Pain
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Randomized Controlled Trial
Cortico-subcortical activation patterns for itch and pain imagery.
The imagery of itch and pain evokes emotional responses and covert motor responses (scratching to itch and withdrawal to pain). This suggests some similarity in cerebral mechanisms. However, itch is more socially contagious than pain, as evidenced by the fact that scratching behaviors can be easily initiated by watching itch-inducing situations, whereas withdrawal is less easily initiated by watching painful situations. ⋯ Connectivity with the aIC was stronger in the primary motor and premotor cortices during pain imagery and stronger in the globus pallidus during itch imagery. These findings indicate that brain regions associated with imagery of itch are the same as those involved in imagery of pain, but their functional networks differ. These differences in brain networks may explain why motor responses to itch are more socially contagious than those related to pain.
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We have modeled the transition from acute to chronic pain in the rat. In this model (termed hyperalgesic priming) a chronic state develops after a prior inflammatory process or exposure to an inflammatory mediator, in which response to subsequent exposure to prostaglandin E2 (PGE2) is characterized by a protein kinase Cε-dependent marked prolongation of mechanical hyperalgesia. To assess the effect of priming on the function of the nociceptor, we have performed in vitro patch clamp and in vivo single-fiber electrophysiology studies using tumor necrosis factor α to induce priming. ⋯ However, 60 minutes after PGE2 administration, the response to mechanical stimulation was further increased in primed but not in control nociceptors. Thus, at the level of the primary afferent nociceptor, it is possible to demonstrate both altered function at baseline and prolonged PGE2-induced sensitization. Intrathecal antisense (AS) to Kv7.2, which contributes to RMP in sensory neurons, reversibly prevented the expression of priming in both behavioral and single-fiber electrophysiology experiments, implicating these channels in the expression of hyperalgesic priming.
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We previously discovered that when faced with a challenging cognitive task in the context of pain, some people prioritize task performance, while in others, pain results in poorer performance. These behaviours, designated respectively as A- and P-types (for attention dominates vs pain dominates), may reflect pain coping strategies, resilience or vulnerabilities to develop chronic pain, or predict the efficacy of treatments such as cognitive behavioural therapy. Here, we used a cognitive interference task and pain stimulation in 80 subjects to interrogate psychophysical, psychological, brain structure and function that distinguish these behavioural strategies. ⋯ Brain imaging revealed structural and functional brain features that characterized these behavioural strategies. Compared to the performance-oriented A group, the P group had (1) more gray matter in regions implicated in pain and salience (anterior insula, anterior midcingulate cortex, supplementary motor area, orbitofrontal cortex, thalamus, caudate), (2) greater functional connectivity in sensorimotor and salience resting-state networks, (3) less white matter integrity in the internal and external capsule, anterior thalamic radiation and corticospinal tract, but (4) were indistinguishable based on sex, pain sensitivity, neuroticism, and pain catastrophizing. These data may represent neural underpinnings of how task performance vs pain is prioritized and provide a framework for developing personalized pain therapy approaches that are based on behaviour-structure-function organization.