Vagal inhibition simply means the reduction of the functions of the vagus nerve to achieve some desired bodily effects. It is a type of neuromodulation which sends stimuli or impulses to inhibit the vagus nerve and hereby reduces the physiological functions of the vagus nerve. This type of treatment is used to alter and reduce the activity of the nerves, especially an overactive vagus nerve. The vagus nerve is the most important part of the ANS (autonomic nervous system). The vagal pathway has a very important function when it comes to the maintenance of metabolic homeostasis. It also plays a major role in the neuroendocrine-immune system to maintain homeostasis through both its efferent and afferent pathways (1). The vagal pathway controls important functions which include but are not limited to heart rate regulation; abdominal movements and digestion; breathing intensity, speed, and pattern regulation; cardiovascular activities; and reflexes like coughing, sneezing, swallowing, and vomiting.
The vagus nerve is one of the cranial nerves - the 10th cranial one. It passes through the neck and it also moves through the chest and other parts of the body such as the abdomen, and the lower parts of the brain. It serves both motor and sensory functions in the esophagus and sinuses (2). In fact, the word "vagus" was derived from the Latin translation of “wanderer”. This explains the course of the vagus nerve as it wanders through the body and is connected to a lot of organs, serving a lot of functions. It is the main aspect of the parasympathetic nervous system. Together, the left and right vagal nerves constitute about 75% of your body’s parasympathetic nervous system’s nerve fibers. These fibers carry information between the brain, heart, and digestive systems. The vagal pathway serves a lot of internal body functions such as saliva and mucus production, immune control, sexual functions like having an orgasm, mood control, muscle sensation, and most importantly - heart rate.
In the case of an overactive vagal pathway. Normal functioning of the vagus nerve is affected. This means over-functioning of the vagus nerve results in alteration of the physiological rate or level of the different functions performed by the vagus nerve. The Vagus nerve is responsible for the stimulation of muscles in different parts of the body such as the pharynx, larynx, and the soft palate (the soft palate is a soft fleshy area at the back of the roof of your mouth). The vagus nerve also stimulates the muscles of the heart thereby helping to lower the heart rate. It also helps digestion by causing involuntary movements in the digestive tract - including the stomach, esophagus, and intestines (2). In this case, over-activity of the vagus nerve means over-relaxation of the heart muscles which means the heart rate gets too low. Sometimes, as a result of over-activity of the vagus nerve, the heart rate could be lowered to dangerously low levels. An overactive vagus nerve will also lead to excessive stimulation of involuntary movement in the digestive tract, leading to improper digestion of food.
Vagus nerve dysfunctions such as over-activity of the vagus nerve are usually caused by a wide variety of factors ranging from previous infection or inflammation. Vagal over-activity can also be caused by physical or psychological stress. Causes of over-stimulation of the vagus nerve are also associated with different parts;
Damage to the vagus nerve can result in a range of symptoms because the nerve is so long and affects many areas. Generally, pathology of the vagus nerve is known to cause any or some of these symptoms: difficulty speaking, loss of voice or voice change (voice changes could manifest as hoarseness and wheezing), swallowing problems, poor or absent gag reflex, hypotension (reduced blood pressure), tachycardia (increased heart rate), bradycardia (reduced heart rate), digestive changes or digestive problems, acid reflux (gastroesophageal reflux disease, GERD), dizziness, abdominal bloating or abdominal pain, vomiting, nausea, loss of appetite, unexplained weight loss, anxiety, and depression.
When the vagus nerve overreacts, it can lead to a sudden reduction in heart rate and blood pressure and can result in fainting. This is called vasovagal syncope. Syncope means fainting, therefore, it can also be referred to as vasovagal fainting - fainting induced by the actions of the vagus nerve. When someone passes out as a result of vasovagal syncope, it is referred to as “vagal out”. This can be triggered by different factors like pregnancy, emotional stress, pain, and nerve damage. Some cases have also been reported without any specific cause. Asides from the sudden drop in heart rate which could result in fainting, other symptoms of an overactive vagus nerve include warmth, nausea, tunnel vision (inability to see things that are not straight or directly in front of you), tinnitus (ringing in the ears), excessive sweating, low blood pressure, and irregular heartbeat. All these are together referred to as vagal response.
Medications are the most effective ways to reduce the parasympathetic effect of the vagus nerve on different organs of the body. These drugs have been found to inhibit muscarinic receptors (anticholinergics). They reduce the action of the vagus nerve on all the organs innervated by the vagus nerve such as the heart, and the digestive tract, among other organs. Acetylcholine (ACh) is a neurotransmitter that is important at the synapses of both the central and peripheral nervous systems. This neurotransmitter is important for the free flow of nervous information. Medications that cause vagal inhibition work by stopping the action of muscarinic receptors which is important for the proper functioning of acetylcholine.
The most common examples of such drugs are atropine and scopolamine (3). These drugs are called vagolytic drugs. Some other vagolytic drugs are Benztropine, Biperiden, Chlorpheniramine, Paroxetine, Dicyclomine, Dimenhydrinate, Diphenhydramine, Doxepin, Doxylamine, Flavoxate, Glycopyrrolate, Glycopyrronium, Hyoscyamine, Ipratropium, Orphenadrine, Oxitropium, Oxybutynin, Promethazine, Propantheline bromide, Solifenacin, Tolterodine, and Tiotropium (9). They are also called antimuscarinic agents.
They reduce the parasympathetic effect of the vagus nerve on the heart thereby speeding up the heart rate. It is especially used in the treatment of patients suffering from bradycardia which means a pathologically low heart rate. However, this is not a prescription, any form of medication to reduce the action of the vagus nerve should be after a thorough examination, diagnosis, and prescription from a physician.
Some other drugs were also purported to have the ability to block the response to postganglionic stimulation of the vagus nerve were measured in isolation, spontaneously beating guinea pig atria. Some of them include Gallamine, Metocurine, Pancuronium, Tubocurarine.
Apart from the use of medications to inhibit the actions of the vagus nerve, one of the best ways to address an overactive vagal system is to address the symptoms. If you have noticed a tendency to experience vasovagal syncope, or you have experienced a recent episode; you can prevent future occurrence of vasovagal fainting in the following ways:
Vagal inhibition as a treatment for the overactive vagus pathway is different from vagal inhibition as a cause of death and should be treated differently. Vagal Inhibition is a disorder that has the potential to cause abrupt death. This happens when there is an abrupt cessation of the parasympathetic functions of the vagus nerve, whereas, vagal inhibition as a treatment of the symptoms of an overactive vagus nerve is a sustained slight and gradual decrease in the parasympathetic effect of the vagus nerve on the organs of the body. It might take place if the neck's vagus nerve is under pressure. The vagus nerve, which originates in the neck vertebra and is the 10th pair of cranial nerves, supplies the heart, lungs, and the gut, among other organs. These organs may stop working if the nerve is effectively inhibited from sending and receiving messages.
There have been numerous reports of people dying suddenly after being submerged in cold water, such as the swimmer who passed away right away after diving into a private swimming pool. Vagal inhibition may result in abrupt death within seconds or minutes from mild injury or harmless peripheral stimulation. Shocking the body into a chilly body of water is one of the potential causes of vagal inhibition. As a result of this shock, cardiac and respiratory centers are suddenly paralyzed with consequent stoppage of heart and respiration resulting in immediate loss of life (4).
A condition where vagal inhibition occurs due to submersion in water is called hydrocution. Cold and temperate regions tend to cause this problem. In this case, drowning is thought to have caused the death owing to cardiac arrest caused by vagal inhibition, which is caused by activation of vagal nerve terminals. This is usually due to the following factors;
You are more at risk of this if you are a young swimmer or if you frequently consume alcohol, have a high level of enthusiasm or emotion, or overeat just before swimming. Death occurs shortly after the practically instantaneous loss of consciousness. On rare occasions, death may occur in a matter of minutes. By ruling out all other possibilities and critically analyzing the situation, a diagnosis can be made (5).
In hanging, A noose is tightened around the neck during hanging because of the victim's body weight. The airways are constricted by the noose, which prevents the lungs from receiving oxygen. The carotid arteries, which deliver blood to the brain, are likewise compressed by it. Both mechanisms result in hypoxia, a condition in which the body and brain lack oxygen. However, in cases of hanging, suffocation is not necessarily the cause of death. Vagal inhibition, a reflex that results in cardiac arrest, may occasionally be brought on by pressure on the vagus nerve in the neck (6).