The psychophysiological phenomenon of pain is of tremendous concern to nurses because of its potential to adversely affect the mental, emotional, and physical health of patients. Increasingly appreciated is the ability of pain to influence immune variables including enumerative and functional measures of leukocyte subsets. In this review, a theoretical model of the role of pain in producing positive changes in the expression of leukocyte cellular adhesion molecules is developed. The model is based on a conceptualization of pain as a perturbing influence on the complex web of neuroendocrine-immune relationships that regulate leukocyte migration. Findings from multiple lines of research are reviewed, including the neurophysiology and psychophysiology of pain, neuroendocrine and proinflammatory cytokine responses to painful stress, animal models linking pain to proinflammatory central immune activation, and pain-specific neurogenic inflammation. Relevant findings are synthesized to develop the physiological pathways from the perspective that pain may alter the balance of this multidirectional system in a proinflammatory direction. Clinical implications and suggestions for further research in the area of painful stress-related inflammation are offered.
A gene pathway analysis highlights the role of cellular adhesion molecules in multiple sclerosis susceptibility
