The pharmaceutical approach to treating anxiety and anxiety disorders is widely used (George et al., 2008). 

In cases where the patient may be resistant to pharmacotherapy treatment or due to the potential of adverse events with short- or long-term use of pharmaceuticals, alternative treatments are considered, for example, vagus nerve (VN) stimulation (George et al., 2008).

The VN acts as a highways for information traveling to various regions of the brain associated with the perception and manifestation of somatic and cognitive symptoms characteristic with anxiety disorders (locus coeruleus, orbitofrontal cortex, insula, hippocampus, thalamus, brainstem, and amygdala).

Stimulating the afferent fibers of the VN sends signals that terminate in the nucleus solitary tract (NTS). From the NTS, the information travels to the locus coeruleus, which is  the primary site of all norepinephrine fibers within the brain (George et al., 2008). 

Norepinephrine (NE) and serotonin are important neurotransmitters involved in the pathogenesis and regulation of mood and anxiety. The VN has been shown to  increase the turnover of serotonin and NE (George et al., 2008). 

These patients with treatment-resistant anxiety disorders generally tolerated VNS treatment, and there was evidence of acute and long-term improvement in some patients.  Although well tolerated, VNS treatment was associated with only modest symptomatic improvement during acute treatment (George et al., 2008).