Potential for Transcutaneous Vagus Nerve Stimulation in Pain Management

Abstract

ISSN 1758-1869 10.2217/PMT.11.27 © 2011 Future Medicine Ltd Pain Manage. (2011) 1(4), 287–289 Currently available therapeutic interven‐ tions for chronic pain disorders are less than ideal. For this reason, new interven‐ tion strategies complementing existing therapeutical approaches are urgently needed. In this context, neurostimulation methods may represent potential success‐ ful tools for managing clinical pain syn‐ dromes. Besides transcranial magnetic stimulation, vagus nerve stimulation (VNS) may open a window for a new pain‐relieving treatment method. Interestingly, the anatomy and physio‐ logy of the vagus nerve (X cranial) is com‐ plex and until recently not well character‐ ized. The vagus nerve was traditionally considered as a purely parasympathetic efferent nerve. However, recent work dem‐ onstrates that approximately 80% of the nerve fibers in the cervical nerve are affer‐ ent fibers [1]. These afferent sensory fibers project via the nucleus tractus solitarius to a variety of distinct brain areas, thereby rep‐ resenting an avenue for providing informa‐ tion into the CNS [2]. In detail, the nucleus tractus solitarius relays information to the parabrachial nucleus, the cerebellum, the periaqueductal gray and via ascending secondary projections to limbic areas such as the amygdalae as well as to paralimbic and cortical regions. This anatomically grounded bottom‐up way of stimulation led to the successful introduction of VNS as a neurostimulation modality affecting the limbic system and thereby associated neuropsychiatric diseases such as epilepsy and treatment‐resistant depression. Based on this potential to reach brain areas such as the periaqueductal gray, thalamic nuclei or limbic areas, which are closely involved in pain processing, it was hypothesized that VNS may bear antinoci‐ ceptive qualities [3]. In fact, neuroimaging studies using SPECT, PET and functional MRI techniques provided additional evi‐ dence that VNS changes cerebral activity in pain‐processing cortical and subcorti‐ cal regions like the dorsal‐rostral medulla, bilateral thalamus, right postcentral gyrus or the anterior cingulate cortex [4]. For this reason, most arguments favor a potential central mode of VNS antinociception, complemented by peripheral mechanisms such as a modulation of primary afferent nociceptors [5]. In this context, animal studies have demonstrated an inhibitory effect of VNS on the electric response of spinal