Pain
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The amygdala is a key subcortical region believed to contribute to emotional components of pain. As opioid receptors are found in both the central (CeA) and basolateral (BLA) nuclei of the amygdala, we investigated the effects of morphine microinjection on evoked pain responses, pain-motivated behaviors, dopamine release in the nucleus accumbens (NAc), and descending modulation in rats with left-side spinal nerve ligation (SNL). Morphine administered into the right or left CeA had no effect on nerve injury-induced tactile allodynia or mechanical hyperalgesia. ⋯ Microinjection of morphine into the BLA had no effects on evoked behaviors and did not produce CPP in nerve-injured rats. These findings demonstrate that the amygdalar action of morphine is specific to the right CeA contralateral to the side of injury and results in enhancement of net descending inhibition. In addition, engagement of mu opioid receptors in the right CeA modulates affective qualities of ongoing pain through endogenous opioid neurotransmission within the rACC, revealing opioid-dependent functional connections from the CeA to the rACC.
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Randomized Controlled Trial
Offset analgesia: somatotopic endogenous pain modulation in migraine.
The complex mechanisms underlying migraine are not entirely understood. It has been suggested that descending endogenous pain modulation is an important contributing factor, although research is controversial. A frequently used method to quantify the inhibitory pain modulation system is offset analgesia (OA), defined as a disproportionally large decrease in pain perception in response to a small decrease of painful stimulation. ⋯ Statistically significant differences between the trigeminal area and the extratrigeminal area were neither observed in healthy controls nor in patients with migraine (P > 0.05). Mechanical detection, mechanical pain threshold, warm detection, and heat pain threshold showed no significant differences between groups or test sites (P > 0.05). In summary, patients with episodic migraine in the headache-free interval exhibited somatotopically specific differences in endogenous pain modulation.
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Approximately 1.7 million youth suffer from debilitating chronic pain in the US alone, conferring risk of continued pain in adulthood. Aberrations in threat-safety (T-S) discrimination are proposed to contribute to pain chronicity in adults and youth by interacting with pain-related distress. Yet, few studies have examined the neural circuitry underlying T-S discrimination in patients with chronic pain or how T-S discrimination relates to pain-related distress. ⋯ In addition, they showed decreased frontal (vmPFC) activation and aberrant frontolimbic connectivity in response to a learned safety cue (CS-). Patients with low pain-related distress and healthy controls appeared strikingly similar across brain and behavior. These findings indicate that altered T-S discrimination, mediated by frontolimbic activation and connectivity, may be one mechanism maintaining pain chronicity in adolescents with high levels of pain-related distress.
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Chronic pain is often associated with changes in brain structure and function, and also cognitive deficits. It has been noted that these chronic pain-related alterations may resemble changes found in healthy aging, and thus may represent accelerated or premature aging of the brain. Here, we test the hypothesis that patients with chronic noncancer pain demonstrate accelerated brain aging compared with healthy control subjects. ⋯ A Bayesian independent-samples t test indicated moderate evidence in favor of the null hypothesis (BF01 = 4.875, ie, group means were equal). Our results provide indirect support for recent models of pain-related changes of brain structure, brain function, and cognitive functions. These models postulate network-specific maladaptive plasticity, rather than widespread or global neural degeneration.