A comparison of pressure pain detection thresholds in people with chronic low back pain and volunteers without pain.

Background and Purpose. Palpation is often utilized in the physical examination of patients with low back pain. The purpose of this study was to compare the pressure pain detection threshold (PPDT) of people with chronic low back pain (CLBP) and subjects without pain. Subjects and Methods. Thirty female subjects with CLBP were recruited from the offices of primary care physicians and physical therapists and compared with 30 female volunteers without pain for differences in PPDT at 6 sites tested bilaterally. Results. A significantly lower mean PPDT was found for all test site groups in subjects with CLBP compared with subjects without pain. A lower global PPDT was found in subjects with CLBP compared with subjects without pain (5.6 lb/[cm.sup.2] versus 6.9 lb/[cm.sup.2]). This also was the case for PPDT for the group of test sites unrelated to the lumbar spine (5.1 lb/[cm.sup.2] versus 6.1 lb/[cm.sup.2]) and for PPDT related to the lumbar spine (5.9 lb/[cm.sup.2] versus 8.0 lb/[cm.sup.2]). Discussion and Conclusion. Neurobiological or biopsychosocial influences may have contributed to the lower PPDT evident in subjects with CLBP. Subjects with CLBP demonstrated a lower global PPDT compared with subjects without pain, which should be taken into account when interpreting findings of pain or tenderness from palpation. [Giesbrecht RJS, Battie MC. A comparison of pressure pain detection thresholds in people with chronic low back pain and volunteers without pain. Phys Ther. 2005;85:1085-1092.]

Key Words: Chronic low back pain, Pain threshold.

Low back pain is a major source of disability and economic burden in Western society. It is one of the most common reasons for disability in people under the age of 45 years and the most frequent symptomatic reason for visiting a physician's office and work absenteeism. (1,2) Epidemiological research has shown a 60% to 80% lifetime prevalence of low back pain in the industrialized world. (3,4) Some investigations (5,6) have shown that 90% to 95% of people with low back pain recover and return to work within 6 to 12 weeks. Yet 5% to 10% of people with low back pain report persistent pain and disability after 3 months and account for 75% to 95% of the costs related to low back pain. (7) Despite the prevalence of low back pain and the tremendous costs associated with it, examination techniques for determining the underlying condition and severity are very limited. Traditionally, the clinical examination of a patient with low back pain relies on a comprehensive physical examination, often involving the evaluation of tenderness. Tenderness is typically assessed with manual palpation, a simple technique for pain provocation to determine the location of painful and pain-free tissues.

There is a physiological basis for such practices. Tissue damage stimulates the release of numerous inflammatory mediators from neurons and immune cells. (8) This activates and excites nociceptors in the area of injury, perpetuating local sensory excitation and nociceptor hypersensitivity. (9) Increased nociceptor sensitivity is expressed through spontaneous firing, enlargement of the neuronal receptive field, increased sensitivity to mechanical stimulation, and a lowered firing threshold. (10) This is known as peripheral sensitization. (11) The pain response to mechanical stimulation in this region is enhanced by a decrease in the nociceptive firing threshold and the activation of previously dormant nociceptors. (12) The activation of silent nociceptors contributes to peripheral sensitization by increasing the amount of neuronal discharge from an area of injury in response to stimulation. (13)

However, the interpretation of pain or tenderness reported during the manual palpation of a patient with low back pain is complex. The nociceptive system is not composed of hardwired pain pathways; rather, it constantly changes, operating in different states of sensitivity or excitability depending on the immediate need and the dominant pain mechanism activated by the central nervous system (CNS). (14) Manual pain provocation may not be directly proportional to the severity of tissue damage and does not necessarily imply damage to tissues beneath the examiner's fingers. (15,16)

Shortly after the onset of injury and pain, alterations in tissue sensitivity may occur in response to neurobiological and biopsychosocial influences. (17) A number of studies (18-21) have demonstrated the development of mechanical hypersensitivity and persistent pain in animals and humans following injury. Pain complaints in unrelated body regions and spontaneous exaggerated pain outside the neuroanatomical sensory distribution of the suspected lesion may follow sensory threshold changes. (22) This shift in pain processing may be responsible for ongoing pain rather than enduring tissue injury or inflammation because ongoing peripheral input is not necessarily required to reinforce persistent pain. (23) Enhanced pain transmission may outlast an initiating noxious input, and only low-level peripheral input may be required to maintain a painful state. (24) The evaluation of tenderness without considering the possible sensory threshold fluctuations influenced by neurobiological and biopsychosocial factors may lead the clinician to misinterpret palpatory tenderness revealed during the physical examination of a patient with chronic low back pain (CLBP).

Furthermore, people with persistent pain may demonstrate secondary hyperalgesia, or hypersensitivity beyond the area of tissue damage, without changes in local nociceptor hypersensitivity. (25) Local nociceptive excitation and peripheral sensitization may coexist with a state of secondary hyperalgesia, resulting in a diffuse, global pain experience. The term "central sensitization" represents this modulation in central pain pathways contributing to diffuse hypersensitivity in regions beyond the damaged tissue. (26) Local and global hypersensitivity also may be influenced by psychosocial factors in people with CLBP.

Previous studies have revealed generalized hyperalgesia in people with chronic whiplash syndrome (27,28) fibromyalgia, (29,30) complex regional pain syndrome, (31) and recurrent headaches. (32) Yet, Peters et al, (33) using a Forgione-Barber pressure stimulator on the middle phalanx of the second finger, found that there was no difference in pressure pain detection threshold (PPDT) between 20 subjects with CLBP and 20 age- and sex-matched subjects without pain. Peters and Schmidt (34) studied the pain threshold of 20 subjects with CLBP compared with 23 subjects without pain using pressure pain threshold measurements from the second finger and electrical pain threshold measurements at the right ankle. The researchers reported that subjects with CLBP were less sensitive to pressure and electrical stimuli than subjects without pain. Unlike the findings of other studies, Peters and Schmidt (34) suggested that people with CLBP might have higher pain threshold levels compared with people without pain.

The primary purpose of this investigation was to determine whether a difference in PPDT exists between people with CLBP and people without pain, using multiple test sites related and unrelated to the lumbar spine. We hypothesized that, compared with volunteers without pain, people with CLBP would demonstrate a lower pain threshold at sites neuroanatomically related and sites clearly unrelated to the lumbar spine. The PPDT differences occurring in people with persistent low back pain and their patterns (eg, within or beyond the neuroanatomical boundaries of the lumbar spine) may provide insights into possible mechanisms of persistent low back pain. Furthermore, knowledge of variations in PPDT in people with CLBP may help clinicians in their interpretation of pain provocation from manual palpation on physical examination.

Method

Subjects

Thirty female subjects with CLBP were recruited for the study from the offices of physicians and physical therapists, and 30 subjects without pain were recruited through posters and word-of-mouth. A sample size calculation was performed for detecting a significant difference between groups using a power index of [alpha] = .05 (2-tailed) and [beta]=.10, which suggested a sample size of 30 subjects per group. (35) Subjects were included in the CLBP group if they reported low back pain with or without leg pain extending below the knee for more than 6 months at a moderate or greater severity on a numeric pain rating scale ([greater than or equal to] 4/10) at the time of testing. The comparison group had experienced no low back or leg pain during the 6 months prior to testing. The history of low back pain beyond 6 months among people without pain is unknown. Additional inclusion criteria for both groups were: age of 20 to 60 years, no spine surgery in the previous 6 months, no involvement in a disability insurance claim, free of concurrent painful conditions, and reported no use of opioid analgesics, benzodiazepine, antidepressant, or anticonvulsant medication within the 3 weeks prior to testing. Subjects also reported no use of nonsteroidal anti-inflammatory drugs or over-the-counter analgesic medications during the 24 hours prior to testing, nor were physical treatments received. Subjects also had to be able to tolerate a prone or side-lying position.

Data Acquisition

We used the International Association for the Study of Pain (IASP) definition of PPDT as the lowest stimulus that gives rise to the earliest perception of pain in an instructed person under given conditions of noxious stimulation. (36) Test sites were measured bilaterally and included the paraspinal muscles of C5, L3, and L5; the wrist extensor muscle belly; the middle phalanx of the second finger; and the calf muscle belly. An electronic pressure threshold meter (Algometer Commander*) with a stimulation surface area of 1 [cm.sup.2] was applied to determine the PPDT at each test site. Prior studies of PPDT reliability have demonstrated Pearson correlation coefficients ranging from .65 to .96 for intrarater reliability (37-39) and from .47 to .89 for interrater reliability. (39,40) This variability in interrater reliability may be related to the tissue consistency beneath the test site and the ability of the examiner to obtain proper perpendicular alignment of the algometer due to the anatomical restrictions related to the test site itself (medial pterygoid muscle). (40) All test sites examined in this study allowed for perpendicular algometer positioning with a stable base of firm subcutaneous tissue directly beneath the site.

Testing took place in a soundproof room of constant temperature between the hours of 3 and 6 PM. Each test session lasted approximately 30 minutes. Prior to testing, participants provided voluntary informed consent and completed a subject questionnaire package consisting of self-report measures with acceptable reliability and validity, including a numeric pain rating scale (correlation coefficient [type not reported] = .63-.99), (41,42) the Roland-Morris Disability Questionnaire (intraclass correlation coefficients = .79-.91), (43-45) a pain drawing (K = .5884), (46,47) and questions concerning demographics, pain location, and employment history. All self-report measures were based on current perceived pain and disability levels. The pain drawing was scored using the penalty point system of scoring. This method was developed by Ransford et al (47) and assigns points for depictions of pain not thought to be associated with lumbar spine disease. High intrarater reliability has been demonstrated with the penalty point system of scoring for pain drawings. (46-48) The participants then joined a female examiner who was unaware of the specific research hypotheses and blinded to the subjects' low back pain status. The examiner was a physical therapist assistant who was trained to properly use the pressure algometer and accurately identify all test points on subjects. Participants assumed a prone or side-lying position for the duration of testing. The applied method of PPDT testing was as described by Hogeweg et al, (49) with a steady pressure rate of 2 lb/s and perpendicular alignment of the pressure threshold meter to the subject's skin. The subject was asked to indicate the PPDT by stating "pain." Three measurements were obtained at each test site with 10 seconds of recovery time allowed between repeated measurements at each test site. The average of the 3 test values was used in the analysis. The order of test site evaluation was randomized for each subject.

Data Analysis

Test sites were grouped to represent body regions for analyses. The global PPDT was regarded as the mean of the 6 points tested bilaterally. Test sites at the L3 and L5 paraspinal muscles were grouped to represent sites anatomically related to the low back region. Test sites at the wrist extensor muscle and finger were grouped to represent sites that were anatomically unrelated to the low back region. The test site at the finger allowed comparison with other studies that tested this site. Independent t tests were done to compare mean values between groups.

Results

The subjects with CLBP had a mean age of 41.6 years (SD = 9.7), and the subjects without pain had a mean age of 42.2 years (SD = 9.5). The subjects with CLBP had a mean pain duration of 11.6 years (SD = 9.2) years and a mean numeric pain rating score of 5.9 (SD = 1.8) out of 10 for current pain. Disability scores on the Roland-Morris Disability Questionnaire ranged from 0 to 20, with a mean score of 7.5 (SD = 5.0) out of 24. Seventy percent of subjects with CLBP reported that low back pain had no effect on their employment status. Only 10% of the subjects with CLBP scored 3 or more on the pain drawing using the penalty point system, such that associations between abnormal pain drawings and global PPDT scores could not be examined. As expected, all subjects without pain reported no pain or disability at the time of testing.

Mean PPDT values tended to be lower at every individual test site in subjects with CLBP compared with subjects without pain (Figure). The mean global pain threshold values (all sites combined) were 5.6 lb/[cm.sup.2] (SD = 2.1) for subjects with CLBP and 6.9 lb/[cm.sup.2] (SD = 2.1) for subjects without pain. Mean pain threshold measurements obtained from regions unrelated to the lumbar spine were 5.1 lb/[cm.sup.2] (SD = 1.6) for subjects with CLBP and 6.1 lb/[cm.sup.2] (SD = 1.6) for subjects without pain. Mean pain threshold measurements obtained from sites anatomically related to the lumbar spine were 5.9 lb/[cm.sup.2] (SD = 3.0) for subjects with CLBP and 8.0 lb/[cm.sup.2] (SD = 2.9) for subjects without pain. Separate analyses of combined test site pain threshold measurements demonstrated significantly lower combined mean PPDT in all test site groupings (Table).

[FIGURE 1 OMITTED]

Discussion

This study identified a lower PPDT in subjects with CLBP compared with those without pain. Study strengths include the degree of control of confounding factors related to PPDT measurement, as well as the sampling of multiple sites to determine global and lumbar pain threshold. The present investigation controlled the potentially confounding influences of medication use, handedness, sex, age, and disability insurance claim involvement. In previous investigations, (33,34) global pain threshold was represented by pain threshold measurements drawn only from the middle phalanx of one hand. The present study compared a sample of 6 points tested bilaterally (global pain threshold), including 2 test sites anatomically unrelated to the lumbar spine and 2 test sites at the lumbar spine. The study subjects with CLBP also represent a group relevant to physical therapist practice as they were care-seekers recruited from physical therapy and primary care clinics.

There also are study limitations to note. Although steps were taken to enhance PPDT measurement reliability through tester training and careful selection of test sites, earlier studies (37,39,40) suggest only moderate to good reliability of the PPDT measurements. Suboptimal measurement reliability, implying some degree of measurement error, can be expected to dilute apparent group differences. Although we believe a 6-month period free of back pain and other painful conditions should be adequate for a pain-free comparison group, it is possible that the subjects without pain in our study may have had undetected earlier long-standing painful conditions that, theoretically, could influence PPDT, which could dilute the magnitude of group differences. Furthermore, it is possible that the strategy to recruit subjects with CLBP from clinics and volunteers without pain from the general population may have affected the homogeneity of the 2 groups on characteristics other than the presence of CLBP that could influence PPDT. However, we are not aware of any specific differences that would be of concern in this regard.

In this investigation, subjects with CLBP had a lower global PPDT and a lower PPDT at combined sites unrelated to the lumbar spine compared with subjects without pain. This finding may be related to the development of central sensitization and maladaptive pain processing involving widespread hypersensitivity. The bombardment of neurons in the dorsal horn of the spinal cord by the primary afferent system stimulates N-methyl-D-aspartate (NMDA) receptors, increasing nociceptive signal transmission to the CNS, and may overwhelm pain control centers. (50) Neuronal plasticity in the dorsal horn and supraspinal regions results from this neuronal barrage and contributes to spontaneous pain and the expansion of receptive fields. Previously subthreshold inputs from the somatosensory system now begin to generate action potentials from the dorsal horn to the CNS. (51) Central sensitization is reinforced by the activation of low-threshold small-diameter primary afferents (A/3--fibers), capable of allowing low-intensity stimulation to be perceived as pain and producing long-term changes in spinal neurons. (52)

Dubner and Ruda (53) suggested that, in the event of prolonged hyperexcitability and hyperalgesia, a pathological state may develop involving excitotoxicity, cellular dysfunction, and loss of descending control mechanisms. Woolf and Doubel1 (54) proposed 3 basic pathological mechanisms that could contribute to central sensitization: increased excitability, decreased inhibition (disinhibition), and structural reorganization of the CNS. Hyperexcitability without adequate descending inhibitory controls may amplify and prolong the pain experience. (55) The combination of excitation and disinhibition might allow pain to persist long after an injury has apparently healed, possible for months or years. (56) Research involving magnetic source imaging has revealed that people with CLPB show enhanced reactivity and reorganization of the somatosensory cortex with a positive relationship between cortical reactivity and chronicity. (57) The clinical effects of altered pain processing may include false positive physical tests, ectopic impulses, nondermatomal spread of pain, and unpredictable pain. (22)

It is possible that biopsychosocial influences may have contributed to the observed differences in pain sensation between the subjects with CLBP and those without pain in our study. Using a biopsychosocial model, Waddell suggested that "pain can no longer be regarded as merely a physical sensation of noxious stimulus and disease, but that the conscious experience of pain may be modulated by mental, emotional, and sensory mechanisms and include both sensory and emotional components. (58) (p637) Flor and Birbaumer (59) demonstrated that patients with chronic pain may overemphasize pain by reporting high levels of physical symptoms and are less able to discriminate muscle tension levels in a stressful laboratory situation compared with control subjects without pain. Flor and Turk (60) found that perceptions of uncontrollability and helplessness were more closely related to pain and disability levels than disease related variables in patients with CLBP. Turk (61) argued that psychosocial factors could interact with biological mechanisms in 2 powerful ways. Biological factors may initiate and maintain physical symptoms, and psychological issues may influence pain perception and appraisal. Patients may react with pain behaviors in response to their perception of pain. Furthermore, psychological elements and cognitive interpretations may alter hormone production, arouse the sympathetic nervous system, and increase levels of muscle tension.

The present study findings contradict those of Peters and colleagues (33,34) by suggesting that people with CLBP are generally more sensitive, rather than less sensitive, than people without pain. The present study involved a greater number of test sites, local and distal to the lumbar spine, compared with the single site at the second finger used by Peters et al, (33) and thus may have been more sensitive in detecting alterations in PPDT. In addition, the present study examined the PPDT of people with CLBP who were seeking health care, whereas the subjects with low back pain in the 2 previous studies (33,34) were recruited through newspaper advertisements, which may represent other differences between the study samples. It is possible that people seeking care for CLBP may vary in the severity of their condition or their attitudes toward pain stimulation compared with non-care-seekers. Detailed comparisons of study samples cannot be made because measures of pain or disability were not reported in either of the earlier studies.

Pressure pain detection threshold also has been studied in subjects with whiplash-associated disorders. Johansen et al (20) found lower PPDT in the neck, shoulder, and tibial regions of subjects with chronic whiplash compared with subjects without pain. In this investigation, test sites were not combined to represent global pain threshold, yet each test site was significantly more sensitive to pressure in the subjects with chronic whiplash than in the subjects without pain. Essentially, the findings are similar to those of the present study on low back pain, suggesting that people with chronic pain may show global hypersensitivity compared with people without pain. However, in a later study, Kasch et al (27) reported apparently conflicting results. They measured and compared PPDT in people with acute whiplash and acute ankle distortion injury at the head and neck region and the left finger at 1 week and 1, 3, and 6 months following injury. Subjects with acute whiplash injury showed higher sensitivity at all head and neck sites until 3 months following injury but no significant difference at 6 months following injury. Pressure pain detection threshold values measured at the distal site (finger) were similar between groups at all examination intervals. Their results suggest that peripheral sensitization in the head and neck region is likely temporary and that hypersensitivity of tissues unrelated to the area of injury may not occur. Among the factors that may have contributed to the dissimilarity in findings from the studies are age, injury acuity, sex, involvement in disability insurance claims, medication usage, and the lack of a pain-free control group.

The results of this investigation have clinical implications. Clinicians should be aware of the possible influence of sensory threshold aberrations on patient responses when performing clinical tests on people with CLBP. Tests involving pain provocation through palpation may suggest the presence of local or global sensory threshold changes but may not be related to musculoskeletal pathology beneath the examiner's fingers, because people with CLBP appear to be more sensitive to pressure than people without pain.

Conclusion

The primary purpose of this investigation was to compare the PPDT of people seeking care for CLBP and volunteers without pain and thereby clarify the presence or absence of a difference in PPDT between groups. The global PPDT of subjects with CLBP, which included a sample of 6 sites tested bilaterally, was significantly lower than that of subjects without pain. In particular, subjects with CLBP demonstrated significantly lower PPDT values at test sites anatomically related to the lumbar spine. Test sites distal to the low back and neuroanatomically unrelated to the lumbar spine also were lower in subjects with CLBP compared with subjects without pain. The results suggest that neurobiological or biopsychosocial influences may account for differences in PPDT demonstrated between subject groups in this study. Further research is needed to elucidate factors responsible for the sensory threshold changes evident in people with CLBP and to identify the time frames in which these sensory changes occur.

* JTech Medical, 4314 ZEVEX Park Ln, Salt Lake City, UT 84123.

References

(1) Kelsey JL, White AA III. Epidemiology and impact of low back pain. Spine. 1980;5:13-142.

(2) Valkenburg HA, Haanen HCM. The epidemiology of low back pain. In: White AA Jr, Gordon SL, eds. Symposium on Idiopathic Low Back Pain. St Louis, Mo: Mosby; 1982:9-22.

(3) Frymoyer JW, Cats-Baril WL. An overview of the incidences and causes of low back pain. Orthop Clin North Am. 1991;22:263-271.

(4) Clinical Standards Advisory Group. Epidemiology Review: The Epidemiology, and Costs of Back Pain, Annex to the Clinical Standards Advisory Group. Report on Back Pain. London, United Kingdom: HMSO; 1994:1-72.

(5) Reid S, Haugh LD, Hazard RG, Tripathi M. Occupational low back pain: recovery curves and factors associated with disability. J Occup Rehab. 1997;7:1-14.

(6) Frymoyer JW. Predicting disability from low back pain. Clin Orthop. 1992;279:101-109.

(7) Nachemson AL. Newest knowledge of low back pain: a critical look. Clin Orthop. 1992;279:8-20.

(8) Dray A. Peripheral mediators of pain. In: Dray A, Dickenson AH, Besson JM, eds. Handbook of Experimental Pharmacology. Berlin, Germany: Springer-Verlag Publishing; 1997:22-41.

(9) Dray A, Urban L. New pharmacological strategies for pain relief. Annu Rev Pharmacol Toxicol. 1996;36:253-280.

(10) Dubner R, Ren K. Endogenous mechanisms of sensory modulation. Pain. 1999; Suppl 6:$45-$53.

(11) Wright A. Recent concepts in the neurophysiology of pain. Man Ther. 1999;4:196-202.

(12) Woolf CJ, Chong M. Pre-emptive analgesia: treating postoperative pain by preventing establishment of central sensitization. Anesth Analg. 1993;77:362-367.

(13) Schmidt RF. The articular polymodal nociceptor in health and disease. In: Kumazawa T, Kruger L, Mizumura K, eds. Progress in Brain Research. Vol. 113. Amsterdam, the Netherlands: Elsevier Science; 1996:53-81.

(14) Woolf CJ. The dorsal horn: state-dependant sensory processing and the generation of pain. In: Wall PD, Melzack R, eds. Textbook of Pain. 3rd ed. New York, NY: Churchill Livingstone; 1994:101-112.

(15) Najm WI, Seffinger MA, Mishra SI, et al. Content validity of manual spinal palpatory exams: a systematic review. BMC Complement Altern Med. May 7, 2003;3(1):1.

(16) Russell R. Diagnostic palpation of the spine: a review of procedures and assessment of their reliability. J Manipulative Physiol Ther. 1983;6: 181-183.

(17) Carr DB, Goudas LC. Acute pain. Lancet. 1999;353:2051-2058.

(18) Song X, Hu S, Greenquist KW, et al. Mechanical and Thermal Hyperalgesia and Ectopic Neuronal Discharge After Chronic Compression of Dorsal Root Ganglion. Rockville, Md: American Physiological Society; 1999:3347-3358.

(19) Woolf CJ. Long term alterations in the excitability of the flexion reflex produced by peripheral tissue injury in the chronic decerebrate rat. Pain. 1984;18:325-343.

(20) Johansen MK, Graven-Nielsen T, Olesen AS, Arendt-Nielsen L. Generalized muscular hyperalgesia in chronic whiplash syndrome. Pain. 1999;83:229-234.

(21) Okifuji A, Turk DC, Marcus DA. Comparison of generalized and localized hyperalgesia in patients with recurrent headache and fibromyalgia. Psychsom Med. 1999;61:771-780.

(22) Cohen ML. The clinical challenge of secondary hyperalgesia. In: Shacklock MO, ed. Moving in on Pain. Marrickville, New South Wales, Australia: Butterworth Heinemann; 1995:21-26.

(23) Urban MO, Gebhart GF. Supraspinal contributions to hyperalgesia. Proc Natl Acad Sci 1999;96:7687-7692.

(24) Woolf CJ, Salter MW. Neuronal plasticity: increasing the gain in pain. Science. 2000;288:1765-1768.

(25) Raja SN, Campbell JN, Meyer RA. Evidence for different mechanisms of primary and secondary hyperalgesia following heat injury to the glabrous skin. Brain. 1984;107:1179-1188.

(26) Woolf CJ. Evidence for a central component of post-injury pain hypersensitivity. Nature. 1983;306:686-688.

(27) Kasch H, Stengaard-Pedersen K, Arendt-Nielsen L, Jensen TS. Pain thresholds and tenderness in neck and head following acute whiplash injury: a prospective study. Cephalalgia. 2001;21:189-197.

(28) Johansen MK, Graven-Nielsen T, Olesen AS, Arendt-Nielsen L. Generalized muscular hyperalgesia in chronic whiplash syndrome. Pain. 1999;83:229-234.

(29) Granges G, Littlejohn G. Pressure pain threshold in pain-free subjects, in patients with chronic regional pain syndromes, and in patients with fibromyalgia syndrome. Arthritis Rheum. 1993;36:642-646.

(30) Mikkelson M, Lattika P, Kautiainen H, et al. Muscle and bone pressure pain threshold and pain tolerance in fibromyalgia patients and controls. Pain. 1992;73:814-818.

(31) Vatine JJ, Tsenter J, Nirel R. Experimental pressure pain in patients with complex regional pain syndrome (reflex sympathetic dystrophy). Am J Phys Med Rehabil. 1998;77:382-387.

(32) Okifuji A, Turk DC, Marcus DA. Comparison of generalized and localized hyperalgesia in patients with recurrent headache and fibromyalgia. Psychsom Med. 1999;61:771-780.

(33) Peters ML, Schmidt AJM, Van den Hout MA. Chronic low back pain and the reaction to repeated acute pain stimulation. Pain. 1989;39: 69-76.

(34) Peters ML, Schmidt AJM. Differences in pain perception and sensory discrimination between chronic low back pain patients and healthy control. J Psychom Res. 1992;36:47-53.

(35) Hassard TJ. Understanding Biostatistics. St Louis, Mo: Mosby-Year Book; 1991.

(36) International Association for the Study of Pain. Pain Supplement 3: Classification of Chronic Pain, Descriptions of Chronic" Pain Syndromes and Definitions of Pain Terms. Amsterdam, the Netherlands: Elsevier Science; 1986.

(37) Merskey H, Spear FG. The reliability of the pressure algometer. BrJ Soc Clin Psychol. 1964;3:130-136.

(38) Nussbaum EL, Dowries L. Reliability of clinical pressure-pain algometric measurements obtained on consecutive days. Phys Ther. 1998; 78:106-168.

(39) Reeves JL, Jaeger B, Graft Radford SB. Reliability of the pressure algometer as a measure of myofascial trigger point sensitivity. Pain. 1986;24:313-321.

(40) Chung SC, Urn BY, Hyung SK. Evaluation of pressure pain threshold in head and neck muscles by electronic algometer: intrarater and interrater reliability. Journal of Mandibular Practice. 1992;10(1):28-34.

(41) Jensen MP, McFarland CA. Increasing the reliability and validity of pain intensity measurement in chronic pain patients. Pain. 1993;55: 195-203.

(42) Jensen MP, Turner JA, Romano JM. What is the maximum number of levels needed in pain intensity measurement? Pain. 1994;58: 387-392.

(43) Stratford PW, Binkley JM. Measurement properties of the RM-18: a modified version of the Roland Morris Disability Scale. Spine. 1997;22: 2416-2421.

(44) Kopec JA, Esdaile JM, Abrahamowicz M, et al. The Quebec Back Pain Disability Scale: measurement properties. Spine. 1995;20:341-352.

(45) Roland M, Morris R. A study of the natural history of back pain, part I: development of a reliable and sensitive measure of disability in low back pain. Spine. 1983;8:141-144.

(46) Ohnmeiss DD. Repeatability of pain drawings in a low back pain population. Spine. 2000;25:980-988.

(47) Ransford AO, Cairns D, Mooney V. The pain drawing as an aid to psychological evaluation of patients with low back pain. Spine. 1976;1: 127-134.

(48) Main CJ. Psychological Factors in Chronic Low Back Pain [doctoral thesis]. Glasgow, United Kingdom: University of Glasgow; 1984.

(49) Hogeweg JA, Langereis MJ, Bernards ATM, et al. Algometry-measuring pain threshold: method and characteristics in healthy subjects. Scand J Rehabil Med. 1992;24:99-103.

(50) Coderre TJ, Katz J, Vaccarino AL, Melzack R. Contribution of central plasticity to pathological pain: review of clinical and experimental evidence. Pain. 1993;52:259-285.

(51) Woolf CJ, King AE. Dynamic alterations in the cutaneous mechanoreceptive fields of dorsal horn neurons in the rate spinal cord. J Neurosci. 1990;10:2717-2726.

(52) Woolf CJ, Thompson SWN. The induction and maintenance of central sensitization is dependent on N-methyl-D-aspartic acid receptor activation: implications for the treatment of post-injury pain hypersensitivity states. Pain. 1991;44:293-299.

(53) Dubner R, Ruda MA. Activity-dependent neuronal plasticity following tissue injury and inflammation. Trends in Neurosciences. 1992;15: 96-103.

(54) Woolf CJ, Doubell TP. The pathophysiology of chronic pain: increased sensitivity to low threshold A[beta]-fibre inputs. Curt Opin Neurobiol. 1994;4:525-534.

(55) Dubner R. Neuronal plasticity and pain following peripheral tissue inflammation or nerve injury. In: Bond MR, Charhon JE, Woolf CJ, eds. Proceedings of the Sixth World Congress on Pain. Amsterdam, the Netherlands: Elsevier Science; 1991:264-276.

(56) William D, Willis. Summary and overview: hyperalgesia and pain. In: Willis WD, ed. Bristol-Myers Squibb Symposium on Pain Research. New York, NY: Raven Press; 1992:1-9.

(57) Flor H, Braun C, Elbert T, Birbaumer N. Extensive reorganization of primary somatosensory cortex in chronic back pain patients. Neurosci Lett. 1997;224: 5-8.

(58) Waddell G. 1987 Volvo award in clinical sciences: a new clinical model for the treatment of low-back pain. Spine. 1987;12:632-644.

(59) Flor H, Birbaumer N. Stress related responses in chronic pain patients. Paper presented at: Annual Meeting of the Society of Psychophysiological Research; October 1988; San Francisco, Calif.

(60) Flor H, Turk DC. Rheumatoid arthritis and back pain: predicting pain and disability from cognitive variables. J Behav Med. 1988;11: 251-265.

(61) Turk DC. The role of psychological factors in chronic pain. Acta Anaesthesiol Scand. 1999;43:885-888.

RJS Giesbrecht, MScPT, BA, is Manager of Rehabilitation Services, Prairie North Health Region, Saskatchewan, Canada. At the time of the study, he was a student in the Department of Physical Therapy, Faculty of Rehabilitation Medicine, University of Alberta, Edmonton, Canada. Address all correspondence to Mr Giesbrecht at Box 12147, Lloydminster, Alberta, Canada, T9V 3C4 ([e-mail]).

MC Battie, PT, PhD, is Professor and Canada Research Chair in Common Spinal Disorders, Faculty of Rehabilitation Medicine, University of Alberta.

Both authors provided concept/idea/research design, writing, and data analysis. Mr Giesbrecht provided data collection, project management, fund procurement, facilities/equipment, and institutional liaisons.

This study was approved by the University of Alberta Health Ethics Research Board (panel B) and the Bioethics Committee of Lloydminster Hospital.

Funding for this study was provided, in part, by the Prairie North Health Region and the Canadian Pain Society.

This article was received December 7, 2004, and was accepted March 15, 2005.

Table.
Mean (Standard Deviation) Regional or Combined Pressure Pain
Detection Threshold (PPDT) Values (in Pounds per Square Centimeter)
for Subjects With Chronic Low Back Pain (CLBP) and Subjects Without
Pain

                                Lumbar      Lumbar
                    Global      Spine-      Spine-
                   PPDT (All   Unrelated    Related
                   6 Points)   PPDT (a)      PPDT

Subjects without   6.9 (2.1)   6.1 (1.6)   8.0 (2.9)
  pain (n = 30)
Subjects with      5.6 (2.1)   5.1 (1.6)   5.9 (3.0)
  CLBP (n = 30)
P (2-tailed)         .0175       .0163       .0083

(a) Includes wrist extensor and second finger sites.