The Very Broad Problem of Pain
When did pain begin? We can trace the evolutionary origin of some receptors–for light and sound, for example–but irritability is a defining feature of life. We might better ask when we began identifying irritability as pain. Few people say that invertebrates have a sense of pain. Fish, birds, and reptiles may have pain without the emotion. Mammals have the full sensory and emotional repertoire.
When does pain begin? Certainly by the time of circumcision in newborn boys. Conscious pain may not be present before 26 weeks of gestation. That is not a scholarly site and may be partisan, but reliable evidence indicates that pain seems not to be present at 24 weeks in humans.
Is pain normal? Pain is a sense that is also a disease. There are many sensory impressions we can categorize as symptoms of an underlying disorder, but pain occurs as a disorder in its own right. Pain is pre-attentive; we rarely have to search to decide whether it’s present, yet it is often elusive and hard to localize—famously so for children.
Where does it hurt? Pain appears to become conscious when messages of tissue injury reach the cerebral cortex. For pain, the focus is on somatosensory cortex, which contains a body map of areas represented in the brain; the insula; and anterior cingulate cortex.
How does it hurt? Specialists distinguish two or three kinds of pain by their origin, with a fourth appearing on the horizon: nociceptive, neuropathic, and inflammatory (sometimes grouped with nociceptive) pain—and maybe another category of central or psychogenic pain should be added. (There is some evidence that chronic pain may turn out to be psychogenic, but there are genetic hypotheses, too.) The pain of combat injuries justifiably dominates many current discussions of pain, but the complexities lie beyond the scope of our textbook.
· Nociceptive pain: e.g., stubbing your toe, often acute
· Neuropathic pain: e.g., multiple sclerosis, always chronic
· Inflammatory pain: e.g., postoperative pain
Anatomists distinguish two peripheral pathways that carry pain signals from the body to the brain. One, the Aδ system, consists of myelinated nerve fibers that transmit signals at around 10 meters per second. We perceive this pain as sharp and localized.
A second pathway is the unmyelinated C-fiber system that carries signals much more slowly at about 1 meter per second. We feel this pain as dull and diffuse. Most of the pain that arises from our internal organs is of this type. This system shows a “windup”phenomenon by which repeated stimulation produces a steadily increasing response that leads eventually to allodynia and central sensitization, which is important in fibromyalgia and chronic fatigue syndrome.
On the skin, both kinds of pain exist. You can perceive the difference when you hit your thumb with a hammer. You become aware of a sharp pain just in time to think “Oh, no” before the dull, aching pain of the C-fibers hits you.
The two pathways are variously labeled as “first”, or lateral; and “second”, or medial, pain sensation. First pain sensation is a discriminative sensory modality resembling touch that terminates at the somatosensory cortex. Unlike touch, second pain sensation brings in an affective or emotional component to pain that makes it aversive. It projects to the anterior cingulate cortex and insula. Another terminus of the second pathway is the insular cortex that lies beneath the lateral fissure. Brain imaging has suggested that the insula may be responsible for empathic pain, which is our tendency to recoil from witnessing someone else’s pain.
Scaling of Pain
Why does pain hurt? We all know that a little pain is very different from a lot of it. Without trivializing the horror of serious pain, let’s admit that we can enjoy hot food but we hate a burned tongue. What makes pain worse?
· Stimulus intensity: Different regions of somatosensory cortex encode stimulus intensity differently.
· Duration: Pain is likely to worsen with prolonged stimulation.
· Heredity: Man or woman, redhead or brunette—your pain betrays your genes. However, gender differences are not necessarily genetic in origin. Psychogenic pain associated with the “neurotic triad” on the MMPI—hypochondriasis, depression, hysteria—breaks down by gender as well.
There are many ways of measuring pain. On the one hand, pain sensation increases with stimulus intensity and unpleasantness increases with sensory magnitude. This much was proved in the days of Fechner.
The problem for psychophysics is to distinguish discriminative, “first” magnitudes from affective, “second” magnitudes. In a hospital, scaling poses a different kind of task. Patients may minimize their pain out of bravado or exaggerate it to get more drugs. Scales are needed for patients with dementia and for young children. While the McGill Pain Questionnaire is in widespread use, the search for a truly objective scale is still going on. The McGill form looks like this and that.
The gate-control model describes two mechanisms for blocking a pain signal, once when it enters the spinal cord (click on “play” or try this animation) and again when the brain inhibits pain input. See if you can pinpoint the synaptic changes that suppress pain.
The control of attention provides another powerful way to reduce pain. Who has not tried to distract a child from the pain of a fall by directing his or her attention to a toy or a piece of candy? For adults, love can accomplish the same end. Although pain was once treated as a body sense, it is increasingly being regarded as a “mind sense”.
Our expectations may increase or decrease pain. The anticipation of a shot may intensify the pain that a child feels from an injection, while the color of a pain-killing pill may allay the soreness of overexertion, as this week’s lab exercises demonstrate. Placebos can have powerful effects. This radio interview and that one describe the phenomenon further.
Questions (please answer one)
1. What flaws do you see in the following pain scales? a. A hospital’s 1 to 10 scale. Patients are asked to rate their pain from 1 to 10 in severity.
b. The Schmidt Sting Pain Index.
2. Is the placebo effect confined to drugs? Can you think of an example in your own life of a placebo effect from something other than a drug?
3. What is pain to you–a sensory signal like touch? A state of consciousness generated by the brain? A disorder or disease? It seems like everyone is thinking about this, but you don’t need research if your own experience offers an answer.