Natural Pain Defenses

We can sense pain because of the presence of nerve cells throughout the body that are activated by painful stimuli. These cells react to a variety of disturbances, including pressure, temperature, and chemical stimuli. There are several kinds of pain receptors for different kinds of stimuli. Once stimulated, a pain receptor sends an impulse along a network of special nerves called afferent nerves to the spinal cord and brain. Signals are transmitted along the afferent nerves by neurotransmitters, including substance P (Guyton AC et al 2001).

In addition to transmitting signals along the nerve pathway, substance P enhances local sensitivity, lowering the pain threshold (Guyton AC et al 2001). Prostaglandin E2 also enhances local sensitivity. During an injury, prostaglandin E2 is increased as a result of the local inflammatory response, which is initiated by the cytokines interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-alpha). Prostaglandin E2 is a target for nonsteroidal pain relievers such as aspirin and ibuprofen.

The body has its own pain-killing system (analgesic system) that blocks pain signals before they reach the brain (Guyton AC et al 2001). Endorphins are a central part of the analgesic system (Guyton AC et al 2001). They are produced by the hypothalamus and secreted into the bloodstream during times of pain or stress (Berne RM et al 1988). Endorphins bind to opioid receptors on the afferent nerves (Guyton AC et al 2001). By stimulating opioid receptors, they prevent neurotransmitters from transmitting the pain signal (Guyton AC et al 2001).