Articles: neuropathic-pain.
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Surgical injury can frequently lead to chronic pain. Despite the obvious importance of this problem, the first publications on chronic pain after surgery as a general topic appeared only a decade ago. This study tests the hypothesis that chronic postsurgical pain was, and still is, represented insufficiently. ⋯ Chronic postsurgical pain is still a neglected topic, except for pain after herniorrhaphy. The change in the attitude toward chronic postsurgical pain is the important first step in the approach to this problem.
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Frontiers in physiology · Jan 2012
Nociceptors as chronic drivers of pain and hyperreflexia after spinal cord injury: an adaptive-maladaptive hyperfunctional state hypothesis.
Spinal cord injury (SCI) causes chronic peripheral sensitization of nociceptors and persistent generation of spontaneous action potentials (SA) in peripheral branches and the somata of hyperexcitable nociceptors within dorsal root ganglia (DRG). Here it is proposed that SCI triggers in numerous nociceptors a persistent hyperfunctional state (peripheral, synaptic, and somal) that originally evolved as an adaptive response to compensate for loss of sensory terminals after severe but survivable peripheral injury. In this hypothesis, nociceptor somata monitor the status of their own receptive field and the rest of the body by integrating signals received by their peripheral and central branches and the soma itself. ⋯ Nociceptor activity generated above the injury level contributes to at- and above-level sensitization and pain (evoked and spontaneous). Thus, SCI triggers a potent nociceptor state that may have been adaptive (from an evolutionary perspective) after severe peripheral injury but is maladaptive after SCI. Evidence that hyperfunctional nociceptors make large contributions to behavioral hypersensitivity after SCI suggests that nociceptor-specific ion channels required for nociceptor SA and hypersensitivity offer promising targets for treating chronic pain and hyperreflexia after SCI.
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Journal of pain research · Jan 2012
Changes in functional properties of A-type but not C-type sensory neurons in vivo in a rat model of peripheral neuropathy.
The aim of this study was to compare primary sensory neurons in controls and in an animal neuropathic pain model in order to understand which types of neurons undergo changes associated with peripheral neuropathy. On the basis of intracellular recordings in vivo from somata, L4 sensory dorsal root ganglion neurons were categorized according to action potential configuration, conduction velocity, and receptive field properties to mechanical stimuli. ⋯ This study provides evidence for defining a potential role of Aβ-fiber low threshold mechanoreceptor neurons that might contribute to peripheral neuropathic pain.
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Int J Clin Exp Patho · Jan 2012
Down-regulation of GAP-43 by inhibition of caspases-3 in a rat model of neuropathic pain.
Neuropathic pain remains a prevalent and persistent clinical problem due to incomplete understanding of its pathogenesis. ⋯ Caspase-3 mediated neuron apoptosis is probably responsible for the neuropathic pain in CCI rats. Inhibition of caspase-3 may serve as a treatment of neuropathic pain.
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Journal of pain research · Jan 2012
Tolerability of NGX-4010, a capsaicin 8% patch, in conjunction with three topical anesthetic formulations for the treatment of neuropathic pain.
The objective of this study was to assess the safety, tolerability, and preliminary efficacy of NGX-4010, a capsaicin 8% patch, following pretreatment with three different topical anesthetics in patients with peripheral neuropathic pain. ⋯ Treatment with NGX-4010 following pretreatment with any of the three topical anesthetics was generally safe and well tolerated; no significant differences in the parameters measured were noted between the pretreatment groups.