Introduction
My name is Dr. Ross Hauser. This video addresses the connection between vagus nerve vasospasm and sudden death syndromes. Lately, the news has featured more and more tragic stories where individuals have died unexpectedly, often with no apparent cause. This trend has drawn attention to a phenomenon known as Sudden Adult Death Syndrome. While many are familiar with Sudden Infant Death Syndrome—where a baby is found deceased in their crib with no clear explanation—there is now growing recognition of similar occurrences in adults, where people die suddenly and unexpectedly.
These alarming patterns inspired me to share a few stories and insights that led me to create this video. But before I delve into those, it is important to define what a vasospasm is and why this topic holds significant meaning for me.
What Is Vasospasm?
A vasospasm occurs when the diameter of an artery suddenly narrows. This narrowing can cause blood cells to accumulate at the site, restricting blood flow much like a traffic jam caused by lane closures on a highway. If one or two lanes are blocked, all the cars must crowd into the remaining open lane, creating congestion. Similarly, when an artery narrows, blood flow may become obstructed, potentially resulting in serious consequences.
If vasospasm affects the heart, it can lead to an ischemic attack, commonly known as angina. The symptoms are identical to those of a heart attack because the underlying pathophysiology is the same: a lack of blood supply to the heart. Often, by the time the person reaches the emergency room, the episode has subsided. However, the danger remains, as a heart attack can occur even without plaque or calcium buildup in the arteries. Vasospasm is an involuntary contraction of the artery, and it can cause death of the organ it supplies. For example, if the blood supply to the liver is cut off due to vasospasm, part or all of the liver may die. This process can affect any organ.
Subarachnoid Hemorrhage and Vagus Nerve Degeneration
Years ago, during my internship at Loyola Medical Center and Hines VA Medical Center in the Chicagoland area, I spent one month in neurosurgery. In this one case a previously healthy gentleman was admitted after losing consciousness. It was discovered that he had suffered a subarachnoid hemorrhage—essentially, a brain bleed. I participated in the emergency surgery, where an artery in his brain had burst. The initial mortality rate for this condition is 50 percent, so the patient had already survived the initial critical phase when he arrived for surgery.
During the procedure, the surgical team carefully entered the brain to locate the ruptured artery. They had to clip the artery, and throughout the operation, there was a risk that the blood clot temporarily sealing the artery could dislodge, which would have resulted in the patient dying instantly on the table. This is considered one of the most challenging brain surgeries. After the artery was clipped, the patient entered recovery. Initially, it seemed that the surgery had been successful and that the patient would recover well. However, sometimes, without any clear explanation, patients begin to experience vasospasm in the brain. In this case, around the second day post-surgery, the patient started to decline. Over several days, I observed the mood of the neurosurgical team and the patient’s family shift from elation at the successful surgery to increasing concern as different parts of the brain began to die. A resident explained to me that, at a certain point, they had to inform the family that their husband and father was now completely brain dead. This conversation has stayed with me many years later.
Research
A January 2025 study in the Journal of neurosurgery (1) investigated the effects of noninvasive transauricular vagus nerve stimulation in patients with subarachnoid hemorrhage. The findings demonstrated that taVNS significantly reduced radiographic vasospasm, decreased inflammatory markers in plasma and cerebrospinal fluid, and improved functional and neurological outcomes. The patients treated with transauricular vagus nerve stimulation had higher rates of favorable outcomes and were less likely to require discharge to care facilities or hospice.
Subarachnoid hemorrhage research has provided valuable insights into vasospasm. Some of the best studies on why vasospasm occurs have involved subarachnoid hemorrhage models in rabbits. These rabbit studies demonstrated a correlation: the degree of vasospasm induced by subarachnoid hemorrhage matched the amount of vagus nerve degeneration observed. This connection between subarachnoid hemorrhage-induced vasospasm and vagus nerve degeneration is a recurring theme in clinical research and practice. When the vagus nerve’s input to the heart is diminished due to degeneration, several cardiac symptoms may develop. These include tachycardia (rapid heart rate), cardiomyopathy (disease of the heart muscle), and arrhythmia (irregular heart rhythm). The right vagus nerve innervates the SA node, while the left vagus nerve innervates the AV node in the heart. If either is compromised, arrhythmias such as atrial fibrillation may develop, even when heart structure appears normal. This suggests that the nerve supply, specifically the vagus nerve, may be the underlying cause.
Case Example: Vagus Nerve Degeneration
The vagus nerve plays a crucial role in regulating various bodily functions. Degeneration of the vagus nerve can have significant health consequences, particularly when it comes to unexplained medical conditions. If you have a history of vasospasm, have been diagnosed with angina, or have experienced necrosis in a lymph node or organ without a clear cause, it is likely that vagus nerve degeneration may be involved.
To illustrate the effects of vagus nerve degeneration, here is the story of a family friend whose daughter was hospitalized with severe symptoms. At just 18 years old, her internal organs began shutting down and atrophying, including her pancreas. This alarming decline prompted a discussion about the possible role of vagus nerve degeneration, which was explained to the family, especially her mother. I told them that it is the right vagus nerve most often implicated, and nerve compression can result from certain body positions.
The mother confirmed that her daughter’s posture in her hospital bed matched the description of nerve compression given. Based on this observation, it was suggested to change the daughter’s posture. Remarkably, after making this adjustment, her digestive tract began functioning properly, and her health improved significantly. She went from being critically ill to thriving at home, demonstrating the profound impact of relieving pressure on the vagus nerve.
Mechanism of Vasospasm and Vagus Nerve Degeneration
Normally, arteries can constrict or dilate to regulate blood flow. Vasoconstriction narrows the lumen, while vasodilation widens it. Vasospasm refers to the narrowing of the arterial lumen without a clear reason. However, evidence suggests that vagus nerve degeneration is a key factor causing this phenomenon. The most common type of vasospasm occurs in the coronary arteries, further linking vagus nerve health to serious cardiac events.
Chest Pain Due to Costochondritis
There are four types of joint instabilities that can lead to chest pain, which are not uncommon occurrences. Ligamentous joint instability may cause severe chest pain, sometimes intense enough for a person to seek emergency care.
One form of instability occurs where the sternum connects to the cartilage, referred to as sternal chondral instability. Another type involves looseness where the rib attaches to the cartilage at the costochondral joint. These joints are supported by ligaments, and acute instability often results in sharp, localized, and superficial pain with tenderness at the site of discomfort. If you experience unresolved chest pain, pressing on the affected area may reveal tenderness associated with conditions such as costochondritis or seed seed syndrome. The pain is usually sharp and tender, and sometimes it resolves with medications like ibuprofen. Treatment can also include Prolotherapy injections directly at the site of instability, which may resolve the pain.
Chest Pain from Intercostal Neuralgia
Another cause of chest pain is thoraco-rib instability, which can result from injury to the costotransverse ligaments or those that attach the ribs to the thoracic vertebrae. This instability can lead to neuritis, affecting the intercostal nerves that provide skin sensation to the thoracic region and chest. Rib instability is often noticeable during movement or deep breathing, sometimes described as slipping rib syndrome. Such instability can irritate the intercostal nerve, causing sharp chest pain and even shortness of breath. Treatment involves Prolotherapy to repair the injured ligaments.
Chest Pain Associated with Cervical Angina
Ligamentous joint instability in the lower neck can cause cervical angina, which may feel like a heart attack. This pain results from a pinched nerve in the lower cervical spine, often due to instability or ligament injury in the neck. Pain can occur in the chest region, especially since the pectoral muscles are innervated by the C5, C6, and C7 nerves. Typically, a pinched nerve in the neck causes pain in the hand, back of the neck, or upper thoracic region, but it can also manifest as chest pain because these nerves serve the pectoral muscles. Diagnosis may be made via MRI or digital motion X-ray, which reveals neural foramina closure during neck movements, particularly extension and rotation toward the painful side. If chest pain worsens with these movements, cervical angina is likely. Treatment focuses on repairing ligaments at the base of the neck with Prolotherapy.
Chest Pain from Vagopathy
Vagopathy-induced vasospasms are another source of chest pain. Instability in the upper cervical ligaments can cause stretch and compression of the vagus nerve. When the vagus nerve degenerates, it can trigger vasospasms in arteries, including the coronary arteries. This pain is typically severe and deep, often described as originating within the heart rather than the ribs, and may be accompanied by a sensation of impending doom. Additional symptoms of vagus nerve degeneration include anxiety, ringing in the ears, digestive problems, sensitive stomach, bloating, constipation, heart palpitations, and shortness of breath. Localized pain may also be present.
Tenderness characterizes costochondritis, while cervical angina can cause pain in the pectoral major and minor muscles, typically presenting as superficial pain. Cervical angina arises when nerves are pinched or stretched, and intercostal neuralgia is marked by pain traveling from the thoracic area to the chest. Thoracic instability may lead to slipping rib syndrome and other thoracic problems, and these tender points are observable during physical exams. To check for thoracic instability, you may ask someone to press different areas to identify soreness in the thoracic region. Thoracic outlet syndrome can also cause chest pain, particularly when the shoulder is abducted and rotated.
What triggers vasospasms?
Several physiological and environmental triggers can lead to vasospasm. These include low-grade inflammation, oxidative stress, and dysfunction of the autonomic nervous system. It is suggested that these factors may ultimately result from degeneration of the vagus nerve. When the vagus nerve degenerates, it becomes smaller, which we measure in our office using ultrasound. Additionally, heart rate variability testing provides insight into the health of the vagus nerve; reduced variability is indicative of vagus nerve degeneration.
Heart Rate Variability (HRV) measures the time variation between consecutive heartbeats (R-R intervals), which can demonstrate the balance between the sympathetic (stress) and parasympathetic (rest) nervous systems. We use HRV to assess vagus nerve function, noting that higher variability indicates a stronger, more resilient nervous system and better stress management.
As vagus nerve function declines, sympathetic nervous system activity becomes dominant, leading to sympathetic hyperactivity. This imbalance is known to cause vasoconstriction—such as when adrenaline surges during stressful situations, resulting in cold, clammy hands. Persistent symptoms like cold hands, cold feet, Raynaud’s phenomenon, or hands turning blue in cold weather are signs of autonomic or sympathetic hyperactivity, which may indicate vagus nerve degeneration.
Other signs include dilated pupils and light sensitivity, both of which are associated with increased sympathetic activity. Comparing one’s pupil response to others may reveal vagus nerve degeneration if dilation is excessive.
More symptoms of Vagus nerve degeneration
Degeneration or dysfunction of the vagus nerve can cause torticollis (abnormal neck position), trigeminal neuralgia (facial nerve pain), and sensitivity to light. Individuals diagnosed with Prinzmetal angina or those who suspect vasospasm may notice additional symptoms, such as clicking or popping in the neck and tension in the upper neck. Other related symptoms include gastroparesis (delayed stomach emptying) and arrhythmias.
Vagus nerve degeneration may also be associated with a range of other conditions. These include dystonia (abnormal muscle tone), depression, double vision, loss of vision, changes in speech, balance problems, and pancreatic insufficiency. If these symptoms are present, it is likely that vagus nerve degeneration may be a contributing factor.
Diagnosis and Treatment of Vasospasm
Matt came to see us after experiencing chest pain soon after his first COVID-19 vaccine in 2020. Initially dismissed as muscle soreness or inactivity, his symptoms persisted, prompting multiple ER visits. While tests were mostly normal, some hinted at acute pericarditis.
Matt was diagnosed with pericarditis and vasospasm. Nitroglycerin quickly relieved his pain, confirming variant angina. He received diltiazem and underwent further diagnostics, including a coronary angiography.
Exploring other causes, Matt researched links to cervical instability and noted posture issues from his work. Additional symptoms—blood in urine and GI distress—led to various scans and endoscopies, revealing a stomach ulcer and H. pylori infection.
Neurological exams showed vagus nerve degeneration and cervical instability. His treatment plan included curve correction and prolotherapy, aiming to gradually reduce medication as his condition improved.
Matt’s journey underscores the complexity of diagnosing vasospasm and related conditions. He credits medical professionals for their support and hopes sharing his story helps others facing similar challenges.
Vasospasm is often diagnosed by administering nitroglycerin, either as a spray or sublingual tablet, to relieve chest pain quickly. If the pain subsides immediately, it is considered diagnostic for vasospastic angina, also known as Prinzmetal angina. Long-term treatment commonly involves calcium channel blockers. However, it is important to address the underlying cause of vasospasm. Treating with calcium channel blockers alone may not resolve issues stemming from vagus nerve degeneration, especially if it is caused by upper cervical instability. While vasospasm may be controlled, symptoms of vagus nerve degeneration, such as heart arrhythmia, may persist and could be severe.
In office settings, diagnosis can include digital motion x-ray to measure vagus nerve function and ultrasound to assess the size of the vagus nerve.
Upper cervical instability
The vagus nerve originates from the brain stem, with the no dose ganglion positioned just in front of the C1 vertebra. It innervates all major organs in the body. Therefore, conditions such as liver disease, pancreas disease, gallbladder disease, small intestine disease, duodenum disease, stomach disease, heart disease, heart arrhythmia, kidney disease, and lung disease may be related to vagus nerve function.
Other conditions like asthma, hyperactive airway, pleural effusion, or pericardial effusion of the heart, as well as long haul COVID, are also likely associated with vagus nerve degeneration. In my opinion, these issues stem from vagus nerve degeneration.
For individuals experiencing angina attacks or unexplained heart issues, vasospasm induced by vagus nerve degeneration—potentially originating from neck problems—may be a contributing factor. At the beginning of this video/article I discussed the role of animal studies. Specifically in rabbits. (x) In these studies, the more vagus nerve degneration, the greater the mortality rate.
Vagus Nerve and the Digestive System
There are approximately one hundred thousand vagus neurons or nerve cells that innervate the five hundred million enteric neurons in the digestive tract. Each time a vagus neuron is lost, it impacts about 5,000 neurons in the digestive tract. This loss leads to increased intestinal permeability.
If you have been diagnosed with leaky gut or believe you have leaky gut, or have been told you have fibromyalgia or excessive inflammation, it is likely due to vagus nerve degeneration.
Immune Surveillance
Vagus nerve cells play a key role in immune surveillance. Research shows that heart rate variability is directly correlated with cancer risk. A strong vagus nerve is associated with a lower risk of cancer, while a weakened vagus nerve increases the likelihood of diseases such as cancer.
The vagus nerve stimulates the immune system and helps regulate nutrient levels, organ function, heart rate, blood pressure, digestion, fluid status, hormone needs, and appetite. It acts as the sensor of the body, communicating information to the brain about stress levels, nutritional status, job satisfaction, and feelings of love or lack thereof.
If the body’s sensor is off due to vagus nerve degeneration, the brain receives incorrect information, resulting in disrupted homeostasis.
Ultrasound Assessment
One way to evaluate the vagus nerve is through ultrasound imaging. In such images, the cross-sectional area of the vagus nerve can be compared with nearby structures like the jugular vein. If a compressed or smaller vagus nerve is visible, this would indicate a state of degeneration.
A simple test involves looking into a mirror with a light and saying “ah.” Normally, both sides of the palate should elevate equally. If one side is lower or the uvula deviates to one side, it may signal vagus nerve dysfunction. Specifically, the levator veli palatini muscle may not be functioning properly, causing the palate to rise less on the affected side.
Pain Modulation and Vagus Nerve Functions
The vagus nerve plays a significant role in pain modulation. It helps control inflammation, calms the sympathetic nervous system, reduces oxidative stress, stimulates calming secretions in the brain, and activates opioid receptors. If someone is eating healthy and taking antioxidants but still experiences excessive oxidative stress, vagus nerve degeneration may be a contributing factor.
For individuals with abnormal stool analyses, genetics, or gut bacteria, fungi, or parasites—and continued symptoms despite a healthy diet—it is likely that vagus nerve degeneration is involved. The vagus nerve innervates key digestive valves and sphincters, such as the ileocecal valve, pyloric valve, sphincter of Oddi, and lower esophageal sphincter. Degeneration can result in malfunctioning valves, leading to issues like small intestinal bacterial overgrowth (SIBO).
Research indicates that people with Parkinson’s disease often have very small vagus nerves. Similarly, those with multiple sclerosis or memory decline should consider vagus nerve assessment. Degeneration often involves not only stretch and compression of the vagus nerve but also of the jugular veins. Since the jugular veins drain the brain and run alongside the vagus nerves, their compression can lead to increased brain pressures, resulting in brain dysfunction and eventual neurodegeneration.
References
1 Huguenard AL, Tan G, Rivet DJ, Gao F, Johnson GW, Adamek M, Coxon AT, Kummer TT, Osbun JW, Vellimana AK, Limbrick DD. Auricular vagus nerve stimulation for mitigation of inflammation and vasospasm in subarachnoid hemorrhage: a single-institution randomized controlled trial. Journal of neurosurgery. 2025 Jan 24;142(6):1720-31. [Google Scholar]