For most of us, pain is mysterious: how does a stubbed toe or backache translate into such an uncomfortable sensation? And why does some pain go on and on? To answer these and other questions, I spoke with three specialists from Stanford's Pain Medicine Division.
Einar Ottestad, MD, director of Stanford's Acute Pain Service, explained that when tissue damage occurs, two different signals communicate the injury to our brains, one after another.
Imagine a person hits their thumb with a hammer, he said. At first, they feel a sharp pain localized to their thumb. This immediate, acute pain in direct response to cell damage is called discriminative pain. It's caused by a signal sent from nerves -- or "A-delta fibers" -- in the injured area through a central control center in the spinal cord, to a part of the brain dedicated to comprehending pain in that region of the body. (In this case, from the thumb to the specific brain region receiving signals from the thumb.)
The exact sensation of pain depends on what sort of external factor damaged the cells, Ottestad told me. For example, thermal receptors detect temperature-related pain (e.g., a burning sensation). In the hammer example, mechanical receptors detect the extreme pressure causing cell destruction. This pain signal is intended to promote a specific action: for example, remove your hand from the hot stove! Or don't hit yourself with a hammer again!
Within a few seconds, the pain of the thumb injury will begin to feel more like a dull ache. The entire hand may feel like it's throbbing, even though only some cells in the thumb were actually damaged. This sensation, Ottestad said, is caused by a slower-moving signal sent via a different pathway -- the "C fiber." This type of pain intensifies when byproducts released from injured cells cause inflammation in the surrounding area.
In the instant following this acute pain, the injured person will experience an emotional reaction, Ottestad said. This reaction is generally an anticipation of additional pain to come, a sense of dread about the magnitude of the injury ("How bad is this? Will I need to see a doctor?"), and/or a feeling of embarrassment or anger ("Of course I hit my thumb with the stupid hammer!"). This type of response is mediated by higher brain centers, such as the amygdala, involved in ascribing an emotional, or affective, quality to pain.
Although affective pain isn't directly caused by injured cells, the signal still plays an important role, said Anuj Aggarwal, MD, an anesthesiologist and pain physician. An anxiety response to pain motivates us to stop doing something that is causing harm to our bodies and to seek help, he said.
However, for people experiencing chronic pain, pain continues for weeks or months, long after the tissue damage has healed. This may be caused in part from changes in the way the neurons connect in the spinal cord, the central control center; and the pain often is accompanied by on-going anxiety, which exacerbates the sensation.
Neuroscientist and anesthesiologist/pain physician Vivianne Tawfik, MD, PhD, studies a condition called complex regional pain syndrome -- an intense form of chronic pain, felt after a minor injury, that is out of proportion with what a patient would be expected to feel.
Tawfik explained that with this syndrome -- and other pain conditions, as well -- an initial pain signal stimulates cells called microglia in the brain and spinal cord. The microglia react by releasing inflammatory signals that then stimulate other microglia; and the feed-forward cycle continues. This likely contributes to a person's persistent sensation of pain, she said.
PET scans and other imaging technologies have been used to measure this type of pain signal in patients with complex regional pain syndrome, Tawfik said. Collecting similar images from other patients could provide information that ultimately leads to a better understanding of chronic pain, she said.
This is the first installment in a two-part series on the physiology and psychology of pain. The conclusion is available here.
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