Articles: neuralgia.
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Conditioned pain modulation (CPM) is a validated measure of the function of endogenous pain inhibitory pathways. Placebo effects reflect top-down inhibitory modulation of pain. CPM and placebo effects are both influenced by expectations, albeit to varying degrees, and are related to neurotransmitter systems such as the endogenous opioid system, and it can be speculated that CPM responses are positively associated with the magnitude of placebo effects. Yet, no studies have tested this. ⋯ Conditioned pain modulation and placebo effects are endogenous pain-modulating phenomena that are influenced by some of the same mechanisms. This study suggests that CPM and placebo effects in neuropathic pain are independent phenomena that may be mediated by different mechanisms.
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The therapeutic influence of somatotopic matching between pain topography and motor cortex stimulation site for neuropathic pain (NP) remains controversial. ⋯ Strict somatotopic targeting of rTMS does not appear warranted for the treatment of upper limb or face NP. Since the hand motor area is easier to target and provides better results, it might be privileged for both types of pain.
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Chemotherapy-induced peripheral neuropathic pain (CIPNP) is a serious dose-limiting neurotoxic effect of cancer drug treatment. The underlying mechanism(s) of this debilitating condition, which lacks effective drug treatment, is incompletely understood. However, neural-immune interactions, involving increased expression and release of cytokines, are believed to be involved. Here, we examined, in the paclitaxel rat model of CIPNP, whether plasma levels of 24 cytokines/chemokines change after paclitaxel treatment, and whether blocking of signalling of some of those cytokines would reverse/attenuate behavioural signs of CIPNP. ⋯ This study demonstrates that paclitaxel-treated rats exhibit, in addition to indices of mechanical and cold hypersensitivity, a behavioural sign of spontaneous pain, the principal compliant of patients with neuropathic pain. This was accompanied by upregulation in plasma levels of key cytokines/chemokines (IL-1α, IL-1β, IL-6, TNF-α, INF-γ and MCP-1) 31 days post-treatment. However, it is noteworthy that cytokine release, rather than nerve injury per se, may be causative of NP in this model of CIPNP. Nevertheless, our findings that pharmacological blockade of TNF-α, IL-1β and MCP-1 attenuated both evoked and spontaneous pain suggest that strategies that target inhibition of these cytokines may be effective in treating CIPNP.
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Pregabalin is a first-line agent for neuropathic pain treatment whose abuse liability remains controversial. Surprisingly, studies exploring the reinforcing properties of pregabalin in operant mouse models are missing. ⋯ This study shows that mice with a nerve injury self-administer pregabalin at doses effective reducing nociceptive hypersensitivity and depressive-like behaviour associated with the neuropathic pain model. Interestingly, mice without neuropathy also develop operant self-administration behaviour, suggesting potential abuse liability of this first-line drug for neuropathic pain treatment.
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Journal of neurosurgery · Apr 2018
Evaluation of surgical treatment for neuropathic pain from neuroma in patients with injured peripheral nerves.
OBJECTIVE Chronic neuropathic pain after peripheral nerve injury is a major clinical problem. Its management is difficult, and therapeutic approaches vary and include oral medication, neurostimulation, and surgery. The aim of this study was to assess the adequacy of surgical nerve revision in a large series of patients with long-term follow-up. ⋯ CONCLUSIONS Bearing in mind that medication achieves satisfying pain relief in only 30%-40% of patients with neuropathic pain, surgery must be considered as an effective alternative therapy. No objective criteria were shown to be factors of poor prognosis. Systematic preoperative clinical mapping of the injured nerves and diagnostic nerve blocks could improve the primary success rate of the surgery.