One of the skin senses deserves special mention—our sense of pain. Pain usually begins with activity in the nociceptors—receptors in the skin that have bare nerve endings and that respond to various forms of tissue damage as well as to temperature extremes. These receptors come in two types: A-delta fibers allow rapid transmission of information and are responsible for the pain you experience when you’re first injured.
The C fibers, in contrast, are unmyelinated and therefore slower in their transmission; they’re the source of the dull ache that remains long after the injury occurs.
Activity in the nociceptors is aversive—obviously, we’d prefer to avoid pain! But pain plays a crucial role for us—as evident in the rare individuals who have medical conditions making them insensitive to pain (Melzack & Wall, 1982). These individuals are constantly at risk: They can’t feel the pain of resting a hand on a hot stove, so they’re in danger of burning themselves. They can’t feel the irritation of an object caught in the throat, so they don’t cough—creating a danger of choking. They don’t notice if they bite their own tongues while chewing food. These (and many other) examples remind us that pain is useful—helping us to avoid a wide range of hazards. Without this “alert system,” ourlikelihood of serious injury would be a lot greater and our life expectancies much shorter.
Let’s be clear, though, that the experience of pain depends on far more than the noci-ceptors themselves because there are circumstances in which people appear to feel no pain despite activity in these receptors. The classic examples come from soldiers who appear not to notice their wounds until the battle ends, or athletes who don’t feel a sprained ankle, or even a broken rib, until the excitement of the game subsides.
How should we think about these observations? Part of the answer involves substances, produced by our bodies, that function as internal medications. These substances—which we first met—are chemically quite similar to drugs like morphine or codeine, and they interfere with the neurotransmission involved in pain sensation. These natural internal painkillers, called endorphins, help us in many cir-cumstances to continue functioning despite a seemingly painful injury.
Pain sensations can also be blocked via a different mechanism: According to the gatecontrol theory, pain sensations must pass through a neural “gate” to reach the brainand can be blocked at that gate by neurons that inhibit signals from the nociceptors, so that these signals are never transmitted to the brain. The gate neurons that provide this inhibition can be triggered in several ways, including counterirritation. This term refers to the phenomenon in which painful sensations from one part of the body trigger the gate neurons and thus decrease the sensitivity to pain elsewhere in the body (e.g., Motohashi & Umino, 2001).
We also know that the experience of pain is influenced by someone’s beliefs and emotions. However, these cognitive factors may be affecting the emotion that accom-panies pain rather than the sensation of pain itself (Melzack & Casey, 1968). These two aspects of pain—the sensation and the emotion—can be distinguished subjec-tively. They can also be distinguished functionally—so that hypnosis (for example) seems to alter the emotional response to pain without decreasing the actual intensity of the sensation. These two aspects of pain can also be distinguished by brain activity—the sensation corresponds mostly to activation in specific areas of the somatosensory cortex, and the emotion corresponds more closely to activity in the anterior cingulate cortex.
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