Insomnia and the Sleep Switch

So what exactly is the “sleep switch,” and how might it figure in insomnia?

This sleep-regulating center in the brain was actually discovered almost 100 years ago.

sleep-attackSo what exactly is the “sleep switch,” and how might it figure in insomnia?

The findings of Dr. Constantin Von Economo, who autopsied victims of sleeping sickness in the 1920s, were prescient. Researchers who went on to study the brains of rats and other lab animals confirmed his theory of a “sleep regulating center” in the brain. While damage to the rear of the hypothalamus sent the animals into a coma, damage to the front gave them a terrific case of insomnia.

Clearly some very important processes took place in the front and rear areas of the hypothalamus, a grape-sized structure deep in the brain.

Sleep Switch at the Front

The front part of the hypothalamus is now known to contain a small cluster of neurons called the VLPO, and they produce GABA and galanin, neurochemicals highly conducive to sleep.

These neurons are mostly off-duty during the daytime. But at night they come alive. When sleep pressure builds up high enough, the VLPO neurons start firing away like mad. Current theory holds that they’re powerful enough to shut the rest of the brain down, in essence functioning like a “sleep switch.”

Alerting Force in the Rear

At the rear of the hypothalamus is an important set of neurons that have the opposite effect: when they’re firing, they help keep you awake. They produce a substance called orexin, and they function “like a ‘finger’ on the (sleep) switch that might prevent unwanted transitions to sleep,” sleep scientist Clifford Saper has said.

The sleep-friendly neurons in the VLPO work to “tranquilize” the orexin neurons at night. But people with a substantial loss of orexin neurons experience narcolepsy. Narcoleptics have irresistible sleep attacks during the day and they also have trouble staying asleep at night. The trusty “finger” on the sleep switch, which helps to maintain a stable waking state, just isn’t there.

How This Relates to Insomnia

A deterioration of orexin neurons may also be a factor in the insomnia of older adults, Saper has hypothesized. Like narcoleptics, older adults tend to nap a lot during the daytime and have frequent wake-ups at night.

A causal factor of insomnia in younger adults, on the other hand, could be a reduced number of GABA neurons in the brain, or an overabundance of orexin neurons. Either condition could interfere with the sleep switch enabling quick, easy transitions to sleep.

These theories aren’t of practical value yet. But stay tuned. The FDA is reviewing a completely new insomnia medication – the first ever “orexin receptor antagonist” – right now.

A Sleep Switch in the Brain

“Scientists Report the Discovery of a Brain ‘Switch’ That Brings On Sleep,” announced the headline of a New York Times article on January 12, 1996. The news marked the beginning of my quest to get to the bottom of my insomnia.

sleep switch“Scientists Report the Discovery of a Brain ‘Switch’ That Brings On Sleep,” announced the headline of a New York Times article on January 12, 1996. The news marked the beginning of my quest to get to the bottom of my insomnia.

“A master switching mechanism for sleep,” I read, “a tiny clump of cells deep in the brain,” in a structure called the hypothalamus. When the switch flipped on, the lights went out. I paused a moment to consider this fascinating tidbit, then read on.

The newly discovered sleep switch turned the lights out pronto. It should not be confused with the process that started people on the somnolent slide. That involved a different mechanism (undiscovered, as yet), a kind of “dimmer switch,” reporter Sandra Blakeslee wrote.

Could the sleep switch be a factor in my insomnia? I wondered. Unlike me, my husband had prodigious ability to fall asleep the minute he lay down or settled himself on an airplane. Was he endowed with a BMW model sleep switch and I, a rusty Ford?

In subsequent years it’s become clear that the sleep switch is one of the most important discoveries in sleep science to occur in the past few decades, and the way it functions does in fact affect people’s sleep.

A Sleep Regulating Center in the Brain

But the idea of a sleep center in the brain was originally proposed nearly a century ago in a context very different from the studies on rats and other lab animals that ultimately proved its existence. It came about during the epidemic of encephalitis lethargica (a kind of sleeping sickness that occurred concurrently with the influenza epidemic) that broke out in the United States and Europe toward the end of World War I. Encephalitis lethargica eventually sent half a million people to early graves.

Disrupted sleep was a common symptom. Some victims fell into a coma-like stupor that persisted for years and sometimes ended in death. A smaller number had the opposite problem. They became very tired but could barely sleep at all. (Sounds familiar, right?) Some of these people with severe insomnia also died.

Dr. Constantin Von Economo, a Viennese neurologist, treated thousands of patients afflicted with the disease. He also autopsied many of his patients who died. And he found a curious thing: in the brains of those who had fallen into a stupor, there was damage at the rear of the hypothalamus; the hypothalamus of those afflicted with insomnia was similarly damaged in the front.

What to make of this information? Von Economo proposed that there was a “sleep regulating center” in the hypothalamus. He was not far off the mark, as will be seen in Monday’s blog.