Nov 3 2008
Scientists at the American Academy of Sleep Medicine have linked insomnia to a neurochemical abnormality in the brain.
In a study which examined primary insomnia in young and middle-aged adults a specific neurochemical difference was seen in the brains of the participants.
The new study, which is the first one to link a specific neurochemical abnormality with insomnia, found that gamma-aminobutyric acid (GABA), the most common inhibitory transmitter in the brain, is reduced by nearly 30% in people who have been suffering from primary insomnia for more than six months.
Primary or chronic insomnia, affects about 10% of all adults in industrialized countries and is the most common sleep disorder - symptoms usually last for at least a month and while most often insomnia is present with another medical illness, mental disorder or sleep disorder, or associated with certain medications or substances, approximately 25% of people suffering from insomnia are considered to have primary insomnia, which is defined as a difficulty falling asleep or maintaining sleep with no coexisting conditions.
The researchers 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.
Lead researcher Dr. John Winkelman of Brigham and Women's Hospital says that GABA is reduced in the brain of individuals with insomnia, suggesting overactivity is present not only at the level of excessive thoughts and emotions, but can also be detected at the level of the nervous system.
Dr. Winkelman says GABA decreases overall activity in many brain areas, helping the brain to "shut down" and having a "racing mind" and an inability to shut down at night is a common complaint of people with primary insomnia.
According to Winkelman, the recognition that primary insomnia is associated with a specific neurochemical deficiency helps validate the often misunderstood complaint of insomnia - he says understanding that insomnia has manifestations in the brain shows that insomnia is not just a phenomenon observed at night, but has daytime consequences for energy, concentration and mood.
The study involved included 8 men and 8 women, age 25 to 55 years who were free of medical and sleep disorders, as well as anxiety and mood disorders, and who were not taking prescription medication.
The participants had difficulty initiating or maintaining sleep resulting in daytime distress or dysfunction for a period of at least six months - the average duration of participants' symptoms was 10 years.
Data was collected and actigraphs and overnight polysomnographs carried out and proton magnetic resonance spectroscopy (1H-MRS) used to determine GABA levels - the study also included a well-matched control group consisting of seven women and nine men.
After adjusting for age, body mass index (BMI) and gender, significant correlations were found between GABA levels and both subjective and objective sleep measures - in subjects with primary insomnia, sleep continuity was strongly associated with GABA levels.
According to the study, reductions in brain GABA levels have also been seen in people suffering from depression and anxiety - they say insomnia shares many features with such disorders, including sleep disturbance, elevation in anxiety, and impairments in concentration and energy.
They also say insomnia is an important risk factor for incident mood and anxiety disorders and suggest the possibility that GABA deficiencies seen in people with mood and anxiety disorders may be based on disturbances in sleep.
The study says many of the hypnotic medications that are most effective in treating insomnia are benzodiazepine receptor antagonists (BzRAs), which increase activity at the GABA neurons and new guideline for the management of chronic insomnia in adults from the Academy suggest that hypnotic treatment should be supplemented with behavioral and cognitive therapies whenever possible.
The study is published in the current in the issue of the journal Sleep.