Sleep Experts Push to Classify Central Hypopneas, the Overlooked Breathing Events That Confuse Apnea Scores

Every night, millions of people experience brief interruptions in their breathing while asleep, and most of those interruptions are tallied in the same column on a sleep study report. A new letter published in the Journal of Clinical Sleep Medicine argues that this practice obscures a clinically meaningful distinction that has persisted for decades: the difference between obstructive and central respiratory events. Naina Kumari of Liaquat University of Medical and Health Sciences in Pakistan, writing in response to a recent call to action from a group of sleep specialists, contends that the field has focused overwhelmingly on identifying and scoring breathing events while paying far less attention to whether those events actually predict the health outcomes patients care about.

The technical problem at the heart of the debate concerns the hypopnea, defined as a partial reduction in airflow during sleep, in contrast to a complete apnea. Standard polysomnography records airflow through nasal pressure cannulas and thermal sensors, alongside respiratory effort belts and oximetry that tracks blood oxygen. Obstructive events are those in which effort continues while the airway collapses; central events are those in which the brain simply stops issuing the neural commands to breathe. Hypopneas, because they are partial, sit awkwardly in this binary scheme. A shallow breath can arise from a partly closed airway, from a weak central drive, or from a combination of the two, and the signal differences on a routine recording can be subtle enough that scorers disagree.

This ambiguity matters because the two categories point to different physiology and, potentially, different treatments. Obstructive events respond to continuous positive airway pressure, oral appliances, and airway-focused interventions. Central events, which reflect instability in the feedback loop that controls ventilation, may respond poorly or even paradoxically to standard pressure therapy, and are managed with different tools entirely, from adaptive servo-ventilation to medications that adjust chemosensitivity. If a hypopnea that is truly central in origin is counted as obstructive, a patient may receive a diagnosis whose treatment pathway is mismatched with the underlying mechanism.

The letter builds on a recent position paper in the same journal in which Ahn, Azarbarzin, Badr, Berry, and colleagues argued that classifying central hypopneas is important enough to warrant coordinated action by the sleep medicine community. Kumari’s contribution extends that argument by asking a more fundamental question: what is the point of identifying an event if knowing its type does not change what happens to the patient next? Drawing on a framework for evaluating diagnostic tests developed by di Ruffano, Hyde, McCaffery, Bossuyt, and Deeks in the British Medical Journal, she frames central hypopnea classification not as a scoring exercise but as a test whose value must be demonstrated in a chain that runs from detection, to differential diagnosis, to treatment selection, to measurable improvement in health.

That framework, originally developed to help researchers design trials of diagnostic technologies, imposes a discipline that sleep scoring has largely escaped. A diagnostic test earns its place in clinical practice by showing that its results lead to better decisions and better outcomes, not merely that it produces numbers. Applied to hypopnea classification, the question becomes whether knowing that a given hypopnea is central rather than obstructive actually alters management in ways that benefit the patient. The letter suggests that the field cannot answer this question with confidence, because the necessary evidence linking event phenotype to treatment response has never been systematically assembled.

The second pillar of the argument comes from a consensus statement led by Malhotra, Ayappa, Ayas, Collop, Kirsch, and McArdle, published in the journal Sleep, on metrics of sleep apnea severity beyond the apnea-hypopnea index. That statement catalogued the shortcomings of the AHI, the single number that has dominated sleep medicine since its inception. The AHI counts all apneas and hypopneas per hour of sleep regardless of type, position, or physiological consequence. Two patients with identical AHI values can carry very different burdens of disease: one may have long, severely desaturating events concentrated in REM sleep, while the other has short, benign events scattered across the night. Collapsing this heterogeneity into one figure discards exactly the information that might guide treatment.

Central hypopneas sit at the sharp edge of this metric problem. Because scoring rules allow hypopneas to be identified through airflow reduction with or without associated desaturation or arousal, depending on the rule set in use, the same recording can yield different AHI values under different guidelines. When central events are lumped together with obstructive ones, the resulting index reflects neither the mechanical burden of airway collapse nor the control-system instability of central apnea. For conditions in which central events predominate, such as heart failure-associated central sleep apnea or opioid-induced respiratory depression, an AHI that blends event types may actively mislead the clinician about both severity and prognosis.

The physiological stakes are considerable. Central respiratory events arise from instability in the loop gain of the ventilatory control system, the sensitivity with which the brain responds to fluctuations in carbon dioxide and oxygen. High loop gain produces overshoot and undershoot in ventilation, creating cyclical patterns such as Cheyne-Stokes breathing. This instability is not a mechanical problem that a splinted airway can fix; it is a control problem with its own pharmacology and its own device solutions. Identifying central hypopneas is therefore a step toward measuring loop gain and control instability in ordinary clinical recordings, which could eventually allow clinicians to select patients for servo-ventilation or other control-targeted therapies on a rational basis rather than by trial and error.

The letter also highlights the human cost of the status quo. Patients whose symptomatic breathing disturbances are scored as mild or equivocal may be denied insurance coverage for therapy, told their sleep study was normal, or left to cycle through ineffective treatments. Conversely, patients whose events are counted but whose event type is misclassified may undergo positive airway pressure trials that fail, reinforcing a cycle of non-adherence and clinical frustration. Kumari argues that rigorous, clinically validated classification of central hypopneas would sharpen the diagnostic pathway at both ends, directing the right patients to the right interventions and sparing others inappropriate treatment.

The path forward, as the letter sketches it, follows the logic of the diagnostic-test framework: define the clinical decision the classification is meant to inform, gather evidence that the distinction changes that decision, and then test whether patients whose management is guided by event type fare better than those managed on AHI alone. That program requires agreement on scoring criteria for central hypopneas, prospectively collected data linking event phenotype to treatment response, and trial designs that treat classification as an intervention in its own right. None of this is easy, and the letter does not pretend otherwise. Its central claim is simpler and harder to dismiss: a measurement that has never been shown to change a clinical decision is a measurement awaiting justification, and for central hypopneas the justification has not yet been built. As sleep medicine moves toward richer phenotyping of sleep-disordered breathing, closing the gap between event identification and clinical utility has become the test that the field’s most familiar number must finally pass.

Subject of Research: Clinical classification of central hypopneas in sleep-disordered breathing diagnosis and the validation of diagnostic utility

Article Title: Central hypopnea classification: bridging the gap between event identification and clinical utility

Article References: Kumari, N. (2026). Central hypopnea classification: bridging the gap between event identification and clinical utility. Journal of Clinical Sleep Medicine, 22(1), Article 172. https://doi.org/10.1007/s44470-026-00202-8

Image Credits: AI Generated

DOI: 10.1007/s44470-026-00202-8

Keywords: central hypopnea, sleep apnea, polysomnography, apnea-hypopnea index, sleep medicine, respiratory events, diagnostic testing, loop gain, positive airway pressure, sleep-disordered breathing, Journal of Clinical Sleep Medicine, Central