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Etiology and treatment of idiopathic trigeminal and atypical facial neuralgias
Etiology and treatment of idiopathic trigeminal and atypical facial neuralgias Alexander M. Roberts, D.D.S., and Philip Person, D.D.S., Clarksburg, W. Va., and Brooklyn, N. Y. DAVIS
MEMORIAL
BROOKLYN,
N.
HOSPITAL,
ELKINS,
W.
VA.,
AND
VETERANS
Ph.D., ADMINISTRATION
HOSPITAL,
Y.
In a series of sixteen patients with idiopathic trigeminal neuralgia and twenty-one patients with atypical facial neuralgia, it was found that the painful phenomena associated with both disorders were, in nearly all instances, closely related to the presence of maxillary or mandibular bone cavities at previous tooth extraction sites. Standard oral surgical procedures for curettage of the cavities, together with administration of antibiotics, were employed in the successful treatment of both the trigeminal and atypical facial neuralgias, with complete pain remissions for periods varying from 2 months (for most recently treated cases) up to 9 years. The observations and results of this study suggest that dental and oral disorders may play a role in the genesis of trigeminal and atypical facial neuralgias.
M
any theories have been proposed to explain the origin and nature of idiopathic trigeminal and atypical facial neuralgias. ‘3 * There is also a wide variety of treatment modalities for these disorders, with varying degrees of success with respect to long-term or permanent relief from pain. 1,2 The purpose of this article is to present observations and data supporting the possibility that pre-existing dental and oral disorders may be major contributing factors in the onset of both idiopathic trigeminal and atypical facial neuralgias. In independent studies, Ratner and Person and their co-workers have made similar observations and arrived at similar conclusions.3-6 Their studies and those reported in this article provide the first evidence to support earlier contentions by such neurologists as Harris’ and Kinnier Wilson and Bruce,* that dental and oral pathosis might be important contributory factors in the onset of trigeminal neuralgia and, on the basis of the present study, we believe, also of atypical facial neuralgia. METHODS
AND PROCEDURES
Criteria for the diagnosis of idiopathic trigeminal and atypical facial neuralgias are those given by White and Sweet.’ Sixteen cases of idiopathic trigeminal neuralgia and twenty-one cases of atypical facial neuralgia will be reported. Dental diagnostic roentgenograms were made by standard intra- and extraoral techniques. While such roentgenograms are usually negative in idiopathic 298
trigeminal and atypical facial neuralgias, we have found that, on the basis of a patient’s history and symptoms one can detect roentgenographic changes in jawbones that might ordinarily be considered within the range of normal variations but which, in these patients with facial pain, reflect the existence of the pain-related bone cavities. In some cases frank radiolucencies may be visible at bone cavity sites which, under other circumstances, might be dismissed as nonrelated to the pain experienced by the patient. Following x-ray detection of such cavities, their digital palpation in nearly all instances elicited the pain patterns and symptoms characteristic of the patient’s complaints. The roentgenographically localized areas were then exposed by standard oral surgical procedures to verify their existence and to permit treatment. Usually, the areas were exposed under local anesthesia via an intraoral surgical approach. In each instance the areas were found to consist of bone cavities at the sites of previous tooth extractions, with dimensions of up to 2 cm. or more in a given axis. Often, narrow fistulous extensions or tracts from the cavity channel led in irregular fashion through adjacent bone for distances up to 2 cm. In the lower jaw, these narrow tracts always opened into the mandibular canal. In the upper jaw, the tracts often ended in a second bone cavity which might be larger than the first, and at times the fistulous tract would continue on into a third cavity. Judicious probing of such areas might disclose communication with the
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Fig. 1. Trigeminal
299
neuralgia, left mandible, premolar and molar regions. A circumscribed radiolucent area
(arrows) is distal to the second premolar. Fig. 2. Trigeminal neuralgia, right mandible, premolar and molar regions. Irregularly shaped radiolucent areas (UWOMS)extend from molar to premolar areas. Fig. 3. Atypical facial neuralgia, left mandible, premolar region. There is an irregularly shaped radiolucency (arrows) distal to the second premolar.
nasal cavity or antrum. Nerve fibers were often exposed in the walls of the cavities as a result of the bone destruction. All tracts and cavities were carefully curetted until
bone of normal consistency was reached. Then, the curetted voids were thoroughly irrigated with sterile distilled water. Next, a solution of chloromycetin in distilled water (250 to 500 mg./ml.) was placed in the cavity, and Gelfoam soaked in the same solution was packed in the cavity. Following this, the overlying gingiva was repositioned and sutured with 3-O silk continuous sutures. In five cases (two cases trigeminal neuralgia and three of atypical facial neuralgia) involving mandibular lesions, an extraoral submandibular (Risdon) approach under general anesthesia was used because (1) it provided more direct and less traumatic
access to the bone cavities and (2) it eliminated the possibility of contamination by intraoral flora of specimens taken for microbial analysis. In a number of cases, after varying periods of time, the patient might experience a recurrence of pain symptoms, usually of much decreased frequency and intensity, and in the old or perhaps a new pattern. If the pain patterns were those originally presented, the original lesion or lesions were re-exposed, recuretted, and treated as described above. If a new pain pattern was emerging, it was usually found to be related to a different bone cavity, perhaps not initially detected. Such a bone cavity would be exposed and treated as described above. Disappearance or decrease of pain occurred immediately or within a week following surgery in most cases. If severe pain persisted, the wound was
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Fig. 4. Atypical facial neuralgia, left maxilla, molar region. Arrows point to an irregular, triangular radiolucency distal to the first molar. Fig. 5. Trigeminal neuralgia, right mandible. Two cavities are present. In the canine and premolar region, an irregular radiolucency is seen, with sparse, thickened, and disorganized trabeculae. Posteriorly, in the molar region, a cavity was found in the area shown by the three arrows.
Fig. 6. Atypical facial neuralgia, left mandible. Distal to the second premolar is a triangular radiolucency. More
posteriorly, in the molar region, a second cavity was found where vestiges of lamina dura are seen. Fig. 7. Atypical facial neuralgia, right mandible, molar region. Vestiges of lamina dura (UP UYTOI~S)are seen. below which is a diffuse radiolucency (douse arrows). A photograph of these areas is shown in Fig. 8.
reopened, re-explored, and re-treated as described above. Irrigation of wounds with 3 percent hydrogen peroxide often appeared to cause the pain to subside. Curetted bone specimens were placed in 10 percent formalin and processed for hematoxylin and eosin staining of demineralized sections by standard methods. When possible, curetted specimens for microbiologic analysis were rapidly transferred into thioglycollate broth. Standard aerobic and anaerobic (BBL-Gas Pak system) culture methods were employed. Histopathologic examinations were made by Dr. G. Shklar, Brackett Professor of Oral Medicine and Oral
Pathology, Harvard School of Dental Medicine, Boston, Massachusetts, and Dr. J. Amorin, pathologist, Davis Memorial Hospital, Elkins, West Virginia. The microbiologic analyses were made in the Laboratory Service of the Davis Memorial Hospital in Elkins, West Virginia. RESULTS Roentgenograms
The appearance of pain-related bone cavities varied considerably. In Figs. 1 to 3, the radiolucencies are discrete, clearly demarcated, and unequivocal. In Figs.
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Fig. 9. Atypical facial neuralgia. On exposure of the area indicated by arrows in Fig. 7, two cavities (arrun~sJ were seen; these were the sockets of extracted molar teeth. Superiorly, they opened onto the surface of the mandible. Inferiorly, they entered the mandibular canal, whose wall was almost entirely destroyed by the disease process. Much necrotic bone was curetted, leaving the mandibular nerve (n) coursing freely through the body of the mandible as shown. Fig. 9. Trigeminal neuralgia, left mandible, premolar and molar regions. Two cavities are shown by arrows. The anterionnost (premolar region) is almost circular, while posteriorly a diffuse, horizontal shadow extends to the border of the anterior cavity. Fig. 10. Trigeminal neuralgia. Photograph of region of mandible corresponding to that shown in roentgenogram of Fig. 9 and madeduring surgical treatmentof the bone cavity. The arrow points to the baseof a cavity that is the remnant of the socket of an extracted tooth. Also, in Fig. 8, the socket communicated directly with the space surrounding the mandibular nerve (tz), whose wall was almost entirely destroyed by the disease process.
4 and 5, the anterior region of Fig. 6, and in Fig. 9, radiolucencies are less clearly demarcated, and might be interpreted as osteoporotic, or as regions of decreased mineral mass not necessarily accompanied by discrete cavity formations. In the posterior region of Fig. 6 and in Figs. 7, 11, and 12 significant changes consisted of distorted bone trabeculations or vestiges of lamina dura. At all roentgenographic sites mentioned above, bone cavities were exposed surgically. None of the above roentgenographic changes are in any way pathognomonic for trigeminal or atypical facial neuralgias, but ail were considered suspicious and worthy
of further exploration. When suspected areas were, in fact, found to be bone cavities, digital pressure over them would elicit characte~stic pain symptoms in most cases. Patient data and clinical results Table I shows that ten of sixteen (63 percent) trigeminal neuralgia patients were women and that, of these, ten were 50 years of age or older. Table II shows that seventeen of twenty-one (81 percent) patients with atypical facial neuralgia were women and that, of these, ten were 50 years of age or older. These sex and
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Fig. 11. Trigeminal neuralgia, upper left premolar and molar regions. Two confluent cavities exist (arrows). There is also a group of random, small radiolucent spots in the premolar area(asterisk). Fig. 12. Trigeminal neuralgia, mandibular left region. Bone trabeculaeform two vertical lines from the alveolar cresttoward the mandibular canal and demarcatethe site of a nonhealedmolar socket.The bottomsof the sockets were continuous with the mandibular canal
age distributions are comparable to those reported in the literature for these disorders.” *. ’ Also, one woman with trigeminal neuralgia (Patient V. P., Table I) also had multiple sclerosis with accompanying symptoms. In the cases of trigeminal neuralgia, either the second or third division was involved; no first division cases were encountered. The pain distributions of the atypical facial neuralgias covered a broad spectrum of both trigeminal and cervical nerve territories as described by White and Sweet.’ Duration of illness prior to treatment was between 1 and approximately 49 years in eleven of the sixteen trigeminal neuralgia cases, and between 2 and 20 years in fourteen of the twenty-one atypical facial neuralgia cases. By means of the treatment described in Methods and Procedures, complete pain abatement to date has been accomplished for periods of up to 9 years in each of the cases listed in both tables. Pain-related bone cavities might be single or multiple, and occasionally they were found diffused throughout the entire jaw, unilaterally or bilaterally. The cavities always encompassed the site of a previously extracted abscessed tooth or a socket previously contaminated by debris and oral microorganisms. Should a tooth be found to be related to experienced pain in such a way that restorative dental procedures cannot remedy the situation, then its extraction is advisable and the alveolus should be examined for a minute fistula which will usually lead into one or more cavities within the spongiosa, involving one or more branches of the trigeminal nerve. As mentioned previously, a frequent phenomenon in both types of facial neuralgia was formation of small fistulas and tunnels
connecting cavities in tandem for varying distances. When arising in the cuspid or premolar areas of the upper jaw, they may progress medially, anteromedially, and inferiorly, or posteriorly and inferiorly to merge, respectively, into the premaxilla or into the posterior palatine fossa. In the former instance, the internal and external nasal branches of the infraorbital nerve may be involved. One such tunnel measured 11 mm. in an anteromedial direction. Tandem cavities were not seen in the lower jaws, where fistulous tracts from the cavities would usually extend inferiorly into the mandibular canal. In some cases in the lower jaw, sclerotic bone may obscure such a fistula penetrating the mandibular canal. In all cases involving the lower jaw, to date, portions of the mandibular canal were found to be destroyed, exposing a nerve with an obviously altered epineurium (Figs. 8 and 10). In one case, on removal of a portion of the wall of the mandibular canal, a shredded epineurium was observed (Patient J. K., Table I; also Case 5 in Case Histories). There was no morbidity or complication following the oral surgical treatment described, with the exception of variable, temporary anesthesia. In all cases, tics, spasms, and lancinating, flashing, and other varieties of pain ceased totally, and patients remained asymptomatic except for occasional recurrences of slight pain. The latter were readily treated in the same fashion as the original pain and usually abated rapidly. In some atypical facial neuralgias, excruciating migrainous headaches involving the vertex, frontal, temporal, and occipital areas were greatly diminished or ceased entirely. All edentulous patients treated for atyp-
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Table I. Trigeminal neuralgia case summary Duration
of Sex
Patient
Trigger zone
symptoms 5 yr.
Trigeminal nerve division(s) involved
Lower left jaw
3
Lower left third molar area
3
I yr.
Lower left molar area
3
F
3 yr.
Lower left molar area
3
55
M
13 yr.
Upper right premolar area
2
N.G.
48
F
22 mo.
Lower left third molar area
3
D.C.
28
F
5 yr.
Lower left second molar area
3
C.F.
74
F
2 mo.
N.M.
62
F
5 mo.
Upper left premolar and left second molar areas Upper left premolar area
E.S.
54
M
H.C.
35
M
G.G.
51
F
K.S.
20
M.M.
2, 3 2
C.B.
63
M
15 yr.
Upper left cuspid; lower left first and second molar areas
H.P.
44
F
I1 yr.
Lower right molar area
3
M.G.
47
F
3 yr.
Upper left lateral incisor
2
L.S.
85
M
Lower left molar area
3
E.S.
83
F
4 yr.
Upper right cuspid area
2
J.K.
45
M
2% yr.
Lower left molar areas; upper left nasolabial fold and left buccal space
Multiple sclerosis V.P.
61
F
49 yr.
Lower left jaw
3
C.F.
14
F
Lower left second molar area
3
2 mo.
ical or trigeminal neuralgia are now wearing their dentures without discomfort. Laboratory results Histologic jndings. Twenty bone-curettage biopsy specimens were taken from eight patients (five trigeminal, three atypical facial neuralgia) with similar histologic pictures in both groups. Typically, there were spicules and fragments of bone (sometimes containing marrow) surrounded by hemorrhagic areas and fields of fibrous connective tissue of varying density, often highly vascularized. Osteoblastic activity or the presence of osteoid was seen in only one of the twenty biopsy specimens. In one trigeminal neuralgia specimen, there was considerable necrosis of bone spicules, but no inflammatory infiltrate. In two specimens (one trigeminal neuralgia and one atypical facial neuralgia)
2, 3
2, 3
Date of surgery
Duration pain free
8-8-74 Intraoral 3- 12-68 Intraoral 5-28-69 Intraoral l-28-76 Intraoral 1l-l-76 Intraoral l-28-76 Intraoral 8-76 Intraoral 12- 16-76 Intraoral
33 mo.
6-17-76
11 mo.
Intraoral IO- 14-75 2-4-76 Intraoral 3-9-76 Intraoral 2-3-16 Intraoral 1-21-17 Intraoral 2-23-76 Intraoral 3-24-17 Intraoral
9- 16-76 Extraoral 12-16-76 Extraoral
9 yr. 8 yr. 16 mo. 6 mo. 16 mo. 9 mo. 5 mo.
I!4 yr. 1.5 mo. 14 mo. 15 mo. 4 mo. 15 mo. 2 mo.
8 mo. 5 mo.
the fibrous connective tissue surrounding bone spicules was infiltrated with lymphocytes. In the trigerninal neuralgia specimen, plasma cells and histiocytes were also present. Microbiologic jindings. Samples for microbial culture were taken from six trigeminal neuralgia and seven atypical facial neuralgia patients. Results are summarized in Table III. Only two organisms were identified in extraoral samplings Staphylococcus epidermidis (growth aerobic and anaerobic) and Peptococcus (growth anaerobic). In intraoral samples, in addition to the above organisms, a-hemolytic streptococci, diphtheroids, and Neisseria were also identified. The absence of o-hemolytic streptococci, diphtheroids, and Neisseria in the extraoral samples suggests that they were probable contaminants of the intraoral samples. In only one patient out of thirteen studied (Patient P. B.,
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Table II. Atypical facial neuralgia case summary Duration
of Patient
Sex
symptoms
Division(s) involved
R.L.
66
F
5 yr.
2
P.B.
65
F
2% yr.
2
A.U.
48
M
2% yr.
W.G.
53
F
5 yr.
2
S.C.
38
F
6 mo.
3
H.B.
38
F
20 yr.
J.J.
35
M
4 yr.
C.F.
74
F
2 mo.
W.G.
34
M
8 mo.
J.H.
31
F
2 mo.
S.N.
37
F
6 yr.
2, 3
H.S.
30
F
2 yr.
2, 3
M.L.
78
F
2 yr.
2, 3
E.L.
65
F
M.B.
55
F
E.P.
50
F
P.B.
54
F
P.S.
33
F
6 mo.
V.L.
35
F
7 yr.
N.G.
48
F
9 yr.
R.S. M.L.
62 78
M F
2 yr. 2 yr.
E.L.
65
F
M.B.
55
F
2, 3
I I yr, 8 mo. 2% yr.
11 yr.
2 2
2 3
Date of surgery
12-2-7 I Intraoral 7-6-75 Intraoral 9- 18-75 Intraoral 2- 17-77 Intraoral 3-3-76 Intraoral 12-30-75 Intraoral 3-25-76 Intraoral 12-16-76 Intraoral I l-8-76 Intraoral 12-13-76 Intraoral 12-17-77 Intraoral 9-9-76 Intraoral 5-4-76 Intraoral 5-23-76 Intraoral 6-16-76 Intraoral 12- 16-76 Intraoral 3-25-77 Intraoral 3-24-77 Intraoral 4-22-77 Intraoral 2- 15-7 1 Intraoral 12-16-76 5-4-76 Extraoral 7-22-76 Extraoral 6- 16-76 Extraoral
Duruiion puin free
5% yr. 22 “IO. 20 mo. 3 mo. 14 mo. 17 mo. 14 mo. 5 mo. 6 mo. 5 mo. 3 mo. 8 mo. I yr. I yr. 11 mo. 5 mo. 2 mo. 2 mo. I mo. 6% yr. 5 mo. 1 yr. 10 mo. 11 mo.
atypical facial neuralgia), neither staphylococcus nor was found in the samples taken from the bone cavity.
and 1 year. Oral surgery was performed at the Davis Memorial Hospital in Elkins, West Virginia. CASE 1
Case histories
Patient M. J. L., a 78-year-old edentulous white woman, was admitted to the hospital on May 13, 1976, in moderate distress.Pain had started5% yearspreviously. For the past 20 months, shehad sufferedfrom intermittent lancinating pain of the left mandible, radiating to the right mandible. Two weeks prior to her visit, the severity of paroxysms increasedmarkedly. Partial relief was obtained by sitting before a hot stove.
Peptococcus
Five cases (three atypical facial neuralgia, two idiopathic trigeminal neuralgia) will be described. Of these, four were treated by the Risdon submandibular (external) approach. All cases have been asymptomatic since treatment, for periods varying between 9 months
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Table III. Microorganisms isolated from jawbone cavities of patients with trigeminal and atypical facial neuralgias Sampling route
Organisms reported
E.S. C.F. C.B.
Intraoral Intraoral Intraoral
cu-hemolyticstreptococcus;Staphylococcus epidermidis Staphylococcus epidermidis Staphylococcus epidermidis; a-hemolytic
H.P. M.G. V.M. C.F.
Intraoral Intraoral Extraoral Extraoral
Patient Trigeminal neuralgia
streptococcus;Peptococcus,diphtheroids a-hemolytic streptococcus Staphylococcus epidermidis Staphylococcus epidermidis Staphylococcus epidermidis
Atypical facial neuralgia
P.B. A.U. W.G. H.B. EL. M.L. E.L. M.B.
Intraoral Intraoral Intraoral Intraoral Intraoral Extraoral Extraoral Extraoral
The patient took eight Percodan tablets daily. The right nasolabial area was involved to a lesser degree. Medical history The patient had arteriosclerotic heart disease with compensated chronic heart failure. Roentgenographically, there was a sclerotic aortic shadow. A positive serologic result was reported for VDRL testing. The above conditions were considered noncontributory. Diagnosis: Atypical facial neuralgia. Intraoral roentgenograms
(not illustrated)
In the upper right canine region, an inverted, irregular, cone-shaped radiolucent area was present in proximity to the floor of the nasal cavity. In the left mandibular molar area, there was an abnormal trabecular pattern, with considerable demineralization and sparse, dense, threadlike bone ramifying throughout the medullary cavity. The boundary between the normal and abnormal spongiosa was demarcated as by a vertical line from the inferior border of the mandible to the crest of the alveolar ridge. Treatment The left face and neck were prepared with Betadine Prep and Scrub, and specimens for microbiologic culture of the skin were taken. The mandible was exposed through a submandibular skin incision and decorticated in the second and third molar area by means of a bur and bone drill. This procedure revealed an underlying cavity in which a segment of the bony mandibular canal had been destroyed for a distance of approximately 1.5 cm. The mandibular nerve coursed freely through this space, which was unlined, and whose walls consisted solely of eroded bone. The nerve was slightly discolored, being of a light brown hue. The cavity wall had the consistency of clumps of dried sugar and crumbled and disintegrated as the curette blade cut through it. There was profuse hemorrhage during curettage. Superficial and deep specimens for microbiologic cultures were taken, including portions of necrotic-appearing bone in close proximity to the mandibular
a-hemolytic streptococcus;Neisseria; diphtheroids ry-hemolytic streptococcus;Staphylococcus epidermidis Staphylococcus epidermidis Staphylococcus epidermidis
a-hemolytic streptococcus;Staphylococcus epidermidis Staphylococcus epidermidis
Peptococcus Staphylococcus epidermidis
nerve. External skin cultures were negative aerobically and anaerobically, while from the cavity interior Staphylococcus epidermidis was cultured aerobically and anaerobically. The bone cavity was thoroughly curetted, and irrigated and packed as described on p. 299, and the wound was closed in layers. On completion of this procedure, the right maxilla (canine area) was treated via an intraoral approach. Recovery from the combined procedures was uneventful, and there has been no pain since treatment. The patient now wears and uses her upper and lower full dentures. CASE 2 Patient M. E. B., a 45year-old edentulous white woman, was admitted to the hospital on June 16, 1976, complaining of “sharp shooting” pain in the right mandible (and on one occasion on the left side) of 6 weeks’ duration. Eleven years previously she had experienced repeated episodes of pain and facial swelling from abscessed teeth in the involved area, which were extracted. Since that time, she had had an almost constant, intractable, dull ache, with irregular periods of remission. The patient was in moderate distress and apprehensive. Medical history The medical history was essentially negative. The patient was not taking any medications. Laboratory work-up results were within normal ranges. Diagnosis: Atypical facial neuralgia. Intraoral roentgenograms Remnants of lamina dura were evident in the mandibular right molar area (up arrows), with suggestive radiolucencies (down arrows) below the alveolar ridge (Fig. 7). Treatment On June 17, 1976, via the external submandibular approach, the bone of the right lower molar area (lateral to the mandibular nerve) was decorticated with a bur and bone drill.
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This exposed two adjacent but separate cavities located immediately above the mandibular canal (Fig. 8), whose superior wall had been completely destroyed. The mandibular nerve was exposed for a length of approximately 2 cm, and was reddish brown in color. The cavity walls were not lined and were of the same necrotic-like, crumbling consistency described in Case 1. This condition extended to the crest of the alveolar ridge. Superficial and deep bone specimens were taken for microbial culture, which was positive for Sraphy/ococcus epidermidis. Following curettage, the wound was irrigated, packed as described on p. 299, and closed in layers. The bone of the left mandibular distal molar area was treated in similar fashion via an intraoral approach. Healing was uneventful, and the patient has been free from pain since treatment. The patient is now wearing and using her full upper and lower dentures. CASE 3 In 1958, following extraction of abcessed teeth, Patient E. V. L., a 65-year-old white woman, noticed the onset of pulsating and “shooting pain” in the lower left jaw. She was treated by an oral surgeon who “cleaned out the bone,” and improvement resulted. The pain had intermittently returned and disappeared since that time. In June, 1974, the left mandibular anterior teeth were removed because of roentgenongraphic findings of bone involvement in the area. There was some improvement in comfort. In December, 1976, the pain became progressively worse in the left anterior mandible, with flashing radiations to the left ear, mental, temporal, and vertex regions. The patient also complained of boring and burning pain in the right mandibular molar area, but of lesser intensity than on the left side. Digital pressure on the gingiva or cheek of the involved sides precipitated the pain. The patient was hospitalized for treatment in May, 1976. The left anterior jaw was successfully treated by an intraoral procedure via a mucoperiosteal flap. However, intraoral treatment of the lower right molar area was unsuccessful. The patient. although relieved of her original complaint on the left side, was now greatly concerned about an increasing intensity of the boring and burning pain in the right lower jaw. On July 21, 1976, she was readmitted to the Davis Memorial Hospital in Elkins, West Virginia for treatment of the right side via a Risdon extraoral procedure. Medical history The patient had a history of hypertensive cardiovascular disease with angina1 syndrome and was taking nitroglycerin, Petitrate, and Librax. Diagnosis: Atypical facial neuralgia. Intraoral roentgenograms
(not illustrated)
There was a large area of distorted bone trabeculations in the right mandibular molar and premolar regions, with striae of sclerotic bone ramifying throughout the area against a translucent background. In the mandibular left cuspid area, an opacity was noted. Treatment The right side of the face and neck was prepared with Betadine Scrub and Prep. The skin was excised 2 mm. below the inferior border of the mandible and retracted. The cortical
Oral Surg. October, 1979 bone of the mandible overlying the premolar and molar areas was removed with buts and bone drill. A small cavity, approximately 0.5 cm. in diameter, was exposed in the first molar area. This cavity communicated with a larger cavity, approximately 1 cm. in diameter, located anteriorly in the premolar area. The walls of the cavities were soft and necrotic. They were thoroughly curetted. The mandibular canal had been totally destroyed in the involved areas, and the mandibular nerve was red in color. Fragments of medullary bone and fluids were taken for microbial culture, which was positive for Peptococcus. Following curettage, the bone cavity was irrigated with sterile water, packed, and closed by layers, as previously described. Healing was uneventful, and there has been no recurrence of pain. CASE 4 Patient V. P., a distraught, 67-year-old edentulous white woman, was seen in August, 1976, complaining of “sharp, shooting” pain in the left posterior mandible. This pain had started 1 year earlier. There were alternating remissions and exacerbations for weeks or months at a time, until 2 weeks prior to examination, when paroxysms of pain became more acute and repetitive. The pain occurred for 5 minutes, remitting for about 1 hour, and then recurring at precisely the same area. It was more intense at night. Talking, eating, face washing, and tactile stimulation triggered the attacks. A careful history revealed that the patient had had abscessed teeth removed from the left lower jaw when she was a young woman, and since that time she had suffered from pain affecting the distribution of the third division on the involved side. When seen, she was taking 50 mg. of Talwin for relief of pain, as required. She was admitted to the hospital on Sept. 15, 1976. Medical history Neurologic findings were normal, except for those associated with multiple sclerosis. There was no sensory deficit in the face to pin prick or light touch, and the cornea1 reflexes were equal. Light touch on the skin of the left face triggered the onset of pain. Laboratory work-up was otherwise within normal limits. Diagnosis: Idiopathic trigeminal neuralgia. intraoral roentgenograms In the left lower molar region there was an irregularly shaped area of trabecular distortion measuring approximately 8 mm. in width and 20 mm. in height (Fig. 9). The area was located above the mandibular canal and traversed by widely dispersed and irregular sclerotic striae. Treatment The left side of the face and neck was prepared with Betadine Prep and Scrub in the usual manner. A 5 cm. incision was made 2 mm. below the inferior border of the mandible, extending from the angle of the jaw to the mental region, and the tissues were retracted. The mandibular cortex in the molar area was removed in toto (2 by 1.5 cm.) and placed in sterile distilled water. The underlying medullary bone appeared extremely porous. It was soft and easily removed with the curette, which left behind a cavity of approximately 1.5 by 2.0 cm. (Fig. 10). The mandibular canal had been destroyed in the involved area. Specimens for cultures were taken, in-
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chiding fragments of necrotic-appearing bone. Cultures were positive for Staphylococcus epidermidis. The mandibular nerve appeared normal, except for reddish brown discoloration, and was not traumatized during curettage of the cavity. Irrigation was performed with approximately 60 ml. of sterile water, and the wound was packed and closed as described in the preceding cases. The patient has been without pain since this operation. CASE 5
When first seen, Patient J. K., a 4%year-old edentulous white man, appeared emaciated, pale, depressed, and extremely apprehensive. He complained of daily, severe, paroxysmal, “electric-like” pain shocks that had begun 2% years previously and in recent weeks had become more intense. The paroxysms occurred spontaneously or were initiated by swallowing, shaving, washing the face, and bending forward. Cold air and tongue contact with the buccal mucosa also triggered the attacks. The latter were preceded by buming and tingling in the left upper lip, which radiated to the left temporal region and vertex and thence anteriorly to the left nasolabial fold and upward through the nasal cavity and left eye, with resulting lacrimation. The patient also complained of severe pain in the left mandible, with lancinating pains “jumping” from the nasolabial fold inferiorly to the mental nerve region. The patient had been previously treated by a physician who injected cortisone into the left temporomandibular joint, with no relief. At a nearby medical center a diagnosis of idiopathic trigeminal neuralgia was made. The patient was given Tegretol, which was discontinued because of intolerance. Later, at the neurosurgical service of the same center, the diagnosis of trigeminal neuralgia was not confirmed. However, when the patient was seen by us, his symptoms were those of idiopathic trigeminal neuralgia. On the morning of March 23, 1977, the patient was admitted to the Davis Memorial Hospital in Elkins, West Virginia. Medical
history
The patient had lost 57 pounds since inception of the present illness. He had occasional severe gastric pains for which no basis could be found. He had suffered a severe injury to the occiput in 1954. He had had no other illnesses or seizures. Valium, 5 mg., and Donnatal were being taken three times daily. The patient’s teeth had been removed 25 years previously, and he stated that at the time many of them were abscessed. The results of the current laboratory work-up were within normal limits, and a chest plate was normal. Diagnosis: Idiopathic trigeminal neuralgia. Intraoral
roentgenograms
In the maxillary left premolar area there was a large circular radiolucency, within which were several small, scattered, darker radiolucencies. The area was anterior to the antrum and 13 mm. above the crest of the alveolar ridge (Fig. 11). In the mandibular left molar area bone trabeculae formed two vertical lines extending from the crest of the alveolar ridge and “fanning out” inferiorly as they approached the mandibular canal, indicating the vestiges of a tooth socket. Superiorly, there was an admixture of radiolucencies and randomly oriented dense or sclerotic bone striations, while in-
Fig. 13. Trigeminal neuralgia. Photograph of maxillary left premolar and molar areas corresponding to the radiolucent areas shown in Fig. I I The anterior circular radiolucent area of Fig. II is represented here by the arrow, and its distal extensions to the tuberosity region are evident. The anteriormost cavity (urrow) existed as such when the area was first exposed. Its distal extension consisted of a soft, necrotic type of very vascular bone which disintegrated during curettage, resulting in the cavity extensions seen in the photograph.
feriorly no bone trabeculae were seen except for a mild opacity. The bottom of the tooth sockets continued into what had been the mandibular canal (Fig. 12). Treatment
The maxillary left premolar area was exposed via an intraoral approach following induction of oroendotracheal general anesthesia. Two confluent cavities were discovered in the premolar and molar areas. The bone cavities were curetted methodically until all soft material was removed and solid bone was reached. This produced a 2.5 cm. cavity (Fig. 13) extending in an anterior, medial, and superior direction. The maxillary tuberosity was also involved. In the bone of the lower left molar area, a cavity approximately 2 cm. in anteroposterior length and 3 cm. in a superior-inferior direction was exposed. Curettage was performed methodically, during which a portion of the wall of the mandibular canal was carefully removed, disclosing a shredded epineurium of reddish brown color. Following irrigation and packing, the mucoperiosteal flaps were sutured. The patient was discharged improved on the third postoperative day. A stormy postoperative course ensued. Lancinating pain was experienced, involving the maxillary left promolar area and radiating to the entire left side of the head and neck. Two extreme episodes were repotted as “explosions” within the head, during which his head forcefully turned to the right side and his feet flew into the air. An antibiotic, Erythrocin, and Demerol for pain, were prescribed, but the pain failed to abate. On the eighth postoperative day, the patient visited the office and was severely depressed and despondent. An attempt was made to locate possibly undetected
3043
Roi7erts
and Person
in\,ljlved areas, and irrigations of the operated areas with hydrogen peroxide were also begun. Following 2 weeks of dally irrigations with hydrogen peroxide, all painful areas improved dramatically, except for one from which sharp shooting pains emanated. This area was located in the maxillary left premolar region, within the fascial and muscle spaces of the nasolabial area. The infraorbital nerve was locally anesthetized and, through a small incision in the nasolabial mucobuccal fold, the fascial spaces in the premolar area were irrigated with 10 ml. of hydrogen peroxide. This produced a sudden and dramatic remission of the remaining pain symptoms. The procedure was repeated on the following day, and on the third day the area was irrigated with 2 ml. of sterile water in which 500 mg. of chlommycetin was dissolved. The pains virtually ceased, except for a small occasional twinge of lancinating pain radiating to the upper left lip. Four weeks later the above procedure was repeated through an intraoral incision of the mucobuccal fold, with delivery of 250 mg. of chloromycetin in solution to the site. Since that time, all pains have ceased totally. The patient speaks now of a slight tenderness in the area, believed to be associated with the healing process. The patient regained 26 pounds in weight and re-
turned to work. At presentall trigeminal symptomsare gone, and his occipital headaches have ceased completely. DISCUSSION
The observations reported in this article support the suggestion that dental and oral pathosis may be important contributing factors in the onset and development of both idiopathic trigeminal neuralgia and atypical facial neuralgia. This contention is supported by (1) disappearance of pain following curettage and antibiotic treatment of the bone cavities at the sites of tooth extractions in afflicted persons and (2) the preliminary microbiologic and histopathologic observations consisting of positive identifications of anerobic staphylococci or Peptococci in thirteen of fifteen cavity samplings. The histopathologic observations of a typical curettage biopsy specimen showed bone spicules and fragments, occasionally necrotic, surrounded by hemorrhagic areas. Fibrous connective tissue of varying density was usually highly vascularized, and often infiltrated with chronic inflammatory cells. The histopathologic observations are similar to those seen in impaired healing of bone but are also perplexing because of the absence of more marked cellular inflammatory changes, such as might be expected in the face of anaerobic bone infections. Strongest support for the belief that the pain of trigeminal and atypical facial neuralgias may be of dental inception comes from the clinical observations and results. The dramatic pain remissions resulting from curettage and antibiotic treatment of the bone cavities support a cause-and-effect relationship between the cavities and the pain. Nevertheless, it must be kept in mind that both deliberate and inadvertent instrumentation of the trigeminal nerve during surgical procedures
Oral Surg. October, I979
produces pain remissions for varying time periods.‘, ’ Although such procedures usually involve more central trigeminal nerve components, it may be that inevitable traumatizations of small peripheral and terminal nerve branches during the oral surgical procedures described here produce similar pain remissions. The present study, together with the work reported by Ratner. Person, and their co-workers,3-6 make it mandatory, we believe, that serious consideration and study be given to the possibility that trigeminal and atypical facial neuralgias may be disorders largely of dental origin. In addition, the present study and the work of the above-mentioned investigators provide, for the first time, a new approach to treatment and management of these afflictions. This may obviate the need for central neurosurgical procedures or the use of medications which interfere with nerve function and often bring with them the threat of serious side effects. Thanks are expressed to Dr. Gerald Shklar, Brackett Pmfessor of Oral Pathology and Oral Medicine, Harvard School of Dental Medicine, Boston, Massachusetts, for his interest and for his advice and assistance with the histopathologic examination of biopsy specimens; Dr. N. B. Chandran, anesthesiologist, Davis Memorial Hospital, Elkins. West Virginia, for skillful professional services and consultations: Dr. James G. Thomas, Professor, Department of Oral Diagnosis and Radiology, West Virginia University Medical Center, Morgantown, West Virginia, for his interest and helpful discussions; and Ms. Beatrice Quigley, Librarian, Veterans Administration Hospital, Clarksburg, West Virginia, for valuable assistance in literature research. REFERENCES
I. White, J. C.. and Sweet, W. S.: Pain and the Neurosurgeon:A Forty Year Experience, Springfield, Ill.. 1969,CharlesC Thomas Publisher, chaps. V. VI, and VIII. 2. Stookey. B., and Ransohoff,J.: Trigeminal Neuralgia: Its History and Treatment, Springfield, Ill., 1959, Charles C Thomas Publisher. 3. Ratner. E. J.. Person, P., and Kleinman, D. J.: Oral Pathology and Trigeminal Neuralgia, I. Clinical Experiences, J. Dent. Res. 55B: 299, 1976. 4. Shklar, G., Person, P., and Ratner, E. J.: Oral Pathology and
Trigeminal Neuralgia, II. Histopathologic Observations.J. Dent. Res. 55B: 299. 1976. 5. Socransky, S. S., Stone, C., Ratner, E., et al.: Oral Pathology and Trigeminal Neuralgia, III. Microbiologic Examination, J. Dent. Res. 55B: 300, 1976. 6. Ratner, E. J.. Person,P., and Kleinman, D. J.: Jaw Bone Cavities and Trigeminal and Atypical Facial Neuralgias, ORAL SURG. 48: 3-20, 1979. 7. Harris, W.: Neuritis and Neuralgia, London, 1926, Oxford Uni-
versity Press, pp. 163-165. 8. Kin&r Wilson: S. A., and Bruce, A. N.: Neurology, Baltimore,
1955. Williams & Wilkins Comuanv. D. 405. 9. Rothman, K. J., andMonson, R.‘R.:‘I$idemiology of Trigeminal
Neuralgia, J. Chron. Dis. 26: 3-12, 1973. Reprint requests to.
Dr. Alexander M. Roberts 704 Union National Center West Clarksburg, W. Va. 26301
MEMORIAL
BROOKLYN,
N.
HOSPITAL,
ELKINS,
W.
VA.,
AND
VETERANS
Ph.D., ADMINISTRATION
HOSPITAL,
Y.
In a series of sixteen patients with idiopathic trigeminal neuralgia and twenty-one patients with atypical facial neuralgia, it was found that the painful phenomena associated with both disorders were, in nearly all instances, closely related to the presence of maxillary or mandibular bone cavities at previous tooth extraction sites. Standard oral surgical procedures for curettage of the cavities, together with administration of antibiotics, were employed in the successful treatment of both the trigeminal and atypical facial neuralgias, with complete pain remissions for periods varying from 2 months (for most recently treated cases) up to 9 years. The observations and results of this study suggest that dental and oral disorders may play a role in the genesis of trigeminal and atypical facial neuralgias.
M
any theories have been proposed to explain the origin and nature of idiopathic trigeminal and atypical facial neuralgias. ‘3 * There is also a wide variety of treatment modalities for these disorders, with varying degrees of success with respect to long-term or permanent relief from pain. 1,2 The purpose of this article is to present observations and data supporting the possibility that pre-existing dental and oral disorders may be major contributing factors in the onset of both idiopathic trigeminal and atypical facial neuralgias. In independent studies, Ratner and Person and their co-workers have made similar observations and arrived at similar conclusions.3-6 Their studies and those reported in this article provide the first evidence to support earlier contentions by such neurologists as Harris’ and Kinnier Wilson and Bruce,* that dental and oral pathosis might be important contributory factors in the onset of trigeminal neuralgia and, on the basis of the present study, we believe, also of atypical facial neuralgia. METHODS
AND PROCEDURES
Criteria for the diagnosis of idiopathic trigeminal and atypical facial neuralgias are those given by White and Sweet.’ Sixteen cases of idiopathic trigeminal neuralgia and twenty-one cases of atypical facial neuralgia will be reported. Dental diagnostic roentgenograms were made by standard intra- and extraoral techniques. While such roentgenograms are usually negative in idiopathic 298
trigeminal and atypical facial neuralgias, we have found that, on the basis of a patient’s history and symptoms one can detect roentgenographic changes in jawbones that might ordinarily be considered within the range of normal variations but which, in these patients with facial pain, reflect the existence of the pain-related bone cavities. In some cases frank radiolucencies may be visible at bone cavity sites which, under other circumstances, might be dismissed as nonrelated to the pain experienced by the patient. Following x-ray detection of such cavities, their digital palpation in nearly all instances elicited the pain patterns and symptoms characteristic of the patient’s complaints. The roentgenographically localized areas were then exposed by standard oral surgical procedures to verify their existence and to permit treatment. Usually, the areas were exposed under local anesthesia via an intraoral surgical approach. In each instance the areas were found to consist of bone cavities at the sites of previous tooth extractions, with dimensions of up to 2 cm. or more in a given axis. Often, narrow fistulous extensions or tracts from the cavity channel led in irregular fashion through adjacent bone for distances up to 2 cm. In the lower jaw, these narrow tracts always opened into the mandibular canal. In the upper jaw, the tracts often ended in a second bone cavity which might be larger than the first, and at times the fistulous tract would continue on into a third cavity. Judicious probing of such areas might disclose communication with the
Idiopathic trigeminal and atypical facial neuralgias
Volume 48 Number 4
Fig. 1. Trigeminal
299
neuralgia, left mandible, premolar and molar regions. A circumscribed radiolucent area
(arrows) is distal to the second premolar. Fig. 2. Trigeminal neuralgia, right mandible, premolar and molar regions. Irregularly shaped radiolucent areas (UWOMS)extend from molar to premolar areas. Fig. 3. Atypical facial neuralgia, left mandible, premolar region. There is an irregularly shaped radiolucency (arrows) distal to the second premolar.
nasal cavity or antrum. Nerve fibers were often exposed in the walls of the cavities as a result of the bone destruction. All tracts and cavities were carefully curetted until
bone of normal consistency was reached. Then, the curetted voids were thoroughly irrigated with sterile distilled water. Next, a solution of chloromycetin in distilled water (250 to 500 mg./ml.) was placed in the cavity, and Gelfoam soaked in the same solution was packed in the cavity. Following this, the overlying gingiva was repositioned and sutured with 3-O silk continuous sutures. In five cases (two cases trigeminal neuralgia and three of atypical facial neuralgia) involving mandibular lesions, an extraoral submandibular (Risdon) approach under general anesthesia was used because (1) it provided more direct and less traumatic
access to the bone cavities and (2) it eliminated the possibility of contamination by intraoral flora of specimens taken for microbial analysis. In a number of cases, after varying periods of time, the patient might experience a recurrence of pain symptoms, usually of much decreased frequency and intensity, and in the old or perhaps a new pattern. If the pain patterns were those originally presented, the original lesion or lesions were re-exposed, recuretted, and treated as described above. If a new pain pattern was emerging, it was usually found to be related to a different bone cavity, perhaps not initially detected. Such a bone cavity would be exposed and treated as described above. Disappearance or decrease of pain occurred immediately or within a week following surgery in most cases. If severe pain persisted, the wound was
300 Roberts and Person
Oral Surg. October, 1979
Fig. 4. Atypical facial neuralgia, left maxilla, molar region. Arrows point to an irregular, triangular radiolucency distal to the first molar. Fig. 5. Trigeminal neuralgia, right mandible. Two cavities are present. In the canine and premolar region, an irregular radiolucency is seen, with sparse, thickened, and disorganized trabeculae. Posteriorly, in the molar region, a cavity was found in the area shown by the three arrows.
Fig. 6. Atypical facial neuralgia, left mandible. Distal to the second premolar is a triangular radiolucency. More
posteriorly, in the molar region, a second cavity was found where vestiges of lamina dura are seen. Fig. 7. Atypical facial neuralgia, right mandible, molar region. Vestiges of lamina dura (UP UYTOI~S)are seen. below which is a diffuse radiolucency (douse arrows). A photograph of these areas is shown in Fig. 8.
reopened, re-explored, and re-treated as described above. Irrigation of wounds with 3 percent hydrogen peroxide often appeared to cause the pain to subside. Curetted bone specimens were placed in 10 percent formalin and processed for hematoxylin and eosin staining of demineralized sections by standard methods. When possible, curetted specimens for microbiologic analysis were rapidly transferred into thioglycollate broth. Standard aerobic and anaerobic (BBL-Gas Pak system) culture methods were employed. Histopathologic examinations were made by Dr. G. Shklar, Brackett Professor of Oral Medicine and Oral
Pathology, Harvard School of Dental Medicine, Boston, Massachusetts, and Dr. J. Amorin, pathologist, Davis Memorial Hospital, Elkins, West Virginia. The microbiologic analyses were made in the Laboratory Service of the Davis Memorial Hospital in Elkins, West Virginia. RESULTS Roentgenograms
The appearance of pain-related bone cavities varied considerably. In Figs. 1 to 3, the radiolucencies are discrete, clearly demarcated, and unequivocal. In Figs.
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Idiopathic trigenzirtal and atypical facial neuralgias
301
Fig. 9. Atypical facial neuralgia. On exposure of the area indicated by arrows in Fig. 7, two cavities (arrun~sJ were seen; these were the sockets of extracted molar teeth. Superiorly, they opened onto the surface of the mandible. Inferiorly, they entered the mandibular canal, whose wall was almost entirely destroyed by the disease process. Much necrotic bone was curetted, leaving the mandibular nerve (n) coursing freely through the body of the mandible as shown. Fig. 9. Trigeminal neuralgia, left mandible, premolar and molar regions. Two cavities are shown by arrows. The anterionnost (premolar region) is almost circular, while posteriorly a diffuse, horizontal shadow extends to the border of the anterior cavity. Fig. 10. Trigeminal neuralgia. Photograph of region of mandible corresponding to that shown in roentgenogram of Fig. 9 and madeduring surgical treatmentof the bone cavity. The arrow points to the baseof a cavity that is the remnant of the socket of an extracted tooth. Also, in Fig. 8, the socket communicated directly with the space surrounding the mandibular nerve (tz), whose wall was almost entirely destroyed by the disease process.
4 and 5, the anterior region of Fig. 6, and in Fig. 9, radiolucencies are less clearly demarcated, and might be interpreted as osteoporotic, or as regions of decreased mineral mass not necessarily accompanied by discrete cavity formations. In the posterior region of Fig. 6 and in Figs. 7, 11, and 12 significant changes consisted of distorted bone trabeculations or vestiges of lamina dura. At all roentgenographic sites mentioned above, bone cavities were exposed surgically. None of the above roentgenographic changes are in any way pathognomonic for trigeminal or atypical facial neuralgias, but ail were considered suspicious and worthy
of further exploration. When suspected areas were, in fact, found to be bone cavities, digital pressure over them would elicit characte~stic pain symptoms in most cases. Patient data and clinical results Table I shows that ten of sixteen (63 percent) trigeminal neuralgia patients were women and that, of these, ten were 50 years of age or older. Table II shows that seventeen of twenty-one (81 percent) patients with atypical facial neuralgia were women and that, of these, ten were 50 years of age or older. These sex and
302
Roberts
urd
Persorl
Oral Surg.
October,1979
Fig. 11. Trigeminal neuralgia, upper left premolar and molar regions. Two confluent cavities exist (arrows). There is also a group of random, small radiolucent spots in the premolar area(asterisk). Fig. 12. Trigeminal neuralgia, mandibular left region. Bone trabeculaeform two vertical lines from the alveolar cresttoward the mandibular canal and demarcatethe site of a nonhealedmolar socket.The bottomsof the sockets were continuous with the mandibular canal
age distributions are comparable to those reported in the literature for these disorders.” *. ’ Also, one woman with trigeminal neuralgia (Patient V. P., Table I) also had multiple sclerosis with accompanying symptoms. In the cases of trigeminal neuralgia, either the second or third division was involved; no first division cases were encountered. The pain distributions of the atypical facial neuralgias covered a broad spectrum of both trigeminal and cervical nerve territories as described by White and Sweet.’ Duration of illness prior to treatment was between 1 and approximately 49 years in eleven of the sixteen trigeminal neuralgia cases, and between 2 and 20 years in fourteen of the twenty-one atypical facial neuralgia cases. By means of the treatment described in Methods and Procedures, complete pain abatement to date has been accomplished for periods of up to 9 years in each of the cases listed in both tables. Pain-related bone cavities might be single or multiple, and occasionally they were found diffused throughout the entire jaw, unilaterally or bilaterally. The cavities always encompassed the site of a previously extracted abscessed tooth or a socket previously contaminated by debris and oral microorganisms. Should a tooth be found to be related to experienced pain in such a way that restorative dental procedures cannot remedy the situation, then its extraction is advisable and the alveolus should be examined for a minute fistula which will usually lead into one or more cavities within the spongiosa, involving one or more branches of the trigeminal nerve. As mentioned previously, a frequent phenomenon in both types of facial neuralgia was formation of small fistulas and tunnels
connecting cavities in tandem for varying distances. When arising in the cuspid or premolar areas of the upper jaw, they may progress medially, anteromedially, and inferiorly, or posteriorly and inferiorly to merge, respectively, into the premaxilla or into the posterior palatine fossa. In the former instance, the internal and external nasal branches of the infraorbital nerve may be involved. One such tunnel measured 11 mm. in an anteromedial direction. Tandem cavities were not seen in the lower jaws, where fistulous tracts from the cavities would usually extend inferiorly into the mandibular canal. In some cases in the lower jaw, sclerotic bone may obscure such a fistula penetrating the mandibular canal. In all cases involving the lower jaw, to date, portions of the mandibular canal were found to be destroyed, exposing a nerve with an obviously altered epineurium (Figs. 8 and 10). In one case, on removal of a portion of the wall of the mandibular canal, a shredded epineurium was observed (Patient J. K., Table I; also Case 5 in Case Histories). There was no morbidity or complication following the oral surgical treatment described, with the exception of variable, temporary anesthesia. In all cases, tics, spasms, and lancinating, flashing, and other varieties of pain ceased totally, and patients remained asymptomatic except for occasional recurrences of slight pain. The latter were readily treated in the same fashion as the original pain and usually abated rapidly. In some atypical facial neuralgias, excruciating migrainous headaches involving the vertex, frontal, temporal, and occipital areas were greatly diminished or ceased entirely. All edentulous patients treated for atyp-
Idiopathic
Volume 48 Number 4
trigeminal
and atypical facial
neuralgias
303
Table I. Trigeminal neuralgia case summary Duration
of Sex
Patient
Trigger zone
symptoms 5 yr.
Trigeminal nerve division(s) involved
Lower left jaw
3
Lower left third molar area
3
I yr.
Lower left molar area
3
F
3 yr.
Lower left molar area
3
55
M
13 yr.
Upper right premolar area
2
N.G.
48
F
22 mo.
Lower left third molar area
3
D.C.
28
F
5 yr.
Lower left second molar area
3
C.F.
74
F
2 mo.
N.M.
62
F
5 mo.
Upper left premolar and left second molar areas Upper left premolar area
E.S.
54
M
H.C.
35
M
G.G.
51
F
K.S.
20
M.M.
2, 3 2
C.B.
63
M
15 yr.
Upper left cuspid; lower left first and second molar areas
H.P.
44
F
I1 yr.
Lower right molar area
3
M.G.
47
F
3 yr.
Upper left lateral incisor
2
L.S.
85
M
Lower left molar area
3
E.S.
83
F
4 yr.
Upper right cuspid area
2
J.K.
45
M
2% yr.
Lower left molar areas; upper left nasolabial fold and left buccal space
Multiple sclerosis V.P.
61
F
49 yr.
Lower left jaw
3
C.F.
14
F
Lower left second molar area
3
2 mo.
ical or trigeminal neuralgia are now wearing their dentures without discomfort. Laboratory results Histologic jndings. Twenty bone-curettage biopsy specimens were taken from eight patients (five trigeminal, three atypical facial neuralgia) with similar histologic pictures in both groups. Typically, there were spicules and fragments of bone (sometimes containing marrow) surrounded by hemorrhagic areas and fields of fibrous connective tissue of varying density, often highly vascularized. Osteoblastic activity or the presence of osteoid was seen in only one of the twenty biopsy specimens. In one trigeminal neuralgia specimen, there was considerable necrosis of bone spicules, but no inflammatory infiltrate. In two specimens (one trigeminal neuralgia and one atypical facial neuralgia)
2, 3
2, 3
Date of surgery
Duration pain free
8-8-74 Intraoral 3- 12-68 Intraoral 5-28-69 Intraoral l-28-76 Intraoral 1l-l-76 Intraoral l-28-76 Intraoral 8-76 Intraoral 12- 16-76 Intraoral
33 mo.
6-17-76
11 mo.
Intraoral IO- 14-75 2-4-76 Intraoral 3-9-76 Intraoral 2-3-16 Intraoral 1-21-17 Intraoral 2-23-76 Intraoral 3-24-17 Intraoral
9- 16-76 Extraoral 12-16-76 Extraoral
9 yr. 8 yr. 16 mo. 6 mo. 16 mo. 9 mo. 5 mo.
I!4 yr. 1.5 mo. 14 mo. 15 mo. 4 mo. 15 mo. 2 mo.
8 mo. 5 mo.
the fibrous connective tissue surrounding bone spicules was infiltrated with lymphocytes. In the trigerninal neuralgia specimen, plasma cells and histiocytes were also present. Microbiologic jindings. Samples for microbial culture were taken from six trigeminal neuralgia and seven atypical facial neuralgia patients. Results are summarized in Table III. Only two organisms were identified in extraoral samplings Staphylococcus epidermidis (growth aerobic and anaerobic) and Peptococcus (growth anaerobic). In intraoral samples, in addition to the above organisms, a-hemolytic streptococci, diphtheroids, and Neisseria were also identified. The absence of o-hemolytic streptococci, diphtheroids, and Neisseria in the extraoral samples suggests that they were probable contaminants of the intraoral samples. In only one patient out of thirteen studied (Patient P. B.,
304
Roberts and Person
Oral Surg. October, 1979
Table II. Atypical facial neuralgia case summary Duration
of Patient
Sex
symptoms
Division(s) involved
R.L.
66
F
5 yr.
2
P.B.
65
F
2% yr.
2
A.U.
48
M
2% yr.
W.G.
53
F
5 yr.
2
S.C.
38
F
6 mo.
3
H.B.
38
F
20 yr.
J.J.
35
M
4 yr.
C.F.
74
F
2 mo.
W.G.
34
M
8 mo.
J.H.
31
F
2 mo.
S.N.
37
F
6 yr.
2, 3
H.S.
30
F
2 yr.
2, 3
M.L.
78
F
2 yr.
2, 3
E.L.
65
F
M.B.
55
F
E.P.
50
F
P.B.
54
F
P.S.
33
F
6 mo.
V.L.
35
F
7 yr.
N.G.
48
F
9 yr.
R.S. M.L.
62 78
M F
2 yr. 2 yr.
E.L.
65
F
M.B.
55
F
2, 3
I I yr, 8 mo. 2% yr.
11 yr.
2 2
2 3
Date of surgery
12-2-7 I Intraoral 7-6-75 Intraoral 9- 18-75 Intraoral 2- 17-77 Intraoral 3-3-76 Intraoral 12-30-75 Intraoral 3-25-76 Intraoral 12-16-76 Intraoral I l-8-76 Intraoral 12-13-76 Intraoral 12-17-77 Intraoral 9-9-76 Intraoral 5-4-76 Intraoral 5-23-76 Intraoral 6-16-76 Intraoral 12- 16-76 Intraoral 3-25-77 Intraoral 3-24-77 Intraoral 4-22-77 Intraoral 2- 15-7 1 Intraoral 12-16-76 5-4-76 Extraoral 7-22-76 Extraoral 6- 16-76 Extraoral
Duruiion puin free
5% yr. 22 “IO. 20 mo. 3 mo. 14 mo. 17 mo. 14 mo. 5 mo. 6 mo. 5 mo. 3 mo. 8 mo. I yr. I yr. 11 mo. 5 mo. 2 mo. 2 mo. I mo. 6% yr. 5 mo. 1 yr. 10 mo. 11 mo.
atypical facial neuralgia), neither staphylococcus nor was found in the samples taken from the bone cavity.
and 1 year. Oral surgery was performed at the Davis Memorial Hospital in Elkins, West Virginia. CASE 1
Case histories
Patient M. J. L., a 78-year-old edentulous white woman, was admitted to the hospital on May 13, 1976, in moderate distress.Pain had started5% yearspreviously. For the past 20 months, shehad sufferedfrom intermittent lancinating pain of the left mandible, radiating to the right mandible. Two weeks prior to her visit, the severity of paroxysms increasedmarkedly. Partial relief was obtained by sitting before a hot stove.
Peptococcus
Five cases (three atypical facial neuralgia, two idiopathic trigeminal neuralgia) will be described. Of these, four were treated by the Risdon submandibular (external) approach. All cases have been asymptomatic since treatment, for periods varying between 9 months
Idiopathic trigeminal and atypical facial neuralgias
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305
Table III. Microorganisms isolated from jawbone cavities of patients with trigeminal and atypical facial neuralgias Sampling route
Organisms reported
E.S. C.F. C.B.
Intraoral Intraoral Intraoral
cu-hemolyticstreptococcus;Staphylococcus epidermidis Staphylococcus epidermidis Staphylococcus epidermidis; a-hemolytic
H.P. M.G. V.M. C.F.
Intraoral Intraoral Extraoral Extraoral
Patient Trigeminal neuralgia
streptococcus;Peptococcus,diphtheroids a-hemolytic streptococcus Staphylococcus epidermidis Staphylococcus epidermidis Staphylococcus epidermidis
Atypical facial neuralgia
P.B. A.U. W.G. H.B. EL. M.L. E.L. M.B.
Intraoral Intraoral Intraoral Intraoral Intraoral Extraoral Extraoral Extraoral
The patient took eight Percodan tablets daily. The right nasolabial area was involved to a lesser degree. Medical history The patient had arteriosclerotic heart disease with compensated chronic heart failure. Roentgenographically, there was a sclerotic aortic shadow. A positive serologic result was reported for VDRL testing. The above conditions were considered noncontributory. Diagnosis: Atypical facial neuralgia. Intraoral roentgenograms
(not illustrated)
In the upper right canine region, an inverted, irregular, cone-shaped radiolucent area was present in proximity to the floor of the nasal cavity. In the left mandibular molar area, there was an abnormal trabecular pattern, with considerable demineralization and sparse, dense, threadlike bone ramifying throughout the medullary cavity. The boundary between the normal and abnormal spongiosa was demarcated as by a vertical line from the inferior border of the mandible to the crest of the alveolar ridge. Treatment The left face and neck were prepared with Betadine Prep and Scrub, and specimens for microbiologic culture of the skin were taken. The mandible was exposed through a submandibular skin incision and decorticated in the second and third molar area by means of a bur and bone drill. This procedure revealed an underlying cavity in which a segment of the bony mandibular canal had been destroyed for a distance of approximately 1.5 cm. The mandibular nerve coursed freely through this space, which was unlined, and whose walls consisted solely of eroded bone. The nerve was slightly discolored, being of a light brown hue. The cavity wall had the consistency of clumps of dried sugar and crumbled and disintegrated as the curette blade cut through it. There was profuse hemorrhage during curettage. Superficial and deep specimens for microbiologic cultures were taken, including portions of necrotic-appearing bone in close proximity to the mandibular
a-hemolytic streptococcus;Neisseria; diphtheroids ry-hemolytic streptococcus;Staphylococcus epidermidis Staphylococcus epidermidis Staphylococcus epidermidis
a-hemolytic streptococcus;Staphylococcus epidermidis Staphylococcus epidermidis
Peptococcus Staphylococcus epidermidis
nerve. External skin cultures were negative aerobically and anaerobically, while from the cavity interior Staphylococcus epidermidis was cultured aerobically and anaerobically. The bone cavity was thoroughly curetted, and irrigated and packed as described on p. 299, and the wound was closed in layers. On completion of this procedure, the right maxilla (canine area) was treated via an intraoral approach. Recovery from the combined procedures was uneventful, and there has been no pain since treatment. The patient now wears and uses her upper and lower full dentures. CASE 2 Patient M. E. B., a 45year-old edentulous white woman, was admitted to the hospital on June 16, 1976, complaining of “sharp shooting” pain in the right mandible (and on one occasion on the left side) of 6 weeks’ duration. Eleven years previously she had experienced repeated episodes of pain and facial swelling from abscessed teeth in the involved area, which were extracted. Since that time, she had had an almost constant, intractable, dull ache, with irregular periods of remission. The patient was in moderate distress and apprehensive. Medical history The medical history was essentially negative. The patient was not taking any medications. Laboratory work-up results were within normal ranges. Diagnosis: Atypical facial neuralgia. Intraoral roentgenograms Remnants of lamina dura were evident in the mandibular right molar area (up arrows), with suggestive radiolucencies (down arrows) below the alveolar ridge (Fig. 7). Treatment On June 17, 1976, via the external submandibular approach, the bone of the right lower molar area (lateral to the mandibular nerve) was decorticated with a bur and bone drill.
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This exposed two adjacent but separate cavities located immediately above the mandibular canal (Fig. 8), whose superior wall had been completely destroyed. The mandibular nerve was exposed for a length of approximately 2 cm, and was reddish brown in color. The cavity walls were not lined and were of the same necrotic-like, crumbling consistency described in Case 1. This condition extended to the crest of the alveolar ridge. Superficial and deep bone specimens were taken for microbial culture, which was positive for Sraphy/ococcus epidermidis. Following curettage, the wound was irrigated, packed as described on p. 299, and closed in layers. The bone of the left mandibular distal molar area was treated in similar fashion via an intraoral approach. Healing was uneventful, and the patient has been free from pain since treatment. The patient is now wearing and using her full upper and lower dentures. CASE 3 In 1958, following extraction of abcessed teeth, Patient E. V. L., a 65-year-old white woman, noticed the onset of pulsating and “shooting pain” in the lower left jaw. She was treated by an oral surgeon who “cleaned out the bone,” and improvement resulted. The pain had intermittently returned and disappeared since that time. In June, 1974, the left mandibular anterior teeth were removed because of roentgenongraphic findings of bone involvement in the area. There was some improvement in comfort. In December, 1976, the pain became progressively worse in the left anterior mandible, with flashing radiations to the left ear, mental, temporal, and vertex regions. The patient also complained of boring and burning pain in the right mandibular molar area, but of lesser intensity than on the left side. Digital pressure on the gingiva or cheek of the involved sides precipitated the pain. The patient was hospitalized for treatment in May, 1976. The left anterior jaw was successfully treated by an intraoral procedure via a mucoperiosteal flap. However, intraoral treatment of the lower right molar area was unsuccessful. The patient. although relieved of her original complaint on the left side, was now greatly concerned about an increasing intensity of the boring and burning pain in the right lower jaw. On July 21, 1976, she was readmitted to the Davis Memorial Hospital in Elkins, West Virginia for treatment of the right side via a Risdon extraoral procedure. Medical history The patient had a history of hypertensive cardiovascular disease with angina1 syndrome and was taking nitroglycerin, Petitrate, and Librax. Diagnosis: Atypical facial neuralgia. Intraoral roentgenograms
(not illustrated)
There was a large area of distorted bone trabeculations in the right mandibular molar and premolar regions, with striae of sclerotic bone ramifying throughout the area against a translucent background. In the mandibular left cuspid area, an opacity was noted. Treatment The right side of the face and neck was prepared with Betadine Scrub and Prep. The skin was excised 2 mm. below the inferior border of the mandible and retracted. The cortical
Oral Surg. October, 1979 bone of the mandible overlying the premolar and molar areas was removed with buts and bone drill. A small cavity, approximately 0.5 cm. in diameter, was exposed in the first molar area. This cavity communicated with a larger cavity, approximately 1 cm. in diameter, located anteriorly in the premolar area. The walls of the cavities were soft and necrotic. They were thoroughly curetted. The mandibular canal had been totally destroyed in the involved areas, and the mandibular nerve was red in color. Fragments of medullary bone and fluids were taken for microbial culture, which was positive for Peptococcus. Following curettage, the bone cavity was irrigated with sterile water, packed, and closed by layers, as previously described. Healing was uneventful, and there has been no recurrence of pain. CASE 4 Patient V. P., a distraught, 67-year-old edentulous white woman, was seen in August, 1976, complaining of “sharp, shooting” pain in the left posterior mandible. This pain had started 1 year earlier. There were alternating remissions and exacerbations for weeks or months at a time, until 2 weeks prior to examination, when paroxysms of pain became more acute and repetitive. The pain occurred for 5 minutes, remitting for about 1 hour, and then recurring at precisely the same area. It was more intense at night. Talking, eating, face washing, and tactile stimulation triggered the attacks. A careful history revealed that the patient had had abscessed teeth removed from the left lower jaw when she was a young woman, and since that time she had suffered from pain affecting the distribution of the third division on the involved side. When seen, she was taking 50 mg. of Talwin for relief of pain, as required. She was admitted to the hospital on Sept. 15, 1976. Medical history Neurologic findings were normal, except for those associated with multiple sclerosis. There was no sensory deficit in the face to pin prick or light touch, and the cornea1 reflexes were equal. Light touch on the skin of the left face triggered the onset of pain. Laboratory work-up was otherwise within normal limits. Diagnosis: Idiopathic trigeminal neuralgia. intraoral roentgenograms In the left lower molar region there was an irregularly shaped area of trabecular distortion measuring approximately 8 mm. in width and 20 mm. in height (Fig. 9). The area was located above the mandibular canal and traversed by widely dispersed and irregular sclerotic striae. Treatment The left side of the face and neck was prepared with Betadine Prep and Scrub in the usual manner. A 5 cm. incision was made 2 mm. below the inferior border of the mandible, extending from the angle of the jaw to the mental region, and the tissues were retracted. The mandibular cortex in the molar area was removed in toto (2 by 1.5 cm.) and placed in sterile distilled water. The underlying medullary bone appeared extremely porous. It was soft and easily removed with the curette, which left behind a cavity of approximately 1.5 by 2.0 cm. (Fig. 10). The mandibular canal had been destroyed in the involved area. Specimens for cultures were taken, in-
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chiding fragments of necrotic-appearing bone. Cultures were positive for Staphylococcus epidermidis. The mandibular nerve appeared normal, except for reddish brown discoloration, and was not traumatized during curettage of the cavity. Irrigation was performed with approximately 60 ml. of sterile water, and the wound was packed and closed as described in the preceding cases. The patient has been without pain since this operation. CASE 5
When first seen, Patient J. K., a 4%year-old edentulous white man, appeared emaciated, pale, depressed, and extremely apprehensive. He complained of daily, severe, paroxysmal, “electric-like” pain shocks that had begun 2% years previously and in recent weeks had become more intense. The paroxysms occurred spontaneously or were initiated by swallowing, shaving, washing the face, and bending forward. Cold air and tongue contact with the buccal mucosa also triggered the attacks. The latter were preceded by buming and tingling in the left upper lip, which radiated to the left temporal region and vertex and thence anteriorly to the left nasolabial fold and upward through the nasal cavity and left eye, with resulting lacrimation. The patient also complained of severe pain in the left mandible, with lancinating pains “jumping” from the nasolabial fold inferiorly to the mental nerve region. The patient had been previously treated by a physician who injected cortisone into the left temporomandibular joint, with no relief. At a nearby medical center a diagnosis of idiopathic trigeminal neuralgia was made. The patient was given Tegretol, which was discontinued because of intolerance. Later, at the neurosurgical service of the same center, the diagnosis of trigeminal neuralgia was not confirmed. However, when the patient was seen by us, his symptoms were those of idiopathic trigeminal neuralgia. On the morning of March 23, 1977, the patient was admitted to the Davis Memorial Hospital in Elkins, West Virginia. Medical
history
The patient had lost 57 pounds since inception of the present illness. He had occasional severe gastric pains for which no basis could be found. He had suffered a severe injury to the occiput in 1954. He had had no other illnesses or seizures. Valium, 5 mg., and Donnatal were being taken three times daily. The patient’s teeth had been removed 25 years previously, and he stated that at the time many of them were abscessed. The results of the current laboratory work-up were within normal limits, and a chest plate was normal. Diagnosis: Idiopathic trigeminal neuralgia. Intraoral
roentgenograms
In the maxillary left premolar area there was a large circular radiolucency, within which were several small, scattered, darker radiolucencies. The area was anterior to the antrum and 13 mm. above the crest of the alveolar ridge (Fig. 11). In the mandibular left molar area bone trabeculae formed two vertical lines extending from the crest of the alveolar ridge and “fanning out” inferiorly as they approached the mandibular canal, indicating the vestiges of a tooth socket. Superiorly, there was an admixture of radiolucencies and randomly oriented dense or sclerotic bone striations, while in-
Fig. 13. Trigeminal neuralgia. Photograph of maxillary left premolar and molar areas corresponding to the radiolucent areas shown in Fig. I I The anterior circular radiolucent area of Fig. II is represented here by the arrow, and its distal extensions to the tuberosity region are evident. The anteriormost cavity (urrow) existed as such when the area was first exposed. Its distal extension consisted of a soft, necrotic type of very vascular bone which disintegrated during curettage, resulting in the cavity extensions seen in the photograph.
feriorly no bone trabeculae were seen except for a mild opacity. The bottom of the tooth sockets continued into what had been the mandibular canal (Fig. 12). Treatment
The maxillary left premolar area was exposed via an intraoral approach following induction of oroendotracheal general anesthesia. Two confluent cavities were discovered in the premolar and molar areas. The bone cavities were curetted methodically until all soft material was removed and solid bone was reached. This produced a 2.5 cm. cavity (Fig. 13) extending in an anterior, medial, and superior direction. The maxillary tuberosity was also involved. In the bone of the lower left molar area, a cavity approximately 2 cm. in anteroposterior length and 3 cm. in a superior-inferior direction was exposed. Curettage was performed methodically, during which a portion of the wall of the mandibular canal was carefully removed, disclosing a shredded epineurium of reddish brown color. Following irrigation and packing, the mucoperiosteal flaps were sutured. The patient was discharged improved on the third postoperative day. A stormy postoperative course ensued. Lancinating pain was experienced, involving the maxillary left promolar area and radiating to the entire left side of the head and neck. Two extreme episodes were repotted as “explosions” within the head, during which his head forcefully turned to the right side and his feet flew into the air. An antibiotic, Erythrocin, and Demerol for pain, were prescribed, but the pain failed to abate. On the eighth postoperative day, the patient visited the office and was severely depressed and despondent. An attempt was made to locate possibly undetected
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in\,ljlved areas, and irrigations of the operated areas with hydrogen peroxide were also begun. Following 2 weeks of dally irrigations with hydrogen peroxide, all painful areas improved dramatically, except for one from which sharp shooting pains emanated. This area was located in the maxillary left premolar region, within the fascial and muscle spaces of the nasolabial area. The infraorbital nerve was locally anesthetized and, through a small incision in the nasolabial mucobuccal fold, the fascial spaces in the premolar area were irrigated with 10 ml. of hydrogen peroxide. This produced a sudden and dramatic remission of the remaining pain symptoms. The procedure was repeated on the following day, and on the third day the area was irrigated with 2 ml. of sterile water in which 500 mg. of chlommycetin was dissolved. The pains virtually ceased, except for a small occasional twinge of lancinating pain radiating to the upper left lip. Four weeks later the above procedure was repeated through an intraoral incision of the mucobuccal fold, with delivery of 250 mg. of chloromycetin in solution to the site. Since that time, all pains have ceased totally. The patient speaks now of a slight tenderness in the area, believed to be associated with the healing process. The patient regained 26 pounds in weight and re-
turned to work. At presentall trigeminal symptomsare gone, and his occipital headaches have ceased completely. DISCUSSION
The observations reported in this article support the suggestion that dental and oral pathosis may be important contributing factors in the onset and development of both idiopathic trigeminal neuralgia and atypical facial neuralgia. This contention is supported by (1) disappearance of pain following curettage and antibiotic treatment of the bone cavities at the sites of tooth extractions in afflicted persons and (2) the preliminary microbiologic and histopathologic observations consisting of positive identifications of anerobic staphylococci or Peptococci in thirteen of fifteen cavity samplings. The histopathologic observations of a typical curettage biopsy specimen showed bone spicules and fragments, occasionally necrotic, surrounded by hemorrhagic areas. Fibrous connective tissue of varying density was usually highly vascularized, and often infiltrated with chronic inflammatory cells. The histopathologic observations are similar to those seen in impaired healing of bone but are also perplexing because of the absence of more marked cellular inflammatory changes, such as might be expected in the face of anaerobic bone infections. Strongest support for the belief that the pain of trigeminal and atypical facial neuralgias may be of dental inception comes from the clinical observations and results. The dramatic pain remissions resulting from curettage and antibiotic treatment of the bone cavities support a cause-and-effect relationship between the cavities and the pain. Nevertheless, it must be kept in mind that both deliberate and inadvertent instrumentation of the trigeminal nerve during surgical procedures
Oral Surg. October, I979
produces pain remissions for varying time periods.‘, ’ Although such procedures usually involve more central trigeminal nerve components, it may be that inevitable traumatizations of small peripheral and terminal nerve branches during the oral surgical procedures described here produce similar pain remissions. The present study, together with the work reported by Ratner. Person, and their co-workers,3-6 make it mandatory, we believe, that serious consideration and study be given to the possibility that trigeminal and atypical facial neuralgias may be disorders largely of dental origin. In addition, the present study and the work of the above-mentioned investigators provide, for the first time, a new approach to treatment and management of these afflictions. This may obviate the need for central neurosurgical procedures or the use of medications which interfere with nerve function and often bring with them the threat of serious side effects. Thanks are expressed to Dr. Gerald Shklar, Brackett Pmfessor of Oral Pathology and Oral Medicine, Harvard School of Dental Medicine, Boston, Massachusetts, for his interest and for his advice and assistance with the histopathologic examination of biopsy specimens; Dr. N. B. Chandran, anesthesiologist, Davis Memorial Hospital, Elkins. West Virginia, for skillful professional services and consultations: Dr. James G. Thomas, Professor, Department of Oral Diagnosis and Radiology, West Virginia University Medical Center, Morgantown, West Virginia, for his interest and helpful discussions; and Ms. Beatrice Quigley, Librarian, Veterans Administration Hospital, Clarksburg, West Virginia, for valuable assistance in literature research. REFERENCES
I. White, J. C.. and Sweet, W. S.: Pain and the Neurosurgeon:A Forty Year Experience, Springfield, Ill.. 1969,CharlesC Thomas Publisher, chaps. V. VI, and VIII. 2. Stookey. B., and Ransohoff,J.: Trigeminal Neuralgia: Its History and Treatment, Springfield, Ill., 1959, Charles C Thomas Publisher. 3. Ratner. E. J.. Person, P., and Kleinman, D. J.: Oral Pathology and Trigeminal Neuralgia, I. Clinical Experiences, J. Dent. Res. 55B: 299, 1976. 4. Shklar, G., Person, P., and Ratner, E. J.: Oral Pathology and
Trigeminal Neuralgia, II. Histopathologic Observations.J. Dent. Res. 55B: 299. 1976. 5. Socransky, S. S., Stone, C., Ratner, E., et al.: Oral Pathology and Trigeminal Neuralgia, III. Microbiologic Examination, J. Dent. Res. 55B: 300, 1976. 6. Ratner, E. J.. Person,P., and Kleinman, D. J.: Jaw Bone Cavities and Trigeminal and Atypical Facial Neuralgias, ORAL SURG. 48: 3-20, 1979. 7. Harris, W.: Neuritis and Neuralgia, London, 1926, Oxford Uni-
versity Press, pp. 163-165. 8. Kin&r Wilson: S. A., and Bruce, A. N.: Neurology, Baltimore,
1955. Williams & Wilkins Comuanv. D. 405. 9. Rothman, K. J., andMonson, R.‘R.:‘I$idemiology of Trigeminal
Neuralgia, J. Chron. Dis. 26: 3-12, 1973. Reprint requests to.
Dr. Alexander M. Roberts 704 Union National Center West Clarksburg, W. Va. 26301