Articles: peripheral-nerve-injuries.
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Comparative Study
Mouse strains that lack spinal dynorphin upregulation after peripheral nerve injury do not develop neuropathic pain.
Several experimental models of peripheral neuropathy show that a significant upregulation of spinal dynorphin A and its precursor peptide, prodynorphin, is a common consequence of nerve injury. A genetically modified mouse strain lacking prodynorphin does not exhibit sustained neuropathic pain after nerve injury, supporting a pronociceptive role of elevated levels of spinal dynorphin. A null mutation of the gamma isoform of protein kinase C (PKCgamma KO [knockout]), as well as an inbred mouse strain, 129S6, also does not manifest behavioral signs of neuropathic pain following peripheral nerve injury. ⋯ However, the PKCgamma KO mice and the 129S6 mice (which express PKCgamma) did not show abnormal pain after SNL; neither strain showed elevated levels of spinal dynorphin. The multiple phenotypic deficits in PKCgamma KO mice confound the interpretation of the proposed role of PKCgamma-expressing spinal neurons in neuropathic pain states. Additionally, the data show that the regulation of spinal dynorphin expression is a common critical feature of expression of neuropathic pain.
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The mechanisms responsible for initiation of persistent neuropathic pain after peripheral nerve injury are unclear. One hypothesis is that injury discharge and early ectopic discharges in injured nerves produce activity-dependent irreversible changes in the central nervous system. The aim of this study was to determine whether blockade of peripheral discharge by blocking nerve conduction before and 1 week after nerve injury could prevent the development and persistence of neuropathic pain-like behavior in the spared nerve injury model. ⋯ Peripheral long-term nerve blockade has no detectable effect on the development of allodynia or hyperalgesia in the spared nerve injury model. It is unlikely that injury discharge at the time of nerve damage or the early onset of ectopic discharges arising from the injury site contributes significantly to the persistence of stimulus-evoked neuropathic pain in this model.
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The consensus is that eversion carotid endarterectomy (CEA) is a safe, effective, and durable surgical technique. Concern remains, however, regarding insertion of a shunt during the procedure. We studied the advisability of shunting with eversion CEA by comparing patients who underwent eversion CEA with and without shunting. ⋯ Shunt insertion can be safely performed during eversion CEA. Perioperative mortality and morbidity after eversion CEA are not statistically modified with shunting.
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PSD-93/chapsin-110 is a neuronal PDZ domain-containing protein that binds to and clusters the N-methyl-D-aspartate receptor (NMDAR) at synapses in the central nervous system. It also assembles a specific set of signaling proteins around the NMDAR and mediates downstream signaling by the NMDAR. Thus, PSD-93/chapsin-110 might be involved in many physiological and pathophysiological actions triggered via the activation of the NMDAR. ⋯ The present results indicate that the deficiency of spinal cord PSD-93/chapsin-110 protein significantly attenuates thermal and mechanical hyperalgesia in complete Freund's adjuvant- or peripheral nerve injury-induced chronic pain. This suggests that spinal cord PSD-93/chapsin-110 might be involved in the central mechanism of chronic pain. Our work might provide a new target for the therapy of chronic pain.
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Saphenous nerve injury has long been recognized as a risk of greater saphenous vein stripping, and it has been suggested by some authors as a reason to avoid stripping below the knee. The rate of injury reported in the literature is extremely variable, with no study adequately addressing the effect of these injuries on patient quality of life. We undertook this study to measure the prevalence of these injuries and quantify their impact on quality of life. ⋯ Signs and symptoms of saphenous nerve injury are common at long-term follow-up after greater saphenous vein stripping to the ankle. However, there appears to be little, if any, significant resultant morbidity. The risk of saphenous nerve injury should therefore not be considered a reason to avoid stripping of the greater saphenous vein to the ankle.