This 35 year old lady struggled for the last few years. An allergist several years ago suggested that gastroesophageal reflux disease (GERD) might be causing her sinus problems. He advised "surgery" and thus not contemplating a major surgical procedure she disregarded his recommendations. When a thoughtful cardiologist commented that her vagus nerve seemed somehow involved she started her own internet search. She found my website and the rest is history. Her recent correspondence follows:
Hi, this is Lilly from Washington state. I contacted you with a case of atypical GERD 3 months ago.
At that time I was suffering from daily, "seizure-like" episodes which left me exhausted and confined to bed for a majority of the time. Quite some time has passed since our phone conversation in December and I wanted to write with an update.
After we talked, I followed your instructions to gradually increase my PPI dose (I think I was taking only 1-2 a day). In addition I began taking the Zantac and Gaviscon nightly. In a matter of a few weeks I was able to increase to six a day (3 Omeprazole @ 20 mg, 3 Lansoprazole@ 15 mg). I take one every two hours because I found that when I doubled them up or took them too close together they made me drowsy. I find also, that if I go beyond two hours, (even 15 mins) I have chest pain and dizziness. I have definitely found that I do much better if I respond immediately to any chest discomfort or dizziness. I have begun taking Gaviscon during the day to supplement the PPIs. I have found that most days I don't need to, but if I have discomfort or heart trouble I take it (occurs a few times a week).
I am excited to report at this time, that I have not had a serious, "seizure-like" episode since December. And I have had a dramatic increase in energy. I am no longer confined to bed. Clearly it will take time for my body to regain strength (it had been nearly three years that I spent most of my time confined to bed), but I am thrilled to regain the health and freedom that I have thus far! I am not yet able to do the more strenuous household duties ie lifting laundry baskets, vacuuming etc., but I have now been able to prepare meals for my family a few nights a week without serious repercussions, which has been one of the most significant improvements.
So, that's where things are at this point. Overall I am very thankful for my improvements! I would be grateful to hear from you and know what your thoughts are as to how I should proceed from here. I feel that I am in a much more stabilized state ie the "attacks" have abated. At the same time, I'd like to see more improvement.
I still seem so incredibly fragile ie if I am late on one PPI dosage, I am a wreck (heart trouble, dizziness, confusion, fatigue etc). Would you expect continued improvement if I proceed at current dosages? Would you suggest I increase? I am not a large person (119 lbs).
Afferents: Implication for Symptom Perception in Patients Across the Gastroesophageal Reflux Disease Spectrum
The Clinical Journal of Pain, 01/25/2013
Szczesniak MM et al. – Esophageal acid infusion sensitizes it to subsequent electrical and chemical stimulation. The acid–related sensitization is greater in gastroesophageal reflux disease than in controls and may influence in part symptom perception in this population. Acid–related sensitization within the gastroesophageal reflux disease population is not dependant on mucosal inflammation.
The implication of the above abstract goes beyond local mucosal “sensitivity” changes since it has previously been shown that “central sensitization” occurs in gastroesophageal reflux disease (GERD). This means that injury (without obvious damage to esophageal tissue) to one area of the body (the esophagus) can cause alteration of pain perception in another part of the body. The example I routinely encounter is a painful response to inflation of the blood pressure cuff due to central sensitization from GERD and then after symptom remission from successful treatment for GERD, the same individual no longer experiences pain with the same blood pressure determination technique.
The autonomic nervous system (ANS or visceral nervous system) is part of the peripheral nervous system that acts as a control system functioning largely below the level of consciousness while it controls visceral (the “inner parts” of the body) functions. The ANS affects heart rate, digestion, respiration rate, salivation, perspiration, diameter of the pupils, urination and sexual arousal. Whereas most of its actions are involuntary, some, such as breathing, work in tandem with the conscious mind.
It is classically divided into two subsystems: the parasympathetic nervous system (PSNS) and the sympathetic nervous system (SNS). Relatively recently, a third subset of neurons have been named ‘non-adrenergic and non-cholinergic’ neurons (because they use nitric oxide as a neurotransmitter) have been described and found to be integral in autonomic function, particularly in the gut and the lungs. The enteric nervous system is sometimes considered part of the autonomic nervous system, and sometimes considered an independent system. Besides output to the various organs of the body, the vagus nerve conveys sensory information about the state of the body's organs to the central nervous system. Up to 80-90% of the nerve fibers in the vagus nerve are sensory nerves communicating the state of the viscera to the brain. The vagus nerve is also called the pneumogastric nerve because it innervates both the lungs and the stomach.
The lower esophagus is richly invested with vagal nerve endings and failure/relaxation of the lower esophageal sphincter allows digestive contents to leak in a retrograde fashion from the intestine and stomach. This allows corrosive digestive juices including acid and proteolytic enzymes to encounter, irritate and stimulate vagal nerve endings which over time become eroded and sensitized.Our brain receives the information via this communication network and, rightly so, becomes alarmed thus triggering involuntary protective reflex responses. Reilly's syndrome confirms that changes in vascular tone, and reticuloendothelial system via neurogenic inflammatory response produces protection in vulnerable tissues. This is where it gets really interesting. Either the severity of the reflux or the intensity of the body’s response to this dangerous insult can result in a clinical syndrome that has manifestations far-reaching beyond the origin of the endangered tissues. Thus regurgitation of digestive/intestinal contents into the lower esophagus can trigger vagal nerve response that results in tissues swelling, injury, scarring and mucus production in the paranasal sinuses as well as the larynx and pharynx without the affected tissues ever having come in direct contact with regurgitated digestive secretions. Artificial placement of acid into the lower esophagus is proven to result in inflammatory reaction of the paranasal sinuses. This is but one example of a myriad of potential effects that can occur anywhere in the distribution of the vagus nerve, or even the entire craniosacral nervous system. This phenomenon of vagal activation in the presence of regurgitated digestive contents explains the resolution of cardiac palpitations with successful therapy for gastroesophageal reflux disorder (GERD).