Polyvagal theory

Polyvagal theory (poly- "many" + vagal "wandering") is a collection of evolutionary, neuroscientific and psychological claims pertaining to the role of the vagus nerve in emotion regulation, social connection and fear response. Due to a lack of evidence and internal coherence, it is not widely accepted in the active neuroscience community, while nevertheless being popular among some clinical practitioners and patients.

Hypothesized phylogenetic subsystems/stages

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

Anatomical conjectures

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. As has been established since the early days of neuroanatomy, the Autonomic nervous system encompasses nerve fibers transmitting information from the body toward the brain, called afferent influences. According to polyvagal theory, this effect has been observed and demonstrated by adaptive reactivity dependent on the neural circuits' phylogenetical development. 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 are claimed to serve different evolutionary stress responses in mammals: the more primitive branch is said to elicit immobilization behaviors (e.g., feigning death), whereas the more evolved branch is said to be linked to social communication and self-soothing behaviors. These functions are claimed to 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)

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. Polyvagal theory calls this the “vegetative vagus” because it sees it as being associated with primal survival strategies of primitive vertebrates, reptiles, and amphibians.[3] Under great stress, these animals "freeze" when threatened, conserving their metabolic resources. This draws on the simplifying claims of the Triune brain theory which are no longer considered accurate due to the many exceptions to this rule (please see Triune brain - Status of the model for more).

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)

With increased neural complexity seen in mammals (due to phylogenetic development) there is said to have 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 speed in responding.[1] Polyvagal theory calls this the “smart vagus” because it associates it with the regulation of sympathetic “fight or flight” behaviors by way of social affiliative behaviors.[3] These behaviors are said to include social communication and self-soothing and calming.[1] In other words, this branch of the vagus is said to inhibit or disinhibit defensive limbic circuits, depending on the situation. Note: Attributing defensive behaviours purely to the limbic system is an oversimplification, as these are triggered by _perceived_ threats, thus requiring an interplay of brain areas performing sensory integration, memory and semantic knowledge with the limbic system to be elicited. Similarly, the regulation of emotions requires a complex interplay of higher cognitive areas with limbic ones. The vagus nerve mediates control of supradiaphragmatic visceral organs, such as the esophagus, bronchi, pharynx, and larynx. It also exerts an 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 according to polyvagal theory, 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] Note: While the vagus nerve's role in downregulating the heart rate is well-established, the notion that a Fight-or-flight response can be triggered without engaging the sympathetic nervous system is not substantiated by any evidence.

Vagal tone as a physiological marker of stress

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, Porges suggests 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 proposed as a measurable, noninvasive way to see how the vagus modulates heart rate activity in response to stress. If true, this method could be 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.[4] Research has shown that amplitude of RSA is an accurate indicator of the efferent influence of the vagus on the heart.[4] 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.[4] These complications may reduce one's capacity to respond to stress appropriately.

Clinical applications of polyvagal theory and vagal tone

Vagal tone has been used in medical and psychological research to better understand the physiological underpinnings of various disorders[5].

Deb Dana goes into great detail about clinical applications in her book, The Polyvagal Theory in Therapy.[6]

Clinical applications in the human fetus

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' theory

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. Corrigan

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]

Other Media

David Puder, M.D. discusses the theory and clinical applications on his podcast, Psychiatry & Psychotherapy Podcast.[10]

Criticism

Critics of the polyvagal theory point out that its premises are not supported by empirical, 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.[11] 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."[12]

Grossman also points out that even the results of Porges' own study on two species of lizard was flawed due to inappropriate measurement of heart rate variability.[13]

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 dissociation, or acute trauma). It has been known for roughly a century that "a differentiation of the visceral efferent column of the vagus nerve into a dorsal motor nucleus and a ventrolateral nucleus (nucleus ambiguus) is first seen in reptiles (Ariens Kappers, '12; Ariens Kappers et al., '36; Addens, '33)"[14]. This contradicts the polyvagal description of the dorsal motor nucleus as being "phylogenetically older" than the nucleus ambiguus, or of the latter being unique to mammals.

In addition, recent findings in lungfish suggest that myelinated vagus nerve fibres leading from the nucleus ambiguus to the heart long precede the evolution of mammals.[15][16]

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.[17] Apart from this, a correlation between vagal tone and stress regulation would not necessarily indicate a causal role of the vagus nerve activity on different stress responses in mammals (see Correlation does not imply causation for more).

By overemphasizing the role of the vagus nerve in deciding between freezing and other fear responses, the theory disregards decades of neuroscientific findings on the origins of the freeze response[18] and fear responses in general[19]. While the vagus nerve undoubtedly plays a role in transmitting emotion-related signals between the brain and the rest of the body (a fact established long before the emergence of polyvagal speculations, see Vagusstoff), there is no evidence to suggest that it has any control over whether a freeze response is triggered or not.

From a methodological perspective, many claims do not meet the criteria of a scientific theory because they are formulated in a manner too vague for empirical testing. For example, the precise functioning of the two proposed distinct "vagal systems" or of the "social engagement system" is not explained,[2] nor is that of the "face-heart connection" supposedly embodied in the ventral branch of the vagus nerve.

While other brain areas known to be involved in fear responses (e. g. the amygdala and periaqueductal gray[18][19]) are mentioned by Porges, he does not integrate them into the description of his own hypothesized systems. Simply observing an anatomical link between two areas of the body is not sufficient for explaining complex social and emotional behaviours as Porges broadly attempts to do.

In addition, polyvagal theory introduces the term "neuroception" for "a neural process that enables humans and other mammals to engage in social behaviors by distinguishing safe from dangerous contexts" [2]. It thus attempts to encompass several categories of psychological phenomena, each one of which constitutes a broad field of research in its own right: fear, threat perception, social behaviour, and emotion regulation. The neural substrates for many of the included phenomena are known at least tentatively, and comprise a large number of brain structures including, but not limited to, the vagus nerve. Polyvagal theory does not explain the mechanism of any of these phenomena with any precision, resulting in an oversimplification rather than an expansion or refinement of existing knowledge.

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See also

References
  1. 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. 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. 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): 174–84. 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. Porges, Stephen W.; Dana, Debra A. (2018). Clinical Applications of the Polyvagal Theory: The Emergence of Polyvagal-Informed Therapies. Norton Series on Interpersonal Neurobiology. W. W. Norton & Company. ISBN 978-1324000518.
  6. Dana, Deb A. (2018). The Polyvagal Theory in Therapy. ISBN 978-0-393-71237-7
  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): 108–18. 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. 80. 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 978-0826106315.
  10. https://psychiatrypodcast.com/psychiatry-psychotherapy-podcast/polyvagal-theory-understanding-emotional-shutdown
  11. 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. PMID 17081672.
  12. "Does anyone know of research documenting large heart-rate decrease during episodes of psychological dissociation?". ResearchGate. Retrieved 2020-01-22.
  13. 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. PMID 17081672.
  14. Barbas-Henry, Heleen (1984). "The Motor Nuclei and Primary Projections of the IXth, Xth, XIth, and XIIth Cranial Nerves in the Monitor Lizard, Varanus exanthematicus". Journal of Comparative Neurology. doi:10.1002/cne.902260409.
  15. Monteiro, Diana (2018). "Cardiorespiratory interactions previously identified as mammalian are present in the primitive lungfish". Science Advances. doi:10.1126/sciadv.aaq0800.
  16. Taylor, E. W. (2010). "Autonomic control of cardiorespiratory interactions in fish, amphibians and reptiles". Brazilian Journal of Medical and Biological Research.
  17. 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.
  18. Roelofs, Karin (2017). "Freeze for action: neurobiological mechanisms in animal and human freezing". Philosophical Transactions of the Royal Society B: Biological Sciences. 372. doi:10.1098/rstb.2016.0206.
  19. Johansen, Joshua (2010). "Neural substrates for expectation-modulated fear learning in the amygdala and periaqueductal gray". Nature Neuroscience. doi:10.1038/nn.2594. PMC 2910797.
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