Pain
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Comparative Study
A prospective identification of neuropathic pain in specific chronic polyneuropathy syndromes and response to pharmacological therapy.
Although many pharmacological agents are used in the therapy of neuropathic pain (NeP) due to polyneuropathy (PN), there are limited comparison studies comparing these agents. We evaluated patients with PN and related NeP in a tertiary care neuromuscular clinic with prospective follow-up after 3 and 6 months for degree of NeP using a Visual Analog Score (VAS). Clinical response to specific open-label pharmacotherapies was measured and compared for those patients not receiving pharmacotherapy. ⋯ Approximated numbers needed to treat were similar between different individual oral pharmacotherapies, trending towards greater treatment efficacy with combination therapy. NeP is common in patients with PN and frequently requires pharmacotherapy management, which may be more effective with combination therapy. Future studies assessing longer duration of follow-up and quality of life changes with the use of various pharmacotherapies for management of NeP due to PN will be important.
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Comparative Study
Retigabine, the specific KCNQ channel opener, blocks ectopic discharges in axotomized sensory fibres.
The M-current has been proposed as a potential target for analgesia under neuropathic pain conditions. M-currents and/or their molecular correlates, KCNQ proteins, have been demonstrated in key elements of the nociceptive system including spinal and dorsal root ganglion neurons. Here we demonstrate that retigabine, a selective KCNQ channel opener, applied at neuromatose endings modulates the excitability of axotomized fibres inhibiting ectopic discharges. ⋯ Application of XE-991 (10 microM), a KCNQ channel blocker, had no effect on responses to stimulation of the neuroma but blocked the effects of retigabine indicating a specific involvement of KCNQ channels. In contrast to the strong effects on ectopic discharges, retigabine did not change responses to stimulation recorded from intact receptors. Results indicate that KCNQ channel opening at axotomized endings may constitute a novel and selective mechanism for modulation of some neuropathic pain symptoms.