Is atypical odontalgia a psychological problem?

oral medicine Editor. H. DEAN MILLARD,

DDS, MS

1205 Glen Lever1 Road Ann Arbor, Michigan 48103

Is atypical odontalgia a psychological problem? Steven B. GrafS-Radford, DDS,” and William K. Solberg, DDS, MS,’ Los Angeles, Calif SECTION

Ot. OROtACIAL

Dtrl’ARTMENT

PAIN,

UCLA

OF ANESTHESIOLOGY

SCHO’OL CEDARS-SINAI

OF DENTISTRY MEDICAL

AND

THE

PAlh

CENTER,

CENTkR

Several authors have asserted that psychological factors are the underlying cause of atypical odontalgia. However, objective evidence is lacking to support this claim. In this study, the Minnesota Multiphasic Personality Inventory was used to assess psychological functioning of an atypical odontalgia population. Means of the standard scores for each Minnesota Multiphasic Personality Inventory scale were within normal ranges. Standard scores for atypical odontalgia profiles compared with standard scores for a chronic: headache group (matched for age, sex, and chronicity) were similar and scales for both groups were within normal ranges. These findings fail to support psychological dysfunction as a primary condition associated with patients suffering from atypical odontalgia. IOR\I.

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St RG ()R.AL

IUED

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P.%TtiOL

1993;75:579..82)

odontalgia (AO) is a diagnosis of exclusion’.’ and is therefore frequently associated with another ill-defined pain syndrome, atypical facial pain (AFP).’ Unfortunately these terms constitute a “wastebasket” for all unexplainable pain in the fasce. Although similar to AFP, A0 is better defined anatomically. 4.6. 7 Several causal theories to explain A0 have been proposed, but little evidence has been found to support these theories. Those problems most commonly described as causal for A0 are: (1) psychological disorders; (2) deafferentation pain; and (3) vascular pain. Of these theories, psychological dysfunction, usually depression, is the most commonly mentioned.‘. ‘-“’ typical

“Section of Orofacial Pain. UCLA School of Dentistry. Pain Center. Department of Anesthesiology. Cedars-Sinai Center. “Section of Orofacial Pain, UCLA School of Dentistry. 1993 by Mosby Year Book, Inc. Copyright 0OY.b4220/9?/$1.00 + .I0 7/13/44211

and The Medical

PSYCHOLOGICAL

DISORDERS

For decades, emotional factors have been claimed to be a cause of chronic facial pain.6,“-” In 1932, Wilson’” reported seven cases of AFP in which he felt that “emotional disturbance and the change in the behavior are out of proportion to the symptoms.” Unfortunately, he did not use any objective means of measuring psychopathologic factors. Engel’” in 195 I described AFP as a hysterical conversion symptom and was quite emphatic that the emotional disturbance was the cause and not the result of the pain. LesseX in 1956 described 18 patients with AFP and eight with primary pain in the teeth (AO). He concluded that the pain complaints were “entirely psychogenic in origin or represented a gross overreaction to a very minor organic deficit which had long since been corrected.” Webb and Lascelles” evaluated depression and facial pain in 1962. They observed a favorable response to antidepressants in an uncontrolled trial. Lascelle@ later completed a controlled study that assessed the effects of treatment 579

with phenelLine versus a placebo. He found that the treated 4FP patients were more severely depressed than a depressed group free of pain or :I group without either depression or pain. These results are of questionable validity because of the choice of statistical methods and ;I lack of objective means of assessment. Smith et al.” in 1969 were the first to use objective tests to assess psychological functioning in persons with AFP. They obtained valid Minnesota Multiphasic Personality Inventory (MMPI) results in 29 of the 31 subjects and compared these data with 50,000 general medical outpatients of the Mayo Clinic. The authors concluded that they saw no ‘-typical MMPI profile” for the AFP patients. When these two groups were compared, elevations (T score >70) in MMPI scales were only IO% more frequent among AFP patients. Considering this small diEerence, the implication of a psychosomatic cause in AFP patients is premature. Lesse”’ made the argument for :I “masked depressive syndrome” as the primary cause of AFP. No ohjective evidence to support the hypotheses was provided, and it is noted that the author relied heavily on the exclusion of organic pathologic factors as the criterion for making the diagnosis. Harris”’ in 1974 was the first to describe ;I dental pain syndrome that he proposed ah being directly linked to a psychological disturbance. He termed this oral pain as “idiopathic periodontalgia.” Harris maintained that a carefully taken history would reveal significant emotional problems in some patients. Later. in 1978. Recs and Harris’ chose another name for the disorder, “atypical odontalgia.” The authors concluded that A0 was a localized form of AFP. In this study, clinical depression was diagnosed in 66% (n = 44 of 66) of patients with the use of intervie\+ methods. This left 34’“; with no established link to clinical depression. Rees and Harris concluded that .A0 was a local disease entity, but one accompanied bq an underlying disorder of afTect.

Remick et ~(1.~ dehned AFP as a nonanatomic. nondermatomal orofacial pain having a duration 01 Ivngcr than 0 months. In their study. ;I specific ps)chiatric disorder \+as diagnosed in 68”; (n = 16 of 6X ) of patients on the basi\ of the Diagnostic and Statist1ca1Manual ot’ Mental Disorders III criteria. Remich. Cl ;I/. suggested that the diagnosis of depreaion ( i 3.2”~. n = I() ijt’68) \vas not as prevalent ;I\ in other studies bccausc they used a more operationall) dc. lined classilication system than previous :Iuthors. I!vcr5olc ct 21 ” jtudicd patients with the diagnosis OI .AFP. m>of:is&l pain. and TMJ internal derangcmerit using the VIMPI. Mean profiles I‘rotn all group\ \Lcrc unelevatecl CT ~chological dysfunction i\ ,I m;t)ol factor that C;IUWS AFP. Although changes in psychological functioning are common in A0 and AFP. there is insufticicnt evidence to support the claim that unique psychological f;1ctor> are the primar:\ CLILW.This study was conducted to better identify the 51 MPI profile seen in the A0 group and to determine an\ unique psychological features Ihut ~.ould qlarate 40 from another chronic pain problem. chronic myot‘ascial pain. METHODS

The MMPI teas administered to 35 consecutive patient5 rcfcrred to the UCLA Clinical Research (‘enter ulth ;I complaint of facial pain. Of these 25 sukjccts. I9 cases of A0 were diagnosed with the use of the criteria modified from the International Association for the Study of Pain Subcommittee on Taxonom\ .lh The criteria are summarized in Table I, lJnher1yin.g organic pathology was ruled out with medical and dental histories and examination of the involved teeth through radiographs, transillumination. thermal and electrical stimulation to the teeth. and percussion and periodontal probing. Myofascial trigger points Lveresystematically palpated to rule out pain from the muscles. The temporornandibular joint and cervical spine were evaluated to exclude these arcas as a source of pain. Myofascial headache was diagnosed \\ith the aid of medical history and evaluation and neurologic evaluation; the most important criteria W;I~ the reproduction of the patient’s headache pain with palpation of trigger points. Confirmation of the diagnosis was made through spray and stretch and triggerpoint injection techniques with at least ;I SO’/; reduction in pain required for inclusion in the heudachc group. After diagnosis. the A0 subjects

GrafS- Radford and Solberg

Out. MEDICINE ORAL PATHOLOGY Volume 75. Number 5

ORAL SLRGEKY

581

MinnesotaMultiphasic PersonalityInventory (MMPI) 120 110

.---a

HA

4

loogo8070 50 60-

4

40-

0

.r 30I L

I F

I K 1234

6

7

8

9

S’i 10

Fig. 1. MMPI Scores of atypical odontalgia and headache for scales L, F, K and 1 through 10. T scores >70 are considered elevated. Solid line = atypical odontalgia; dotted line = headache. No statistical differencesbetween the mean values were found for atypical odontalgia and headache.

Table II. Frequency of MMPI scale elevations in A0 and HA patients: Group comparisons M‘MPI I 2 3 4 6 7 8 9 0 1-3

A0 (n = 1917 i%i

HA (n = 19) l%i

31.6 42. I 31.6 5.3 5.3 21.1 5.3 S.3 5.3 63.2

26.3 36.8 41.4 15.8 15.8 26.3 I .5.x 0.0 5.3 51.9

were matched for age, sex, and duration of pain with a headache population seen at the UCLA Pain Management Center. Mean demographic data for the A0 and Headache (HA) groups are summarized in Fig. 1. To help confirm that the A0 and HA groups were indeed not the same clinical entity, the McGill Pain Questionnaire was administered at the initial appointment and compared with the use of paired t tests. RESULTS The mean MMPI profiles of the 19 A0 patients were essentially unelevated (Table II). The compara-

Table III. Mean demographic data for A0 and HA subjects A0 (n = iO)--MEAN (S.E.) :

Age Duration of pain Men Women

45.68 (3.19) 25.47 (5.02) 4 = 21.05% I5 = 78.9%

HA in = 191 MEA ,v (S.E.)

.-

45.89 (3.19) years 25.1 (5.14) months 4 = 21.05% I5 = 78.95%)

S.E. = standard error

ble profiles of the HA group were similarly within normal ranges. Normal is defined as a T score below 70. T tests for each of the mean MMPI scale scores ( I - 10 excluding 5) failed to show significant differences between the two groups (Table III). The frequency of patients in each diagnostic category with scores elevated above 70 is summarized in Table II. Scale 2 (depression) was the most commonly elevated scale in the A0 group with 42% of this scale being elevated. In the HA group, scale 3 was the second most frequent elevated scale (36.8%) and scale 2 in the HA group was the third most frequent scale to be elevated with 3 1.6% above the standard score of 70. Smith et al.” report scale 2 elevations in 42% of 50,000 general medical outpatients. This supports the opinion that depression is not the cause of AO.

DISCUSSION

The tindings in this study fail to support the popular notion that psychological dysfunction is the cause of 40. One could argue that the A0 and HA groups in this study were the same clinical entity because ot the similarities in the MMPI results (Fig. 1). To test this possibility, the McGill Pain Questionnaire’” M’;I~ used to compare word descriptors between the two groups. T tests for the sensor!. ult‘ective, evaluative. and miscellaneous subgroups of the questionnaire revealed significant differences between groups in scnsory subgroups 4 and I0 as well as the evaluative suhgroup 16. These findings support that A0 and HA are clinically different despite having similar MMPI proliles. k’ordyce” has pointed out that too often a paticnt”s pain experiences are labeled “psychogenic pain” Mhen repeated failures with the biomedical model result in the persistence of pain.“’ He suggests it is the medical system that has not provided adequate treatment and that assuming that it is the patient’s fault is incorrect. Fordyce asserts that the termp,s)“‘hogenic, pin may he interpreted in several ways. Some clinicians consider pain to be psychogenic when the pain behavior is overrepresented in tams of evident pathologic factor\. A more stringent definition of psychogenic pain is one that requires emotional and ps) chological factors to bc the primary cause of the pain complaint. The latter alternative requires positive criteria for classilication and maq hc divided into I’ou~ groups: ( 1) somatic delusions. (2) homatizltion disorder, (3) conversion. (4) depression. Fordyce points out that the basis 01‘ the psychogenic diagnosis is ;L philosophical one. Typical and characteristic psychological profiles arc evident in chronic pain regardless of the pathologq.” “ Whether this characteristic protile is premorhid has yet to he determined. In summary. we conclude that psychological functioning among an A0 population does not differ from a matched chronic pain group diagnosed with tnyofascial headaches. Observed changes in the psychological functioning in A0 patients ma!. he related to manifestations of pain common to many chronic medical disorders. The findings of this study direct the clinician away from implicating psychological factors as the cause of AO.

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