Pain is indeed an unpleasant experience; the perception of pain feels like damage or injury. Whether such damage is actual or potential, pain is usually described with the idioms of injury, including inflammation. The word itself conjures flames, fire, burning, redness, swelling…ouch! As students of the body, we know that inflammation refers to a complex biochemical process and is not a colloquialism to be used loosely. How often do patients describe their pain as swelling or fire, or ask “is it inflammation?” or “will this injection make the disc swelling go down?” How often are treatments variations of anti-inflammatories? Is inflammation truly there? This chapter serves as a review of evidence that there is a process of inflammation involved in some of the major conditions seen in the pain clinic: musculoskeletal pain and neuropathic pain. The general principles applicable are illustrated in detail by the specific examples of intervertebral disc disorders and complex regional pain syndrome.
Celsus’ ancient description of the cardinal signs of inflammation includes rubor, calor, tumor, and dolor. These are, respectively, redness, heat, swelling, and pain. Others, including Virchow, later added loss of function as part of the cardinal descriptors of inflammation. Two thousand years after Celsus, we are beginning to understand the biochemical substrates underlying the cardinal properties of inflammation. Increasingly, inflammatory biochemical profiles are being discovered in association with all afflictions, from Alzheimer's to zoster. While disorders such as rheumatoid arthritis or gout have long been managed as inflammatory conditions, new knowledge of the inflammatory mechanisms underlying “noninflammatory” disorders gives hope that new treatments may be on the horizon.
Inflammation types include acute and chronic. The inflammation response may result from a variety of types of damage to body tissue; inflammation itself may perpetuate damage. Vascular response is a critical component of inflammation and includes vasodilation, increased small blood vessel flow adjacent to tissue damage, and increased permeability of blood vessels. These vascular changes are caused by chemical mediators histamine and prostaglandin, and the kinin and complement enzyme systems. Polymorphonuclear lymphocytes migrate first, then macrophages, through permeable blood vessels, and into the damaged tissue. Plasma proteins flow through permeable vessels into tissue, resulting in increased osmotic pressure there, and tissue edema by a process of exudation. Fibrinogen is converted into fibrin, which forms acute inflammatory exudate (and aids in clotting).
Chemical mediators are numerous in inflammation. Histamine causes the immediate dilation of vessels. Histamine is stored in mast cells, basophils, eosinophils, and platelets. Histamine release is activated by complement C3a and C5a and lysosomal protein from neutrophils. Complement proteins are glycoproteins that may form a membrane attack complex, and may amplify immune response. Serotonin is also a vasoactive mediator released by mast cells and basophils. Phospholipase, contained in cell membranes, produces arachadonic acid during inflammation. Arachadonic acid is rapidly formed into (1) prostaglandins, prostacyclins, thromboxanes, via the cyclooxygenase pathway, and ...