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Referred pain from an asymptomatic impacted mandibular third molar
Section
of the
Federal dental services Referred pain from an asymptomatic impacted mandibular third molar Report
of a case
Ronald D. Baker, Commander (DC) USN,* Howard B. Marble, Jr., Captain (DC) USN ,I+ William R. Martin, Commanck (DC) USN,C*+ and Nicholas R. Rafaelly, Lieutenant Commander (MC) USN***” NAVAL
DENTAL
SCHOOL,
NATIONAL
NAVAL
MEDICAL
CENTER,
BETHESDA,
MD.
T
he dental literature prior to 1940 is replete with descriptions of cures of various physical and mental ailments effected by the removal of impacted teeth.l+’ Some of the resolutions reported could be accepted today on the basis of present concepts of referred pain. Other reported “cures” of reflex loss of normal function of arms and legs, nervous or mental disorders, gastrointestinal disturbances, and dysmenorrhea would be difficult to explain physiologically. It is an accepted fact that referred pain can and does occur. In 1940, McCouch1° wrote that “ . . . the teeth, like the viscera, may give pain referred to characteristic areas of the face and neck.” Few would dispute that statement. The dental literature contains well-documented cases in which the elimination of dental pathosis has resulted in the resolution of deep-seated ear pain, headache, and facial neuralgia.ll-I4 Referred pain is not randomly distributed but is anatomically ordered or segmented. The following case illustrates that a dental site may give rise to nerve im-
The opinions or assertions contained herein are the private ones of the writers and are not to be construed as official or reflecting the views of the Navy Department or the naval service at large. *Chief of Dental Service, United States Naval Hospital, Camp Lejeune, N. C.; formerly Oral Surgery Resident, Naval Dental School. **Head, Oral Surgery Department, Naval Dental School. ***Senior Dental Officer, U.S.S. Essex; formerly Oral Surgery Resident, Naval Dental School. United States Naval Hospital, ****Senior Resident, Otorhinolaryngology Service, National Naval Medical Center, Bethesda, Md.
273
274
Baker et al.
OS., O.M. & O.P. February, 1968
pulses strong enough to cause markedly severe referred pain while remaining asymptomatic itself. It also demonstrates that one must be alert to the possibility that two or more simultaneously occuring, but distinct and unrelated, conditions may give rise to a multitude of symptoms in a circumscribed anatomic location. Finally, it emphasizes the value of the dental diagnostician on the health service team. CASE REPORT A 3%year-old Caucasian housewife was admitted to the Otorhinolaryngology Service of the Naval Hospital, National Naval Medical Center, Bethesda, Maryland, on Jan. 13, 1966. Her chief complaints were (1) severe headaches, recently increasing in intensity and causing loss of consciousness, (2) deafness of the left ear, progressive during the 2 years prior to admission, (3) blurred vision at the peak of the headaches, as if a mist were present, (4) “dead feeling” of the left auditory canal, (5) paresthesia of the left preauricular area, and (6) recurrent unsteadiness on turning. History
The patient had been completely well until 4 years prior to admission, when she developed tinnitus of the left ear. This was accompanied by a fullness and deep pressure ache of the left side of the head, with nausea but no vomiting. Initially, the attacks lasted only 1 day but recurred at intervals of 3 to 4 weeks. The patient did not remember nor could she recall any paresthesia or anesthesia at being unsteady or having vertigo; that time. She was admitted to the Naval Hospital at Great Lakes, Illinois, where a myringotomy was performed. The operation gave no noticeable relief, but several months later the attacks ceased for approximately 1 year. In 1964 the patient developed a symptom complex consisting of a low-pitched tinnitus, a feeling of fullness in the left ear, and a gradually increasing, deep, steady, left-sided aching which, at its peak, caused unsteadiness (without vertigo), nausea, pressure vomiting, and then anesthesia of the skin anterior to the left ear. The symptoms might be present when the patient awoke in the morning, but at times they commenced during the day. Initially, Cafergot seemed to attenuate the symptoms, but later it had no effect. By September, 1965, the symptom complex manifested itself at intervals of 1 to 2 weeks. Subsequently, the attacks increased in frequency, with a concomitant increase in severity. During the 2 weeks preceding admission, the headaches were almost continuous and so severe that five or six times the patient lost consciousness for periods of unknown duration. Treatment with Actifed, Darvon, Donnatal, and codeine gave no appreciable relief. Deafness of the left ear, insidious in onset about 2 years prior to admission, became progressively worse in 1965. In the months preceding admission, the patient noted a “dead feeling” of the left auditory canal. Past medical history revealed a chronic nasal congestion of 10 years’ duration, suggestive of allergic rhinitis. Physical
examination
Physical examination on admission revealed a well-developed, well-nourished, alert Caucasian woman. Vital signs were within normal limits. There was no tenderness over the scalp and no facial muscle weakness. Nystagmus was not present, nor was there any cornea1 anesthesia. Otoscopic examination was noncontributory, except for the decreased sensation to instrumentation, touch, or pain in the left auditory canal. There was a moderate mixed hearing loss on the left side, as measured by air and bone conduction. The results of caloric examination of the right and left ears were considered to be within normal limits. The Romber sign was absent. Examination of the cranial nerves was negative, except for the noted deficiencies of the trigeminal and auditory nerves.
Volume 25 Number 2 Laboratory
Referred
pain from
asymptomatic
impacted
molar
275
examination
Initial laboratory examinations, including complete blood count, urinalysis, glucose, and total serum protein determinations, were all within normal limits.
VDRL,
blood
including a chest film, a sinus The results of roentgenographic examinations, a cervical spine study, and skull roentgenograms with views of the internal auditory were within normal limits.
series. canal,
Roentgonographic
Hospital
course
examination
and
treatment
Otorhiaolaryngology Service. After the initial admission medical workup, the patieut was examined in consultation with the United States Army Audiology and Speech Center. The diagnosis was hearing loss of the left ear, mixed type, severe. There was no evidence of a retrocochlear lesion. Examination of the right ear revealed no abnormalities. The cause of the complete symptom complex was undetermined. It was tentatively suggesteil that a unilateral otosclerosis of the left ear caused the deafness and that some unrelated disease process, such as central nervous system pathosis, caused the headaches and left auricular paresthesia. Nezlrological examination. An electroencephalogram on January 20 was within normal limits. A RISA I-131 brain scan on January 28 revealed no evidence of abnormal uptake view disclosed a midline area of in the region of the acoustic nerve, but the lateral uptake in the parietal-occipital area. A Technetium 99” scan was interpreted as normal. A repeat RISA scan on February 10 was also normal, and a lumbar puncture on the same date revealed normal cerebrospinal fluid findings, Examination by the Neurology Bramh of the Neuropsychiatric Service for pathosis of the nervous system was negative. Dental Service. Since none of the indicated examinations elicited any pathologic condition consistent with the symptoms, the patient was referred to the Oral Diagnosis Department of the Naval Dental School to rule out the slight possibility of a temporomandibular joist syndrome. On February 11 a thorough clinical examination revealed the additional symptoms of paresthesia of the left long buceal nerve and partial lingual anesthesia, localized along the extreme left side of the tongue and extending onto the floor of the mouth. There was also a loss of sensation in the area of the left retromolar triangle. The patient had not been aware of these altered sensations until clinical examination revealed them. Roentgenograms disclosed an unerupted left mandibular third molar, impacted mesioangula,l anal with the apex in close proximity to, if not in actual contact with, the mandibular canal. No pathologic processes affecting the second molar or the adjacent bony structures were demonstrated. The patient was referred to the Oral Surgery Department for further evaluation. Although the impaction was considered to be a remote etiologic possibility, the patient was scheduled for removal of this tooth as well as a distoangularly impacted right mandibular third molar. A general nasotracheal anesthetic was administered on February 21, and the two impacted molars were surgically removed by sectioning with a high-spoecl air-turbine handpiece. The left third molar was found to be eroded, or grooved, in such a way that the contents of the mandibular canal lay directly on the root surface near the tip. On the first postoperative day, the patient had minimum discomfort, slight trisnbus, and a suggestion of returning sensation in the left preauricular area. Headache was absent, and remained so despite the development of alveolar osteitis. There was a progressive return of sensation to all previously affected intraoral areas, the preauricular region, and all of the auditory canal except the anterior border of the external autlitor:, meatus. Otorhinobyngology Service. On March 3, the patient underwent a left middle ear exploration which revealed ostosclerosis of the foot plate. An anterior stapes crurotomy produced immediate improvement in hearing. The postoperative course was uneventful, anrl there was only a mild residual sensorineural loss.
276 Baker et al.
OS., O.M. & 02. February, 1968
Consultation with the Allergy Branch of the Medical Service revealed that the patient had significant allergies to foods, molds, dust, and other inhalants. Desensitization was not accomplished at that time. The patient was discharged on March 24, 1966, asymptomatie except for slight deafness. Follow-up
Communication with the patient in April, 1967, indicated that she “never felt better in her life,” and had been completely free of the headaches that had incapacitated her more than a year previously. She was then undergoing injection desensitization therapy for her allergies.
DtSCUSSION
KennedyI stated : “Those casesin which action has been taken against alleged evil, and good results seem to have followed, are reported and remembered, whereas a multitude of cases in which no good result followed, are buried in decent obscurity.” It might be that Kennedy’s philosophy is illustrated by this case, in which recurrent and severe headaches, partial lingual anesthesia, and paresthesias of the buccal and auriculotemporal nerves were resolved after removal of an impacted mandibular third molar. Recovery in this case can be explained logically. Trigeminal nerve involvement has widespread effects, including referred pain. WolP states : “Malposed teeth, notably the third molars, sometimes induce pain, which results from direct pressure upon afferent nerves. The pa.in of such ischemic neuritis may be of high intensity, but usually it is moderate. It is sometimes continuous, though usually intermittent.” He asserts that the referred pain spreads to predictable sites in the same segment and that the pain may spread to involve all areas of distribution of the trigeminal nerve. Wolff also notes that electrical stimulat.ion of a mandibular second premolar or first molar caused pain within ‘the anterior wall of the auditory canal. In the evaluation of any patient for the possibility of referred pain, the anatomic location of pain and the distribution and pathways of the nerves must be kept in mind. Concerning the present case, it should be noted that the third division of the trigeminal nerve (mandibular nerve) sends a recurrent branch to the dura mater, arising in the infratemporal fossa and re-entering the skull through the foramen spinosum, while its auriculotemporal branch supplies the preauricular-temporal area and also sends branches to the anterosuperior part of the outer ear and to the external auditory meatus.17 No patient should be dismissed as a neurotic simply because his complaints are unusual and do not follow a conventional pattern. The diagnostician must realize that referred pain may cause disabling and severe effects without local symptoms. He must also keep in mind the fact that impacted teeth may cause bizarre symptoms. Obviously, no guarantee should even be implied that vague or recurring neuralgias in the facial area will be cured by the removal of impacted teeth, but the possibility must be considered. There are enough other well-recognized indications for removing impacted teeth to make surgical treatment beneficial to the patient. If the operation also relieves the neuralgia or other unconventional symptoms, the patient will be exceedingly grateful and the
Vulume 25 Number 2
Referred
pain from asymptomatic impacted
molar
277
surgeon will earn respect for his diagnostic acuity. As in this case, the relief of symptoms is also a source of genuine pleasure, not only to the surgeon but to others who have seen the patient in the throes of his misery. SUMMARY
We have presented the case of a patient with an unusual symptom complex, which complete and thorough neurologic and oral examinations revealed to be due to two completely unrelated disease processes: (I) otosclerosis and (2) referred pain and paresthesias within the left mandibular nerve distribution. Removal of an impacted mandibular third molar that was in intimate contact with the neurovascular contents of the mandibular canal dramatically relieved the patient’s disabling syndrome of headaches and paresthesias. REFERENCES
1. Upson, H. S.: Insanity Caused by Painless Dental Disease, Dental Cosmos 52: 526, 1910. 2. Main, L. R.: Nerve Reflex Disturbances of Dental Origin, J. Am. Dent. A. 20: 870, 1933. 3. Douglas, C. M.: The Teeth in Relation to Mental Diseases, J. Am. Dent. A. 25: 1260, 1938. 4. Kuntz, 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15.
A., and Main, L. R.: The Neural Basis of Certain Syndromes Associated With Dental Lesions, Arch. Clin. Path. 4: 333, 1940. Engel, A. C.: Alleviation of Reflex Disturbances Following the Removal of an Impacted Mandibular Third Molar, Arch. Clin. Path. 4: 355, 1940. Facial Pain Following the Removal of Christiansen, G. W.: The Relief of Unilateral an Impacted Mandibular Third Molar! Arch. Clin. Path. 4: 357, 1940. Wahl, J. P.: Relief From Neurologic Symptoms Following Removal of an Impacted Mandibular Third Molar, Arch. Clin. Path. 4: 359, 1940. Molt, F. F.: Why Do We Remove Impacted Teeth? Arch. Clin. Path. 4: 275, 1940. Callahan, V. D.: Relief From Neuralgic Symptoms Following Removal of an Impacted Mandibular Third Molar, Arch. Clin. Path. 4: 367, 1940. M&ouch, G. P.: The Physiology of Pain. In Appleton, J. L. T. (editor) : Control of Pain in Dental Practice, Philadelphia, 1940, J. B. Lippincott Company, p. 55. Incisive Canal Cyst as Source of Facial Vianna, M. R., and Horizonte, B.: Infected and Head Pain: Report of a Case, J. Oral Sure.. Anesth. & Hosp. D. Serv. 21: 345, 1963. Report of a Case, URAL SCRG., ORAL &ED. & Carnes, J. C.: headache of Dental Origin: ORAL PATH. 13: 1314, 1960. Logan. T. H.: Pain ADDfi.renth Referred Across the Midline From a Perforated Lower Secon6 Molar, ORAL S&G., ORAL MED. & ORAL PATH. 18: 593,1964. Atterbury, R. A., and Vazirani, S. J.: Headache and the Source of Pain, ORAL Sn~c., ORAL MED. & OR& PATE. 12: 175, 1959. Kennedy, F.: Neurological Implications of Impacted Wisdom Teeth, Arch. Clin. Path.
4: 345, 1940. 16. Wolff, H. G.: Headache
and Other Head Pain, ed. 2, New York, 1963, Oxford University Press, pp. 35-36, 520, 529. ed. 3, St. Louis, 1960, The C. 1’. Mosby Company, pp. 361. 17. Sicher, H.: Oral Anatomy, 363,
376.
of the
Federal dental services Referred pain from an asymptomatic impacted mandibular third molar Report
of a case
Ronald D. Baker, Commander (DC) USN,* Howard B. Marble, Jr., Captain (DC) USN ,I+ William R. Martin, Commanck (DC) USN,C*+ and Nicholas R. Rafaelly, Lieutenant Commander (MC) USN***” NAVAL
DENTAL
SCHOOL,
NATIONAL
NAVAL
MEDICAL
CENTER,
BETHESDA,
MD.
T
he dental literature prior to 1940 is replete with descriptions of cures of various physical and mental ailments effected by the removal of impacted teeth.l+’ Some of the resolutions reported could be accepted today on the basis of present concepts of referred pain. Other reported “cures” of reflex loss of normal function of arms and legs, nervous or mental disorders, gastrointestinal disturbances, and dysmenorrhea would be difficult to explain physiologically. It is an accepted fact that referred pain can and does occur. In 1940, McCouch1° wrote that “ . . . the teeth, like the viscera, may give pain referred to characteristic areas of the face and neck.” Few would dispute that statement. The dental literature contains well-documented cases in which the elimination of dental pathosis has resulted in the resolution of deep-seated ear pain, headache, and facial neuralgia.ll-I4 Referred pain is not randomly distributed but is anatomically ordered or segmented. The following case illustrates that a dental site may give rise to nerve im-
The opinions or assertions contained herein are the private ones of the writers and are not to be construed as official or reflecting the views of the Navy Department or the naval service at large. *Chief of Dental Service, United States Naval Hospital, Camp Lejeune, N. C.; formerly Oral Surgery Resident, Naval Dental School. **Head, Oral Surgery Department, Naval Dental School. ***Senior Dental Officer, U.S.S. Essex; formerly Oral Surgery Resident, Naval Dental School. United States Naval Hospital, ****Senior Resident, Otorhinolaryngology Service, National Naval Medical Center, Bethesda, Md.
273
274
Baker et al.
OS., O.M. & O.P. February, 1968
pulses strong enough to cause markedly severe referred pain while remaining asymptomatic itself. It also demonstrates that one must be alert to the possibility that two or more simultaneously occuring, but distinct and unrelated, conditions may give rise to a multitude of symptoms in a circumscribed anatomic location. Finally, it emphasizes the value of the dental diagnostician on the health service team. CASE REPORT A 3%year-old Caucasian housewife was admitted to the Otorhinolaryngology Service of the Naval Hospital, National Naval Medical Center, Bethesda, Maryland, on Jan. 13, 1966. Her chief complaints were (1) severe headaches, recently increasing in intensity and causing loss of consciousness, (2) deafness of the left ear, progressive during the 2 years prior to admission, (3) blurred vision at the peak of the headaches, as if a mist were present, (4) “dead feeling” of the left auditory canal, (5) paresthesia of the left preauricular area, and (6) recurrent unsteadiness on turning. History
The patient had been completely well until 4 years prior to admission, when she developed tinnitus of the left ear. This was accompanied by a fullness and deep pressure ache of the left side of the head, with nausea but no vomiting. Initially, the attacks lasted only 1 day but recurred at intervals of 3 to 4 weeks. The patient did not remember nor could she recall any paresthesia or anesthesia at being unsteady or having vertigo; that time. She was admitted to the Naval Hospital at Great Lakes, Illinois, where a myringotomy was performed. The operation gave no noticeable relief, but several months later the attacks ceased for approximately 1 year. In 1964 the patient developed a symptom complex consisting of a low-pitched tinnitus, a feeling of fullness in the left ear, and a gradually increasing, deep, steady, left-sided aching which, at its peak, caused unsteadiness (without vertigo), nausea, pressure vomiting, and then anesthesia of the skin anterior to the left ear. The symptoms might be present when the patient awoke in the morning, but at times they commenced during the day. Initially, Cafergot seemed to attenuate the symptoms, but later it had no effect. By September, 1965, the symptom complex manifested itself at intervals of 1 to 2 weeks. Subsequently, the attacks increased in frequency, with a concomitant increase in severity. During the 2 weeks preceding admission, the headaches were almost continuous and so severe that five or six times the patient lost consciousness for periods of unknown duration. Treatment with Actifed, Darvon, Donnatal, and codeine gave no appreciable relief. Deafness of the left ear, insidious in onset about 2 years prior to admission, became progressively worse in 1965. In the months preceding admission, the patient noted a “dead feeling” of the left auditory canal. Past medical history revealed a chronic nasal congestion of 10 years’ duration, suggestive of allergic rhinitis. Physical
examination
Physical examination on admission revealed a well-developed, well-nourished, alert Caucasian woman. Vital signs were within normal limits. There was no tenderness over the scalp and no facial muscle weakness. Nystagmus was not present, nor was there any cornea1 anesthesia. Otoscopic examination was noncontributory, except for the decreased sensation to instrumentation, touch, or pain in the left auditory canal. There was a moderate mixed hearing loss on the left side, as measured by air and bone conduction. The results of caloric examination of the right and left ears were considered to be within normal limits. The Romber sign was absent. Examination of the cranial nerves was negative, except for the noted deficiencies of the trigeminal and auditory nerves.
Volume 25 Number 2 Laboratory
Referred
pain from
asymptomatic
impacted
molar
275
examination
Initial laboratory examinations, including complete blood count, urinalysis, glucose, and total serum protein determinations, were all within normal limits.
VDRL,
blood
including a chest film, a sinus The results of roentgenographic examinations, a cervical spine study, and skull roentgenograms with views of the internal auditory were within normal limits.
series. canal,
Roentgonographic
Hospital
course
examination
and
treatment
Otorhiaolaryngology Service. After the initial admission medical workup, the patieut was examined in consultation with the United States Army Audiology and Speech Center. The diagnosis was hearing loss of the left ear, mixed type, severe. There was no evidence of a retrocochlear lesion. Examination of the right ear revealed no abnormalities. The cause of the complete symptom complex was undetermined. It was tentatively suggesteil that a unilateral otosclerosis of the left ear caused the deafness and that some unrelated disease process, such as central nervous system pathosis, caused the headaches and left auricular paresthesia. Nezlrological examination. An electroencephalogram on January 20 was within normal limits. A RISA I-131 brain scan on January 28 revealed no evidence of abnormal uptake view disclosed a midline area of in the region of the acoustic nerve, but the lateral uptake in the parietal-occipital area. A Technetium 99” scan was interpreted as normal. A repeat RISA scan on February 10 was also normal, and a lumbar puncture on the same date revealed normal cerebrospinal fluid findings, Examination by the Neurology Bramh of the Neuropsychiatric Service for pathosis of the nervous system was negative. Dental Service. Since none of the indicated examinations elicited any pathologic condition consistent with the symptoms, the patient was referred to the Oral Diagnosis Department of the Naval Dental School to rule out the slight possibility of a temporomandibular joist syndrome. On February 11 a thorough clinical examination revealed the additional symptoms of paresthesia of the left long buceal nerve and partial lingual anesthesia, localized along the extreme left side of the tongue and extending onto the floor of the mouth. There was also a loss of sensation in the area of the left retromolar triangle. The patient had not been aware of these altered sensations until clinical examination revealed them. Roentgenograms disclosed an unerupted left mandibular third molar, impacted mesioangula,l anal with the apex in close proximity to, if not in actual contact with, the mandibular canal. No pathologic processes affecting the second molar or the adjacent bony structures were demonstrated. The patient was referred to the Oral Surgery Department for further evaluation. Although the impaction was considered to be a remote etiologic possibility, the patient was scheduled for removal of this tooth as well as a distoangularly impacted right mandibular third molar. A general nasotracheal anesthetic was administered on February 21, and the two impacted molars were surgically removed by sectioning with a high-spoecl air-turbine handpiece. The left third molar was found to be eroded, or grooved, in such a way that the contents of the mandibular canal lay directly on the root surface near the tip. On the first postoperative day, the patient had minimum discomfort, slight trisnbus, and a suggestion of returning sensation in the left preauricular area. Headache was absent, and remained so despite the development of alveolar osteitis. There was a progressive return of sensation to all previously affected intraoral areas, the preauricular region, and all of the auditory canal except the anterior border of the external autlitor:, meatus. Otorhinobyngology Service. On March 3, the patient underwent a left middle ear exploration which revealed ostosclerosis of the foot plate. An anterior stapes crurotomy produced immediate improvement in hearing. The postoperative course was uneventful, anrl there was only a mild residual sensorineural loss.
276 Baker et al.
OS., O.M. & 02. February, 1968
Consultation with the Allergy Branch of the Medical Service revealed that the patient had significant allergies to foods, molds, dust, and other inhalants. Desensitization was not accomplished at that time. The patient was discharged on March 24, 1966, asymptomatie except for slight deafness. Follow-up
Communication with the patient in April, 1967, indicated that she “never felt better in her life,” and had been completely free of the headaches that had incapacitated her more than a year previously. She was then undergoing injection desensitization therapy for her allergies.
DtSCUSSION
KennedyI stated : “Those casesin which action has been taken against alleged evil, and good results seem to have followed, are reported and remembered, whereas a multitude of cases in which no good result followed, are buried in decent obscurity.” It might be that Kennedy’s philosophy is illustrated by this case, in which recurrent and severe headaches, partial lingual anesthesia, and paresthesias of the buccal and auriculotemporal nerves were resolved after removal of an impacted mandibular third molar. Recovery in this case can be explained logically. Trigeminal nerve involvement has widespread effects, including referred pain. WolP states : “Malposed teeth, notably the third molars, sometimes induce pain, which results from direct pressure upon afferent nerves. The pa.in of such ischemic neuritis may be of high intensity, but usually it is moderate. It is sometimes continuous, though usually intermittent.” He asserts that the referred pain spreads to predictable sites in the same segment and that the pain may spread to involve all areas of distribution of the trigeminal nerve. Wolff also notes that electrical stimulat.ion of a mandibular second premolar or first molar caused pain within ‘the anterior wall of the auditory canal. In the evaluation of any patient for the possibility of referred pain, the anatomic location of pain and the distribution and pathways of the nerves must be kept in mind. Concerning the present case, it should be noted that the third division of the trigeminal nerve (mandibular nerve) sends a recurrent branch to the dura mater, arising in the infratemporal fossa and re-entering the skull through the foramen spinosum, while its auriculotemporal branch supplies the preauricular-temporal area and also sends branches to the anterosuperior part of the outer ear and to the external auditory meatus.17 No patient should be dismissed as a neurotic simply because his complaints are unusual and do not follow a conventional pattern. The diagnostician must realize that referred pain may cause disabling and severe effects without local symptoms. He must also keep in mind the fact that impacted teeth may cause bizarre symptoms. Obviously, no guarantee should even be implied that vague or recurring neuralgias in the facial area will be cured by the removal of impacted teeth, but the possibility must be considered. There are enough other well-recognized indications for removing impacted teeth to make surgical treatment beneficial to the patient. If the operation also relieves the neuralgia or other unconventional symptoms, the patient will be exceedingly grateful and the
Vulume 25 Number 2
Referred
pain from asymptomatic impacted
molar
277
surgeon will earn respect for his diagnostic acuity. As in this case, the relief of symptoms is also a source of genuine pleasure, not only to the surgeon but to others who have seen the patient in the throes of his misery. SUMMARY
We have presented the case of a patient with an unusual symptom complex, which complete and thorough neurologic and oral examinations revealed to be due to two completely unrelated disease processes: (I) otosclerosis and (2) referred pain and paresthesias within the left mandibular nerve distribution. Removal of an impacted mandibular third molar that was in intimate contact with the neurovascular contents of the mandibular canal dramatically relieved the patient’s disabling syndrome of headaches and paresthesias. REFERENCES
1. Upson, H. S.: Insanity Caused by Painless Dental Disease, Dental Cosmos 52: 526, 1910. 2. Main, L. R.: Nerve Reflex Disturbances of Dental Origin, J. Am. Dent. A. 20: 870, 1933. 3. Douglas, C. M.: The Teeth in Relation to Mental Diseases, J. Am. Dent. A. 25: 1260, 1938. 4. Kuntz, 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15.
A., and Main, L. R.: The Neural Basis of Certain Syndromes Associated With Dental Lesions, Arch. Clin. Path. 4: 333, 1940. Engel, A. C.: Alleviation of Reflex Disturbances Following the Removal of an Impacted Mandibular Third Molar, Arch. Clin. Path. 4: 355, 1940. Facial Pain Following the Removal of Christiansen, G. W.: The Relief of Unilateral an Impacted Mandibular Third Molar! Arch. Clin. Path. 4: 357, 1940. Wahl, J. P.: Relief From Neurologic Symptoms Following Removal of an Impacted Mandibular Third Molar, Arch. Clin. Path. 4: 359, 1940. Molt, F. F.: Why Do We Remove Impacted Teeth? Arch. Clin. Path. 4: 275, 1940. Callahan, V. D.: Relief From Neuralgic Symptoms Following Removal of an Impacted Mandibular Third Molar, Arch. Clin. Path. 4: 367, 1940. M&ouch, G. P.: The Physiology of Pain. In Appleton, J. L. T. (editor) : Control of Pain in Dental Practice, Philadelphia, 1940, J. B. Lippincott Company, p. 55. Incisive Canal Cyst as Source of Facial Vianna, M. R., and Horizonte, B.: Infected and Head Pain: Report of a Case, J. Oral Sure.. Anesth. & Hosp. D. Serv. 21: 345, 1963. Report of a Case, URAL SCRG., ORAL &ED. & Carnes, J. C.: headache of Dental Origin: ORAL PATH. 13: 1314, 1960. Logan. T. H.: Pain ADDfi.renth Referred Across the Midline From a Perforated Lower Secon6 Molar, ORAL S&G., ORAL MED. & ORAL PATH. 18: 593,1964. Atterbury, R. A., and Vazirani, S. J.: Headache and the Source of Pain, ORAL Sn~c., ORAL MED. & OR& PATE. 12: 175, 1959. Kennedy, F.: Neurological Implications of Impacted Wisdom Teeth, Arch. Clin. Path.
4: 345, 1940. 16. Wolff, H. G.: Headache
and Other Head Pain, ed. 2, New York, 1963, Oxford University Press, pp. 35-36, 520, 529. ed. 3, St. Louis, 1960, The C. 1’. Mosby Company, pp. 361. 17. Sicher, H.: Oral Anatomy, 363,
376.