INFLAMMATORY PAIN

Inflammatory pain is precipitated by an insult to the integrity of tissues at a cellular level. This can happen with penetration wounds, burns, extreme cold, fractures, arthritis, autoimmune conditions, excessive stretching, infections and vasoconstriction. Multiple chemicals mediate the inflammatory process. There are chemicals that act directly and those that act as precursors for other more direct acting substances. There are vascular components, fibroblastic components and tissue cell components. Blood vessels carry circulating precursor that are released into the area of injury and are enzymatically activated. Mast cells release histamines and 5HT. Macrophages activate fibroblasts, which in turn release Interleukin and Tumor Necrosis Factor. Cycoloxygenase activates prostaglandin and leukotrienes. (Arnoff p 14)

This chemical soup of inflammatory mediators can directly affect nociceptors or may sensitize them to touch or movement, even some distance from the inflammatory field. In this way one inflammatory mediator may sensitize more distant pain receptors to another inflammatory mediator.

Chronic inflammation occurs when Aß touch sensitive nerve fibers, which normally do not transmit pain, become activated by chronically inflamed nociceptors. In the meantime the nociceptors pass a constant and powerful signal to cell bodies in the dorsal root ganglion cells causing them to become highly activated. The result is that the newly activated touch fibers pass signals to the highly sensitized cells in the dorsal root ganglion and the signal is passed to the spinal cord as pain. This pain to touch is called allodynia. If this increased pain lasts it can cause wind up pain in the cell bodies of the dorsal horn interneurons and further induce wide dynamic range neurons to stimulate sympathetic coupling. The path from the anatomical to the microscopic to the molecular level of chronic inflammatory pain can be traced by clicking the next animation

Nonsteroidal anti-inflammatory drugs are the most efficacious treatment for inflammatory pain and are all aimed at the interdiction of prostaglandin production though cycoloxygenase (COX) inhibition. Problems with NSAIDs have mostly been related to side effects caused by inhibiting Cox1 as opposed to COX 2. COX 1 is involved in vegetative and restorative activity of tissues, while COX 2 is involved in inflammatory pain. The reason COX 2 selective anti-inflammatories are effective, with lower gastropathy and other side effects is because they are such weak inhibitors of COX 1. Until the release of COX 2 specific anti-inflammatories, the risk of serious side effects and mortality were significant, but the newer anti-inflammatories appear to lower these risks dramatically. It is important to know that while older anti-inflammatories have their uses, risks to patients are higher on this class of medications and they should not be seen as interchangeable with COX 2 selective medications.

Use of corticosteroids can be highly effective. These can be delivered to the site of the inflammation, such as facet joint blocks in the spine, or they can be given systemically in steroid tapers. Caution must be taken in the frequency of use of these types of medications as they can cause serious problems with side effects, ranging from osteoporosis to disruption of the hypophoseal hypothalamic axis.