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Myelin Damage (myelin + damage)
Selected AbstractsNerve perforation with pencil point or short bevelled needles: histological outcomeACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 8 2010T. STEINFELDT Background: In the case of needle nerve contact during peripheral blocks, pencil point needles are considered less traumatic compared with bevelled needles. However, there are not enough data to prove this notion. Therefore, the aim of this study was to challenge the hypothesis that nerve perforation with short bevelled needles is associated with major nerve damage compared with pencil point needles. Methods: In five anaesthetised pigs, the brachial plexus was exposed bilaterally. Up to eight nerves underwent needle nerve perforation using a pencil point needles cannula or an short bevelled needle. After 48 h, the nerves were resected. The specimens were processed for visual examination and the detection of inflammatory cells (haematoxylin,eosin, i.e. CD68-immunohistochemistry to detect macrophages), myelin damage (Kluver,Barrera staining) and intraneural haematoma. The grade of nerve injury was characterised by an objective score ranging from 0 (no injury) to 4 (severe injury). Results: Fifty nerves were examined. According to the injury score applied, there was no significant difference between the pencil point needles [median (inter-quartile range) 2.0 (2.0,2.0)] and the short bevelled-needle group [median 2.0 (2.0,2.0) P=0.23]. No myelin damage was observed. Signs of post-traumatic inflammation were equally distributed among both groups. Conclusions: In the present study, the magnitude of nerve injury after needle nerve perforation was not related to one of the applied needle types. Post-traumatic inflammation rather than structural damage of nerve tissue is the only notable sign of nerve injury after needle nerve perforation with either needle type. However, neither the pencil point- nor the short bevelled needle can be designated a less traumatic device. [source] Postinjury estrogen treatment of chronic spinal cord injury improves locomotor function in ratsJOURNAL OF NEUROSCIENCE RESEARCH, Issue 8 2010Eric A. Sribnick Abstract Spinal cord injury (SCI) causes loss of neurological function and, depending on serverity, may cause paralysis. The only recommended pharmacotherapy for the treatment of SCI is high-dose methylprednisolone, and its use is controversial. We have previously shown that estrogen treatment attenuated cell death, axonal and myelin damage, calpain and caspase activities, and inflammation in acute SCI. The aim of this study was to examine whether posttreatment of SCI with estrogen would improve locomotor function by protecting cells and axons and reducing inflammation during the chronic phase following injury. Moderately severe injury (40 g · cm force) was induced in male Sprague-Dawley rats following laminectomy at T10. Three groups of animals were used: sham (laminectomy only), vehicle (dimethyl sulfoxide; DMSO)-treated injury group, and estrogen-treated injury group. Animals were treated with 4 mg/kg estrogen at 15 min and 24 hr postnjury, followed by 2 mg/kg estrogen daily for the next 5 days. After treatment, animals were sacrificed at the end of 6 weeks following injury, and 1-cm segments of spinal cord (lesion, rostral to lesion, and caudal to lesion) were removed for biochemical analyses. Estrogen treatment reduced COX-2 activity, blocked nuclear factor-,B translocation, prevented glial reactivity, attenuated neuron death, inhibited activation and activity of calpain and caspase-3, decreased axonal damage, reduced myelin loss in the lesion and penumbra, and improved locomotor function compared with vehicle-treated animals. These findings suggest that estrogen may be useful as a promising therapeutic agent for prevention of damage and improvement of locomotor function in chronic SCI. © 2010 Wiley-Liss, Inc. [source] Insulin-like growth factor-I ameliorates demyelination induced by tumor necrosis factor-, in transgenic miceJOURNAL OF NEUROSCIENCE RESEARCH, Issue 4 2007Ping Ye Abstract Our groups have reported that tumor necrosis factor-, (TNF-,) causes myelin damage and apoptosis of oligodendrocytes and their precursors in vitro and in vivo. We also have reported that insulin-like growth factor-I (IGF-I) can protect cultured oligodendrocytes and their precursors from TNF-,-induced damage. In this study, we investigated whether IGF-I can protect oligodendrocytes and myelination from TNF-,-induced damage in vivo by cross-breeding TNF-, transgenic (Tg) mice with IGF-I Tg mice that overexpress IGF-I exclusively in brain. At 8 weeks of age, compared with those of wild-type (WT) mice, the brain weights of TNF-, Tg mice were decreased by ,20%, and those of IGF-I Tg mice were increased by ,20%. The brain weights of mice that carry both TNF-, and IGF-I transgenes (TNF-,/IGF-I Tg mice) did not differ from those of WT mice. As judged by histochemical staining and immunostaining, myelin content in the cerebellum of TNF-,/IGF-I Tg mice was similar to that in WT mice and much more than that in TNF-, Tg mice. Consistently, Western immunoblot analysis showed that myelin basic protein (MBP) abundance in the cerebellum of TNF-,/IGF-I Tg mice was double that in TNF-, Tg mice. In comparison with WT mice, the number of oligodendrocytes was decreased by ,36% in TNF-, Tg mice, whereas it was increased in IGF-I Tg mice by ,40%. Oligodendrocyte number in TNF-,/IGF-I Tg mice was almost twice that in TNF-, Tg mice. Furthermore, IGF-I overexpression significantly reduced TNF-,-induced increases in apoptotic cell number, active caspase-3 abundance, and degradaion of MBP. Our results indicate that IGF-I is capable of protecting myelin and oligodendrocytes from TNF-,-induced damage in vivo. © 2007 Wiley-Liss, Inc. [source] Peripheral neuropathy associated with mitochondrial disorders: 8 cases and review of the literatureJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 4 2002S. Bouillot Abstract Forty-three cases of peripheral neuropathy (PN) have been reported in the literature with a proven mitochondria (mt) DNA mutation, and 21 had a peripheral nerve biopsy (PNB). We studied 8 patients, 1 of whom had severe sensory PN, 3 mild PN, and 4 subclinical PN. Nerve biopsy was performed in every case; all patients showed axonal degeneration and 4 showed features of primary myelin damage. In addition, there were 2 crystalline-like inclusions in the Schwann cell cytoplasm of a patient with MERRF, and 1 in a patient with multiple deletions on the mtDNA. There are 11 cases of PNB in the literature with axonal lesions, 5 with demyelination, and 4 with mixed lesions. One PNB was not modified. A few crystalline-like inclusions were seen in 1 case of MERRF. Such inclusions were first reported in the Schwann cell cytoplasm of unmyelinated fibers in a patient with Refsum disease and were considered to be modified mitochondria. However, their mitochondrial origin remains debatable. [source] Assessing optic nerve pathology with diffusion MRI: from mouse to humanNMR IN BIOMEDICINE, Issue 9 2008Junqian Xu Abstract The optic nerve is often affected in patients with glaucoma and multiple sclerosis. Conventional MRI can detect nerve damage, but it does not accurately assess the underlying pathologies. Mean diffusivity and diffusion anisotropy indices derived from diffusion tensor imaging have been shown to be sensitive to a variety of central nervous system white matter pathologies. Despite being sensitive, the lack of specificity limits the ability of these measures to differentiate the underlying pathology. Directional (axial and radial) diffusivities, measuring water diffusion parallel and perpendicular to the axonal tracts, have been shown to be specific to axonal and myelin damage in mouse models of optic nerve injury, including retinal ischemia and experimental autoimmune encephalomyelitis. The progression of Wallerian degeneration has also been detected using directional diffusivities after retinal ischemia. However, translating these findings to human optic nerve is technically challenging. The current status of diffusion MRI of human optic nerve, including imaging sequences and protocols, is summarized herein. Despite the lack of a consensus among different groups on the optimal sequence or protocol, increased mean diffusivity and decreased diffusion anisotropy have been observed in injured optic nerve from patients with chronic optic neuritis. From different mouse models of optic nerve injuries to the emerging studies on patients with optic neuritis, directional diffusivities show great potential to be specific biomarkers for axonal and myelin injury. Copyright © 2008 John Wiley & Sons, Ltd. [source] | ||||||||||