Documentary on Sleep Paralysis this May

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Stephanie Pappas, LiveScience Senior Writer

When filmmaker Carla MacKinnon started waking up several times a week unable to move, with the sense that a disturbing presence was in the room with her, she didn’t call up her local ghost hunter. She got researching. Now, that research is becoming a short film and multiplatform art project exploring the strange and spooky phenomenon of sleep paralysis. The film, supported by the Wellcome Trust and set to screen at the Royal College of Arts in London, will debut in May.

Sleep paralysis happens when people become conscious while their muscles remain in the ultra-relaxed state that prevents them from acting out their dreams. The experience can be quite terrifying, with many people hallucinating a malevolent presence nearby, or even an attacker suffocating them. Surveys put the number of sleep paralysis sufferers between about 5 percent and 60 percent of the population. “I was getting quite a lot of sleep paralysis over the summer, quite frequently, and I became quite interested in what was happening, what medically or scientifically, it was all about,” MacKinnon said.

Her questions led her to talk with psychologists and scientists, as well as to people who experience the phenomenon. Myths and legends about sleep paralysis persist all over the globe, from the incubus and succubus (male and female demons, respectively) of European tales to a pink dolphin-turned-nighttime seducer in Brazil. Some of the stories MacKinnon uncovered reveal why these myths are so chilling.

One man told her about his frequent sleep paralysis episodes, during which he’d experience extremely realistic hallucinations of a young child, skipping around the bed and singing nursery rhymes. Sometimes, the child would sit on his pillow and talk to him. One night, the tot asked the man a personal question. When he refused to answer, the child transformed into a “horrendous demon,” MacKinnon said.

For another man, who had the sleep disorder narcolepsy (which can make sleep paralysis more common), his dream world clashed with the real world in a horrifying way. His sleep paralysis episodes typically included hallucinations that someone else was in his house or his room — he’d hear voices or banging around. One night, he awoke in a paralyzed state and saw a figure in his room as usual. “He suddenly realizes something is different,” MacKinnon said. “He suddenly realizes that he is in sleep paralysis, and his eyes are open, but the person who is in the room is in his room in real life.” The figure was no dream demon, but an actual burglar.

Sleep paralysis experiences are almost certainly behind the myths of the incubus and succubus, demons thought to have sex with unsuspecting humans in their sleep. In many cases, MacKinnon said, the science of sleep paralysis explains these myths. The feeling of suffocating or someone pushing down on the chest that often occurs during sleep paralysis may be a result of the automatic breathing pattern people fall into during sleep. When they become conscious while still in this breathing pattern, people may try to bring their breathing under voluntary control, leading to the feeling of suffocating. Add to that the hallucinations that seem to seep in from the dream world, and it’s no surprise that interpretations lend themselves to demons, ghosts or even alien abduction, MacKinnon said.

What’s more, MacKinnon said, sleep paralysis is more likely when your sleep is disrupted in some way — perhaps because you’ve been traveling, you’re too hot or too cold, or you’re sleeping in an unfamiliar or spooky place. Those tendencies may make it more likely that a person will experience sleep paralysis when already vulnerable to thoughts of ghosts and ghouls. “It’s interesting seeing how these scientific narratives and the more psychoanalytical or psychological narratives can support each other rather than conflict,” MacKinnon said.

Since working on the project, MacKinnon has been able to bring her own sleep paralysis episodes under control — or at least learned to calm herself during them. The trick, she said, is to use episodes like a form of research, by paying attention to details like how her hands feel and what position she’s in. This sort of mindfulness tends to make scary hallucinations blink away, she said. “Rationalizing it is incredibly counterintuitive,” she said. “It took me a really long time to stop believing that it was real, because it feels so incredibly real.”

http://www.livescience.com/28325-spooky-film-explores-sleep-paralysis.html

The brain’s natural valium

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Hitting the wall in the middle of a busy work day is nothing unusual, and a caffeine jolt is all it takes to snap most of us back into action. But people with certain sleep disorders battle a powerful urge to doze throughout the day, even after sleeping 10 hours or more at night. For them, caffeine doesn’t touch the problem, and more potent prescription stimulants aren’t much better. Now, a study with a small group of patients suggests that their condition may have a surprising source: a naturally occurring compound that works on the brain much like the key ingredients in chill pills such as Valium and Xanax.

The condition is known as primary hypersomnia, and it differs from the better known sleep disorder narcolepsy in that patients tend to have more persistent daytime sleepiness instead of sudden “sleep attacks.” The unknown cause and lack of treatment for primary hypersomnia has long frustrated David Rye, a neurologist at Emory University in Atlanta. “A third of our patients are on disability,” he says, “and these are 20- and 30-year-old people.”

Rye and colleagues began the new study with a hunch about what was going on. Several drugs used to treat insomnia promote sleep by targeting receptors for GABA, a neurotransmitter that dampens neural activity. Rye hypothesized that his hypersomnia patients might have some unknown compound in their brains that does something similar, enhancing the activity of so-called GABAA receptors. To try to find this mystery compound, he and his colleagues performed spinal taps on 32 hypersomnia patients and collected cerebrospinal fluid (CSF), the liquid that bathes and insulates the brain and spinal cord. Then they added the patients’ CSF to cells genetically engineered to produce GABAA receptors, and looked for tiny electric currents that would indicate that the receptors had been activated.

In that first pass, nothing happened. However, when the researchers added the CSF and a bit of GABA to the cells, they saw an electrical response that was nearly twice as big as that caused by GABA alone. All of this suggests that the patients’ CSF doesn’t activate GABAA receptors directly, but it does make the receptors almost twice as sensitive to GABA, the researchers report today in Science Translational Medicine. This effect is similar to that of drugs called benzodiazepines, the active ingredients in antianxiety drugs such as Valium. It did not occur when the researchers treated the cells with CSF from people with normal sleep patterns.

Follow-up experiments suggested that the soporific compound in the patients’ CSF is a peptide or small protein, presumably made by the brain, but otherwise its identity remains a mystery.

The idea that endogenous benzodiazepinelike compounds could cause hypersomnia was proposed in the early 1990s by Elio Lugaresi, a pioneering Italian sleep clinician, says Clifford Saper, a neuroscientist at Harvard Medical School in Boston. But several of Lugaresi’s patients later turned out to be taking benzodiazepines, which undermined his argument, and the idea fell out of favor. Saper says the new work makes a “pretty strong case.”

Based on these results, Rye and his colleagues designed a pilot study with seven patients using a drug called flumazenil, which counteracts benzodiazepines and is often used to treat people who overdose on those drugs. After an injection of flumazenil, the patients improved to near-normal levels on several measures of alertness and vigilance, the researchers report. Rye says these effects lasted up to a couple hours.

In hopes of longer-lasting benefits, the researchers persuaded the pharmaceutical company Hoffmann-La Roche, which makes the drug, to donate a powdered form that can be incorporated into dissolvable tablets taken under the tongue and a cream applied to the skin. One 30-something patient has been taking these formulations for 4 years and has improved dramatically, the researchers report in the paper. She has resumed her career as an attorney, from which her hypersomnia had forced her to take a leave of absence.

The findings are “certainly provocative,” Saper says, although they’ll have to be replicated in a larger, double-blind trial to be truly convincing.

Even so, says Phyllis Zee, a neurologist at Northwestern University in Evanston, Illinois: “This gives us a new window into thinking about treatments” for primary hypersomnia. “These patients don’t respond well to stimulants,” Zee says, so a better strategy may be to inhibit the sleep-promoting effects of GABA—or as Rye puts it, releasing the parking brake instead of pressing the accelerator.

The next steps are clear, Rye says: Identify the mystery compound, figure out a faster way to detect it, and conduct a larger clinical trial to test the benefits of flumazenil. However, the researchers first need someone to fund such a study. So far, Rye says, they’ve gotten no takers.

http://news.sciencemag.org/sciencenow/2012/11/putting-themselves-to-sleep.html