GATSBY COMPUTATIONAL NEUROSCIENCE UNIT

Psychological modulation of pain and brain processing of pain

Brain processing of pain in humans is based on multiple ascending pathways and brain regions that are involved in several pain components, such as sensory, immediate affective, and secondary affective dimensions. These dimensions are processed both serially and in parallel. They include spinal ascending pathways that directly target limbic and brainstem structures involved in pain-related emotions as well as a pathway proceeding from the somatosensory cortices to limbic cortical areas. Superimposed on this neural organization structure is the capacity to process the dimensions of pain in multiple ways, as in patients who lack one cerebral hemisphere but can nevertheless locate and rate pain intensity and pain unpleasantness on both sides of the body. Neuroplasticity in pain processing is also shown by the capacity of human beings to learn to psychologically modulate pain in multiple ways. This modulation is accompanied by corresponding changes in relevant brain structures. Understanding psychological modulation of pain and pain-related brain activity is optimized by a scientific framework that integrates principles of neuroscience and analysis of human experience.

An example of a learned modulation of pain is the placebo analgesic effect, the measured difference between pain intensity in the natural history or untreated baseline condition and pain intensity in the placebo condition. The placebo analgesic effect is a phenomenon that is different than changes due to natural history. Placebo effects are associated with perception of being given a therapeutically effective agent. The magnitude of placebo analgesia varies enormously as a function of environmental factors, including past history with effective analgesics (conditioning), and psychosocial factors. These factors influence psychological mediators of placebo effects: desire for pain relief, increased expectation of pain relief, and sometimes memory distortion. In our studies of placebo analgesia, both desire for pain relief and expected pain intensity decrease throughout the placebo condition, leading to an increase in the placebo effect over time. This increase is enhanced by feedback that reinforces a perception that the agent is “working”. These psychological factors relate to multiple neural mechanisms and possibly multiple types of placebo analgesic effects, some of which are related to endogenous opioids and others that are unrelated to opioids. There is increasing evidence that placebo analgesia is accompanied by corresponding reductions in pain-related activity of the brain. For example, brain activity of irritable bowel syndrome patients was measured in response to painful rectal distension by a balloon barostat. Large reductions in pain and in brain activation within pain-related regions (thalamus, somatosensory cortices, insula, and anterior cingulate cortex) occurred during the placebo condition, whereas increases occurred in rostral/subgenual ACC, amygdala, ventral striatum, and PAG in the placebo condition. Although many factors influence placebo analgesia, it is accompanied by reduction in pain processing within the brain. The placebo analgesic effect is a psychologically and biologically event that is learned. Its effect size can be large or quite small depending on the presence or absence of several environmental and psychological factors that mediate it.

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