Happy 57th Birthday to the Beast Known as Sleep Apnea!

Dr. David E. McCarty discusses the history of sleep apnea, its evolution, and changing perceptions over the past 57 years — and the nuances and complexities for diagnostics.

History of sleep apneaThe Monster Has left The Building. What Do We D0? 

by David E. McCarty, MD, FAASM

If Sleep Apnea – as a construct – can be said to have a birthday, you could say it happened in February 1966. That would make this year Sleep Apnea’s 57th birthday.

It was during that cold winter that French epileptologist Henri Gastaut and colleagues strapped electrodes to a patient with Pickwickian syndrome, with a specific intent to study his sleep, finding a certain breathing pattern that would later spawn a new specialty of medicine, a multi-billion-dollar industry, and ongoing feuds between providers with differing opinions for how the problem should be managed.

But I’m getting ahead of myself.

By 1966, the concept of Pickwickian Syndrome had been puzzled over by scientists for various reasons for over half a century. It was well-understood that patients with a combination of snoring, obesity, and daytime somnolence tended to die younger. Their mode of exit was typically cardiovascular: right heart failure, pulmonary hypertension, strokes, cardiac arrhythmias.

The pattern was called “Pickwickian Syndrome” because the great Dr. William Osler noticed a similarity his patients shared with a character created by Charles Dickens for his first novel The Posthumous Papers of the Pickwick Club, first published in serial form in 1836-1837. In the story, an obese young lad (often called “Fat Joe”) makes his appearance to the other characters by literally falling asleep on his feet while knocking at the door.

Back in 1966, Sleep Apnea didn’t have a name, because nobody even knew it existed. Nobody ever thought to study Pickwickian sleep before. Back then, there was only the knowledge that obesity and sleepiness often went together.

To hear Dr. Osler describe it in 1918: “A remarkable phenomenon associated with excessive fat in young persons is an uncontrollable tendency to sleep – like the fat boy in Pickwick.”1

In 1956, Burwell reported a case involving an obese patient with excessive sleepiness, who was found to be in heart failure with chemical evidence of respiratory acidosis.2 From this case, a new mindset emerged.

Burwell’s case definitively demonstrated a link between sleepiness and inadequate clearance of CO2.

After Burwell’s report, the prevailing presumption in the medical community was that, in Pickwickian patients, excess abdominal fat acted as a barrier to pulmonary excursion, thus limiting proper ventilation. The follow up logic was that the hypoventilation (i.e.: lack of clearance of CO2) was the mechanism for the daytime hypersomnia. In other words, patients like Fat Joe were sleepy, they reasoned, because the arterial CO2 level was constantly too high.

Obesity-hypoventilation syndrome, nice to make your acquaintance!

In 1966, Henri Gastaut was known to his peers as a diligent and highly intelligent man, possessing a voracious appetite for learning and exploring, and a supernatural talent for seeing patterns within patterns. Gastaut’s observations of squiggles obtained by the relatively new technique known as electroencephalography (EEG) – the science of interpreting brain waves – established the new field of epileptology as a legitimate science, putting him on the international map as a medical pioneer and a force to be reckoned with.

Gastaut’s work to understand seizure semiology must have prepared him to think about medical challenges with a different frame of mind than his peers. Perhaps the experience of having seen seizures that transition to a state indistinguishable from sleep positioned him to challenge the dominant paradigm, the one that said that sleepiness in Pickwickian patients was chemical in nature, the result of persistent hypercapnia.

In the winter of 1965, Gastaut seized the idea to apply his genius for pattern recognition and his familiarity with EEG patterns, to scientifically deconstruct the sleep of a person suffering from Pickwickian Syndrome.

History of sleep apnea

The beast known as Sleep Apnea opened its eyes and choked its first breaths in February 1966, when Gastaut, Tassarini, and Duron published a case report in the second issue of the journal Brain Research, entitled “Polygraphic study of the episodic diurnal and nocturnal (hypnic and respiratory) manifestations of the pickwick syndrome”.3

It says a lot for Gastaut’s prominence that he was afforded an astonishing 19 pages to tell the story of a single patient with “authentic Pickwickian syndrome, the symptomotology may be confined to obesity and diurnal drowsing epsiodes of the type described by Dickens in his novel.”

You can almost feel the glee of discovery as Gastaut describes the pattern he found. He was smart enough to know he was seeing something no one had ever described before:

“Nocturnal polygraphic registrations disclosed respiratory pauses which occurred in the initial phase of sleep… so rapid and pronounced that the tongue moves back and causes the obstructive apnoea responsible for a hypoxia, which arouses the subject, who returns to sleep after a short while. The cyclic repetition of arousal and slumber reduces the nocturnal sleep to 2-3 hours a night. This loss of nocturnal sleep is held responsible for the diurnal somnolence.”

Cue crash of thunder, as lightning flashes reveal a silhouette of a brash young neurologist crying out into the night, as the creature opens its eyes: “C’est vivant!….VIVANT!!”. Meanwhile a nearby transistor radio plays the number one pop song on the planet, over and over: Lou Christie’s falsetto-infused teen anthem Lightnin’ Strikes Again.

The concept of “Sleep Apnea” as a cause of daytime sleepiness wouldn’t enter the public consciousness until over two decades later, because, quite frankly, there wasn’t much one could do about it, back then. The prevailing wisdom at the time was for doctors to tell Pickwickian patients to lose weight, because…what else was there? For those who had problems deemed too severe to live with, a tracheostomy was a last-ditch option that almost no one wanted to talk about.

For nearly three decades following his birth, Sleep Apnea lived primarily behind closed doors, the diagnosis mostly being made in academic institutions, populated by nerdy eggheads who idolized people like Henri Gastaut enough to spend two years of their life learning how to decode the erratic squiggles of a polysomnogram.

It would take a treatment strategy more appealing than tracheostomy and more immediate than diet advice to propel Sleep Apnea into the public consciousness. That strategy wouldn’t arrive until Sleep Apnea’s 25th birthday.

In April 1981, while fellow Aussies The Bee Gees established their own falsetto chart supremacy, Dr. Colin Sullivan quietly published a case series of five patients with “severe obstructive sleep apnea,” who experienced complete remediation of the breathing pauses and restoration of “an entire night of uninterrupted sleep” as a result of using a device he cobbled together from ventilator parts and an emancipated vacuum cleaner pump, a treatment he called Continuous Positive Airway Pressure.3

Almost overnight, a new paradigm of medical treatment was born, and not surprisingly, much debate would ensue in the coming years about what does and does not constitute Sleep Apnea, much of it initiated by insurance payors, having done the math to find out how expensive it could get, if every sleepy person on their “covered life” list decided they needed a sleep study and wanted treatment.

The disease we call “obstructive sleep apnea” is an end stage of a long process.

I felt compelled to tell the story of Sleep Apnea’s birthday, because his origin story – the very notion of the construct known as Sleep Apnea – creates strange new ways for individuals to suffer. The concept itself creates siloed thinking that can ironically block patients suffering with airway problems from obtaining care, whilst simultaneously placing vulnerable people in a situation of being offered treatments that they don’t necessarily need.

To understand how the construct of Sleep Apnea can ironically become a barrier to care, I spoke with Katy, an outspoken physical therapist and mother of four who has Sleep Apnea with a respiratory effort related arousal (RERA) predominance. In other words, she has obstructive events which ONLY cause arousals from sleep, not oxygen desaturations. Katy says she literally had to lie to her doctor to obtain access to polysomnographic testing.

“The problem was: I’m young, and my breathing events don’t cause desaturations. On the oximetry test, my oxygen levels were normal, and didn’t drop. My doctor told me that I couldn’t possibly have Sleep Apnea because I was slender, and my oxygen level was normal. Meanwhile I was snoring and feeling terrible, and I couldn’t breathe through my nose. I knew something was wrong, and the doctor just made me feel like it was all in my head.”

Dr. Barry Raphael, an Airway Centered Orthodontist in New Jersey, agrees that the construct known as Sleep Apnea can sometimes represent a barrier to care. “I think we are seeing a different phenotype of the larger problem. The disease we call “obstructive sleep apnea” is an end stage of a long process that involves chronic airflow limitation. Patients we see have difficulty with their breathing not just during sleep, but during the daytime, too. We are just more susceptible to the consequences of suboptimal breathing during sleep.”

Raphael says that patients seen by Airway Centered Dentists are fundamentally different than the Pickwickian patient studied by Gastaut that fateful winter, so long ago: “Patients we see are not just overweight old men, but may be thin, fit women, with evidence of upper airway resistance and sympathetic overdrive…they have fragmented sleep, headaches, TMJ dysfunction, dental breakdown, and comorbidities that aren’t mentioned in the ICSD-3, like migraine headaches, and we are seeing these signs and symptoms improve when we work on the airway.”

These obvious differences aside, these patients are still labeled with Sleep Apnea, if they happen to undergo testing in the sleep lab. The label, it seems, now represents problems that are decidedly not Pickwickian.

I think it’s fair to say that even the great Dr. Osler wouldn’t recognize the connection between Raphael’s patients and Dickens’ character.

If a Pickwickian lens applied to the diagnostic process is capable of blocking slender, RERA-predominant cases from being recognized, a culture of relying on the apnea-hypopnea index (AHI) as the gold-standard indicator of “disease” creates another potential problem: needless overtreatment of vulnerable patients, at the expense of an algorithmic payor.

In 2008, Milena Pavlova and colleagues published a paper that blew my mind, revealing that, in a group of seniors (over age 65) who specifically denied any sleep-wake complaints and had ZERO evidence of medical disease, more than half had an AHI greater than 15 per hour – a metric which, according to the ICSD-3, allows the diagnosis of “obstructive sleep apnea” to be awarded with no other supportive information.

Let that sink in.

When Sleep Apnea was confined to his nerdy academic home (that is to say, when the world was young, and the diagnosis was still rare) the discussion of the WHY? of therapy could be a lot more nuanced. Scientific investigators are often the first to tell you what they don’t know.

The truth of the matter is: nobody knows what to do with the inconvenient truth that more than half of “perfectly well” seniors would test positive for Sleep Apnea, if somebody just bothered to screen them. Nobody knows whether treating a person like this with CPAP (or anything else) will prolong life, prevent disease, or enhance cognition. It’s quite possible that “treatment” in this setting could make a person’s life worse. Those are the facts.

It really should be presented that way.


That’s not how it goes, in the “real world,” where patients are seen on a rotating 15-minute schedule, where providers are overworked and stressed, and defensive medicine is on display. A 65-year-old who raises objections to being treated is quite likely to be subjected to an “educational” session about the “risks of non-treatment,” which inevitably includes a crisp discussion on how untreated Sleep Apnea raises the risk for stroke, a process which feels a lot like a browbeating.

In my experience, this sort of algorithmic approach pushes many patients to reject the system altogether, after only a short introduction, and never…ever, come back.

If that’s not harm, what is?

Help the patient understand that if there are no reasons to treat, there is no reason to treat.

We are Poised on the Brink of a New Age in Sleep Medicine

Sleep Apnea is no longer confined to an academic dungeon, but indeed has “escaped” to the consideration of the individual patient, who is presented with an increasing array of options for how to proceed. Sleep Apnea diagnostic testing has likewise escaped from the nerdy laboratory to the realm of wearable technology, making the diagnostic test more efficient and available than ever before, and making access to Sleep Apnea treatment almost as easy as stepping up to a vending machine.

So, what’s missing? While we providers who have watched the beast grow and mature understand the nuance and complexity that exist under the black and white rules of diagnostic classifications and event scoring criteria, new trainees have internalized these rules as core beliefs, as ground truth.

The construct has become the reality. The monster is fully awake.

To Katy’s provider, her absence of daytime sleepiness constituted an “evidence-based reason” to deny her access to a sleep study. “I practice evidence-based medicine,” he said, the evidence apparently being the rules he had memorized.

To a senior citizen who feels perfectly well and has no evidence of medical disease, on the other hand, a well-intentioned “screening test” has more than a coin-flip’s chance of disclosing a “disease” that will require a hefty amount of counseling to understand (and may only represent a natural consequence of aging). The growing trend towards more algorithmic delivery of treatments for Sleep Apnea will doubtless see many more individuals talked into starting therapy for dubious reasons, by inexperienced providers reading from an algorithm provided by the company they work for.

So, if the current definition of Sleep Apnea can’t be trusted not to exclude atypical patients with non-Pickwickian phenotypes, nor can it be trusted to prevent well persons from being exposed to unnecessary treatments, where does that leave us?

In other words: What Do We Do?

My answer: Empower the patient.

Educate the patient early in the process about the Five Reasons to Treat Sleep Apnea: (1) risk, (2) snoring, (3) sleep, (4) wake, (5) comorbidities.5 Help the patient understand that if there are no reasons to treat, there is no reason to treat.

Help the patient understand that the discussion about the first reason – risk – is a nuanced one, requiring attentive deliberation to the types of breathing events that the patient experienced, a review of the patient’s comorbid conditions, as well as the patient’s perceived medical vulnerability. Help the patient understand that there is no “one size fits all” solution. Give the patient guidance in the creation of goals of therapy, based upon the reasons to treat that matter to them. Help the patient along on their journey towards achieving those goals.

Above all: Create the expectation that you will care for the person, not for the label.

That’s what you do.

So raise a glass with me, as I toast a happy 57th birthday to the beast known as Sleep Apnea, as he emerges to walk amongst us, with a life of his own.

May we someday truly understand him, in all his glory, beyond the lens of his Pickwickian origins, for the better health of our patients!

In the meantime… Brace yourself.

Check out Dr. Gilles Lavigne’s insights on some of the history of sleep apnea and its impact on dental sleep medicine. https://dentalsleeppractice.com/thoughts-current-future-practice-dental-sleep-medicine/

History of sleep apneaDavid E McCarty, MD, FAASM is a Sleep Medicine clinician, author, cartoonist, and podcast creator/host. He is the co-author of Empowered Sleep Apnea: A Handbook for Patients and the People Who Care About Them, and the creator and co-host of Empowered Sleep Apnea: THE PODCAST.

  1. Osler W. The Principle and Practice of Medicine. Eighth Edition. 1918.
  2. Burwell CS, Robin ED, Whaley RD, Bickelman AG. Extreme obesity associated with alveolar hypoventilation—A Pickwickian Syndrome. Am J Med. 21:811, 1956
  3. Sullivan CE, Berthon-Jones M, Issa FG, Eves L. Reversal of obstructive sleep apnea by continuous positive airway pressure applied through the nares. The Lancet. 1981. 317, 8225: 862-865
  4. Pavlova MK, Duffy JF, Shea SA. Polysomnographic Respiratory Abnormalities in Asymptomatic Individuals. SLEEP 2008;31(2):241-248
  5. McCarty DE, Stothard E. Empowered Sleep Apnea: A Handbook for Patients and the People Who Care About Them. Bookbaby Press, 2022.

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