The theme of this issue of Psychosomatic Medicine is “The Neuroscience of Pain,” with a focus on biobehavioral, developmental, and psychosocial mechanisms that are relevant to intervention. In the introduction to the special issue, Guest Editors Lauren Y. Atlas and Mustafa al’Absi focus on the following themes: (1) risk factors and early adversity as related to chronic pain; (2) the role of expectations in shaping pain perception; and (3) mechanisms of interventions targeting pain modulation. The article concludes by outlining new targets for research, including the neurobiology of pain, important methodological challenges, and targets for personalized pain interventions.
Cotton et al. compared perceptual and autonomic responses to pain between yoga practitioners and controls. Autonomic responses to pain, including skin conductance and heart rate, differed between people who had been practicing yoga on a regular basis for at least 6 years and physically healthy active volunteers, despite having similar pain ratings. These findings suggest that autonomic reactivity to pain may be altered by factors common to yoga practice, such as deep breathing, relaxation, and mindfulness.
Because of the potential for mindfulness-based meditation to alleviate the experience of anxiety, perceived stress, and pain, the practice has drawn the interest of the scientific community. In an experimental setting, Taylor et al. explored the pain modulating impact of classical fear learning in meditation practitioners and control participants. Experienced meditators showed decreased effects of fear conditioning on pain at a higher-order perceptual level of processing. These findings highlight potential mechanisms underlying mindfulness-related hypoalgesia, relevant to clinical conditions in which repeated pain exposure might reinforce hyperalgesic processes through fear-conditioning.
Studies have consistently shown that long-term meditation practice is associated with reduced pain, but the neural mechanisms by which long-term meditation practice reduces pain remain unclear. In healthy experienced meditation practitioners, May et al. tested endogenous opioid involvement in meditation analgesia in a double-blind, placebo-controlled, cross-over design. Naloxone not only failed to eliminate meditation analgesia, it enhanced meditation analgesia, suggesting that long-term meditation practice does not rely on endogenous opioids to reduce pain.
Contextual factors can transform how people experience pain, particularly if pain is associated with positive outcomes. In a study from López-Solà et al., participants were given the opportunity to choose to receive pain on behalf of their romantic partners. Placing pain in a context of prosocial meaning reduced its unpleasantness but not its intensity and increased positive thoughts and pleasant feelings during pain. Positive effects were stronger in participants with greater willingness to accept their partner’s pain and were associated with augmented activity in the ventromedial prefrontal cortex, a region involved in affective meaning representations.
The aim of a functional magnetic resonance imaging study by Koenen et al. was to compare behavioral and neural anticipatory responses to cues predicting either somatic or visceral pain in an associative learning paradigm. For the visceral modality, enhanced negative emotional learning and higher engagement of the posterior insula during cued pain anticipation were found, suggesting greater salience of interoceptive, visceral pain. The article provides directions for future research on the pathophysiology and neurobiology of chronic pain conditions, especially chronic visceral pain.
Effects of expectations on pain perception have been well documented, yet the generalizability of these effects on intensity perception of non-painful somatosensory sensations remains unclear. Zaman et al. used a fear-conditioning paradigm to induce different expectations about the probability of pain occurrence and found that the expectation of pain biased intensity perception of non-painful somatosensory sensations but only when the threat of pain remained present due to partial reinforcement. Results also indicate that the expectation of pain affects perception of non-painful bodily stimuli. These findings are relevant to a wide range of clinical pain conditions.
High blood pressure (BP) is associated with reduced pain sensitivity (BP-related hypoalgesia). The underlying neural mechanisms remain uncertain. In individuals with BP in the normal range, Ottaviani et al. used functional neuroimaging and pain stimulation during distinct phases of the cardiac cycle to test the hypothesized neural mediation of baroreceptor-induced attenuation of pain. Results support the existence of a significant association between elevated BP and reduced pain perception. Neural substrates associated with baroreceptor/BP-related hypoalgesia include regions typically involved in the cognitive aspects of pain experience.
Naturalistic observations suggest that expectation of adverse experiences exerts strong effects on anxious youth, which is also relevant to pain perception. In adults, expectation influences the experience of thermal pain. Michalska et al. compared effects of expectation on pain among 23 adults, 20 healthy youth, and 20 anxious youth. All participants showed strong effects of expectancy on pain. No influences of development or anxiety arose, indicating that the modulation of pain experience by anticipatory cues in adults is similarly observed in healthy and anxious youth.
Sexual assault is associated with an increased risk for chronic pain and psychological distress, but the mechanisms for this relationship are unknown. Hellman et al. measured the ability to modulate pain and nociceptive flexion reflex, a measure of spinal cord pain processing, in individuals who had experienced sexual assault. The participants underwent validated procedures to change emotional states. Results suggested reduced descending inhibition in the brain in individuals who experienced sexual assault relevant to the modulation of pain signals at the spinal level, leaving the ascending signal unchecked and promoting pain.
You et al. investigated the association of childhood adversity with hypersensitivity on measures of central pain facilitation. Larger areas of secondary allodynia were observed in individuals with high childhood adversity compared to those with low adversity. The difference was explained in part by adult PTSD symptoms. No difference was observed, however, in temporal summation of second pain. Childhood adversity may be closely linked to the enhancement of central pain facilitation that can spread pain hypersensitivity, and to adult PTSD symptoms, which may underlie the association between childhood adversity and generalized widespread pain.
Lane et al. hypothesize that early adversity is associated with a compromised ability to understand and regulate negative affect. Biased attention toward somatic pain may then be reinforced (and become habitual) because it removes attention from more intolerable (poorly understood/regulated) social-affective distress. The neural basis for this hypothesized mechanism and relevant research and clinical implications are discussed.