Diagnosis and Management of Facial Pain: Two Case Reports of Unusual Presentations

by Bruce V. Freeman DDS, D.Ortho, M.Sc., Michael B. Goldberg MSc., DDS, Dip. Perio

The diagnosis of the origin of facial pain is a convoluted, complicated issue. Few patients present with an unrestored dentition and a clear history as to the nature of their problem. The origins of orofacial pain can range from neoplasms to syndromes of psychogenic origin. It is incumbent upon the clinician to consider all alternatives from the obvious to the esoteric.


The patient presented to the Mt. Sinai dental clinic with a complaint of “pain in my jaw joint on the right”. The medical history was non-contributory. There had been a negative neurology evaluation due to episodes of migraine with aura. The problem had been present for approximately fifteen years but only recently had become annoying enough to seek treatment. The patient stated the pain was like an inflamed, “pumped-up” sensation, similar to a swollen knee. The pain was often present in the morning and was not usually exacerbated with jaw function. Tylenol was used to no effect. A limitation of mandibular opening was also noted. The patient is a mechanic and when bending during work he felt discomfort and a restriction in jaw movement. Right-sided clicking was noted by the patient and had worsened in recent months. There were no reports of altered sensation within the head/neck region.

The extraoral and intraoral examinations were non-contributory with regard to sites of tenderness to palpation. Condylar translation was equal. There were inconsistent, reciprocal joint sounds associated with the right TMJ. The range of mandibular opening was within normal limits and was not associated with discomfort. The dentition was heavily restored and the level of care was suboptimal (Fig. 1). Due to the patient’s complaint of a change in his symptoms with different head postures, the original differential diagnosis was “TMD-like symptoms complicated by possible vascular abnormality.”

The patient was convinced as to the origin of his problem, stating that his right TMJ was sore, like “any sore joint”. Attempts at symptom management with anti-inflammatory and muscle-relaxant medications was suggested on the condition that the patient attend an appointment for a neurology consultation, as the nature of his symptoms did not support a diagnosis of a TMD alone.

Upon re-evaluation, the TMD-like symptoms had subsided somewhat but the sensation of the chief complaint had not changed. The patient stated that he had already seen a neurologist and that he would not seek another consultation, as he was insistent on the diagnosis of a “TMJ problem”. A referral was then made to an otolaryngological surgeon as the patient was told yet again that there could be a serious, underlying problem that was not related to his self-diagnosis.

The patient attended the ENT consultation where the surgeon stated he could not account for the complaint of right preauriciular pain and swelling. An ultrasound was ordered and the results suggested “cystic spaces and calcium deposits”, which could be representative of a phlebolith. Thus, the possibility of a hemangiomatous-type lesion was suspected. The ultrasound also revealed a 3cm heterogeneous mass located along the deep surface of the right masseter muscle. The lesion appeared to invaginate into the muscle superiorly, extending under the zygoma to lie medial to it and adjacent to the head of the temporalis muscle.

A second, abnormal area was found lying along the medial border of the lateral pterygoid muscle. There were calcifications within the lesion. The final diagnosis was that of a hemangioma with at least two foci. The patient underwent percutaneous embolization therapy. Embolization is a treatment used in an attempt to terminate or reduce blood flow to a lesion in the head, neck, or skull base region. The procedure is usually performed in conjunction with diagnostic angiography and most often is completed in one session.1 Percutaneous embolization in this case involved injection of approximately 3cc of absolute alcohol into the malformations.


Establishing a diagnosis for orofacial pain can almost be as difficult as trying to manage the patient. In this instance patient management and his resistance to seek further opinions was part of the problem. The first impression of the patient’s symptoms coupled with his insistence as to the nature of the problem could easily have sent his treatment down the wrong course. There are a myriad of causes of orofacial pain and many are not obvious. The reason for the original differential diagnosis was unfortunately not solely based on objective findings but a combination of the patient’s complaints and the fact that the whole picture did not ‘make sense’. The patient could open without discomfort and his pain was not exacerbated with jaw function–definitely not hallmarks of a “garden variety” TMD. It is important when diagnosing orofacial pain conditions to first, not fall prey to the ‘tyranny of the obvious’ and to also acknowledge when you may have reached the limits of your own knowledge base and seek the opinions of others.


Ms. JK is a 43-year-old female with no contributory medical history. She presented to our clinic with a chief complaint of chronic pain in the right maxilla, which had been present for approximately 12 months. She initially went to her dentist in order to deal with pain that was thought to be associated with tooth 48. A carious lesion was discovered and was apparently of moderate depth. Given that 18 had been extracted many years previously, it was decided that 48 should be extracted. This was accomplished without incident.

However, during the recovery period, the patient claimed that her discomfort persisted, beyond the time with which pain should have dissipated. She returned to her dentist who referred her to an endodontist to assess 47. Endodontic therapy was completed on 47 however this did not diminish the pain in any way. Ultimately, 47 was extracted. Again, there was no relief of pain from this treatment.

Ms. JK noted that her discomfort was gradually migrating anteriorly after each tooth was extracted. The patient continued treatment, with the assumption that the origin of the problem was dental in nature. The general practitioner and endodontist proceeded to endodontically treat and extract 17, 16, 15, 14, 46, 45 and 44. Finally, it was felt that a non-dental origin might be contributing to the pain complaint. JK was ultimately referred to the Wasser Pain Management Centre at Mount Sinai Hospital.

Ms. JK claimed that her current pain was localized to the 12/11 region, and that “when she tapped on the tooth, it felt different”. On occasion, that sensation would come on spontaneously. In most cases the pain was worse after meals. However, there was “always a constant, dull ache present”. The pain would occasionally radiate to the temporal region. Ms. JK denied any parafunctional activity. She noted that her sleep patterns had worsened after the pain had been present for 6 months.

Of note was the fact that Ms. JK’s family physician elected to send her to a neurologist in order to investigate the situation further. Although there was no overt neurological deficit, Ms. JK’s doctor suggested that she be placed on Nortriptyline, 10 mg, prior to bed. Ms. JK noted that her pain became markedly reduced for a period of three to four weeks. After that, her pain would gradually increase. She noted that if she increased her Nortriptyline dose, her response patterns would be similar. At the time of presentation, she was taking 30mg of Nortriptyline nightly.

Clinical examination revealed no palpation tenderness in either the temporomandibular joints or the muscles of mastication. No joint noises were noted, and maximum interincisal opening was well within normal limits and pain free. An intra-oral examination revealed no overt signs of pathology. Palpation of the edentulous ridge did not produce any discomfort. What was noteworthy was the fact that percussion of the remaining right maxillary
teeth did not produce any discomfort. However, when Ms. JK percussed her own teeth, she noted that they felt “different”. A panoramic radiograph (Fig. 2) identified no overt pathology.

From the examination, we suggested that the differential diagnosis is likely topped by an Atypical Facial Neuralgia (AFP). JK enquired if there was any way to “definitively” rule out the possibility of dental pathology still being associated with the pain condition. We suggested the use of a Technitium and Gallium bone scan, which would be able to detect subtle areas of infection or inflammation. This was ordered, which proved negative. This further substantiated our diagnosis of neuropathic pain. Given that Ms. JK was being well-controlled with Nortriptyline, we did not feel that changing the medications was appropriate at that time. However, we referred Ms. JK to our group neurologist for further assessment and treatment.

It was suggested by the neurologist that a change in medication from Nortriptyline to Desiprimaine be made. Ms. JK was titrated to a 25mg dose of Desipramine. Her pain condition has been stable for four months. Future intervention will include an attempt at reducing her medication intake. As well, a solution to the partial edentulism will be needed. Although a temporary removable partial denture is currently in place, future surgical intevention with implant therapy will need to be evaluated carefully, given the past history.


There are many important issues surrounding the management of a patient suffering from Atypical Facial Neuralgia. First and foremost, an early and proper diagnosis is essential in order to avoid the pitfalls that befell this case. Had this occurred, many more teeth may have been salvaged before undergoing what appeared to be unnecessary endodontic treatment and extraction. The use of local anaesthetics as a diagnostic tool will often assist in differentiating dental from neuropathic pain.2 Infiltration of local anaesthetic into the site of perceived pain will oftentimes not diminish the chief complaint in any manner, although the dental site itself will be completely anaesthetized.

Once a diagnosis has been made, the use of tricyclic anti-depressants is often the first line of therapy in the management of these conditions.3 Low-dose TCA’s have been shown to be effective in the management of chronic pain symptoms. These doses are sub-therapeutic in the management of clinical depression. However, although the doses may be smaller, side reactions can often be quite severe. Patients often complain of dry mouth and drowsiness. Patients with a history of cardiac disease may suffer arrythmias and tachycardia. It is important that should a need for tricyclic antidepressant therapy be required, the patient’s family physician should be the prime administrator of these medications. Patients will often have a pre-treatment cardiogram and liver enzyme levels assessed prior to starting, what oftentimes is, long-term pharmacotherapy.

The most important point of this case as a dentist is to discontinue further dental interventions until the pain has been managed for a substantial period of time. AFP may be aggravated by repeated interventions and even when stable, the chances of recurrent problems will always be present. However, if appropriate management strategies have been undertaken and an appropriate period of time is allowed to pass, slow, methodical re-introduction of dental treatment (ie: implant therapy) may be considered.

Dr. Freeman maintains a private orthodontic practice in Toronto and is a member of the Facial Pain Clinic in the Department of Dentistry, Mount Sinai Hospital.

Dr. Goldberg maintains a private periodontics practice in Downtown Toronto and is an Assistant Professor in the Department of Periodontics, University of Toronto. He is also a member of the Facial Pain Clinic in the Department of Dentistry, and the Wasser Pain Management Centre, Mount Sinai Hospital.

Oral Health welcomes this original article.


1.Canter HI, Vargel I, Mavill, ME, Gokoz A, Erk Y. Tissue response to N-butyl-2-cyanoacrylate after percutaneous injection into cutaneous vascular lesions. Ann Plast Surg. 2002;49(5):520-526.

2.Graff-Radford SB, Solberg WK. Atypical odontalgia, J Craniomandib Disord. 1992; 6(4):260-265.

3.Melis, M, Lobo SL, Ceneviz C, Zawawi K, Al-Badawi E. Maloney G, Mehta N. Atypical odontalgia: a review of the literature. Headache, 2003;43(10):1060-1074.