In 1884, considering how the emotional processes work, William James put forward the argument that emotional experiences arise from direct perceptions of bodily change. This meant that we do not feel our emotions because we choose them, but because of some neurological process that causes them. This idea that emotional experience does not start with a conscious experience but our experience of bodily changes was shared by Carl Lange (1885). Both James and Lange believed that bodily and behavioral responses precede the conscious experience of emotion, resulting in what it today known as the James–Lange theory of emotion.
In 1927, Walter B. Cannon critiqued the James–Lange theory arguing that visceral changes do not always result in the presence of an emotion. This meant that the first theory could not be entirely true, otherwise we would experience a new emotion anytime our heart rate changed or breathing slowed or sped up, for example. He suggested that the range of visceral changes in the body resulted in too little differentiation to explain the range and variety of emotions experienced by most people under normal circumstances.
In 1983, Cannon’s claims were questioned with evidence suggesting that emotional responses may at least in part be distinguished on the basis of patterns of autonomic activity (Ekman, Levenson, & Friesen), that separation of the body from the brain can in fact reduce the intensity of emotional experience (e.g., following spinal injury, Montoya & Schandry, 1994), and that artificial stimulation of the viscera (e.g., via intravenous injection of peptides) can induce emotions (Harro & Vasar, 1991).
Then, in 1994, neuroscientist Stephen Porges proposed the Polyvagal Theory. Polyvagal Theory offers an explanation regarding how the vagus nerve, which connects the brain, to the heart, to the viscera (the organs of the belly), relates to our human ability to connect and communicate with each other. Learning about the vagus nerve helps us understand our physiologic responses to perceived safety and danger. The latin root of “vagus,” means “wander,” and is used for this nerve because of how it runs throughout the body.
Picture from Wikipedia, of Stephen Porges in white shirt and tie. He has dark hair, a light beard, and is looking to the left smiling.
In 2011, he released his book The Polyvagal Theory: Neurophysiological Foundations of Emotions, Attachment, Communication, and Self-regulation (Norton). This was a year after the National Institute of Mental Health changed their funding to neuroscience only, and researchers latched on to his two decade old breakthrough theory as a foundation for further research and application to treatment model development.
Blue cover of Porges’s book reads “The Polyvagal Theory” at the top right, with brain structure picture in the middle and with subtitle written below. Author’s name is at the bottom center.
His work has been a breakthrough in the field of trauma study, giving neurological evidence for the trauma response experience. It’s been huge for clinicians and huge for survivors alike. Though the research is still filtering down into common clinical practice, it has profound implications for understanding and treating trauma - including attachment and dissociative disorders.
In 2018, Deb Dana released her book, The Polyvagal Theory in Therapy, which brought the application of the polyvagal theory to psychological treatment to the forefront. Now the latest research and most popular explanation of trauma responses, it has also provided a way to reconnect trauma treatment back to funding sources. These applications also correlate with shame theory, in regards to connection with others being one critical - even necessary - aspect of healing.
Orange and white book cover, with “Polyvagal Theory in” in orange letters, and “Therapy” in blue letters, with author’s name beneath.
WHAT IS THE POLYVAGAL THEORY?
It’s a theory that explains the connection between the vagus nerve and trauma response, emotional regulation, attachment, and self-expression.
The vagus nerve is the tenth cranial nerve, the longest and most complex of 12 pairs of nerves that go from the brain (CLICK HERE for an illustration). It runs from the brain to every major organ in the body, branching off along the way into “accessory” nerves. So when there are many vagus nerves, they call it “poly” vagal nerve as a whole unit because there is more than nerve that branches off the main nerve as it runs to the organs of the body.
It’s a “theory” because they don’t know for sure that what Porges proposes is true.
Specifically, the theory proposes that there is a connection between this nerve (and all its branches) is the source of visceral experiences and the main body organs: the lungs, heart, and gut - even just in response to the facial expressions or voice tones of others - and is expressed in your own facial expressions and tone of voice, as well.
In The Body Keeps Score, Bessel van der Kolk explained:
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 explained why a kind face or a soothing tone of voice can dramatically alter the way we feel. It clarified 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 focused attunement with another person can shift us out of disorganized and fearful states. In short, Porges’s theory made us look beyond the effects of fight or flight and put social relationships front and center in our understanding of trauma. It also suggested new approaches to healing that focus on strengthening the body’s system for regulating arousal.
Thus, the polyvagal theory attempts to combine physiology, behavior, and psychosocial processes in a unified framework (Berntson et al., 2007). According to Porges, evolutionary developments over time have linked together neuroanatomical and neurophysiological connections between the vagal regulation of the heart and the neural regulation of the striated muscles of the face and head (Porges, 1995, 2003a, 2007b). This, Porges proposes, means that the vagal influence on the heart is also related to behaviors that are involved in social engagement (Porges, 2003a). It is important to note that Porges also argues that social engagement is not a learned behavior, but an emergent behavior of neurophysiology - an idea contrary to many of the already established prevailing theories today.
However, he explains his case using fetal development. The vagal nerve originates in the brain stem, and during fetal development projects to and from the striated muscles of the face and head (Patestas & Gartner, 2006). These fibers function to regulate the facial muscles (for facial expressivity), muscles of mastication (for ingestion), neck muscles (for looking behavior), laryngeal and pharyngeal muscles (for vocalization and intonation), as well as the middle ear muscles (for listening to human voice). Porges notes that all of these muscles are also observed to be used in socialization behaviors such as maintaining eye contact, listening to speech, and making appropriate facial expressions (1995). He then makes the polyvagal theory conclusion: that social engagement is contingent upon the self-soothing physiological states - which, he says, are ultimately determined by the vagus nerve (Porges, 2003b, 2009a; Porges & Lewis, 2010). He implies, then, that when it feels like you can’t control your emotions, it’s because you really actually can’t - not without stimulating, or activating, the vagal nerves in some way.
Because it is still just a theory, we must be careful not get swept up in the excitement of its popularity. Taking a critical look, the polyvagal theory has many tenets that have not actually be empirically verified yet. It also has challenges that must be addressed. Some of these are:
the term polyvagal is a misnomer, as polyvagal theory divides the vagal system into two efferent systems not many; Ritz (2009) has suggested that “bivagal theory” would be a more accurate description;
the term nucleus ambiguous perfectly represents the perplexity of the brainstem, as the name reflects the ill-defined borders of this region (Loewy & Spyer, 1990);
current techniques are unable to ascertain where the vagal outflow originates (Berntson et al., 2007; Grossman & Taylor, 2007), and this has made it impossible to verify Porges’ claims regarding potential functional differences between the vagal efferent systems, at both psychophysiological and behavioral levels (Berntson et al., 2007; Ritz, 2009), which leaves his entire theory hanging without actual evidence;
much of the research used to substantiate polyvagal theory has been carried out with juvenile rather than adult populations (for example, vagal regulation has been associated with self-soothing in neonates (Huffman et al., 1998), facial expressivity in infants (Stifter, Fox, & Porges, 1989), and emotion regulation in infants and pre-school aged children (Hastings et al., 2008; Porges, Doussard-Roosevelt, Portales, & Greenspan, 1996; Stifter & Jain, 1996)), while the research on adults has been much more subjective (Lower resting (tonic) high-frequency HRV has been linked to decreased regulation of negative affect and maladaptive coping (Fabes & Eisenberg, 1997; Pu et al., 2010), as well as poorer romantic attachment and marital quality (Diamond & Hicks, 2005; Smith et al., 2010). Further to this, smaller changes in high-frequency HRV in response to laboratory stressors have been associated with emotion regulation difficulties (Austin, Riniolo, & Porges, 2007; Hughes & Stoney, 2000; Sahar, Shalev, & Porges, 2001), and inferior social functioning (Egizio et al., 2008));
there is also research that actually refutes the polyvagal theory (for example Gyurak and Ayduk (2008) did not find a direct relationship between resting HRV and emotion control, and Demaree and colleagues have reported that cardiac vagal control does not predict emotional expressivity in response to film clips (Demaree, Robinson, et al., 2004; Demaree, Pu, et al., 2006), although this could be explained by methodology and by how the vagal nerve itself actually works - supporting evidence in healthy adult populations tends to emerge during highly emotional situations (e.g., increased levels of daily stress, Fabes & Eisenberg, 1997), and not situations that do not warrant substantial emotional responses (e.g., passively viewing film clips, Demaree, Pu, et al., 2006), and so it may only be under conditions of actual danger or threat that relationships between ANS function and socio-emotional behaviors clearly emerge in healthy adults;
the polyvagal framework neglects the occurrence of situations where mobilization occurs without fear, such as during play and exercise (Porges now (2009b) attributes this to defensive fight–flight arousal coupled with dynamic VVC activation to insure safe interactions; and
researchers are unable to distinguish the vagal efferents originating from the NA and the DVNX (Berntson et al., 2007; Grossman & Taylor, 2007). This means it is currently impossible to verify Porges’ claims regarding the different qualitative functions of the vagal efferent systems.
It’s application to therapy appears to be useful, however, regardless of whether this is because of the neuroscience behind eye contact and facial expressions or because of the very separate and distinct shame theories regarding the processes of connection and attachment. It may turn out that these do, indeed overlap and explain each other, or it may be coincidence and shame theory is just on target in regards to developmental trauma and chronic shame.
HOW DOES IT WORK?
Both research and personal experience have long shown that our behaviors are guided by our emotions (Davidson & Irwin, 1999). Experiencing emotions biologically means changes in subjective experience, appraisal, expression, physiological arousal, and goal-directed behavior. Still, emotions are not a tangible thing we can touch outside ourselves or even always immediately or easily recognize within ourselves. Experiencing emotions involves several processes: the perception of an emotional stimulus, the production of an affective state and emotional behavior, and the regulation of that affective state and emotional behavior (Phillips, Drevets, Rauch, & Lane, 2003). When emotional stimuli are perceived, messages are sent from the central nervous system (CNS) to the rest of the body, either by nerve cells or chemical hormones. These initiate changes in autonomic, neuroendocrine, and somatic systems. Thus, the experience of an emotion is exclusively internal unless it is expressed outwardly through behaviors. Because of this, the only way to “measure” emotional responses in another person is through facial, vocal, and postural cues. (Hugdahl, 1996; Gross & John, 1995). Recognizing, comprehending, interpreting, and responding to these cues in others are all a vital part of social interactions (Darwin, 1872/2009). We will come back to this piece later, when we talk more about the impact of chronic trauma and related shame.
Any nervous system tissue outside of the brain and spinal cord is referred to as the peripheral nervous system. This second system carries motor and sensory information from the brain to the body and then relays information back to the CNS. Although the peripheral nervous system and CNS are theorized as being anatomically separate, they are functionally interconnected (Jessell, 1995). The peripheral nervous system has been further divided into the somatic system, which controls muscular activities, and the autonomic nervous system (ANS), which controls the body’s internal environment: breathing, heartrate, digestion. (Sequeira, Hot, Silvert, & Delplanque, 2009).
We don’t have to think about these. They just happen. It’s unconscious, and not a choice.
It’s also important to remember that the term “autonomic” is actually misleading. The CNS can actually inhibit or bypass lower reflex mechanisms of the ANS via activity in areas such as the hypothalamus, amygdala, and prefrontal cortex (Jessell, 1995). This piece will come up again later when we talk about trauma response in the brain.
What makes the polyvagal theory unique is that Porges proposes that emotional dysregulation and psychopathology result with abnormalities in how the ANS functions, rather than something being wrong with its structure. To over-simplify, when Porges talks about the “myelinated” vagal nerve, he is referring to the ANS. There are two branches of the ANS: the sympathetic (SNS) and the parasympathetic (PNS). When he talks about the “unmyelinated” vagal nerve, he is referring to the PNS. He uses this terminology because his theory is based on the writings of John Hughlings Jackson back in 1884, which is based on evolutionary theory. Regardless, the vagal nerve communicates with and connects to all the major organs.
Sympathetic responses include fight and flight in response to danger, and parasympathetic responses include calming back down again when you are safe.
This is why things like taking slow, deep breaths helps so much: not only does it literally slow down your breathing and heart rate, but it also tells your body to slow it down, too. It shifts that panic cycle to the positive, giving a feedback loop for feelings of safety and calm in the same way anxiety escalated into panic. Further, slow deep breaths activate different parts of your ANS, bringing an actual neurobiological balance back to your body as you breathe in and out.
Every ANS response is in service of survival. It is completely natural, expected to happen, and should be happening. It’s supposed to happen. It’s what helps you get out of danger and keeps you safe and then gets you well again as you recover after danger.
We often think of the flight-or-fight as part of the response to trauma, and as survivors who dissociate, we are also familiar with “freeze”. But in 2004, Bracha added the terms “fright” and “faint” to the acute stress response spectrum, making a distinction between tonic immobility (fright) and flaccid immobility (faint). This was important because prior to this distinction, Porges (1995, 2004a, 2007b) and Gray (1987; Gray & McNaughton, 2000) both used the term freeze response, but there is confusion as to what point in the defense repertoire “freezing” should refer to (in Porges’ work, freezing refers to refers to the DVC being up-regulated and resulting in vasovagal syncope, whilst Gray encapsulated freezing as being analogous to the orienting response (which occurs higher up the hierarchy).
Bracha made a clear distinction between these responses by proposing a freeze–flight–fight–fright–faint hierarchy. The three initial responses in the hierarchy reflect normal responses to acute stress. The initial orienting response involves “stop, look, and listen” behaviors and Bracha termed this as the freeze response (in the polyvagal hierarchy orienting occurs when the vagal brake is removed, prior to activation of the SNS). This is followed by flight and fight responses (commonly attributed to SNS activation). The next response according to Bracha is fright, also known as tonic immobility, which is less common as a response to acute stress, and will be discussed below.
This response evolved as an alternative to flight–fight tendencies (Alboni et al., 2008). During fright the body is immobile, but should the chance to escape arise the body will be able to rapidly initiate a mobilization response. This form of immobility can be distinguished from the last stage of the hierarchy which involves flaccid immobility. This last stage Bracha termed faint, and it corresponds to Porges’ description of the body when the DVC is up-regulated, resulting in vasovagal syncope (i.e., a temporary loss of consciousness). This final stage in the response hierarchy is the least common form of reaction to acute stress and is usually only initiated in times of severe life threat, with the exception of some clinical disorders.
Later, Schauer and Elbert (2010) added “flag” and “faint” to the response process. Flag is associated with slow heart rate, low blood pressure, corresponding cognitive failure, and emotional numbing. As the flag state progresses further emotional involvement is thought to decrease, which is consistent with a dissociative shut-down response (Schauer & Elbert, 2010). The final stage of the hierarchy, faint, occurs when the PNS (DVC) is up-regulated without SNS activation, which can result in vasovagal syncope. Bracha terms this as flaccid immobility because the body is now shut down and no longer prepared to protect from or mobilize away from danger (2004).
In her 2012 doctoral thesis, Megan Christine Barnsley combines these into the following model:
Figure 2.4. Diagram of Porges’ (1995, 2004a, 2007b) polyvagal hierarchy integrated with Gray and McNaughton’s (2000) revised reinforcement sensitivity theory, and Schauer and Elbert’s (2010) defence cascade. VVC = ventral vagal complex. SNS = sympathetic nervous system. BIS = behavioural inhibition system. BAS = behavioural activation system. FFFS = fight–flight–freeze system. DVC = dorsal vagal complex.
In this way, human beings, like all other mammals, are able to automatically adjust to various levels of safety or danger, whether that is internally or externally or even just perceiving threats or dangers. But this is more than just an automatic response: the vagal nerve also acts as a helper in overriding even the automatic response for emergencies when your body needs to respond even more quickly because of danger. So for example, if the vagal nerve withdraws from the heart, that can stimulate the heart rate to increase much more quickly than a message from the SNS can tell the heart rate to increase (Berntson, Cacioppo, & Quigley, 1993a) - that way by the time your muscles get the message to run, your heart is already beating fast and ready to go.
Simplified, your body uses the nervous system to initiate the fight-or-flight response, but the vagal nerve can beat it to the punch, so that all your organs are ready to go at the starting line by the time the race begins.
The vagal nerve can also do the opposite of flight-or-fight, which is known as rest-and-digest, to alert the body when the race is over and you are safe, so it’s okay to calm down. This is sometimes referred to as the “vagal brake” in reference to the myelinated vagal nerve, because it “stops” the flight-or-fight response. In our previous example with the heart, activation of the vagal nerve back to the heart again is what tells it to slow down.
Literally and metaphorically, it is the touching of the heart that brings healing and peace.
Some research seems to support Porges and his theory regarding the vagal brake. Examples confirmed are the process of self-soothing in infants (Huffman et al., 1998), and higher self-regulation in adults (Fabes & Eisenberg, 1997). However, research has not yet confirmed any link between the vagal brake and actual emotional expressivity (Demaree, Pu, Robinson, Schmeichel, & Everhart, 2006; Demaree, Robinson, Everhart, & Schmeichel, 2004; Pu, Schmeichel, & Demaree, 2010). Further, it cannot be assumed that greater vagal activity relates to greater health, because there are clear examples where too much really is too much: infant death syndrome, stress-induced asthma, stress-induced gastric ulcerations, and vasovagal syncope (see Ritz, 2009). The question remains, then, regarding the actual influence of the vagal nerve.
The changes in heart rate variability, or HRV, are one way to measure this influence. When a person has developmental trauma, chronic shame and/or chronic stress, or other experiences that induce repeated patterns of the flight-or-fight response, the power in the low-frequency domain of HRV tends to increase whilst the high-frequency power decreases (Berntson & Cacioppo, 2004). This effect is noted to be associated with anxiety, depression, chronic illness, and autoimmune disorders (Berntson & Cacioppo, 2004; Thayer & Friedman, 1997). However, it’s also true that the same effect happens when either the SNS or the PNS are out of balance, one being used more than the other. This complicates understanding the true impact of the vagal nerve itself, but also explains why safe touch and sensorimotor therapies such as EMDR, equine therapy, progressive muscle relaxation, grounding skills, etc. work so effectively with survivors. We will discuss this further in a bit, but it implies that what needs to be integrated is not actually so much the personality as the mind-body experience itself.
So researchers focus on exactly that: what integrates these systems to work together, in balance, to keep the entire system online.
Thayer and Lane (2000, 2009) proposed a general model of neurovisceral integration for the brain, visceromotor, neuroendocrine, and behavioral responses to explain how the body rapidly responds to environmental stimulation. This model focuses on the function of the entire autonomic network as being implicated in goal-directed behavior and adaptability (Benarroch, 1993; Thayer & Brosschot, 2005). This emphasizes the brain’s link to emotional responding (Benarroch, 1993), and gives the prefrontal cortex the stage in a top-down effect in integrating the mind-body experience.
This is what you experience in traditional talk therapy. You are able to share your experience, think about it, reflect on it, and make meaning from those experiences. It works because engaging the cortex activates the vagal nerve to the heart, sending safety signals back to your brain ((Wong, Massé, Kimmerly, Menon, & Shoemaker, 2007; Milad, Quirk, et al., 2007; Milad, Wright, et al., 2007).
However, it’s also what can make talk therapy difficult. When you have a new therapist that you are still unfamiliar with, or while still establishing safety, or when confronting difficult material, or if you have a therapist who is not attentive or maintaining attachment-connection or who is otherwise unresponsive in some way, it disrupts the process. Literally. Much like the attunement/misattunement research from shame theory, which we will discuss in a moment, there is a same kind of disconnect that actually happens in the brain during attachment rupture or when the frontal cortex gets kicked offline.
A withdrawal of parasympathetic activation and an increase in sympathetic activation, which is consistent with defensive responding, is what causes dysregulation. Dysregulation of these cortical pathways may result in prolonged increases in sympathetic activation, which in the long term could result in potential autonomic imbalance. Prolonged action readiness and SNS over-activity have been linked to deficits in self-regulation and psychopathology (Thayer & Brosschot, 2005). For specific and extensive literature review application to each specific diagnoses, please CLICK HERE for Megan Christina Bensley’s doctoral thesis on the social consequences of physiologic states.
Aside from specific application to DSM-5 diagnoses, Porges explains how these neurophysiological adjustments in our bodies have consequences for daily living. These physiologic states, or “modes”, can be categorized primarily into three groups of purpose or functioning:
Safe and Social (engagement) – located in our face and our heart;
Flight and Fight (mobilization) – located in our lungs and limbs; and
Shutdown (immobilization) – located in our stomach.
We don’t choose to do these. It’s a sequence. It happens in a certain order.
We start out in the safe zone, and then when exposed to trauma or a threat of any kind (even perceived), we drop down the “ladder” into flight to try and get away. When we cannot get away, we drop down to fight. When fighting doesn’t keep us safe, we drop down to shutdown. This is the sequence in response to any kind of danger perceived by the body as a threat.
Behaviorally, we see this expressed in many ways. When we are safe, and our body feels safe, then our affects are bright and there is a great deal of range in our tone of voices and in our facial expressions. As we drop down the ladder, the changes in the vagal nerve literally flatten our affect by withdrawing signals to the facial muscles, our voices become more monotone, and our facial expressions are more limited. In the same way, as we move back up the ladder, our affects brighten and our voices and facial expressions have more range in presentation.
Further, they are responses to our external world, our internal world, and the way we perceive the world around us, but they also are the filters through which we see our world - which makes them reinforcing and happen in patterns for some people. This is especially true when we get stuck in one of these “modes”, and begin to filter all experiences through them.
For example, someone stuck in “fight” mode will perceive the world as a more dangerous place than it may be, and/or may find themselves in actual dangerous situations (or reenacting traumas) because they are focused on and looking for those situations that verify their internal experience of the world.
Or, someone in “flight” mode may have difficulty making eye contact, establishing relationships, or connecting with others even in superficial ways.
Trauma survivors experience these modes through triggers. They may feel safe and connected with their partner, or with their therapist, or in their own home, but if they have a sensory trigger like a smell or a sound or something that looks like something from the past, it may trigger a literal change in mode. The survivor then shifts from “safe and social” to “flight and fight”, with increased heart rate and panicked breathing, and maybe even literal running away or fighting against something familiar, or even to complete shutdown and being nonresponsive in a “freeze” or dissociated response.
The insight comes in understanding that switching or a “meltdown” or “spacing out” or some other trauma response may really not be coming from nowhere, but an actual physiological response to a particular trigger.
This perception at a neurological level was described by Porges when he coined the new term “neuroception”. Neuroception refers to how neural circuits in the brain and body distinguish whether situations or people or environments or experiences are safe or whether they are dangerous - such as why we may appreciate a hug from a friend, but not from a stranger. So basically, when this neuroception is faulty, there is an incongruence between whether you feel that you are safe and whether you actually are safe. This faulty neuroception, then, explains the neurobiological process of everything from autism to schizophrenia to anxiety disorders to reactive attachment disorder to dissociative disorders.
Neuroception is our body’s ability to detect risk outside of our body, bring that information in, and accurately and appropriately respond to that risk.
Each “mode” has its own neuroception “key” that unlocks specific behaviors. The safety and socialization mode has the neuroception key that encourages eye contact, prosocial behaviors, smiling, conversation, full range of voice, closer proximity of bodies, and safe touch. The neuroception of danger unlocks fight and flight behaviors such as being mobilized for running away or getting aggressive. But when something is life-threatening, that neuroception unlocks the behaviors of immobilization, or “freeze”, like dissociation.
And, when you are in one mode, you lose access to the behaviors in the other mode. Neuroception unlocks some behaviors in response to what is happening or perceived to be happening. But it also inhibits alternate behaviors that you could choose if you were in a different mode.
That is why, when you are dissociating, it is hard to maintain eye contact. It is hard to follow conversation. It is hard to perceive others around you as safe. It is hard to remember now time.
This is part of why, they think, that trauma survivors are so often abused or violated in different ways again and again as they become adults and even into adulthood. Once they are already dissociated, they lose access to the behaviors that would get them away from danger now that they are an adult - even if they could not get away while they were a child.
It’s also why those younger parts or child alters can be so difficult to orient to the present place and time.
This is why, in your therapist office, during your appointment, you may feel connected and strong and present and confident, and then later while on your own feel such a rush of panic or fear or do the opposite of what you had agreed on during safety planning.
This is why it takes domestic violence survivors so many times to actually leave such abusive situations.
When in the mode where your life is being threatened, or you feel (perceive) that your life is being threatened (even if only a trigger of memory time intruding into now time), you literally do not have access to the behaviors that you are able to do just fine when feeling safe and secure.
That’s unhealthy neuroception, when there is incongruence in any of those areas. Someone may be in danger but not recognize it. Someone may be safe, but think they are in danger.
Healthy neuroception is when there is congruence between what is happening and how your body is responding. It means that you are able to accurately to detect whether you are safe or in danger (in the present moment), correctly shift into the appropriate mode for that level of safety or danger, and then respond in a way that matches that mode and that level of safety or danger.
Healthy neuroception looks like connecting with someone safe when you are falling in love. It looks like mutual friendship and connection. It looks like recognizing the right therapist when you finally find them.
It also looks like recognizing red flags and acting accordingly, instead of dismissing what your intuition is telling you to do about it. It looks like setting boundaries when someone is being too intrusive, or when your workload is too much, or in ways that protect your Self, your time, and your energy. It looks like appropriate self-disclosure, by not sharing too much to everyone but also making an effort to connect with your sacred few.
THE CONNECTION BETWEEN TRAUMA AND POLYVAGAL THEORY
When someone experiences trauma, they shift into either immobilization or mobilization, unlocking behaviors of flight, fight, or freeze. We know this. But what we are learning from polyvagal theory, is that these behaviors are neurobiological responses.
When someone grows up with chronic trauma, or ongoing trauma, or gets stuck in one of those modes like dissociation, then that in and of itself becomes traumatic. Now, not only is there incongruence between what is actually happening and what it feels like is happening, but it also feels like you have no choice in how to respond or may even be unable to respond even if you wanted to try.
Here is Stephen Porges explaining it himself, in this video from The National Institute for the Clinical Application of Behavioral Medicine:
So like in his example of having a panic attack even though he wanted to get his MRI, and even though he was really actually interested in the results because of research he studies, he was unable to do it.
Once we are mobilized, or immobilized, it is difficult to shift back into safe mode.
This is why nightmares are so disturbing well into the next day. This is why flashbacks interfere with our functioning. This is why it is so hard to remember that now time is safe, and that memory time really is in the past.
Further, specifically in regards to dissociation, “shutdown” mode (immobilization, or dissociation) is different for human beings than it is with wild animals.
There are two words used to describe immobilization behavior in wild animals: tonic immobility and thanatosis.
Thanatosis is when an animal perceives a predator and “plays dead” - in Texas, we see this with armadillos on the side of the road. It is sometimes called “playing possum” in English. It can resemble a state of shock, but from which the animal can spontaneously recover with no apparent trauma symptoms.
Tonic immobility is a little different, and often called “animal hypnosis”. We see this survival technique everywhere from a kitten being carried by its mother’s mouth to a tiger frozen behind prairie grass ready to pounce its prey. This state of tonic immobility may last from minutes to hours, and again, the animal recovers spontaneously with no apparent trauma symptoms.
If you want to see a more extreme example of this, search “tonic immobility shark” on YouTube, and watch videos of divers seemingly putting sharks to sleep while they are diving. The shark is not actually sleeping, but demonstrating tonic immobility: it is neither fighting for its life or trying to get away. The shark, and the example of the kitten in its mother’s mouth, recover completely and quickly without any adverse affects because they never entered an actual fear response. They are able to jump from immobilization right back into safety mode.
Humans, however, have an added layer of consciousness and awareness, so that when danger happens or they perceive danger happening, they also experience fear. This is a fear-induced tonic immobility, which leaves the body in that state much longer and comes out of that state very slowly. Further, humans cannot move as far as quickly, not enough to flush out all of those chemicals from the parasympathetic response to trauma.
So then, when the trauma itself involves some sort of being pinned down or any kind of confinement, there is even a great degree of immobilization that becomes quite literal externally and not just internally.
Awareness of this is further complicated by other abuse dynamics, including neglect, shame, not being rescued, having no one to tell, and having no one externally intervene.
These are the roots of dissociation from a neurological standpoint: that when in a fear-induced state of tonic immobility, you are also aware of the parasympathetic response to fight or run away even though you cannot physically do so, and those neural circuit signals get sent to your brain because all that information - the sensory input experience, the physical input experience, the memory itself, the parasympathetic response - all of it has to go somewhere.
This is where Bessel van der Kolk writes in The Body Keeps Score, that:
Trauma results in a fundamental reorganization of the way mind and brain manage perceptions. It changes not only how we think and what we think about, but also our very capacity to think… [There are] automatic physical and hormonal responses of bodies that remain hypervigilant, prepared to be assaulted or violated at any time…
When we live in a constant state of hypervigilance, it is because of the amygdala, a part of the limbic system in the brain. The amygdala is “a cluster of brain cells that determines whether a sound, image, or body sensation is perceived as a threat” (ibid, p. 33). It warns us of danger and activates the stress response, including the vagal nerves.
When this is activated, another part of our brain, Broca’s area in the frontal lobe, is shut off. That part of our brain is what helps us put our thoughts and feelings into words. This is why it is so difficult to tell our stories, and why it was so difficult to ask for help even if you ever got the chance, and why it is so difficult to jump into talk therapy even once you do find a therapist you feel safe with and trust.
This also disrupts sequencing, which makes it difficult not only to put pieces of the story together, but is part of why memory time and now time can be so confusing. It’s also why we think we are intelligent people, but then in trauma response moments behave in ways that are impulsive instead of logical. It’s why the past feels present, how Littles get frozen in time, and where time goes when we lose it.
The polyvagal theory explains why so many years later, we still organize our lives “as if the trauma were still going on - unchanged and immutable - as every new encounter or event is contaminated by the past” (ibid, p. 53).
Our brains literally do not know that we are safe now, and because of the polyvagal nerves, we don’t, either.
So when we have external information that tells us we are in danger, or internal information (such as a trigger that takes us to memory time instead of staying in now time), all of that sensory information comes into our body through the limbic system, and another part of our brain - the thalamus - is what makes sense of it and sends it on to the amygdala for quick responses and to the frontal cortex for slower responses.
What we learned from the polyvagal theory is how the thalamus can kind of mix up where that information needs to go. The amygdala can process danger signals from the thalamus before we are consciously aware of what’s happening in the frontal cortex, and when this happens memory processing gets split up into separate pieces instead of metabolized as a whole experience. This is when it feels like time freezes, when sensory memories get stored separately from the emotional or physical memory, and the experience of the memory may get stored somewhere else. This is dissociation.
Now we have our experiences separated into “parts”. Some might hold memories, but without the context, or maybe it doesn’t feel like ours. Sometimes we might feel an emotional response, but not have the memory it’s connected to, and the same thing happens with body memories. Or maybe it is something you should remember, but don’t at all remember it. Regardless, the brain is doing this before you are even conscious of it, before the frontal cortex is ever engaged to make choices about how to process what you are experiencing or how to understand what you are remembering.
It means dissociating is something your brain did on its own, not something you did wrong.
It means dissociating is something that’s an automatic process under the right conditions, not because you failed or didn’t try hard enough or weren’t strong enough.
It means dissociating is something your brain did when it was trying to protect itself and your body, which is how it is designed, and not at all “crazy”.
It’s not about logic. It’s not about reason. It’s not something you can think about and decide to do differently. It’s literally the wiring of the brain in response to what is happening to the body in an actual attempt to survive.
This is also why what van der Kolk said (p. 66) is so true: “Flashbacks and reliving are in some ways worse than the trauma itself. A traumatic event has a beginning and an end - at some point it is over. But… a flashback can occur at any time… There is no way of knowing when it’s going to occur again or how long it will last.”
The amygdala is not able to discern between past and present, and so when the polyvagal nerves are sending danger signals to the organs of the body, and the brain gets the message that something life-threatening may be happening, there’s no stopping to ask the frontal cortex to sort it out first.
When the processing by the thalamus is interrupted by the danger signals from the vagal nerves, there is no story of the experience “with a beginning, middle, and end, but isolated sensory imprints: images, sounds, and physical sensations accompanied by intense emotions, usually terror and helplessness” (ibid, p. 70).
When Broca’s area is shut down so that there are no words to describe that terror and helplessness, and no means to connect those sensory imprints, that terror and helplessness becomes very real, with no sense of time to wait it out, sort it out, or crawl out of it back into the present.
But this is also why understanding Polyvagal Theory is so important: because while it explains what goes so terribly wrong internally, and it describes the horrific experience survivors endure, it also gives us hope.
Falling “down the ladder” is a metaphor created by Dana in her book that applied the polyvagal theory to the therapeutic process. What she meant was that we “fall” down from safe mode into danger mode (mobilization, or flight and fight), and then even further into life-threatening mode (immobilization, or dissociation itself). But that also means we can go back UP the ladder, too.
Using the sensory input and connection to engage the vagal nerves, we can use our own bodies as a resource to help us move from immobilization back into safe mode.
That’s powerful.
There are some formal ways of doing this that many are already familiar with: yoga, sensorimotor, deep breathing, progressive muscle relaxation, EMDR, pet therapy, equine therapy, grounding skills, diffusing oils, and other techniques that utilize sensory input to engage the vagal nerves.
And, as it turns out, these all have some things in common: deep breathing, connection with an Other, and some version of physical touch or processing.
And they work, because the vagal nerves don’t just warn us of danger.
They confirm safety, too.
This is why it’s so jolting to look your therapist in the eyes, until you are already regulating more in safe mode on your own. This is why safe touch when appropriate is so powerful and grounding. This is why you don’t just read a note from your therapist or a friend or a partner, but you hold it and touch it. This is why you rub your face or your hands together when you are trying to stay present. This is why petting a puppy or touching a horse is so difficult and first, and feels so far away, and then so intense when you do.
Connecting these aspects to the neurological processes understood by polyvagal opened the door to shame theory, which explains the patterns of negativity and dismissal of anything good in connection to ourselves.
Guilt is feeling bad for something you DID.
Shame is feeling bad for who you ARE.
This goes all the way back to infancy and early years growing up, whether our needs were met or not, and whether or not our caregivers acknowledged our emotional responses by mirroring them, and whether or not they engaged with us in all of those connecting ways: eye contact, facial expressions, and safe touch.
That’s “attunement”, and the vagal nerves were built for it. That’s what confirms safety.
You can see the old video about this “attunement” and what happens when it isn’t given, if you look up the “Still Face Experiment” on YouTube.
A mother and baby are playing.
The mother has good eye contact, mimics the faces the baby is making, and they are touching with their hands.... that's all "attunement".
But then, as part of the experiment, the mother looks away and puts her hands down. Then she turns back to the baby with a flat affect and doesn't make any expressions at all.
The baby does three things: First, the baby tries hard to touch and reach and make the same sounds and faces they were just doing that was so happy for them both.
When that doesn't work, the baby gets angry and tries to push the mother away, because what is happening is so unpleasant.
When she won't go away, but still isn't tuned in, the baby can only resolve the misattunement by matching her, which he does by physically turning away and also making a flat face without expression.
It's so sad, and may even be triggering to some. But it shows how this works, and what is so distressing when we do not have that connection.
For the sake of the baby, at the end of the experiment, the mother does "repair" the misattunement by turning back to the baby and reengaging, so you can feel the relief and the baby is okay.
But if you had a caregiver who was flat and turned away your whole life, or neglectful, or dismissive, or otherwise disengaged, and you had to match that, then it makes sense that these pieces are really hard for your brain. It also explains why you “act out” the way you do sometimes, just like that baby, even though you are grown: asking for help, pushing help away, or matching the unavailability of help by pretending you don’t need it.
Because that’s what is under shame: that your infant self still depended on your caregiver for survival, which is what kicked in the vagal nerves. Because you depended on them for survival, you couldn’t think they were “bad” even when they were not meeting your needs. Instead, you thought YOU were bad for needing in the first place.
But thanks to the vagal nerves, we know that healing comes the same way, and that this can be repaired. Eye contact. Emotional connection. Mirroring back your experience. Being present with you in those trauma responses. Reciprocity of caring and response. Safe touch when it’s appropriate. That’s the stuff of healing.
This matters in your choice of therapist. This matters in your choice of spouse. This matters in choosing healthy and safe friendships. This matters in your choice of parenting style that you so desperately want to be different than what your own experience was like.
This matters because not only do we understand our world through neuroception, but there is also a process called introception - which is our own awareness of our own life, body, and potential to control both.
This is the birthplace of presence, the ability to be oriented to time and place. It is a state of existence, rather than avoidance. It is the ability to reassure yourself, and to know how to connect when you need reassurance from others.
This grows into emotional regulation, which then grows into your internal and external experiences being more congruent.
Only then do we know when we are safe, and where we are safe, and with whom we are safe.
Only then are we safe enough to remember.
Because isn’t just the talking that heals us.
It’s the connection with whom we are talking that confirms safety and holds us in the present, even when we start to remember.
And that’s what helps us connect our Selves.
REFERENCES:
Adolphs R. Trust in the brain. Nature Neuroscience. 2002;5:192–193.
Ahern GL, Sollers JJ, Lane RD, Labiner DM, Herring AM, Weinand ME, Hutzler R, Thayer JF. Journal of Clinical Child Psychology. 2001;25:388–397.
Austin MA, Riniolo TC, Porges SW. Borderline Personality Disorder and Emotion Regulation: Insights from the Polyvagal Theory. Brain and Cognition in press.
Barnsley, Megan Christina. August 2012. The Social Consequences of Defensive Phsyiological States. Doctoral Thesis at the University of Exeter. Retrieved from https://core.ac.uk/download/pdf/12826597.pdf on 21 March 2019.
Beauchaine TP, Bell Z, Knapton E, McDonough‐Caplan H, Shader T, Zisner A. Respiratory sinus arrhythmia reactivity across empirically based structural dimensions of psychopathology: A meta‐analysis. Psychophysiology. 2019.
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.
Berthoud, H. R.; Neuhuber, W. L. (2000). "Functional and chemical anatomy of the afferent vagal system". Autonomic Neuroscience. 85 (1–3): 1–17.
Berntson GG, Bigger JT, Eckberg DL, Grossman PG, Kaufmann M, Malik HN, Nagaraja HN, Porges SW, Saul JP, Stone PH, van der Molen MW. Heart rate variability: Origins, methods, and interpretive caveats. Psychophysiology. 1997;34:623–648.
Blair C, Peters R. Physiological and Neurocognitive Correlates of Adaptive Behavior in Preschool among Children in Head Start. Developmental Neuropsychology. 2003;24:479–497.
Blass EM, Watt LB. Suckling and sucrose-induced analgesia in human newborns. Pain. 1999;83:611–623.
Calkins SD, Keane SP. Cardiac vagal regulation across the preschool period: Stability, continuity, and implications for childhood adjustment. Developmental Psychobiology. 2004;45:101–112.
Carter CS. Neuroendocrine perspectives on social attachment and love. Psychoneuroendocrinology. 1998;23:779–818.
Chambers AS, Allen JJB. Vagal tone as indicator of treatment response in major depression. Psychophysiology. 2002;39:861–864.
Cheng Z, Powley TL. Nucleus ambiguus projections to cardiac ganglia of rat atria: An anterograde tracing study. Journal of Comparative Neurology. 2000;424:588–606.
Cohen J. Statistical Power Analysis for the Behavioral Sciences. 2. Lawrence Erlbaum Associates; Hillsdale, NJ: 1988.
Cole PM, Zahn-Waxler C, Fox NA, Usher BA, Welsh JD. Individual differences in emotion regulation and behavior problems in preschool children. Journal of Abnormal Psychology. 1996;105:518–529.
Craig AD. Forebrain emotional asymmetry: A neuroanatomical basis? Trends in Cognitive Sciences. 2005;9:566–571.
Critchley HD. Neural mechanisms of autonomic, affective, and cognitive integration. Journal of Comparative Neurology. 2005;493:154–166.
Córdova, E; et al. (April 2010). "Neurological manifestations of Chagas' disease". Neurological Research. 32 (3): 238–44.
Denver JW, Reed SF, Porges SW. Methodological issues in the quantification of respiratory sinus arrhythmia. Biological Psychology. 2006.
Dutschmann, Mathias; Bautista, Tara G.; Mörschel, Michael; Dick, Thomas E. (2014). "Learning to breathe: Habituation of Hering–Breuer inflation reflex emerges with postnatal brainstem maturation". Respiratory Physiology & Neurobiology. 195: 44–49.
Eckberg DL. The human respiratory gate. Journal of Physiology. 2003;548:339–352.
Eljamel, Sam (2011). Problem Based Neurosurgery. p. 66.
Mandal, Ananya (25 September 2013). "Vomiting Mechanism". News Medical. Archived from the original on 4 January 2015. Retrieved 27 June 2015.
Berthoud HR (2008). "The vagus nerve, food intake and obesity". Regulatory Peptides. 149 (1–3): 15–25.
Dana, Deb. 2014. The Polyvagal Theory in Therapy: Engaging the Rhythm of Regulation (Norton).
de Lartigue G, Ronveaux CC, Raybould HE (2014). "Deletion of leptin signaling in vagal afferent neurons results in hyperphagia and obesity". Molecular Metabolism. 3 (6): 595–607.
Fabes RA, Eisenberg N. Regulatory control and adults’ stress-related responses to daily life events. Journal of Personality and Social Psychology. 1997;73:1107–1117.
Fox NA. If it’s not left, it’s right: Electroencephalography asymmetry and the development of emotion. American Psychologist. 1991;46:863–872.
Friedman BH, Thayer JF. Autonomic balance revisited: Panic anxiety and heart rate variability. Journal of Psychosomatic Research. 1998;44:133–151.
Graham FK, Clifton RK. Heart rate change as a component of the orienting response. Psychological Bulletin. 1966;65:305–320.
Grippo AJ, Lamb DG, Carter CS, Porges SW. Autonomic and cardiac regulation in the prairie vole: implications for translational research investigating brain. unpublished.
Grossman P, Karemaker J, Wieling W. Prediction of tonic parasympathetic cardiac control using respiratory sinus arrhythmia: the need for respiratory control. Psychophysiology. 1990a;28:201–216.
Grossman P, Svebak S. Respiratory sinus arrhythmia as an index of parasympathetic cardiac control during active coping. Psychophysiology. 1987;24:228–235.
Grossman P, van Beek J, Wientjes C. A comparison of three quantification methods for estimation of respiratory sinus arrhythmia. Psychophysiology. 1990b;27:702–714.
Grossman P, Wilhelm FH, Spoerle M. Respiratory sinus arrhythmia, cardiac vagal control, and daily activity. American Journal of Physiology, Heart and Circulatory Physiology. 2004;287:H728–H734.
Haselton JR, Solomon IC, Motekaitis AM, Kaufman MP. Bronchomotor vagal preganglionic cell bodies in the dog: An anatomic and functional study. Journal of Applied Physiology. 1992;73:1122–1129.
Hatfield BD, Santa Maria DL, Porges SW, Potts JT, Spalding T, Byrne EA. Respiratory sinus arrhythmia during exercise in aerobically trained and untrained men. Medicine and Science in Sports and Exercise. 1998;30:206–214.
Hayano J, Sakakibara Y, Yamada M, Ohte N, Fujinami T, Yokoyama K, Watanabe Y, Takata K. Decreased magnitude of heart rate spectral components in coronary artery disease: Its relation to angiographic severity. Circulation. 1990;81:1217–24.
Hayano J, Yasuma F, Okada A, Mukai S, Fujinami T. Respiratory sinus arrhythmia. A phenomenon improving pulmonary gas exchange and circulatory efficiency. Circulation. 1996;94:842–847.
Hering HE. A functional test of heart vagi in man. Menschen Munchen Medizinische Wochenschrift. 1910;57:1931–1933.
Hirsch JA, Bishop B. Respiratory sinus arrhythmia in humans: how breathing pattern modulates heart rate. American Journal of Physiology. 1981;241:H620–629.
Hnatiow M, Lang J. Learned stabilization of cardiac rate. Psychophysiology. 1965;1:330–336.
Hofer MA. Cardiac respiratory function during sudden prolonged immobility in wild rodents. Psychosomatic Medicine. 1970;32:633–647.
Houle MS, Billman GE. Low-frequency component of the heart rate variability spectrum: a poor marker of sympathetic activity. American Journal of Physiology. 1999;276:H215–223.
Insel TR, Young LJ. The neurobiology of attachment. Nature Reviews Neuroscience. 2001;2:129–136.
Jackson JH. Evolution and dissolution of the nervous system. In: Taylor J, editor. Selected Writings of John Hughlings Jackson. Stapes Press; London: 1958. pp. 45–118.
Jackson JC, Kantowitz SR, Graham FK. Can newborns show cardiac orienting? Child Development. 1971;42:107–121.
Kalsbeek JWH, Ettema JH. Scored irregularity of the heart pattern and the measurement of perceptual or mental load. Ergonomics. 1963;6:306–307.
Katona PG, Jih F. Respiratory sinus arrhythmia: noninvasive measure of parasympathetic cardiac control. Journal of Applied Physiology. 1975;39:801–805.
Katz LF, Gottman JM. Vagal tone protects children from marital conflict. Development and Psychopathology. 1995;7:83–92.
Keay KA, Bandler R. Parallel circuits mediating distinct emotional coping reactions to different types of stress. Neuroscience and Biobehavioral Reviews. 2001;25:669–678.
Kennedy AE, Rubin KH, Hastings PD, Maisel B. Longitudinal relations between child vagal tone and parenting behavior: 2 to 4 years. Developmental Psychobiology. 2004;45:10–21.
Kryter KD. The Effects of Noise on Man. Academic Press; New York: 1985.
Lacey JI. Somatic response patterning and stress: Some revisions of activation theory. In: Appley MH, Trumbull R, editors. Psychological Stress: Issues in Research. Appleton-Century-Crofts; New York: 1967. pp. 14–37.
Lacey JI, Lacey BC. Verification and extension of the principle of autonomic response stereotypy. American Journal of Psychology. 1958;71:50–73.
Lang PJ, Sroufe LA, Hastings JE. Effects of feedback and instructional set on the control of cardiac rate variability. Journal of Experimental Psychology. 1967;75:425–431.
Langley JN. The Autonomic Nervous System. Heffer & Sons; Cambridge, England: 1921.
Leary A, Katz LFD. Coparenting, family-level processes, and peer outcomes: The moderating role of vagal tone. Development and Psychopathology. 2004;16:593–608.
Leckman JF, Grice DE, Boardman J, Zhang H, Vitale A, Bondi C, Alsobrook J, Peterson BS, Cohen DJ, Rasmussen SA, Goodman WK, McDougle CJ, Pauls DL. Symptoms of obsessive-compulsive disorder. American Journal of Psychiatry. 1997;154:911–917.
Leite-Panissi CR, Coimbra NC, Menescal-de-Oliveira L. The cholinergic stimulation of the central amygdala modifying the tonic immobility response and antinociception in guinea pigs depends on the ventrolateral periaqueductal gray. Brain Research Bulletin. 2003;60:167–178.
Lonstein JS, Stern JM. Site and behavioral specificity of periaqueductal gray lesions on postpartum sexual, maternal, and aggressive behaviors in rats. Brain Research. 1998;804:21–35.
Luo ZX, Crompton AW, Sun AL. A new mammaliaform from the early Jurassic and evolution of mammalian characteristics. Science. 2001;292:1535–1540.
Lyonsfield JD, Borkovec JD, Thayer JF. Vagal tone in generalized anxiety disorder and the effects of aversive imagery and worrisome thinking. Behavior Therapy. 1995;26:457.
Malliani A, Pagani M, Lombardi F, Cerutti S. Cardiovascular neural regulation explored in the frequency domain. Circulation. 1991;84:1482–1492.
Mendelowitz D. Firing properties of identified parasympathetic cardiac neurons in nucleus ambiguus. American Journal of Physiology. 1996;271:H2609–H2614.
Mendelowitz D, Kunze DL. Identification and dissociation of cardiovascular neurons from the medulla for patch clamp analysis. Neuroscience Letters. 1991;132:217–221.
Miller NE. Biofeedback and visceral learning. Annual Review of Psychology. 1978;29:373–404.
Morris JL, Nilsson S. The circulatory system. In: Nilsson S, Holmgren S, editors. Comparative Physiology and Evolution of the Autonomic Nervous System. Chur, Switzerland: Harwood Academic Publishers; 1994.
Morris JS, Ohman A, Dolan RJ. A subcortical pathway to the right amygdale mediating “unseen” fear. Proceedings of the National Academy of Sciences. 1999;96:1680–1685.
Movius HL, Allen JJB. Cardiac vagal tone, defensiveness, and motivational style. Biological Psychology. 2005;68:147–162.
Komisaruk BR, Whipple B, Crawford A, Liu WC, Kalnin A, Mosier K (2004). "Brain activation during vaginocervical self-stimulation and orgasm in women with complete spinal cord injury: fMRI evidence of mediation by the vagus nerves". Brain Res. 1024 (1–2): 77–88.
Pocai, A; TK Lam; Gutierrez-Juarez R (2005). "Hypothalamic K(ATP) channels control hepatic glucose production". Nature. 434 (7036): 1026–31.
Pagotto, U. (2009). "Where does insulin resistance start? The brain". Diabetes Care. 32 (2): S174–77.
Nemeroff, Charles B.; et al. (2006). "VNS therapy in treatment-resistant depression: clinical evidence and putative neurobiological mechanisms". Neuropsychopharmacology. 31 (7): 1345–55.
Eisenstein, Michael (2013). "Neurodevice startups target peripheral nervous system". Nature Biotechnology. 31 (10): 865–66.
"Feedback on Nexium Side Effects and Usage, page 54". www.askdocweb.com. Archived from the original on 28 December 2017. Retrieved 28 December 2017. Clinical trials are currently underway in Antwerp, Belgium using VNS for the treatment of tonal tinnitus. This came from a breakthrough published in 2011 by researchers at the University of Texas, Dallas. They found that tinnitus could be successfully suppressed in rats when tones were paired with brief pulses of stimulation of the vagus nerve.
Monteiro, D. A., Taylor, E. W., Sartori, M. R., Cruz, A. L., Rentin, F. T., and LEite, C. A.C. 2018. Cardiorespiratory interactions previously identified as mammalian are present in the primitive lungfish. Evolutionary Biology (2018) 4.
"Nerve Stimulation Highly Effective in Battling Tinnitus, Nature Study Reports - UT Dallas News". Archived from the original on 24 February 2011. Retrieved 25 March 2011.
Noesselt T, Driver J, Heinze HJ, Dolan R. Asymmetrical activation in the juamn brain during processing of fearful faces. Current Biology. 2005;15:424–429.
Phillips ML, Drevets WC, Rauch SL, Lane R. Neurobiology of emotion perception I: The neural basis of normal emotion perception. Biological Psychiatry. 2003a;54:504–514.
Phillips ML, Drevets WC, Rauch SL, Lane R. Neurobiology of emotion perception II: Implications for major psychiatric disorders. Biological Psychiatry. 2003b;54:515–528.
Pine DS, Wasserman GA, Miller L, Coplan JD, Bagiella E, Kovelenku P, Myers MM, Sloan RP. Heart period variability and psychopathology in urban boys at risk for delinquency. Psychophysiology. 1998;35:521–529.
Porges, Stephen. 2011. The Polyvagal Theory: Neurophysiological Foundations of Emotions, Attachment, Communication, and Self-regulation (Norton).
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.
Porges, Stephen W (October 2001). "The polyvagal theory: phylogenetic substrates of a social nervous system". International Journal of Psychophysiology. Elsevier. 42 (2): 123–146.
Porges SW. Heart rate variability and deceleration as indices of reaction time. Journal of Experimental Psychology. 1972;92:103–110.
Porges SW. Heart rate variability: An autonomic correlate of reaction time performance. Bulletin of the Psychonomic Society. 1973;1:270–272.
Porges SW. Peripheral and neurochemical parallels of psychopathology: A psychophysiological model relating autonomic imbalance to hyperactivity, psychopathy, and autism. In: Reese HW, editor. Advances in Child Development and Behavior. Vol. 11. Academic Press; New York: 1976. pp. 35–65.
Porges SW. Method and Apparatus for Evaluating Rhythmic Oscillations in Aperiodic Physiological Response Systems. United States Patent Number. 4,510,944 1985.
Porges SW. Orienting in a defensive world: Mammalian modifications of our evolutionary heritage: A Polyvagal Theory. Psychophysiology. 1995;32:301–318.
Porges SW. Emotion: An evolutionary by-product of the neural regulation of the autonomic nervous system. In: Carter CS, Kirkpatrick B, Lederhendler I, editors. The Integrative Neurobiology of Affiliation, Annals of the New York Academy of Sciences. Vol. 807. 1997. pp. 62–77.
Porges SW. Love: An emergent property of the mammalian autonomic nervous system. Psychoneuroendocrinology. 1998;23:837–861.
Porges SW. The Polyvagal Theory: Phylogenetic substrates of a social nervous system. International Journal of Psychophysiology. 2001a;42:123–146.
Porges SW. Is there a major stress system at the periphery other than the adrenals? In: Broom DM, editor. Dahlem Workshop on Coping with Challenge: Welfare in Animals including Humans. Dahlem University Press; Berlin: 2001b. pp. 135–149.
Porges SW. Social engagement and attachment: A phylogenetic perspective. Roots of Mental Illness in Children, Annals of the New York Academy of Sciences. 2003;1008:31–47.
Porges SW, Bohrer RE. Analyses of periodic processes in psychophysiological research. In: Cacioppo JT, Tassinary LG, editors. Principles of Psychophysiology: Physical, Social, and Inferential Elements. Cambridge University Press; New York: 1990. pp. 708–753.
Porges SW, Bohrer RE, Keren G, Cheung MN, Franks GJ, Drasgow F. The influence of methylphenidate on spontaneous autonomic activity and behavior in children diagnosed as hyperactive. Psychophysiology. 1981;18:42–48.
Porges SW, Byrne EA. Research methods for measurement of heart rate and respiration. Biological Psychology. 1992;34:93–130.
Porges SW, Doussard-Roosevelt JA, Maiti AK. Vagal tone and the physiological regulation of emotion. Emotion Regulation: Behavioral and Biological Considerations. In: Fox NA, editor. Monograph of the Society for Research in Child Development. Vol. 59. 1994. pp. 167–186. 2–3, Serial No. 240.
Porges SW, Doussard-Roosevelt JA, Portales AL, Greenspan SI. Infant regulation of the vagal "brake" predicts child behavior problems: A psychobiological model of social behavior. Developmental Psychobiology. 1996;29:697–712.
Porges SW, McCabe PM, Yongue BG. Respiratory-heart rate interactions: Psychophysiological implications for pathophysiology and behavior. In: Cacioppo J, Petty R, editors. Perspectives in Cardiovascular Psychophysiology. Guilford; New York: 1982. pp. 223–264.
Porges SW, Raskin DC. Respiratory and heart rate components of attention. Journal of Experimental Psychology. 1969;81:497–503.
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.
Sachis PN, Armstrong DL, Becker LE, Bryan AC. Myelination of the human vagus nerve from 24 weeks postconceptual age to adolescence. Journal of Neuropathology and Experimental Neurology. 1982;41:466–472.
Tyler, Richard; Cacace, Anthony; Stocking, Christina; Tarver, Brent; Engineer, Navzer; Martin, Jeffrey; Deshpande, Aniruddha; Stecker, Nancy; Pereira, Melissa; Kilgard, Michael; Burress, Chester; Pierce, David; Rennaker, Robert; Vanneste, Sven (20 September 2017). "Vagus Nerve Stimulation Paired with Tones for the Treatment of Tinnitus: A Prospective Randomized Double-blind Controlled Pilot Study in Humans". Scientific Reports. 7 (1): 11960.
Truex RC, Carpenter MB. Human Neuroanatomy. 6. Williams and Wilkins; Baltimore, MD: 1969.
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.
Vibhuti N, Singh; Monika Gugneja (22 August 2005). "Supraventricular Tachycardia". eMedicineHealth.com. Archived from the original on 16 December 2008. Retrieved 28 November 2008.