DR.

GETÚLIO AMARAL

Originally published on Plenya Blog. Read at the source ↗

Circadian RhythmApril 2026 · 6 min

Apnea in those who don't snore — the invisible female form

A 42-year-old woman, lean, no snoring, treated for years for "anxiety." Polysomnography comes back with a low AHI and the apparent diagnosis is "no apnea." But the RDI tells a different story — and its name is UARS.

Apnea in those who don't snore — the invisible female form

Patrícia is 42. Lean (BMI 22.8). She doesn't snore — her husband confirms it. She came to me for anxiety, referred by a colleague. She has been on sertraline for four years, prescribed by a competent psychiatrist. Some afternoons she takes alprazolam as rescue. Even so, she describes life this way: Doctor, I wake up tired. My head feels scrambled all day. At night it takes me a while to fall asleep because my heart races. When I sleep, it's light. I have neck pain, jaw pain, queasiness.

Cláudio's wife, from the office one floor up, described the same thing five years before the diagnosis that changed her life.

I ordered a Type I polysomnography, in lab, with specific channels that don't come standard: nasal pressure cannula, thermistor flow sensor, and — this is the critical point — analysis of RERAs (respiratory effort-related arousals) and calculation of the RDI (respiratory disturbance index), not just the AHI.

The result: AHI 3 events/hour (“no apnea”). RDI 24 events/hour. 86% of the events were RERAs, not classical apneas. Bruxism appeared in 47% of sleep time. Minimum saturation was 92% — “normal.”

Patrícia had upper airway resistance syndrome (UARS). The disease conventional polysomnography does not see.

The apnea we have seen our whole life — and the one we miss

“Classical” obstructive sleep apnea was described in middle-aged men, overweight, thick neck, loud snoring, witnessed pauses by the wife, severe daytime sleepiness. AHI (apnea-hypopnea index) is the standard metric: pauses and marked reductions in airflow, with desaturation or arousal.

The HypnoLaus study, published in 2015 in Lancet Respiratory Medicine by Heinzer and colleagues, performed polysomnography in 2,121 adults from the Swiss general population. The numbers shocked the community: 49.7% of men and 23.4% of women had AHI ≥15 (moderate to severe apnea). The earlier datum from the Wisconsin cohort (Young et al., 1993) underestimated female prevalence by three to five times — because it screened by snoring and sleepiness, the male symptoms.

Apnea in women exists. And when the severe form exists, it is usually underdiagnosed. But there is an additional, more subtle problem: the UARS form — in which the AHI is low, saturation is preserved, but increased respiratory effort fragments sleep into micro-arousals invisible to a superficial reading of the report.

What UARS is, mechanically

Christian Guilleminault, of Stanford, first described UARS in the 1990s. In 1996, he published in Chest the observation that patients with increased upper airway resistance showed elevated nocturnal blood pressure and neurocognitive symptoms, even without classical apnea criteria.

In 2003, Gold and colleagues, also in Chest, formalized the picture: UARS patients frequently present with chronic fatigue, paradoxical insomnia (they sleep but do not recover), chronic pain (head, jaw, neck), bruxism, rhinitis, restless legs syndrome, functional disorders of the gastrointestinal tract, and — the point that matters — psychiatric diagnoses of anxiety and depression that do not respond well to medication.

The Bonsignore, Saaresranta, and Riha review (European Respiratory Review, 2019) consolidated what each gender study had pointed to: women with sleep-disordered breathing more frequently present with insomnia, fatigue, morning headache, anxiety, depression, palpitations — and less often with snoring and excessive daytime sleepiness. The classical male presentation, for decades, became the operational definition. Women fell outside it.

Mechanically, UARS involves:

  • Narrow upper airways — high palate, mild retrognathia, large tongue relative to space, septal deviation, turbinate hypertrophy.
  • Increased dilator muscle tone — keeping airflow “normal” but with elevated respiratory effort.
  • Successive cortical micro-arousals fragmenting deep sleep and REM, even without apnea.
  • Autonomic response — nighttime sympathetic firing, tachycardia, vasoconstriction, falling heart rate variability, altered morning cortisol.

What the patient feels: she sleeps the hours, doesn't recover. She thinks it is in her head.

Why “ordinary” polysomnography misses it

The AHI is a metric designed for obstructive apnea. It counts apneas (cessation of flow) and hypopneas (marked flow reduction with desaturation or arousal). It does not count RERAs — respiratory events that cause cortical arousal without reaching hypopnea criteria.

The RDI sums AHI + RERAs. It is the honest metric for UARS. But it requires:

  • Nasal pressure cannula (not just a thermistor — the thermistor is less sensitive for detecting flow limitation).
  • Esophageal pressure sensor (gold standard, rarely available) or careful analysis of the nasal flow envelope and EEG arousals.
  • Technical staff trained to score RERAs — many centers do not score them.

In women, it is common for polysomnography to come back with “AHI = 4” and the patient to leave with “no apnea.” Without the RDI, the picture remains invisible. That is why, when ordering the exam, it is important to write on the request: “Type I polysomnography, with nasal pressure cannula and RDI calculation; suspicion of UARS.”

What to treat, and how

UARS responds, generally well, to non-CPAP-dependent approaches — which changes adherence.

Targeted ENT and oral-maxillofacial assessment. Cephalometry. Awake nasofibroscopy and, in some cases, drug-induced sleep endoscopy (DISE). Dental assessment of palate, arch, and mandibular position.

Mandibular advancement intraoral appliance (MAD), made by a sleep-specialist dentist. In UARS, frequently first-line. Comfortable, effective, with adherence >70%.

Two profiles of obstructive apnea. On the left, the classical profile (overweight man, loud snoring, marked daytime sleepiness, high AHI) that the standard protocol knows how to recognize. On the right, the invisible profile (woman with normal weight, modest snoring, fatigue instead of sleepiness, low AHI but elevated RDI — UARS) that escapes screening.
Two profiles of obstructive apnea. On the left, the classical profile (overweight man, loud snoring, marked daytime sleepiness, high AHI) that the standard protocol knows how to recognize. On the right, the invisible profile (woman with normal weight, modest snoring, fatigue instead of sleepiness, low AHI but elevated RDI — UARS) that escapes screening.

Orofacial myofunctional therapy. Muscular re-education of the tongue, lips, and palate, with a specialized speech-language pathologist. Randomized studies show RDI reduction in selected populations.

Positional therapy. For patients worse in the supine position, positional devices or postural adjustments can help.

Treatment of nasal obstruction. Allergic rhinitis, septal deviation, turbinate hypertrophy — anything that increases nasal resistance worsens UARS. ENT assessment is mandatory.

Low-pressure CPAP, in selected cases — especially when there is clear symptomatic response. In UARS, pressures of 4–7 cmH₂O usually suffice, against the 8–12 of classical apnea.

Serious sleep hygiene. Alcohol out or drastically reduced (relaxes the airway, worsens it). Sleeping on the side. Cool room. Avoiding heavy meals in the 3 hours before bed.

Treatment of associated bruxism. A myorelaxant occlusal splint — not as treatment for UARS, but to protect dentition and reduce jaw pain.

The reading the Continuum makes

UARS is a clear example of the kind of diagnosis lost in a 30-minute visit with a short complaint list. It demands a long-form history — asking about teeth grinding, morning pain, sleep position, frequency of nighttime awakenings to urinate (the nocturia of UARS is classical, a sign of sympathetic firing), mouthguard use, mouth-breathing pattern.

In Continuum Plenya, the initial panel includes structured screening for sleep-disordered breathing (STOP-BANG and the Berlin Questionnaire, but, critically, we do not take them as the only filter), the Epworth Sleepiness Scale, the Pittsburgh Sleep Quality Index, and when the picture asks — especially in women with chronic fatigue, refractory anxiety, or chronic head/jaw pain — direct referral to Type I polysomnography with a specific request for RDI.

The Patrícia from the beginning of the story fitted a mandibular advancement intraoral appliance 14 months ago. She reduced sertraline in conversation with the psychiatrist (she did not cut it — she reduced it, with judgment). At six months, she stopped alprazolam entirely. At ten months, she described in the visit the sentence I hear when the diagnosis was right: I didn't know one could wake up rested.

The “anxiety” was never just anxiety. It was a trachea working too hard at night, a brain fragmented by micro-arousals, and four years of treatment on the wrong avenue.

A tired woman at 42 is not always hormones. Sometimes it is a breath no one listened to properly.

Clinical review. Medical content authored by Dr. Getúlio Amaral Filho · CRM-PR 21,876 · RQE 16,038 (Nephrology). Originally published at plenyasaude.com.br/en/blog.

Educational notice

This content is educational and does not constitute medical prescription. Each case is unique — for individual evaluation and care, consult a physician.