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Relationship Between Clinical Pain Complaints and Pain Sensitivity in Patients With Depression and Panic Disorder

From the Department of Psychiatry and Psychotherapy, Philipps-University of Marburg, Marburg, Germany.

Address reprint requests to: PD Dr. S. Lautenbacher, Department of Psychiatry and Psychotherapy, Philipps-University of Marburg, Rudolf-Bultmann-Str. 8, 35033 Marburg, Germany. Email: lautenba{at}post.med.uni-marburg.de

	ABSTRACT

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OBJECTIVE: There is evidence that depression and panic disorder are both associated with an increased frequency of clinical pain complaints. A change in pain sensitivity is alleged to be involved in this phenomenon. However, few studies have assessed clinical pain complaints and pain sensitivity in the same group of patients.

METHODS: Thirteen patients with a major depressive disorder, 13 patients with a panic disorder (diagnoses based on the Diagnostic and Statistical Manual of Mental Disorders, fourth edition), and 13 healthy control subjects were investigated. None of the subjects were taking medications. Body maps were used to measure the number of painful sites as well as the intensity and unpleasantness of pain complaints in the previous 6 months. Furthermore, pain thresholds for pressure, cold, and heat were assessed at the forearm or hand.

RESULTS: Patients with depression and panic disorder had significantly more frequent, more intense, and more unpleasant pain complaints than healthy control subjects. Despite this similarity, patients with depression had significantly higher pain thresholds than patients with panic disorder in two (pressure and cold) of three stimulus modalities and significantly higher pressure pain thresholds than the healthy control subjects. There were no differences between the pain thresholds of patients with panic disorder and healthy control subjects. The correlations between clinical pain measures and pain thresholds were generally weak.

CONCLUSIONS: These findings suggest that the clinical pain complaints of patients with depression and panic disorder cannot simply be explained by changes in pain sensitivity.

Key Words: panic disorder • depression • clinical pain • pain threshold

Abbreviations: DSM-IV = Diagnostic and Statistical Manual of MentalDisorders, fourth edition; HAMA = Hamilton Anxiety Scale; HAMD = Hamilton Depression Scale; HC = healthy control; MDD = major depressive disorder; PD = panic disorder; VAS = visual analog scale.

	INTRODUCTION

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Both depression and panic disorder (PD) have been found to be associated with an increased frequency of clinical pain complaints. Roughly half of the patients with these two disorders seem to suffer from pain (1–3). In depression, widely dispersed pain is very common and more typical than pain at particular localizations (eg, headache) (4, 5). Patients with functional chronic pain syndromes, such as low back pain, fibromyalgia, and primary headache, often suffer from depression, a fact that further points to a link between depression and pain (6). In PD, widespread pain is also very common, although headache and unexplained chest pain are also major complaints of patients with PD (2, 7). Altogether, depression and PD seem to be conditions with an increased likelihood of suffering from pain.

The underlying mechanisms of this association are far from clear. It is tempting to assume that the pathopsychophysiology of both conditions includes an increased sensitivity to pain, that is, an augmentation of "pain" signals at physiological and/or psychological levels. However, earlier studies have not provided much corroboration for such a point of view. Whereas patients with PD have been observed to be normalgesic in a few studies (8, 9), considerable evidence has accumulated that patients with depression are hypalgesic rather than hyperalgesic (10–13). However, many of these studies have had a main shortcoming, namely, that clinical pain and pain sensitivity had not been assessed together in the groups of patients investigated.

According to our knowledge, there are only few exceptions. In a study by Merskey (14) on various groups of psychiatric patients, the level of pain sensitivity were shown to be clearly dependent on the occurrence of clinical pain. Patients with depression and concurrent pain had lower pressure pain thresholds than depressed patients without such pain complaints, whereas patients with anxiety neurosis and concurrent pain had higher pressure pain thresholds than those without pain. This finding might indicate different relationships between clinical pain and pain sensitivity in depression and anxiety disorder. Pin-prick reactions and motor reactions to electrocutaneous stimulation did not distinguish the diagnostic groups in Merskey’s study, suggesting variance due to the method of experimental pain induction. However, the diagnoses of mental disorders in Merskey’s study did not rely on current standards, and the assessment of clinical pain did not include quantitative measures. Similar objections apply to a study by von Knorring (15). Among his depressed patients, 60% suffered from acute pain. These patients did not differ in their pain sensitivity from the patients without pain. Davis et al. (10) reported on a pilot study in which depressed patients with pain complaints in the last few days before investigation were even less sensitive to pain. Consequently, the relationship between clinical pain and pain sensitivity in depression needs clarification.

The aims of the present study in patients with depression and PD, diagnosed according to contemporary criteria (ie, DSM-IV), were to measure 1) clinical pain in the recent past, assessed quantitatively by its frequency, intensity, and unpleasantness; and 2) pain sensitivity, assessed by using three experimental methods for assessing pressure, cold, and heat pain thresholds. Clinical pain in the recent past was assessed instead of present pain for two reasons. First, the prevalence of present pain in patients with depression and patients with PD is around 50% (1, 3) and, although considerable, is very likely too low to allow this parameter to be subjected to a correlation analysis because half of the patients showed no variance in the data. Second, the pain threshold is thought to covary with the pathopsychophysiological basis of depression and PD, which varies in terms of weeks and months rather than days. The spurious relationships between clinical pain and pain sensitivity in earlier studies (10, 14, 15) might have been due to correlating a quickly fluctuating present pain with a more stable pain threshold. Because the assessment of "typical" or "usual" pain instead of "present" pain was recommended to reduce variability (16), the time frame for the measure of clinical pain was widened to reflect the recent past, although we acknowledge that the memory of pain may be erroneous (17). The use of three physically different pain induction techniques for assessment of the pain thresholds was due to the findings of Merskey (14) and many others (eg, 18) that there is considerable divergence among these methods. Hence, only a multiple-method approach would permit generalization.

	METHODS

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Subjects
Participants included 13 inpatients with a current MDD, 13 inpatients with a current PD, either with (N = 9) or without (N = 4) agoraphobia (DSM-IV diagnoses; Ref. 19), and 13 HC subjects. The patients were consecutively recruited on admission for inpatient treatment in a psychiatric hospital. Mean age was 35.4 years (SD = 10.1) for the MDD group, 29.8 years (SD = 7.5) for the PD group, and 32.9 years (SD = 7.9) for the HC group, which did not differ significantly (F(2,36) = 1.359, p = .270). Each group had eight women and five men. The severity of the two disorders was quantified with use of the HAMD (20) and HAMA scales (21). Mean scores for the HAMD were 23.8 (SD = 7.5) for the MDD group and 18.6 (SD = 7.8) for the PD group, which did not differ significantly (t = 1.74, p = .094). Mean scores for the total HAMA were 23.2 (SD = 10.4) for the MDD group and 34.8 (SD = 9.3) for the PD group, which differed significantly from each other (t = -3.00, p = .006).

Patients were diagnosed by an experienced psychiatrist by applying the International Checklist for DSM-IV (22). One major focus of the diagnostic procedure was to exclude a present and lifetime comorbidity of depression and PD in every case. Because all patients were admitted to open wards, suicidal tendencies were estimated to be minimal. Furthermore, any indication of a change in the diagnosis during inpatient treatment led to a posteriori exclusion. Further exclusion criteria were present or lifetime diagnoses of an additional mental disorder, neuropathies, disk diseases, nerve injuries at the upper extremities, endocrine disorders, and dermatosis at the upper extremities. No patients were taking medications. In cases of prior medication, patients underwent a washout period of a minimum of 6 days; the exact duration was at least three times the half-life of the drug and its active metabolites. All patients were studied during the first 2 weeks after admission. Patients that were potentially eligible for inclusion were referred to the investigator from all wards for verification of the diagnosis and explanation of the study. Two thirds of the preselected patients approached were either not eligible because of additional or unclear diagnoses or refused to participate in the study. The same exclusion criteria as used for the MDD and PD patients were applied by the same rater for the HC subjects; this time, of course, the presence of MDD or PD also led to exclusion. HC subjects were staff members and were paid for participation.

The protocol was approved by the ethics committee of the medical faculty of the University of Marburg, Marburg, Germany; all subjects gave written informed consent.

Apparatus and Procedure
Sessions always started at 3:00 PM; at the beginning of the sessions, subjects filled out questionnaires.

The pain questionnaire was designed by the first author (S.L.) because no validated and standardized instruments for pain assessment in psychiatric patients were available. On two schematic drawings of a body, showing the front and the rear, the subjects were asked to mark each location in which they had experienced pain during the previous 6 months. This allowed for counts of the number of painful sites. Thereafter, subjects were asked to rate the intensity and unpleasantness of pain for each site at separate horizontal VASs of 100 mm. To assess overall pain intensity and overall pain unpleasantness, the VAS ratings of all sites were summed for each of the two pain dimensions. This means, for example, that 10 sites with VAS ratings of 50 mm each and 5 sites with VAS ratings of 100 mm each result in the same total score of 500 mm. This approach to summing pain ratings from multiple sites was introduced by Lautenschläger et al. (23) as a sensitive tool for the assessment of widespread fibromyalgia pain and was also used successfully by us (24) for the same purpose. Because we assumed that pain in depression and PD is also often widespread and polytopic, making it difficult to rate on only one scale, we adopted this approach for the present study. The pain questionnaire was designed to be simple enough to allow also the assessment of pain in severely mentally disordered subjects. Meanwhile, it has also been shown to be suitable for studying pain in schizophrenic patients (Lautenbacher, Roscher, Krieg, unpublished data, 1994).

During the second part of the session, the assessment of pain thresholds was conducted. There were two runs, during which the pain thresholds for pressure, cold, and heat were measured in a randomized order; the order was the same for both runs. The two runs differed in respect to the body side tested. The order of body side was randomized for each of the three pain thresholds. The mean of the two sides for each of the three pain thresholds was used in further evaluations.

To assess the pressure pain threshold, a variable pressure dolorimeter (25) with a footplate surface of 0.8 cm² and a scale range of 0 to 17 kg was used. The footplate was positioned for the first trial at the volar forearm, just between the proximal crease of the wrist and the transverse crease of the elbow. In the second and the third trials, the footplate was moved slightly distally and proximally to minimize local sensitization. The investigator was trained to raise the pressure at a constant rate of 1 kg/second. The pressure was raised until the subjects signaled pain. The mean of the three trials was used as the threshold measure.

The thresholds for cold pain were assessed by using the cold-pressor test. Subjects immersed their hands to a level of 10 cm above the wrist in a cold-water bath held at 5°C. The water temperature was controlled with a precision of 0.01°C by a thermostat (Variostat, Peter Huber Kältemaschinenbau GmbH, Offenburg, Germany), and the water was whirled by a force and suction pump to prevent local warming around the subject’s hand. The time until the subjects signaled pain was recorded as the pain threshold. There was only one trial because the tonic cold-pressor pain readily triggers inhibitory processes (26), which may cause erroneous data in later trials.

Heat pain thresholds were measured using a computer-controlled thermal stimulator with a contact thermode of 1.6 x 3.6 cm² (for details, see Ref. 27). The thermode was attached with a constant pressure of 0.4 N/cm² at the same site at which the pressure pain thresholds were taken. Beginning at a temperature of 38°C, eight heat stimuli were applied with a rate of temperature change of 0.7°C/second. Subjects signaled pain by pressing a button, at which time the temperature returned to baseline. There were eight trials, which were visually and acoustically announced. The measure of the pain threshold was the mean calculated during the last five trials because including the first few trials leads to erroneously low pain threshold estimates (27).

Statistics
Differences among all three groups were evaluated by one-factorial analyses of variance, and Duncan’s multiple range tests were used to compare two groups. Relationships between two variables were examined with Pearson correlation coefficients. Two-tailed tests were used throughout because directed hypotheses were available only for a small number of the tests. The level was set at 0.05. Because we investigated untreated, severely ill inpatients who had to fulfill stringent inclusion and exclusion criteria, sample sizes were limited. To overcome this limitation and to give an idea of the relevance of the findings, power calculations were added to determine the sample sizes required for significant effects.

	RESULTS

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There were highly significant differences among patients with MDD, patients with PD, and HC subjects with respect to clinical pain complaints in the recent past (Table 1). This concerns the number of painful sites as well as the intensity and unpleasantness of pain. In all three measurements, both the MDD and PD groups had significantly higher scores than the HC group. There were no differences between the two groups of patients.

To investigate in greater detail the seemingly incompatible results for clinical pain complaints and pain sensitivity, Pearson correlations for the relationship between the two sets of variables were computed. Although none of the correlation coefficients were significant (Table 2), some thought-provoking findings appeared. In the MDD group, there was no coefficient greater than 0.17 for absolute size. In the HC subjects, a similar finding was obtained (maximum = 0.26). This points to a complete lack of a substantial relationship between pain thresholds and clinical pain complaints. However, in the PD group, the coefficients describing the relationship between pain thresholds for pressure, cold, and heat and the unpleasantness of pain were -0.39, -0.47, and -0.54, respectively. Because we had small samples and could therefore have missed substantial relationships, the sample sizes, which would make these coefficients significant, were estimated (power = 80%, = 0.05): These were N = 46, N = 30, and N = 21 for pressure, cold, and heat, respectively. This finding suggests that the expectation of a substantial relationship between pain threshold and unpleasantness of clinical pain is not far-fetched in patients with PD. Indeed, we were not able to verify that the correlation coefficients differed among the groups because much larger samples are required (a difference between two correlation coefficients of 0.50 would become significant with power = 50% and = 0.05 if at least 57 subjects are investigated in each group).

	DISCUSSION

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A number of studies corroborate the view that patients with depression or PD suffer from pain problems (1–3). Furthermore, patients with PD have been found to be normalgesic (8, 9), and depressive patients have been found to be hypalgesic (10–13). Most of these findings, however, stem from different samples, so the contrast between increased pain complaints and normal or even reduced pain sensitivity could be attributed to the fact that pain complaints and pain sensitivity had been assessed in different subgroups of patients. This objection does not concern our study because the divergence between pain complaints and pain sensitivity was observed in the same group of patients.

The association of increased clinical pain and decreased pain sensitivity suggests that these two domains are independent of each other in depression. This assumption is corroborated by our correlation analysis, which did not show a substantial relationship between clinical pain and pain threshold. Only speculations are possible at the moment to explain this lack of relationship. The expression of pain in depressive patients may be only slightly influenced by perceptual factors, as delineated by the pain threshold, but more so by emotional factors, such as catastrophizing cognitions and fears related to one’s own body. Furthermore, the pain threshold assessed by brief stimuli does not reflect disturbances in endogenous pain inhibition because long-term stimulation is needed for that. If so, a lack of pain inhibition in depressive patients might have remained undetected for methodological reasons.

In the PD patients who seemed to be normalgesic but nevertheless suffered exceedingly from pain, there seems to be some relationship between clinical pain and pain sensitivity, as ascertained by our correlation analysis. Because the correlation was most pronounced for the unpleasantness of clinical pain, one might speculate that the relationship results from the intense scanning for unpleasant events in patients with PD as part of the general anxiety sensitivity. This could explain why such a relationship between clinical pain complaints and pain sensitivity might be typical for PD patients but not present in healthy individuals or depressed patients. The study of Merskey (14) also suggested different relationships between clinical pain and pain sensitivity in depression and anxiety disorder because patients with depression had lower pain thresholds when suffering concurrently from pain, whereas patients with anxiety neurosis had higher ones under the same condition. However, further speculations need corroboration of our finding.

Finally, some methodological comments are necessary. First, one might argue that our pain questionnaire does not measure pain but memory of pain. This is true, as is the fact that the memory of patients with emotional problems can be selectively biased toward the recall of negative events such as pain (28). However, it is also true that an increased likelihood of remembering painful events in the past seems to be associated with an increased likelihood of suffering from pain in the present (29). Thus, the selective bias of recalling pain in patients with depression and PD could be a potential cause of current pain problems. Second, one might argue that the questionnaire does not measure pain but its expression. However, the new definitions of pain do not exclude pain expression from pain (30) because it has turned out to be very difficult to draw a line between the two concepts. Although we have to acknowledge such objections regarding our pain questionnaire, we did not have the alternative of a validated pain questionnaire for mentally ill individuals. Furthermore, the data thus obtained corroborated those that were gathered using other nonstandardized instruments, suggesting more pain in patients with depression and PD than in healthy individuals. Finally, we once again found that different tests for pain sensitivity do not necessarily lead to the same results. This is probably due to the well-known weak correlations among various experimental tests for pain sensitivity (18). Hence, one must either use multiple tests, as done in the present study, or have a theory to deduce the appropriate test for a given question.

In summary, the present examinations performed in the same group of subjects provided evidence that patients with depression and those with PD suffer exceedingly from pain, although the latter present as normalgesic and the former even as hypalgesic individuals in experimental tests for pain sensitivity. This puzzle may be solved in the future by studying endogenous pain inhibitory processes in addition to primary pain sensitivity in patients with depression and PD because a dysfunction of the pain inhibitory systems also seems to be an important factor in the development of clinical pain complaints.

	ACKNOWLEDGMENTS

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This study was supported by the Wilhelm Sander-Stiftung (Grant 92.040.2). We thank the Max-Planck-Institute of Psychiatry, Munich, Germany, for its generous support with technical devices.

Received for publication September 15, 1998.

Revision received June 30, 1999.

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