Today’s TMD specialist must think and act beyond the inadequate biomechanical aspects, explanations, and theories of TM pain and dysfunction which was anchored in the mechanical model of pain. He/she must enter the field of neurophysiology and acknowledge the interrelationship of the physical and psychological dimensions of craniofacial pain and join with the medical specialists who are now recognizing neuromuscular and musculoskeletal pain contained in the stomatognathic system. It has been noted that common symptomatology is frequently observed in the otic symptoms and TMD during daily clinical practice and should be understood by each discipline from the broad anatomical and clinical perspective as described in this article. It is incumbent on clinicians treating pain in the head, neck and facial areas to become familiar with the less common pain disorders to assist in the differential review. An early intervention in these conjugated anatomical areas of pain can be provided by a unique monomodal treatment protocol utilizing a passive intra-oral device (maxillary anterior passive appliance; MAPA).1
When we consider the amount of anatomical structures included in the cranial-maxillofacial area and the complexity of the pathophysiologies, it can be concluded that only a multi-disciplinary approach to orofacial pain symptoms is effective. Four less-common pain disorders were described and ruled out in the case report described in this article. Reciprocity among the disciplines of ENT and the orofacial pain doctor should be brought together by the TMD and otic-referred mutual symptomathology. These type of cases should promote the principles of successful team effort.
Developing good communication skills and establishing therapeutic relationships with patients is a priority for physicians and dentists involved in head, neck and facial pain. The diagnostic background of the case study—as well as the patient’s observations—may demonstrate that an inadequate team effort may have occurred resulting in a lack of trust by the patient as well as indecision by the doctors. The lessons learned from this case study should hopefully contribute to a stronger proactive relationship between the TMD and ENT specialists.
Although otomandibular syndrome is seldom described in the literature, it exists in many patients that are seen every day in ENT offices as well as dental offices. “Patients suffering from otomandibular syndrome present one or more symptoms without ear, nose, or throat pathology but have one or more masticatory muscles in a state of constant spasm.”2
Ear pain (otalgia) is found in many pains of the craniofacial mandibular area, and is one of the most frequently encountered in TMD pain. It is often associated with hearing loss, tinnitus, fullness in the ear and disorders of balance. Pain arising from the external ear structures is usually not difficult to recognize. Often there is history of trauma, or manipulation of the ear (e.g., from the use of Q-tips, blunt trauma or water exposure). Scuba divers will easily understand and appreciate the anatomy and physiology of this article. The most common problem in their first dive can be ear damage as a result of the inability of the diver to equalize pressure between the middle and the outer ear. ENT doctors frequently see these divers since as much as 80% of divers show observable tympanic membrane damage during the first few dives. Hyperbaric oxygen is sometimes used because the equalization process (“clearing ears” in the ascent from the depths) was not mastered. If the clearing of the ears does not occur, the water pressure pushing against the eardrum may cause it to rupture.
A more dramatic illustration of this equalization process occurred in World War II, when German Stuka bomber pilots needed an instant opening of the eustachian tube the moment they completed a successful dive on their target. The Stuka bomber attacks were the most precise form of bombing. The pilots, having both hands on the stick, would put their plane into a steep dive aimed directly at their target. Just before crashing into their target they would release their bomb and pull out of the dive. The bomb followed the launch trajectory and fell into the target. There were no computer adjusted hydraulics available and so the pilot needed to instantly balance the eustachian/middle ear connection or face possible deafness. It was imperative that a hands-free, rapid, effective and safe method of clearing ears was used. The technique they used was developed in 1938 by a German physician named Herman Frenzel.
Head and neck pain patients are often suspected of having sinusitis, dental disease symptoms or both since they may, at least in part, mimic an underlying neurologic disorder. Invasive surgical procedures should be avoided in cases of less than fully conclusive evidence. Detailed advanced diagnosis based on new knowledge and experience may also avoid excessive opioid medication for previously undiagnosed conditions. Another, perhaps most important reason for this differentiation, is proper identification and diagnosis so that definitive therapy can be given.
Both ENT and dental specialties have often observed that the eustachian tube and the palatine muscles display a fascinating array of cranial interneuron connections, and that these connections reveal an often-overlooked neurological pain and dysfunction genesis. As we discuss this fascinating array of interneuron connections, the rationale leads one to believe that this very common objective finding in temporomandibular joint dysfunction is spasm of the internal pterygoid muscle. Embryologically, the same nerve that innervates the internal pterygoid muscle directly innervates the tensor timpani muscle. It is therefore stands to reason that if a stimulation along the nerve that innervates the internal pterygoid muscle places that much stress and reactivity in the jaw muscles then it can affect the adjacent network of nerve and muscle response in the middle ear and the pharyngotympanic tube.
The interaction of the craniomandibular posture and gravity is demonstrated by the patients who complain of ear pain, jaw pain, or both. Muscle or nerve dysfunction in the maxillofacial area, especially around the palatal vault and the temporomandibular area, is responsible for many resulting signs and symptoms easily misdiagnosed as Menieare’s disease, positional vertigo, or other otologic maladies.
The following case report will present a critical review of the craniofacial anatomy and the neuromuscular anatomy, as well as the central nervous system connections involved in vertigo, temporomandibular disorders and co-morbid otologic disease. This author’s intraoral exam of head, neck or facial pain patients routinely includes a close look at the palatine muscles, uvula, the posterior border of the maxillae, and the hamular notch.
Thirty years ago dentists were prone to use an all-inclusive theory of temporomandibular disorder to explain the cause of chronic pain.3 Since then it has been well stated that temporomandibular joint disorder can mimic neurological disease. Accepting that premise will require that we understand that neurological disease can create symptoms of temporomandibular joint disorder. Therefore temporomandibular joint disorder with chronic pain and dysfunction can co-exist with otologic pain and dysfunction—and they are not mutually exclusive. Is it possible that jaw opening or closing or swallowing could have an effect or response in the ear structures? Is there a relationship between temporomandibular pain disorders and otologic pain disorders? Can they be mutually provocative?
The pathognomonic triggers in craniofacial pain seem to arise in multiple areas of nociception and the sensory branches of a number of cranial nerves are involved in this reaction. The reflex arc of pain transmission is commensurate in the ear structures and the jaw mechanisms that receive pain stimulus. Close observation of the proximity of major nerves in this area will reveal the reasoning developed in this case study. It will also help clinicians by revealing the composite anatomy of this major maxillofacial area and reveal the embryological development of these structures.
As with most illnesses, the patient history holds the key to a majority of diagnosis. Examining clinicians have to remember, however, that a chief complaint my falsely localize the lesion to a particular organ when the pathologic lesion maybe elsewhere.
Eighteen patients (58%) reported wrists with incomplete range of motion before prolotherapy. After prolotherapy, only six (19%) patients reported incomplete range of motion in their wrists (see Figure 3). Patients average wrist crepitation was 2.8 before prolotherapy, but only 1.5 after prolotherapy.
The patient is a very intelligent 52-year-old female U.S. Navy retired Chief Petty Officer who is currently employed as an Office Manager. This patient’s problem began in October 1998 with her initial complaint of left ear pain. She developed chronic sinus problems and pain and has had seven sinus surgeries over the past ten years. Following these surgeries for recurring pain, she was followed by her otolaryngologist and received antibiotics and analgesics and re-examinations for the sinus-type pain. The left ear pain did not appear as paramount to the ENT evaluations. In June 2000—the second year of her dilemma—an oral maxillofacial surgeon at the U.S. Naval Hospital stated that the patient displayed no obvious pathology with the exception of a small 2x2mm area of petechia and possible ulcer on the left posterior-superior pharyngeal wall viewed only with nasal endoscophy. The assessment was that this was not TMJ or dental and that the area of the ulcer was the most probable cause of the pain.
She was given I.V. antibiotics for infection which she self-injected into an I.V. catheter at home. Findings were consistent with an uncomplicated otitis media. However, antihistamines, decongestants, and steroid inhalants did not change the symptomathology. Tympanostomy tubes were placed but did not alter the pain level. Shortly thereafter, the patient began to experience progressive pain in, and around, the left ear. A sense of fullness developed as well as clicking and popping of the left temporomandibular joint. A follow-up ENT examination also raised the possibility of TMJ dysfunction.
This history of injury appeared to reveal an inordinate amount of miscommunication with all doctors with the exception of the otolaryngologist who saw the ulcer again in 2007 prior to my examination. The patient in this study felt vulnerable, frightened and depressed, which made a coherent description of clinical and personal aspects of her pain difficult. Clinicians in a commanding role with a patient need to convey understanding of the patients experience and accept that experience with some empathy. In the Fall 2008 issue of the Pain Practitioner, Lennie Duensing wrote an editor’s piece titled “Communicate!” in which she described a cogent message with a brilliant example of what may be missing in the clinician-patient relationship. While she was working on that issue and speaking with both clinicians and patients, the words, “what we’ve got here is a failure to communicate,” kept running through her head.4
Open lines of communication between the patient and the clinician are essential in pain management. In the head, neck and facial pain practice, an honest and personal discourse—talking to patients about their pain and listening actively—is absolutely vital to understand pain as it is experienced by patients. This open dialogue was lost along the way as revealed in this case study. Effective communication between the clinician and patient also reduces risks of misdiagnoses, improper treatment, and other undesirable outcomes such as malpractice lawsuits. There is an inherent imbalance of power in these relationships as the clinician is usually in command when it comes to structuring the interaction with patients.
In this case, it appeared that both dental and medical specialists became focused on the turbinates and nasopharynx and the recurrent infection in these areas. This focus culminated in seven successive operations in the left nasal sinus—including removing parts of the left hamulus as well as degenerated and degraded soft tissue and bone. The patient’s focus was on an area around the Fossa of Rosenmuller that she was convinced was the source of pain in her left ear. May the reader be reminded that the eustachian tube is a passage between the oropharynx and the middle ear. The recurrent soft tissue infections with swelling caused compression of the auditory tube by continuous palatine muscle hyperactivity and started the heterogeneous referred pain to the TMJ mechanisms. Compaction of the anterior-posterior length of the palatal shelves and maxillary bone caused severe retrusion and over-closure. This is a typical extraction-retraction scenario that sometimes results from extraction of the first bicuspid teeth. Although this patient had these teeth removed when she was 16 years old, the adult malocclusion that she exhibits now is a result of gradual tooth and boney changes over the years. The maxillae and the mandibular malrelation may not have caught the attention of the ear doctors or the orofacial pain specialists.
In October 2006, my office provided this patient an initial clinical evaluation including a complex TMJ, head and neck examination. The patient’s predominate complaint was pain in the left ear, soft palate, Eustachian tube, and hearing loss.
In the initial examination of this patient, the author reviewed all the previous accumulated data of the otolaryngologist and dentist consultants. In the interim years between 2000 and 2007, only very limited etiology was revealed and the patients stress level was not reduced. In February of 2007, an otolaryngologist stated that review of the records also showed surgery of the left hamulus. The outside record also showed that there was an area of ulceration in the same area noticed on endoscopic exam at the posterior aspect of her nasal cavity above her soft palate.
Physical examination revealed moderate TMJ pain on opening, closing and lateral excursions and the left TM joint exhibited barely audible crepitus on opening and left lateral excursions. The mandibular range of motion (ROM) was a 47mm maximum opening with a deviation first to the left then to the right. Lateral excursion was six to the left and four to the right. The patient has a class III molar occlusion on the right side, and a class I bicuspid occlusion on the left side with a faulty anterior guidance with an end-to-end position on the laterals. All four bicuspids were removed. Further examination revealed moderate-to-severe TM degenerative joint disease of both right and left sides. Imaging data included corrected tomograms (SMV) of both TM joints, lateral and frontal cephalometric films, and a townes view. The left TMJ radiographics showed severe flattening and bone loss on the head of the condyle and posterior jamming of the condyle in the fossa and also against the ear canal.
Observing the obvious foreboding and psychological issues that this patient presented at the initial examination required an immediate intervention. This clinician intuitively felt a need to give the patient a sign of hope by demonstrating some pain relief and a tentative treatment plan. The pain relief began during the diagnosis and utilized the anterior passive appliance (MAPA) to verify a mandibular position that would release the pain of the closed lock and decrease joint compression. The success of this initial examination and treatment was confirmed by the patient’s statement that the previous pain from speaking, eating, swallowing, coughing and laughing, was immediately gone. Diagnostic injections, physical therapy, acupuncture, biofeedback, craniosacral manipulation, and other diagnostic procedures have not been necessary or requested by the patient since the initial diagnostic passive appliance successfully removed the neurological and psychological pain and dysfunction that the patient had suffered for the previous ten years.
The author became the last health care professional to evaluate the patient and was number 26 on the list of doctors seen by the patient. All TMD pain and dysfunction was initially reduced and a lesion near the proximal end of the Eustachian tube remains in continuous pain and is being handled by her ENT doctor whom she trusts implicitly because of his ability to listen to and communicate with her. Since her hyperbaric chamber of two months duration was not successful, the lesion is unchanged and it will be pursued by this Otolaryngologist. The patient needs irrigation of the area but may possibly be cleared of the pain associated with this lesion by radio frequency thermonucleosis (RFN).
The patient’s history of injury includes nearly ten continuous years of chronic left ear pain which has produced tinnitus, hearing loss, disequilibrium that was accompanied by significant psychosocial and neurological pain. The endless pain, anxiety and frustration from 10 years of specialty consultations to find and correct an ENT/TMD disorder appeared fruitless.
Combined efforts of several medical and dental experts—ranging from a single visual oral examination, to a trial of six weeks on intravenous antibiotics for infection to eight weeks of hyperbaric chamber treatments—did not provide relief. She also had seven sinus surgeries. After ten years with no pain relief or doctors who could find the cause of her pain, she became depressed and almost lost hope of ever getting well. In the first year of her dilemma, a dentist located a 2mm ulcer in the nasal cavity near the “Fossa of Rosenmuller” and the eusta-chian tube that he thought was the source of her pain. This information was relayed to her ENT doctor who could not confirm the diagnosis. She was sent to numerous dentists and ENT doctors throughout the years. She tried to tell them where the ulcer was and that the pain was in that area. No one could find anything. She believed that since she had seen numerous doctors they began to stigmatize her. She would get comments like “You have seen some good doctors and they couldn’t find it, so how do you expect me to find it?” On several appointments, she was told that she should see a psychologist. It was about seven years into her search for pain relief that she made an appointment with yet another ENT specialist. She did not give him much information about the doctors she had seen in the previous years. She described where she thought the pain was coming from and this doctor went right to where the ulcer was located near the eustachian tube. Finally, here was a doctor who saw this ulcer again and hopefully could give her some pain relief.
She was also referred to this author and the diagnostic protocol used will be described below. The unique passive appliance treatment plan provided immediate pain relief verifying a passive appliance treatment (MAPA) as an expedient and prudent way to begin treatment and confirm the initial diagnosis. As demonstrated in Dr. Danny Crout’s poster presentations at many national meetings, the MAPA confirms the notion that the brain’s proprioceptive sense cannot comprehend a jaw position that has been manually manipulated or provided by a mechanical device. A passive appliance, as utilized in this patient’s treatment, eliminates chronic microtrauma to the TM joints by removing or reducing the constant compression and negative movement caused by excess muscle activity. Therefore there will be minimum muscle activity to cause disc compression or displacement. This passive appliance can establish a release position in “a place in space” unimpeded in any way by contact, pressure or weight—and meets the demand of gravity as expressed in total body posture. The position established in this manner is directed by the homeostatic balancing of neurotransmitters in the ANS. Comprehensive coverage of this unique appliance will be described in a separate article. The author puts great importance at this point on the fact that this appliance has the distinguishing capability of providing pain treatment during the diagnosis of combined dual-pain generators of ENT and TMD.
What followed this breakthrough in the otomandibular pain was attention to the affective pain represented by the patient’s central activation. It was at this point that the originating pain condition crossed over the line into chronic pain having affective pain arising by central activation. It was the first time the patient’s biopsychosocial pain had been recognized.
“Temporomandibular disorders and co-morbid otological disease reveal the depth of the urgent need to understand TM disorders and craniofacial referred symptomatology contained in the stoma-tognathic system.”
Now, following the successful passive appliance treatment, the patient wears a neutral bionator appliance at night. All original pains have been drastically reduced. The patient takes one pain medication at night prescribed by a pain management doctor but all other neuropathic medications have been eliminated.
In her words: “After years of anger, frustration, and being doubted that there was a valid reason for my pain, I realized that my only reason to continue my search for pain relief was the pain itself... I have seen several doctors who could not locate the area I was concerned with and kept telling me there was nothing wrong. Throughout the years, I had seven sinus surgeries. Parts of my sinuses were taken out during some of the surgeries and I constantly had sinus infections. One doctor said that I had too much taken out of my sinuses. I asked him to please make a note of that in my record and his comment was “I’m not looking for a law suit.” Another doctor asked me what was the worst thing anyone had said to me concerning my situation, and I responded “have you seen a psychologist?” The next question was what was my biggest fear about all of this? My answer was “that I would have to live with this pain for the rest of my life.” I once asked a doctor if the area of concern was a dental or ENT specialist area? I did not get a clear answer. A dentist said that everything above the soft palate was an ENT doctor’s area and everything below the soft palate was a dentist’s area. The soft palate seemed to be the divider. What if the soft palate was part of the problem? This is an area that both specialties should share. Both specialties need to communicate.
“This led to my frustration, anger, and my obvious disappointment with dentistry and medicine in their ability to work together to come up with a diagnosis to help with my pain. After years of being stigmatized, I learned not to get too excited about seeing any doctors because I would probably just be let down again. I think that was my way of protecting myself from the psychological pain.
“I have many other stories I could share about my search to get well. My hope is that through this article doctors will learn the importance of working together to come up with a diagnosis and not to stigmatize patients. Maybe patients in the future won’t have to experience what I experienced for the past ten years. I believe that a lot of what I went through could have been prevented if doctors worked more as a team instead of independently.”
Temporomandibular disorders and co-morbid otological disease reveal the depth of the urgent need to understand TM disorders and craniofacial referred symptomatology contained in the stoma-tognathic system. This author’s clinical exam of head, neck or facial pain patients routinely include a close look at the palatine muscles, the uvula, the posterior border of the maxillae, and hamular notch.
When students ask this author why these areas are so important in the examination, the reply is that tenderness in the palatine muscles with accompanying redness and swelling often indicate deflective incisor guidance either by anterior malalignment or an appliance that does not give cuspid guidance in a passive manner. TMD produces contraction and tension of the masticatory muscles and reflex contraction tensor veli palatine and tensor tympani muscles due to common innervations from the trigeminal mandibular branch. Otalgia can be felt by tympanic membrane tension due to constant tensor tympani muscle contracture. This suggests a frequent relationship between orofacial, chewing and middle ear muscle operation. TMD can be produced with increased emotional tension and dysfunctional muscle activity. This complex neuromuscular interaction between the muscles of mastication and the ear was referred to as otognatic syndrome by Myrhaug in 19645 and otomandibular syndrome by Arlen in 1977.6 As indicated earlier, this author has had significant experience in cleft palate surgery and rehabilitation which allowed visualization of the eustachian tube and paratubal muscles. Patients with repaired or unrepaired palates suffered from a functional obstruction of the eustachian tube. This inability to actively open the eustachian tube is demonstrated by patients with a bifed uvula and submucous clefts as well. The abnormality was presumably due to abnormal relations between the craniofacial defects and the tensor villae palatine muscles. This has illustrated the need for an intact palatopharyngeal composite anatomy since the neuro-patterns of these muscles were integrated early in the embryologic development.
Investigators have hypothesized that eustachian tube dysfunction and masticatory muscle dysfunction occurs secondary to abnormal stimulation of autonomic nerves of the TM joint. It is hypothesized that structural effects induce oral symptoms—including mandibular over-closure and posterior displacement of the condyle—that secondarily puts pressure on craniofacial nerves, the eustachian tube, and erosion of the tympanic plate. Reflex disturbance of the tensor timpanea, villae palatini muscles, as well as the otomandibular ligaments, are among the structural causes for aural symptoms. Ear, nose and throat consultants often fail to find any objective pathologic condition to explain ear symptoms. Nevertheless, it is well documented that TMD patients with otalgia or tinnitus have higher pain and dysfunction than do patients without otologic symptoms.
In his September 2007 article “Patulous Eustachian Tube,” Dr. Edwin Ernest stated “…if we look only for what we know we will usually not see or recognize anything else.”7 Dr. Ernest’s insightful comment is an appropriate description of the dilemma that developed in this case study.
The graduate students in advanced prosthodontists in the 1970s were getting extensive first hand experience with temporomandibular disorders. Thorough examination of the maxillary and mandibular arches were routine and often revealed muscle and soft tissue impingement by removable dentures which caused speech, hearing and swallowing problems. Overextended removable dentures may cause temporomandibular pain as well as pain and dysfunction in the anatomical areas that include the posterior palate, hamulus, soft palate and pharyngeal area (including the dysfunctional palatine muscles that are responsible for the otomandibular symptoms discussed in this article).
As described briefly above, less common disorders were ruled out beginning with the complex pterygoid hamular area pain. Doctors Dupont and Brown, who recognized that pterygoid hamular pain is an uncommon disorder, described comorbidity of pterygoid hamular area pain.8 However, prosthodontists encounter the hamular complex frequently because over extension of an upper full denture will immediately create hamular pain and dysfunction. This patient fit the typical symptoms of hamular bursitis. Consequently, it was difficult to rule this diagnosis out. However pterygoid humular syndrome was ruled out because the patient had responded immediately to the passive intraoral appliance and palpation of the hamulus was painless.
Glossopharyngeal neuralgia can be precipitated by a variety of stimulae such as swallowing, chewing, coughing, talking or occasionally eating cold or highly spiced foods. This diagnosis—as opposed to the otomandibular syndrome—frequently occurs at night and may present with syncope or convulsions. The second uncommon neuralgic diagnosis associated with the eustachian tube, middle ear and oropharinx and external auditory canal can be mistaken for otalgic pain episodes. The latter is exceedingly uncommon—with the left side affected more than the right side, together with the typical sharp stabbing pain—and was not identified in this patient.
A third very infrequent neuralgic pain symptom is called nervus intermedius neuralgia (NIN). This sensory branch of the facial nerve is an uncommon disorder producing very intense and stabbing pain localized in the depth of the ear canal. This is an extremely rare condition thought to be similar to trigeminal neuralgia but involving a sensory branch of the facial nerve that innervates the external ear canal. This patient failed to qualify for this diagnosis because Q-tip palpation in the deep external auditory canal on both right and left sides caused momentary discomfort and not paroxysms of intermittently occurring pain. Eagles’ Syndrome and other TMJ disorders were also ruled out.
A fourth unusual and interesting possibility, the patulous eustachian tube diagnosis as described by Dr. Ernest,7 was ruled out because the patient’s eustachian tube opening was easily identified. This was verified with the Frenzel technique for ear clearing.
The original sinus, eustachian tube and TMD pain began by a noceceptive signal arising from neuropathic stimulation of the 5th cranial nerve and other cranial extensions. Hyperactive palatine muscle activity is constantly occurring due to the clashing of the upper and lower anterior teeth causing compression against the heavily innervated muscles, tendons, ligaments and discs of the TMD apparatus and the auditory tube. This cycle of pain was negated in this patient’s case by utilizing the maxillary anterior passive appliance (MAPA). This passive appliance instantly removed the compression in the fossa by opening the vertical dimension and providing relief to the sympathetic pain by eliminating tooth contact in the incisors and the posterior teeth.
The art and science of dentistry—often mentioned by Dr. Edwin Ernest in this journal—includes the study and clinical practice of dental medicine. Head and neck pain disorders are often addressed by physicians and dentists who have considerable background in the study of chronic pain as well as clinical experience in neuropathology associated with TMD. Dentists practicing orofacial pain management are cross-referring these patients with ENT physicians, pain management doctors and other physicians specialists in neurology, orthopedics, and psychology and psychiatry, to name a few. An analytical review of the craniofacial anatomy and neuromuscular anatomy was presented above, as well as the central nervous system connections involved in vertigo, temporomanibular disorders and co-morbid otological disease.
The author has described a very non-traditional diagnostic treatment protocol utilizing the MAPA to intercept the afferency in the sympathetic part of the ANS and provide relief through the parasympathetic response. The author has also explained the need to interrupt the nerve-muscle activity in the palatine muscles associated with the eustachian tube and middle ear as demonstrated in the case study. The intimate nexus between dysfunctional masticatory activity—such as bruxism—TMD and emotional stress can lead to a cause-effect relationship between them.
The anatomical area described in this article is a veritable professional “no man’s land.” Neither medicine nor dentistry stake claim to this controversial anatomical territory. Common symptomatology is frequently observed in otic symptoms and TMD during daily clinical practice in both medicine and dentistry. Conflicting and overlapping symptoms can present a confusing clinical picture in the diagnosis of craniofacial pain and can prove a frustrating and difficult event for both the examiner and the patient. Therefore, it is incumbent on clinicians treating pain in the head, face and neck areas to become familiar with the less common pain disorders to assist in the differential review.
This author has observed TM joint disease and otalgia as being traumatic, inflammatory, and frequently as a referred pain that may accompany pain from some other site. A significant number of these ear pain victims are non-otogenic in causation. The author’s professional community is blessed with numerous otolaryngologists with outstanding scholarly credentials. There is a luminary ENT physician amongst them who frequently refers patients on the basis of mysterious ear pain syndromes that don’t respond to the usual treatments provided for auricular pain. Besides the patient in this case report, referred patients have included those suffering from otic shock from electronic devices, chronic TMD pain patients with untreated whiplash or jaw lash, neuropathic (complex reflex pain pyndrome), old diving accidents, and unresolved air sickness. Professionals that join in successful diagnosis and treatment of such patients most frequently include otolaryngologists, neurologists, psychiatrists, dentists, and oral maxillofacial surgeons.