Articles: neuralgia.
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Neuropathic pain is a debilitating symptom reported by patients presenting with postherpetic neuralgia (PHN). Efforts to alleviate this pain have been projected to lie in individualization of pharmacological treatment through pain phenotyping and subsequent investigations into the genetic basis of PHN therapy. ⋯ Knowledge and application of genetic variations in PHN, structural proteins, and genes can aid in ascertaining risk, susceptibility to, severity of, and protection from PHN. This review summarizes the most recent information that has been published on phenotypes and genotypes with possible clinical applications and directions for future research.
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Observational Study
Long-term neuropathic pain behaviors correlate with synaptic plasticity and limbic circuits alteration: a comparative observational study in mice.
Neuropathic pain has long-term consequences in affective and cognitive disturbances, suggesting the involvement of supraspinal mechanisms. In this study, we used the spared nerve injury (SNI) model to characterize the development of sensory and aversive components of neuropathic pain and to determine their electrophysiological impact across prefrontal cortex and limbic regions. Moreover, we evaluated the regulation of several genes involved in immune response and inflammation triggered by SNI. ⋯ On the other hand, a reduced neural activity was recorded in the lateral entorhinal cortex-dentate gyrus pathway in the 1-month SNI mice, but not in the 12-month SNI mice. Finally, we observed the upregulation of specific genes involved in immune response in the hippocampus of 1-month SNI mice, but not in the 12-month SNI mice, suggesting a neuroinflammatory response that may contribute to the SNI phenotype. These data suggest that distinct brain circuits may drive the psychiatric components of neuropathic pain and pave the way for better investigation of the long-term consequences of peripheral nerve injury for which most of the available drugs are to date unsatisfactory.
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The authors estimate the probability of successful development and duration of clinical trials for medications to treat neuropathic and nociceptive pain. The authors also consider the effect of the perceived abuse potential of the medication on these variables. ⋯ The authors' data suggest that the unique attributes of pain medications, such as their abuse potential and intended pathology, can influence the probability of successful development and duration of development.
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Observational Study
Capsaicin 8% Dermal Patch for Neuropathic Pain in a Pain Unit.
Pain units manage approximately 20% of the patients with neuropathic pain, usually presenting with severe uncontrolled pain associated with substantial impairment of quality-of-life and disability. We aimed to analyze the experience with the capsaicin 8% dermal patch for managing patients with neuropathic pain in a pain unit. ⋯ Our results suggest that the capsaicin 8% dermal patch is a useful and well-tolerated treatment option for managing peripheral neuropathic pain in pain units.
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Neuropathic pain in rodents can be driven by ectopic spontaneous activity (SA) generated by sensory neurons in dorsal root ganglia (DRG). The recent demonstration that SA in dissociated human DRG neurons is associated with reported neuropathic pain in patients enables a detailed comparison of pain-linked electrophysiological alterations driving SA in human DRG neurons to alterations that distinguish SA in nociceptors from SA in low-threshold mechanoreceptors (LTMRs) in rodent neuropathy models. Analysis of recordings from dissociated somata of patient-derived DRG neurons showed that SA and corresponding pain in both sexes were significantly associated with the three functional electrophysiological alterations sufficient to generate SA in the absence of extrinsic depolarizing inputs. ⋯ These findings suggest that conserved physiological mechanisms of SA in human nociceptor somata can drive neuropathic pain despite documented cellular differences between human and rodent DRG neurons. PERSPECTIVE: Electrophysiological alterations in human sensory neurons associated with patient-reported neuropathic pain include all three of the functional alterations that logically can promote spontaneous activity. The similarity of distinctively altered spontaneous depolarizations in human DRG neurons and rodent nociceptors suggests that spontaneously active human nociceptors can persistently promote neuropathic pain in patients.