A research team at the Department of Mathematics of Boston University in collaboration with the divisions of Sleep Medicine, Endocrinology, Diabetes and Hypertension from the Brigham and Women’s Hospital identified a potential target to restore normal sleep in patients with fibromyalgia (FM). The study entitled “Thalamic Mechanisms Underlying Alpha-Delta Sleep with Implications for Fibromyalgia” was published August 5, 2015 in Journal of Neurophysiology.
Fibromyalgia is a syndrome characterized by chronic widespread pain from an unidentified source. Patients with fibromyalgia also have chronic daytime fatigue and sleep disturbances. Previous studies indicate that sleep and pain are associated, supporting the role of sleep disruption in the development of fibromyalgia symptoms.
When healthy, middle-aged women were sleep deprived for three days, they showed a decreased tolerance for pain and increased fatigue similar to fibromyalgia patients. Researchers have also reported that fibromyalgia is associated with an alteration of slow wave sleep, the deepest stage of sleep characterized by delta waves in an electroencephalogram (ECG). In FM patients, there is an interference of brain alpha waves, known as alpha activity, typical of wakefulness. Since there are no available animal models of fibromyalgia to address drug’s efficacy and their effect in sleep disturbances, this research team established a biophysically-based mathematical model.
They based their model in the neural abnormalities observed in fibromyalgia and in the molecular targets of drugs reported to improve patients’ sleep. Using this model, the team addressed the interference of alpha activity into the delta activity that occurs normally during slow wave sleep. By focusing their model on sodium oxybate, they found that altering the activity of its targets—GABAB receptor-activated currents, the potassium leak currents and hyperpolarization-activated thalamic currents—restored normal sleep patterns. They further concluded that changing just the potassium leak currents or the hyperpolarization-activated thalamic currents was sufficient to restore normal deep sleep.
These results suggest the potential of drugs acting on one of such targets in the thalamus, a brain region that regulates sleep, to prevent disrupted sleep and fatigue in patients with fibromyalgia.
It is still unclear how the interference of alpha activity in delta sleep causes pain in fibromyalgia patients. One of the functions of delta sleep is to decrease the intensity of the interaction between neurons involved in pain transmission. Therefore, normal downscaling of intensity may not occur in fibromyalgia patients due to the disruption of normal delta activity by alpha activity. Future studies using EEG may further explain why alpha-delta activity could have deleterious effects in fibromyalgia patients.
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