Sleep was consuming Anna Sumner’s life. Her yearning for sleep first emerged in the early 1990s when she was a high school senior. Later, as a Princeton undergraduate, she alarmed her parents by spending large chunks of the holidays at home in bed, asleep.
Her flexible schedule, which continued through law school at Duke, allowed her to conceal her prodigious sleep needs from herself and others. Still, she knew something was badly wrong: Regularly forgoing breakfast or a shower to gain a few extra minutes of shut-eye and sleeping away a friend’s wedding after traveling cross country for the event just weren’t normal behaviors.
The demands of the workforce finally forced a reckoning. By the time Anna sought me out at Emory University’s Sleep Center in 2005, she was devoting at least 12 hours a day to sleep. Yet it never felt like enough. Her cravings for sleep rivaled an addict’s compulsions for a fix.
The generic name for Anna’s persistent sleepiness, which no amount of sleep could erase, is hypersomnia. More colorful terms include the German Schlaftrunkenheit and the French ivresse de sommeil, both of which translate as “sleep drunkenness,” a moniker that captures the insatiable sleep needs of the hypersomniac and the blackouts and hangovers that follow.
For most people, whatever brain fog, or sleep inertia, that lingers after a good night’s sleep burns off quickly. Hypersomniacs, in contrast, resort to extraordinary means to clear the fog: multiple alarm clocks, some outfitted with sonic booms; phantasmagorical flying or crawling contraptions designed to coax their woozy owners into moving; or even physical harassment from a roommate or a visiting nurse. Nothing less would work.
As one hypersomniac put it, “I don’t take naps. I take comas.”
Examining Anna, our care team ruled out common causes for hypersomnia, including medications, illicit drugs, anemia, depression and sleep apnea, as well as deficiencies of thyroid hormones, vitamin B12 or iron. Capitulating to the reality that the cause of her condition was unknown, we diagnosed her with idiopathic hypersomnia.
I prescribed the default drugs that boost brain concentrations of wake-promoting neurotransmitters, such as dopamine and noradrenaline. These helped briefly, but it wasn’t long before Anna’s tolerance for the medications prompted higher dosages, and she experienced side effects including twitchiness, elevated blood pressure and a diminished appetite.
Then things began to unravel. At least once each week, Anna would sleep for 30 straight hours; during one stretch, she topped out at 53 hours. She awoke from these sleeping marathons like Rip van Winkle, befuddled as to the time or date.
A Permanent Anesthetic?
Anna’s condition defied conventional wisdom. I was taught to approach hypersomnia as an inability to stay awake; such loss of function, it logically followed, originated from a deficiency of wake-promoting neurochemicals. In other words, there was not enough gas in the car.
But Anna’s extreme condition forced me to depart from conventional wisdom. What if her extraordinary need for sleep were caused not by an absence of wakefulness, but by the presence of sleepiness induced by some other biochemical agent — the Sandman’s mythical dust?
If so, then bathing Anna’s brain with high doses of wake-promoting drugs would be like flooring the gas pedal with the parking brake engaged. Such a strategy might bring physical alertness — as evidenced by the twitchiness and high blood pressure caused by the medications we prescribed her — but a disabling mental dullness lingered.