The Effect of Vagus Nerve Stimulation on Temporomandibular Joint Dysfunction
Condition: Temporomandibular Joint Dysfunction Syndrome; Autonomic Nervous System Imbalance
MeSH terms: Joint Diseases; Temporomandibular Joint Disorders; Temporomandibular Joint Dysfunction Syndrome; Syndrome
Study type: Interventional

Summary: 
      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.
    

Detailed description: 
      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.
    

Intervention name(s): Auricular Non-Invazive Vagus Nerve Stimulation + Traditional Rehabilitation Program for TMD; Traditional Rehabilitation Program
Intervention type(s): Other; Other
Intervention description(s): In this application, vagus nerve stimulation is applied to the patients in addition to the traditional rehabilitation program. In our research, vagal nerve stimulation will be applied with the "Vagustim" Device and all applications will be applied at a frequency of 10 Hz, a pulse amplitude of 300 microseconds and for 20 minutes.; This intervention includes: Deep Friction Massage, Myofascial Trigger Point Compression Therapy, Temporomandibular Joint Mobilization, Rocabado Exercises, Muscle-Energy Techniques.
Allocation: Randomized
Intervention model: Parallel Assignment
Intervention model description: All groups will be involved physical therapy and both groups will have traditional rehabilitation program for TMD. Only the group 1 will also have auricular non-invasive vagus nerve stimulation.
Masking: Single (Participant)
Primary purpose: Treatment
Keywords: Vagus Nerve Stimulation; Neuromodulation