Vagus Nerve Stimulation

Vagus nerve stimulation (VNS) has been commercially available in the United States with an indication for treatment-resistant partial onset seizures in epilepsy since 1997. VNS is achieved in the NCP system (Cyberonics, Houston) by coiling an electrode around the left vagus nerve in the neck near the carotid artery. A subcutaneous line connects the stimulating electrode to a bipolar pulse generator implanted in the left chest wall. The vagus nerve is composed of 80 percent afferent sensory fibers. These sensory fibers terminate in the nucleus tractus solitarus (NTS). The NTS sends information to the forebrain, hypothalamus, and thalamus through the LC and parabrachial nucleus (George et al., 2000). Animal studies have demonstrated that the LC must be intact for VNS to achieve an anticonvulsant effect (Krahl et al., 1998). The role of the LC in the treatment of depression with medications has been noted above. Brain imaging studies in epilepsy patients have shown VNS to cause an initial increase in the perfusion of the rostral medulla, hypothalamus, and thalamus bilaterally and a decrease at the hippocampus, amygdala, and posterior cingulate gyri bilaterally (Henry et al., 1998). The decrease in perfusion of the hippocampus and amygdala has been shown to be present after 6 months with chronic VNS (Van Laere et al., 2002). The decrease in perfusion to the hippocampus has been reported to differentiate a response to an active drug in the treatment of depression from a placebo response (Mayberg et al., 2002).

The first observations of the positive effect of VNS on mood were in epilepsy patients. Improvements in overall well-being were reported by the patients that were not entirely explained by improvements in seizure frequency (Handforth et al., 1998). In a study of 30 nonepileptic patients with treatment-resistant depression, a response rate of 40 percent was obtained with 10 weeks of VNS (Rush et al., 2000). These improvements were shown to be stable over a 1-year period on the same 30 patients with 91 percent of the original responders continuing to show a response with continued VNS. Of the 18 original nonresponders 41 percent showed a response at 6 months of VNS (Marangell et al., 2002). The most frequent side effect was voice alteration in 21 percent of the patients. No patient discontinued due to clear adverse effects, even though one patient elected to be explanted after failure to respond following 1 year of therapy, which may have been due to VNS-induced dysphoric hypomania.

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