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In Some Insomnia Patients, Brain Just Won't Shut Down

HealthDay news imageTUESDAY, June 9 (HealthDay News) -- Adults with primary insomnia have a neurochemical abnormality that makes it difficult to "shut down" the mind at night for sleep, new research has found.

Researchers measured the levels of gamma-aminobutyric acid (GABA) in 16 adult men and women with primary insomnia and 16 men and women deemed normal sleepers.

Primary insomnia is difficulty falling sleep or staying asleep at night for over a period of at least one month, according to the American Academy of Sleep Medicine. Unlike most cases of insomnia, primary insomnia can't be attributed to a psychiatric, medical or environmental cause.

The new study found that people who had suffered from primary insomnia for more than six months had 30 percent lower levels of GABA.

GABA, the most common inhibitory transmitter in the brain, slows overall activity in many brain areas.

The research was to be presented June 9 at the annual meeting of the Associated Professional Sleep Societies, in Seattle.

The findings suggest that primary insomnia is the result of a neurobiological state of hyperarousal, and that this state remains throughout the day and night, affecting the individual's mind and body, according to a news release from the American Academy of Sleep Medicine. About one-quarter of people with insomnia have this type, the Academy stated.

Understanding that primary insomnia is associated with a specific neurochemical deficiency helps validate the often-misunderstood complaint of insomnia, explained lead study author Dr. John Winkelman of Brigham and Women's Hospital at Harvard Medical School in Boston.

"Recognition that insomnia has manifestations in the brain may increase the legitimacy of those who have insomnia and report substantial daytime consequences," Winkelman said. "Insomnia is not just a phenomenon observed at night, but has daytime consequences for energy, concentration and mood."


SOURCE: American Academy of Sleep Medicine, news release, June 9, 2009

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