Vagus nerve stimulation
Also Known As: Vagus nerve stimulation, VNS
Vagus, the tenth cranial nerve, arises from the medulla and carries both afferent and efferent fibers. The afferent vagal fibers connect to the nucleus of the solitary tractwhich in turn projects connections to other locations in the central nervous system. Little is understood about exactly how vagal nerve stimulation modulates mood and seizure control but proposed mechanisms include alteration of norepinephrine release by projections of solitary tract to the locus coeruleus, elevated levels of inhibitoryGABA related to vagal stimulation and inhibition of aberrant cortical activity by reticular system activation.
Randomized control trials indicated that thirty-percent of patients would have a greater than fifty-percent reduction of seizures. On average, about fifty-percent of patients experience a forty percent or greater reduction in seizure frequency and severity. About 75% of patients choose to have the battery replaced (continue with the therapy).
In 1997, the United States Food and Drug Administration (FDA) approved the use of VNS as an adjunctive therapy for partial-onset epilepsy. In 2005, the FDA approved the use of VNS for treatment-resistant depression.
Although the use of VNS for refractory depression has been endorsed by the American Psychiatric Association, the FDA's approval of VNS for refractory depression remains controversial. According to Dr. A. John Rush, vice chairman for research in the Department of Psychiatry at the University of Texas Southwestern Medical Center at Dallas, results of the VNS pilot study showed that 40 percent of the treated patients displayed at least a 50 percent or greater improvement in their condition, according to the Hamilton Depression Rating Scale. Many other studies concur that VNS is indeed efficacious in treating depression. However, these findings do not take into account improvements over time in patients without the device. In the only randomized controlled trial VNS failed to perform any better when turned on than in otherwise similar implanted patients whose device was not turned on.