The polyvagal perspective

Abstract

The polyvagal theory introduced a new perspective relating autonomic function to behavior, that included an appreciation of the autonomic nervous system as a "system," the identification of neural circuits involved in the regulation of autonomic state, and an interpretation of autonomic reactivity as adaptive within the context of the phylogeny of the vertebrate autonomic nervous system. The paper has two objectives: first, to provide an explicit statement of the theory; and second, to introduce the features of a polyvagal perspective. The polyvagal perspective emphasizes how an understanding of neurophysiological mechanisms and phylogenetic shifts in neural regulation leads to different questions, paradigms, explanations, and conclusions regarding autonomic function in biobehavioral processes than peripheral models. Foremost, the polyvagal perspective emphasizes the importance of phylogenetic changes in the neural structures regulating the autonomic nervous system and how these phylogenetic shifts provide insights into the adaptive function and the neural regulation of the two vagal systems.

Figures

Figure 1. Phylogenetic stages of the Polyvagal Theory

Figure 2. The Social Engagement System

Social communication is determined by the cortical regulation of medullary nuclei via corticobulbar pathways. The Social Engagement System consists of a somatomotor compnent (i.e., special visceral effernt pathways that regulate the striated muscles of the face and head) and a visceromotor component (i.e., the myelinated vagus that regulates the heart and bronchi). Solid blocks indicate the somatomotor component. Dashed blocks indicate the visceromotor component.

Figure 3. Atropine sulfate dose response curve

HP (heart period in msec), RSA (respiratory sinus arrhythmia amplitude in ln msec2) and LF(low frequency amplitude ln msec2). Atropine dose is per 75 kg of body weight. A placebo was used for the 0 mg dose.

Figure 4. Atropine sulfate dose response curve: Size of effect

Cohen’s d is calculated for the effect size for each variable contrasting placebo condition (0 mg) with each of the four doses.