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Trigeminal neuralgia and endodontically treated teeth
0099-2399/88/1407-0360/$02.00/0 JOURNAL OF ENDODONTICS Copyright 9 1988 by The American Association of Endodontists
Printed in U.S.A.
VOL. 14, NO. 7, JULY 1988
Trigeminal Neuralgia and Endodontically Treated Teeth Frank Francica, DMD, Josh Brickman, DMD, Carmine J. LoMonaco, DDS, and Louis M. Lin, BDS, DMD, PhD
of the pain. The medical history of the patient indicated that he was epileptic and had been taking dilantin for almost 9 yr. Review of other systems was noncontributory. The dental history revealed that he had initial root canal treatment of the maxillary left first premolar by his dentist several years before (Fig. 1), and the tooth started to hurt him 2 months before. He was referred to an endodontist and conventional root canal treatment was redone on that tooth (Fig. 2). However, the pain did not subside. He went back to see his dentist. According to his dentist, because the maxillary left canine was also very sensitive to percussion and palpation, he subsequently opened the canine which had a vital pulp (Fig. 3). Nevertheless, the severe pain continued to agonize the patient. He was again referred to the endodontist who could not find the cause of the pain. The endodontist completed the root canal treatment of the canine and prescribed Tylenol with codeine every 4 h to relieve the pain. The pain continued to persist. Finally, the endodontist performed endodontic surgery of the maxillary left first premolar because this tooth apparently had an ill-defined periapical lesion (Fig. 3). He also prescribed Keflex (500 mg every 6 h for 1 wk) and Percordan (every 6 h for pain). However, the pain was still not alleviated. The biopsy report of the tissue removed during the endodontic surgery was consistent with a periapical granuloma. A clinical examination at the postgraduate endodontic clinic of the UMDNJ-New Jersey Dental School demonstrated that both the maxillary left canine and first premolar were sensitive to percussion. Palpation of the periapical area of these two teeth induced severe pain but no periapical swelling was present. The surgical wound of the first premolar had healed well. A radiographic examination showed that the maxillary left canine had a root canal filling and the first premolar had root canal fillings and retrofillings (Fig. 4). The patient was asked about the intensity, frequency, and duration of the pain. He stated "the pain was severe and occurred several times a day and lasted for several minutes." Based on the dental history and clinical and radiographic examinations, the patient was informed that the exact cause of the severe pain could not be determined. Since the endodontic surgery was performed 3 wk previously, it might take a few more weeks for the tissue to heal. Tylenol with codeine every 4 h was prescribed for the patient, and he was instructed to come back 1 wk later for examination. Unfortunately, there was no improvement in the level of pain after 1 wk. The maxillary left canine and first premolar were still sensitive to percussion. Palpation of the periapical area of the first premolar was not
A case of trigeminal neuralgia that occurred in the area of endodontically treated teeth is presented. The pain caused by trigeminal neuralgia may sometimes simulate the pain caused by endodontically involved teeth. However, the characteristic features of trigeminal neuralgia, such as intensity, duration and location of pain as well as triggering areas of pain should be used to differentiate trigeminal neuralgia from dental pain.
Trigeminal neuralgia is defined as "Severe, paroxysmal bursts of pain in one or more branches of the trigeminal nerve; often induced by touching trigger areas in or around the mouth" (1). The mandibular and maxillary divisions are most commonly involved (2). Typically, the pain occurs as paroxysms of shocking, burning or lightning-like sharp stabs that last from a few seconds to a few minutes (3, 4). It occurs predominantly during middle and old age, and more frequently in women (4, 5). The pain can be provoked by sensory stimulations, such as touching and washing of the face, tooth brushing, shaving, chewing, talking, or by thermal change (2). It usually is unilateral and remains in the anatomical distribution of the affected nerve regardless of intermission or remissions. The peripheral nerve fibers seem to be the receptor areas because the pain and triggering can be effectively arrested by analgesic blocking of these nerve fibers (4). The etiology of trigeminal neuralgia is still unknown, although pathological bone cavities have been found in the jawbones of some patients with trigeminal neuralgia (6, 7). The purpose of this report is to describe a case of trigeminal neuralgia which occurs in the area of endodontically treated teeth. CASE R E P O R T A 55-yr-old Caucasian was referred to the postgraduate endodontic clinic at the University of Medicine and Dentistry of New Jersey, New Jersey Dental School, for consultation. The chief complaint of the patient was pain of the maxillary left canine and first premolar. The patient stated "he had root canal treatment and surgery of these two teeth 3 weeks earlier, and the severe pain kept him awake for several nights." He appeared to be in great stress and desperate to seek any relief
360
Vol. 14, No. 7, July 1988
Trigeminal Neuralgia
361
FIG 1. Maxillary left first premolar. Root canal treatment was done by patient's dentist several years before. The tooth started to hurt the patient 2 months before his appointment.
FiG 3. Maxillary left canine that had a vital pulp was opened by the patient's dentist.
FIG 2. Conventional root canal treatment was redone on maxillary left first premolar by endodontist about 2 months before his appointment.
very sensitive, but palpation of the canine suddenly provoked the severe pain which was described by the patient as electric shock-like pain radiating to the lower eyelid and the side of the nose. The pain lasted for only a few minutes and then disappeared. Because the canine did not have a periapical lesion or swelling, the severe pain suddenly provoked by palpation of the periapical area was considered most likely not to be endodontically related. The patient was further questioned as to whether the pain could be caused by any other means. He stated "sometimes when he stretched or rubbed his upper lip with his fingers, pain occurred." Occasionally, the pain could be relieved by rubbing the upper lip hard. While sitting in the dental chair, he experienced a pain attack, he was immediately injected with xylocaine anesthetic solution containing l:100,000 epinephrine into the mucobuccal fold just above the canine. The severe pain immediately disappeared. The patient remained pain free for almost 3 h, and the pain could not be reproduced by palpating the periapical area of the canine or rubbing the left upper lip. Based on the findings described above, trigeminal neuralgia involving the infraorbital branch was suspected. The patient was
FIG 4. Conventional root canal treatment and endodontic surgery were performed on maxillary left canine and first premolar, respectively, by an endodontist about 3 wk before.
362
Journal of Endodontics
Francica et al.
referred to a neurologist at the UMDNJ-New Jersey Medical School for consultation; diagnosis oftrigeminal neuralgia was confirmed. The patient discontinued dilantin and has been taking 800 to 1000 mg of Tegretol daily prescribed by the neurologist. He has been symptom free for more than 2 months. Follow-up dental examination showed that the periapical area of the maxillary left canine and first premolar was not sensitive to palpation.
DISCUSSION Trigeminal neuralgia has been reported to be associated with dental extractions (6, 7), multiple sclerosis (5, 8) or malignancy of the head (4). It has never been described as being associated with endodontically treated teeth. The occurrence of trigeminal neuralgia in the area of endodontically involved teeth in this patient was a coincidence. Nevertheless, it presented some difficulty in diagnosis for dental practitioners. The trigeminal neuralgia was present before any endodontic treatment of the maxillary left canine and first premolar. The maxillary left canine was treated without conclusive evidence of pulpal involvement. The maxillary left first premolar apparently had a periapical lesion. It is possible that the pain caused by the pulpal-periapical pathosis may have stimulated the pain caused by the trigeminal neuralgia (9), and thus confused the dentists. This is because the tooth is part of the sensory receptor system of the affected nerve trunk (4). However, it should be remembered that the pain of trigeminal neuralgia is triggered by stimulation of non-nociceptors (I0, 11), while the pain of pulpal-periapical pathosis is stimulated by nociceptors (t 2-14). In addition, the pain of trigeminal neuralgia is paroxysmal and electric or lightning like (3, 4). It lasts for only a few seconds to a few minutes and has periods of intermissions without symptoms. Typically, the pain of trigeminal neuralgia can be provoked by stimulation of the trigger area (3, 4, 15), and that is not a characteristic feature of pulpal-periapical pathosis. In pulpal-periapical disease, the pain usually can be controlled by complete canal debridement and analgesics or a combination of analgesics and antibiotics. This is not the treatment regimen for trigem-
inal neuralgia which is administered by a neurologist. Although the epileptic seizures and trigeminal neuralgia are sometimes treated with the same medication (dilantin), these two disease entities are not related (3). This case report emphasizes the importance of making a correct diagnosis or a proper consultation prior to treatment. Otherwise, the patient may suffer unnecessary trauma Dr complication.
Dr. Francica is a postgraduate student, Department of Endodontics, University of Medicine and Dentistry of New Jersey, New Jersey Dental School, Newark, NJ. Dr. Brickman is a postgraduate student, Department of Endodontics, University of Medicine and Dentistry of New Jersey, New Jersey Dental School. Dr. LoMonaco is professor of endedontics and biodental science and associate dean of student affairs, university of Medicine and Dentistry of New Jersey, New Jersey Dental School Dr. Lin is associate professor and director of the Postgraduate Program in Endodontics, Department of EndedonUcs, University of Medicine and Dentistry of New Jersey, New Jersey Dental School.
References 1. Rasmajian JV, Burke MD, Burnett GW, et aL (eds). Stedman's Medical Dictionary. 23rd ed. Baltimore: Williams & Wilkins, 1976. 2. Ingle JI, Taintor JF(eds). Endodontics. 3rd ed. Philadelphia: Lea & Febiger, 1985:547-8. 3. Ailing CC, Mahan PE(eds). Facial pain. 2rid ed., Philadelphia: Lea & Febiger, 1977:71-93. 4. Bell WE. Orotacial pain: classification, diagnosis, management. 3rd ed. Chicago: Year Book Medical Publishers, Inc., 1985:280-6. 5. Lynch MA, Brightman VJ, Greenberg MS(eds). Burket's oral medicine: diagnosis and treatment. 8th ed. Philadelphia: JB Lippincott, 1984:507. 6. Ratner EJ, Person P, Kleinman DJ, Shklar G, Socransky SS. Jawbone cavities and trigeminal and atypical facial neuralgias. Oral Surg 1979;48:3-20. 7. Roberts AM, Person P. Etiology and treatment of idiopathic trigeminal and atypical facial neuralgia. Oral Surg 1979;48:298-308. 8. Harris W. Paroxysmal trigeminal neuralgia in relation to disseminated sclerosis. Br Met J 1950;2:1015-9. 9. Pinsawasdi P, Seltzer S. The induction of trigeminal neuralgia-like symptoms by pulp-pedapJcal pathosis. J Endodon 1986;12:73-5. 10. Loeser JD. What to do about tic douloureux. J Am Med Assoc 1978;239:1153-5. 11. Sessle BJ. Recent developments in pain research: central mechanisms of orofacial pain and its control, J Endedon 1986;12:435-44. 12. Seltzer S, Bender IB (eds). The dental pulp: biologic considerations in dental procedures. 3rd ed. Philadelphia: JB Lippincott, 1984;131-51. 13. Trowbridge HO. Intradental sensory units: physiological and clinical aspects. J Encro~on 1985;11:489-98. 14. Trowbridge HO. Review of dental pain--histology and physiology. J Endedon 1986; 12:445-52. 15. Shafer WG, Hine MK, Levy BM(eds). A textbook of oral pathology. 4th ed. Philadelphia: WB Saunders, 1983:854-6.
Printed in U.S.A.
VOL. 14, NO. 7, JULY 1988
Trigeminal Neuralgia and Endodontically Treated Teeth Frank Francica, DMD, Josh Brickman, DMD, Carmine J. LoMonaco, DDS, and Louis M. Lin, BDS, DMD, PhD
of the pain. The medical history of the patient indicated that he was epileptic and had been taking dilantin for almost 9 yr. Review of other systems was noncontributory. The dental history revealed that he had initial root canal treatment of the maxillary left first premolar by his dentist several years before (Fig. 1), and the tooth started to hurt him 2 months before. He was referred to an endodontist and conventional root canal treatment was redone on that tooth (Fig. 2). However, the pain did not subside. He went back to see his dentist. According to his dentist, because the maxillary left canine was also very sensitive to percussion and palpation, he subsequently opened the canine which had a vital pulp (Fig. 3). Nevertheless, the severe pain continued to agonize the patient. He was again referred to the endodontist who could not find the cause of the pain. The endodontist completed the root canal treatment of the canine and prescribed Tylenol with codeine every 4 h to relieve the pain. The pain continued to persist. Finally, the endodontist performed endodontic surgery of the maxillary left first premolar because this tooth apparently had an ill-defined periapical lesion (Fig. 3). He also prescribed Keflex (500 mg every 6 h for 1 wk) and Percordan (every 6 h for pain). However, the pain was still not alleviated. The biopsy report of the tissue removed during the endodontic surgery was consistent with a periapical granuloma. A clinical examination at the postgraduate endodontic clinic of the UMDNJ-New Jersey Dental School demonstrated that both the maxillary left canine and first premolar were sensitive to percussion. Palpation of the periapical area of these two teeth induced severe pain but no periapical swelling was present. The surgical wound of the first premolar had healed well. A radiographic examination showed that the maxillary left canine had a root canal filling and the first premolar had root canal fillings and retrofillings (Fig. 4). The patient was asked about the intensity, frequency, and duration of the pain. He stated "the pain was severe and occurred several times a day and lasted for several minutes." Based on the dental history and clinical and radiographic examinations, the patient was informed that the exact cause of the severe pain could not be determined. Since the endodontic surgery was performed 3 wk previously, it might take a few more weeks for the tissue to heal. Tylenol with codeine every 4 h was prescribed for the patient, and he was instructed to come back 1 wk later for examination. Unfortunately, there was no improvement in the level of pain after 1 wk. The maxillary left canine and first premolar were still sensitive to percussion. Palpation of the periapical area of the first premolar was not
A case of trigeminal neuralgia that occurred in the area of endodontically treated teeth is presented. The pain caused by trigeminal neuralgia may sometimes simulate the pain caused by endodontically involved teeth. However, the characteristic features of trigeminal neuralgia, such as intensity, duration and location of pain as well as triggering areas of pain should be used to differentiate trigeminal neuralgia from dental pain.
Trigeminal neuralgia is defined as "Severe, paroxysmal bursts of pain in one or more branches of the trigeminal nerve; often induced by touching trigger areas in or around the mouth" (1). The mandibular and maxillary divisions are most commonly involved (2). Typically, the pain occurs as paroxysms of shocking, burning or lightning-like sharp stabs that last from a few seconds to a few minutes (3, 4). It occurs predominantly during middle and old age, and more frequently in women (4, 5). The pain can be provoked by sensory stimulations, such as touching and washing of the face, tooth brushing, shaving, chewing, talking, or by thermal change (2). It usually is unilateral and remains in the anatomical distribution of the affected nerve regardless of intermission or remissions. The peripheral nerve fibers seem to be the receptor areas because the pain and triggering can be effectively arrested by analgesic blocking of these nerve fibers (4). The etiology of trigeminal neuralgia is still unknown, although pathological bone cavities have been found in the jawbones of some patients with trigeminal neuralgia (6, 7). The purpose of this report is to describe a case of trigeminal neuralgia which occurs in the area of endodontically treated teeth. CASE R E P O R T A 55-yr-old Caucasian was referred to the postgraduate endodontic clinic at the University of Medicine and Dentistry of New Jersey, New Jersey Dental School, for consultation. The chief complaint of the patient was pain of the maxillary left canine and first premolar. The patient stated "he had root canal treatment and surgery of these two teeth 3 weeks earlier, and the severe pain kept him awake for several nights." He appeared to be in great stress and desperate to seek any relief
360
Vol. 14, No. 7, July 1988
Trigeminal Neuralgia
361
FIG 1. Maxillary left first premolar. Root canal treatment was done by patient's dentist several years before. The tooth started to hurt the patient 2 months before his appointment.
FiG 3. Maxillary left canine that had a vital pulp was opened by the patient's dentist.
FIG 2. Conventional root canal treatment was redone on maxillary left first premolar by endodontist about 2 months before his appointment.
very sensitive, but palpation of the canine suddenly provoked the severe pain which was described by the patient as electric shock-like pain radiating to the lower eyelid and the side of the nose. The pain lasted for only a few minutes and then disappeared. Because the canine did not have a periapical lesion or swelling, the severe pain suddenly provoked by palpation of the periapical area was considered most likely not to be endodontically related. The patient was further questioned as to whether the pain could be caused by any other means. He stated "sometimes when he stretched or rubbed his upper lip with his fingers, pain occurred." Occasionally, the pain could be relieved by rubbing the upper lip hard. While sitting in the dental chair, he experienced a pain attack, he was immediately injected with xylocaine anesthetic solution containing l:100,000 epinephrine into the mucobuccal fold just above the canine. The severe pain immediately disappeared. The patient remained pain free for almost 3 h, and the pain could not be reproduced by palpating the periapical area of the canine or rubbing the left upper lip. Based on the findings described above, trigeminal neuralgia involving the infraorbital branch was suspected. The patient was
FIG 4. Conventional root canal treatment and endodontic surgery were performed on maxillary left canine and first premolar, respectively, by an endodontist about 3 wk before.
362
Journal of Endodontics
Francica et al.
referred to a neurologist at the UMDNJ-New Jersey Medical School for consultation; diagnosis oftrigeminal neuralgia was confirmed. The patient discontinued dilantin and has been taking 800 to 1000 mg of Tegretol daily prescribed by the neurologist. He has been symptom free for more than 2 months. Follow-up dental examination showed that the periapical area of the maxillary left canine and first premolar was not sensitive to palpation.
DISCUSSION Trigeminal neuralgia has been reported to be associated with dental extractions (6, 7), multiple sclerosis (5, 8) or malignancy of the head (4). It has never been described as being associated with endodontically treated teeth. The occurrence of trigeminal neuralgia in the area of endodontically involved teeth in this patient was a coincidence. Nevertheless, it presented some difficulty in diagnosis for dental practitioners. The trigeminal neuralgia was present before any endodontic treatment of the maxillary left canine and first premolar. The maxillary left canine was treated without conclusive evidence of pulpal involvement. The maxillary left first premolar apparently had a periapical lesion. It is possible that the pain caused by the pulpal-periapical pathosis may have stimulated the pain caused by the trigeminal neuralgia (9), and thus confused the dentists. This is because the tooth is part of the sensory receptor system of the affected nerve trunk (4). However, it should be remembered that the pain of trigeminal neuralgia is triggered by stimulation of non-nociceptors (I0, 11), while the pain of pulpal-periapical pathosis is stimulated by nociceptors (t 2-14). In addition, the pain of trigeminal neuralgia is paroxysmal and electric or lightning like (3, 4). It lasts for only a few seconds to a few minutes and has periods of intermissions without symptoms. Typically, the pain of trigeminal neuralgia can be provoked by stimulation of the trigger area (3, 4, 15), and that is not a characteristic feature of pulpal-periapical pathosis. In pulpal-periapical disease, the pain usually can be controlled by complete canal debridement and analgesics or a combination of analgesics and antibiotics. This is not the treatment regimen for trigem-
inal neuralgia which is administered by a neurologist. Although the epileptic seizures and trigeminal neuralgia are sometimes treated with the same medication (dilantin), these two disease entities are not related (3). This case report emphasizes the importance of making a correct diagnosis or a proper consultation prior to treatment. Otherwise, the patient may suffer unnecessary trauma Dr complication.
Dr. Francica is a postgraduate student, Department of Endodontics, University of Medicine and Dentistry of New Jersey, New Jersey Dental School, Newark, NJ. Dr. Brickman is a postgraduate student, Department of Endodontics, University of Medicine and Dentistry of New Jersey, New Jersey Dental School. Dr. LoMonaco is professor of endedontics and biodental science and associate dean of student affairs, university of Medicine and Dentistry of New Jersey, New Jersey Dental School Dr. Lin is associate professor and director of the Postgraduate Program in Endodontics, Department of EndedonUcs, University of Medicine and Dentistry of New Jersey, New Jersey Dental School.
References 1. Rasmajian JV, Burke MD, Burnett GW, et aL (eds). Stedman's Medical Dictionary. 23rd ed. Baltimore: Williams & Wilkins, 1976. 2. Ingle JI, Taintor JF(eds). Endodontics. 3rd ed. Philadelphia: Lea & Febiger, 1985:547-8. 3. Ailing CC, Mahan PE(eds). Facial pain. 2rid ed., Philadelphia: Lea & Febiger, 1977:71-93. 4. Bell WE. Orotacial pain: classification, diagnosis, management. 3rd ed. Chicago: Year Book Medical Publishers, Inc., 1985:280-6. 5. Lynch MA, Brightman VJ, Greenberg MS(eds). Burket's oral medicine: diagnosis and treatment. 8th ed. Philadelphia: JB Lippincott, 1984:507. 6. Ratner EJ, Person P, Kleinman DJ, Shklar G, Socransky SS. Jawbone cavities and trigeminal and atypical facial neuralgias. Oral Surg 1979;48:3-20. 7. Roberts AM, Person P. Etiology and treatment of idiopathic trigeminal and atypical facial neuralgia. Oral Surg 1979;48:298-308. 8. Harris W. Paroxysmal trigeminal neuralgia in relation to disseminated sclerosis. Br Met J 1950;2:1015-9. 9. Pinsawasdi P, Seltzer S. The induction of trigeminal neuralgia-like symptoms by pulp-pedapJcal pathosis. J Endodon 1986;12:73-5. 10. Loeser JD. What to do about tic douloureux. J Am Med Assoc 1978;239:1153-5. 11. Sessle BJ. Recent developments in pain research: central mechanisms of orofacial pain and its control, J Endedon 1986;12:435-44. 12. Seltzer S, Bender IB (eds). The dental pulp: biologic considerations in dental procedures. 3rd ed. Philadelphia: JB Lippincott, 1984;131-51. 13. Trowbridge HO. Intradental sensory units: physiological and clinical aspects. J Encro~on 1985;11:489-98. 14. Trowbridge HO. Review of dental pain--histology and physiology. J Endedon 1986; 12:445-52. 15. Shafer WG, Hine MK, Levy BM(eds). A textbook of oral pathology. 4th ed. Philadelphia: WB Saunders, 1983:854-6.