ABSTRACT
Stimulation of the vagal nerve was shown in the 1960s to influence EEG activity in laboratory animals,1,2 and in 1972 by Zabara to block induced vomiting in a dog.3
Zabara subsequently demonstrated that stimulation of the left vagal nerve controlled seizures induced in dogs with intravenous phenylenetetrazol.4 A similar effect was shown by others in different animal models of epilepsy.5-8 The left vagal nerve was used because its fibers are predominantly afferent. Following an open pilot study of 16 refractory patients,9 two doubleblinded, active control studies in patients at least 12 years old with intractable partial seizures showed the efficacy of vagal nerve stimulation (VNS).10,11 In the long-term studies and in postapproval reports, the number of patients with at least a 50 per cent reduction in seizures approaches 50 per cent.12,13
The mechanism of action of VNS is poorly understood. Fos staining of rats undergoing VNS demonstrates synaptic activation of thalamus, hypothalamus and amygdala, areas that can inhibit epileptic discharges.14
Efficacy of the VNS in rats is lost if the nucleus ceruleus is chemically ablated.15 PET in humans has shown changes in blood flow to specific forebrain and brainstem nuclei.16 There was a correlation between the alteration of blood flow in the thalamus and suppression of
