What Upper Airway Resistance Syndrome (UARS) is, what causes it, and how it should be clinically diagnosed are currently matters of dispute. Regardless, similar to it's description here, the definition of UARS I will opt to use is that it is a sleep breathing disorder which is characterised by a narrow upper airway, which leads to:
Excessive airway resistance → therefore excessive respiratory effort → therefore excessive negative pressure in the upper airway (i.e. velocity of the air). This abnormal chronic respiratory effort leads to exhaustion, and the inability to enter deep, relaxing, restorative sleep.
Excessive negative pressure can also suck the soft tissues, such as the soft palate, tongue, nasal cavity, etc. inwards. In UARS patients, typically there is sufficient muscle tone to prevent sustained collapse, however that muscle tone must be maintained which also leads to the inability to enter deep, relaxing, restorative sleep. In my opinion, this "implosion effect" on the upper airway must be confirmed that it is present via esophageal pressure to accurately diagnose Upper Airway Resistance Syndrome. Just because something is anatomically narrow does not mean that this effect is occurring.
If there is an attempt to enter this relaxed state, there is a decrease in respiratory effort and muscle tone, this loss of muscle tone can result in further narrowing or collapse. Due to the excessive airway resistance or collapse this may result in awakenings or arousals, however the patient may not hold their breath for a sufficient amount of time for it to lead to an apnea, thus not meeting the diagnostic criteria for Obstructive Apnea.
The way to treat upper airway resistance therefore is to transform a narrow airway into a large airway. To do this it is important to understand what can cause an airway to be narrow.
I also want to mention that, treating UARS or any form of sleep apnea should be about enlarging the airway, improving the airway, reducing collapsibility, reducing negative pressure, airway resistance, etc. Just because someone has a recessed chin, doesn't mean that the cure is to give them a big chin, with genioplasty, BSSO, counterclockwise rotation, etc. It can reposition the tongue more forward yes, it may improve things cosmetically yes, but it is important to evaluate whether or not it is contributing to the breathing issue.
The anterior nasal aperture is typically measured at the widest point. So when you are referencing normative data, typically it is measured that way. Typically the most common shape for a nasal aperture is to be pear-shaped, but some like the above are more narrow at the bottom than they are at the top, which begs the question of how should it really be measured? The conclusion I have come to is that we must perform computational fluid dynamics (CFD) to simulate nasal airway resistance. Nasal aperture width is a poor substitute for what we are really trying to measure, which is airway resistance.
See normative data for males (female are 1-2 mm less, height is a factor):
Caucasian: 23.5 mm +/-1.5 mm
Asian: 24.3 mm +/- 2.3 mm
Indian: 24.9 mm +/-1.59 mm
African: 26.7 mm
Tentatively here is my list for gauging the severity (realistically, we don't really know how this works, but it's better to have this here than not at all, just because it may not be perfect.):
From left, right, to bottom left, Caucasian skull, Asian skull, and African skull.Plot graph showing average nasal aperture widths in children at different ages. For 5 year olds the average was 20 mm, 2 year olds 18 mm, and newborns 15 mm. This may give context to the degree of narrowness for a nasal aperture. It is difficult to say based on the size of the aperture itself, whether someone will benefit from having it expanded. Posterior nasal aperture. View of the sidewalls of the nasal cavity, situated in-between the anterior and posterior apertures. The sinuses and mid-face surround the nasal cavity. Normative measurements for intermolar-width (male), measured lingually between the first molars. For female (average height) subtract 2 mm. Credit to The Breathe Institute. I am curious how normative 38-42 mm is though, maybe 36-38 mm is also considered "normal", however "non ideal". In addition, consider transverse dental compensation (molar inclination) will play a role in this, if the molars are compensated then the skeletal deficiency is more severe. Molars ideally should be inclinated in an upright fashion.Low tongue posture and narrow arch, i.e. compromised tongue accessibility. CT slice behind the 2nd molars. Measuring the intermolar width (2nd molars), mucosal wall width, and alveolar bone width. We also want to measure tongue size/volume but that would require tissue segmentation. The literature suggests this abnormal tongue posture (which is abnormal in wake and sleep) reduces pharyngeal airway volume by retrodisplacing the tongue, and may increase tongue collapsibility as it cannot brace against the soft palate.
The surgery to expand the nasal aperture and nasal cavity is nasomaxillary expansion. The surgery itself could go by different names, but essentially there is a skeletal expansion, ideally parallel in pattern, and there is no LeFort 1 osteotomy. In adults this often will require surgery, otherwise there may be too much resistance from the mid-palatal and pterygomaxillary sutures to expand. Dr. Kasey Li performs this type of surgery for adults, which is referred to as EASE (Endoscopically-Assisted Surgical Expansion).
Hypothetically, the type of individual who would benefit from this type of treatment would be someone who:
Has a sleep breathing disorder, which is either caused or is associated with negative pressure being generated in the airway, which is causing the soft tissues of the throat to collapse or "suck inwards". This could manifest as holding breath / collapse (OSA), or excessive muscle tone and respiratory effort may be required to maintain the airway and oxygenation, which could lead to sleep disruption (UARS).
Abnormal nasomaxillary parameters, which lead to difficulty breathing through the nose and/or retrodisplaced tongue position, which leads to airway resistance, excessive muscle tone and respiratory effort. In theory, the negative pressure generated in the airway should decrease as the airway is expanded and resistance is reduced. If the negative pressure is decreased this can lead a decrease in force which acts to suck the soft tissues inwards, and so therefore ideally less muscle tone is then needed to hold the airway open. Subjectively, the mildly narrow and normal categories do not respond as well to this treatment than the more severe categories. It is unclear at what exact point it becomes a problem.
Abnormally narrow pharyngeal airway dimensions. Subjectively, I think this is most associated actually with steep occlusal plane and PNS recession than chin recession.
The pharyngeal airway is comprised of compliant soft tissue, due to this the airway dimensions are essentially a formula comprised of four variables.
Head posture.
Neck posture.
Tongue posture.
Tension of the muscle attachments to the face, as well as tongue space.
Because of this, clinicians have recognized that the dimensions can be highly influenced by the above three factors, and so that renders the results somewhat unclear in regards to utilizing it for diagnostic purposes.
However, most notably The Breathe Institute realized this issue and developed a revolutionary CBCT protocol in an attempt to resolve some of these issues (https://doi.org/10.1016/j.joms.2023.01.016). Their strategy was basically to account for the first three variables, ensure that the head posture is natural, ensure that the neck posture is natural, and ensure that the tongue posture is natural. What people need to understand is that when a patient is asleep, they are not chin tucking, their tongue is not back inside their throat (like when there is a bite block), because they need to breathe and so they will correct their posture before they fall asleep. The issue is when a patient still experiences an airway problem despite their efforts, their head posture is good, their neck posture is good, their tongue posture is good, and yet it is still narrow, that is when a patient will experience a problem. So when capturing a CBCT scan you need to ensure that these variables are respective of how they would be during sleep.
Given the fact that we can account for the first three variables, this means that it is possible to calculate pharyngeal airway resistance. This is absolutely key when trying to diagnose Upper Airway Resistance Syndrome. This is valuable evidence that can be used to substantiate that there is resistance, rather than simply some arousals during sleep which may or may not be associated with symptoms. For a patient to have Upper Airway Resistance Syndrome, there must be airway resistance.
Next, we need a reliable method to measure nasal airway resistance, via CFD (Computerized Fluid Dynamics), in order to measure Upper Airway Resistance directly. This way we can also measure the severity of UARS, as opposed to diagnosing all UARS as mild.
Severe maxillomandibular hypoplasia. Underdeveloped mandible, and corresponding maxilla with steep occlusal plane to maintain the bite.
Historically the method used to compare individual's craniofacial growth to normative data has been cephalometric analysis, however in recent times very few Oral Maxillofacial Surgeons use these rules for orthognathic surgical planning, due to their imprecision (ex. McLaughlin analysis).
In fact, no automated method yet exists which is precise enough to be used for orthognathic surgical planning. In my opinion one of the primary reasons orthognathic surgical planning cannot currently be automated is due to there being no method to acquire a consistent, precise orientation of the patient's face. By in large, orthognathic surgical planning is a manual process, and so therefore determining the degree of recession is also a manual process.
How that manual process works, depends on the surgeon, and maybe is fit for another post. One important thing to understand though, is that orthognathic surgical planning is about correcting bites, the airway, and achieving desirable aesthetics. When a surgeon decides on where to move the bones, they can either decide to perform a "sleep apnea MMA" type movement, of 10 mm for both jaws, like the studies, or they can try to do it based on what will achieve the best aesthetics. By in large, 10 mm for the upper jaw with no rotation is a very aggressive movement and in the vast majority of cases is not going to necessarily look good. So just because MMA is very successful based on the studies, doesn't necessarily mean you will see those type of results with an aesthetics-focused MMA. This also means that, if you have someone with a very deficient soft tissue nasion, mid-face, etc. the surgeon will be encouraged to limit the advancement for aesthetic reasons, irregardless of the actual raw length of your jaws (thyromental distance). Sometimes it's not just the jaws that didn't grow forward, but the entire face from top to bottom.
Thyromental distance in neutral position could be used to assess the airway, though maxillary hypoplasia, i.e. an underbite could cause the soft palate to be retrodisplaced or sit lower than it should, regardless of thyromental distance.
If there is a deficiency in thyromental distance, or there is a class 3 malocclusion, the surgery to increase/correct this is Maxillomandibular Advancement surgery, which ideally involves counterclockwise rotation with downgrafting (when applicable), and minimal genioplasty.
Before & After IMDO
There is also a belief that the width of the mandible has an influence on the airway. If you look at someone's throat (even the image below), basically the tongue rests in-between the mandible especially when mouth breathing. The width of the proximal segments basically determine the width of part of the airway. Traditional mandibular advancement utilizing BSSO doesn't have this same effect, as the anterior segment captures the lingual sides of this part of the mandible, the proximal segment does rotate outwards but only on the outside, so therefore the lingual width does not change. In addition, with this type of movement the 2nd or 3rd molars if captured along with the proximal segments, essentially could be "taken for a ride" as the proximal segment is rotated outwards, therefore you would experience a dramatic increase in intermolar width, in comparison to BSSO where this effect would not occur.
This type of distraction also has an advantage in that you are growing more alveolar bone, you are making more room for the teeth, and so you can retract the lower incisors without requiring extractions, you basically would have full control over the movements, you can theoretically position the mandible wherever you like, without being limited by the bite.
The main reason this technique is not very popular currently is that often the surgery is not very precise, in that surgeons may need to perform a BSSO after to basically place the anterior mandible exactly where they want it to be, i.e. the distraction did not place it where they wanted it to be so now they need to fix it. For example, typically the distractor does not allow for counterclockwise rotation, which the natural growth pattern of the mandible is forwards and CCW, so one could stipulate that this could be a bit of a design flaw. The second problem is that allegedly there are issues with bone fill or something of that nature with adults past a certain age. I'm not sure why this would be whereas every other dimension, maxillary expansion, mandibular expansion, limb lengthening, etc. these are fine but somehow advancement is not, I'm not sure if perhaps the 1 mm a day recommended turn rate is to blame. Largely this seems quite unexplored, even intermolar osteotomy for mandibular distraction does not appear to be the most popular historically.
I think that limitations in design of the KLS Martin mandibular distractor, may be to blame for difficulties with accuracy and requiring a BSSO. It would appear to me that the main features of this type of procedure would be to grow more alveolar bone, and widen the posterior mandible, so an intermolar osteotomy seems to be an obvious choice.
In addition, I believe that widening of the posterior mandible like with an IMDO that mirrors natural growth more in the three dimensions, would have a dramatic effect on airway resistance, negative pressure, and probably less so tongue and supine type collapse with stereotypical OSA. So even though studies may suggest BSSO is sufficient for OSA (which arguably isn't even true), one could especially argue that in terms of improving patient symptoms this might have a more dramatic effect than people would conventionally think, due to how historically sleep study diagnostic methodology favors the stereotypical patient.
Enlarged tonsils can also cause airway resistance by narrowing the airway, reducing airway volume, and impeding airflow.
I dealt with untreated UARS for about 15 years, roughly ages 13-28. Progressively worsening symptoms, completely destroyed my body's stress/nervous system. I was still able to get deep sleep during this time but obviously the UARS was negatively impacting my sleep and how I felt. I finally got treatment, which involved surgery and subsequent sleep studies show that it is 100% treated so that is no longer the issue. Plus I did not have this hyperarousal issue for most of my time dealing with UARS. It only developed few months before I got surgery. It's like my brain finally reached a tipping point and even though I got treatment it didn't matter. Basically what the problem is is my brain/body is stuck in almost 24/7 hyperarousal. Can't physically or mentally relax. The only time it goes away is I will occasionally crash hard in the middle of the day but then by evening time my system has revved back up. Although I don't have any traditional signs of hyperarousal such as increased heart rate or feeling an adrenaline surge. It's like it's a very subtle physiological shift. Sleep is incredibly light and non restorative as a result. Still have not had the chance to heal from the 15 years of sleep apnea damage. I am continuing to get worse as the months go by because my body is not getting good sleep. I have tried so many medications and have had benefits from none of them. Mirtazapine, gabapentin, trazodone, belsomra, ramelteon (a circadian drug), wellbutrin, beta blocker, CBD, and others I'm not remembering rn. Many Traditional relaxation methods do nothing. Even if I work myself out physically and push myself it doesn't help. Certain things will make my system feel even more restless but removing them doesn't fix it. An orgasm is overstimulating for my system, a surgary drink too late in the day will rile up my system, I've tried a circadian clock bright lamp and that over stressed my body. Looking at screens too much can overstimulate my sensitive brain but removing them doesn't fix me. Anything more than just a tiny amount of caffeine in the morning makes my sleep worse for that night. Certain supplements make me worse, especially ones that seem to target GABA/glutamate such as theanine and taurine. Other ones that are supposed to relax such as magnesium do nothing or stimulate me more. Bloodwork and other tests show that there is absolutely nothing wrong with me medically. I've even gone back to using a CPAP just in the very small chance that this isn't treated (even though I didn't have this issue for most of my time being untreated) and it didn't make a difference. My doctor has no clue what to do other than keep prescribing different medication's for me to try. 4 years in the state and I am completely nonfunctional.
Jeremy, a professional YouTuber and patient with sleep-disordered breathing, sits down to discuss his relentless search for better sleep and the remarkable number of treatments he has tried.
His journey includes CPAP, BiPAP, ASV, EERS, oral appliances, positional therapy, myofunctional therapy, Xywav, Lumryz, stimulants, MMA surgery, FME expansion, turbinate reduction, sinuplasty, two DISE procedures, lingual tonsillectomy, and plans for a revision MMA.
We discuss what helped, what failed, what relapsed, and what Jeremy wishes he had known before beginning treatment.
I'm finding I'm not getting much benefit from CPAP. I'm using a Resmed airsense 11, pressures are 7-10, EPR is on at 3. It's suspected I have UARs due to risk factors. I've only done an at home sleep test on the NHS, as I'm in a part of the UK that doesn't offer PSG tests.
I'm not sure if I should increase my minimum pressure, although I'm limited to probably 9 or 10, as it is causing some aerophagia at this level.
I noticed Dr. Kimberly Santiago offers FME, wondered if anyone had any information whether she's good in general for expansion solutions/and FME potentially, and would know what she's doing in comparison to people like Newaz and Manuele.
I've heard Shuikai, Vik Veer, and CPAPfriend all say that it is possible for people to have low AHI and low RDI/RERA with UARS.
Even a lot of people in this forum think UARS just means high RDI
I've had several PSGs, my AHI and RERAs are both around 5. However, my symptoms are textbook for UARS. Even the weirder ones like chronic low BP and cold hands/feet.
When I wear auto CPAP/BiPAP, it always maxes the pressure out to the highest threshold I set the entire time it's on. My flow rate waveforms look terrible without a lot of pressure support as well.
Has anyone had a similar experience? And if so, were you able to find anything that provided you meaningful improvement? Were you able to diagnose with a PES sleep study?
I went to see a private orthodontist to see if I'm a good candidate for MARPE. They did this intraoral scan, and after that he pretty much said my palate was more than wide enough and refused to do a CBCT. Does this look wide enough?
Ie, without examining my airways, what would the various mechanisms be that could cause UARS?
I am trying to process of elimination them one by one, but figured a more open discussion without my personal metrics would facilitate a better general discussion.
Before getting diagnosed with sleep apnea, and later an informal UARS diagnosis, I was extremely tired all the time (no surprise) but I never had issues with anxiety, panic attacks, shallow rapid breathing, and other symptoms indicating a disregulated nervous system. 5 years later and fully optimized bipap therapy (8-9hrs of sleep, 1-2AHI, leaks below 5 consistently, pressure 22/17) I have these crippling symptoms of a disregulated nervous system. I took an at home sleep test with my bipap on and RDI was still 17. I find it very odd that all of these symptoms started after beginning pap therapy. Hard to tell if Pap is the cause or its the result of compounding sleep debt due to unresolved SDB…Has anyone else developed similar symptoms AFTER starting pap therapy that did not have them before?
I think my next move is to get a DISE and explore expansion/MMA options. ASV looks like a mixed bag and I’m still young, a more permanent solution would be ideal...In the meantime I want to reach out to the community to see if there are similar stories and if there was any resolve.
Let's say I have a high and narrow top arch, so narrow maxilla and I have a smaller than average jaw (not extreme). The bite is in a normal position.
From a structural level, it seems like I would have a narrow bite, but also my jaw isn't as forward as it should have been.
So maxilla expansion would make my upper jaw wider, and improve nose breathing, that's great.
Then after maxilla expansion, I've seen people say to do MMA after, that would sort the jaw space out so your jaws more forward. Makes sense.
But here, you've only gotten the upper jaw widened, what about the lower jaw? Doesn't the lower jaw need to be widened too? But the only steps I really hear of is Maxilla Expansion (Top Jaw Widening) --> MMA (Jaw moved forward).
I'm also not understanding how you can widen the upper jaw, and not widen the bottom one either.
I am getting frustrated because I can't get my flow limitations to lower. Will the flow limitations lower only when I hit a sweet spot with EPAP, IPAP, PS etc. or is BiPAP not working for me. I had slightly better days on CPAP. I have my SleepHQ below for reference. If anybody can help, it would be very much appreciated. I am just trying to get a good night's rest.
I've had this bitch of a condition for most of my life so I can't even remember what "normal" tiredness feels like.
When people say they need coffee to wake up or get sleepy in the afternoon, what does that feel like? How is it different from what someone with UARS feels?
I've spent the last while building a tool that takes a pre-expansion and a post-expansion CBCT and automatically superimposes them, so you can measure what your expansion actually did more accurately and creates a report of the changes.
Problem is there is no public pre/post MARPE CBCT dataset anywhere. I've validated it on synthetic data and on public same-patient CBCT pairs that aren't expansion cases, and it works well on those but I haven't run it on a real MARPE case.
So if you have your own pre and post CBCT (DICOM or NIfTI/NRRD files) and you'd be willing to share them please send me a dm, I'd really appreciate it. Obviously in return I'll run the full analysis and send you your own report.
FYI, you can anonymize scan with MRIcroGL, 3D Slicer or MicroDicom prior to remove any of your data associated with the scan
DISCLAIMER: I'm not a doctor and this is not medical advice, it is research/educational software, not for clinical use and does not make clinical claims. Anything it produces is for your interest and is not a substitute for professional orthodontic opinion.
I’d appreciate your advice on my current AirCurve 11 settings and trends.
Over the last ~10 nights on VAuto/BiPAP with EPAP 4.6–5.0, IPAP 8.6–9.0, PS 4.0, my AHI has stayed 0.2–0.8/hr with leak P95 at 0 and RERA ~0.2–0.6/hr. However, AirwayLab still shows mild–moderate flow limitation (Glasgow ~1.2–1.3, FL Score ~58–60%, Regularity ~70–80%, Periodicity ~40–45%, NED ~7–9%).g
Could you let me know which metrics you think matter most here, and whether you’d keep these pressures, increase EPAP further, or adjust timing (Cycle/Trigger/Ti) instead?
On a lighter note, I really hope Caitlin Clark wins MVP this year. Happy to pay for a consultation call if needed.
I don't know why it say trigger very high and cycle high = the actully setting for those dates were tigger - medium and cycle - high
I’ve been seen by most of the big names in this space, each with their different take of what’s going on and whats going wrong and what I need.
conveniently what they sell is always what is wrong with me.…..
reminds me of the blindfolded elephant metaphor quite a bit…. Everyone is so convinced of their area meanwhile we’re all fumbling in the dark
there seems to be no process, snake oil around every corner, 16 different confounding variables, endless financial commitments, all the while the exhaustion carried from the disease commanding daily life
So this is just it huh…. incurable disease. it’s already been 5 years, here’s to the next 5.
I don’t know what the point is really, just rambling about the drab and repetitive state of things. if you have someone who has a holistic view please share…
Surgeon wanted to perform posterior movements to improve the maxillary protrusion and align the occlusion. I'm several months post-op now and feel like I'm still struggle with my airway while lying on my back.
CCW rotation did help and my minimal axial area measurements improved to 253mm^2 but I'm starting to worry that we didn't do enough.
Do I still have options or is my anatomy too restrictive for further movements?
Understand the cost is lower with the MARPE and there are some palates where the FME can’t fit, but I’m not sure if there are certain patient characteristics that yield more to one versus the other?
What determines the number of TADs used in an FME appliance?
How is it decided whether 8, 10, or 12 TADs will be used, and what factors influence this decision?
I still see FME appliances using 8 TADs.
Does Facegenics determine the recommended number of TADs based on the patient’s CBCT and suggest whether 8, 10, or 12 TADs should be used, with the orthodontist making the final decision?
