Browsing by Subject "Sciatic Neuropathy"

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    Gluteal compartment syndrome with sciatic nerve palsy caused by traumatic rupture of the inferior gluteal artery: a successful surgical treatment.
    (BMJ case reports, 2017-01) Rocos, Brett; Ward, Anthony
    Gluteal compartment syndrome is a rare entity, usually caused by direct trauma. This occurrence with sciatic nerve palsy caused by inferior gluteal artery laceration and compressive haematoma has not been reported in the literature. We describe such a case treated successfully by urgent surgical decompression and resolution of the sciatic nerve palsy. A man aged 41 years sustained blunt trauma to the right gluteal region causing a rupture of the inferior gluteal artery, gluteal compartment syndrome and rapidly progressive sciatic nerve palsy. The condition was treated urgently with interventional radiology, open surgical decompression and debridement. Recovery was complicated by recurrent haematoma formation, treated successfully with subsequent complete resolution of the sciatic nerve palsy. A review of the literature of traumatic gluteal compartment syndrome is presented with discussion of the clinical diagnosis, multidisciplinary treatment and recommendations for treatment of this injury.
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    Neuropathic pain activates the endogenous kappa opioid system in mouse spinal cord and induces opioid receptor tolerance.
    (J Neurosci, 2004-05-12) Xu, Mei; Petraschka, Michael; McLaughlin, Jay P; Westenbroek, Ruth E; Caron, Marc G; Lefkowitz, Robert J; Czyzyk, Traci A; Pintar, John E; Terman, Gregory W; Chavkin, Charles
    Release of endogenous dynorphin opioids within the spinal cord after partial sciatic nerve ligation (pSNL) is known to contribute to the neuropathic pain processes. Using a phosphoselective antibody [kappa opioid receptor (KOR-P)] able to detect the serine 369 phosphorylated form of the KOR, we determined possible sites of dynorphin action within the spinal cord after pSNL. KOR-P immunoreactivity (IR) was markedly increased in the L4-L5 spinal dorsal horn of wild-type C57BL/6 mice (7-21 d) after lesion, but not in mice pretreated with the KOR antagonist nor-binaltorphimine (norBNI). In addition, knock-out mice lacking prodynorphin, KOR, or G-protein receptor kinase 3 (GRK3) did not show significant increases in KOR-P IR after pSNL. KOR-P IR was colocalized in both GABAergic neurons and GFAP-positive astrocytes in both ipsilateral and contralateral spinal dorsal horn. Consistent with sustained opioid release, KOR knock-out mice developed significantly increased tactile allodynia and thermal hyperalgesia in both the early (first week) and late (third week) interval after lesion. Similarly, mice pretreated with norBNI showed enhanced hyperalgesia and allodynia during the 3 weeks after pSNL. Because sustained activation of opioid receptors might induce tolerance, we measured the antinociceptive effect of the kappa agonist U50,488 using radiant heat applied to the ipsilateral hindpaw, and we found that agonist potency was significantly decreased 7 d after pSNL. In contrast, neither prodynorphin nor GRK3 knock-out mice showed U50,488 tolerance after pSNL. These findings suggest that pSNL induced a sustained release of endogenous prodynorphin-derived opioid peptides that activated an anti-nociceptive KOR system in mouse spinal cord. Thus, endogenous dynorphin had both pronociceptive and antinociceptive actions after nerve injury and induced GRK3-mediated opioid tolerance.