Patients with reflex sympathetic dystrophy (RSD) often present with pain and disability that cannot be explained on the basis of objective physical findings. This has led some to speculate that RSD may be caused or mediated by non-organic factors. Unfortunately, there have been few studies using standardized measures of mood and illness behavior that have compared patients with RSD to patients with other chronic pain disorders. The goal of the present study, therefore, was to compare the pattern of psychological dysfunction in patients with RSD to the pattern of dysfunction in patients with chronic back pain and local neuropathic pain. Patients with back pain resemble those with RSD in that both may report symptoms that cannot be reconciled with objective physical findings. Patients with local neuropathy, by contrast, report pain that is both circumscribed and consistent with a known organic cause. The records of 253 patients attending a tertiary pain service were retrospectively reviewed and three distinct (non-overlapping) diagnostic groups were formed: 25 were assigned to the RSD group; 44 to the back pain group; and 21 to the local neuropathy group. Using a set of stringent criteria to diagnose RSD and an analysis of covariance to control for differences in symptom duration and age, the present study found no evidence to suggest that patients with RSD were psychologically unique. Instead, RSD patients were remarkably similar to those with local neuropathy in terms of their symptom reporting, illness behavior, and psychological distress. The only exception was that RSD patients had more disability days during the preceding 6 months than those with local neuropathy (P < 0.05). The back pain group, on the other hand, presented with more diffuse pain complaints (P < 0.05) and had a greater number of non-specific medical symptoms (P < 0.05) compared to either the RSD or local neuropathy group. In contrast to previous research using less stringent diagnostic criteria, there was no evidence of higher pain scores or lower levels of psychological distress among patients with RSD. In addition, a validated survey of childhood trauma found that sexual abuse, physical abuse, emotional abuse, and cumulative trauma were evenly distributed among all three diagnostic groups. The burden of proof would appear to be upon those who advocate the non-organic hypothesis to provide credible evidence of psychological involvement in the etiology of RSD.
Patients with chronic non-malignant pain are often suspected of reporting medical symptoms that have non-organic as opposed to purely organic origins. According to the somatization hypothesis, non-organic reporting occurs when affective or other benign physical sensations are misconstrued as symptoms of physical disease [corrected]. Psychological tests purporting to assess somatization are limited by their self-report format and may be confounded in patients with physical disease or injury. Measures of somatization may also be influenced or biased by underlying differences in depression or anxiety. In order to obtain an unbiased estimate of somatization, therefore, it is necessary to control for the influence of extraneous variables. In the present study, symptom report scales designed to assess somatization, symptom amplification, and disease conviction were administered to a group of 100 patients with chronic non-malignant pain. The strategy was to determine whether any of these tests could account for individual differences in illness behavior. Specifically, the set of dependent measures included: length of disability; frequency of medical visitation; activity level; and level of domestic functioning. The most successful predictor of patient behavior was the Somatization Scale (Derogatis et al. 1974) which correlated positively and significantly with each dependent measure. In order to examine the possibility that scores on this test were biased by differences in organic pathology, three physician pain specialists were asked to rate the morbidity of each item on the scale. A multiple regression analysis was then performed to examine whether differences in symptom morbidity, depression, or anxiety could account for the correlation between symptom ratings and illness behavior. The analysis showed that while depression and anxiety were significantly correlated with measures of illness behavior, the Somatization Scale still accounted for a significant amount of unique variance in three out of five dependent variables. Symptom morbidity was significantly correlated with only one measure of illness behavior (Activity Level). In view of these findings, scores on the Somatization Scale were used to classify 25 patients as Symptom Minimizers and another 25 as Symptom Amplifiers. When compared to Minimizers, Amplifiers were disabled for a significantly greater number of days, reported significantly more impairment in domestic functioning, were significantly less active, visited the doctor significantly more often, and were significantly more distressed. The results suggest that substantial differences in disability and medical visitation may exist among patients who may not differ appreciably in their level of organic pathology. Instead, differences in illness behavior may, to some extent, be mediated by differences in somatization.
There is still controversy surrounding the use of opioid medication for patients with chronic nonmalignant pain. Schofferman has argued that long-term opioid use leads to a "downhill spiral" associated with loss of functional capacity and a corresponding increase in depressed mood. The present study was a retrospective comparison of opioid users vs. non-users to determine whether: (a) users have higher levels of disability, medical visitation, depression, and pain; (b) the behavioral problems associated with opioid use persist after controlling for the influence of other medication; (c) opioid use is in fact a predictor of illness behavior; and (d) higher levels of opioid consumption are associated with higher levels of disability and depression. A consecutive series of 243 patients with nonmalignant pain about to enroll at a tertiary clinic were retrospectively assigned to either an Opioid User (n = 87) or Non-User (n = 156) group. Compared to Non-Users, Opioid Users were more likely to be physically disabled ( P <0.05) and depressed ( P<0.05), as well as more likely to report pain at higher levels (P<0.001) and in more locations ( P<0.05). Despite the appearance of a downhill spiral, we were unable to demonstrate an association between opioid use and any measure of illness behavior after controlling for benzodiazepine use (with the possible exception of domestic disability). Instead, we found that benzodiazepine use was significantly associated with activity level ( P<0.05), medical visitation ( P<0.01), domestic disability ( P<0.01), depression ( P <0.01), and to a lesser degree, disability days (P<0.1). Using somatization as a reference variable, we found that opioid use failed to explain a comparable amount of variance in illness behavior. Finally, there was no evidence that higher levels of opioid use were associated with higher levels of disability or depression.
Economic and social rewards were both associated with increased disability and depression, but only social rewards were associated with increased symptom reporting. Exposure to economic and social rewards may account for unique variance in illness behavior that cannot be explained by differences in medical diagnosis, symptom duration, pain intensity, depression, or somatization.
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