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Chronic Pain Disorder Following Physical Injury
Chronic Pain Disorder Following Physical Injury JON STRELTZER, M.D., BYRON A. ELIASHOF, M.D. AMY E. KLINE, PH.D., DEBORAH GOEBERT, DR.P.H.
Pain disorders that are primarily associated with psychological factors are of great clinical concern, but they are difficult to study because of the inability to make valid or reliable diagnoses by structured interview alone. The authors confront this difficulty by using an injured subject population that had extensive psychiatric and medical evaluations. Those who developed somatoform pain disorder (SPD) were compared with a control group who did not. The SPD group had distinctive associated factors: more sites of pain, spread of pain beyond area of original injury, and substantially more opiate and benzodiazepine use. Compensation/litigation influenced symptoms more in the SPD group. Psychotherapists often supported the patient’s viewpoint that the pain was physical and to be endured. (Psychosomatics 2000; 41:227–234)
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hronic pain is a poorly understood condition subject to a variety of interpretations and theories with respect to its etiology and persistence.1 The duration and degree of pain and disability following physical injury may be unrelated to the apparent severity of the injury,2,3 especially if compensation is involved.4–6 Patients suffering severe trauma often experience substantial pain only until their injuries stabilize and begin to heal. If the pain persists, it is ordinarily manageable without opiate analgesics. In contrast, among patients who develop chronic pain, a history of relatively minor trauma is common. Chronic pain has been described as a syndrome or process with many dysfunctional features not explained by physical pathology.7 Psychological factors are considered important, including depression, hypochondriasis, medication dependence, and situational factors.2,8–11 Assessment of these factors is difficult, and they are often inadequately appreciated in clinical management.12 A multidisciplinary approach to treatment is generally advocated,9,13 but results may be less than satisfactory.14,15 DSM-III-R and DSM-IV recognize a chronic pain disorder that is predominantly psychological and classify it within the group of somatoform disorders. Presumably, this is a specific type of chronic pain disorder, but its epidemiology is unknown. Population surveys, even those asPsychosomatics 41:3, May-June 2000
sessing chronic pain patients, usually do not attempt to assess a somatoform pain disorder (SPD),11,16,17 probably because diagnosis does not seem amenable to self-report, and medical evaluations are required to rule out organic explanations of the pain. The Structured Clinical Interview for DSM-III-R (SCID) has not been shown to reliably diagnose SPD.18 A study designed to assess “somatization,” a concept that includes various somatoform disorders (including chronic pain disorder), reported a prevalence of 9%–20% in the general population,19 suggesting that pain disorder may be common. Another study of 1,000 patients in primary care clinics found somatoform disorders in 14% of the patients; these disorders frequently included unexplained pain symptoms.20 On the basis of clinical experience with chronic pain patients, we hypothesized that if adequate medical information were available, many of these patients would be diagnosed as having somatoform pain disorders. We predicted that they would have a number of characteristics that would distinguish them from injured patients who did not Received March 4, 1999; revised September 23, 1999; accepted October 22, 1999. From the Department of Psychiatry, John A. Burns School of Medicine, Honolulu, Hawaii. Address reprint requests to Dr. Streltzer, Department of Psychiatry, 1356 Lusitana St., Honolulu, HI 96813. Copyright 䉷 2000 The Academy of Psychosomatic Medicine.
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Chronic Pain develop a chronic pain disorder. These characteristics included more frequent depression, the use of more dependency-producing medications, the use of more surgery for the pain,21 and an increased susceptibility to the influence of compensation or litigation on maintaining symptoms. To test these hypotheses, we studied a population of injured workers, all of whom were referred for psychiatric evaluation. Some of these workers developed a chronic pain disorder, and they were compared with those who did not. Because all of these patients were litigating or seeking benefits, their past medical records (sometimes lifetime) were available. This presented a unique opportunity to compare chronic somatoform pain patients to a control group. METHODS Cases were selected from independent psychiatric evaluations conducted on workers’ compensation and automobile accident claimants seen between January 1, 1989, and June 30, 1992. They were examined by two board-certified psychiatrists who have experience with psychiatric impairment evaluations. Each subject received a comprehensive psychiatric evaluation along the lines of London et al.22 and recommended by the state of California, Division of Industrial Accidents.23 This included a 2- to 5-hour interview, sometimes supplemented by questionnaires and psychological tests. Extensive medical records were reviewed in all cases. These records were not limited to treatment of a specific injury. Records were obtained by insurance adjusters and attorneys by voluntary release and by subpoena. The psychiatrists generated a detailed report of 18–30 single-spaced pages. At the time of evaluation, the examiners were unaware that a study of pain disorders would occur. Each report was screened by one or another of the reviewers (JS or BE) to determine if a physical injury occurred. Two groups were generated from the screening: an “SPD” group, if a diagnosis of an SPD was present (DSMIII-R); and a “control” group, if no somatoform diagnosis was present. Fifty-four cases were initially screened into each group. This represented all of the potential control subjects and most of the potential SPD subjects who were chosen alphabetically. All data were obtained from the reports. For the SPD group, both reviewers had to agree that the case unequivocally met DSM-III-R criteria for somatoform pain disorder. The diagnosis was accepted only if the medical records documented the absence of physical or laboratory findings that could explain the pain, or if pain complaints were grossly disproportionate to any objective 228
findings that may have been present. Borderline cases, including cases of suspected malingering, were excluded. The criteria for malingering were obvious inconsistencies in behavior documented in the medical records or by surreptitious surveillance. For the control group, both reviewers had to agree that somatoform pain disorder or any other somatoform disorder was not a diagnosis. If physical pain was present, it had to be explained by objective findings in the medical records. After eliminating cases in which both reviewers had not concluded that the subject unequivocally fit into one of the groups, 47 SPD cases and 43 control subjects remained for study. Data collected included demographic information, duration of pain complaints, number of pain sites, location of pain and its relation to the site of initial injury, types of treatments, and medications. Use of opiates, benzodiazepines, and barbiturates was considered positive if used daily for at least 6 months at the time of evaluation. Illicit drug use was also recorded. Significant alcohol use was considered present if there was a history of three or more drinks daily or binge drinking. Nonphysiological findings were considered present if medical records revealed nonanatomical sensory findings, nonphysiological weakness, inconsistent range of motion, or positive Waddell’s signs.24,25 Reviewers tabulated the following: anger at working conditions pre- and postinjury, whether pain prevented work, prior history of significant pain problem, history of child abuse, number of specialized imaging and electrodiagnostic tests [e.g., magnetic resonance imaging (MRI), computed tomography (CT) scan, electromyogram (EMG)], number of surgeries, and number of medical consultants who did or did not consider the pain symptoms explainable by objective findings. Subject reports were also evaluated to determine whether DSM-III criteria for psychogenic pain disorder and DSM-IV criteria for pain disorder were met. Other psychiatric diagnoses were accepted only if DSM-III-R criteria were met. Again, both reviewers had to agree. For the SPD group, records of psychotherapists were scrutinized to determine working diagnosis. Particular attention was paid to see if the pain was conceptualized as part of a psychological pain disorder or whether the pain was considered a natural result of a physical disorder. A compensation/litigation scale was developed.26 Examples of rated items included aggravation of symptoms in response to events associated with litigation, such as scheduling of a hearing or independent medical examination. The scale was tested for interrater reliability, which was fair (3 raters for 13 subjects; kappa⳱ 0.21, P⬍0.01). Psychosomatics 41:3, May-June 2000
Streltzer et al. A scale was developed to assess the severity of SPD as measured by objective behaviors. The scale failed to meet a satisfactory standard of reliability, however, and it was not used in the analyses. This quasi-experimental design27 examined differences between SPD subjects and control subjects using Student’s t-tests on continuous variables, and v2 and Fisher exact tests on categorical variables. Because multiple comparisons were being made, a Bonferroni correction was applied, and P values were adjusted accordingly. RESULTS Demographic and medical characteristics are presented in Table 1. Although women seemed to be overrepresented in the SPD group compared with injured control subjects, this was not significant. Further analysis also indicated that the variables distinguishing SPD from control subjects were not influenced by gender. Overall, the two groups were remarkably similar. Medical data strongly differentiated the two groups, however, confirming their diagnostic distinctiveness. Pain variables are presented in Table 2. Pain had notably different characteristics in the SPD group. Pain ocTABLE 1.
curred in two or more distinct sites for all SPD subjects except one. Almost half the control subjects (20 of 43) had pain complaints in only one site. Particularly striking was the finding that pain usually spread from the original site(s) of injury to new areas in the SPD group, but this never occurred in the control group. Treatment variables are presented in Table 3. Physical therapy had been particularly common, and many SPD subjects had several courses. No treatment had any lasting effect on pain complaints or associated disability in SPD patients. Daily opiate and benzodiazepine use were rare in the control group but common in the SPD group. Daily barbiturates, used by five SPD patients, consisted of butalbital preparations prescribed for headaches (headaches were never the original painful symptom from the injury). Antidepressant use was common overall. No case was found in which antidepressants clearly improved pain, although depression sometimes improved. Historical factors did not differentiate the two groups. These included a history of alcohol abuse (17% vs. 14%, NS), child abuse (21% vs. 12%, NS), and prior pain problems (53% vs. 37%, NS). Comorbid diagnoses, which fulfilled DSM-III-R criteria, were common (Table 4). There
Comparisons of demographic characteristics and medical evaluation in somatoform pain disorder and injured control groups
Mean age Gender Mean education Time from injury to evaluation Mean # of MDs who cannot medically explain cause of pain Mean # of MDs who can explain cause of pain Mean # of special tests (MRI, CT, EMG) Nonphysiological findings on physical exam, n(%)
Somatoform Pain Disorder Group (nⴔ47)
Injured Control Group (nⴔ43)
Statistic Degrees of Freedom Bonferroni-corrected P
39.3 years 21 M / 26 F 12.6 years 30.9 months 2.9 0.6 1.9 26 (55%)
38.7 years 31 M / 12 F 12.2 years 32.0 months 0.5 1.9 0.7 3 (7%)
NS NS NS NS t⳱ⳮ6.38, df⳱80, P⬍0.001 t⳱4.15, df⳱82, P⬍0.001 t⳱(3.95, df⳱86, P⬍0.001 X2⳱21.87, df⳱1, P⬍0.001
Note: NS⳱not significant; MRI⳱magnetic resonance imaging; CT⳱ computed tomography scan, EMG ⳱ electromyogram.
TABLE 2.
Comparisons of pain characteristics in somatoform pain disorder and injured control groups
Mean duration of pain Mean # of pain sites Two or more pain sites, n(%) Spread of pain from site of injury, n(%) Pain prevents work, n(%)
Somatoform Pain Disorder Group (nⴔ47)
Injured Control Group (nⴔ43)
Statistic Degrees of Freedom Bonferroni-corrected P
Odds Ratio (95% Confidence Interval)
40.7 months 5.2 46 (98%) 43 (91%) 39 (83%)
21.5 months 2.3 23 (53%) 0% (0) 9 (23%)
t⳱3.21, df⳱86, P⳱0.005 t⳱ⳮ6.11, df⳱86, P⬍0.001 X2⳱22.31, df⳱1, P⬍0.001 X2⳱71.71, df⳱1, P⬍0.001 X2⳱32.29, df⳱1, P⬍0.001
NA NA OR⳱40.00 (5.50, 1692.69) OR⳱451.50 (43.35, 11652.57) OR⳱18.42 (5.76, 62.25)
Note: NA⳱not applicable; OR⳱odds ratio.
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Chronic Pain was a trend toward more Axis I diagnoses (other than SPD) in the control group, and a trend toward more Axis II diagnoses in the SPD group. Compensation/litigation issues were found to have major influence in 40% of the SPD group, moderate influence in 9%, and minimal influence in 51%. In contrast, the control group had 7% major, 16% moderate, and 77% minimal influence (v2 ⳱13.72, df⳱1, P⳱0.007). The cases were also reviewed to see if they fulfilled criteria for DSM-III and DSM-IV pain disorders. Of the SPD group, 57% qualified for DSM-III psychogenic pain disorder (and no control subjects). Of the SPD group, 100% had a DSM-IV Axis I pain disorder: 64% qualified for pain disorder associated with psychological factors, and the other 36% qualified for pain disorder associated with both psychological factors and a general medical condition (medical factors were significant at the onset of the disorder TABLE 3.
but not at the time of evaluation). Seven percent of the control subjects also fulfilled DSM-IV criteria. Scrutiny of the psychotherapists’ records for the SPD patients revealed that 47% of the therapists viewed the pain complaints as appropriate to a physical illness, 32% did not, and 21% could not be determined from the records.
Case Reports
To portray the strikingly different impression given by subjects in the two groups, the following case vignettes are presented. Case example from the SPD group: A 48-year-old divorced woman employed as a clerical worker complained of pain in her wrists, forearms, and upper arms related to the use of her
Comparisons of treatment and medication types in somatoform pain disorder(nⴔ47) and injured control groups(nⴔ43) Somatoform Pain Disorder Group n (%)
Injured Control Group n (%)
Statistic Degrees of Freedom Bonferroni-corrected P
Odds Ratio (95% Confidence Interval)
Treatments Biofeedback Chiropractor Massage Physical Therapy Psychotherapy Surgery TENS
8 22 15 39 36 10 14
(17%) (47%) (32%) (83%) (77%) (21%) (30%)
1 14 3 20 36 16 2
(2%) (33%) (7%) (47%) (84%) (37%) (5%)
NS NS X2⳱7.24, df⳱1, P⳱0.025 X2⳱11.66, df⳱1, P⳱0.002 NS NS X2⳱8.06, df⳱1, P⳱0.016
NA NA OR⳱8.70 (1.76, 82.47) OR⳱5.61 (1.95, 16.94) NA NA OR⳱8.70 (1.76, 82.47)
Medication Opiates Benzodiazapines Barbituates Antidepressants
23 16 5 28
(49%) (34%) (11%) (60%)
4 2 0 15
(9%) (5%) (0%) (35%)
X2⳱14.96, df⳱1, P⬍0.001 X2⳱10.36, df⳱1, P⳱0.006 NS NS
OR⳱9.34 (2.61, 36.60) OR⳱10.58 (2.18, 99.30) NA NA
Note: NS⳱not significant; NA⳱not applicable, OR⳱odds ratio; TENS⳱transcutaneous electrical nerve stimulation.
TABLE 4.
Comparisons of psychiatric diagnoses in somatoform pain disorder (nⴔ47) and injured control groups (nⴔ43) Somatoform Pain Disorder Group n (%)
Injured Control Group n (%)
Statistic Degrees of Freedom Bonferroni-corrected P
Comorbid diagnoses (DSM-III-R) Axis I Any Depression Major Depression Anxiety Disorder Substance Abuse Any Diagnosis Axis II
22 19 2 7 29 14
(47%) (40%) (4%) (15%) (61%) (30%)
23 14 11 7 38 3
(53%) (30%) (23%) (16%) (88%) (7%)
NS NS NS NS X2⳱7.05, df⳱1, P⳱0.024 NS
Note: NS ⳱ not significant
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Psychosomatics 41:3, May-June 2000
Streltzer et al. arms in packing and unpacking boxes at work. She described her overall pain as constant at an 8/10 level and often reaching 10. She had developed the pain while at work 7 years before. She had been out of work on workers’ compensation disability about half the time since then. She stated she was working now only because her doctor would not certify her as currently disabled. At the time of injury she complained only of bilateral upper arm soreness after moving heavy boxes at work. She saw a physician who prescribed anti-inflammatory medication and 2 days off work. The pain increased, however, and eventually involved the forearms, wrists, fingers, and shoulders. At times she also complained of constant headaches and back pain. She considered herself to be in good health, otherwise. She reported that she was not supposed to drive because of her hand problems, but because she “had to,” she did anyway. She took several codeine tablets per day for her pain and for sleep. She stated she had to be careful not to take too much, or she would appear “giddy” at work. Medical records revealed that she had complained of headaches, back pain, neck pain, shoulder pains, foot pain, and other somatic symptoms on and off for years before her work injury claim. Subsequent to the injury claim, several medical consultants found the complaints to be remarkably dramatic and inconsistent with activity or physical exam. She had bilateral carpal tunnel operations performed despite the fact that her symptoms covered many areas not explained by carpal tunnel syndrome, and despite normal nerve conduction studies, and the opinions of a neurologist and a hand specialist that the patient did not have carpal tunnel syndrome. The surgeon’s progress notes revealed that he operated based on subjective complaints only, and he documented the strong possibility that her symptoms may not be relieved. In fact, symptoms increased following each surgery. For 18 months, she had been treated in a chronic pain clinic with group therapy, fluoxetine (60 mg per day), and trazodone (100 mg at bedtime). Case example from the control group: A 45-year-old carpenter was evaluated 1 year after breaking his ankle when a wooden beam fell on it. The patient reported that his ankle was crushed and was surgically repaired the same day. He had pain for several months, taking 2 or 3 oxycodone tablets per day and drinking 4–5 beers. After 3 months he underwent physical therapy, which helped, and he gradually returned to work. At one point, a screw was removed from the ankle, and the pain greatly diminished. Three months after the injury, he developed an attack of “shaking,” associated with extreme anxiety. He then saw a psychiatrist and began medication. He still uses occasional diazepam when he fears another attack. He no longer is concerned about the pain in his ankle. His ankle aches after working for several hours, but he manages this with aspirin. Medical records were consistent with the patient’s history. They revealed some cocaine and alcohol abuse prior to age 30, but only minor medical problems until the ankle fracture. Surgery reduced and immobilized the fracture on the day of injury. The subsequent course was complicated by swelling of the ankle and difficulties with the cast. Oxycodone was prescribed in steadily decreasing amounts for the first two postoperative Psychosomatics 41:3, May-June 2000
months. A screw was removed 6 months after injury with no further complications, except for anxiety attacks.
DISCUSSION Establishing the validity of somatoform diagnoses is a particularly daunting task in psychiatry.20 The availability of extensive medical records allowed us to study a group of SPD patients with greater diagnostic certainty than previously possible. The opportunity to compare these SPD patients with a control group also provided this study with unique advantages. Requiring complete agreement between raters gives confidence that two distinct groups were achieved and that the study has internal consistency. Similarities in age, education, and length of time from injury to evaluation suggest that the control group eliminated many potentially confounding influences, allowing the characteristics of SPD to be delineated. An argument could be made that the ideal control group would have been derived from the population of all subjects injured on the job or in motor vehicle accidents, regardless of referrals for psychiatric evaluation. The infeasibility of obtaining all medical records from such individuals, and subjecting them to a prolonged, intensive psychiatric evaluation, however, has resulted in a lack of studies of chronic pain disorder patients despite the importance in terms of disability and use of medical resources.28 The control group, while perhaps not being ideal, matched the pain disorder group in that psychiatric disorders were involved or suspected in association with the physical injury. Thus, the SPD group could be examined for whether characteristics specific to the pain disorder were present, which differed from injured patients in general who also had psychiatric disorders. A striking finding was the number of distinct sites of pain in the SPD group. The presence of multiple pain sites has been shown to correlate with psychiatric disturbance and dysfunctional pain status.29 Multiple sites of pain and spread of pain from the site of original injury to new locations strongly differentiated the SPD group from the control subjects whose pain was not grossly disproportionate to objective findings. In contrast, a history of alcohol or substance abuse did not differentiate the groups, nor did a history of child abuse. Although a childhood history of physical and sexual abuse was sought in all cases, it is possible that the true frequency is higher than what was found, since patients may be reluctant to report such information. Our prevalence rates for child abuse were quite similar to the 14%–15% rate found in a large community 231
Chronic Pain sample.30 However, with a larger sample size, the difference between the SPD and control groups may have become significant, but in our study, findings indicate that child abuse is not a major antecedent of SPD. Comorbid psychiatric diagnoses, particularly depression, were common in the SPD group, but with the possible exception of personality disorders, they were less common than the control group. Personality disorder diagnoses tend to be unreliable no matter how they are diagnosed.31 Strict comparison with the control group, however, lends confidence to the conclusion that personality disorders may be more prevalent in SPD than with those who do not develop SPD. Our finding that 30% of the SPD group had personality disorders is comparable to a previously reported 37% personality disorder rate in chronic pain patients.32 These rates are substantially higher than those found in the general population.33 Daily use of prescription opiates and benzodiazepines was far more common in the SPD group. Use was rare in the control group, despite the fact that the injuries in this group were often substantial. Chronic pain patients are known to underestimate their medication use,34 but because of the medical record availability, we believe this was accurately assessed. In many cases, opiate intake was particularly high, exceeding 10 pills per day. There has been a trend in recent literature to recommend opiate maintenance for selected patients with chronic, noncancer pain.35–37 There is increasing evidence, however, that chronic opioid intake can produce hypersensitivity to pain and perhaps foster ongoing pain.38–42 Our findings suggest that it is the patients with minimal objective findings who are most likely to be maintained on dependency-producing drugs. Antidepressant use was common in both groups, often with apparent success in alleviating depression. Remarkably, we found no case in which antidepressant therapy had any lasting effect on pain complaints, even when depression improved. The SPD group often had several courses of antidepressant therapy, typically reaching dose levels equivalent to 20 mg of fluoxetine or 150 mg of amitriptyline for 1 month or longer. Antidepressants are frequently recommended as adjunctive treatment for chronic pain,43 and controlled trials have demonstrated efficacy in a few specific pain syndromes.9 Controlled studies have not consistently reported antidepressant efficacy in alleviating chronic pain in general; however, they have not been attempted specifically for SPD.44,45 The role of compensation/litigation in causing or in maintaining chronic pain has been unresolved and subject 232
to strong and conflicting opinions.6,9,46–49 We developed a simple scale with face validity and reasonable reliability in an attempt to objectify this controversial area. We found that for about half the SPD group, compensation/litigation was an important factor in maintaining symptomatology, but in the other half this was not the case. The control group had the same opportunities for workers’ compensation or personal injury litigation, but this substantially influenced only 23%. These results are consistent with a meta-analytic review in which financial incentives were found to be more influential when prolonged disability followed less severe injury.4 Similarly, disability from work after lower back injury has been found to be strongly related to compensation status but not to severity of injury.50 Most subjects had been referred for psychotherapy. Subjects frequently accepted this on the grounds that the chronic pain was very stressful and disruptive in their lives. Therapists’ records indicated that all too frequently the patient’s explanation of the pain was accepted at face value. These therapists supported their patients’ view of themselves as pain-ridden and disabled due to physical causes. These therapists often encouraged further medical workup and even surgery as a treatment option. Overall, SPD patients presented in a rather typical manner, which contrasted sharply with the control group. After a minor or trivial injury, pain developed, became more severe with time, and then spread to new locations. The symptoms were not limited to or characteristic of areas of potential pathology. Descriptions of the pain tended to be extreme, and nonphysiological findings were present on physical exam. Objective physical findings were lacking; and CT scans, MRIs, and nerve conduction studies were often performed in a vain attempt to demonstrate pathology. The patient often focused on minor degenerative changes found on MRI or CT as proof of an objective and medical basis for the pain. Such changes were usually not different from the norm found in the general nonsymptomatic population.51–54 Numerous types of treatment were attempted and repeated; none of which provided any lasting relief of pain. Passive physical therapies, chiropractic manipulation, and massage were most likely to be appreciated by the SPD patient, who might report pain relief lasting from minutes to hours, but relief was always temporary. The patient often seemed to desire acknowledgment of disability more than encouragement about the potential benefits of treatment. In conclusion, the SPD group had several associated features that distinguished it from the control group. These features included nonphysiological findings on physical Psychosomatics 41:3, May-June 2000
Streltzer et al. exam, increased use of diagnostic tests, multiple sites of pain which spread to new locations, frequent use of dependency-producing medications, and lack of response to all types of treatment. This study supports the use of SPD as a distinct diagnostic category, at least within the injury population studied. Further studies might determine if the associated features are predictive in order to enable diagnosis without the availability of extensive medical records.
Implications for treatment include recognizing the features of SPD, emphasizing function rather than focusing on pain complaints, and minimizing interventions that risk introducing complications.55 This study was presented at the 151st Annual Meeting of The American Psychiatric Association, Toronto, May 30–June 4, 1998.
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49. Allaz AF, Vannotti M, Desmeules J, et al: Use of the label “litigation neurosis” in patients with somatoform pain disorder. Gen Hosp Psychiatry 1998; 20:91–97 50. Greenough CG: Recovery from low back pain. Acta Orthop Scand 1993; 64 (Suppl 254):1–34 51. Jensen MC, Brandt-Zawadzki MN, Obuchowsi N, et al: Magnetic resonance imaging of the lumbar spine in people without back pain. N Engl J Med 1994; 331:69–73 52. Boden SD, Davis DO, Dina TS, et al, Abnormal magnetic-resonance scans of the lumbar spine in asymptomatic subjects. J Bone Joint Surg 1990; 72A:403–408 53. Wiesel SW, Tsourmas N, Feffer HL, et al: A study of computerassisted tomography I. The incidence of positive CAT scans in an asymptomatic group of patients. Spine 1984; 9:549–551 54. Deyo RA: Magnetic resonance imaging of the lumbar spine—terrific test or tar baby? New Engl J Med 1994; 331:115–116 55. Streltzer J: Chronic pain, in Biopsychosocial Approaches in Primary Care: State of the Art and Challenges for the 21st Century, edited by Leigh H, New York, Plenum Press, 1997
Psychosomatics 41:3, May-June 2000
Pain disorders that are primarily associated with psychological factors are of great clinical concern, but they are difficult to study because of the inability to make valid or reliable diagnoses by structured interview alone. The authors confront this difficulty by using an injured subject population that had extensive psychiatric and medical evaluations. Those who developed somatoform pain disorder (SPD) were compared with a control group who did not. The SPD group had distinctive associated factors: more sites of pain, spread of pain beyond area of original injury, and substantially more opiate and benzodiazepine use. Compensation/litigation influenced symptoms more in the SPD group. Psychotherapists often supported the patient’s viewpoint that the pain was physical and to be endured. (Psychosomatics 2000; 41:227–234)
C
hronic pain is a poorly understood condition subject to a variety of interpretations and theories with respect to its etiology and persistence.1 The duration and degree of pain and disability following physical injury may be unrelated to the apparent severity of the injury,2,3 especially if compensation is involved.4–6 Patients suffering severe trauma often experience substantial pain only until their injuries stabilize and begin to heal. If the pain persists, it is ordinarily manageable without opiate analgesics. In contrast, among patients who develop chronic pain, a history of relatively minor trauma is common. Chronic pain has been described as a syndrome or process with many dysfunctional features not explained by physical pathology.7 Psychological factors are considered important, including depression, hypochondriasis, medication dependence, and situational factors.2,8–11 Assessment of these factors is difficult, and they are often inadequately appreciated in clinical management.12 A multidisciplinary approach to treatment is generally advocated,9,13 but results may be less than satisfactory.14,15 DSM-III-R and DSM-IV recognize a chronic pain disorder that is predominantly psychological and classify it within the group of somatoform disorders. Presumably, this is a specific type of chronic pain disorder, but its epidemiology is unknown. Population surveys, even those asPsychosomatics 41:3, May-June 2000
sessing chronic pain patients, usually do not attempt to assess a somatoform pain disorder (SPD),11,16,17 probably because diagnosis does not seem amenable to self-report, and medical evaluations are required to rule out organic explanations of the pain. The Structured Clinical Interview for DSM-III-R (SCID) has not been shown to reliably diagnose SPD.18 A study designed to assess “somatization,” a concept that includes various somatoform disorders (including chronic pain disorder), reported a prevalence of 9%–20% in the general population,19 suggesting that pain disorder may be common. Another study of 1,000 patients in primary care clinics found somatoform disorders in 14% of the patients; these disorders frequently included unexplained pain symptoms.20 On the basis of clinical experience with chronic pain patients, we hypothesized that if adequate medical information were available, many of these patients would be diagnosed as having somatoform pain disorders. We predicted that they would have a number of characteristics that would distinguish them from injured patients who did not Received March 4, 1999; revised September 23, 1999; accepted October 22, 1999. From the Department of Psychiatry, John A. Burns School of Medicine, Honolulu, Hawaii. Address reprint requests to Dr. Streltzer, Department of Psychiatry, 1356 Lusitana St., Honolulu, HI 96813. Copyright 䉷 2000 The Academy of Psychosomatic Medicine.
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Chronic Pain develop a chronic pain disorder. These characteristics included more frequent depression, the use of more dependency-producing medications, the use of more surgery for the pain,21 and an increased susceptibility to the influence of compensation or litigation on maintaining symptoms. To test these hypotheses, we studied a population of injured workers, all of whom were referred for psychiatric evaluation. Some of these workers developed a chronic pain disorder, and they were compared with those who did not. Because all of these patients were litigating or seeking benefits, their past medical records (sometimes lifetime) were available. This presented a unique opportunity to compare chronic somatoform pain patients to a control group. METHODS Cases were selected from independent psychiatric evaluations conducted on workers’ compensation and automobile accident claimants seen between January 1, 1989, and June 30, 1992. They were examined by two board-certified psychiatrists who have experience with psychiatric impairment evaluations. Each subject received a comprehensive psychiatric evaluation along the lines of London et al.22 and recommended by the state of California, Division of Industrial Accidents.23 This included a 2- to 5-hour interview, sometimes supplemented by questionnaires and psychological tests. Extensive medical records were reviewed in all cases. These records were not limited to treatment of a specific injury. Records were obtained by insurance adjusters and attorneys by voluntary release and by subpoena. The psychiatrists generated a detailed report of 18–30 single-spaced pages. At the time of evaluation, the examiners were unaware that a study of pain disorders would occur. Each report was screened by one or another of the reviewers (JS or BE) to determine if a physical injury occurred. Two groups were generated from the screening: an “SPD” group, if a diagnosis of an SPD was present (DSMIII-R); and a “control” group, if no somatoform diagnosis was present. Fifty-four cases were initially screened into each group. This represented all of the potential control subjects and most of the potential SPD subjects who were chosen alphabetically. All data were obtained from the reports. For the SPD group, both reviewers had to agree that the case unequivocally met DSM-III-R criteria for somatoform pain disorder. The diagnosis was accepted only if the medical records documented the absence of physical or laboratory findings that could explain the pain, or if pain complaints were grossly disproportionate to any objective 228
findings that may have been present. Borderline cases, including cases of suspected malingering, were excluded. The criteria for malingering were obvious inconsistencies in behavior documented in the medical records or by surreptitious surveillance. For the control group, both reviewers had to agree that somatoform pain disorder or any other somatoform disorder was not a diagnosis. If physical pain was present, it had to be explained by objective findings in the medical records. After eliminating cases in which both reviewers had not concluded that the subject unequivocally fit into one of the groups, 47 SPD cases and 43 control subjects remained for study. Data collected included demographic information, duration of pain complaints, number of pain sites, location of pain and its relation to the site of initial injury, types of treatments, and medications. Use of opiates, benzodiazepines, and barbiturates was considered positive if used daily for at least 6 months at the time of evaluation. Illicit drug use was also recorded. Significant alcohol use was considered present if there was a history of three or more drinks daily or binge drinking. Nonphysiological findings were considered present if medical records revealed nonanatomical sensory findings, nonphysiological weakness, inconsistent range of motion, or positive Waddell’s signs.24,25 Reviewers tabulated the following: anger at working conditions pre- and postinjury, whether pain prevented work, prior history of significant pain problem, history of child abuse, number of specialized imaging and electrodiagnostic tests [e.g., magnetic resonance imaging (MRI), computed tomography (CT) scan, electromyogram (EMG)], number of surgeries, and number of medical consultants who did or did not consider the pain symptoms explainable by objective findings. Subject reports were also evaluated to determine whether DSM-III criteria for psychogenic pain disorder and DSM-IV criteria for pain disorder were met. Other psychiatric diagnoses were accepted only if DSM-III-R criteria were met. Again, both reviewers had to agree. For the SPD group, records of psychotherapists were scrutinized to determine working diagnosis. Particular attention was paid to see if the pain was conceptualized as part of a psychological pain disorder or whether the pain was considered a natural result of a physical disorder. A compensation/litigation scale was developed.26 Examples of rated items included aggravation of symptoms in response to events associated with litigation, such as scheduling of a hearing or independent medical examination. The scale was tested for interrater reliability, which was fair (3 raters for 13 subjects; kappa⳱ 0.21, P⬍0.01). Psychosomatics 41:3, May-June 2000
Streltzer et al. A scale was developed to assess the severity of SPD as measured by objective behaviors. The scale failed to meet a satisfactory standard of reliability, however, and it was not used in the analyses. This quasi-experimental design27 examined differences between SPD subjects and control subjects using Student’s t-tests on continuous variables, and v2 and Fisher exact tests on categorical variables. Because multiple comparisons were being made, a Bonferroni correction was applied, and P values were adjusted accordingly. RESULTS Demographic and medical characteristics are presented in Table 1. Although women seemed to be overrepresented in the SPD group compared with injured control subjects, this was not significant. Further analysis also indicated that the variables distinguishing SPD from control subjects were not influenced by gender. Overall, the two groups were remarkably similar. Medical data strongly differentiated the two groups, however, confirming their diagnostic distinctiveness. Pain variables are presented in Table 2. Pain had notably different characteristics in the SPD group. Pain ocTABLE 1.
curred in two or more distinct sites for all SPD subjects except one. Almost half the control subjects (20 of 43) had pain complaints in only one site. Particularly striking was the finding that pain usually spread from the original site(s) of injury to new areas in the SPD group, but this never occurred in the control group. Treatment variables are presented in Table 3. Physical therapy had been particularly common, and many SPD subjects had several courses. No treatment had any lasting effect on pain complaints or associated disability in SPD patients. Daily opiate and benzodiazepine use were rare in the control group but common in the SPD group. Daily barbiturates, used by five SPD patients, consisted of butalbital preparations prescribed for headaches (headaches were never the original painful symptom from the injury). Antidepressant use was common overall. No case was found in which antidepressants clearly improved pain, although depression sometimes improved. Historical factors did not differentiate the two groups. These included a history of alcohol abuse (17% vs. 14%, NS), child abuse (21% vs. 12%, NS), and prior pain problems (53% vs. 37%, NS). Comorbid diagnoses, which fulfilled DSM-III-R criteria, were common (Table 4). There
Comparisons of demographic characteristics and medical evaluation in somatoform pain disorder and injured control groups
Mean age Gender Mean education Time from injury to evaluation Mean # of MDs who cannot medically explain cause of pain Mean # of MDs who can explain cause of pain Mean # of special tests (MRI, CT, EMG) Nonphysiological findings on physical exam, n(%)
Somatoform Pain Disorder Group (nⴔ47)
Injured Control Group (nⴔ43)
Statistic Degrees of Freedom Bonferroni-corrected P
39.3 years 21 M / 26 F 12.6 years 30.9 months 2.9 0.6 1.9 26 (55%)
38.7 years 31 M / 12 F 12.2 years 32.0 months 0.5 1.9 0.7 3 (7%)
NS NS NS NS t⳱ⳮ6.38, df⳱80, P⬍0.001 t⳱4.15, df⳱82, P⬍0.001 t⳱(3.95, df⳱86, P⬍0.001 X2⳱21.87, df⳱1, P⬍0.001
Note: NS⳱not significant; MRI⳱magnetic resonance imaging; CT⳱ computed tomography scan, EMG ⳱ electromyogram.
TABLE 2.
Comparisons of pain characteristics in somatoform pain disorder and injured control groups
Mean duration of pain Mean # of pain sites Two or more pain sites, n(%) Spread of pain from site of injury, n(%) Pain prevents work, n(%)
Somatoform Pain Disorder Group (nⴔ47)
Injured Control Group (nⴔ43)
Statistic Degrees of Freedom Bonferroni-corrected P
Odds Ratio (95% Confidence Interval)
40.7 months 5.2 46 (98%) 43 (91%) 39 (83%)
21.5 months 2.3 23 (53%) 0% (0) 9 (23%)
t⳱3.21, df⳱86, P⳱0.005 t⳱ⳮ6.11, df⳱86, P⬍0.001 X2⳱22.31, df⳱1, P⬍0.001 X2⳱71.71, df⳱1, P⬍0.001 X2⳱32.29, df⳱1, P⬍0.001
NA NA OR⳱40.00 (5.50, 1692.69) OR⳱451.50 (43.35, 11652.57) OR⳱18.42 (5.76, 62.25)
Note: NA⳱not applicable; OR⳱odds ratio.
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Chronic Pain was a trend toward more Axis I diagnoses (other than SPD) in the control group, and a trend toward more Axis II diagnoses in the SPD group. Compensation/litigation issues were found to have major influence in 40% of the SPD group, moderate influence in 9%, and minimal influence in 51%. In contrast, the control group had 7% major, 16% moderate, and 77% minimal influence (v2 ⳱13.72, df⳱1, P⳱0.007). The cases were also reviewed to see if they fulfilled criteria for DSM-III and DSM-IV pain disorders. Of the SPD group, 57% qualified for DSM-III psychogenic pain disorder (and no control subjects). Of the SPD group, 100% had a DSM-IV Axis I pain disorder: 64% qualified for pain disorder associated with psychological factors, and the other 36% qualified for pain disorder associated with both psychological factors and a general medical condition (medical factors were significant at the onset of the disorder TABLE 3.
but not at the time of evaluation). Seven percent of the control subjects also fulfilled DSM-IV criteria. Scrutiny of the psychotherapists’ records for the SPD patients revealed that 47% of the therapists viewed the pain complaints as appropriate to a physical illness, 32% did not, and 21% could not be determined from the records.
Case Reports
To portray the strikingly different impression given by subjects in the two groups, the following case vignettes are presented. Case example from the SPD group: A 48-year-old divorced woman employed as a clerical worker complained of pain in her wrists, forearms, and upper arms related to the use of her
Comparisons of treatment and medication types in somatoform pain disorder(nⴔ47) and injured control groups(nⴔ43) Somatoform Pain Disorder Group n (%)
Injured Control Group n (%)
Statistic Degrees of Freedom Bonferroni-corrected P
Odds Ratio (95% Confidence Interval)
Treatments Biofeedback Chiropractor Massage Physical Therapy Psychotherapy Surgery TENS
8 22 15 39 36 10 14
(17%) (47%) (32%) (83%) (77%) (21%) (30%)
1 14 3 20 36 16 2
(2%) (33%) (7%) (47%) (84%) (37%) (5%)
NS NS X2⳱7.24, df⳱1, P⳱0.025 X2⳱11.66, df⳱1, P⳱0.002 NS NS X2⳱8.06, df⳱1, P⳱0.016
NA NA OR⳱8.70 (1.76, 82.47) OR⳱5.61 (1.95, 16.94) NA NA OR⳱8.70 (1.76, 82.47)
Medication Opiates Benzodiazapines Barbituates Antidepressants
23 16 5 28
(49%) (34%) (11%) (60%)
4 2 0 15
(9%) (5%) (0%) (35%)
X2⳱14.96, df⳱1, P⬍0.001 X2⳱10.36, df⳱1, P⳱0.006 NS NS
OR⳱9.34 (2.61, 36.60) OR⳱10.58 (2.18, 99.30) NA NA
Note: NS⳱not significant; NA⳱not applicable, OR⳱odds ratio; TENS⳱transcutaneous electrical nerve stimulation.
TABLE 4.
Comparisons of psychiatric diagnoses in somatoform pain disorder (nⴔ47) and injured control groups (nⴔ43) Somatoform Pain Disorder Group n (%)
Injured Control Group n (%)
Statistic Degrees of Freedom Bonferroni-corrected P
Comorbid diagnoses (DSM-III-R) Axis I Any Depression Major Depression Anxiety Disorder Substance Abuse Any Diagnosis Axis II
22 19 2 7 29 14
(47%) (40%) (4%) (15%) (61%) (30%)
23 14 11 7 38 3
(53%) (30%) (23%) (16%) (88%) (7%)
NS NS NS NS X2⳱7.05, df⳱1, P⳱0.024 NS
Note: NS ⳱ not significant
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Psychosomatics 41:3, May-June 2000
Streltzer et al. arms in packing and unpacking boxes at work. She described her overall pain as constant at an 8/10 level and often reaching 10. She had developed the pain while at work 7 years before. She had been out of work on workers’ compensation disability about half the time since then. She stated she was working now only because her doctor would not certify her as currently disabled. At the time of injury she complained only of bilateral upper arm soreness after moving heavy boxes at work. She saw a physician who prescribed anti-inflammatory medication and 2 days off work. The pain increased, however, and eventually involved the forearms, wrists, fingers, and shoulders. At times she also complained of constant headaches and back pain. She considered herself to be in good health, otherwise. She reported that she was not supposed to drive because of her hand problems, but because she “had to,” she did anyway. She took several codeine tablets per day for her pain and for sleep. She stated she had to be careful not to take too much, or she would appear “giddy” at work. Medical records revealed that she had complained of headaches, back pain, neck pain, shoulder pains, foot pain, and other somatic symptoms on and off for years before her work injury claim. Subsequent to the injury claim, several medical consultants found the complaints to be remarkably dramatic and inconsistent with activity or physical exam. She had bilateral carpal tunnel operations performed despite the fact that her symptoms covered many areas not explained by carpal tunnel syndrome, and despite normal nerve conduction studies, and the opinions of a neurologist and a hand specialist that the patient did not have carpal tunnel syndrome. The surgeon’s progress notes revealed that he operated based on subjective complaints only, and he documented the strong possibility that her symptoms may not be relieved. In fact, symptoms increased following each surgery. For 18 months, she had been treated in a chronic pain clinic with group therapy, fluoxetine (60 mg per day), and trazodone (100 mg at bedtime). Case example from the control group: A 45-year-old carpenter was evaluated 1 year after breaking his ankle when a wooden beam fell on it. The patient reported that his ankle was crushed and was surgically repaired the same day. He had pain for several months, taking 2 or 3 oxycodone tablets per day and drinking 4–5 beers. After 3 months he underwent physical therapy, which helped, and he gradually returned to work. At one point, a screw was removed from the ankle, and the pain greatly diminished. Three months after the injury, he developed an attack of “shaking,” associated with extreme anxiety. He then saw a psychiatrist and began medication. He still uses occasional diazepam when he fears another attack. He no longer is concerned about the pain in his ankle. His ankle aches after working for several hours, but he manages this with aspirin. Medical records were consistent with the patient’s history. They revealed some cocaine and alcohol abuse prior to age 30, but only minor medical problems until the ankle fracture. Surgery reduced and immobilized the fracture on the day of injury. The subsequent course was complicated by swelling of the ankle and difficulties with the cast. Oxycodone was prescribed in steadily decreasing amounts for the first two postoperative Psychosomatics 41:3, May-June 2000
months. A screw was removed 6 months after injury with no further complications, except for anxiety attacks.
DISCUSSION Establishing the validity of somatoform diagnoses is a particularly daunting task in psychiatry.20 The availability of extensive medical records allowed us to study a group of SPD patients with greater diagnostic certainty than previously possible. The opportunity to compare these SPD patients with a control group also provided this study with unique advantages. Requiring complete agreement between raters gives confidence that two distinct groups were achieved and that the study has internal consistency. Similarities in age, education, and length of time from injury to evaluation suggest that the control group eliminated many potentially confounding influences, allowing the characteristics of SPD to be delineated. An argument could be made that the ideal control group would have been derived from the population of all subjects injured on the job or in motor vehicle accidents, regardless of referrals for psychiatric evaluation. The infeasibility of obtaining all medical records from such individuals, and subjecting them to a prolonged, intensive psychiatric evaluation, however, has resulted in a lack of studies of chronic pain disorder patients despite the importance in terms of disability and use of medical resources.28 The control group, while perhaps not being ideal, matched the pain disorder group in that psychiatric disorders were involved or suspected in association with the physical injury. Thus, the SPD group could be examined for whether characteristics specific to the pain disorder were present, which differed from injured patients in general who also had psychiatric disorders. A striking finding was the number of distinct sites of pain in the SPD group. The presence of multiple pain sites has been shown to correlate with psychiatric disturbance and dysfunctional pain status.29 Multiple sites of pain and spread of pain from the site of original injury to new locations strongly differentiated the SPD group from the control subjects whose pain was not grossly disproportionate to objective findings. In contrast, a history of alcohol or substance abuse did not differentiate the groups, nor did a history of child abuse. Although a childhood history of physical and sexual abuse was sought in all cases, it is possible that the true frequency is higher than what was found, since patients may be reluctant to report such information. Our prevalence rates for child abuse were quite similar to the 14%–15% rate found in a large community 231
Chronic Pain sample.30 However, with a larger sample size, the difference between the SPD and control groups may have become significant, but in our study, findings indicate that child abuse is not a major antecedent of SPD. Comorbid psychiatric diagnoses, particularly depression, were common in the SPD group, but with the possible exception of personality disorders, they were less common than the control group. Personality disorder diagnoses tend to be unreliable no matter how they are diagnosed.31 Strict comparison with the control group, however, lends confidence to the conclusion that personality disorders may be more prevalent in SPD than with those who do not develop SPD. Our finding that 30% of the SPD group had personality disorders is comparable to a previously reported 37% personality disorder rate in chronic pain patients.32 These rates are substantially higher than those found in the general population.33 Daily use of prescription opiates and benzodiazepines was far more common in the SPD group. Use was rare in the control group, despite the fact that the injuries in this group were often substantial. Chronic pain patients are known to underestimate their medication use,34 but because of the medical record availability, we believe this was accurately assessed. In many cases, opiate intake was particularly high, exceeding 10 pills per day. There has been a trend in recent literature to recommend opiate maintenance for selected patients with chronic, noncancer pain.35–37 There is increasing evidence, however, that chronic opioid intake can produce hypersensitivity to pain and perhaps foster ongoing pain.38–42 Our findings suggest that it is the patients with minimal objective findings who are most likely to be maintained on dependency-producing drugs. Antidepressant use was common in both groups, often with apparent success in alleviating depression. Remarkably, we found no case in which antidepressant therapy had any lasting effect on pain complaints, even when depression improved. The SPD group often had several courses of antidepressant therapy, typically reaching dose levels equivalent to 20 mg of fluoxetine or 150 mg of amitriptyline for 1 month or longer. Antidepressants are frequently recommended as adjunctive treatment for chronic pain,43 and controlled trials have demonstrated efficacy in a few specific pain syndromes.9 Controlled studies have not consistently reported antidepressant efficacy in alleviating chronic pain in general; however, they have not been attempted specifically for SPD.44,45 The role of compensation/litigation in causing or in maintaining chronic pain has been unresolved and subject 232
to strong and conflicting opinions.6,9,46–49 We developed a simple scale with face validity and reasonable reliability in an attempt to objectify this controversial area. We found that for about half the SPD group, compensation/litigation was an important factor in maintaining symptomatology, but in the other half this was not the case. The control group had the same opportunities for workers’ compensation or personal injury litigation, but this substantially influenced only 23%. These results are consistent with a meta-analytic review in which financial incentives were found to be more influential when prolonged disability followed less severe injury.4 Similarly, disability from work after lower back injury has been found to be strongly related to compensation status but not to severity of injury.50 Most subjects had been referred for psychotherapy. Subjects frequently accepted this on the grounds that the chronic pain was very stressful and disruptive in their lives. Therapists’ records indicated that all too frequently the patient’s explanation of the pain was accepted at face value. These therapists supported their patients’ view of themselves as pain-ridden and disabled due to physical causes. These therapists often encouraged further medical workup and even surgery as a treatment option. Overall, SPD patients presented in a rather typical manner, which contrasted sharply with the control group. After a minor or trivial injury, pain developed, became more severe with time, and then spread to new locations. The symptoms were not limited to or characteristic of areas of potential pathology. Descriptions of the pain tended to be extreme, and nonphysiological findings were present on physical exam. Objective physical findings were lacking; and CT scans, MRIs, and nerve conduction studies were often performed in a vain attempt to demonstrate pathology. The patient often focused on minor degenerative changes found on MRI or CT as proof of an objective and medical basis for the pain. Such changes were usually not different from the norm found in the general nonsymptomatic population.51–54 Numerous types of treatment were attempted and repeated; none of which provided any lasting relief of pain. Passive physical therapies, chiropractic manipulation, and massage were most likely to be appreciated by the SPD patient, who might report pain relief lasting from minutes to hours, but relief was always temporary. The patient often seemed to desire acknowledgment of disability more than encouragement about the potential benefits of treatment. In conclusion, the SPD group had several associated features that distinguished it from the control group. These features included nonphysiological findings on physical Psychosomatics 41:3, May-June 2000
Streltzer et al. exam, increased use of diagnostic tests, multiple sites of pain which spread to new locations, frequent use of dependency-producing medications, and lack of response to all types of treatment. This study supports the use of SPD as a distinct diagnostic category, at least within the injury population studied. Further studies might determine if the associated features are predictive in order to enable diagnosis without the availability of extensive medical records.
Implications for treatment include recognizing the features of SPD, emphasizing function rather than focusing on pain complaints, and minimizing interventions that risk introducing complications.55 This study was presented at the 151st Annual Meeting of The American Psychiatric Association, Toronto, May 30–June 4, 1998.
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