A small study is demonstrates a specific neurochemical abnormality in adults with primary insomnia, providing greater insight to the limited understanding of the condition’s pathology.
Primary insomnia is sleeplessness that cannot be attributed to an existing medial, psychiatric or environmental cause. Secondary insomnia is when symptoms of insomnia arise from a primary medical illness, mental disorders or other sleep disorders.
The research results indicate that gamma-aminobutyric acid (GABA), a naturally occurring neurotransmitter that inhibits the activity of certain nerve systems, is reduced by nearly 30 percent in individuals who suffer from primary insomnia for more than six months.
These findings suggest that primary insomnia is a manifestation of a neurobiological state of hyperarousal, which is present during both waking and sleep at physiological and cognitive levels.
According to principal investigator Dr. John Winkelman, the recognition that primary insomnia is associated with a specific neurochemical deficiency helps validate the often misunderstood complaint of insomnia.
“Recognition that insomnia has manifestations in the brain may increase the legitimacy of those who have insomnia and report substantial daytime consequences,” he said. “Insomnia is not just a phenomenon observed at night, but has daytime consequences for energy, concentration and mood.”
The study included 16 non-medicated individuals (eight of whom were women) with primary insomnia and 16 individuals (seven women) who were deemed normal sleepers. Global brain GABA levels were measured in both groups. Primary insomnia was established through clinical interviews, sleep diary, actigraphy use and polysomnograpy.
References:
1. John Winkelman, et al. Reduced brain GABA in primary insomnia: preliminary data from 4T proton magnetic resonance spectroscopy (1H-MRS). American Academy of Sleep Medicine. Abstract ID: 0768.
2. Image by louise-knight.
