Figure 3

Schematic representation of the theoretic reflex-based "somatovisceral disease" model put forth by Korr and others around the middle of the century [3-12].

This theory maintained that afferent nociceptive signals generated by dysfunction involving various paraspinal somatic structures, once having arrived in the central nervous system, then acted to facilitate the activities of segmentally related somatomotor as well as visceromotor (autonomic) neuronal cell bodies. These reflex-induced increases in autonomic activity, particularly that of the sympathetic division, were then postulated to induce pathophysiologic vasoconstriction responses in their respective segmentally-correlated internal organs. The states of ischemia thought to be produced by this somato-visceral "vasoconstrictor attack" were then presumed to lead to the eventual demise of any organs which might be susceptible to them.

Admittedly, such reflexbased theories certainly represented a substantial improvement over the "pinched nerve" notions which preceded them (see Figure 1). However, since that time, major scientific advances regarding the roles that the autonomic nervous system is now known to play in both health and disease have made the existence of a segmentally-related "somato-visceral disease" mechanism far less tenable than it might have seemed when Korr and others first envisioned it more than fifty years ago.