Articles: sciatic-neuropathy-pathology.
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Currently a wide variety of polymer materials are being applied to fabricate nerve guide tubes to repair injured peripheral nerves. In this study we have examined whether collagen-chitosan nerve guides promotes nerve repair compared to chitosan nerve guides using histological analysis. ⋯ Collagen-chitosan guides improved axonal maturation measured by a significant increase in axon diameter and axon area. These findings indicate that the collagen-chitosan nerve guides can be applied to repair severed peripheral nerve ends.
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Experimental neurology · Aug 2008
Magnetic resonance imaging of mouse skeletal muscle to measure denervation atrophy.
We assessed the potential of different MRI measures to detect and quantify skeletal muscle changes with denervation in two mouse models of denervation/neurogenic atrophy. Acute complete denervation and chronic partial denervation were examined in calf muscles after sciatic nerve axotomy and in transgenic SOD1(G93A) mice, respectively. Serial T(2), diffusion tensor, and high resolution anatomical images were acquired, and compared to behavioral, histological, and electrophysiological data. ⋯ Changes in T(2) and muscle volume were first observed in medial gastrocnemius and later in other calf muscles. Alterations in secondary and tertiary eigenvalues obtained from DTI were first observed in tibialis anterior and medial gastrocnemius muscles at age 12 weeks. We propose that MRI of skeletal muscle is a sensitive surrogate outcome measure of denervation atrophy in animal models of neuromuscular disorders, with potential applicability in preclinical therapeutic screening studies in rodents.
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Foot drop is a common and distressing problem that can lead to falls and injury. Although the most frequent cause is a (common) peroneal neuropathy at the neck of the fibula, other causes include anterior horn cell disease, lumbar plexopathies, L5 radiculopathy and partial sciatic neuropathy. And even when the nerve lesion is clearly at the fibular neck there are a variety of causes that may not be immediately obvious; habitual leg crossing may well be the most frequent cause and most patients improve when they stop this habit. ⋯ Nerve conduction and electromyographic studies are useful adjuncts in localising the site of injury, establishing the degree of damage and predicting the degree of recovery. Imaging is important in establishing the cause of foot drop be it at the level of the spine, along the course of the sciatic nerve or in the popliteal fossa; ultrasonography, CT and MR imaging are all useful. For patients with a severe foot drop of any cause, an ankle foot orthosis is a helpful device that enables them to walk better and more safely.
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Neuropathic pain is a major clinical problem, and several animal models have been developed to investigate its mechanisms and its treatment. In this report, the role of the rostral ventromedial medulla (RVM) in the early events of the chronic constriction injury (CCI) model was investigated in behavioral and electrophysiological experiments. Placing the 4 CCI ligatures around the sciatic nerve induced large discharges and residual ongoing activity in spinal nociceptive neurons. Two weeks after CCI ligation, the rats showed behavioral hyperalgesia and allodynia as well as increased ongoing activity and responsiveness of spinal nociceptive neurons to innocuous and noxious stimuli. Blockade of excitatory synapses in the RVM by a kynurenate microinjection (2 nmol in 0.5 muL) 5 minutes before placement of the sciatic ligatures had no immediate effect on spinal neuronal activity but largely prevented the activation of spinal neurons. In kynurenate microinjected rats, behavioral hyperalgesia and allodynia developed slowly and incompletely, which corresponded with an incompletely developed hyperexcitability of spinal neurons. To the best of our knowledge, these results show for the first time that the initial response to nerve damage requires facilitation from the RVM. ⋯ The present and previous findings indicate that descending facilitation from brainstem nuclei critically contributes to the spinal hyperexcitability that underlies neuropathic pain. The present results indicate that this contribution begins at the very moment the nerve is damaged and should be prevented and treated accordingly.
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Recent data indicate that peripheral T-type Ca2+ channels are instrumental in supporting acute pain transmission. However, the function of these channels in chronic pain processing is less clear. To address this issue, we studied the expression of T-type Ca2+ currents in small nociceptive dorsal root ganglion (DRG) cells from L4-5 spinal ganglia of adult rats with neuropathic pain due to chronic constrictive injury (CCI) of the sciatic nerve. ⋯ CCI-induced neuropathy did not significantly change the pharmacological sensitivity of T-type current in these cells to nickel. Collectively, our results indicate that CCI-induced neuropathy significantly increases T-type current expression in small DRG neurons. Our finding that T-type currents are upregulated in a CCI model of peripheral neuropathy and earlier pharmacological and molecular studies suggest that T-type channels may be potentially useful therapeutic targets for the treatment of neuropathic pain associated with partial mechanical injury to the sciatic nerve.