Depression, Depressionen

Vagus Nerve Stimulation:

The History of Vagus Nerve Stimulation (VNS)

Another, less invasive means of directly affecting central function is to stimulate the cranial nerves that are direct extensions of the brain. For years, scientists have been interested in whether and how autonomic functions modulate activity in the limbic System and higher cortex. Numerous studies have identified extensive projections of the vagus nerve via its sensory afferent connections in the nucleus tractus solitarius (NTS) to many brain areas (Bailey and Bremer 1938: Dell and Olson 1951; Maclean 1990). As early as 1938, Bailey and Bremer reported that VNS in the cat elicited synchronized activity in the orbital cortex. In 1949, MacLean and Pribram stimulated the vagus nerve and recorded electroencephalograms from the cortical surface of anesthetized monkeys and found inconsistent slow waves generated from the lateral frontal cortex (Maclean 1990, p. 468). Moreover, Dell and Olson (1951) found that VNS evoked a slow-wave response in the anterior rhinal sulcus, as well as in the amygdala, in awake cats with high cervical spinal section.

Reasoning from this body of literature, Zabara demonstrated the anticonvulsant action of VNS on experimental seizures in dogs (Zabara l985a, l985b). Although the vagus is an autonomic nerve, Zabara, basing his conclusions on known anatomy, hypothesized that VNS could prevent or control the motor, autonomic, and conscious components of epilepsy. Interestingly, he also observed that the inhibitory effect on seizures outlasted the VNS period by approximately a factor of four in the acute model, and probably would be much longer in a chronic model. Zabara (1992) initially hypothesized that VNS had two distinct antiepileptic mechanisms of action: 1) a direct inhibition terminating the beginning or ongoing seizure and 2) a long-lasting inhibition that increased with continued periods of stimulation to prevent seizures. Dr. Kiffin Penry (Penry and Dean 1990) and others (Rutecki 1990) ushered in the modern use of VNS with the first human implant for the treatment of epilepsy in 1988