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ARTICLE ABSTRACT A variety of pathologic conditions can cause orofacial pain. Establishing the etiology of the pain is key to providing appropriate treatment. Trigeminal neuralgia (TN) is a relatively uncommon condition and can present a diagnostic challenge to even the experienced dental practitioner. The authors discuss two cases of TN that exhibited intraoral trigger points, which initially resulted in confusion regarding the establishment of a correct diagnosis and treatment.
KEY WORDS:
trigeminal neuralgia,
tic douloureax
Trigeminal Neuralgia with Intraoral Trigger Points: Report of Two Cases Jude A. Fabiano, DDS1*; Andrew J. Fabiano, MD2; Patrick L. Anders, DDS3; Terrence J. Thines, DDS, MS4 Associate Professor and AEGD Program Director, Dept. of Restorative Dentistry, School of Dental Medicine, University at Buffalo, Buffalo, New York; 2Resident, Neurosurgery Residency Program, School of Medicine and Biomedical Sciences, University at Buffalo; 3Associate Professor, Dept. of Oral Diagnostic Sciences, School of Dental Medicine, University at Buffalo; 4Associate Professor and GPR Program Director, Dept. of Oral Diagnostic Sciences, School of Dental Medicine, University at Buffalo; *Corresponding author: jaf1@buffalo.edu Spec Care Dentist 25(4): [pagex-pagexx], 2005 1
Introduction The International Association for the Study of Pain defines “neuralgia” or “neuropathic pain” as pain “initiated or caused by a primary lesion or dysfunction in the nervous system.”1 Further, the group describes trigeminal neuralgia (TN) as unilateral facial pain, characterized by brief electric shock-like (lancinating) pain limited to the distribution of one or more of the three divisions of the trigeminal nerve (see Figure 1). The pain of TN is commonly evoked by trivial stimuli including washing, shaving, smoking, talking and brushing the teeth, but also may occur spontaneously. The pain is abrupt in onset and termination, and may remit for varying periods.2 The intensity of the pain is such that individuals with a severe, uncontrolled neuralgia have become suicidal.3 Although it is unilateral, the same nerve on both sides of the face may be affected independently in an individual. Formerly known as tic douloureax, TN affects the fifth cranial nerve, which transmits sensory impulses (touch, pressure, pain and temperature) from the orofacial region to the brain. It is the most common facial neuralgia, affecting
Figure 1: Dermatomes of the three divisions of the trigeminal nerve.
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4.3 per 100,000 people, with women being slightly more affected than men by a 3:2 ratio.4 Although it occurs more often in the sixth decade of life, TN has been reported in infants and children.4,5 Two categories of TN exist: idiopathic and symptomatic. Idiopathic TN is characterized by unilateral facial pain that corresponds to the distribution of the fifth cranial nerve, a “trigger point” that, when stimulated, will evoke pain and an unremarkable clinical neurological examination.6 Symptomatic TN is diagnosed when the neurological examination reveals an organic cause or when additional cranial nerves are involved.6 The identification of a “trigger point” is paramount in establishing the presence of TN. A non-painful stimulus such as a light touch, facial movement or draft of air to a specific, ipsilateral area innervated by the trigeminal nerve may provoke or trigger” the pain.2,6 Additional stimuli that may initiate an attack include chewing, applying make-up and swallowing.
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Attacks usually last several seconds but may become rapidly repeating or fused, thereby incapacitating the patient. Interestingly, pain associated with TN does not occur during sleep.6,7
Etiology No anatomic abnormalities of the peripheral branches of the trigeminal nerve have been observed in studies of individuals with TN.7,8 8,9 A literature review9,10 concluded that TN appears to have both a central and a peripheral etiology. The authors state that the central pathogenesis occurs due to decreased inhibition of nociceptive input and that peripherally focal demyelination of the trigeminal nerve results in abnormal action potentials that cause increased afferent input. This combination results in a perceived sensation of pain triggered by a non-painful stimulus. Areas of demylination may result in faulty transmission or generation of nerve impulses, and have been implicated as the cause of the pain associated with TN. Indeed, multiple sclerosis (MS), which is characterized by demylination in the central nervous system, has a higher incidence in patients with TN, and TN has a higher incidence in individuals with MS when either group was compared to the general population. Patients with TN should undergo an appropriate imaging study of the brain to rule out the presence of MS10 because TN associated with MS may have a more varied presentation, including bilateral pain, no trigger point and an earlier onset.11 Most clinical evidence suggests that TN is caused by compression of the trigeminal nerve root resulting in abnormal nerve conduction along the nerve.9, 10, 11,12 The compression usually occurs at the root-entry area but also may occur at the trigeminal ganglion. Causes of compression include tumors, cysts and blood vessels. It is thought that the compression initiates the demyelination process.13 In the case of vessel compression, blood flow may further irritate the nerve root. Surgical decompression of the blood vessel has been effective in resolving TN in 75%-80% of such cases, with follow-up of 20 years.12,13
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Differential Diagnosis The diagnosis of TN must be differentiated from other conditions that may cause pain in the orofacial area. Attention to the patient’s description and history of his/her symptoms and a thorough clinical examination often will lead to the correct diagnosis. A thorough history is the key to an accurate diagnosis of TN. A patient’s complaints of paroxymal, unilateral, excruciating pain confined to the innervation of one or more branches of the trigeminal nerve is characteristic of TN. The presence of a trigger point and the avoidance by the patient of activities
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that stimulate the trigger point also distinguishes TN from other orofacial pain conditions. Patients may report with clusters of pain attacks that blend into a continuous episode, which may last hours or days. Spontaneous remission that results in pain-free periods lasting weeks or months has been reported by many individuals.13,14 A percentage of patients initially experience pre-trigeminal neuralgia, a condition that is symptomatically different but pathophysiologically the same as TN and may contribute to the difficulty in diagnosing TN. Pre-trigeminal neuralgia
is characterized by a dull, continuous, aching pain, usually in the maxilla or mandible, and can easily be confused with odontogenic pain.14-16 6,15,16 Other than the trigger point or points, results of clinical examination have been negative in the majority of people with TN. It is important to rule out the presence of an anatomic or organic cause. Magnetic resonance imaging (MRI) is most useful in identifying structural and compressive lesions affecting the trigeminal nerve and has resulted in many idiopathic cases being reclassified as symptomatic. By using MRI testing, the investigator may establish whether a compressed blood vessel is associated with the trigeminal nerve.14-15 15,16 A dental evaluation is essential, as dental pathology can be a trigger for TN. A thorough clinical and radiographic examination must be performed to eliminate oral pathology as the source of pain. It is essential to avoid irreversible dental treatment until a definitive diagnosis has been established. Clinicians may be lead to diagnose TN when there is an absence of clinical signs, pathologic findings or other trigeminal nerve dysfunction. At times, however, a patient’s interpretations and reactions to pain can be variable or inaccurate, and other conditions must be considered and ruled out to establish the correct diagnosis. Table 1 summarizes the characteristics of the more common conditions that cause orofacial pain. Zakrzewska16,6 has published a thorough review of the differential diagnosis of TN.
Treatment and Management of TN Medical treatment of TN is the first treatment of choice and is directed at pain relief.17-19 It is well recognized that effective medical treatment reinforces the diagnosis of TN. Trosseau20 proposed in 1853 that the episodes of pain suffered by patients with tic douloureux, as TN was then called, were due to paroxysmal depolarization in the trigeminal pathways and were reminiscent of the paroxysmal depolarization that occurred in patients with epilepsy. Attempts to find a drug that would effectively manage TN
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pain were unsuccessful until the 1960s, when Swedish neurologist Blom21 found carbamazepine to be highly effective in the majority of his TN patients, and Campbell and colleagues22 performed the first successful clinical trial utilizing the drug. Carbamazepine (Tegretol®), an anticonvulsant medication well tolerated by most individuals, remains the primary
drug of choice for the medical management of TN, often providing relief of symptoms within 12 to 48 hours. The usual dose is 100 milligrams (mg) two or three times a day, with a maximum daily dose of 1200mg. The dose may be increased incrementally, on a three-timesper-day basis, until pain relief is obtained. Once the pain is controlled for two to
three months, the dosage should be slowly decreased to the lowest level that maintains pain control or, if possible, discontinued completely. Patients should have blood serum levels of carbamazepine evaluated every two to three weeks after the start of therapy and at regular intervals as long as the patient is taking the medication. Complete blood
Table 1. Differential Diagnosis of Facial Pain. Eliciting/Accompanying Factors
Character of Pain
Duration of Pain
Neuralgias (trigeminal or glossopharyngeal)
• Sudden onset • Trigger point in dermatome of affected nerve
• Sharp, knife-like, sudden, excruciating, lancinating • Severe
• Very Brief – seconds (may be recurrent)
Odontogenic Pain
• May be intermittent or continuous • Spontaneous in nature • May be affected by temperature or pressure on offending tooth
• Dull aching, throbbing, lancinating • Mild/Moderate/Severe
• Brief – minutes/hours
Sinusitis
• Change in head position • Valsalva maneuver • Pain involving the posterior maxillary dentition
• Nonpulsating, aching, pressure • Mild/Moderate/Severe
• Short-days
Migraine
• • • •
Usually unilateral Spontaneous onset Nausea & vomiting Sensoriphobia
• Throbbing • Severe
• Short-hour/days
Cluster Headache
• • • • •
High prevalence in men Spontaneous, repetitive Seasonal (?)a Tearing, ptosis, nasal obstruction Occurs at same time of day, often during sleep
• Boring, sharp, burning, excruciating • Severe
• Brief - minutes/hours
Tempromandibular Disorder
• • • • •
History of trauma and/or bruxism Trismus Deviation TMJ sounds/pain on palpation Dental occlusal discrepancies
• Dull/Ache • Mild/Moderate/Severe
• Long-weeks/months
Temporal Arteritis
• • • •
Pain in the scalp (when combing hair) Orbital pain Claudication of the masticatory muscles Sudden onset
• Deep, aching, throbbing, burning • Moderate/Severe
• Short - hours/days
Post-Herpetic Neuralgia
• Previous Herpes zoster infection • May be scarring
• Mild/Moderate/Severe
• Long – weeks/months
Tension-type Headache
• Usually bilateral • Nausea & vomiting are rare • May be related to stress, anxiety & depression
• Dull, non-pulsating, pressure, tightness • Mild/Moderate
• Short – hours/days
Atypical Facial Pain
• Non-specific diagnostic term often used when no other diagnosis corresponds to symptom description • Usually unilateral and continuous • May spread to a large area of the face • Relationship between the pain source and site of pain may be absent
• Constant, pulling, deep, aching • Mild/Moderate/Severe
• Long – weeks/months
There is no evidence based data to support this as a cause of cluster headaches.
a
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cell counts also are indicated periodically, as the drug has been associated with aplastic anemia.23 Other medications with central nervous system effects have been used alone or in various combinations to treat TN, including phenytoin (Dilantin®), baclofen (Lioresal®), valproic acid (Epilim®) and clonazepam (Rivotril®), with mixed success.24 Newer medications, including topiramate (Topamax®), lamotrigine (Lamictal®) and gabapentin (Neurontin®), have demonstrated effectiveness in managing TN, especially in cases found to be refractory to traditional drug therapy.25-31 Oxcarbazepine, a keto-analong of carbamazepine, has shown therapeutic promise with improved tolerability and fewer side-effects, and may be an important addition to the neuropathic pain armamentarium.32
Surgical Management Surgical therapy for the management of TN is reserved for patients who do not respond to drug management or those who experience severe side effects to medications prescribed for TN. Surgical management can be divided into three general categories: 1.Peripheral surgery; 2.Surgery at the trigeminal ganglion; and 3.Posterior fossa surgery. Peripheral surgery includes neurectomy of a portion of the trigeminal nerve, alcohol injection, cryotherapy and radiofrequency thermocoagulation. All peripheral methods have a high recurrence but low mortality and morbidity rates. These procedures present an option for cases refractory to medical therapy and for patients who refuse more invasive surgery.33-35 Surgery at the level of the trigeminal ganglion involves techniques utilized at the peripheral nerve level. Radiofrequency thermocoagulation of and injection of alcohol or glycerin into the gasserian ganglion are the two most frequently performed procedures in the treatment of TN.36-39 Fromm40 states that both procedures meet the criteria of ideal surgical procedures, resulting in prolonged pain relief with minimal neurologic deficit. But, he adds, injection techniques should
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be eliminated as they result in a higher postoperative complication rate. Anesthesia dolorosa (facial anesthesia with severe paresthesia) may complicate both radiofrequency thermocoagulation and injection techniques, but does not occur following microvascular decompression.12 The major operative procedures for the management of TN are microvascular decompression and rhizotomy. Microvascular decompression is the most often performed of these procedures and focuses on eliminating vascular compression, usually caused by the superior cerebellar
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artery of the trigeminal nerve at the root entry zone. Rhizotomy involves sectioning of part or all of the sensory division of the trigeminal nerve, sparing the motor division. Because it is curative, nondestructive, does not result in a sensory deficit and has proven to be more effective, microvascular decompression is considered the surgical treatment of choice for trigeminal neuralgia in otherwise healthy individuals.12, 41-45 The reader is again referred to a text authored by Zakrzewska,46 who has compiled a thorough review of the medical and surgical management on TN.
Case Repor ts Case Report 1 A 63-year-old woman sought treatment from her general dentist with a chief complaint of toothache in the area of the right mandibular teeth. Her medical history was unremarkable, and she reported taking no medications. She stated that she had recently experienced mild, intermittent, jabbing pain that was present on rising in the morning and at bedtime. She said that she had not experienced any dental sensitivity to temperature changes or when chewing. The extraoral examination was within normal limits, and the dentist found no lymphadenopathy or other soft tissue lesions. The intraoral examination was within normal limits, and the dentist did not see any soft tissue lesions. The dental structures were without caries and in good repair. Examination of the teeth in the mandibular right quadrant revealed a negative response to percussion, cold and touch with a dental instrument to exposed root surfaces. No abnormal periodontal pockets (>3 millimeters) were detected. Review of the patient’s dental record indicated that tooth #28 (mandibular, right, first premolar) had a history of a direct pulp cap. An evaluation of a periapical radiograph of that tooth did not show any pathology. The initial differential diagnosis was reversible pulpitis of an as-yet-unidentified tooth or irreversible pulpitis of #28. The patient was informed of the findings, and it was agreed that she would return in three days for a re-evaluation to better localize her symptoms. At the re-examination appointment, the patient described her pain as an intermittent “electric shock,” saying that this pain was different from that she had previously experienced with an abscess. She again noted no sensitivity to temperature or when chewing, although sweet apples and toothpaste caused the pain to start. The dentist made a tentative diagnosis of reversible pulpitis due to root surface sensitivity and instructed her to use a desensitizing toothpaste. She also was instructed to return for an assess-
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ment in 10 days or to contact the office if symptoms increased before the next visit. The patient returned to the dental office two days later, reporting pain that was localized to tooth #28 during chewing and stimulated by heat. The affected tooth was sensitive to percussion, and the dentist diagnosed acute apical abscess of the mandibular right first premolar. An endodontic access cavity was prepared, which revealed a necrotic pulp. The tooth was instrumented to a no. 40 file, irrigated, dried and temporized. The patient returned eight days later for obturation of the canal in tooth #28. She reported that she was pain-free for approximately 10-11 hours after the previous appointment, until normal sensation returned to the area affected by local anesthesia. She experienced pain on her first bite of food at supper. She stated that the pain did not arise from chewing pressure but rather contact of the food bolus with the right side of her mouth. Since that time, she had not been able to chew on the right side, as anything that touched that area instantaneously (within one to four seconds of contact) resulted in bursts of “electrical” pain. The patient also said that she could not wash or dry the right side of her face, as this also would also trigger the pain. She outlined the area affected by the pain, and it followed the distribution of the third division of the right trigeminal nerve. The symptoms associated with tooth #28 were no longer present. Because the patient was very protective of the affected area, the dentist was not able to examine her intraorally. Using mepivicaine, a right, inferior alveolar nerve block was given, which eliminated any triggering of pain when the affected area was manipulated and palpated. No swelling or other soft tissue abnormalities were present. The dentist diagnosed TN and obturated the root canal on tooth #28 without incident. A temporary restoration was placed to close the access cavity, and the patient was referred to a neurologist for evaluation, diagnosis confirmation and TN management. Three weeks following the obturation appointment, the patient returned for
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restoration of tooth #28. At that time, she had not yet seen the neurologist. She was continuing to experience the “electric” pain but had not had a recurrence of symptoms associated with tooth #28. The need to have a neurologic consultation was emphasized to the patient, and she stated she would do so. The area was anesthetized, the tooth was restored with a prefabricated stainless steel post and amalgam in anticipation of a fullcoverage restoration, and the patient was dismissed. After examining the patient, the neurologist confirmed the diagnosis of
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TN and prescribed carbamazepine 100 mg twice a day, which eliminated the patient’s TN symptoms. She reported no significant side effects regarding the medication. Laboratory testing conducted three months after the patient started using the medication showed a carbamazepine level of 3.1, normal liver function and a normal complete blood count. The neurological examination was within normal limits. The patient has been pain-free for more than two months. Her neurologist planned to gradually decrease the medication dose to determine whether spontaneous
remission of the TN had occurred.
Case Report 2 A 74-year-old woman sought care from her general dental practitioner with a chief complaint of irritation of the lower right lip and right side of her tongue from a recently fabricated mandibular complete denture. The complete dentures she was using had been made 11 months prior to this visit and were the second set made by her previous dentist. This second set of dentures was made of hypoallergenic materials, as her previous dentist thought the irritation of her lip and tongue was an allergic reaction to a material used in the initial dentures. The patient had worn the first set of dentures for approximately two years before the fabrication of the second set. The patient complained of constant soreness on her lower right lip and on the right side of her tongue, with intermittent sharp pain when either her lip or tongue (or both) touched her lower denture or each other. This sharp pain occurred even when the denture was not in her mouth. The patient’s medical history was significant for a penicillin allergy, an “inner ear problem,” a kidney stone that had been passed and diet-controlled diverticulitis. The patient reported medication use that included Antivert® (25 mg taken as needed for the inner ear condition) and erythromycin prescribed by her previous dentist to resolve the tongue and lip irritation. She reported a negative history of herpes zoster. The extraoral examination was within normal limits, with no lymphadenopathy or facial swelling. The intraoral examination revealed mild inflammatory changes on the right side of the tongue. No ulceration, swelling or other abnormalities were observed associated with the tongue or lower lip. There were no signs of traumatic injury. The patient experienced pain when the lower lip was palpated on the right side but not on the left side. The dentures were evaluated and were found to be well-fitting with appropriate border extensions. The occlusion was small and clinically acceptable, and retention was
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adequate. No denture pressure sores were observed, and no oral lesions were found. The following differential diagnosis was developed: • TN of the mandibular division; • odontogenic or phantom pain; or • atypical facial pain. The signs, symptoms and differential diagnosis were discussed with the patient and with her primary physician, who in turn referred her to a neurologist for evaluation. The neurologist confirmed the diagnosis of TN. The patient was prescribed Tegretol XR 200® one per day, with instructions to increase to two per day if necessary to control the pain. Reevaluation of the patient one month later revealed a significant improvement, with a report of an occasional “twinge” of very mild discomfort in the lower lip. The patient did not wish to increase the medication dose from one to two tablets per day and reported no medication-related side effects.
Discussion This article discusses two patients diagnosed with TN with intraoral trigger points, which are unusual in TN; trigger points associated with TN typically are perioral.47-49 An intraoral trigger point can make the diagnosis of TN difficult because the dental practitioner must eliminate an odontogenic etiology, as illustrated by the first case report. The first patient had been a patient of record for several years with no signs of TN. The TN symptoms she reported arose a few days after the odontogenic symptoms began. Indeed, this patient had symptoms of both an acute alveolar abscess (tooth #28) and TN. After endodontic therapy of tooth #28, the odontogenic symptoms (temperature and chewing sensitivity) resolved, but the TN symptoms (shock-like pain) remained except when the trigger-point area was anesthetized. An innocuous stimulus, such as chewing or swallowing, may initiate TN pain and may be misinterpreted as a stimulus of dental pain. This type of response can mislead the dental practitioner in assessing the complaint and result in unwarranted and unnecessary
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treatment. One study examining patients with orofacial pain symptoms found that 61 percent were treated initially with ineffective dental interventions.50 It is critical that the practitioner not assume that the site of the pain is also the source of the pain. The location, character and intensity of TN pain may appear to be similar to pain of odontogenic origin, such as that caused by a split or cracked tooth, a periapically involved tooth or primary occlusal trauma; however, only reversible treatment should be rendered until a definitive diagnosis can be determined. The diagnosis of TN made in
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Case Report 1 was based on the history of symptoms, negative clinical findings and elimination of pain during periods of local anesthesia affecting the trigger point area. Case Report 2 involved a patient with similar overlapping symptoms. After the fabrication of a set of complete dentures, the patient began to experience pain and soreness that was assumed to have been caused by the new dentures. An association between the symptoms of TN and the new dentures was, in hindsight, coincidental. It was not unreasonable, however, for the dentist to assume this cause-and-
effect association given the circumstances; however, further investigation into the cause of the pain was indicated because the patient experienced characteristic TN pain when the trigger site was stimulated without the dentures in her mouth and without any clinical signs of denture irritation. In both cases, a general dental practitioner made the diagnosis of TN; however, concern regarding the long-term and refractory nature of the treatment of TN and the potential need for additional testing to rule out other neurologic conditions, such as multiple sclerosis, resulted in the referral of these patients to a neurologist. When a challenging clinical situation presents, the practitioner must consider the multiple etiologies of orofacial pain in developing a differential diagnosis, including: • intracranial pain disorders (neoplasm, aneurysm, hemorrhage, hematoma, abscess); • primary headache disorders (migraine, cluster headache, cranial arteitis, carotidyna, tension headache); • neurogenic pain disorders (TN, glossopharyngeal neuralgia, post-herpetic neuralgia, posttraumatic and post-surgical neuralgias); • intraoral pain disorders (dental, periodontal, mucogingival, tongue pain); • temporomandibular disorders (masticatory muscle, temporomandibular joint and associated structures); • referred pain (paranasal sinuses, ears, eyes, nose, throat, salivary glands, neck and associated lymph nodes); and • mental disorders (somatoform disorders, pain of psychogenic origin)51 Israel et al.52 concluded that misdiagnosis and multiple failed treatments were common in patients with chronic orofacial pain. Shankland53 recommends a differential approach in determining a diagnosis. Multiple reports in the dental and medical literature52-63 illustrate the diagnostic puzzle that TN symptoms may produce, the number of other conditions TN may mimic, and the importance of a thorough history and clinical and radiographic evaluation in reaching a correct diagnosis before any treatment begins. Arriving at the diagnosis of TN is
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often a process of eliminating other pain-provoking conditions so that confirmation that the diagnosis is correct may be demonstrated by the reduction or elimination of pain following the administration of an appropriate medication, such as carbamazepine.16 In both patients presented here, relief of symptoms occurred after they had received therapeutic doses of carbamazepine, substantiating the clinical diagnosis of TN. Although current pharmacotherapy allows most patients at least some degree of comfort, there remains a significant number who do not experience adequate pain management. This may arise as a consequence of the disorder proving to be refractory to drug treatment in an individual, or as the manifestation of drug-induced side effects at proper therapeutic doses. When this occurs, surgical procedures—with the increased risk of morbidity and mortality—are the next options in management. Thus, research for effective anti-neuralgic medications is essential and must continue.31 If doubt exists regarding the proper diagnosis, only reversible treatment should be provided. Vague symptoms often will localize over a short time and allow accurate assessment and diagnosis. If the diagnosis is not clear, consultation with a dental and/or medical specialist may help establish a definitive diagnosis, provide appropriate treatment and properly manage any developing complications.64
Conclusion Trigeminal neuralgia is the most common neuropathic cause of facial pain. The correct diagnosis of the pain source is critical and is made by obtaining a thorough and accurate history, along with negative clinical and radiographic examinations for odontogenic or other pathology. Medical treatment often is effective in relieving the symptoms of TN and usually reaffirms the diagnosis. Surgical options are available if the patient is refractory to medical treatment.
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Two patients with TN, who had intraoral trigger points, are presented here to illustrate the importance of obtaining a detailed and precise history, and of performing a thorough clinical and radiographic examination to establish a definitive diagnosis and provide effective treatment.
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