratory events per hour = 36.2
Average Arousals per hour = 26.9
Oxygen saturation = 89%
Severe Sleep Apnea present

These results came as quite a shock to me but obviously something I have to deal with. Could this be the case for a large majority of people starting threads about brain fog? I must have acclimatized myself to the fatigue and recognized this as my norm. I do have a penchant for stimulant type supplements and this makes sense to me now.

How many people out there have sleep apnea without knowing it? Stats shows that if sleep tested 1 in 5 Americans will come up with at least mild obstructive sleep apnea. Could this be causing the brain fog that you have? A new lease on life could be as simple as getting a sleep study done to asses whether you have sleep apnea. Sleep apnea that could be causing the brain fog that you experiance from day to day.

I'm being treated for sever sleep apnea with CPAP. I will be having another sleep study next week with the CPAP attached. If the CPAP can keep my airways open then I should experiance a dramatic increase in energy and clarity from here on. It's bad news that I have to wear a CPAP to bed every night but great news that I will be finally getting a normal nights sleep.

[drmz]

Man I gotta tell you that the last year has been an eye opener for me. An eye opener because I am so particular about my health and do what I can to keep myself in tip top shape but recently had a bomb shell dropped on me. I'll get back to this.

I've lost count of the amount of times that I've read threads about people suffering from brain fog. There seems to be a new person reaching out for answers every other day about they can deal with their brain fog and general lack energy. Well if you are one of these people then ask yourself:

• do you snore
• choking or gasping for breath when you are asleep
• do you have an elevated arterial blood pressure?
• daytime sleepiness
• Morning headaches
• Memory or learning problems
• increased heart rate
• Feeling irritable
• Not being able to concentrate on your work
• Mood swings or personality changes; perhaps feeling depressed
• Dry throat when you wake up
• Frequent urination at night
• decreased libido

The first 2 in bold you may not notice and you may only notice when a family member or your partner points it out to you. Well if you have any of the above signs and symptoms there could be a chance that you have sleep apnea.

From wikipedia.....
Sleep apnea, sleep apnoea or sleep apnœa is a sleep disorder characterized by pauses in breathing during sleep. These episodes, called apneas (literally, "without breath"), each last long enough so one or more breaths are missed, and occur repeatedly throughout sleep. .......

There are three distinct forms of sleep apnea: Central, Obstructive and Complex (complex is a combination of central and obstructive) with 0.4%, 84% and 15% making up their respective percentages of cases^[1]. Breathing is interrupted by the lack of effort in central sleep apnea; in obstructive sleep apnea, breathing is interrupted by a physical block to airflow despite effort. In mixed sleep apnea, there is a transition from central to obstructive features during the events themselves. .....

Regardless of type, the individual with sleep apnea is rarely aware of having difficulty breathing, even upon awakening. Sleep apnea is recognized as a problem by others witnessing the individual during episodes or is suspected because of its effects on the body (sequelae). Symptoms may be present for years, even decades without identification, during which time the sufferer may become conditioned to the daytime sleepiness and fatigue associated with significant levels of sleep disturbance.

The last paragraph pretty much describes me. I have been a tosser and turner for years but do not snore. I can fall asleep quite easily but rarely wake up feeling refreshed. I toss and turn so much that my partner often sleeps in another bed. I can't stop the tossing and turning because I don't know that I am doing it. It's pretty much out of my control.

Anyhow.....I'm at the writing up stage of my Ph.D and am finding it hard to read and concentrate. I thought I was just being lazy but that's not the case. In trying to resolve problems related to my lack of focus I went to see a Neurologist/sleep specialist to get a prescription for modafinil. I thought that the modafinil will help me 1. get my focus back and 2. deal with the shiftwork. Well to cut a long story short a sleep study was conducted. A sleep study, or other wise known as polysomnography (PSG), is a test that is often done in a sleep center or sleep laboratory, which may be part of a hospital. You may stay overnight in the sleep center, although sleep studies are sometimes done in the home. I took my test at home. The study/test records:

• Brain activity
• Eye movement
• Muscle activity
• Breathing and heart rate
• How much air moves in and out of your lungs while you are sleeping
• The percentage of oxygen in your blood

A PSG is painless. You will go to sleep as usual. The results of your PSG will be analyzed by a sleep medicine specialist to see if you have sleep apnea, how severe it is, and what treatment may be recommended.


Anyhow.....I had my sleep study and it was the worst nights sleep of my life. I had all these electrodes attached to my body from head to tow, I was wearing a heart rate monitor, a respiratory bely, had tubes stuck up my nose and something attached to my finger tip to measure oxygen stauration.


from wiki again......The standard definition of any apneic event includes a minimum 10 second interval between breaths, with either a neurological arousal (3-second or greater shift in EEG frequency, measured at C3, C4, O1, or O2), or a blood oxygen desaturation of 3-4 percent or greater, or both arousal and desaturation.
.....
An "event" can be either an apnea, characterised by complete cessation of airflow for at least 10 seconds, or a hypopnea in which airflow decreases by 50 percent for 10 seconds or decreases by 30 percent if there is an associated decrease in the oxygen saturation or an arousal from sleep (American Academy of Sleep Medicine Task Force, 1999). To grade the severity of sleep apnea the number of events per hour is reported as the apnea-hypopnea index (AHI). An AHI of less than 5 is considered normal. An AHI of 5-15 is mild; 15-30 is moderate and more than 30 events per hour characterizes severe sleep apnea.

My result blew me away. They blew me away so much that I refused to believe them. I explained that the results are most likely just an artifact resulting from my bad nights sleep but the sleep technicial explained that the test was a technically acceptable test. I'm still in denial to be honest. The results are pretty conclusive.

I have severe sleep apnea.

My results:
Onset of sleep
= 4.5 minutes. Average is 15 minutes. It's understandible that I would fall asleep quickly considering that I'm not sleeping well

Respiratory events:(RDI/AHI)
Cylclical in phase hypopnoeas were observed during Non-REM (NREM) and REM sleep, in particular in the supine REM (supine REM AHI: 44.5/hr). These events were occasionally in association with leg movements, oxygen desturation and arousal

ECG:
Dominant sinus rhythm with an average heart rate of 50 bpm. No arrhythmias were present

Conclusion:
Average Respiratory events per hour = 36.2
Average Arousals per hour = 26.9
Oxygen saturation = 89%
Severe Sleep Apnea present

These results came as quite a shock to me but obviously something I have to deal with. Could this be the case for a large majority of people starting threads about brain fog? I must have acclimatized myself to the fatigue and recognized this as my norm. I do have a penchant for stimulant type supplements and this makes sense to me now.

How many people out there have sleep apnea without knowing it? Stats shows that if sleep tested 1 in 5 Americans will come up with at least mild obstructive sleep apnea. Could this be causing the brain fog that you have? A new lease on life could be as simple as getting a sleep study done to asses whether you have sleep apnea. Sleep apnea that could be causing the brain fog that you experiance from day to day.

I'm being treated for sever sleep apnea with CPAP. I will be having another sleep study next week with the CPAP attached. If the CPAP can keep my airways open then I should experiance a dramatic increase in energy and clarity from here on. It's bad news that I have to wear a CPAP to bed every night but great news that I will be finally getting a normal nights sleep.

I'm going for such a PSG myself in x weeks to check if it can cause my dizzyness and even AV Block.Seems that AV blocks occur when having sleep apnea and that those blocks can continue during the day.
I can't imagine how i will sleep with all those things connect to me because i'm a belly sleeper.How can they make the sleep situation the same as @home, i assume i cannot sleep on my belly when being monitored ?
I don't think i'm a candidate for sleep apnea, but it's always good to check.I go to the toilet 2,3,4 times a night and i seem to keep my breath when sleeping.I do not wake up during sleep.I usually feel very bad till about 13:00 in the afternoon, then the fog disappears.2.5 years ago i tried alot of noops to counter this, but they made things worse (esp in pointing the finger to the cause)
I always know when i have a "bad" day when i wake up, i just feel it in my head.

so we'll see what comes out of the psg.Glad you found " your problem" and i hope the cpap thing wil lkeep the airways open.A good night of sleep is very important to perform the next day.I'll post my results when i had the psg.

Edited by drmz, 28 November 2007 - 02:32 PM.

[zoolander]

I can't imagine how i will sleep with all those things connect to me because i'm a belly sleeper.How can they make the sleep situation the same as @home, i assume i cannot sleep on my belly when being monitored ?

Well if it's a home study they will brief you on how to attached all the gear. I did it by myself and used a mirror to find the exact locations for the electrodes on the head, face and neck. It took my about an hour to attach everything. You have to securely tape everything down. In some areas you will have long chords that run down the leg to the foot. These have to be taped down every 5 cms or so. Same with the upper body cords. It's important that you tape everything secured so that you don't catch it with your hand and rip it off sometime during the sleep. My advice to you would be to get someone to help you. I'm going to make sure I have someone helping me when I attach all the cords next week. It should not be a problem if you sleep on your stomach. Just be sure to wear something light over the cords and belts.

I don't think i'm a candidate for sleep apnea

That's how I was. Didn't even consider but thought it would be good to see how I'm sleeping and then I found out.

go to the toilet 2,3,4 times a night

That's a sure sign. It's called Nocturia

and i seem to keep my breath when sleeping.I do not wake up during sleep.

Same here. Unfortunately most people are unaware of how many times they wake during the evening. I had an average of 26.9 arousals per hour but if you asked me in the morning I would categorically tell you that I fell asleep and then woke without any disturbances during the night.

I usually feel very bad till about 13:00 in the afternoon, then the fog disappears

Another sign. You shouldn't be feeling that way. I don't have any of the signs that you have and I have severe sleep apnea. You should rate yourself on the Epworth Sleepiness Scale.

I always know when i have a "bad" day when i wake up, i just feel it in my head.

Some days for me I just have to call off. I thought this was because I am so busy with shiftwork plus Uni but it's most likely related to the quality of sleep. I know these days because my brain fog is so bad that I literally can focus enough to get out of bed. Coincidentially my partner will always comment on how much I was tossing and turning on that particular night.

I look forward to seeing how your PSG goes DrMz

[Jacovis]

Thanks for the starting this thread zoo!

I had a sleep study as well recently at a sleep clinic as I don't trust myself following the instructions properly - correctly putting all the wires together in the correct spots, etc.

Anyway my symptoms are similar to those of ADD inattentive type (have had them all my life).

My doctor's report said:
"Long latency to sleep and mild sleep-disordered breathing seen. Mild hypopneas seen causing an increase in EEG arousals and mild oxygen desaturdations to 89% at times. Only moderate snoring heard. No periodic leg movements.

These findings are not severe but could cause daytime symptoms (upper airways resistance syndrome). Should discuss further management with [personal GP] or one of us. Mandibular advancement splint could be considered."

My results were:
Total RDI = 13.6
SaO2 awake average = 95%
Average SaO2 desaturation = 3%
Mean Apnea/Hypopnea duration = 36.9 sec
Longest apnea = 21.6 sec
Longest Hypopnea = 67.5 sec

It looks like my average SaO2 was 96% though.

I am interested in anyone's opinions of these results. From my reading, upper airways resistance syndrom (UARS), is not well understood and I could have it. While it isn't as 'severe' as Sleep Apnea to the doctor's eye, the daytime symptoms (like sleepiness) may well be the same for the patient. So even if someone doesn't have full blown sleep apnea, UARS may well be contributing to their daytime sleepiness.

Here are three articles from 2007 which include information on UARS...

1: Sleep. 2007 May 1;30(5):641-7.Links
Comment in:
Sleep. 2007 May 1;30(5):553-5.
The cyclic alternating pattern demonstrates increased sleep instability and correlates with fatigue and sleepiness in adults with upper airway resistance syndrome.Guilleminault C, Lopes MC, Hagen CC, da Rosa A.
Stanford University Sleep Medicine Program, Stanford, CA 94305, USA. cguil@stanford.edu

OBJECTIVE: To clarify the relationship between sleep instability and subjective complaints in patients with upper airway resistance syndrome (UARS). METHODS: Thirty subjects (15 women) with UARS and 30 age- and sex-matched controls in a prospective, single-blind, case-control study. Blinded cyclic alternating pattern (CAP) electroencephalogram analysis and scales of fatigue and sleepiness were completed. ANALYSIS: Mann-Whitney U tests for independent, nonparametric variables between groups and chi2 tests for nonparametric variables with defined standard values. RESULTS: Patients with UARS had significantly more complaints of fatigue and sleepiness, compared with controls, demonstrated on their Fatigue Severity Scale (P < 0.001) and Epworth Sleepiness Scale (P < 0.001). By design, the mean apnea-hypopnea index was normal in both groups, whereas the respiratory disturbance index was greater in patients with UARS than in those without (14.5 +/- 3.0 vs 9 +/- 5.2, respectively [P < 0.001]). CAP analysis demonstrated abnormal non-rapid eye movement sleep with abnormally increased CAP rate, electroencephalogram arousals, A2 index, and A3 index. Decreased A1 index in controls was consistent with their more normal progression of sleep. CAP rate correlated with both the Epworth Sleepiness Scale (r = 0.38, P < 0.01) and the Fatigue Severity Scale (r = 0.51, P < 0.0001), and there was a positive trend between the Fatigue Severity Scale and phase A2 index (r = 0.29, P < 0.05). CONCLUSION: Compared with age- and sex-matched controls, patients with UARS have higher electroencephalogram arousal indexes and important non-rapid eye movement sleep disturbances that correlate with subjective symptoms of sleepiness and fatigue. These disturbances are identifiable with sensitive measures such as CAP analysis but not with traditional diagnostic scoring systems.

PMID: 17552380 [PubMed - indexed for MEDLINE]


1: Sleep Med. 2007 Jul 16; [Epub ahead of print] Links
Differences in clinical features of upper airway resistance syndrome, primary snoring, and obstructive sleep apnea/hypopnea syndrome.Stoohs RA, Knaack L, Blum HC, Janicki J, Hohenhorst W.
Somnolab – Dortmund Sleep Disorders Center, Hörder Burgstr. 18, 44263 Dortmund, Germany; Somnolab – Essen Sleep Disorders Center, Essen, Germany.

BACKGROUND: The clinical features of patients with upper airway resistance syndrome (UARS) have previously been compared to patients with obstructive sleep apnea/hypopnea syndrome (OSAHS). No data regarding differences between patients with primarysnoring (PS) or patients with obstructive sleep apnea/hypopnea without daytime sleepiness (OSAH) are available. We conducted a study to investigate clinical features of UARS, comparing them to those in patients with PS, OSAH, and OSAHS. METHODS: Retrospective chart analysis of 157 patients with PS, 424 patients with UARS, 562 patients with OSAH, and 1610 patients with OSAHS seen in two sleep disorders clinics between 1996 and 2006. All patients had a diagnostic polysomnography (PSG) and a comprehensive clinical history taken by board-certified sleep specialists. RESULTS: PS and UARS patients were significantly younger, less overweight and had lower weight gain during the past 5years. The female-to-male ratio was highest in the UARS group. UARS patients had significantly less stage non-rapid eye movement sleep (NREM) 1 and NREM 2 and significantly more NREM 3 and NREM 4 sleep than OSAH and OSAHS patients. Arousal indices between PS/UARS and OSAH/OSAHS patients were significantly lower, with no significant difference within these diagnostic categories. Patients with UARS presented the highest degree of subjective impairment. CONCLUSIONS: UARS patients share some clinical features of patients with OSAHS and PS, although these two groups differ in their presentation of clinical sleepiness. Patients with UARS were most impaired in terms of their daily functioning and perception of sleep quality. This finding could not be corroborated by objective measures.

PMID: 17644425 [PubMed - as supplied by publisher]


1: Sleep Med. 2007 Nov 15; [Epub ahead of print] Links
Hypersomnolence, insomnia and the pathophysiology of upper airway resistance syndrome.Gold AR, Gold MS, Harris KW, Espeleta VJ, Amin MM, Broderick JE.
Division of Pulmonary/Critical Care Medicine, Stony Brook University School of Medicine, Stony Brook, DVA Medical Center, Northport, NY 11768, USA.

OBJECTIVE: In order to test the hypothesis that upper airway resistance syndrome (UARS) is merely an extension of the pathophysiology of obstructive sleep apnea/hypopnea (OSA/H) to less severe pharyngeal collapse during sleep, we compared the severity of hypersomnolence and the prevalence of insomnia in UARS patients to the patterns observed for OSA/H patients. Our goal was to determine whether the severity of hypersomnolence and the prevalence of insomnia observed in UARS patients could have been predicted from the patterns observed among OSA/H patients. METHODS: We performed a retrospective study of a large consecutive patient series evaluated at an academic sleep disorders center, including 220 OSA/H patients and 137 UARS patients. Patients had no other sleep-related diagnosis and underwent an initial evaluation that included a measure of hypersomnolence [a multiple sleep latency test (MSLT); 95%] or insomnia questionnaire (87%). Patients were characterized by anthropometric data, polysomnographic descriptive measures of sleep, MSLT data and insomnia questionnaire data. RESULTS: Severity of hypersomnolence decreased over the continuum from severe to mild OSA/H. A model fit to the OSA/H patients to predict severity of hypersomnolence significantly underestimated hypersomnolence in UARS patients, which was comparable in severity to that of patients with mild OSA/H. The frequency of sleep-onset insomnia increased over the continuum from severe to mild OSA/H and increased further in UARS. CONCLUSIONS: UARS is, in some respects, an extension of OSA/H to less severe pharyngeal collapse, but this does not adequately account for the symptom profile of patients with UARS. A physical model is proposed to account for the excess somnolence in UARS relative to expectations and the increasing frequency of sleep-onset insomnia along the continuum from severe OSA/H to UARS.

PMID: 18024168 [PubMed - as supplied by publisher]

[david ellis]

Zoolander,

Is there a profile for sleep apnea sufferers? I too was astonished by your diagnosis. I thought you were too young, too healthy, got plenty of exercise to fit the profile I had.

[sentinel]

Zoo

Really sorry to hear you've got this to deal with but well done for facing up to it and allowing others to benefit from your experience. I have just forwarded the list to a colleague who exhibits at least half of those symptoms and will encourage her to get it checked out properly.

Looking on the bright(er) side, now that you have identified and are treating your condition, and given your great current level of health and achievement, just think of what you'll be capable of as you gain control over your apnea!

Best of luck :thumb:

sentinel

[nushu]

Zoo, how is the quality of your sleep now? I think I'm going to have a study done, but I would not have considered it before reading this post. My wife has told me many times that I snore- I've never thought much of it since I exercise and I'm not obese/no smoking etc. But almost every morning when it's time to wake up I feel like someone has been kicking my ass the entire night, despite sleeping 8-9 hrs! I often don't feel normal till the afternoon. Something's just not adding up here.

[zoolander]

I am currently doing a trail with CPAP. Wearing the mask does not bother me that much at all however I'm finding it very hard to fall asleep with the mask on. At the moment my sleep quality is worse than it's ever been. I will have to wait to see if I can get used to the mask

[rhodan]

Sorry to read about your apnea problems.

I recall having read about some positive results from diggeridoo practising : didgeridoo study

As you live in Australia, you should not have difficulties finding some courses. Maybe worth trying.

[zoolander]

Yes I have also heard some pretty good stuff about cyclic breathing. I'll have a look into it a bit more

[jaydfox]

Hmm, I never really considered this. I know I snore, because I've been told. I've only in the last couple months become aware that when I'm really tired and trying to fall asleep, I stop breathing, which wakes me up. I'm probably not a reliable witness, but on several occassions I had the distinct impression that I simply stopped trying to breathe (the central type). I would actually be aware that I just stopped trying, and it usually felt like I was just tired and took a little "break" because I was so tired, only to be woken up when I gasped for air all of the sudden.

But there could be blockage as well, and given the percentages listed in the first post, that'd likely make it of of the complex variety. My sleeping in the last two months, and especially the last month, has been very broken by travelling and working long hours. That could be making an existing condition worse. I suppose I ought to get checked out.

[liorrh]

what about looking at your histmaine levels and otehr factors causing respetory sensetivity?

PS I found that tianeptine really helps with sleep apnea, YMMV.

[zoolander]

Jay, please do get it checked out. There are other alternatives to the full PSG. You can rent a pulse oximeter and look at oxygen saturation. As far as I know all apnea types will show some degree of oxygen desaturation when oxygen intake is inhibited.

I know one thing for sure. The CPAP, even though I have only used it for a short period (make 4 hours of sleep) has made a substantial difference to many aspects of my life.

[graatch]

Update? How are you doing, zoolander?

[luv2increase]

I need at least 10 hours to feel rested. I do not snore, but I wake up twice in the night at least to piss. I also notice that when trying to fall asleep, or even deeply relaxing, I inadvertently stop breathing. I will catch myself, then start again. I also experience bouts of sleep paralysis which are sh*tty as all get out! I wonder if that is somehow related to sleep apnea?

Edited by luv2increase, 17 December 2007 - 05:18 PM.

[zoolander]

Update? How are you doing, zoolander?

Umm....not good actually. The CPAP is pretty hard to tolerate. The CPAP was given for obstructive sleep apnea (OSA) but now it appears that at higher pressures on the CPAP we see the emergence of central apneas. Central apneas are neurological whereas the obstructive are physiological.

I think I know why I'm getting the central apneas. At higher pressures on the CPAP I start to hyperventilate. This blows off CO2. MOre CO2 than usual and in doing so my blood CO2 levels go below my CO2 set point. Those of you who know a little about physiology will know that it isn't O2 that regulates breathing. It's CO2 that drives breathing. When CO2 are high in the blood you hyperventilate or should I say, your respiratory frequency increases to blow off the excess. This is what occurs during exercise. The cells produce more CO2 and the respiration rate increase.

Well.....I know that my respiratory rate increae at higher pressures because I have seen it on the graph. Additionally I woke a few times in the first few days and noticed that my breathing was being controlled somehow by the CPAP.

So I'm not sleep well at all. NOthing that I am not use to already but it's getting me down a little because I thought the CPAP was going to help alleviate a few of the issues. Oh well.

I need to find a pressure on the CPAP that keeps my airways open without causing central apneas.

[wayside]

Have you looked into getting a mandibular advancement device (MAD)?

Apparently MADs work for many people, and they seem much less intrusive than the face mask.

[shuffleup]

Update? How are you doing, zoolander?

Umm....not good actually. The CPAP is pretty hard to tolerate. The CPAP was given for obstructive sleep apnea (OSA) but now it appears that at higher pressures on the CPAP we see the emergence of central apneas. Central apneas are neurological whereas the obstructive are physiological.

I think I know why I'm getting the central apneas. At higher pressures on the CPAP I start to hyperventilate. This blows off CO2. MOre CO2 than usual and in doing so my blood CO2 levels go below my CO2 set point. Those of you who know a little about physiology will know that it isn't O2 that regulates breathing. It's CO2 that drives breathing. When CO2 are high in the blood you hyperventilate or should I say, your respiratory frequency increases to blow off the excess. This is what occurs during exercise. The cells produce more CO2 and the respiration rate increase.

Well.....I know that my respiratory rate increae at higher pressures because I have seen it on the graph. Additionally I woke a few times in the first few days and noticed that my breathing was being controlled somehow by the CPAP.

So I'm not sleep well at all. NOthing that I am not use to already but it's getting me down a little because I thought the CPAP was going to help alleviate a few of the issues. Oh well.

I need to find a pressure on the CPAP that keeps my airways open without causing central apneas.

I'm kind of surprised you are changing the pressure on the machine versus having a pressure prescribed which is set in the CPAP. I have sleep apnea and I've been using the CPAP for about 6 months - I notice much better moods, less anxiety, more rested. My pressure was prescribed to 6 which is relatively low. I have no problems with central apneas but it's enough pressure to make a difference.

[zoolander]

My prescribed pressure is/was set at 10-11cm H2O by my sleep physician. This is the pressure that keeps my airways open without stimulating a central apnea. I spoke with my sleep physician and he explained that all of the central apneas appear post event. He think that they may just be a response to a respiratory event. Sort of like a gasp.

My problem is finding the rigfht mask that I can stick with. I swapped over from a full face mask to a nasal mask and started to mouth breath. This resulting in an extremely dry and sore throatr the next day. It's a shame because the nasal mask was very comfortable. I'm back on the full face mask again but this time it's a slightly different mask. I used it for the first time last night and for the first time since my trial I didn't rip it off after the first hour. It stayed on for about 6 hours I think and today I'm very awake and feel great.

[shuffleup]

My prescribed pressure is/was set at 10-11cm H2O by my sleep physician. This is the pressure that keeps my airways open without stimulating a central apnea. I spoke with my sleep physician and he explained that all of the central apneas appear post event. He think that they may just be a response to a respiratory event. Sort of like a gasp.

My problem is finding the rigfht mask that I can stick with. I swapped over from a full face mask to a nasal mask and started to mouth breath. This resulting in an extremely dry and sore throatr the next day. It's a shame because the nasal mask was very comfortable. I'm back on the full face mask again but this time it's a slightly different mask. I used it for the first time last night and for the first time since my trial I didn't rip it off after the first hour. It stayed on for about 6 hours I think and today I'm very awake and feel great.

Cool - hope you're finding something that will work. I use the nasal mask myself and it works fine. I did some mouth breathing myself but found that if I use a breath-rite strip in addition to the nasal mask my mouth stays shut. Works wonders as i have a deviated septum and basically get like 25% of the air in my right nostril as I do through the left. Breath rite strips level the playing field.

[zoolander]

Here are my results for my initial and then post (with CPAP) sleep tests


Age: 36
Height: 181cm
Weight: 78kg
Body Fat %: 10
Blood pressure: 105/60
Resting Heart Rate: 45-50 bpm.

Here are the result of my first study (before CPAP trial) Date: 15/03/2007
Sleep Latency: 4.5 minutes
Sleep Efficiency: 81.9%
Total Arousal Index: 26.9/hr
Respiratory events: SaO2 baseline: Awake=96-98% Asleep = 95-98%
Cyclical in phase hypopnoeas were observed during NREM and REM sleep, in particular in supine REM (Supine REM RDI: 44.5/hr). These events were observed occasionally in association with leg movements, oxygen desaturation and arousal

Average oxygen desaturation: NREM 2%, REM 2%
Oxygen desaturation range: NREM 0-4 %, REM 0-4 %
SaO2 Nadir: NREM 89%, REM 94%
RDI: Total 36.2/hr NREM 35.6/hr, REM 37.6/hr

Periodic Leg Movement: Occasionally associated with arousal and respiratory events
Snoring: mild
ECG: dominant rhythm is sinus with and average of 50bpm. No arrhythmias were present
Conclusion: Severe Sleep Apnea


Here are the result of my first study (before CPAP trial) Date: 05/12/2007
Sleep Latency: 8.5 minutes
Sleep Efficiency: 84.2%
Total Arousal Index: 24.6/hr
CPAP Treatment: SaO2 baseline: Awake=98% Asleep = 94%
CPAP titrated between 4-15cmH2O. Despite CPAP pressure central apneas persisted throughout the study. These were associated with arousal and oxyheamoglobin desaturation. It would appear pressures greater than 10cmH2O are required to control obstructive components, however anything over 12-13cmH2O elicits a significant degree of continuous central events. Response does not seem to be positional or stage dependant. May require review at CPAP clinic to assess for mask/mouth leakage

Average oxygen desaturation: NREM 4%, REM 3%
Oxygen desaturation range: NREM 2-9 %, REM 2-7 %
SaO2 Nadir: NREM 85%, REM 92%
RDI: Total 44.0/hr NREM 43.7/hr, REM 46.3/hr

Periodic Leg Movement: Nil
Snoring: Nil
ECG: dominant rhythm is sinus with and average of 53bpm. No arrhythmias were present
Conclusion: CPAP at 10-11cmH2O appears satisfactory for the control of snoring and obstructive respiratory events. Oxygen saturations are improved on CPAP. Higher pressures are associated with arousals and central events (some post arousal)

[liorrh]

wait a sec youre taking ahsitload of long HL stims like modafinil, cocoa etc and surprised about your sleep quality?

anyway I had nose surgery to correct my septum. apparently I had like 10% going through in one nostril and 70=80 on teh other. nto really great. the surgery went fine. we will see how my breathing during sleep will be.

[liorrh]

to add to the point about histmaine, allergy, nasal conegestion and noradrenergic transmition:
from:
Nasal congestion: A review of its etiology, evaluation, and treatment.
Author: Ng, Bernard A.
Publication: Ear, Nose and Throat Journal
Article Type: Brief Article
Geographic Code: 1USA
Date: Sep 1, 2000

Nasal obstruction and sleep disturbance

The part that nasal obstruction plays in sleep disturbance is controversial. Some authors believe nasal obstruction can cause frank obstructive sleep apnea syndrome, while others minimize its role.

In the normal awake state, nasal airway resistance markedly exceeds that of oral airway resistance. During sleep, the relaxation of the oral and pharyngeal musculature leads to a reversal of the resistance patterns of the nose and oral cavity, and oral airway resistance increases. Breathing through an inefficient oral cavity requires increased effort, which leads to greater negative pressures in the pharynx and a higher risk of collapse. The resistance in the nasal cavity, which has a more rigid frame, is more constant during both the awake and asleep states. The pharynx still connects the nose to the trachea, but the lower resistance to airflow makes a collapse of the pharynx less likely. The nose appears to be the more efficient route of breathing during sleep. [16]

Although the effects of sleep on the nose are less than its effects on the oral cavity, changes in nasal patency do occur. Nasal resistance is known to increase during recumbency, as mucosal congestion takes place. [17] An underlying limitation of nasal airflow, which can be subclinical during the daytime while the patient is upright, can manifest at night shortly after the patient becomes recumbent. Any process that produces nasal congestion while the patient is awake will have an additive effect on nasal airflow during sleep.

Studies have demonstrated a significant correlation between nasal resistance and snoring. [16, 18] Patients who snore habitually are more likely to complain of nighttime nasal congestion, nasal discharge, and congestion caused by allergic rhinitis.

Upper airway resistance syndrome (UARS) is characterized by an increase in the amount of work that is required to breathe during sleep in order to overcome the elevated airway resistance. UARS causes numerous microarousals that fragment sleep and diminish its quality. Sleep fragmentation has been shown to lower patients' subjective assessments of wakefulness, mood, and attention. [19] Patients with UARS often complain of daytime somnolence, which can be assessed objectively with instruments such as the multiple sleep latency test.

It appears that the nose might play a significant role in the development of UARS. The nasal obstruction associated with allergic rhinitis has been found to fragment sleep and significantly increase the incidence of microarousals. [20] The effects of allergic rhinitis can be alleviated with medical therapy to reduce allergic inflammation. Intranasal topical corticosteroids significantly reduce nasal congestion in patients with allergic rhinitis, which improves the quality of their sleep and alleviates daytime sleepiness . [21]

Patients with UARS do not have frequent enough apneic episodes to meet the criteria for obstructive sleep apnea syndrome (OSAS). Some authors believe that UARS might be a precursor to OSAS and suggest that a continuum exists between normal nocturnal breathing, occasional snoring, habitual snoring, UARS, and OSAS. For example, patients might progress from one point to another on the continuum as their weight fluctuates. Similarly, nasal obstruction might move a patient up or down the continuum.

A direct linear correlation between nasal resistance and the respiratory disturbance index (RDI) has not been observed, although the two indices do seem to have an association. [16,18] Complete obstruction from nasal packing has long been suspected of causing apneic episodes. Studies that provide evidence both for and against packing as a cause of OSAS have been published. [22-25] It might be that patients who undergo nasal packing in addition to having other risk factors make up the primary population of those who experience apneic episodes. [26]

Patients who are allergic to ragweed have longer and more frequent episodes of obstructive apnea during their acute season than they do during their off season, which might be attributable to increased nasal resistance. [27] Fixed anatomic obstructions, such as a deviated nasal septum, might contribute to OSAS. Surgical repair can improve the RDI. [28] Nasal obstruction can be at least partly responsible for the development of OSAS.

I saw you also have low BP and take alot of flavones. it all makes sense to me that nightly nasal congestion caused by vasodilitation and low adrenergic tone. (prob from all that stim abuse , constant daily SNS tone)

I'm stuck at teh same boat. my BP is extremley low. I have sleep apnea basically from waking up with stuffed nose. although my deviated shitty septum didnt help taht. we will see how I will correct that after the surgery. I think this is no OSAS but UARS as describd before. unfortunately it is jsut as nasty.

[emery54]

Hi there,

I'm a 28 year old female that has recently suffered from what I believe to be brain fog. Does anyone else have this? and if so do you know what causes it?
The only time i've ever gotten it is when i've went out and drank and smoked all night long. I will wake up and of course with a hangover and then by the next day it will start....and the worse part is....it lasts for 14 days...always 2 weeks. I know its one of those two things or both that cause it or perhaps it just compounds another issue that is wrong with me.

Any information would be greatly appreciated.

thank you!

[Jacovis]

Another option if CPAP is not working well is the Pillar Implant Procedure. Search Pubmed for studies on this procedure - it is quite effective, free of side effects, and seems to have decent relatively long term outcomes. It is only recommended for MILD Sleep Apnea though and Snoring. I read though on a sleep apnea forum that some with a strong version of the condition were able to be virtually 'cured' by combining the Pillar Implant Procedure with a Mandibular Advancement Device. It might be worth a try combining these two treatments for a milder version of the condition if you have strong apnea and don't want to use a CPAP your entire life.

[Wens]

You're not the only one with this problem. I have sleep apnea but not severe one. I was pretty afraid of going to sleep at the beginning and almost got into anxiety but no it's ok. I asked my doctor if I should use oxygen mask at night and he told me it's not my case and that I just have a very light apnea.

[abolitionist]

I work at a sleep lab (I'm working right now) and we get all ages. There is an idea that it's all fat overweight Americans who have sleep apnea - and while this is true to some extent : we get all ages, sizes, and body styles.

sometimes it's just the way your airway is formed genetically

[Jacovis]

http://www.scienceda...80611071037.htm

Memory Loss Linked To Common Sleep Disorder
ScienceDaily (June 13, 2008) — For the first time, UCLA researchers have discovered that people with sleep apnea show tissue loss in brain regions that help store memory. Reported in the June 27 edition of the journal Neuroscience Letters, the findings emphasize the importance of early detection of the disorder, which afflicts an estimated 20 million Americans.

Sleep apnea occurs when a blocked airway repeatedly halts the sleeper's breathing, resulting in loud bursts of snoring and chronic daytime fatigue. Memory loss and difficulty focusing are also common complaints. Prior studies have linked the disorder to a higher risk of stroke, heart disease and diabetes.

"Our findings demonstrate that impaired breathing during sleep can lead to a serious brain injury that disrupts memory and thinking," said principal investigator Ronald Harper, a distinguished professor of neurobiology at the David Geffen School of Medicine at UCLA.

The study focused on structures called mammillary bodies, so named because they resemble small breasts, on the underside of the brain.

The UCLA team scanned the brains of 43 sleep apnea patients, using magnetic resonance imaging (MRI) to collect high-resolution images of the entire brain, including slices of the mammillary bodies.

The structures' small size and proximity to bone and fluid make them difficult to measure by conventional MRI. So the researchers manually traced the mammillary bodies from the high-resolution scans and calculated their volumes from the hand-drawn outlines.

When they compared the results to images of 66 control subjects matched for age and gender, the scientists discovered that the sleep apnea patients' mammillary bodies were nearly 20 percent smaller, particularly on the left side.

"The findings are important because patients suffering memory loss from other syndromes, such as alcoholism or Alzheimer disease, also show shrunken mammillary bodies," said lead author Rajesh Kumar, a UCLA assistant researcher in neurobiology.

"Physicians treat memory loss in alcoholic patients with massive amounts of thiamine, or vitamin B1," he added. "We suspect that the dose helps dying cells to recover, enabling the brain to use them again."

The scientists' next step is to determine how sleep apnea causes tissue loss in the mammillary bodies.

Harper hypothesizes that repeated drops in oxygen lead to the brain injury. During an apnea episode, the brain's blood vessels constrict, starving its tissue of oxygen and causing cellular death. The process also incites inflammation, which further damages the tissue.

"The reduced size of the mammillary bodies suggests that they've suffered a harmful event resulting in sizable cell loss," Harper said. "The fact that patients' memory problems continue despite treatment for their sleep disorder implies a long-lasting brain injury."

In a future study, Harper and Kumar will explore whether taking supplemental vitamin B1 helps restore sleep apnea patients' memory. The vitamin helps move glucose into the cells, preventing their death from oxygen starvation.

"UCLA researchers used sophisticated imaging technology to identify brain lesions associated with impaired memory in individuals with obstructive sleep apnea," said Elizabeth G. Nabel, director of the National Heart, Lung and Blood Institute, which funded the study. "These results underscore the importance of early diagnosis and treatment of sleep-disordered breathing, which can have long-term effects on patients' health and well-being."

Obstructive sleep apnea occurs when the muscles in the throat, soft palate and tongue relax during sleep and sag, narrowing the airway. The tongue slides to the back of the mouth, blocking the windpipe and cutting off oxygen to the lungs.

The sleeper wakes up, gasping for air, and falls back into a fitful sleep. The cycle can repeat itself hundreds of times per night.

Study co-authors included Bramley Birrer, Paul Macey, Mary Woo and Frisca Yan-Go of UCLA, and Rakesh Gupta from the Sanjay Gandhi Institute of Medical Sciences, India.


--------------------------------------------------------------------------------

Adapted from materials provided by University of California - Los Angeles, via EurekAlert!, a service of AAAS.

[jCole]

I used to have Sleep apnea... I would wake up in the middle of the night choking and grasping for air at least once a week. It would scare the shit of out me every time.

I just sleep on my side now, never on my back, which greatly helped. Then got in shape and lost about 70 lb's, that pretty much did it for me. Snoring/breathing heavy also stopped too.

I do still wake up at least once or twice a night to use my inhaler tho, but that's been chronic my whole life, I'm used to that.


But seedless to say now, I leap out of bed every morning....

Edited by jCole, 05 August 2008 - 01:02 PM.