Skip to main content
. Author manuscript; available in PMC: 2015 Sep 1.
Published in final edited form as: J Fluency Disord. 2014 Jul 6;0:12–31. doi: 10.1016/j.jfludis.2014.06.002

Table 1.

Phylogentic stages of the Polyvagal Theory, with I = earliest phylogenetically developed and III = most recent phylogenetically developed (after Figure 1, Porges, 2007).

Behavioral function Physiological action ANS component
III Social communication, self-soothing and calming, inhibits “arousal” Parasympathetic activity mediated by vagal pathways to the heart producing increases in RSA, slowing heart rate, and dampening sympathetic reactivity (i.e., vagal brake). Myelinated vagal pathways originating in nucleus ambiguus (i.e., ventral vagal complex)
II Mobilization (active avoidance), fight-flight behaviors Withdrawal of the vagal brake followed by sympathetic and endocrine activation to increase metabolic output (observed as increases in SCL) (see Dale et al., 2011) Sympathetic neural pathways with ganglion paralleling the spinal cord and a neuroendocrine regulated adrenal system producing catecholamines and cortisol
I Immobilization (death feigning, passive avoidance) Parasympathetic activity mediated by vagal pathways to the heart and primarily to subdiaphragmatic organs (e.g., gut) producing cessations of breathing, large drops in heart rate and blood pressure potentially causing vasovagal syncope (i.e., fainting) Unmyelinated vagal pathways originating in the dorsal motor nucleus of the vagus (i.e, dorsal vagal complex)