u/sleepapnea25

A 2025 review, “Epiglottis Collapse in Individuals With Obstructive Sleep Apnea,” takes a detailed look at one of the more overlooked causes of airway obstruction in OSA: epiglottic collapse.

The reported prevalence varies enormously, from 11.5% to 73.5%, partly because examining the airway while someone is awake can miss what happens during sleep. Drug-induced sleep endoscopy (DISE) is particularly useful because it can directly reveal epiglottic collapse occurring during a sleep-like state.

The CPAP part is particularly interesting

CPAP remains the main treatment for OSA, but the review explains that it may have limited benefit in some patients with epiglottic collapse.

The proposed mechanical problem is:

CPAP pressure → pushes the epiglottis backward → narrows the laryngeal inlet → potentially worsens obstruction or contributes to CPAP intolerance

The authors specifically state that CPAP pressure can push the epiglottis backward into the laryngeal inlet, narrowing the airway and potentially exacerbating OSA symptoms or contributing to CPAP intolerance. Nasal CPAP may also produce an uncomfortable choking sensation in people with epiglottic collapse.

Later in the review, the authors describe CPAP as having “suboptimal efficacy” in OSA associated with epiglottic collapse.

Their conclusion also states that people with epiglottic collapse often exhibit low tolerance for CPAP.

Important distinction

This does not mean CPAP worsens epiglottic collapse in every patient.

Instead, the review suggests that epiglottic collapse may help explain why some patients:

• cannot tolerate CPAP • experience choking or uncomfortable breathing with PAP • continue to have obstruction despite treatment • may not improve simply by increasing CPAP pressure

This is one reason DISE can be valuable in CPAP failure, because the epiglottis may look relatively normal during an awake examination but collapse during sleep.

What can be done instead?

The review discusses several approaches depending on the type of collapse, including positional therapy, mandibular advancement devices, epiglottis stiffening operation, partial epiglottidectomy, epiglottopexy, glossoepiglottopexy, and upper airway stimulation.

Interestingly, lateral sleeping can substantially reduce epiglottic collapse in some patients, while jaw thrust during DISE can help determine whether mechanically advancing the airway improves the obstruction.

The main takeaway: If CPAP seems to make breathing more difficult, produces a choking sensation, or simply fails despite adequate treatment attempts, the problem may not always be insufficient pressure. Epiglottic collapse is one anatomical cause worth considering, and DISE may reveal something that an awake airway examination misses.

📄 Article: Epiglottis Collapse in Individuals With Obstructive Sleep Apnea World Journal of Otorhinolaryngology - Head and Neck Surgery, 2025

🔗 https://doi.org/10.1002/wjo2.70061

A 2026 systematic review and meta-analysis looked at whether lateral throat wall collapse seen during DISE affects the success of hypoglossal nerve stimulation (Inspire) for obstructive sleep apnea.

In the main analysis of 502 patients, complete oropharyngeal lateral wall collapse was associated with significantly lower odds of successful HNS treatment (OR 0.43, 95% CI 0.28–0.64). Interestingly, simply having some lateral wall collapse was not clearly associated with worse outcomes—the strongest negative effect was seen with complete collapse.

The authors emphasize that complete lateral wall collapse is NOT an absolute contraindication to HNS, but it may be an important factor when predicting response and counseling patients before implantation.

Study: https://doi.org/10.1177/01455613261477450

Title: Oropharyngeal Lateral Wall Collapse as a Predictor of Hypoglossal Nerve Stimulation Response: A Systematic Review and Meta-Analysis

Has anyone here actually had hyoid suspension for sleep apnea? Did it help? How was the recovery, and would you do it again?

A new study published in JAMA Otolaryngology–Head & Neck Surgery evaluated 3,786 patients who underwent Inspire hypoglossal nerve stimulation (HGNS) for obstructive sleep apnea.

Key findings

• After more than 2 years, HGNS was associated with:

• A significantly lower risk of new-onset diabetes.

• A significantly lower risk of new-onset hypertension.

• For major cardiovascular events—including:

  • Heart attack (myocardial infarction)
  • Stroke
  • Heart failure the study did not demonstrate a clear reduction during the first 2 years. However, event rates began to trend downward with longer follow-up, although the evidence is not yet strong enough to conclude that HGNS provides definite cardiovascular protection.

Takeaway

This large cohort study suggests that Inspire HGNS may offer long-term health benefits beyond improving obstructive sleep apnea, particularly by reducing the risk of developing diabetes and hypertension. However, longer-term studies are still needed to determine whether it truly lowers the risk of major cardiovascular events such as heart attack and stroke.

A new 2026 review highlights how obstructive sleep apnea (OSA) care is becoming increasingly personalized. While CPAP remains the first-line treatment, newer options—including hypoglossal nerve stimulation (Inspire), transoral robotic surgery (TORS), radiofrequency treatments, and maxillomandibular advancement (MMA)—are expanding choices for carefully selected patients.

The review also emphasizes that AHI alone doesn't tell the whole story. Emerging metrics such as hypoxic burden, time spent below 90% oxygen (T90), and ventilatory burden may better predict cardiovascular risk and help tailor treatment. Drug-induced sleep endoscopy (DISE) and the PALM endotyping framework are also gaining importance in identifying why a patient's airway collapses and which therapy is most likely to work.

Bottom line: Sleep apnea management is moving away from a "one-size-fits-all" approach toward precision medicine, where treatment is selected based on each patient's anatomy and physiology—not just their AHI score.

A study examined whether the shape of the upper dental arch is associated with obstructive sleep apnea severity in adults. Researchers compared 50 adults with OSA with 50 controls. All participants underwent hospital-based polysomnography, and digital dental scans were used to measure the width and depth of the upper palate.

The study measured intermolar distance, which is the width between the upper first molars, and palatal height, which represents the depth of the roof of the mouth. Participants without OSA had an average palate width of 41.50 mm and palatal height of 20.72 mm. In mild OSA, the averages were 35.83 mm and 23.74 mm; in moderate OSA, 35.62 mm and 24.48 mm; and in severe OSA, 31.39 mm and 26.89 mm.

Overall, worsening OSA was associated with a progressively narrower and deeper palate. Each additional 1 mm of palate width was associated with approximately 0.76 fewer AHI events per hour, while each additional 1 mm of palatal height was associated with approximately 2.81 more AHI events per hour. Together, these two measurements explained about 76% of the variation in AHI within this selected study sample.

However, this was a retrospective observational study, so it shows an association rather than causation. It does not prove that a narrow or deep palate directly causes OSA, or that adult maxillary expansion will necessarily reduce AHI. The sample was also relatively small, with only eight participants in the severe OSA subgroup.

Has anyone here had their palate dimensions measured or undergone adult maxillary expansion and seen an objective improvement in their sleep study results?

Study: Correlation Between Severity of Obstructive Sleep Apnea and Dental Arch Form in Adults

I came across a recent narrative review on loop gain in obstructive sleep apnea (OSA):

“Loop Gain in Obstructive Sleep Apnea: From Physiological Endotype to Clinical Translation” PMID: 42445695

The main idea is that two patients can have the same AHI, but very different disease behavior and treatment responses, partly because of different underlying physiology.

Loop gain refers to the stability of the ventilatory control system. In simple terms, it describes how strongly the body reacts to changes in oxygen and carbon dioxide during sleep. If loop gain is high, breathing control may become unstable, making apneas/hypopneas more likely to repeat.

The review argues that loop gain could become clinically useful, especially for:

• Predicting who may respond better or worse to surgery or oral appliances
• Identifying patients who may benefit from oxygen or medications targeting ventilatory control
• Understanding residual breathing instability even when using CPAP
• Moving beyond AHI-only interpretation of OSA severity

The authors note that research-grade testing is still the reference standard, but raw PSG-based modeling may be the most practical route for clinical use. Other simplified tools using polygraphy, photoplethysmography, or respiratory belts may also help in the future.

My takeaway: loop gain is probably not useful as a standalone number, but it may be valuable as part of a broader OSA endotyping approach, especially in patients whose symptoms or treatment response do not match their AHI.

Severe house dust mite allergy and moderate cat allergy here. Tried Xolair, no help at all.

Has anyone used Dupixent for dust mite or cat allergies? Did it actually work — especially if Xolair failed you first?

Thanks

MMA basically zeroed my NREM (0.9) but REM-AHI won't budge (10.6).

For a REM-only residual, which device actually normalizes it? Leaning bilevel (PS for REM atonia), but I've had centrals twice so nervous about unmasking loop gain → ASV.

Anyone fix REM-predominant disease on bilevel, or did you need ASV?

Came across this new one from the RICCADSA trial (Sleep Medicine, 2026).

Basically: in people with coronary artery disease + OSA who aren't sleepy (Epworth <10), a year of CPAP did nothing for their exercise autonomic stuff — heart rate recovery, peak HR, chronotropic response all unchanged Vs. no CPAP. What actually mattered? BMI and beta-blocker use.

TL;DR: if you've got heart disease + apnea but no symptoms, CPAP alone probably isn't fixing your cardiovascular risk. Diet and exercise still carry the load. (Doesn't apply if you're symptomatic.)

TL;DR: Acarizax works best in people with moderate-to-severe HDM disease, high HDM-specific IgE, and HDM as their dominant allergen. It underperforms in mild, well-controlled patients and in those whose main allergic driver isn’t HDM. Daily compliance for 3 years is non-negotiable.

The Acarizax Phase III programme has studied ~9,000 patients, and the subgroup analyses consistently identify the same responder profile. Top responders are patients with moderate-to-severe disease at baseline.

In the MT-02 asthma trial, partly controlled asthmatics on 400–800 µg ICS showed a 327 µg/day ICS reduction vs placebo, far larger than the broader population effect. The Japanese MT-08 trial made the same point in reverse: it missed its primary endpoint because the enrolled patients were too well-controlled, but the uncontrolled subgroup matched MITRA’s exacerbation reduction. The MT-02 post-hoc ROC analysis added a biomarker signal — lower FEV1, thicker airway walls, higher FeNO, and higher HDM-specific IgE all predicted response. Allergen dominance also matters: patients whose symptoms are clearly HDM-driven (perennial pattern, high Der p/Der f sIgE, no major pollen or mould co-driver) consistently do better than polysensitised patients where HDM is a minor contributor. Age is not a meaningful modifier. MATIC (children 5–11) and the adolescent subgroup of TO-203-3-2 both showed ~22% TCRS reduction, matching adult MERIT and P001 results.

Lowest responders are patients with mild, well-controlled disease (less symptom burden to relieve, often failing the WAO 20% clinical relevance threshold), patients whose dominant allergen isn’t HDM, and patients who can’t sustain daily dosing — real-world cohorts show meaningful first-year dropout, and early discontinuers lose both symptomatic and disease-modifying benefit. The ideal candidate: moderate-to-severe perennial HDM AR uncontrolled on nasal steroids + antihistamines, or HDM allergic asthma on moderate ICS still symptomatic, with elevated Der p/Der f sIgE, HDM as the dominant allergen, and willing to commit to 3 years of daily treatment. Summary of published evidence — not medical advice.

References Virchow JC, et al. MITRA trial. JAMA. 2016;315(16):1715–1725. Demoly P, et al. MERIT trial. J Allergy Clin Immunol. 2016;137(2):444–451. Mosbech H, et al. MT-02 trial. J Allergy Clin Immunol. 2014;134(3):568–575. Mosbech H, et al. MT-02 post-hoc analysis. Respir Med. 2015;109(7):870–877. Okamoto Y, et al. MT-08 (Japan). J Allergy Clin Immunol Pract. 2019;7(8):2628–2638. Roberts G, et al. MATIC trial. Lancet Respir Med. 2024;12(12):993–1004. Sidenius K, et al. Real-life Scandinavian study. Pulm Ther. 2021;7(1):221–235. Demoly P, et al. Real-life French study. Clin Transl Allergy. 2022;12(3):e12129. ACARIZAX 12 SQ-HDM SmPC. emc UK, 2024.​​​​​​​​​​​​​​​​

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5-year journey. Septoplasty, UPPP, MAD trial, MMA. Now on CPAP, AHI below 1. Sleep still broken — multiple awakenings, never restorative.

My Oct 2023 PSG: total arousal index 45/h, spontaneous 40.4/h against AHI 7.5 — a 6× disproportion. Post-MMA in Feb 2025 that collapsed to total arousal 4.3/h, spontaneous 2.5/h. So the 2023 hyperarousal was airway-mediated, not primary insomnia. But REM-AHI is still 10.6 post-MMA, and symptoms persist on CPAP.

Five of six PSGs scored RERAs as zero. Without proper RERA scoring there's no way to know if residual symptoms are undertreated UARS or a COMISA overlay needing CBT-I.

Comparison table of all six studies attached.

Note: I am currently also treating my severe dust mites allergies using immunotherapy

Given REM-AHI 10.6 post-MMA with persistent symptoms but near-zero AHI on CPAP — would you push for an in-lab PSG on CPAP with proper RERA scoring? Would you also request the raw EDF data upfront and have it independently re-scored afterward? Anyone in a similar post-MMA residual-UARS spot — what moved the needle?

Thanks

My total IgE is in the 1300s, driven mainly by dust mite sensitization.

Currently on Acarizax (SLIT). Beyond the usual rhinitis symptoms, I deal with persistent fatigue and brain fog that don’t fully respond to antihistamines or CPAP.

For those with similar IgE levels, do you experience fatigue or brain fog? What actually helped — SLIT, SCIT, environmental control, diet, something else?

And how long until you noticed real energy improvement?

Trying to get a sense of realistic timelines from people who’ve been through it. Thanks.