There’s a condition that makes people chronically exhausted, gives them fragmented sleep, and can closely mimic insomnia — but it isn’t insomnia. It’s caused by breathing, it responds to the same treatments as sleep apnea, and most doctors have never heard of it. It’s called upper airway resistance syndrome, or UARS, and it’s one of the most underdiagnosed conditions in sleep medicine.

What UARS Actually Is

UARS sits on the spectrum of sleep-disordered breathing, somewhere between benign snoring and frank obstructive sleep apnea. Here’s the distinction: in obstructive sleep apnea, the airway collapses enough to cause measurable drops in airflow (hypopneas) or complete cessation of breathing (apneas), typically with associated oxygen desaturation. In UARS, the airway narrows but doesn’t collapse. Airflow continues, oxygen levels stay relatively normal, but the increased effort required to breathe through that narrowed airway causes brief arousals from sleep — what we call respiratory effort-related arousals, or RERAs.

The person doesn’t stop breathing. They don’t desaturate. Their AHI (apnea-hypopnea index) comes back normal or near-normal. But they’re waking up dozens of times per hour because their brain detects the increased breathing effort and briefly surfaces toward consciousness. They never reach sustained deep sleep. They wake up feeling like they didn’t sleep at all.

Why It Gets Missed

The fundamental problem is that standard polysomnography, as typically scored using AASM criteria, was designed to detect apneas and hypopneas. The scoring rules for RERAs exist, but they require oesophageal manometry (a pressure catheter placed through the nose into the oesophagus) to definitively measure inspiratory effort. Most sleep labs don’t routinely perform oesophageal manometry because it’s uncomfortable for patients and adds complexity to the study.

Without that direct effort measurement, RERAs are identified using surrogate markers — nasal pressure flattening, increased respiratory effort bands, and associated EEG arousals. But these are subtler signals that are easy to miss, especially when the technologist is primarily looking for the more dramatic events that define obstructive sleep apnea.

The result: a patient with significant UARS comes in for a sleep study, gets an AHI of 3 (normal), and is told “your sleep study is fine.” They leave confused, frustrated, and still exhausted.

The Typical UARS Patient

UARS has a different demographic profile than classic obstructive sleep apnea. The typical patient is:

• Often female (UARS has a more equal gender distribution than OSA)
• Younger and thinner than the average OSA patient
• Presenting with fatigue, non-restorative sleep, or insomnia rather than daytime sleepiness
• Frequently diagnosed with other conditions: fibromyalgia, irritable bowel syndrome, chronic fatigue syndrome, anxiety, depression, orthostatic intolerance

That last point is particularly interesting. Dr. Christian Guilleminault, who first described UARS at Stanford, published extensively on the overlap between UARS and functional somatic syndromes. His work suggested that chronic sleep fragmentation from undiagnosed UARS could drive sympathetic nervous system dysregulation, contributing to the constellation of symptoms seen in conditions like IBS, fibromyalgia, and POTS (postural orthostatic tachycardia syndrome).

How to Actually Detect It

If oesophageal manometry is the gold standard but rarely performed, what’s the practical alternative?

Nasal pressure transducer with careful scoring. A high-quality nasal cannula signal can show the characteristic inspiratory flow limitation — the flattening of the inspiratory waveform that indicates increased upper airway resistance. This requires a technologist (or sleep physician) who knows what to look for and takes the time to look.

RERA index calculation. Some labs calculate a Respiratory Disturbance Index (RDI) that includes RERAs in addition to apneas and hypopneas. If the AHI is 4 but the RDI is 18, that tells a very different story.

The key is awareness. If the referring physician doesn’t ask about UARS and the sleep lab doesn’t look for it, it won’t be found.

Treatment Options

The good news is that UARS responds to many of the same treatments as obstructive sleep apnea:

CPAP. Even at low pressures (typically 5-8 cmH2O), CPAP can eliminate upper airway resistance and dramatically improve sleep quality. The challenge is adherence — it’s a harder sell to a thin, young woman who’s been told she doesn’t have sleep apnea than to an overweight man who snores like a freight train.

Oral appliances. Mandibular advancement devices can be very effective for UARS, often better tolerated than CPAP in this population. A study published in the Journal of Clinical Sleep Medicine showed significant improvement in RERA index and subjective sleep quality with oral appliance therapy in UARS patients.

Nasal surgery or nasal dilators. Many UARS patients have subtle nasal obstruction — deviated septum, turbinate hypertrophy, nasal valve collapse — that increases the upstream resistance contributing to the problem. Addressing nasal patency can be curative or can make CPAP/oral appliance therapy more effective.

Why This Matters

UARS isn’t rare. It’s under-recognised. The patients it affects often suffer for years, collecting misdiagnoses and unnecessary medications, when a proper sleep evaluation with attention to respiratory effort could identify the problem and lead to effective treatment.

If you’re someone who sleeps “enough hours” but never feels rested, who’s been told your sleep study was normal, who maybe also deals with IBS or chronic pain or unexplained fatigue — it might be worth asking a sleep specialist specifically about UARS. Not every doctor will know what it is. But the ones who do can make a real difference.