The Polyvagal theory (gr. 'polus', “‘many’” + 'vagal', "'vagus nerve'") is a theory that posits that the Vagus nerve is interconnected with and sensitive to influences that flow from the body toward the brain.

Phylogenetic subsystems/stagesEdit

The vagus nerve is a primary component of the autonomic nervous system. Polyvagal theory outlines the structure and function of the two distinct branches of the vagus, both of which originate in the medulla.[1] More specifically, each branch is associated with a different adaptive behavioural strategy, both of which are inhibitory in nature via the parasympathetic nervous system. The vagal system is in opposition to the sympathetic-adrenal system, which is involved in mobilization behaviours. According to polyvagal theory, these opposing systems are phylogenetically arranged.[1]


The vagus, or tenth cranial nerve serves to identify the relationship between visceral experiences and the vagus nerve's parasympathetic control of the heart, lungs, and digestive tract. The theory was introduced in 1994 by Dr. Stephen Porges, director of the Brain-Body Center at the University of Illinois at Chicago. According to the theory and its increasing evidence base[2], the autonomic nervous system is interconnected with and sensitive to influences that flow from the body toward the brain, called afferent influences. This effect has been observed and demonstrated by adaptive reactivity dependent on the neural circuits' phylogenetical development. It builds on the study of what Charles Darwin referred to as the “pneumogastric nerve." The polyvagal theory claims that humans have physical reactions, such as cardiac and digestive changes, associated with their facial expressions[2]. Porges argues this theory with observations from both evolutionary biology and neurology.

The branches of the vagal nerve serve different evolutionary stress responses in mammals: the more primitive branch elicits immobilization behaviors (e.g., feigning death), whereas the more evolved branch is linked to social communication and self-soothing behaviors. These functions follow a phylogenetic hierarchy, where the most primitive systems are activated only when the more evolved functions fail. These neural pathways regulate autonomic state and the expression of emotional and social behaviour. Thus, according to this theory, physiological state dictates the range of behaviour and psychological experience. Polyvagal theory has many implications for the study of stress, emotion, and social behaviour, which has traditionally utilized more peripheral indices of arousal, such as heart rate and cortisol level. The measurement of vagal tone in humans has become a novel index of stress vulnerability and reactivity in many studies of populations with affective disorders.

The dorsal vagal complex (DVC)Edit

The dorsal branch of the vagus originates in the dorsal motor nucleus and is considered the phylogenetically older branch.[3] This branch is unmyelinated and exists in most vertebrates. This branch is also known as the “vegetative vagus” because it is associated with primal survival strategies of primitive vertebrates, reptiles, and amphibians.[3] Under great stress, these animals “freeze” when threatened, conserving their metabolic resources.

The DVC provides primary control of subdiaphragmatic visceral organs, such as the digestive tract. Under normal conditions, the DVC maintains regulation of these digestive processes. However, prolonged disinhibition can be lethal for mammals, as it results in apnea and bradycardia.[1]

The ventral vagal complex (VVC)Edit

With increased neural complexity seen in mammals (due to phylogenetic development) evolved a more sophisticated system to enrich behavioral and affective responses to an increasingly complex environment.[1] The ventral branch of the vagus originates in the nucleus ambiguus and is myelinated to provide more control and speed in responding.[1] This branch is also known as the “smart vagus” because it is associated with the regulation of sympathetic “fight or flight” behaviors in the service of social affiliative behaviors.[3] These behaviors include social communication and self-soothing and calming.[1] In other words, this branch of the vagus can inhibit or disinhibit defensive limbic circuits, depending on the situation. The VVC provides primary control of supradiaphragmatic visceral organs, such as the esophagus, bronchi, pharynx, and larynx. The VVC also exerts important influence on the heart. When vagal tone to the heart’s pacemaker is high, a baseline or resting heart rate is produced. In other words, the vagus acts as a restraint, or brake, limiting heart rate. However, when vagal tone is removed, there is little inhibition to the pacemaker, and so rapid mobilization (“fight/flight”) can be activated in times of stress, but without having to engage the sympathetic-adrenal system, as activation comes at a severe biological cost.[1]

Vagal tone: a physiological marker of stressEdit

In order to maintain homeostasis, the central nervous system responds constantly, via neural feedback, to environmental cues. Stressful events disrupt the rhythmic structure of autonomic states, and subsequently, behaviors. Since the vagus plays such an integral role in the peripheral nervous system via regulation of heart rate, it follows that the amplitude of respiratory sinus arrhythmia (RSA) is a good index of parasympathetic nervous system activity via the cardiac vagus.[4] That is, RSA is a measurable, noninvasive way to see how the vagus modulates heart rate activity in response to stress. This method is useful to measure individual differences in stress reactivity.

RSA is the widely used measure of the amplitude of heart rate rhythm associated with rate of spontaneous breathing.[5] Research has shown that amplitude of RSA is an accurate indicator of the efferent influence of the vagus on the heart.[5] Since inhibitory effects of the VVC branch of the vagus allow for a wide range of adaptive, prosocial behaviors, it has been theorized that individuals with greater vagal tone are able to exhibit a greater range of such behaviors. On the other hand, decreased vagal tone is associated with illnesses and medical complications that compromise the CNS.[5] These complications may reduce one's capacity to respond to stress appropriately.

Clinical applications of polyvagal theory and vagal toneEdit

Vagal tone has been used in medical and psychological research to better understand the physiological underpinnings of various disorders[6].

Clinical applications in the human fetusEdit

Healthy human fetuses have a high variability in heart rate, which is mediated by the vagus.[7] On the other hand, heart rate decelerations, which are also mediated by the vagus, are a sign of fetal distress. More specifically, prolonged withdrawal of vagal influence on the heart creates a physiological vulnerability to the influence of the Dorsal Vagal Control, which in turn produces bradycardia (very low heart rate). However, the onset of this deceleration is commonly preceded by transitory tachycardia, which is reflective of the immediate effects of Ventral Vagal Control withdrawal.

Results of Porges' TheoryEdit

As described by Bessel van der Kolk, professor of psychiatry at the Boston University School of Medicine:[8]

The Polyvagal Theory provided us with a more sophisticated understanding of the biology of safety and danger, one based on the subtle interplay between the visceral experiences of our own bodies and the voices and faces of the people around us. It explains why a kind face or a soothing tone of voice can dramatically alter the way we feel. It clarifies why knowing that we are seen and heard by the important people in our lives can make us feel calm and safe, and why being ignored or dismissed can precipitate rage reactions or mental collapse. It helped us understand why attuning with another person can shift us out of disorganized and fearful states. In short, Porges’s theory makes us look beyond the effects of fight or flight and put social relationships front and centre in our understanding of trauma. It also suggested new approaches to healing that focus on strengthening the body’s system for regulating arousal.

Frank M. CorriganEdit

In 2011, Frank M. Corrigan and colleagues published Neurobiology and Treatment of Traumatic Dissociation Toward an Embodied Self, in which they added flight and feign polyvagal responses to Porges' work. Unlike previous work, they tagged the dissociative disorders using PET and fMRI rather than relying on subjective measures.[9]


Critics of the polyvagal theory point out that it's premises are not supported by scientific research. Prof. Paul Grossman of University Hospital Basel argues that there is no evidence that the dorsal motor nucleus (DMN) is an evolutionarily more primitive center of brainstem parasympathetic system than the nucleus Ambiguus (NA), and that no evidence supports the claim that sudden decrease in heartrate elicited by extreme emotional circumstances (like trauma-related dissociation) is due to DMN efferent activity to the heart.[10] In fact, there seems no evidence that such decrease happens in trauma-related dissociation in the first place.

"There is consensus among evolutionary biologists that there are huge species differences among fishes, reptiles (and birds) with respect to whether dorsal brainstorm centers (corresponding to DMN) or ventral centers (corresponding to NA) are responsible for parasympathetic control of heart rate."[11]

Grossman also points out that even the results of Porge's own study on two species of lizard was flawed due to inappropriate measurement of heart rate variability.[12]

While the criticism does not address the clinical speculations of the polyvagal theory directly, it contradicts its premises. In particular it pulls the rug from under the suggestion that there is a phylogenetic hierarchy, where one vagal system is more primitive than the other, and therefore is activated only when the more evolved one fails (as in dissocation, or acute trauma).

In polyvagal theory the term vagal tone is equated with respiratory sinus arrhythmia (RSA), which is suggested to be linked to dimensions of psychopathology. A number of research studies have evaluated RSA responses across a range of dimensions of psychopathology, but a comprehensive meta-analysis has shown that no clinically meaningful relation can be found between psychopathology and RSA reactivity.[13]

See alsoEdit


  1. ^ a b c d e f g Porges, Stephen W (October 2001). "The polyvagal theory: phylogenetic substrates of a social nervous system". International Journal of Psychophysiology. Elsevier. 42 (2): 123–146. doi:10.1016/S0167-8760(01)00162-3. ISSN 0167-8760. PMID 11587772.
  2. ^ a b Porges, Stephen W (April 2009). "The polyvagal theory: New insights into adaptive reactions of the autonomic nervous system". Cleveland Clinic Journal of Medicine. 76 (Supplement 2): S86–S90. doi:10.3949/ccjm.76.s2.17. ISSN 1939-2869. PMC 3108032. PMID 19376991.
  3. ^ a b c Beauchaine, Theodore P; Gatzke-Kopp, Lisa; Mead, Hilary K (February 2007). "Polyvagal Theory and developmental psychopathology: Emotion dysregulation and conduct problems from preschool to adolescence". Biological Psychology. Elsevier. 7 (2): 176. doi:10.1016/j.biopsycho.2005.08.008. ISSN 0301-0511. PMC 1801075. PMID 17045726.
  4. ^ Porges, Stephen W (2011). The Polyvagal Theory: Neurophysiological Foundations of Emotions, Attachment, Communication, and Self-regulation. W. W. Norton & Company. ISBN 978-0-3937-0700-7.
  5. ^ a b c Porges, Stephen W (2011). The Polyvagal Theory: Neurophysiological Foundations of Emotions, Attachment, Communication, and Self-regulation. W. W. Norton & Company. p. 69. ISBN 978-0-3937-0700-7.
  6. ^ Porges, Stephen W.; Dana, Debra A. (2018). Clinical Applications of the Polyvagal Theory: The Emergence of Polyvagal-Informed Therapies (Norton Series on Interpersonal Neurobiology). WW Norton & Company. ISBN 1324000511.
  7. ^ Reed, Shawn F; Ohel, Gonen; David, Rahav; Porges, Stephen W (September 1999). "A neural explanation of fetal heart rate patterns: A test of the polyvagal theory". Developmental Psychobiology. Wiley. 35 (2): 109. doi:10.1002/(SICI)1098-2302(199909)35:2<108::AID-DEV4>3.0.CO;2-N. ISSN 1098-2302. PMID 10461125.
  8. ^ Van Der Kolk, Bessel (2014). The body keeps the score: brain, mind, and body in the healing of trauma. New York: Viking Penguin. p. 81. ISBN 9780670785933. Retrieved 3 February 2018.
  9. ^ Corrigan, Frank E. M. (2014). Neurobiology and treatment of traumatic dissociation toward an embodied self. New York: Springer. p. 510. ISBN 0826106315.
  10. ^ Grossman, Paul; Taylor, Edwin W. (2007-02-01). "Toward understanding respiratory sinus arrhythmia: Relations to cardiac vagal tone, evolution and biobehavioral functions". Biological Psychology. Special Issue of Biological Psychology on Cardiac Vagal Control, Emotion, Psychopathology, and Health. 74 (2): 263–285. doi:10.1016/j.biopsycho.2005.11.014. ISSN 0301-0511.
  11. ^ "Does anyone know of research documenting large heart-rate decrease during episodes of psychological dissociation?". ResearchGate. Retrieved 2020-01-22.
  12. ^ Grossman, Paul; Taylor, Edwin W. (2007-02-01). "Toward understanding respiratory sinus arrhythmia: Relations to cardiac vagal tone, evolution and biobehavioral functions". Biological Psychology. Special Issue of Biological Psychology on Cardiac Vagal Control, Emotion, Psychopathology, and Health. 74 (2): 263–285. doi:10.1016/j.biopsycho.2005.11.014. ISSN 0301-0511.
  13. ^ Beauchaine, Theodore P.; Bell, Ziv; Knapton, Erin; McDonough‐Caplan, Heather; Shader, Tiffany; Zisner, Aimee (2019). "Respiratory sinus arrhythmia reactivity across empirically based structural dimensions of psychopathology: A meta-analysis". Psychophysiology. 56 (5): e13329. doi:10.1111/psyp.13329. ISSN 1469-8986. PMC 6453712. PMID 30672603.

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