Trigeminal neuralgia mistaken as temporomandibular disorder

E V I D E N C E -B A S E D C A S E C O N F E R E N C E

Trigeminal neuralgia mistaken as temporomandibular disorder Mark Drangsholt, DDS, MPH,a,b and Edmond L. Truelove, DDS, MSDa From the Departments of Oral Medicine,a Dental Public Health Sciences,b School of Dentistry, University of Washington, Seattle

A 40-year-old woman was admitted to the clinical service with a report of “exquisite” left facial pain of 3 months’ duration. She had been healthy with no significant complaints before the onset of pain, except for a similar episode of the same symptoms 1 year earlier that persisted for 3 weeks and then stopped without treatment. She described her pain as being severe and brief, and she said it was commonly brought on by rapid movement of her jaw, face, lips, and tongue. Usual opening and closing of her jaw did not initiate the pain, and when the pain was not present, chewing and eating were not affected. The pain was located in several areas of her face, all on the left side, and included her face, gingiva, tongue, upper jaw, temporomandibular joint, and mandible. Her jaw also felt stiff, and the pain limited her ability to open wide. She described her pain as sharp, splitting, shooting, and exquisite, and rated the severity as 10 on a scale of 0 to 10. Physical exercise seemed to help decrease her symptoms, but the pain was not reduced with the use of any analgesic medications, including opioids. At the time of the first episode she was examined by her dentist, who found no specific dental pathology and referred her to a dental specialist. Her symptoms were inconsistent at the time of that examination, and the pain stopped before a diagnosis could be established. During the recurrence of her pain, she was referred to an endodontist, who was unsure of the origin of the symptoms and referred her to a TMJ specialist. This specialist conducted a history and physical examination that took several hours and concluded that she had had a temporomandibular disorder. Treatment was initiated, which included upper and lower acrylic splints, carisoprodol (350 mg, 4 tablets/d), and amitriptlyine (50 mg, hs). After using the splints and taking these medications as prescribed, her symptoms increased in both severity and frequency, and, after several weeks she became dissatisfied with the failure of this treatment. Her general dentist then referred her to our clinical service. J Evid Base Dent Pract 2001;1:41-50 Copyright © 2001 by Mosby, Inc 1532-3382/2001/$35.00 + 0 77/1/116846 doi:10.1067/med.2001.116846

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Fig 1. Panoramic films showed no obvious dental or maxillofacial pathology.

HISTORY AND EXAMINATIONS MEDICAL AND DENTAL HISTORY She had a medical history notable for a fractured tibia from a sports injury, and current complaints of fatigue, arm weakness, changes in handwriting, sleep difficulties, and earaches. Her menstrual cycle had also become irregular. Otherwise, she rated her health as excellent and engaged in regular vigorous exercise daily, occasionally consumed wine, and had never smoked. Her most recent physical examination by a physician had taken place 6 months before, and the findings were unremarkable. Her family history was positive for cancer and heart disease. She was not taking any medications and did not report any allergies. Her past dental care had been routine, with regular 6-month checkups for many years, and she had had no dental restorative treatment for over 5 years. She said she had not had any toothaches recently.

PSYCHOSOCIAL HISTORY The patient, who was single and living alone, had a postgraduate education and worked as a university faculty member. No significant family problems had occurred while she was growing up, and she reported excellent relationships with both her mother and her father. Mild stress was reported as a result of family concerns and social relationships, and she reported that she had had a minor physical assault 8 months ago with no permanent injury. Moderate 42 Drangsholt and Truelove

stress was related to concerns about her health. Data gathered from a structured database revealed sleep problems, including restless sleep, weakness in her extremities, and feelings that most things were a strain. In addition, she identified the feeling that something was seriously wrong with her body. The Symptom Checklist-90 questionnaire was used to identify possible psychosocial distress, and it indicated that she was unlikely to have depression, anxiety, or somatization disorders.1

PHYSICAL EXAMINATION A physical examination revealed a normal morphology of the face, neck, eyes, and oral structures, with no obvious lesions of soft tissue or osseous structures. Temperature was 98.8°F, pulse was 68 beats/min, respiration was 12 breaths/min, and blood pressure was 118/71 mm Hg. Unassisted mandibular opening was 41 mm, and rapid opening and closing caused severe left facial pain, but slow opening and closing movements caused no pain. Neurological assessment of the cranial nerves revealed no abnormalities, with normal motor and sensory function, as tested, except for pain generated when the left side of the face was palpated with light pressure over the region of the upper aspect of the masseter and temporalis. Firm (2-lb) palpation of the muscles of mastication (temporalis and masseter) was rated as non-painful by the patient and palpation of the temporomandibular joints and cervical muscles also did not elicit any pain complaints. Palpation of Journal of Evidence-Based Dental Practice July 2001

the labial mucosa of the maxilla on the left triggered her pain. Between the brief episodes of the severe pain during the examination, she was pain free. Percussion of all of the teeth in both arches revealed brief and variable pain upon percussion of the left maxillary teeth. Upon repeat percussion a few minutes later, none of her teeth were painful to percussion. Electric pulp and thermal testing of the maxillary and mandibular teeth on the left showed all of her teeth to be vital and none that were hypersensitive to cold. Her periodontal status was excellent, with no pockets in excess of 3 mm and no evidence of infection. Salivary function was also within normal limits, and all 4 major glands were noted to actively produce clear saliva.

RADIOGRAPHIC EXAMINATION Full-mouth dental radiographs, a panoramic film of the jaws (Fig 1), and tomograms of the temporomandibular joints revealed no obvious pathologic condition. No significant carious lesions or periodontal defects were evident, and no existing restorations were in close approximation to the pulp chamber. All 4 of her third molars had been extracted several years earlier, and the extraction sites had healed normally. Root canal therapy had been successfully performed on tooth 15 about 20 years earlier. The maxillary sinuses also appeared to be normal. The temporomandibular joints were seen to be normal on tomograms, except for faint flattening of the condylar heads bilaterally.

DIFFERENTIAL DIAGNOSIS The complex nature of her symptoms and the failure of her dentist and the endodontist to detect specific odontogenic pathology suggested that a less common etiology could be present.

In patients with similar symptoms, the differential diagnosis would include neuropathic pain arising along the distribution of the trigeminal nerve, including the possibility of classic trigeminal neuralgia (TN) or a trigeminal neuropathy resulting from damage caused by trauma or dental treatment; chronic pulpitis or pulpitis resulting from a cracked or fractured tooth; myofascial pain of the muscles of mastication; an internal derangement of the left TMJ; or sinus pathology, including sinusitis or a sinus lesion.

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Classic historical features of TN, negative radiographic findings, repeated pulp testing including electrical and cold tests, along with challenge with percussion, all failed to provoke the symptoms, thus reducing the likelihood of pain from odontogenic origin. The failure to detect the presence of pain through use of biting pressure on the cusp tips further decreased the possibility that symptoms were caused by a cracked tooth. Usually, a symptomatic cracked tooth that causes pain other than on biting has an accompanying pulpitis and reacts to percussion or cold testing. The failure to provoke pain and the pattern of pain, including triggered symptoms upon the rapid opening and closing of the mouth, whether the teeth were brought into occlusion or not, suggested another source. Pain stimulated by light, but not firm, palpation of the masseter and temporalis muscles indicated that neurological stimulation of superficial sources of innervation were involved in the initiation of pain. The lack of pain with slow, but not fast, opening also suggests neurological versus muscle-based pain. The lack of percussion pain but severe pain upon palpation of the alveolar tissues also pointed toward neurological pain.

Muscle tenderness with palpation suggested she also had myofascial pain that was the result of jaw splinting, done in an effort to reduce the jaw mobility that triggered her neurological symptoms. On the basis of these observations, the patient was reexamined. Considerable attention was devoted to pain provocation from very light tactile stimulation of the left trigeminal distribution. Stroking of the skin over the temporalis, masseter, TMJ, and gingival/oral mucosa with the jaw held in a stationary position caused brief episodes of severe pain. Topical anesthesia of the gingiva and oral mucosa completely prevented the triggering of the pain. These responses essentially ruled out pulpal disease, sinus pathology, and myofascial pain as the primary etiology, and indicated that TN was the most likely diagnosis. Although the patient was only 40 years old, her age was still within the common range for TN. Muscle tenderness with palpation suggested that she also Drangsholt and Truelove 43

Fig 2. Likely sites of triggering TN pain. (Reprinted from Bonica’s Management of Pain. 3rd ed. By permission.)

dosage slowly over the next week until her pain was no longer present, could not be triggered, or she reached a daily dosage of 1200 mg. On return to the clinic, she reported that all her pain had stopped when she reached a dose of 150 mg 3 times a day and that reducing the dosage caused re-initiation of the her symptoms. This positive response to carbamazepine helped to confirm the diagnosis of TN. The patient decided to delay the MRI scan since she was doing well and was lost to follow up for several years. A subsequent MRI taken at a later date showed no pathologic findings. Consulting neurosurgeon’s diagnosis: left second and third division classical TN

DISCUSSION

had myofascial pain that was the result of jaw splinting, which was done in an effort to reduce jaw mobility that triggered her neurological symptoms. Preliminary clinical diagnosis: TN, left division 1, 2, and 3; secondary myofascial pain, left masseter and temporalis muscles. Because there are a number of possible causes for TN, additional diagnostic testing and consultation was in order. The patient was recommended for MRI evaluation of the brain and distribution of the greater part of the trigeminal nerve, as well as soft tissue in the distribution of the nerve that could be involved in nerve impingement. She was also referred to a neurosurgeon at the university who was an expert in TN and neuropathy. Dental films were reevaluated to ensure that occult disease was not present, and panoramic films were assessed for evidence of obvious sinus disease that might affect the trigeminal nerve (Fig 1). Because her pain was severe, consultation with the neurosurgeon resulted in a joint decision to initiate a therapeutic medication trial at pain control, with the aim of improving comfort and providing more data about the diagnosis. Carbamazepine was therefore initiated, and appropriate laboratory studies were ordered. Her medication trial was initiated at 100 mg of carbamazepine every 8 hours, and she was asked to increase the 44 Drangsholt and Truelove

Dentists often play an important role in the diagnosis and appropriate management of TN, since patients often approach them early in the course of the condition with complaints of facial, dental, or oral pain. Making the correct diagnosis is important, because errors invariably result in initiation of invasive and irreversible treatments that often compound the symptoms. The resulting condition of the patient then becomes more complex and can mislead the treating clinicians into thinking that the pain after initial therapy is the result of a treatment failure. In addition, since peripheral etiologies for neurological pain can occur and odontogenic pain often manifests with a severity equivalent to neuralgia, dentists have a great responsibility to rule out local pathology and to guide the patient toward appropriate medical evaluation. One often-overlooked aspect of TN is the manifestation of pain triggered by use of the jaws, including while eating and talking. When the presenting complaint is associated with such activities, an error in diagnosis is possible by confusing symptoms that might occur with myofascial pain or a disorder within the TMJ. Clinicians mistaking TN for TMD have been reported by other authors.3,4 Furthermore, because TN occurs in older patients, and since the rate of TMJ remodeling from osteoarthritis or TMJ sounds (either crepitus or clicking) are common in patients above 50 years of age, it is easy to see how one might arrive at a diagnosis of TMD and misdirect therapy.

EVIDENCE-BASED REVIEW OF THE DIAGNOSIS OF TN The diagnosis of TN is usually made from a characteristic history of the patient, coupled with Journal of Evidence-Based Dental Practice July 2001

normal head and neck findings on examination and radiographic imaging. TN is characterized by the following: 1. Electric shock–like, brief pains 2. Pain-free intervals between attacks, when the patient is completely asymptomatic 3. Unilateral pain during any one attack 4. Pain of abrupt onset and equally abrupt termination 5. Pain restricted to the trigeminal nerve distribution 6. Minimal or no sensory loss in the trigeminal distribution 7. Non-nociceptive triggering of pain, almost always ipsilateral to the pain, usually from the perioral region (Fig 2)5 A proportion of TN patients, perhaps a fourth to a third, may have some atypical features, such as pain lasting longer than a few seconds, and the condition these patients have is termed atypical TN. Although few other facial pain entities have these characteristic symptoms, the scientific literature and the 27-year experience from our own facial pain clinic indicate that many, if not most, cases of TN are initially misdiagnosed and incorrectly treated.3 One author indicated that 80% of 36 patients referred to a dental specialty clinic were initially thought to have a dental problem and were treated as such.6 Another recent series of cases showed that the average delay in diagnosis for both typical and atypical TN referred to a tertiary pain clinic was 6 years.7 Although these findings may just illustrate that the most difficult to diagnose cases are referred on to specialty clinics, and shows the so-called referral bias of these tertiary care settings, we postulate that this is unlikely, for 3 reasons: (1) we see many “classic” presentations of TN in our clinic, not just the atypical cases; (2) informal surveys of local neurologists and neurosurgeons show that a primary referral of a probable TN patient from a dentist is extremely rare without prior treatment attempts, such as root canal or tooth extraction; and (3) almost every TN case we have seen that was initially seen by a dentist resulted in some sort of irreversible dental treatment. This is somewhat puzzling, considering that the diagnosis of TN has been taught in both dental and medical school curriculums for at least the past 50 years. But the prevalence estimates of TN show that a dentist in the United States will likely see, on average, only 1 to 4 TN patients over their 35- to 40-year practice, and that these people will be mixed in with thousands of patients with Journal of Evidence-Based Dental Practice Volume 1, Number 1

pain of dental or myofascial origin. Furthermore, some patients with true TN may also have concomitant dental problems that could further cloud the diagnosis, or may have had initial dental treatment to treat the confusing symptoms. Finally, some patients may have atypical symptoms, such as a prolonged burning quality of their pain or pain triggered every few seconds over several hours, and a clinician may mistakenly diagnose that their pain is long lasting or continuous.

HOW CAN DENTAL PRACTITIONERS BETTER DIAGNOSE TN? ANSWERABLE CLINICAL QUESTION The main question of this report is, How can dental practitioners better diagnose TN? The question could be phrased in PICO format as “In patients with TN [Patient/problem], do specific questions in the history or specific examination findings [Intervention] do better than a standard dental history and physical [Comparison intervention] to increase the likelihood of a correct diagnosis [Outcomes]?”

ARTICLE SEARCHES To answer this question, the following databases were searched: (1) PubMed (1965-February 2001) for scientific articles, and OCLC WorldCat (1950-February 2001) for books. The terms trigeminal neuralgia and tic doloroureux were the search terms used during the indicated periods. These searches resulted in locating 2194 articles in PubMed, which used “trigeminal neuralgia” as the primary indexing term, 1 systematic review of treatment, and 1261 books or other materials. After reviewing these initial lists, the major MeSH terms “trigeminal neuralgia/diagnosis” was used to limit the number of articles to 282. By excluding articles that did not have English abstracts, the list was reduced to about 140. We limited our book searches to English books that were available in the University of Washington library but also searched recent textbooks on pain, orofacial pain, and neurology.

ARTICLE SELECTION The titles, abstracts, and indexing terms were read to determine relevance and initially screen for study quality. Because the main question is one of diagnosis, cross-sectional studies using a defined gold standard for the diagnosis for TN are among the best study designs to answer this Drangsholt and Truelove 45

Table I. Diagnostic features of condition

Diagnostic feature

Source of criteria

Test value (TN vs pulpitis)

History Refractory period of pain observed after stimulation for at least 1 minute Opioids in usual doses do not provide >50% pain relief Electric-shock–like, stabbing, or shooting pains that last only seconds to less than 1 minute* Non-nociceptive triggering of pain almost always the same side as the pain, and usually from the perioral region* Pain of abrupt onset and equally abrupt termination* Pain-free intervals between attacks when patient is completely asymptomatic* Minimal or no sensory loss in the trigeminal distribution* Pain restricted to the trigeminal nerve distribution* Unilateral pain during any one attack*

Fromm15

High

Fromm Loeser/Rasmussen5,10

High Medium

Loeser5

Medium

Loeser Loeser

Low Low

Loeser Loeser Loeser

Useless Useless Useless

Loeser

Medium

Examination Normal cranial nerve exam* Dental examination Hot/cold sensitivity of teeth when ice/heat is applied Percussion sensitivity of teeth on side of pain Palpation sensitivity of periapical region No response to EPT of teeth on side of pain TMD examination At least 2 sites with pain on palpation of masticatory muscles or TMJ Abnormal mandibular range of motion (<35 mm males, <30 mm females)

Medium Useless Useless Medium Dworkin16

Very low

Dworkin

Very low

Diagnostic Tests: Panoramic Radiograph Deep caries approaching the pulp Radiographic evidence of periapical infection Other radiographically apparent lesions

High Low Low

*Diagnostic criteria for TN from Loeser JD.5 Legend Yes Usually

Probability

Score

>95%

5

70%

4

Likely

50%

3

Sometimes

30%

2

Not usually

10%

1

No

<5%

0

question.8 However, only one such study was located, and it used the McGill Pain Questionnaire to help differentiate TN patients from patients with atypical facial pain. It found 46 Drangsholt and Truelove

that 90% of patients could be correctly classified just by the type of pain descriptor that they chose.9 Other studies located were case-series that listed the prevalence of clinical findings in their Journal of Evidence-Based Dental Practice July 2001

Estimated Likelihood Ratio +

TMD-ID/TMJ internal derange ment

Estimated likelihood ratio –

Classic TN

Irreversible pulpitis due to caries

9.5

0.05

Yes

No

No

0.11 4.95

9.0 0.01

Yes Yes

Not usually Sometimes

Not usually Sometimes

2.33

0.43

Usually

Sometimes

Sometimes

1.8 1.8

0.20 0.20

Yes Yes

Likely Likely

Sometimes Yes

1.0 1.0 1.0

1.0 1.0 1.0

Yes Yes Yes

Yes Yes Yes

Yes Yes Yes

0.74

6.0

Usually

Yes

Yes

0.5 1.0 1.0 0.5

5.00 1.0 1.0 0.13

Not usually Sometimes Sometimes Not usually

Yes Sometimes Sometimes Sometimes

Not usually Sometimes Not usually Not usually

1.0

1.0

Not usually

Not usually

Yes

1.0

1.0

Not usually

Not usually

Likely

0.14 0.5 1.0

3.0 0.13 1.0

Not usually Not usually Not usually

Usually Sometimes Not usually

Not usually Not usually Not usually

patients. For example, a large series of 1052 patients showed that 99.1% of classic TN patients report pain that lasts seconds to less than 1 minute, while only 23% of atypical TN patients, and 0 of 570 (0%) of the non-neuralgiaform facial Journal of Evidence-Based Dental Practice Volume 1, Number 1

pain (atypical facial pain) patients reported the same short time course.10 We were able to find only 4 articles of case series that reported the clinical findings of their subjects in numerical form.6,7,10,11 Drangsholt and Truelove 47

Definition and calculations for a diagnostic test and use of likelihood ratios in clinical diagnosis.

ARTICLE EVALUATION The cross-sectional study by Melzack could be evaluated with accepted criteria for diagnostic studies.9 For example, was the new test (the McGill Pain Questionnaire) tested compared with an accepted gold standard (complete history and physical and imaging by a neurologist/neurosurgeon), and were both tests applied in a uniformly blind fashion? Yes, this article met this first criterion. Did the patient sample include an appropriate spectrum of patients to whom the diagnostic test will be applied in clinical practice (with similar signs and symptoms)? No, since there were no patients with dental conditions commonly mistaken for TN, such as irreversible pulpitis and TMD. The other 4 criteria were not applied, since this second critical criterion was not met. Since only 1 of the articles was of the usual study type to answer our question, and it was judged to be inadequate for our purposes, we created our own “quasi–cross-sectional study” by estimating the prevalence of various diagnostic features of the history and physical examination for orofacial pain conditions that may be confused with TN in dental practice (Table I). These conditions included classic TN, irreversible pulpitis, and internal derangement–type of TMD. Although we did the same for other orofacial conditions commonly considered on the differential diagnosis for TN—such as glossopharyngeal neuralgia,

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cluster-tic syndrome, post-herpetic neuralgia, and CTconfirmed sinusitis—we have not included these entities, since they are rare in dental practice and the treatment would be essentially the same, such as initiation of drug therapy or referral to a specialist. Since much of these data are not available, we estimated many of the probabilities from clinical experience on a 5-point scale (>95%, 70%, 50%, 30%, 10%, <5%), although some of the key probabilities are from published studies, such as a national cross-sectional study of orofacial pain conditions,12 and case series of TN patients.10 Then, these probabilities can be put into a simulation of a cross-sectional study of, say, 100 TN and 1000 irreversible pulpitis or myofascial pain patients to estimate the sensitivity, specificity, and likelihood ratios of a positive and negative test (Fig 3). This simulation method is well illustrated with examples in a recent text.13 By comparing the likelihood ratios of a positive test, we were able to find the specific questions in the history and examination findings that can best distinguish between TN and other common orofacial pain disorders. For example, a refractory period of pain after stimulation of the trigger area (meaning that you cannot elicit pain again with touching or pushing right after a painful attack) is a highly predictive feature of TN, and a person with this feature is about 9 times more likely to have TN than irreversible pulpitis. By comparing Table I with our present case, you

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Fig 3. Simulation results for 40- to 80-year-old patients (n=1100) when asked the above question.

can see that our subject meets 7 of 7 diagnostic criteria from the history (eg, non-nociceptive triggering, abrupt onset and termination, pain described as sharp, shooting) and all 3 of other historical features (eg, inadequate pain reduction with opioids) and has no positive findings on examination or radiographs, except for possibly pain on palpation of the muscles of mastication. Since our patient was seen in an orofacial specialty clinic where TN is initially diagnosed in about 8 of 800 new patients, then the pretest prevalence before the patient’s chief complaint is known is 8/800 or 0.01. As discussed in the sidebar, the likelihood ratio of a specific test (a question in the history, in this case) can be multiplied by the pretest odds of a disorder to obtain the posttest odds or probability. Thus, if the estimated likelihood ratio for each of the historical features ranges from 9.5 (highly valuable) to 1.0 (useless), then the pretest odds of (.01/(1 – 0.01) is multiplied by the likelihood ratios of all the questions: .01 × 9.5 × 9.0 × 4.9 × 2.3 × 1.8 × 1.8 × 1.8 × 1.0 × 1.0 = 31.2, posttest probability = 31.2/1 + 31.2 = 0.97 or 97% probability of the disorder. Just using 3 of the most valuable features, such as nonnociceptive triggering, sharp, shooting pain lasting only a few seconds, and opioids not adequately reducing pain would increase the probability from 0.010 to 0.809 (0.010 × 9.5 × 9.0 ×

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4.9 = 4.23, posttest probability = 4.23/(1 + 4.23) = 0.809, or 81% probability of the disorder. This numerical demonstration attests how powerful history taking alone is in differentiating between these orofacial pain conditions.

EVIDENCE SUMMARIZATION The evidence presented helps to answer the question “In patients with TN, do specific questions in the history or specific examination findings perform better than a standard dental history and physical in increasing the likelihood of a correct diagnosis?” Key questions in the history were found to have a powerful ability to differentiate between irreversible pulpitis, myofascial pain, and TN. Because TN is uncommon in dental practice, and patients are initially seen with severe pain in the region of their teeth, it is imperative that these specific questions be asked of patients with atypical presentations of severe orofacial pain to avoid misdiagnosis and maltreatment.

STRENGTH OF EVIDENCE The level of evidence is a low 4 out of 5 levels (1 is the highest) because it is based on evidence from a case series, or a simulated cross-sectional study.14 Because many of the probabilities for each condition were esti-

Drangsholt and Truelove 49

mated, it is possible that data from new studies could alter the likelihood ratios and the value of the diagnostic features. An actual cross-sectional study of TN and other common orofacial pain conditions describing these history and examination findings is badly needed to confirm or refute many of these estimated probabilities.

SUMMARY Trigeminal neuralgia is an uncommon neuropathic pain condition that is frequently misdiagnosed. A case of TN that was mistakenly diagnosed and treated as a temporomandibular disorder was presented. An evidence-based evaluation of the diagnostic problems of this disorder was presented. Specific features of the history and examination were found to be of moderate to high value in differentiating TMD and pulpal pain from patients with TN. These include the short duration and character of pain, whether opioid medications reduce pain, whether non-painful stimulation provokes pain, and whether a refractory period of pain is observed. REFERENCES 1. Derogatis LR. SCL90-R: Administration, scoring, and procedures manual-ii for the revised version. Towson (MD): Clinical Psychometric Research; 1983. 2. Sobotka JL, Alexander B, Cook BL. A review of carbamazepine’s hematologic reactions and monitoring recommendations. DICP 1990;24:1214-9.

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3. Merrill RL, Graff-Radford SB. Trigeminal neuralgia: how to rule out the wrong treatment. J Am Dent Assoc 1992;123:63-8. 4. Bell WE. Neurogenous pains, orofacial pains. Chicago: Year Book Medical Publishers; 1989:377-416. 5. Loeser JD. The management of tic douloureux. Pain 1977;3:155-62. 6. Kennett S, Cohen L. Paroxysmal trigeminal neuralgia: a review of thirty-six cases. Oral Surg Oral Med Oral Pathol 1968;25:374-9. 7. Juniper RP, Glynn CJ. Association between paroxysmal trigeminal neuralgia and atypical facial pain. Br J Oral Maxillofac Surg 1999;37:444-7. 8. Jaeschke R, Guyatt GH, Sackett DL. Users’ guides to the medical literature. III. How to use an article about a diagnostic test. B. What are the results and will they help me in caring for my patients? The Evidence-Based Medicine Working Group. JAMA 1994;271:703-7. 9. Melzack R, Terrence C, Fromm G, Amsel R. Trigeminal neuralgia and atypical facial pain: use of the McGill Pain Questionnaire for discrimination and diagnosis. Pain 1986;27:297-302. 10. Rasmussen P. Facial pain. II. A prospective survey of 1052 patients with a view of: character of the attacks, onset, course, and character of pain. Acta Neurochir (Wien) 1990;107:121-8. 11. Katusic S, Beard CM, Bergstralh E, Kurland LT. Incidence and clinical features of trigeminal neuralgia, Rochester, Minnesota, 19451984. Ann Neurol 1990;27:89-95. 12. Lipton JA, Ship JA, Larach-Robinson D. Estimated prevalence and distribution of reported orofacial pain in the United States. J Am Dent Assoc 1993;124:115-21. 13. Elmore JG, Boyko EJ. Assessing accuracy of diagnostic and screening tests. In: Geyman JP, Deyo RA, Ramsey SD, editors. Evidence-based clinical practice. Boston: Butterworth-Heinemann; 2000. p. 83-93. 14. Ball C, Sackett DL, Phillips B, Haynes RB, Straus S. Levels of evidence and grades of recommendations. Oxford Centre for Evidence-based Medicine, 1. 2001. 15. Terrence CF. Differential diagnosis of trigeminal neuralgia. In: Fromm GH, editor. The medical and surgical management of trigemninal neuralgia. Mount Kisco (NY): Futura; 1987-44. 16. Dworkin SF, LeResche L. Research diagnostic driteria for temporomandibular disorders: review criteria, examinations and specifications, critique. Craniomandib Disord Facial Oral Pain 1992;6: 301-55.

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