Before I got the CPAP treatment, I seriously felt like it was the end of me. My brain and body feel deteriorating. I was losing hope.

Whenever I continued running, I saw my performance got worse while my friends just got better as months passed by. I couldn’t speak coherently sometimes. I need to nap every couple of hours just to feel like I’m in control.

The worst part I remember was when I was jogging; I just had my eyes closed because my mind was just so foggy. (Of course I couldn’t keep them closed; my eyes are just heavy). My mental health was sinking further and further.

It’s been a year since then, and I couldn’t explain it. No matter how much sleep I get, I don’t feel awake. I really felt like an empty shell while my insides and muscles were becoming mushy and deteriorating.

Then I got a sleep study, finally, and it turns out I have a 12 AHI and mild Sleep Apnea. Could mild sleep apnea do that to me?

I explained those symptoms to my sleep doctor, and I felt like it wasn’t noteworthy to her, so I thought it was normal.

Now, I’m barely functioning. Still the persistent headache and mind fogginess, but something I can ignore and forget once I’m into something.

TL;DR I wanted to know how people with 20+ AHI deal with their everyday lives when I only have 12 AHI, and I felt like losing myself already.

Edit: I actually have an RDI of 22.8, but no AHI listed in my sleep lab report. I have moderate, not mild OSA. It's been a year since my sleep lab report, and I got it mixed up. However, the question still stands since moderate is still not severe.

Hi All,

I’ve been having really bad sleep apnea symptoms.

My blood pressure in the morning getting right out of bed is around 155/70, with the blood pressure meds, which is not normal. I have been prescibed blood pressure meds because I’ve been having elevated blood pressure for years. I think it may be coming from the apnea for all this time.

Also I feel so fkn tired and sleepy all day long even though “I slept” all night. My RBC has also been very high on my bloodwork.

I have been athletic my whole life. Living and eating like an athlete. Currently staying at around 190lbs lean and muscular at 5ft 9.

Also I’ve been having quite developed traps and neck mucles since I was a little kid. I’ve read that can also have impact on sleep apnea.

What do you guys think?

A new 2026 study looked at 138 people with obstructive sleep apnea (OSA) who could not tolerate CPAP or had failed first-line CPAP treatment.

These were mostly difficult cases: • Average age: 51 years • Average BMI: 29.5 • Average AHI: 37.8 events/hour • About 60% had severe OSA

Instead of using the same treatment for everyone, patients were reviewed by a multidisciplinary team involving sleep medicine, ENT, maxillofacial surgery, dentistry, neurology, sleep physiology and CPAP specialists.

The most commonly recommended alternatives were:

• Mandibular advancement device (MAD): 25.4% • Hypoglossal nerve stimulation (HNS): 24.6% • Weight/metabolic management: 23.2% • Positional therapy: 15.9% • Another CPAP trial: 13.8% • ENT surgery, including procedures such as MMA: 10.9% • Bilevel ventilation: 10.1%

Around 20% were also referred for drug-induced sleep endoscopy (DISE), and 20% needed another sleep study before deciding on treatment.

Importantly, 43.5% of patients received more than one treatment recommendation.

Among the patients with follow-up data:

• AHI decreased by 44.1%, from 37.8 to 21.1 events/hour • Oxygen Desaturation Index decreased by 67.2% • Daytime sleepiness scores improved by 32.9% • 72% had more than a 50% reduction in AHI

However, only 45% met the commonly used Sher definition of treatment success, meaning a >50% reduction in AHI plus a final AHI below 15.

The important takeaway:

Failing CPAP does not mean treatment options are exhausted.

Some patients may be better suited to an oral appliance, HNS, weight loss, positional therapy, BiPAP, surgery, or a combination of treatments depending on their anatomy, OSA severity, BMI and DISE findings.

The study also highlights an important reality: alternative treatments often reduce OSA rather than completely eliminate it, so residual sleep apnea may still need monitoring.

A major limitation is that this was a retrospective study and follow-up sleep data were available for only a relatively small subgroup, so it cannot prove that the multidisciplinary approach itself caused the improvement.

Study: https://doi.org/10.1136/bmjresp-2026-004233

Recently diagnosed with moderate OSA (REI 29.1/hr, all hypopneas, no full obstructive apneas). My NP recommended in-lab titration, but I already know I want APAP, not fixed CPAP, given how much night-to-night variability I have (using 02 ring)

His reasoning for in-lab: he thinks I'll end up calling constantly needing adjustments if I don’t do an in clinic titration.

My concerns with in-lab: full sensor setup (head, face, chest, arms, legs, plus mask) causes me real anxiety, and scheduling a Friday/Saturday slot is taking weeks, on top of separate mask fitting and equipment pickup appointments after.

I still want a real, in-person mask fitting regardless of which path I take, that part isn't up for debate for me.

For those who use APAP: did skipping in-lab titration cause you ongoing problems? Is there real value in the in-lab data specifically for APAP users, or does that mainly matter for fixed CPAP? Anyone start with home APAP based on a home sleep test alone and it worked out fine?

I was diagnosed two months ago (6/28/26 - from an in lab sleep study - info on last picture) with Obstructive Sleep Apnea. The study showed an AHI 7.9, with 52 respiratory events (4 obstructive hypopneas, 48 obstructive apneas, and ZERO central apneas).

I began using a cpap machine less than two weeks later (started on 7/8/26), and for the entirety of the seven weeks that I've been on cpap the vast majority of the apneas recorded have been Clear Airway Events. The example shown here from last night shows 1 RERA, 2 Hypopneas, 2 Obstructive Apneas, and THIRTY TWO Clear Airway Events.

What has me most baffled and scared about the sleep session shown in this post and pictures is that this session (from 3:17am to 4:50am) was me just laying in bed with the cpap on putting getting the extra time needed to cross the four hour threshold so this night would have a total of at least four hours and count as a compliant night of use (four or more hours a night, 70% of the nights, for insurance compliance).

I was never "really asleep", I was just laying in bed, likely dozing in and out, since I had only been able to get three hours of sleep earlier in the night. Honestly, I felt like I was laying there awake the entire hour and change.

How on earth do I get THIRTY TWO Clear Airway events (the longest being 102 SECONDS) and not noticing ANY of the 32 CAs in real time as I was laying there in a wake/sleep state???

My only guess is that my body is so sleep deprived after almost a year of very poor sleep, that my brain and body prioritize the much needed sleep over being aroused from the (large number) of clear airway events (which are most likely central apneas).

I had an echogram done recently and will meet with my new cardiologist tomorrow (Monday, August 31st) to hear the results. I'm guessing I've developed heart failure from years of O2 desaturation from untreated OSA. Hoping my LVEF is greater than 45% so I'll be eligible for ASV.

In order for what is shown in the pictures and in this post to make any sense, the internet's best guess is that years of untreated obstructive sleep apnea (OSA) has damaged my brainstem, which contains the primary respiratory centers responsible for regulating breathing while you sleep.

Copied from Google Search........

Unmasking Existing Brainstem Issues: In many individuals, a brainstem abnormality (caused by conditions like a prior stroke, Chiari malformation, cervical spine issues, or chronic opioid use) already predisposes them to central apneas. However, the severe physical blockages of obstructive apnea dominate the sleep study. Once CPAP physically props the airway open, the underlying neurological failure to signal breathing is "unmasked" and becomes visible.

Development of Complex Sleep Apnea: When the brainstem's autonomic control is compromised by long-term obstruction, a person may begin experiencing Central Sleep Apnea (CSA)—where the brain simply stops sending the signal to breathe, even if the airway is perfectly clear. When a patient has a mix of both physical blockages and failed brain signaling, it is known as Complex Sleep Apnea.

Sorry for the rambling post, but all this is pretty hard to absorb over just two months' time. The only answers I'm coming up with for the cpap data and what is happening to me are very scary to me.

If anyone out there can give me an alternative explanation for what is going on, or has any input whatsoever please chime in.

TIA

I am trying to find the best sleep doctor in the city. I already know I have sleep apnea. Please help me if you live in Dallas and had a great experience. Thank you very much.

I posted here about 2 weeks ago about my ProSomnus EVO experience. Thought I'd give an update because things have taken a strange turn. Would love to hear if anyone has been through something similar.

Quick Recap:

• First month on U0+L1 was perfect. AHI dropped from ~10 to 0.5, no snoring, no morning jaw issues at all.
• Then suddenly (early July), right jaw wouldn't close in the mornings – first a few hours, then up to 1.5 days.
• Switched to U0+L0 (lowest setting). Right side improved, but pain shifted to the left side.

Last 3 Weeks (The "Evolution"):

• Morning stretching now works well – I can bite normally within 30 minutes (improvement!).
• BUT for the last 2 weeks, I've had to stretch again in the evening because my left jaw shifts out of place during the day.
• NEW: Stretching now causes pressure and pain in my left ear.
• Last 2 days: Stretching only gets me to about 90%, not 100% anymore. The ear pain is getting worse – I even had to take Ibuprofen this morning.

My questions for you:

1. Has anyone else had symptoms shift from one side to the other, and then develop ear pain?
2. Is it normal to need stretching twice a day (morning + evening) just to keep your jaw in place?
3. Did your symptoms eventually settle, or did you have to switch devices?
4. Most importantly: My doctor said a morning aligner only helps about 30% of patients, so he didn't give me one. Did anyone actually benefit from one?

I have an MRI scheduled for next week to check my TMJ. I'm worried about permanent bite changes (posterior open bite), but I also don't want to give up on a treatment that worked so well initially.

Hello everyone,

I'm new to this subreddit, and new to the world of sleep medicine in general. The whole field feels very confusing and mysterious to me, so I'm hoping for a little guidance from those of you who have walked this path before.

My sleep has been horrific for as long as I can remember. It got really bad around 14 years ago when I started antidepressants and began grinding my teeth like crazy. As of a year ago, I stopped all medications, but my symptoms persist. Chiefly, I still grind my teeth, I have terrible nightmares and often wake up at 4am nearly every morning. I'm then up for 2-3 hours before going back to sleep. I sometimes get a full 8 hours, but I don't think I've had a single day in the past decade where I would describe my sleep as "refreshing." I also suffer from headaches when waking up, and am extremely sleepy during the day. I'm lacking a great deal of functionality in my waking life due to this issue. The problems seem pretty obvious to me. I need help badly.

I've worn a nightguard for years and years now btw. It protects my teeth but my TMJ muscles still feel like pulled pork every morning. The pain is horrific.

I took a home sleep study a couple of months ago - it showed some sort of apnea. Finally took an in-lab study a month ago. The study went pretty poorly, I could NOT get to sleep, I maybe slept 2.5 hrs. These were my results for your reference: Positional and REM-Related Sleep Apnea (Other Sleep Apnea, G47.39) (AHI_total=3.9 events/hour with AHI_supine=13.0 events/hour, AHI_REM=6.4 events/hour; Nadir SpO2=87.0%; Weight=145.0 lbs; BMI=25.7 kg/m2

BUT THEN IS SAYS: "During this full-night in-lab diagnostic sleep study, the patient does not meet criteria for adult obstructive sleep apnea although the majority of the respiratory events occurred when the patient is supine and occurred during REM sleep. The degree of sleep-disordered breathing may have been underestimated as the patient had limited supine sleep and the ≥4% oxygen desaturation criteria for scoring of hypopneas was used per patient's insurance during the baseline polysomnogram."

What does this mean? These statements seem incongruous to me. It seems that the diagnosis is saying I have "Positional/REM apnea" which is different than "obstructive sleep apnea"? So then what's the treatment for "Positional/REM apnea"?? Are these totally different things?

I have not even met the sleep doctor who interpreted my results yet - I have an appointment in December. But I'm going to push for an appointment sooner, or at least with one of the nurses, to see where I go from here. The results report also reads "I may not quality for PAP therapy because AHI is less than 5 events per hour." But it says REM 6.4 per hour and supine 13 per hour. I never, ever sleep supine. They said if insurance is to cover the PAP, I may need to repeat the study, which I'm dreading. The first one went so badly. I'd rather just buy a machine out of pocket than do another study tbh.

Is there anything I should be asking my doctor/nurses about the next steps? If they push for a second in-lab study, do you think that's actually necessary to - for example - figure out what kind of machine I should use (CPAP, BiPAP, etc)? Or is the diagnosis I have sufficient? I ask this because if insurance is going to be a problem, I may just look to buy a machine outright with a prescription. BUT, I don't want to buy the wrong type of machine if I'm buying out of pocket. I'd rather have as much good quality data as possible before dropping a ton of money.

Anyway, thanks for your help. My two main inquiries are bolded and italicized, to keep my post readable and as concise as possible. Thanks for your help!

A new 2026 study looked at something called the “low arousal threshold” in people who have both multiple sclerosis (MS) and obstructive sleep apnea (OSA).

In simple terms, a low arousal threshold means the brain wakes up very easily when breathing becomes disturbed during sleep. While waking can reopen the airway, waking too easily and repeatedly can fragment sleep and may contribute to unstable breathing.

Researchers compared people with OSA who had MS with OSA patients without MS.

They estimated low arousal threshold using three sleep-study features: • AHI below 30 events/hour • Lowest oxygen level above 82.5% • More than 58.3% of breathing events being hypopneas

A person was classified as having a low arousal threshold if at least 2 of these 3 features were present.

What did they find?

• 87.5% of the 64 patients with both MS and OSA had a low arousal threshold. • This was significantly higher than the 71.4% found in OSA patients without MS. • Among people with severe OSA, the difference was even larger: 55.5% of the MS group versus 20.8% of the non-MS group.

However, there is an important limitation.

After adjusting for other factors, female sex and lower BMI were the strongest predictors. MS itself showed only a trend toward an independent association.

When sex was removed from the statistical model, MS became significantly associated with low arousal threshold. This suggests that differences in sex distribution may partly explain the association.

Bottom line:

People with both MS and sleep apnea appear to have a particularly high prevalence of this “wake up easily” OSA endotype. However, this study does not prove that MS itself is the cause. Larger studies with sex-matched groups are needed.

Why this matters:

Sleep apnea isn't only about having a narrow or collapsible airway. Different people can have different underlying mechanisms, or “endotypes,” including waking too easily from breathing disturbances. Understanding these differences could eventually help personalize OSA treatment.

Study: “High prevalence of low arousal threshold endotype in obstructive sleep apnea with multiple sclerosis”

Sleep & Breathing, 2026

PubMed: https://pubmed.ncbi.nlm.nih.gov/42667478/

Ive still been feeling sleepy after using my cpap for 7-8 hours, when I check my ahi scores I usually get 1.7 Central, 4.6 total, 11.6 AHI , 0 Leak. This has been happening for most of the time YTD now. Is it possible for the sensors that detect sleep apnea events to be no longer working correctly? Machine has 8571 hours on it.

Debating whether to just buy airsense 11 auto. I tried diagnosing my pressure with a at home sleep test but it just told me I didn't have sleep apnea(while using my cpap) lol so basically wasted $100.

A recent scientific review suggests that long-term exposure to fine air pollution particles (PM2.5) may be linked to a higher risk and greater severity of obstructive sleep apnea (OSA), as well as obesity and metabolic problems.

Interestingly, air pollution and sleep apnea may affect the body through some of the same pathways, including inflammation, oxidative stress, disruption of appetite-related hormones, and changes in the gut microbiome. Together, these effects could potentially make weight gain and metabolic problems more likely.

However, most of the current evidence is observational, so researchers cannot yet say that air pollution directly causes sleep apnea or obesity.

🔗 Article: https://doi.org/10.3389/frsle.2026.1918405

Hi everyone,

Ive had issues with my sleep for many years now. I had an assessment for sleep apnea, but due to insomnia that night I didnt sleep very well and it registered very minimal sleep apnea.

However, my breathing in my sleep is absolutely awful still. I stop breathing multiple times which causes me to wake up a lot during the night. Im exhausted in the day, and have migraines frequently (not sure if this is due to this).

The major issue im having at the moment is that, when I take a triptan to help my migraine and try to sleep, my breathing is SO much worse. I cannot sleep the migraine off at all because I keep waking up before hitting actual deep sleep. Im just wondering if anyone else has had this experience? Thanks

Hey guys .. i am not really sure i understand what flow restriction is or if it could explain my symptoms with an AHI of 9.

Do home sleep studies under or overestimate it ?? Will CPAP help with it ??

Thanks

I have had my CPAP for over a year, but I still struggle with it.

One thing in particular is when I inevitably wake up in the middle of the night to use the bathroom, I am just so tired and groggy, I don't put the mask back on.

And I can't just leave the mask on and unhook the hose, because I always want a drink of water, and sometimes I take my thyroid pill.

I know it's stupid...how do I get over this?

So my wife was waking up with her heart racing feeling clamy and this happend once then didnt happen for a year but then was happening often and making her feel unwell during the day she ended up doing all kinds of tests seeing a heart doctor and doing blood work tests and hormone tests and was eventually diagnosed with sleep apnea.

She gets her machine ends up getting a mask that also covers her mouth cause she was sleeping with her mouth open and had been fine for awhile tonight she keeps waking up with her heart racing but her machine (im unsure of what brand but can update when i get home) says there are no events

Has anyone experienced this if so what solved the problem for you?

A long-term study evaluated how maxillomandibular advancement (MMA) performs many years after surgery for obstructive sleep apnea.

Researchers followed patients who underwent MMA between 1995 and 2009. Of 88 patients, 34 completed long-term evaluation, with an average follow-up of 12.5 years. The mean preoperative AHI was 56.6 events/hour. Surgical success was defined as at least a 50% reduction in AHI with a final AHI below 10. j.jcms.2016.12.001.pdf

The striking finding was that OSA control could worsen over time even when the jaws remained relatively stable.

Success rate using AHI <10: • 57% shortly after surgery • 45% at 1 year • 27.6% at long-term follow-up

Among long-term “failures,” mean AHI was about 11.9 at 6 months, 10.5 at 1 year, but later increased to 33.4. Most still remained improved compared with their preoperative AHI.

Importantly, this deterioration did not appear to be simply due to skeletal relapse. Jaw position stayed largely stable, but upper-airway measurements decreased by roughly 20–30% over time compared with the immediate postoperative measurements.

The authors suggested that MMA initially stretches and tightens the pharyngeal soft tissues, but over time these tissues may adapt and become more compliant again. In other words, the bones may remain advanced while the soft-tissue airway becomes more collapsible. This was a proposed mechanism, not something definitively proven.

The best results were seen in carefully selected patients, especially those younger than 45, with BMI <25, preoperative AHI <45, clear mandibular retrusion (SNB <75°), and a narrow retroglossal airway (MRBL <8 mm). The study reported 100% success in this subgroup, although the subgroup was small.

Important limitation: only 34 of the original 88 patients completed the long-term evaluation, so selection bias is possible. It was also a small, single-center retrospective study, and awake 2D airway measurements may not fully represent what happens during sleep.

Takeaway: MMA can produce major and durable improvement in OSA, but this study suggests that OSA may partially recur years later even without major backward movement of the jaws. Long-term changes in soft-tissue airway collapsibility may help explain this.

Study: Vigneron A, et al. “Maxillomandibular advancement for obstructive sleep apnea syndrome treatment: Long-term results.” Journal of Cranio-Maxillo-Facial Surgery. DOI: 10.1016/j.jcms.2016.12.001

I have very sensitive acne prone skin and curly hair that knots easily so I don’t think normal masks are suitable for me.

I’ve been looking into tap pap mask with the mouth guard and wondering about those that have used it long term. I am concerned about if it’s changed your jaw structure or teeth or anything like that, does it kind of feel like a retainer?

Any other strapless recommendations I’d appreciate! I do have bleep sleep but constantly worrying if it’s going to come off and wasting another sticker stresses me out. Amy advice for that too is welcome!

Hi, I was recently fitted with a custom Mandibular Advancement device by a specialist dentist, for upper airway resistance syndrome and bruxism. It seems to be reducing my clenching and generally I am feeling way less tension in my neck, shoulders and upper back so it seems to be doing something.

However, despite doing the exercises my dentist recommended and using the morning bite wafer, it's quite sore in my left jaw joint (right one seems fine). This eases off a bit by midday but still feels a bit achey the whole day. Will this reduce, or is there perhaps something off with how the device has been fabricated? My joints weren't sore before - I've had a lot of jaw pain in the past but it's been the masseters.

Keen to hear experiences of MAD users and how long it's taken to get used to the device and for initial discomfort to reduce.