In my previous article,
I introduced the Vagus Nerve in the context of its role in Parkinson's Disease. There, I noted that
"...there are actually two major branches of the Vagus Nerve, and this 'polyvagal' feature of the nerve in humans is incredibly important for understanding Parkinson's Disease. This is because the more primitive, or 'reptilian', branch of the VN governs 'playing dead' - the 'Freeze' stress response - which is the state in which people with PD appear to be stuck. However, the details of this are quite involved, so in this first article on the subject, I shall concentrate on the role of the more evolved, or 'mammilian', branch of the VN..."
and then, like virtually every other article you will find on the subject, including the vast majority of those I cite in the above article, I proceeded to describe ways to stimulate "the" Vagus Nerve, and espoused its benefits.
I subsequently expanded on the polyvagal characteristics of the Vagal system in
and we began to understand it actually has somewhat of a "Jekyll and Hyde" nature.
In this article, I would like to return to this topic, and concentrate this time on that primitive, reptilian branch of the Vagus Nerve, and its potentially central role in Parkinson's Disease.
The Dorsal Vagus Nerve
Let's first summarize the two branches. and their important roles in the Nervous System's regulation of our bodies. The following is adapted from
while a collection of peer reviewed technical science articles on this by Dr Stephen Porges and co-workers can also be found in
THE POLYVAGAL THEORY: NEUROPHYSIOLOGICAL FOUNDATIONS OF EMOTIONS, ATTACHMENT, COMMUNICATION, AND SELF-REGULATION.
The Vagus Nerve includes a more primitive set of fibers which evolved with ancient, extinct reptiles: the Dorsal Vagus [aka: vegetative; reptilian; unmylinated; subdiaphragmatic].
The Vagus Nerve also includes a more advanced set of fibers which evolved with appearance of mammals: the Ventral Vagus [aka: smart; mammalian; mylinated; suprediaphragmatic].
One in six of the Vagus Nerve fibers are of the mylinated (advanced) type.
Most of the unmylinated (primitive) fibers regulate organs below the diaphragm such as the gut.
The Dorsal Vagus fibers connect the gut to the brain [most of which transmit signals from the gut to the brain], and is responsible for gut motility and neuropeptides.
The Dorsal Vagus is activated, but with the Ventral Vagus inhibited, when the Nervous System is in Survival mode, and is responsible for the freeze/shutdown/death feigning response of mammals to life-threatening dangers.
The Enteric Nervous System is a mesh of neurons which regulate the gastrointestinal system, embedded in lining of digestive tract from esophagus to anus, capable of functioning independently, but receives considerable information from autonomic nervous system (ANS).
This Enteric Nervous System is optimal when functioning with Ventral Vagus active and in control, such that Dorsal Vagus is not in defensive mode.
People who experience immobilization (freeze/shutdown behaviours) almost invariably experience gut problems: the two are not independent because both are functions of the Dorsal Vagus.
When the Dorsal Vagus is activated for a immobilization defence, gut and gastric problems will occur.
Problems also occur when fight/flight the defence system is activated chronically, and the activated sympathetic nervous system also dampens the Dorsal and Ventral Vagus Nerve's ability to support healthy digestive functions.
If the Dorsal Vagus has been used to immobilize the system, this may have knock on effect disturbing its function, causing to it surge or become too quiescent, leading to long term medical problems in the gut, such as IBS, fibromalgia, obesity.
People who have had both branches of their Vagus Nerves severed surgically were found to have a significant protection from Parkinson's Disease diagnosis later in life.
Immobilization due to Dorsal Vagus Activation
Next, we consider in depth the Freeze/Shutdown/Death Feigning function of the human Nervous System which results in immobilization. Again, the following is adapted from Dr Stephen Porges' work.
Death Feigning is an adaptive response of the Nervous System to life threatening situations.
Occurs once options for fight-or-flight response is eliminated/unavailable, such as when restrained or no obvious escape routes.
A primitive response, which evolved in extinct reptilian progenitors, characterized by appearing to be inanimate/dead.
Triggered when our "neuroception" (innate sense of danger/safety) deems lethal threat, imminent death.
Biological mechanism is via activation of the primitive branch of the Vagus Nerve (the Dorsal or Subdiaphragmatic branch), creating a "shutdown" state of the autonomic functions, resulting in low respiration and heart rate.
As humans require very significant amounts of oxygen, time spent in the shutdown state is dangerous and damaging, due to inability to oxygenate the blood and deliver enough oxygen to the brain.
Shutdown now may result in apnea (cessation of breathing), bradycardia (abnormally slow heart action), vasovagal syncope (fainting), defecation and/or dissociation (detachment from physical or emotional reality).
An episode of Death Feigning can have very long term affects, and is strongly implicated in trauma of many kinds.
Shutdown is not a conscious or voluntary response, in the same way passing out in fear is not voluntary, it is a visceral reaction due to inability to fight or flee from perceived lethal danger.
Our Nervous System is constantly evaluating risk below the conscious level, and different people will have different responses to the same event, due to different sensitivities of their Nervous System. Some people can shutdown in the same situations as others may be able to stay calm.
Unlike other mammals, humans appear to have unique difficulty recovering from a Death Feigning event, and our Nervous System can get easily stuck, causing lasting biobehavioural responses which prevent normalization.
These biobehavioural responses are observable in traumatized individuals, due to hyperactivity of the Dorsal Vagus Nerve thereafter, which impacts on the digestive tract, breathing and heart, and brain activity due to hypoxia.
The Dorsal immobilization circuit can however, be co-opted by the Ventral Vagus nerve and associated Social Engagement nervous system, under conditions of safety, especially in intimate or oxytocin generating situations, such as cuddling up.
From the understandings we have gleaned above, I therefore strongly believe that people with Parkinson's Disease have become permanently stuck in the Freeze response of the Nervous System, through the activation of the Dorsal Vagus Nerve. This is the only explanation for Parkinson's Disease that I have come across which is capable of describing and predicting, in a simple and robust way, all the symptoms, peculiarities and real lives of people affected by the condition. This includes not just motor symptoms, but also the issues with the gut and functions of the head, neck and face, for examples. See
for further details of these aspects.
Mechanisms of Shutdown via Dorsal Vagus Activation
More evidence for the role of Dorsal Vagus Nerve activation in Parkinson's Disease comes from the book
Accessing the Healing Power of the Vagus Nerve: Self-Help Exercises for Anxiety, Depression, Trauma, and Autism,
by Stanley Rosenberg, which provides biophysical mechanisms for how the Dorsal Vagus shifts the physiology of the body to create a shutdown state:
"Social engagement is not a fixed state, nor should the position of C1 [the first cervical vertebra or Atlas] and C2 [the second cervical vertebra or Axis] stay fixed. These bones move the instant that our psychological state shifts in moments of happiness, satisfaction, fear, anger, or withdrawal, or when our physiological state shifts among social engagement, dorsal vagus activation, or spinal sympathetic chain activation. A rotation of C1 and C2 can put pressure on the vertebral artery, which supplies the frontal lobes and the brainstem, where the five nerves necessary for social engagement originate."
This helps explain why people with Parkinson's Disease faces go blank, and their voices diminish, when symptomatic: the arteries/nerves supplying the head get pinched.
"It only takes one negative thought to bring C1 and C2 out of joint, affecting our posture and physiology. Our nervous system is quick to be upset, it takes a longer time to settle down when we are safe again. Ten small muscles connect the occipital bone at the base of the skull with C1 and C2. Inappropriate tensions in any of these ten muscles are enough to shift and hold C1 and C2 out of joint."
"Our autonomic nervous system is constantly scanning both our external and internal environments. When everything is good, C1 and C2 come into place, and we get adequate blood flow to the brainstem. When there is a dorsal vagal state, or activity of the spinal sympathetic chain, C1 and C2 rotate out of position, reducing blood flow to the origin of the five cranial nerves in the brainstem and to some areas of the brain. This physiological mechanism takes us away from social engagement, but it also enables us to react when we are challenged or endangered. This mechanism is instinctive, immediate, and bypasses conscious thought. Usually we are not aware of the change."
This also helps to explain why people with Parkinson's Disease do indeed suffer from lack of oxygen to the brain when symptomatic, and indeed ties together various threads of research I discovered previously in:
This mechanism also explains why medicated people with PD seem to "deflate" as a dose of drugs where off - our necks can visibly shorten, our heads move forward and down, our shoulders slump. On the other hand, some people with PD can get symptom relief by exaggerating the head position, and tucking their chin tightly against their chest, opening up the vertebrae at the back of the neck, as exampled in the following video of Michael J. Fox playing the guitar.
"Interventions can release imbalances in the tension of the small muscles that hold the skull and the first two vertebrae in relation to each other, and this repositions the atlas and the occiput. Improved alignment of the vertebrae, especially C1 and C2, improves blood flow to the brain and usually brings a rapid improvement in the function of the five nerves necessary for the state of social engagement."
"If we can give the body the right information with a soft touch at the right place, the body will balance itself. Because we cannot put C1 and C2 into place and expect them to stay that way permanently, we should repeat balancing techniques frequently, or as needed. Since there is no such thing as a fixed state of balance, it is more useful to think of balancing, an ongoing process."
The concept of long term strategies to mobilize the C1 and C2 joints, in order that they can move back into place more easily, also matches my own empirical experiences of the types of exercises and positions that I've found which alleviate my symptoms, and can encourage the next dose of medication to kick in earlier: see my two videos I've included above, for examples.
The activation of the human Nervous System's immobilization (Freeze) response via the role of the Dorsal Vagus Nerve provides a robust and elegant framework for explaining Parkinson's Disease, including not only the major motor symptoms, but also those associated with the digestive tract and social functions. This framework also supports the concept of specific "neural exercises" as a long term strategy for progressive reduction of symptoms, which help the Nervous System feel safe and return to a Parasympathetic state much more readily. See
for more details and lists of specific exercises which I have found have helped me, based on this concept.
The Dorsal Vagus Nerve framework, however, also sets on us on the path towards exploring and understanding the role of trauma in Parkinson's Disease, and therefore to seek the connections with other conditions such as Post-Traumatic Stress Disorder (PTSD) and Dystonia. Indeed, in speaking to very many people affected by PD around the world about their history before diagnosis, I've found that there is almost universally a major physical (injury to neck, back, shoulder, legs, feet abound) or emotional trauma lurking in the background.
Update 7th July 2019
Recently, a couple more scientific journal articles have been published which lend support to the idea.
Transneuronal Propagation of Pathologic α-Synuclein from the Gut to the Brain Models Parkinson’s Disease,
scientists abused mice to discover if the problem protein which is a signature of PD (alpha-synuclein) can get to the brain from the gut via the subdiaphragmatic (dorsal) vagus nerve bundle. They injected the mice with alpha-synuclein into their guts. In some of the mice they also severed the dorsal vagus beforehand. In the mice with intact nerve, they found alpha-synuclein in the brains of mice some time later, and these displayed typical mouse Parkinson's symptoms. On the other hand, the mice with severed dorsal vagus nerves did not show signs of alpha-synuclein in the brain and behaved like "normal" mice.
So this points to the vagus nerve having a principle role in the development of the disease. We can tie this in with another paper experimenting on rodents, which showed that a malfunctioning dorsal vagus nerve results in dopamine deficiency in the brain,
Chronic impairment of the vagus nerve function leads to inhibition of dopamine but not serotonin neurons in rat brain structures,
“… suggests a close relationship between the [dorsal] vagus nerve impairment and the inhibition of dopamine system in the brain structures. This is the first report of such relationship which may suggest that mental changes (pro-depressive) could occur in the first stage of Parkinson's disease far ahead of motor impairment.”
I also came across a scientific role of the role of the dorsal vagus nerve in digestive and gut process, and in regulating pancreatic excretions,
Again, given that digestive and gut issues abound in Parkinson’s Disease, this is another significant link between dorsal vagus dysregulation and the condition. Here, a direct link between dorsal vagus nerve issues and diabetes is also made, in regards to insulin production,
Glutamatergic drive facilitates synaptic inhibition of dorsal vagal motor neurons after experimentally induced diabetes in mice.
A more recent paper expands on this link:
The article is very technical and somewhat impenetrable, so I have attempted to extract the more digestible parts:
"The brain orchestrates peripheral responses to changes in blood glucose concentration. Several recent studies have identified insulin-independent pathways for regulating glucose metabolism and the role of the brain as a glucose regulatory organ is gaining acceptance. Multiple ‘preautonomic’ areas of the brain contribute to systemic glucose [balance]. Much work describing the glucose regulatory function of the brain focuses on the hypothalamic microcircuitry necessary for feeding and satiety, but ample evidence indicates that the brainstem dorsal vagal complex (DVC) plays an important role in modulating plasma glucose and insulin levels, feeding, and energy balance."
"Vagally-mediated parasympathetic output critically regulates visceral functions related to metabolic [balance]... insulin release requires an intact vagus nerve and [damage to the] vagus nerve potently suppresses effects of central insulin... Neurons in the DVC clearly influence blood glucose concentration, yet little is known about the circuitry underlying this effect."
"Neurons throughout the DVC are directly responsive to a wide range of nutrient and satiety signals, including leptin, insulin, lactate, and glucose. GABA release in the dorsal motor nucleus of the vagus (DMV) [part of the brain] is also significantly elevated after the induction of diabetes, consistent with diabetes-induced plasticity of DMV neuronal function, particularly of GABA [cell] receptor activity."
(Supplemental notes from Wikipedia:
"gamma-Aminobutyric acid (GABA) is the chief inhibitory neurotransmitter in the central nervous system. Its principal role is reducing neuronal excitability throughout the nervous system. GABA is also directly responsible for the regulation of muscle tone.")
"Taken together, the DVC, particularly its GABAergic circuitry, appears ideally situated to regulate peripheral glucose metabolism. Despite our appreciation of fundamental autonomic pathways and principles, the role of parasympathetic output in metabolic regulation, including maintenance of blood glucose concentration, is not well understood.”
Dorsal vagus activation or dysregulation may therefore help explain the often proposed links between PD and diabets too, such as the recent article in Psychology Today, which posits that excessive glucose in the brain may be causal of PD and Alzheimer’s.
Update 12th October 2018
Since the publication of the original article below, from May 2018, which proposed that Parkinson's Disease essentially occurs when the Dorsal (subdiaphragmatic, unmylinated) Vagus Nerve is permanently stuck in mediating the "Death Feigning" or immobilazation/freeze stress response, newer research appears to support this concept.
THE GUT-BRAIN-AXIS, THE DORSAL VAGUS NERVE AND DOPAMINE
A scientific journal paper,
actually establishes a direct link of the Vagus Nerve endings in the gut with dopamine production in the Substantia Nigra part of the brain!
•Critical role for the vagal gut-to-brain axis in motivation and reward
• Optogenetic (light) stimulation of the vagal gut-to-brain axis produces reward behaviors
• Asymmetric brain pathways [from right side of gut only] of vagal origin mediate motivation and dopamine activity
• Gut-innervating vagal sensory neurons are major components of the reward circuitry”
"The gut is now recognized as a major regulator of motivational and emotional states."
for a synopsis on some background research on this aspect.
"However, the relevant gut-brain neuronal circuitry remains unknown. We show that optical activation of gut-innervating vagal sensory neurons [create] the hallmark effects of stimulating brain reward neurons. Specifically, right, but not left, vagal sensory [nerve] activation sustained self-stimulation behavior, conditioned both flavor and place preferences, and induced dopamine release from Substantia Nigra."
Parkinson's Disease, in particular, is linked to a lack of dopamine release precisely in this area of the brain.
"Our findings establish the vagal gut-to-brain axis as an integral component of the neuronal reward pathway. They also suggest novel vagal stimulation approaches to affective disorders."
So this seems to help explain the "how" of the mechanism by which the Dorsal [subdiaphragmatic] Vagus branch actually activates freeze/immobilzation in response to stress, perhaps by cutting off or inhibiting the signals from the gut to supply dopamine to the Subtantia Nigra, shutting down self-stimulating reward feedback from the gut/enteric nervous system.
This would seem to indicate that not only does Parkinson's Disease “begin in the gut”, but also that onset of a symptom attack begins in the gut, through right sided Dorsal Vagus activation of its immobilzation function, as proposed below. This matches my own daily experience: when my gut goes quiet and I lose the sensation of my digestive tract, my symptoms are worse. It also helps explains why those who have had their Dorsal Vagus surgically cut get a strong protection from PD, presumably because then the inhibitory communications between gut and Substantia Nigra are also severed.
Another interesting aspect of this research is the asymmetry, in that only the right branch of the Dorsal Vagus is found to be connected with dopaminergic substantia nigra activity in this way. Through the contra-lateralization aspect of the Nervous System, this implies the resulting issue is in the left hemisphere of the brain. We know from the "Divided Brain" work of Iain McGilchrist, see
that the left brain, in particular and in a wider sense, runs mainly on dopamine. We will explore the links with the Divided Brain further in a sequel.
While stimulation of the right Dorsal Vagus has potential therapeutic value, as mentioned in the research, some care will need to be taken in people who experience freezing problems. The stimulation needs to enhance the dopamine reward system from the gut, but not stimulate the freeze response even more, worsening the issues. For example, an older article,
suggests that some forms of stimulation of the Vagus Nerve in the right side (only) of the neck can cause bradycardia, a critical slowing down of heart and breathing rate, a state which will be so familiar for people with PD. Interestingly, this article also finds significant differences in the way the left and right vagus nerves interact with the heart:
“Left vagal projections … course primarily along and between the right pulmonary artery and left superior pulmonary vein. Right vagal projections … are somewhat more diffuse but concentrate around the right pulmonary vein complex and adjacent segments of the right pulmonary artery. We conclude there are parallel, yet functionally distinct, inputs from right and left vagi.”
Another study of September 2018 actually measured the cross-sectional area of the left and right vagus nerve bundles,
and revealed that the Vagus Nerve is indeed significantly smaller in cross-section in people with Parkinson’s Disease than the general population. Interestingly, the right side vagus is found to be more significantly atrophied. Moreoever, the degree of atrophy correlated to symptom severity, and
“…the right vagus nerve [atrophy] but not of the left vagus nerve correlated with the parasympathetic [decrease] of heart rate variability [a measure of robustness to stress]… “
The study concludes that is the unmyelinated Vagus Nerve fibers which atrophy, corresponding to the subdiaphragmatic Dorsal Vagus. Thus this research also suggests that normal communication between the gut and the brain via the Dorsal Vagus Nerve is significantly disrupted and hence a major factor in PD.