Pain is real, but also subjective. Perception of pain can vary among different people. Pain
can be perceived with different intensities at different times. These factors have made it
difficult to establish a firm physiological understanding of pain. It is useful to distinguish
. We have specific receptors that cause the perception of
pain when activated. A physiological definition of a nociceptor is a receptor activated by
a stimulus that causes tissue damage or would cause damage if continued.
Nociceptors are the least differentiated of the sensory receptors in the skin. They
generally have free nerve endings. There are several classes of cutaneous pain receptors.
nociceptors have small-diameter, thinly myelinated A
conduct at 5-30 m/s. Activation of these nociceptors is associated with sensations of
sharp prickly pain.
nociceptors are activated by a variety of high intensity
mechanical, chemical, or thermal stimuli, and have small diameter, unmyelinated C fibers
that conduct at 0.5-2 m/s. These make up about 40% of all C fibers.
Under pressure block we first loose touch sensation, then the sharp pain carried by
fibers, and finally the duller, slow pain carried by C fibers. The sharp pain is more
easily tolerated than the dull pain. Similarly, electrical stimulation activates the largest
fibers first, and sharp pain is perceived before dull pain as the stimulus intensity is
increased. Local anesthetics, on the other hand, first affect the smallest fibers. Therefore,
they block dull pain first. The fact that different kinds of pain are carried over fibers with
different transmission velocities is responsible for the idea of “first and second pain,”
when, for example, we stub our toe.
Pain or nociception usually does not adapt. In fact, the response to the pain-
inducing stimulus often sensitizes. This is called
. The sensitization of
nociceptors after injury or inflammation often results from local tissue damage and the
release of a variety of chemical mediators. Tissue damage releases bradykinin and
prostaglandins that sensitize the free nerve endings. The effectiveness of aspirin as a
painkiller is partly because it interferes with the synthesis of prostaglandins. Also,
activation of the nerve endings cause them to release substance P which acts on mast
cells to release histamine which can, in turn, act on the nerve endings to increase their
sensitivity. This arrangement is unusual. In most cases, receptor nerve endings are not
also releasing endings. In addition, substance P and other agents can cause local
vasodilation and edema, which, in turn, releases more substance P over a wider area.