Fibromyalgia is characterized by chronic pain from no clear source. Patients with fibromyalgia frequently have sleep problems: Their deep sleep brain wave patterns are often disrupted by brain waves that correspond to wakefulness. Previous studies have suggested that these irregular wave patterns worsen and may cause the pain. In a new study in Journal of Neurophysiology, researchers constructed a computational model that recreated the sleep patterns observed in patients with fibromyalgia to understand how the abnormal patterns arose.
The research team focused on the molecular targets of sodium oxybate, a drug reported to improve sleep in patients with fibromyalgia. They found that altering the activity of three specific targets—GABAB currents, the potassium leak currents and hyperpolarization-activated thalamic currents—restored sleep patterns in their model. Surprisingly, altering just the potassium leak currents or the hyperpolarization-activated thalamic currents could also restore normal deep sleep wave patterns. According to the researchers, drugs acting on one of these targets in the thalamus, a region in the brain that regulates sleep, might be enough to prevent disrupted sleep and its related adverse effects and provide relief to patients with fibromyalgia. In addition, "since no animal models of fibromyalgia exist, our model provides a much-needed tool for understanding what makes current fibromyalgia drugs efficacious and for finding more effective drugs," the researchers wrote.