Ross Hauser, MD.
Research into the vagus nerve is expanding rapidly. Once discussed primarily in relation to heart rate, digestion, and the parasympathetic nervous system, the vagus nerve is now being investigated for its potential roles in inflammation, myocardial injury, cardiac regeneration, arrhythmia susceptibility, autonomic balance, and recovery following myocardial infarction. This research raises an interesting question from our perspective at Caring Medical: If researchers are investigating ways to stimulate the vagus nerve to improve cardiovascular regulation and protect the injured heart, should doctors also investigate conditions that may interfere with the normal function of the vagus nerve itself?
This question is at the center of our published research in the journal Frontiers in Neurology (1). Here we coined the term “cervicovagopathy,” a proposed condition in which cervical ligament instability, loss of the normal cervical curve, and abnormal cervical structure may subject the vagus nerve to chronic stretch or compression as it travels through the neck
Vagal activity can influence the environment in which injured heart muscle attempts to survive and recover.
Note: Research has not demonstrated that cervical instability causes myocardial infarction, nor has it demonstrated that treating cervical instability improves recovery following a heart attack. Acute myocardial infarction requires established emergency and cardiovascular treatment. What the emerging research does demonstrate is that the vagus nerve is an important component of cardiovascular physiology. This makes the causes and consequences of impaired vagal function an increasingly relevant area of investigation. Let’s look at some of this research.
A January 2026 review published in iScience (2) examined vagus nerve stimulation as a potential therapeutic approach to myocardial ischemia-reperfusion injury (MIRI). Ischemia occurs when heart muscle does not receive adequate blood and oxygen. Reperfusion occurs when circulation is restored, as may happen after treatment for an acute myocardial infarction. While restoring circulation is essential, reperfusion itself can trigger additional inflammation, oxidative stress, cellular injury, mitochondrial dysfunction, and cardiomyocyte death.
This secondary process is known as myocardial ischemia-reperfusion injury.
The researchers reviewed evidence suggesting that vagus nerve stimulation may potentially reduce this injury through several mechanisms, including suppression of inflammatory cascades, modulation of the vagus nerve-spleen pathway, improvement in mitochondrial function, reduction of oxidative stress and apoptosis, and regulation of autonomic activity associated with arrhythmia risk. The authors nevertheless emphasized that VNS remains investigational in this setting. However, the growing cardiovascular interest in vagus nerve stimulation tells us something significant: vagal activity can influence the environment in which injured heart muscle attempts to survive and recover.
After myocardial infarction, this vagal balance can become disrupted.
The heart is regulated by a continuous interaction between the sympathetic and parasympathetic nervous systems. The sympathetic nervous system increases heart rate and cardiac activity during physical or physiological stress. Parasympathetic influence, much of which is conveyed through the vagus nerve, provides an important counter-regulatory influence. After myocardial infarction, this vagal balance can become disrupted.
Cardiovascular researchers have therefore become interested in whether increasing parasympathetic or vagal activity could reduce some of the harmful physiological responses that occur during and after myocardial ischemia.
A 2024 review in Bioelectronic Medicine (3) specifically examined vagal nerve stimulation in myocardial ischemia-reperfusion injury. The authors described a strong rationale for neuromodulation strategies capable of reducing excessive sympathetic activity and/or increasing vagal tone. They reviewed both invasive cervical vagus nerve stimulation and noninvasive transcutaneous auricular vagus nerve stimulation.
The progression of this research from experimental models toward less-invasive methods demonstrates the growing interest in targeting the autonomic nervous system as part of cardiovascular medicine.
The vagus nerve and inflammation after myocardial injury
One of the most important proposed mechanisms involves the cholinergic anti-inflammatory pathway. The vagus nerve participates in neural regulation of immune and inflammatory activity. Vagal signaling can stimulate acetylcholine-mediated pathways that suppress excessive production of inflammatory cytokines. Inflammation is necessary for clearing damaged tissue and initiating repair, but an excessive or prolonged inflammatory response can contribute to additional myocardial injury and unfavorable ventricular remodeling. VNS research therefore does not propose simply “turning inflammation off.” Instead, the concept is that the nervous system may help regulate the magnitude and duration of inflammatory signaling. This neuroimmune connection is one reason the vagus nerve is the focus in new cardiovascular research.
Noninvasive stimulation of the cervical vagus nerve protected the heart in an experimental model
A study published in Cardiovascular Drugs and Therapy (4) investigated a noninvasive approach using focused ultrasound stimulation of the cervical vagus nerve during myocardial ischemia-reperfusion. In an experimental model, focused ultrasound was directed at the right cervical vagus nerve during early reperfusion. The researchers assessed inflammatory markers, arrhythmias, cardiac pathology, oxidative stress, fibrosis, apoptosis, cardiac function, and infarct size. The results supported a cardioprotective effect and implicated the cholinergic anti-inflammatory pathway as an important mechanism. This remains preclinical research and cannot be interpreted as proof that focused ultrasound VNS should be used clinically after myocardial infarction.
What it does show is that researchers are increasingly targeting the cervical portion of the vagus nerve as a potential pathway through which cardiovascular physiology can be influenced. In our research, that focus on anatomical location is of great interest.
What happens to the vagus nerve before it reaches the heart and other organs. Can an abnormal mechanical environment in the cervical spine interfere with vagus nerve function?
The vagus nerve originates in the brainstem and travels through the jugular foramen before descending through the neck. Within the cervical region, the vagus nerve travels in close relationship to the internal jugular vein and carotid artery within the carotid sheath. It then continues into the chest, where vagal branches participate in cardiovascular, pulmonary, and visceral regulation. We have focused an aspect of our research on what may happen to the vagus nerve before it reaches the heart and other organs and we ask “can an abnormal mechanical environment in the cervical spine interfere with vagus nerve function?”
The cervicovagopathy theory
In July 2025, our team published the paper: “Cervicovagopathy: ligamentous cervical instability and dysstructure as a potential etiology for vagus nerve dysfunction in the cause of human symptoms and diseases.” which I cited above.
Here we proposed the term cervicovagopathy for vagus nerve dysfunction arising from cervical spine pathology. The theory proposes a progression beginning with weakening or stretching of the posterior cervical ligaments. As these ligaments lose their ability to adequately stabilize the cervical vertebrae, excessive or abnormal movement may develop. Over time, this can be accompanied by forward head posture and deterioration of the normal cervical lordotic curve—a process the authors describe as cervical dysstructure.
According to the “Hauser hypothesis,” these changes can alter the physical environment surrounding the carotid sheath. Because the internal jugular veins and vagus nerves travel immediately anterior to the cervical spine, forward displacement of the upper cervical vertebrae and deterioration of normal cervical alignment could potentially contribute to stretch or compression of the vagus nerve. Our study further proposed that chronic mechanical stress could initially interfere with nerve conduction and, if persistent, potentially contribute to vagus nerve degeneration.
Cardiology researchers are attempting to increase beneficial vagal signaling.
The theory of cervicovagopathy becomes more interesting when considered alongside the cardiovascular VNS literature. Cardiology researchers are attempting to increase beneficial vagal signaling. Based on what we see that in certain patients, we ask: “can overlooked structural problems in the neck can be reducing normal vagal signaling?”
These are different research questions, but they converge on the same anatomical structure. One research pathway asks: Can we stimulate the vagus nerve to help restore autonomic balance? We ask: Could there be a mechanical reason the vagus nerve is not functioning normally?
Myocardial infarction may itself alter parasympathetic function
Now let’s add another aspect of this line of research. Myocardial infarction does not only injure cardiac muscle. Research has shown that MI can also produce pathological alterations throughout the cardiac autonomic nervous system. Experimental work has documented parasympathetic dysfunction following myocardial infarction and abnormalities in neural activity within cardiac parasympathetic pathways. Increasing parasympathetic drive through VNS has, in experimental models, reduced susceptibility to ventricular arrhythmias.
This creates a potentially self-reinforcing problem: Cardiac injury may disrupt autonomic regulation, while impaired autonomic regulation may make the injured heart more susceptible to further electrical and physiological instability. That is one reason restoration of autonomic balance has become an important target of cardiovascular neuromodulation research.
Could the vagus nerve participate in cardiac regeneration?
A 2025 review published in Cardiology (5) examined the importance of neural regulation and innervation following myocardial infarction. The authors discussed evidence that the vagus nerve may positively influence cardiomyocyte proliferation and regeneration, ventricular remodeling, and cardiac function after myocardial infarction. The autonomic nervous system may not simply control how fast the heart beats. Neural signaling may also participate in the biological environment governing cardiac repair and remodeling. This is experiment and evolving research.
Vagus nerve stimulation may reduce arrhythmia susceptibility
One of the more consistent themes in VNS research is its potential influence on cardiac electrical stability. A 2026 study (6) of VNS preconditioning found reductions in infarct size, arrhythmia burden, inflammatory responses, and apoptosis, together with preservation of cardiac function following ischemia-reperfusion injury.
Earlier pooled analysis of preclinical studies also found VNS to be associated with reduced myocardial infarct size following ischemia-reperfusion injury, although there was substantial heterogeneity between the studies. These findings may help reinforce the idea that parasympathetic-vagal signaling influences cardiac electrophysiology and the myocardial response to injury.
Caring Medical / Hauser research
Our 2025 cervicovagopathy paper developed concepts initially described in our 2024 Frontiers in Neurology publication examining ligamentous cervical instability and the effects of forward head posture and cervical dysstructure. (7) Here we proposed that progressive loss of cervical structure can bring the upper cervical vertebrae into closer mechanical relationship with structures contained within the carotid sheath, particularly the internal jugular veins and vagus nerves. We hypothesized that compression of the internal jugular veins could affect cerebral venous drainage, while stretch or compression of the vagus nerve could contribute to autonomic dysfunction. Again, this is best understood as a proposed mechanism rather than an established cause of systemic disease.
We also published original research in Frontiers in Neurology (8) in May 2026 involving 227 consecutive patients evaluated at an outpatient neck center for chronic brain-based symptoms.
Within this selected clinical population:
- 100% had radiologically identified forward head posture.
- 90% had decreased cervical lordosis.
- 87% had C1-C2 ligamentous cervical instability.
- 95% had decreased vagus nerve cross-sectional areas.
- 98% had decreased internal jugular vein cross-sectional areas.
- 99% had elevated optic nerve sheath diameters.
We also found statistically significant but weak relationships between certain measures of upper cervical instability and vagus nerve cross-sectional area. This was a retrospective, cross-sectional study in a symptomatic population presenting to our neck center. It cannot establish for certainty that cervical instability caused the abnormal vagus nerve measurements, nevertheless, the study provides objective imaging and ultrasound findings that allow the cervicovagopathy hypothesis to be investigated beyond symptom reporting alone.
Heart rate variability and the cervical vagus nerve
One way researchers attempt to assess autonomic balance is through heart rate variability (HRV). HRV evaluates variations in the interval between heartbeats. Although HRV cannot diagnose cervical vagus nerve compression and should not be viewed as a direct measurement of vagal nerve function, certain HRV parameters provide information about autonomic regulation. We have incorporated HRV into our evaluation of patients suspected of having cervicovagopathy. Cardiology has long recognized autonomic imbalance and altered HRV as important markers in cardiac populations, while our research asks whether abnormalities in the cervical portion of the vagus nerve could represent one structural contributor to autonomic imbalance in certain patients.
Summary
There are no clinical trials showing that correction of cervical instability prevents myocardial infarction, reduces infarct size, prevents cardiac arrhythmias after MI, or improves post-MI survival. But there is now substantial evidence that the autonomic nervous system—and particularly vagal signaling—plays an important role in cardiovascular physiology and myocardial injury. At the same time, we have published a testable hypothesis and preliminary clinical findings suggesting that abnormal cervical mechanics may influence the anatomical environment of the vagus nerve in a subgroup of patients.
The Caring Medical perspective
At Caring Medical, patients are not evaluated for cervical instability because they have cardiovascular disease alone. Patients considered for a cervical instability evaluation generally have a broader clinical picture that may include chronic neck pain, history of cervical trauma, abnormal neck motion, forward head posture, loss of cervical lordosis, dizziness, palpitations, digestive symptoms, exercise intolerance, orthostatic symptoms, or other complaints suggestive of autonomic dysfunction.
The goal is to determine whether there is objective evidence of cervical ligament instability, cervical dysstructure, or abnormalities involving structures within the carotid sheath. This represents a very different clinical question from treating coronary artery disease or myocardial infarction.
Related articles
Ross Hauser, MD Reviews Cervical Spine Instability and Potential Effects on Brain Physiology
Chronic Neck Pain: Making the Connection Between Capsular Ligament Laxity and Cervical Instability
References
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