TMJ Derangement and SUNCT Syndrome Co-morbidity
The patient who suffers head and or neck pain is often a complex pain patient, meaning that the suffering can be the result of multiple, often unrelated conditions. It is also common for an ear, nose and throat specialist to examine a patient with headache and ear-related complaints that are often determined to be of TMJ or TMJ/Bite origin. Complaints related to the Ear/TMJ/Bite are based on first branchial arch embryology and proximity, common neural innervation, a ligamentous physical connection from mandible to TMJ and to the middle ear cavity. The term ‘Ear/TMJ/Bite’ simply ascribes a relationship that can influence many areas in the head and neck. The “bite” aspect of the term describes the influence of the upper and lower teeth. This influence includes the “fit” of the upper and lower teeth and whether that fit helps to support or hinder the articulation of the jaw joint and thus its stability.
In fact, it is accurate to describe each tooth in the maxillary bone and in the mandible to also be a “joint.” In the human adult, anywhere from 28 to 32 teeth normally play a pivotal role in the health and or disease of the TMJ—that is, excluding extrensic trauma or developmental abnormalities. Each tooth is normally suspended in its bony socket by a series of many fine ligaments that allow for minor lateral movement. It is this ligamentous connection of tooth to bone that often plays a contributing role in TMJ arthrokinesis.
Arthrokinesis is the ligamento-neuro-muscular reflex mechanism that allows a movable joint anywhere in the body to work either effectively or to exhibit some degree of dysfunction, injury, or disease. Since the primary role of a ligament is to protect its companion joint, the 28 to 32 normally occurring teeth with numerous suspensory ligaments represent a complex portion of the ligamentous structures that are responsible for good mandibular joint function and arthrokinesis. The remaining non-tooth ligaments that are connected to the mandible include the stylomandibular, sphenomandibular, lateral capsular ligament, and the temporomandibular ligament (often blended in the capsular ligament). In arthrokinesis, it is the ligament—via its mechano-receptors—that directs spinal and CNS activity that serves to protect as well as signal joint-related injury. Joint-related injury often results in muscular reflex restriction and pain, and the pain often includes pain referral to distant sites.
An injury to a tooth affecting its position or height, maloccluded teeth, tooth extraction and progressive dental instability, extrensic injury to the muscles or ligaments that move the joint, or internal derangement within the joint can all alter normal joint arthrokinesis. The result can be trismus or muscle spasm, slipping or locking of the disc in the jaw joint, degeneration or perforation of disc and disc ligaments, spurring or degenerative changes within the TM joint, ear pain, headache, and pain of the axial muscles of the neck. The affected axial muscles influenced by the TMJ and muscles of mastication have been demonstrated by Mehta (at Tufts University School of Dental Medicine)1 to include the trapezius, and sternocleidomastoid muscles.
A slipped TMJ articular disc carries with it a potential host of nociceptive, neural, vascular, autonomic, and head and neck postural changes with accompanying painful symptoms. The autonomic influence is thought to be affected by the post-ganglionic, parasympathetic fibers that invest the lateral capsular ligament of the temporomandibular joint. Research has shown there is a physical connection between the articular disc and the lateral capsular ligament.
The trigeminal nerve is the dominant sensory/motor nerve in the region with interconnects to facial nerve branches, occipital nerve branches, and glossopharyngeal nerves. Equally significant is that trigeminal nerve cells in the trigeminal spinal nucleus interface with spinal nerve cells in the first three cervical vertebrae. Additionally, recent EMG research is demonstrating that postural stability of the head on the neck can be influenced by a TMJ problem or, conversely, the TMJ can be affected by changes in the axial cervical structures.1 Clearly there is an abundance of complexity.
A neurologic condition (SUNCT syndrome) that may be caused, affected, or influenced by a TMJ internal derangement will be seen in the following case report. As a reminder, this case report is not intended to be a proof of cause and effect. However, since “observation” is the first of the five steps in the scientific method, this case is worth considering as having a possible cause and effect. Whether this case of suspected association between the TMJ slipped disc and SUNCT will be reproduced in the future is yet to be determined. Whether it is or not, at least this case’s treatment will stand as having been therapeutic for this particular patient.
Short-lasting Unilateral Neuralgiform Headache Attacks with Conjunctival Injection and Tearing (SUNCT)
While TMJ has been discussed at some length, more needs to be disclosed concerning the nature of SUNCT syndrome and its painful symptoms. SUNCT is classified as one of a number of paroximal trigeminal autonomic hemicranias (TAC’s) that can occur with autonomic features. The attacks occur in spasms or bursts of paroxysmal pain. The condition is noted to occur most commonly in men over age 50, though women too may suffer from this condition. The attacks are described as being marked by rapid bursts of moderate to very severe burning, stabbing, or throbbing pain, mostly on one side of the head, around the eye or the temple. Some cases also report eye lid drooping or ptosis during the episodes.2
The literature reports the attacks typically occurring in the daytime hours and lasting from five seconds to four to five minutes. Frequency of attacks is generally seen to be five or six per hour. The National Institutes of Health report these autonomic responses include:
watery eyes, reddish or bloodshot eyes caused by dilation of blood vessels, nasal congestion, runny nose, sweaty forehead, swelling of the eyelids, and increased pressure within the eye on the affected side of head. Systolic blood pressure may rise during an attack. Movement of the neck may trigger these headaches... SUNCT may be a form of trigeminal neuralgia and is considered one of the trigeminal autonomic cephalgias, or TACs.4
NIH further states that there is currently no cure for SUNCT.3
Oxford University’s Institute of Neurology divides the short lasting headaches into those with autonomic activation (SUNCT) and those without autonomic activation. The cases with autonomic activation have an attack frequency from five to forty attacks a day. The pain is a severe pain and has autonomic symptoms such as conjunctivaal injection, lacrimation, nasal congestion, rhinorrhea, as well as ptosis or eyelid edema. Some cases respond to indomethacin and other medications, including IV Lidocaine. Currently there is no medication that has been reported to cure the attacks. Some researchers believe that the similarity of the symptoms of both autonomic and non-autonomic activation may suggest a shared pathophysiology.