The Effect of Application of Vagus Nerve Stimulation on the Treatment Efficiency in Temporomandibular Joint Dysfunction Caused by Myofascial Pain Syndrome
The Effect of Application of Vagus Nerve Stimulation on the Treatment Efficiency in Temporomandibular Joint Dysfunction Caused by Myofascial Pain Syndrome
Temporomandibular joint dysfunction (TMD) is a broad clinical picture involving the TMJ and its disc, masticatory musculature, ligament tissue, and autonomic nervous system (ANS). TMD symptoms include decrease or excessive increase in joint range of motion (ROM), clicking sound or crepitation in the joint, pain around the joint or muscle group, chewing and swallowing problems. Pain caused by MPS, trigger point, fatigue, limitation of ROM, and ANS dysfunction cause TMD. With the inclusion of habits such as clenching and bruxism, pain, spasm and disability develop in the chewing muscles. Exposure to repeated trauma and excessive use of chewing muscles may cause the formation of tight bands and trigger points, which are characterized by MPS. When the relationship between TMD and ANS was examined, it was observed that increased sympathetic activity and decreased parasympathetic activity were effective in the severity of TMD symptoms. Auricular vagus nerve stimulation is a peripheral, non-pharmacological and non-invasive neuromodulation technique that modifies signal processing in the CNS, activates reflex circuits, exploits brain plasticity for different therapeutic purposes, thereby affecting very different areas of the brain. Non-invasive or transcutaneous Vagus Nerve Stimulation delivery systems provide stimulation in the auricular branch of the vagus nerve in the outer ear, thus eliminating the need for surgical implantation. The aim of our study is to reveal the extent to which Auricular Vagus Nerve Stimulation, applied in addition to the conventional rehabilitation program, affects the results of the treatment by stimulating the parasympathetic nervous system in patients with Temporomandibular Joint Dysfunction caused by Myofascial Pain Syndrome.
The temporomandibular joint (TMJ) is a ginglymoarthrodial joint, a term derived from ginglymus, meaning a hinge joint that allows only forward and backward movement in one plane, and arthrodia, a joint that allows gliding motion, and right and left TMJ are similar to knee articulation. It forms the ellipsoid variety of bicondylar articulation and synovial joints. TMJ movements are defined as elevation, depression, protrusion, retrusion, and lateralization. Primary muscle groups that reveal these joint movements m. masseter, m. temporalis, medial and lateral pterygoid, suprahyoid (digastricus, mylohyoid, geniohyoid, stylohyoid) and infrahyoid (thyrohyoid, sternohyoid, sternothyroid, omohyoid). The TMJ ligament complex consists of superficial and deep collateral ligament, sphenomandibular ligament and stylomandibular ligament. While the sensory nerves of the TMJ branch from the Trigeminal (V. Cranial nerve) nerve, they receive sympathetic innervation from the cervical ganglion (C8-T3). Temporomandibular joint dysfunction (TMD) is a broad clinical picture involving the TMJ and its disc, masticatory musculature, ligament tissue, and autonomic nervous system (ANS). TMD symptoms include decrease or excessive increase in joint range of motion (ROM), clicking sound or crepitation in the joint, pain around the joint or muscle group, chewing and swallowing problems. TMD is considered in two groups as articular and non-articular disorders: articular disorders express the dislocation of the disc with and without reduction, while non-articular disorders express the problems caused by myofascial pain syndrome (MPS). Pain caused by MPS, trigger point, fatigue, limitation of ROM, and ANS dysfunction cause TMD. With the inclusion of habits such as clenching and bruxism, pain, spasm and disability develop in the chewing muscles. Exposure to repetitive trauma and overuse of chewing muscles may cause the formation of tight bands and trigger points, which are characterized by MPS.
ANS is part of the peripheral nervous system (PSS), which regulates involuntary physiological processes such as heart rate, blood pressure, respiration, and digestion, and is anatomically composed of 3 parts: the sympathetic, parasympathetic, and enteric nervous systems. The sympathetic nervous system (SNS) and parasympathetic nervous system (PNS) contain afferent and efferent pathways that provide sensory and motor stimulation, and these pathways consist of preganglionic neurons in the central nervous system (CNS) and postganglionic neurons in the periphery. The SNS enables the body to handle stressors through the "fight or flight" response, and this reaction primarily regulates the blood vessels. The vessels are tonically innervated and in most cases an increase in sympathetic signals leads to vasoconstriction. SNS activation increases heart rate and contraction force. The PNS exits the SNS via cranial nerves III, VII, IX, and X, as well as via S2-4 nerve roots. The vagus nerve (Cranial Nerve X), together with the sacral parasympathetic fibers, provides parasympathetic input to most of the thoracic and abdominal organs and has four cell bodies: Dorsal nucleus (parasympathetic stimulation of viscera), Nucleus ambiguous (preganglionic neurons innervating the heart), Nucleus solitarius (taste sense) and Trigeminal nucleus (outer ear circumference receives touch, pain and temperature information). The vagus nerve is responsible for the "resting and digesting" processes. By providing cardiac relaxation, the vagus nerve reduces contraction in the atria and ventricles and decreases the conduction velocity through the atrioventricular node. The vagus nerve also has a significant effect on the respiratory cycle, and its activity increases during expiration, constricting and stiffening the airways to prevent lung collapse.
When the relationship between TMD and ANS was examined, it was observed that increased sympathetic activity and decreased parasympathetic activity were effective in the severity of TMD symptoms. It has been shown that TMD patients may show changes in the sympathoadrenal and inflammatory cytokine function resulting from their response to the stressor, and that the increase in the sympathetic activity of these patients in the long term may cause decreased interleukin-6 (IL-6) and norepinephrine response. It is thought that IL-6 may be an important factor related to the increased morbidity and mortality in people with chronic stress and may play a pathogenic role in the course of stress-reactive chronic diseases. Another mechanism thought to cause TMD is that the junctional region between the trigeminal subnucleus caudalis (Vc) and the upper cervical spinal cord, called the Vc/C1-2 region, is the primary site for synaptic integration of sensory input from TMJ nociceptors, and Vc/C1- It is known that estrogen hormone is effective on the processing of nociceptive stimulus by neurons in region 2. Especially in the post-menopausal period, the decrease in the level of estrogen in the blood causes an increase in sympathetic activity and causes pain and disability around the TMJ. Another method of evaluating the relationship between TMD and ANS is the measurement of heart rate variability (HRV). In a study, it was observed that HRV, which is a marker of ANS dysfunction, decreased in patients with myofascial temporomandibular disorder (TMD) compared to healthy individuals.
Auricular vagus nerve stimulation is a peripheral, non-pharmacological and non-invasive neuromodulation technique that modifies signal processing in the CNS, activates reflex circuits, exploits brain plasticity for different therapeutic purposes, thereby affecting very different areas of the brain. Modulation of the afferent vagus nerve affects numerous physiological processes and bodily states associated with the transfer of information between the brain and the body. These include disease mitigating effects and sustainable therapeutic practices ranging from chronic pain diseases, neurodegenerative and metabolic disorders to inflammatory and cardiovascular diseases. Non-invasive or transcutaneous Vagus Nerve Stimulation delivery systems provide stimulation in the auricular branch of the vagus nerve in the outer ear, thus eliminating the need for surgical implantation. One of the non-invasive Vagus Nerve Stimulators in use today, NEMOS®, stimulates the outer ear turbinate and is European Conformity (CE) marked for the European Union for the management of epilepsy. The electrode is connected to a stimulation box and the stimulation intensity can be adjusted by the patient, caregiver, or treating healthcare professional. During use, it is increased in 0.1 milliamperes(mA) steps until the detection threshold of electrical stimulation is reached; the stimulation frequency was defined as 25 Hz. Another non-invasive Vagus Nerve Stimulator gammaCore® is used for transcutaneous stimulation of the cervical branch of the vagus nerve and is FDA approved for the treatment of episodic cluster headache. The device generates a wave in the form of a pulse. It creates impulses with a 1 ms transition time of an electrical current with a frequency of 25 Hz. The recommended stimulation time is 2 minutes and can be applied up to 12 times a day.
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