The prevalence and cost of chronic pain is a major physical and mental health care problem in the United States today. As a result, there has been a recent explosion of research on chronic pain, with significant advances in better understanding its etiology, assessment, and treatment. The purpose of the present article is to provide a review of the most noteworthy developments in the field. The biopsychosocial model is now widely accepted as the most heuristic approach to chronic pain. With this model in mind, a review of the basic neuroscience processes of pain (the bio part of biopsychosocial), as well as the psychosocial factors, is presented. This spans research on how psychological and social factors can interact with brain processes to influence health and illness as well as on the development of new technologies, such as brain imaging, that provide new insights into brain-pain mechanisms.

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The Biopsychosocial Approach to Chronic Pain: Scientific Advances and Future Directions

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Descending control of pain.

Structure and function of the brain serotonin system.

The study of pain in awake animals raises ethical, philosophical, and technical problems. We review the ethical standards for studying pain in animals and emphasize that there are scientific as well as moral reasons for keeping to them. Philosophically, there is the problem that pain cannot be monitored directly in animals but can only be estimated by examining their responses to nociceptive stimuli; however, such responses do not necessarily mean that there is a concomitant sensation. The types of nociceptive stimuli (electrical, thermal, mechanical, or chemical) that have been used in different pain models are reviewed with the conclusion that none is ideal, although chemical stimuli probably most closely mimic acute clinical pain. The monitored reactions are almost always motor responses ranging from spinal reflexes to complex behaviors. Most have the weakness that they may be associated with, or modulated by, other physiological functions. The main tests are critically reviewed in terms of their sensitivity, specificity, and predictiveness. Weaknesses are highlighted, including 1) that in most tests responses are monitored around a nociceptive threshold, whereas clinical pain is almost always more severe; 2) differences in the fashion whereby responses are evoked from healthy and inflamed tissues; and 3) problems in assessing threshold responses to stimuli, which continue to increase in intensity. It is concluded that although the neural basis of the most used tests is poorly understood, their use will be more profitable if pain is considered within, rather than apart from, the body's homeostatic mechanisms.

Animal Models of Nociception

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The induction of pain: an integrative review

We have recently developed, in the rat, a model with a limited arthritic process for chronic pain studies. Intra-articular injection (0.05 ml) of complete adjuvant containing 300 micrograms Mycobacterium butyricum in the tibio-tarsal joint produces a predictable monoarthritis stable clinically and behaviourly from weeks 2 through 6 post-injection. This model appears to be a suitable alternative for the polyarthritic rat for chronic studies based on both its ethical and scientific advantages. In the present work we report results of experiments on the effects of exercise on the pain behaviour and development of arthritis in this model. A group of rats prepared with the above protocol was submitted at 2 weeks post-inoculation to mild exercise (swimming [water 37 degrees C] three times per week) increasing from 5 to 15 min during 4 weeks. As revealed by analyses of the arthritis score, the stiffness score and the mobility score, no aggravation of arthritis occurred in these rats. However the threshold for struggle in response to paw pressure was further decreased (as compared to control arthritic rats) in these animals. These results are discussed in view of observations made in human studies.

F. Godefroy

Papers

Increase in "pain sensitivity" induced by exercise applied during the onset of arthritis in a model of monoarthritis in the rat.

Absence of long-term changes in biochemical markers of monoaminergic systems afferent to the excitotoxically neuron-depleted somatosensory thalamus.

Changes in total and free tryptophan levels in serum following acute morphine administration in arthritic rats.

Regional distribution of 3-O-methyl-DOPA in the cortex and subcortical structures in the rat: effect of aging.

Production of a limited arthritic model for chronic pain and inflammation studies in rats