Both personality and biology have been proposed as linkages in the relatively strong correlation between depression and chronic pain. We propose that difficulty expressing anger and difficulty controlling intense emotions are predisposing factors linked to these two conditions. Chronic pain and depression may be disturbances or failures to process intensely emotional information, with concomitant disturbances both in the body's immune system and in interpersonal relationships. Depletions of amines and neurotransmitters and dysfunctions of the endogenous opioid system may be variable actions that contribute to both pain and depression. From an exploration of diverse models and proposals, we present a unifying theory of arousal with a view toward developing research questions and paradigms.It is estimated that from 13% to 20% of the U.S. population has clinically significant symptoms of depression and that 3% of the men and nearly 10% of the women have diagnosahle, full blown depressive syndromes (Romano & Turner, 1985). Among patients with medical problems, however, these prevalence rates are consistently higher, reaching their most critical levels among patients with chronic pain. For example, studies suggest that 50% of medical patients have significant depressive symptoms (Nielsen & Williams, 1980) and that well over 20% warrant a diagnosis within the spectrum of depressive syndromes (Raft, Davidson, Towney, Spencer, & Lewis, 1975); additionally, among chronic pain patients a major depressive syndrome can be ruled out only in one-third of the cases (Romano & Turner).Whereas a relation between chronic pain and depression has often been observed, the source, strength, and nature of the linkage between these two conditions remains uncertain. Numerous mechanisms have been proposed as causal links, and the empirical evidence that is available has been invoked as support with various amounts of certitude. Indeed, Romano and Turner (1985) concluded that there is research support for virtually all (often contradictory) hypotheses about the nature of the pain-depression relation: depression provokes pain by increasing pain sensitivity and by lowering pain tolerance thresholds; pain becomes an interchangeable equivalent of depression among patients with certain dispositions; pain serves as a stressor that evokes subsequent depression; and finally, pain and depression are simultaneously occurring experiences that are related only because of coincidentally similar psychological or biological foundations.

The relationship among therapeutically induced affective arousal, depressive symptoms, pain and beta-endorphin levels were explored on 6 patients with chronic, active rheumatoid arthritis. An ABA, n of 1 study methodology was utilized, replicated 5 times. This procedure allowed the analysis of individualized changes across time in response to the therapeutic regimen. The results indicated that the treatment regimen activated the beta-endorphin system, particularly during the early and late phases of treatment. However, beta-endorphin response had little effect on reports of subjective pain. Depressive symptoms were affected positively by the treatment but were not strongly correlated to the beta-endorphin response. The results suggest that pain and depression represent independent systems and that beta-endorphin levels serve more as stress markers than analgesics in chronic, organic pain.

Fourteen school counselors were systematically and intensively trained to provide two varieties of parent-focused instruction. Six of the counselors were subsequently followed as they provided such training. Three elected to base their training procedures upon principles of operant conditioning and three elected to provide training in effective communication. One hundred and thirty-seven mothers were followed through the course of these training sessions. The findings suggested that neither the behavior modification nor effective communication programs produced substantially better results. Neither was there evidence that the two procedures exerted their effects upon mothers who were distinguished by differing need systems. There was some suggestion, however, that those who dropped out of training tended to have lower needs for social inclusion than those who remained. Moreover, the communication training module had its greatest impact in reducing affectional needs, although this was relatively independent of improvement or felt benefit from the program. The findings were discussed both as they relate to attempts to tailor parent training to specific problems and as they relate to methodological issues in this area.