- Email: [email protected]
The spatial distribution, intensity and unpleasantness of acute dental pain
363
Purn, 20 (1984) 363-370 Elsevier
PA1 00699
The Spatial Distribution, Intensity and Unpleasantness of Acute Dental Pain Y. Sharav, E. Leviner, A. Tzukert
and P.A. McGrath
’
Department of Oral Diagnosis, Oral Medicine and Radiology, School of Dental Medicine, The Hebrew University - Hadassah, Jerusalem (Israel) (Received
9 May 1984, accepted
4 July 1984)
Summary The distribution, intensity and unpleasantness of acute dental pain were studied in 196 patients. Dental pain was classified by source according to 7 anatomical sites: dentinal, pulpal, pulpal and periapical, periapical, pericoronal, papillar, and periodontal. The distribution of dental pain was classified by the frequency of pain spread throughout the sample, by the extent of pain spread for a particular pain source, that is, the number of vectors of spread, and by the pain reference locations in the face and head. Pain-intensity and pain-unpleasantness were assessed on Visual Analogue Scales. The frequency and extent of pain spread varied as a function of source. However, specific patterns of pain spread were not associated with particular pain sources. There was considerable overlap in patterns of spread between maxillary and mandibular pain sources. The frequency and extent of pain spread was correlated positively with both pain intensity and pain unpleasantness. The correlation between pain ratings and pain spread may be attributed to central mechanisms and interactions between trigeminothalamic neurons. Spatial overlap of pain from maxillary and mandibular pain sources may be due to the large receptive fields of wide dynamic range neurons, that can extend beyond one trigeminal division. These observations indicate that the spatial distribution of acute dental pain is not sufficient as a diagnostic tool for indentifying pain source.
’ Present address: University gramme, Children’s Hospital, 1 B8, Canada. 0304-3959/84/$03.00
of Western Ontario, Department of Paediatrics, Paediatric and Pain Research Unit, Department of Oral Biology, London,
0 1984 Elsevier Science Publishers
B.V.
Pain ProOnt. N6B
364
Introduction Although acute oral pain originates from many oral structures, most pain originates in the teeth and in the immediate surrounding structures. The pain is primarily the result of inflammation that is confined to a relatively small area, such as the tooth pulp 1131. Much of our knowledge for how pain spreads in the face is derived from studies of experimentally induced pain [2,9,16], in which the patterns of pain spread are fairly consistent. However, previous trauma, pain intensity. and pain duration may alter the pattern of pain spread and subsequently the site of pain [2,8,9]. Also, the pain source, that is, the anatomical site in the oral cavity from which pain originates may affect the extent and distribution of pain spread. For example, dental pain originating from the tooth pulp is poorly localized [4,10,17] and may be considered to spread to adjacent sites more readily [3,5] white pain originating from the periodontal tissue, that surrounds the teeth, is well localized [I] and may therefore be assumed to spread less. Recently, the spatial distribution of pain has been proposed as a possible diagnostic tool for chronic pain [ 151. The purpose of our study was to investigate the pattern of pain spread for acute dental pain in order to evaluate the utility of pain spread as a diagnostic tool. The following questions were addressed: (1) Is there an association between the frequency of pain spread, that is, number of occurrences, and pain source? (2) Is there an association between the extent of pain spread, that is, the number of vectors of spread per occurrence, and pain source? (3) Is there an association between the distribution of pain spread, that is, the pain reference location and pain source? (4) Is there an association between the pattern of pain spread and the intensity and/or unpleasantness of the pain?
Methods One hundred and ninety-six patients, who presented to the Dental Clinic with acute dental pain, participated in the study. Mean patient age was 26.0 + 9.0 years; 82 (42%) were men; and 114 (58%) were women. Patients had an average of 11.6 f 3.3 years of formal education. All patients consented to be in the research study. Each patient was interviewed about several characteristics of his/her pain in order to determine the pain source, pain distribution, and the intensity and unpleasantness of the pain sensation. Pain source
Patients were divided into 7 diagnostic categories according to the intraoral source of their pain 1131: (1) Dentinal - in which pain was due to stimulation of dentine, such as that caused by caries or defective restorations. Pain was not spontaneous, it was evoked principally by heat, cold, and sweet foods. When evoked. pain subsided immediately with no overshoot. The pulp was intact and the tooth was not sensitive to percussion. (2) Pulpal - in which pain was associated with acute
365
pulpitis. The pain was spontaneous, and exacerbated by heat and cold, with an overshoot of more than 30 sec. The tooth was not sensitive to percussion. (3) Pulpal and periapical - in which the pain had similar characteristics to pulpal pain, but in which the tooth was also sensitive to percussion. (4) Periapical - in which pain was associated with an acute inflammatory process of the periapical tissue. The tooth was not sensitive to heat and cold, but was very sensitive to pressure and percussion. (5) Pericoronal - in which pain was associated with an acute inflammatory process of the gingiva overlaying a partially erupted lower molar. The pain was spontaneous and was exacerbated by pressure to the area. (6) Papillar - in which pain was associated with an acute inflammatory process of a gingival papilla. Pain was either spontaneous or was evoked by food impaction and pressure to the area. (7) Periodontal in which pain was associated with an acute lateral periodontal abscess. The pain was spontaneous, and exacerbated by pressure to the area and by percussion applied to the tooth. The pain was not evoked by heat or cold. Patients were excluded from the study if they had more than one pain source, for example, dentinal and papillar. Pain spread Patients pointed to any painful areas. Seven locations were then categorized: (1) maxillary region; (2) mandibular region; (3) cheek; (4) angle of mandible; (5) ear; (6) temple; and (7) general orbital region. If the pain was localized to a small area (1 or 2 teeth) at the pain source, then there was no pain spread. When pain spread from a source to one of the 7 reference areas, the spread was defined as a vector. No distinction was made as to whether the pain was referred or radiating. Although a patient could have only one pain source, he/she could have several different vectors. Pain intensity and unpleasantness The patients used a 150 mm visual analogue scale to rate the intensity and unpleasantness of their dental pain. Intensity was defined as the strength of the pain; unpleasantness was defined as the uncomfortable, bothersome quality of the pain [12]. Addirional pain d~~ensians Pain was described also according to whether it was: (1) external or internal; (2) the time of day at which it was maximal {morning, afternoon, night or during meals); and (3) spontaneous or evoked.
Results Pain source The distribution of the 196 patients according to the source of their acute dental pain is listed in Table I. Pain sources are equally distributed between upper and lower jaws and between sexes, except for pain of pericoronal origin. Pain unpleasantness is rated consistently higher than pain intensity. Pain intensity and pain unpleasantness are significantly correlated (r = 0.60; P < 0.~1).
TABLE
I
PERCENTAGE
OF PATIENTS
Source
N
ACCORDING
Mean age+ SD.
TO PAIN SOURCE Men
Women
Maxillary
Mandibular
(years) Denlinal
43
25+
42
S8
Pulpal Pulpal +
33
28klO
42
58
51 45
49 55
periapical Periapieal Pericoronai
33 51 16
27+10 26iIO 23+ 4
48 43 19
52 57 81
54 57 0
Papillar Periodontal
11 9
26If- 5 31+12
45 44
55 56
45 56
46 43 100 55 44
26i_
42
sx -
40
60
196
Total
I
9
--___
Puin spread The frequency of pain spread, the percentage of occurrences across patients, and the extent of pain spread, the mean number of vectors of spread, are listed in Table II as a function of pain source. As shown, both the frequency and extent of spread are associated with pain source, with minimal spread for pain of papillar origin and maximal spread for pain of pericoronal origin. Mean intensity ratings for each pain source are also listed in Table II. Intensity ratings were correlated positively with pain spread, as shown in Fig. 1. The mean intensity for the pain sources that did not spread (61.3 f 23) was significantly lower than the mean intensity (74.4 & 21) for sources that did spread (P -c0.001). The distribution of pain reference locations from maxillary and mandibular sources is listed in Table III. Although the distribution of pain reference locations from maxillary teeth differs from those of mandibular teeth (P < O.Ol), there is considerable overlap in pain reference locations for maxillary and mandibular sources, as shown in Fig. 2. There is no difference in pain intensity between pain
TABLE
II
FREQUENCY
AND EXTENT
OF PAIN SPREAD
Svurce
N
Frequency
Extent of spread ’
Pain intensity
Papillar Dentinal Periodontal Periapical
11 43 9 51
27 30 44 65
0.27 0.44 0.89
I .h3
56 58 66 71
Pulp + periapical Pulpal Pericoronal
33 33 16
61 73 87
1.70 2.18 2.25
76 76 69
of spread ’
’ Percentage of patients who had at least 1 vector of pain spread. h Mean number of vectors of pain spread.
367 TABLE
III
DISTRIBUTION Pain reference
1. 2. 3. 4.
OF PAIN SPREAD area
Number
Mandibular region Maxillary region Ear Cheek
5. Angle of mandible
6. Temple 7. Orbital region Total a Pain distribution
INTO THE VARIOUS
of vectors (%)
Maxillary
AREAS
teeth a
IN THE FACE AND
Mandibular
(55)
(56)
55 (19.9) 54 (19.6) 43 (15.6) 39 (14.1) 38 (13.8) 26 (9.4) 21 (7.6)
17 33 21 13 22 17 13
38 21 22 26 16 9 8
276 (100.0)
136
140
from maxillary
source differs from that of mandibular
teeth
HEAD
Mean pain intensity 75.7 f 19 79.5 f 18 76.9+21 77.3 k 20 74.6 f 23 81.8+ 19 74.1 f 21
source (x2 =19.59;
P < 0.01).
reference areas that are closer to the pain source, i.e., lower and upper jaws and those that are more distant, i.e., temple, ear, eye (77.5 and 77.7 respectively). Additional pain dimensions
Most patients (92%) described their pain as internal, deep pain. The time of maximal pain was significantly associated with the source of pain (P < 0.0001). For example, 91% of dentinal pain was maximal at meals whiIe 95% of maximal pulpal pain did not occur at mealtimes. Sixty patients (30%) reported that pain woke them from sleep and this was found to be significantly associated with pain intensity (P < 0.001). Sixty percent of the patients who had evoked pain described the pain as
O--
Pain Intensity
C- --
Pain Unpleasantness
PAIN SPREAD
Fig. 1. Pain intensity of vectors.
(vectors)
and pain unpleasantness
ratings
as a function
of pain spread,
shown by the number
368
Spread of pain from 56 mandibular teeth
Spread of pain from 55 maxillary teeth
Fig. 2. Spread of pain to the following areas in the face: (1) upper jaw; (2) lower jaw: (3) cheek: (4) angle of mandible; (5) ear: (6) orbital region; and (7) temple. Each dot represents a vector.
localized; 60% of those with spontaneous non-localized pain ( P c 0.001).
pain
described
the pain
as a diffuse,
Discussion The spread, intensity, and unpleasantness of acute dental pain were evaluated as a function of pain source. Pain spread was noted when a patient experienced pain in a region distant (> 2 teeth) from the pain source. Both the frequency and extent of pain spread varied with pain source. However, there was no consistent pattern or distribution of pain spread that was associated with a particular pain source. Pain spread was correlated positively with pain intensity and pain unpleasantness. Our observation, that the frequency and extent of pain spread are correlated with pain intensity, is consistent with the finding that for chronic pain patients there was a significant association between the number of pain locations and the sensory-ranksum of the McGill Pain Questionnaires [1.5]. Although in general, pain associated with the teeth and their supporting structures is rated as moderate to severe pain 1141, pain unpleasantness was consistently higher than pain intensity for all pain sources. This observation indicates that clinical pain has a higher affective component than experimentally induced pain, such as that reported for electrical tooth pulp stimulation and noxious cold stimulation of exposed dentine [7]. Since pain sources were classified according to the anatomical site of the pathological process [13], we were able to examine pain spread as a function of anatomical structures that have different modes of innervation. Pulp and dentine are supplied principally by AS and C fibers while the other, periodontal, sources contain also A@ fibers f3]. Our results indicate that this anatomical classification alone.
369
albeit important for the practicing clinician, is not sufficient to distinguish pain intensity, unpleasantness, or pattern of pain spread. For example, equivalent high pain intensities may be associated either with pulpal (dental) or periapical origin (periodontal), similarly, equivalent low pain intensities may represent dentinal (dental) or papillar (periodontal) pain sources. The nociceptive mechanisms that are responsible for oral facial pain spread are probably of central origin, resulting from interactions that occur between primary nociceptive afferents and trigeminothalamic neurons [6,11]. The positive correlation between pain intensity and pain spread (Fig. 1) may be related to the transmission of nociceptive information in nucleus caudalis [6]. Two factors which may be important for this pain spread are: the large receptive fields of wide dynamic range neurons with extensive gradient sensitivity and the somatotopic organization. As pain intensity increases, neurons whose receptive field centers lie directly within the source of pain would increase their activity and presumably activate a larger receptive field. Consequently, more nociceptive neurons would be activated since the increased stimulation would also lie within the peripheral zone of receptive fields of other, somatotopically adjacent, neurons [6,11]. Our observation that pain from a maxillary source spreads into the region supplied by the mandibular division and vice versa (Fig. 2) is consistent with the observation that wide dynamic range neurons often have large receptive fields that extend across trigeminal divisions [6]_ This extensive spread with the increased pain accounts for the inability to precisely localize the pain source given information about the spatial distribution of the pain. Consequently, it is unlikely that maps of facial pain spread patterns would be sufficient for the unequivocal diagnosis of pain source in the oral facial region.
This study was partially supported by the David Epelbaum Fund for Pain Research. The authors express thanks to Mary Rooke for here secretarial assistance.
References 1
Anderson, D.J., Hannam, A.G. and Matthews, A., Sensory mechanisms in mammalian teeth and their supporting structures, Physiol. Rev., 50 (1970) 171-195. 2 Dalessio, D.J., Wolff’s Headache and Other Head Pain, 3rd ed., Oxford University Press, New York, 1972, pp. 463-476. 3 Dubner, R., Sessle, B.J. and Storey, A.T., The Neural Basis of Oral and Facial Function, Plenum Press, New York, 1978. 4 Friend, L.A. and Glenwright, H.D., An experimental investigation into the localization of pain from the dental pulp, Oral Surg., 25 (1968) 765-774. 5 Click, D.H., The interpretation of pain of dental origin, Dent. C&n. N. Amer., 11 (1967) 535-548. 6 Hayes, R.L., Price, D.D. and Dubner, R., Behavioral and physiological studies of sensory coding and
370
modulation of trigeminal nociceptive input. In: J.J. Bonica, J.C. Liebeskind and D.G. Albe-Fessard (Eds.), Advances in Pain Research and Therapy. Raven Press, New York. 1979, pp. 219.-243. 7 Heft, M.W., Sharav, Y. and Gracely. R.H., Assessment of chronic pain using verbal descriptor scaling procedures, J. dent. Res., 58 (1979) 216. 8 Hockaday. 481-.496.
J.M. and Whitty.
C.W.M.,
Patterns
of referred
pain in the normal
subject,
Brain. 90 (1967)
9 Hutchins, H.C. and Reynolds, E.O.. Experimental investigations of the referred pain or aerodontalgia, J. dent. Res., 26 (1947) 3-8. IO Mumford. J.M.. Oralfacial Pain: Aetiology, Diagnosis. and Treatment, 3rd ed., Churchill Livingstone. Edinburgh, 1982. 11 Price, D.D., Hayes, R.L., Ruda, M. and Dubner R., Spatial and temporal transformation of input to spinothalamic tract neurons and their relation to somatic sensations. J. Neurophysiol., 41 (1978) 933-947. 12 Price, D.D., McGrath, P.A. and Rafii, A,. The validation of visual analogue scales as ratio scale measures for chronic and experimental pain, Pain, 17 (1983) 45-56. 13 Sharav, Y.. Orofacial pain. In: P.R. Wall and R. Melzack (Eds.), Textbook of Pain, Churchill Livingstone, London, 1984, pp. 338-349. 14 Stembach, R.A., Pain Patients: Traits and Treatment, Academic Press, New York, 1974. 15 Toomey, T.C.. Gover. V.F. and Jones, B.N., Spatial distribution of pain: a descriptive characteristic of chronic pain, Pain, 17 (1983) 289-300. 16 Travell, J., Temporomandibular joint pain referred from muscles of the head and neck, J. prosth. Dent., 10 (1960) 745-763. 17 Van Hassel, H.J. and Harrington. G.W., Localization of pulpal sensation. Oral Surg.. 28 (1969) 753-760.
Purn, 20 (1984) 363-370 Elsevier
PA1 00699
The Spatial Distribution, Intensity and Unpleasantness of Acute Dental Pain Y. Sharav, E. Leviner, A. Tzukert
and P.A. McGrath
’
Department of Oral Diagnosis, Oral Medicine and Radiology, School of Dental Medicine, The Hebrew University - Hadassah, Jerusalem (Israel) (Received
9 May 1984, accepted
4 July 1984)
Summary The distribution, intensity and unpleasantness of acute dental pain were studied in 196 patients. Dental pain was classified by source according to 7 anatomical sites: dentinal, pulpal, pulpal and periapical, periapical, pericoronal, papillar, and periodontal. The distribution of dental pain was classified by the frequency of pain spread throughout the sample, by the extent of pain spread for a particular pain source, that is, the number of vectors of spread, and by the pain reference locations in the face and head. Pain-intensity and pain-unpleasantness were assessed on Visual Analogue Scales. The frequency and extent of pain spread varied as a function of source. However, specific patterns of pain spread were not associated with particular pain sources. There was considerable overlap in patterns of spread between maxillary and mandibular pain sources. The frequency and extent of pain spread was correlated positively with both pain intensity and pain unpleasantness. The correlation between pain ratings and pain spread may be attributed to central mechanisms and interactions between trigeminothalamic neurons. Spatial overlap of pain from maxillary and mandibular pain sources may be due to the large receptive fields of wide dynamic range neurons, that can extend beyond one trigeminal division. These observations indicate that the spatial distribution of acute dental pain is not sufficient as a diagnostic tool for indentifying pain source.
’ Present address: University gramme, Children’s Hospital, 1 B8, Canada. 0304-3959/84/$03.00
of Western Ontario, Department of Paediatrics, Paediatric and Pain Research Unit, Department of Oral Biology, London,
0 1984 Elsevier Science Publishers
B.V.
Pain ProOnt. N6B
364
Introduction Although acute oral pain originates from many oral structures, most pain originates in the teeth and in the immediate surrounding structures. The pain is primarily the result of inflammation that is confined to a relatively small area, such as the tooth pulp 1131. Much of our knowledge for how pain spreads in the face is derived from studies of experimentally induced pain [2,9,16], in which the patterns of pain spread are fairly consistent. However, previous trauma, pain intensity. and pain duration may alter the pattern of pain spread and subsequently the site of pain [2,8,9]. Also, the pain source, that is, the anatomical site in the oral cavity from which pain originates may affect the extent and distribution of pain spread. For example, dental pain originating from the tooth pulp is poorly localized [4,10,17] and may be considered to spread to adjacent sites more readily [3,5] white pain originating from the periodontal tissue, that surrounds the teeth, is well localized [I] and may therefore be assumed to spread less. Recently, the spatial distribution of pain has been proposed as a possible diagnostic tool for chronic pain [ 151. The purpose of our study was to investigate the pattern of pain spread for acute dental pain in order to evaluate the utility of pain spread as a diagnostic tool. The following questions were addressed: (1) Is there an association between the frequency of pain spread, that is, number of occurrences, and pain source? (2) Is there an association between the extent of pain spread, that is, the number of vectors of spread per occurrence, and pain source? (3) Is there an association between the distribution of pain spread, that is, the pain reference location and pain source? (4) Is there an association between the pattern of pain spread and the intensity and/or unpleasantness of the pain?
Methods One hundred and ninety-six patients, who presented to the Dental Clinic with acute dental pain, participated in the study. Mean patient age was 26.0 + 9.0 years; 82 (42%) were men; and 114 (58%) were women. Patients had an average of 11.6 f 3.3 years of formal education. All patients consented to be in the research study. Each patient was interviewed about several characteristics of his/her pain in order to determine the pain source, pain distribution, and the intensity and unpleasantness of the pain sensation. Pain source
Patients were divided into 7 diagnostic categories according to the intraoral source of their pain 1131: (1) Dentinal - in which pain was due to stimulation of dentine, such as that caused by caries or defective restorations. Pain was not spontaneous, it was evoked principally by heat, cold, and sweet foods. When evoked. pain subsided immediately with no overshoot. The pulp was intact and the tooth was not sensitive to percussion. (2) Pulpal - in which pain was associated with acute
365
pulpitis. The pain was spontaneous, and exacerbated by heat and cold, with an overshoot of more than 30 sec. The tooth was not sensitive to percussion. (3) Pulpal and periapical - in which the pain had similar characteristics to pulpal pain, but in which the tooth was also sensitive to percussion. (4) Periapical - in which pain was associated with an acute inflammatory process of the periapical tissue. The tooth was not sensitive to heat and cold, but was very sensitive to pressure and percussion. (5) Pericoronal - in which pain was associated with an acute inflammatory process of the gingiva overlaying a partially erupted lower molar. The pain was spontaneous and was exacerbated by pressure to the area. (6) Papillar - in which pain was associated with an acute inflammatory process of a gingival papilla. Pain was either spontaneous or was evoked by food impaction and pressure to the area. (7) Periodontal in which pain was associated with an acute lateral periodontal abscess. The pain was spontaneous, and exacerbated by pressure to the area and by percussion applied to the tooth. The pain was not evoked by heat or cold. Patients were excluded from the study if they had more than one pain source, for example, dentinal and papillar. Pain spread Patients pointed to any painful areas. Seven locations were then categorized: (1) maxillary region; (2) mandibular region; (3) cheek; (4) angle of mandible; (5) ear; (6) temple; and (7) general orbital region. If the pain was localized to a small area (1 or 2 teeth) at the pain source, then there was no pain spread. When pain spread from a source to one of the 7 reference areas, the spread was defined as a vector. No distinction was made as to whether the pain was referred or radiating. Although a patient could have only one pain source, he/she could have several different vectors. Pain intensity and unpleasantness The patients used a 150 mm visual analogue scale to rate the intensity and unpleasantness of their dental pain. Intensity was defined as the strength of the pain; unpleasantness was defined as the uncomfortable, bothersome quality of the pain [12]. Addirional pain d~~ensians Pain was described also according to whether it was: (1) external or internal; (2) the time of day at which it was maximal {morning, afternoon, night or during meals); and (3) spontaneous or evoked.
Results Pain source The distribution of the 196 patients according to the source of their acute dental pain is listed in Table I. Pain sources are equally distributed between upper and lower jaws and between sexes, except for pain of pericoronal origin. Pain unpleasantness is rated consistently higher than pain intensity. Pain intensity and pain unpleasantness are significantly correlated (r = 0.60; P < 0.~1).
TABLE
I
PERCENTAGE
OF PATIENTS
Source
N
ACCORDING
Mean age+ SD.
TO PAIN SOURCE Men
Women
Maxillary
Mandibular
(years) Denlinal
43
25+
42
S8
Pulpal Pulpal +
33
28klO
42
58
51 45
49 55
periapical Periapieal Pericoronai
33 51 16
27+10 26iIO 23+ 4
48 43 19
52 57 81
54 57 0
Papillar Periodontal
11 9
26If- 5 31+12
45 44
55 56
45 56
46 43 100 55 44
26i_
42
sx -
40
60
196
Total
I
9
--___
Puin spread The frequency of pain spread, the percentage of occurrences across patients, and the extent of pain spread, the mean number of vectors of spread, are listed in Table II as a function of pain source. As shown, both the frequency and extent of spread are associated with pain source, with minimal spread for pain of papillar origin and maximal spread for pain of pericoronal origin. Mean intensity ratings for each pain source are also listed in Table II. Intensity ratings were correlated positively with pain spread, as shown in Fig. 1. The mean intensity for the pain sources that did not spread (61.3 f 23) was significantly lower than the mean intensity (74.4 & 21) for sources that did spread (P -c0.001). The distribution of pain reference locations from maxillary and mandibular sources is listed in Table III. Although the distribution of pain reference locations from maxillary teeth differs from those of mandibular teeth (P < O.Ol), there is considerable overlap in pain reference locations for maxillary and mandibular sources, as shown in Fig. 2. There is no difference in pain intensity between pain
TABLE
II
FREQUENCY
AND EXTENT
OF PAIN SPREAD
Svurce
N
Frequency
Extent of spread ’
Pain intensity
Papillar Dentinal Periodontal Periapical
11 43 9 51
27 30 44 65
0.27 0.44 0.89
I .h3
56 58 66 71
Pulp + periapical Pulpal Pericoronal
33 33 16
61 73 87
1.70 2.18 2.25
76 76 69
of spread ’
’ Percentage of patients who had at least 1 vector of pain spread. h Mean number of vectors of pain spread.
367 TABLE
III
DISTRIBUTION Pain reference
1. 2. 3. 4.
OF PAIN SPREAD area
Number
Mandibular region Maxillary region Ear Cheek
5. Angle of mandible
6. Temple 7. Orbital region Total a Pain distribution
INTO THE VARIOUS
of vectors (%)
Maxillary
AREAS
teeth a
IN THE FACE AND
Mandibular
(55)
(56)
55 (19.9) 54 (19.6) 43 (15.6) 39 (14.1) 38 (13.8) 26 (9.4) 21 (7.6)
17 33 21 13 22 17 13
38 21 22 26 16 9 8
276 (100.0)
136
140
from maxillary
source differs from that of mandibular
teeth
HEAD
Mean pain intensity 75.7 f 19 79.5 f 18 76.9+21 77.3 k 20 74.6 f 23 81.8+ 19 74.1 f 21
source (x2 =19.59;
P < 0.01).
reference areas that are closer to the pain source, i.e., lower and upper jaws and those that are more distant, i.e., temple, ear, eye (77.5 and 77.7 respectively). Additional pain dimensions
Most patients (92%) described their pain as internal, deep pain. The time of maximal pain was significantly associated with the source of pain (P < 0.0001). For example, 91% of dentinal pain was maximal at meals whiIe 95% of maximal pulpal pain did not occur at mealtimes. Sixty patients (30%) reported that pain woke them from sleep and this was found to be significantly associated with pain intensity (P < 0.001). Sixty percent of the patients who had evoked pain described the pain as
O--
Pain Intensity
C- --
Pain Unpleasantness
PAIN SPREAD
Fig. 1. Pain intensity of vectors.
(vectors)
and pain unpleasantness
ratings
as a function
of pain spread,
shown by the number
368
Spread of pain from 56 mandibular teeth
Spread of pain from 55 maxillary teeth
Fig. 2. Spread of pain to the following areas in the face: (1) upper jaw; (2) lower jaw: (3) cheek: (4) angle of mandible; (5) ear: (6) orbital region; and (7) temple. Each dot represents a vector.
localized; 60% of those with spontaneous non-localized pain ( P c 0.001).
pain
described
the pain
as a diffuse,
Discussion The spread, intensity, and unpleasantness of acute dental pain were evaluated as a function of pain source. Pain spread was noted when a patient experienced pain in a region distant (> 2 teeth) from the pain source. Both the frequency and extent of pain spread varied with pain source. However, there was no consistent pattern or distribution of pain spread that was associated with a particular pain source. Pain spread was correlated positively with pain intensity and pain unpleasantness. Our observation, that the frequency and extent of pain spread are correlated with pain intensity, is consistent with the finding that for chronic pain patients there was a significant association between the number of pain locations and the sensory-ranksum of the McGill Pain Questionnaires [1.5]. Although in general, pain associated with the teeth and their supporting structures is rated as moderate to severe pain 1141, pain unpleasantness was consistently higher than pain intensity for all pain sources. This observation indicates that clinical pain has a higher affective component than experimentally induced pain, such as that reported for electrical tooth pulp stimulation and noxious cold stimulation of exposed dentine [7]. Since pain sources were classified according to the anatomical site of the pathological process [13], we were able to examine pain spread as a function of anatomical structures that have different modes of innervation. Pulp and dentine are supplied principally by AS and C fibers while the other, periodontal, sources contain also A@ fibers f3]. Our results indicate that this anatomical classification alone.
369
albeit important for the practicing clinician, is not sufficient to distinguish pain intensity, unpleasantness, or pattern of pain spread. For example, equivalent high pain intensities may be associated either with pulpal (dental) or periapical origin (periodontal), similarly, equivalent low pain intensities may represent dentinal (dental) or papillar (periodontal) pain sources. The nociceptive mechanisms that are responsible for oral facial pain spread are probably of central origin, resulting from interactions that occur between primary nociceptive afferents and trigeminothalamic neurons [6,11]. The positive correlation between pain intensity and pain spread (Fig. 1) may be related to the transmission of nociceptive information in nucleus caudalis [6]. Two factors which may be important for this pain spread are: the large receptive fields of wide dynamic range neurons with extensive gradient sensitivity and the somatotopic organization. As pain intensity increases, neurons whose receptive field centers lie directly within the source of pain would increase their activity and presumably activate a larger receptive field. Consequently, more nociceptive neurons would be activated since the increased stimulation would also lie within the peripheral zone of receptive fields of other, somatotopically adjacent, neurons [6,11]. Our observation that pain from a maxillary source spreads into the region supplied by the mandibular division and vice versa (Fig. 2) is consistent with the observation that wide dynamic range neurons often have large receptive fields that extend across trigeminal divisions [6]_ This extensive spread with the increased pain accounts for the inability to precisely localize the pain source given information about the spatial distribution of the pain. Consequently, it is unlikely that maps of facial pain spread patterns would be sufficient for the unequivocal diagnosis of pain source in the oral facial region.
This study was partially supported by the David Epelbaum Fund for Pain Research. The authors express thanks to Mary Rooke for here secretarial assistance.
References 1
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