Medical Discovery News
By Norbert Herzog and David Niesel
"And when he saw her looking so lovely in her sleep, he could not turn away his eyes; and presently he stooped and kissed her, and she awaked, and opened her eyes, and looked very kindly on him.”
So the Grimm Brothers ended their tale of “The Sleeping Beauty.” But for people suffering from primary hypersomnia, life is no fairy tale. Fortunately, they may have found a fairy godmother in the form of a neurologist named David Rye, M.D.
Hypersomnia causes symptoms such as difficulty waking up from a long sleep, an increased need for sleep during the day even when working or engaged in a task, no relief from daytime naps, and a pattern of sleeping 14-18 hours per day. Hypersomnia is different from narcolepsy in that it does not come on suddenly and patients do not fall completely asleep, but function in a half-awake state. It is also quite rare.
Rye and his colleagues at Emory University in Atlanta have discovered a possible cause of hypersomnia. Certain drugs such as Valium or Xanax cause sleepiness by stimulating receptors for a chemical in the brain called gamma-amino butyric acid, or GABA. As a result, when this chemical is absorbed through receptors, it inhibits activity in the brain, slowing down functions in a way that leads to sleep. The scientists hypothesized that there might be a substance in the cerebral spinal fluid — CSF — of hypersomnia patients that also stimulates these receptors, leading to excessive sleepiness.
They collected CSF samples from 32 people with hypersomnia and from a control group of those without the disorder. This CSF fluid was added to cells that had been engineered with GABA receptors and could produce electrical activity. Scientists hoped to measure the absorption of GABA through the amount of electricity the engineered cells gave off when receptors were activated. At first, nothing happened. Then the scientists added a little GABA to the mix. Suddenly, the electric signals were twice as strong! The CSF from hypersomnia patients caused the receptors of engineered cells to be twice as sensitive to GABA. This suggests that hypersomnia patients have something in their CSF that enhances the effects of GABA, therefore dampening brain function.
Rye didn’t know what this special something in the CSF of hypersomnia patients was, but guessed that it might be a small protein made in the brain. So he created another study with a treatment in mind. Seven hypersomnia patients were injected with a drug called flumazenil, which is used to treat overdoses of Valium and related drugs. Rye thought that since hypersomnia patients’ brains act as if they are on such sedatives, why not try giving them an antidote? It worked – patients’ symptoms were reduced and they were more alert and vigil for up to a couple of hours.
The next step is to conduct a bigger study to verify these exciting findings and identify the cause of hypersomnia. This is the first real hope for a treatment for hypersomnia; after all, a kiss from a prince is hard to come by.
Professors Norbert Herzog and David Niesel are biomedical scientists at the University of Texas Medical Branch. Learn more at medicaldiscoverynews.com.