The pain of being sick: Implications of immune-to-brain communication for understanding pain

Author(s): Maier, S. F.

Journal/Book: Annu Rev Psychol. 2000; 51: 4139 El Camino Way, PO Box 10139, Palo Alto, CA 94303-0139, USA. Annual Reviews Inc. 29-57.

Abstract: This review focuses on the powerful pain facilitatory effects produced by the immune system. Immune cells, activated in response to infection, inflammation, or trauma, release proteins called proinflammatory cytokines. These proinflammatory cytokines signal the central nervous system, thereby creating exaggerated pain as well as an entire constellation of physiological, behavioral, and hormonal changes. These changes are collectively referred to as the sickness response. Release of proinflammatory cytokines by immune cells in the body leads, in turn, to release of proinflammatory cytokines by glia within the brain and spinal cord. Evidence is reviewed supporting the idea that proinflammatory cytokines exert powerful pain facilitatory effects following their release in the body, in the brain, and in the spinal cord. Such exaggerated pain states naturally occur in situations involving infection, inflammation, or trauma of the skin, of peripheral nerves, and of the central nervous system itself. Implications for human pain conditions are discussed.

Note: Review Watkins LR, Univ Colorado, Dept Psychol, Campus Box 345, Boulder,CO 80309 USA

Keyword(s): review; interleukin-1; tumor necrosis factor; nerve growth factor; hyperalgesia; allodynia; TUMOR-NECROSIS-FACTOR; NERVE GROWTH-FACTOR; LONG-TERM POTENTIATION; SPINAL-CORD INJURY; NOCICEPTIVE NEURONAL RESPONSES; MELANOCYTE-STIMULATING HORMONE; CHRONIC CONSTRICTION INJURY; CONDITIONED ANTI-ANALGESIA; FIBRILLARY ACIDIC PROTEIN; HIV-1 GP120 GLYCOPROTEIN

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