Articles: neuropathic-pain.
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Pain is aversive, and its relief elicits reward mediated by dopaminergic signaling in the nucleus accumbens (NAc), a part of the mesolimbic reward motivation pathway. How the reward pathway is engaged by pain-relieving treatments is not known. Endogenous opioid signaling in the anterior cingulate cortex (ACC), an area encoding pain aversiveness, contributes to pain modulation. ⋯ In neuropathic, but not sham-operated, rats, systemic doses of morphine that did not affect withdrawal thresholds elicited CPP and NAc dopamine release, effects that were prevented by blockade of ACC opioid receptors. The data provide a neural explanation for the preferential effects of opioids on pain affect and demonstrate that engagement of NAc dopaminergic transmission by non-opioid pain-relieving treatments depends on upstream ACC opioid circuits. Endogenous opioid signaling in the ACC appears to be both necessary and sufficient for relief of pain aversiveness.
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To study the relationship between expected pain and future outcomes along with the moderating effects of expected pain in neuropathic pain patients. ⋯ In neuropathic pain patients whose pain does not respond to therapy, high levels of expected pain may relate to relatively lower catastrophizing scores by shifting focus away from futile attempts at "curing" pain toward focusing on achievement of more realistic personal goals.
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Clinical therapeutics · May 2015
Meta AnalysisExamining the Time to Therapeutic Effect of Pregabalin in Spinal Cord Injury Patients With Neuropathic Pain.
In 2 large-scale, placebo-controlled trials, pregabalin improved both pain and pain-related sleep interference in patients with neuropathic pain due to spinal cord injury (SCI). In both trials, pregabalin found statistically significant improvement compared with placebo after 1 week of treatment. However, the effects of pregabalin in the days immediately after initiation of treatment are unknown. The purpose of the present analysis was to determine timing of pregabalin's therapeutic effect in the days after initiation of treatment. ⋯ Treatment with pregabalin results in rapid time to significant improvement in both pain and pain-related sleep interference in patients with neuropathic pain due to SCI. These findings should only be used as a guide to physicians and patients as to when clinical response to pregabalin may be expected.
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Brain research bulletin · May 2015
CB1 receptors modulate affective behaviour induced by neuropathic pain.
Patients suffering from chronic pain are often diagnosed with a psychiatric condition, in particular generalized anxiety and major depression. The underlying pathomechanisms contributing to this comorbidity, however, are not entirely clear. In this manuscript we have focussed on the potential role of the cannabinoid receptor CB1, because it is known to modulate neuronal circuits contributing to chronic pain states and affective behaviours. ⋯ Our results show that the development of mechanical hypersensitivity was similar in CB1 deficient mice and wild type controls. However, CB1 knockouts showed much more pronounced behavioural manifestations of anxiety-related behaviours in the light-dark and zero-maze tests, sucrose anhedonia, and disturbed home-cage activity. These results indicate that the endocannabinoid system affects chronic pain-induced mood changes through CB1 receptors.
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Evidence of nonopioid analgesic effectiveness exceeds that for long-term opioids in chronic noncancer pain (CNCP), most with lower risk. Non-drug therapies such as cognitive behavioral therapy and physical activation are safer and also effective. ⋯ Antidepressants with noradrenergic activity (such as tricyclics and seroton-norepinephrine reuptake inhibitors) and neuromodulating anticonvulsant drugs (gabapentinoids and sodium-channel blockers) are proven to be effective for neuropathic and centralized pain. Ketamine and cannabinoids are other studied analgesics but have a less well-proven role in CNCP.