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PubMed1978

Studies on myelin proteins in human peripheral nerve.

The myelin fraction from human peripheral nerve was prepared. Two basic protein fractions (BF-P2 and PB) were isolated from acid extracts of the myelin fraction and three glycoproteins (BR-PO, PASII and Y protein) were purified from its acid-insoluble residue. In biochemical analysis the human BF-P2 protein (M.W.13,000) showed similar but not identical properties to bovine BF-P2 protein. The PB fraction was suggested to include the encephalitogenic CNS-BP (M.W.18,000) and another, new protein of similar molecular weight. Both the human BR-PO protein (M.W.28,000) and PASII protein (M.W.13,000) showed similar biochemical properties to the corresponding myelin proteins of bovine peripheral nerve, while they both are clearly different from other myelin proteins. Close relationship between the BR-PO protein and the Y protein (M.W.22,000) was suggested by amino acid analysis. Injection of the myelin fraction of bovine peripheral nerve with the complete adjuvant produced EAN while the CNS-BP induced EAE in laboratory animals. However, all three purified proteins, BF-P2, BR-PO and PASII, from bovine peripheral nerve myelin were inactive in inducing demyelinating diseases.

Amino Acids↗
PubMed2000

BDNF is involved in sympathetic sprouting in the dorsal root ganglia following peripheral nerve injury in rats.

Peripheral nerve injury results in sympathetic sprouting around large diameter sensory neurons in the dorsal root ganglia (DRG). The mechanism underlying this pathological phenomenon is not known. Brain-derived neurotrophic factor (BDNF) is up-regulated in large sensory neurons and ensheathing satellite cells following a sciatic nerve injury. In the present study, we investigated the effects of BDNF on the sympathetic sprouting in the DRG, by delivering BDNF antibody or antisense oligodeoxynucleotide to injured DRGs, or by delivering exogenous BDNF to intact DRGs. The sheep antibody to BDNF, characterized by bioassays and dot blots, specifically reacted with BDNF but not other neurotrophins. Noradrenergic fibers were visualized by immunostaining of tyrosine hydroxylase (TH) and quantified by an NIH Imaging program. Two weeks following L5 spinal nerve lesion, a dramatic increase in TH-immunoreactive (-ir) fibres was observed in both ipsi- and contralateral DRGs in normal sheep IgG treated rats. BDNF antibody significantly reduced the sprouting of sympathetic nerves in both ipsi- and contra-lateral DRGs by 67% and 42% respectively. BDNF antisense oligodeoxynucleotide, by inhibiting BDNF synthesis in DRGs, also significantly suppressed the sprouting by 67% and 60% respectively in the ipsi- and contra-lateral DRGs. Delivery of exogenous BDNF into an intact L5 DRGs resulted in an increase in the sprouting by 4.2-fold. Our results clearly indicate that BDNF, synthesized in and secreted from the DRGs, is involved in the sympathetic sprouting in the DRG following the peripheral nerve injury.

Journal Article↗
PubMed2003

Effects of human amniotic fluid on peripheral nerve scarring and regeneration in rats.

OBJECT: Peripheral nerve repair surgery is still replete with challenges. Despite technical improvements in microsurgery, classic methods of nerve repair have failed to provide satisfactory results. The purpose of this study was to investigate the effects of amniotic fluid from humans on peripheral nerve scarring and regeneration in rats. METHODS: Forty adult Sprague-Dawley rats were used in this study. After the right sciatic nerve in each rat was transected and repaired using an epineural suture procedure, the nerves were divided into two groups according to the solution applied around the repair site: experimental group, 0.3 ml human amniotic fluid (HAF); and control group, 0.3 ml saline. Macroscopic and histological evaluations of peripheral nerve scarring were performed 4 weeks postsurgery. Nerves treated with HAF demonstrated a significant reduction in the amount of scar tissue surrounding the repair site (p < 0.05). No evidence of a reaction against HAF was noted. Functional nerve regeneration was measured once every 2 weeks by using a sciatic function index until 12 weeks postsurgery. Functional recovery in nerves treated with amniotic fluid occurred significantly faster than that in nerves treated with saline (p < 0.05). Peripheral nerve regeneration was evaluated histomorphologically at 12 weeks postsurgery. Nerves treated with amniotic fluid showed significant improvement with respect to the indices of fiber maturation (p < 0.05). CONCLUSIONS: Preliminary data show that HAF enhances peripheral nerve regeneration. The preventive effect of HAF on epineural scarring and the rich content of neurotrophic and neurite-promoting factors possibly contribute to this result.

Adjuvants, Immunologic↗
PubMed2002

Nogo-A expressed in Schwann cells impairs axonal regeneration after peripheral nerve injury.

Injured axons in mammalian peripheral nerves often regenerate successfully over long distances, in contrast to axons in the brain and spinal cord (CNS). Neurite growth-inhibitory proteins, including the recently cloned membrane protein Nogo-A, are enriched in the CNS, in particular in myelin. Nogo-A is not detectable in peripheral nerve myelin. Using regulated transgenic expression of Nogo-A in peripheral nerve Schwann cells, we show that axonal regeneration and functional recovery are impaired after a sciatic nerve crush. Nogo-A thus overrides the growth-permissive and -promoting effects of the lesioned peripheral nerve, demonstrating its in vivo potency as an inhibitor of axonal regeneration.

Animals↗
PubMed1992

The location and distribution of neural crest-derived Schwann cells in developing peripheral nerves in the chick forelimb.

The location and distribution of neural crest-derived Schwann cells during development of the peripheral nerves of chick forelimbs were examined using chick-quail chimeras. Neural crest cells were labeled by transplantation of the dorsal part of the neural tube from a quail donor to a chick host at levels of the neural tube destined to give rise to brachial innervation. The ventral roots, spinal nerves, and peripheral nerves innervating the chick forelimb were examined for the presence of quail-derived neural crest cells at several stages of embryonic development. These quail cells are likely to be Schwann cells or their precursors. Quail-derived Schwann cells were present in ventral roots and spinal nerves, and were distributed along previously described neural crest migratory pathways or along the peripheral nerve fibers at all stages of development examined. During early stages of wing innervation, quail-derived Schwann cells were not evenly distributed, but were concentrated in the ventral root and at the brachial plexus. The density of neural crest-derived Schwann cells decreased distal to the plexus, and no Schwann cells were ever seen in advance of the growing nerve front. When the characteristic peripheral nerve branching pattern was first formed, Schwann cells were clustered where muscle nerves diverged from common nerve trunks. In still older embryos, neural crest-derived Schwann cells were evenly distributed along the length of the peripheral nerves from the ventral root to the distal nerve terminations within the musculature of the forelimb. These observations indicate that Schwann cells accompany axons into the developing limb, but they do not appear to lead or direct axons to their targets. The transient clustering of neural crest-derived Schwann cells in the ventral root and at places where axon trajectories diverge from one another may reflect a response to some environmental feature within these regions.

Animals↗
PubMed2002

Very early activation of m-calpain in peripheral nerve during Wallerian degeneration.

Peripheral nerve injury results in a series of events culminating in degradation of the axonal cytoskeleton (Wallerian degeneration). In the time period between axotomy and cytoskeletal degradation (24-48 h in rodents), there is calcium entry and activation of calpains within the axon. The precise timing of these events during this period is unknown. In the present study, antibodies were generated to three distinct peptide epitopes of m-calpain, and a fusion protein antibody was generated to the intrinsic calpain inhibitor calpastatin. These antibodies were used to measure changes in these proteins in mouse sciatic nerves during Wallerian degeneration. In sciatic nerve homogenates and cultured dorsal root ganglion (DRG) neurites, m-calpain protein was significantly reduced in transected nerves very early after nerve injury, long before axonal degeneration occurred. Levels of m-calpain protein remained low as compared to control nerves for the remainder of the 72-h time course. No changes in calpastatin protein were evident. Systemic treatment of animals with the protease inhibitor leupeptin partially prevented the rapid loss of calpain protein. Removal of calcium in DRG cultures had the same effect. These data indicate that m-calpain protein is lost very early after axonal injury, and likely reflect activation and degradation of this protein long before the cytoskeleton is degraded. Calpain activation may be an early event in a proteolytic cascade that is initiated by axonal injury and culminates with axonal degeneration.

Animals↗
PubMed1985

Electromyographic evaluation of a novel surgical preparation to enhance nerve-muscle specificity that follows mammalian peripheral nerve trunk transection.

Previous studies indicated that axons from proximal stumps of transected peripheral nerves "prefer" to grow through Silastic tubes attached to their native (originally associated) rather than foreign (not originally associated) distal stumps. We determined whether or not this specificity is expressed at the level of the neuromuscular junction. Proximal stumps of transected rat sciatic nerves (peroneal and tibial branches) were attached to single inlet ends of 6-mm-long, Y-shape Silastic implants. One outlet was attached to the distal peroneal and the other to the distal tibial stump. Ten weeks later, innervation of the anterior tibialis and interosseous muscles (normally innervated predominantly by peroneal and tibial nerve fibers, respectively) was assessed by measuring compound muscle action potential amplitudes and latencies that follow supramaximal peroneal and tibial nerve stimulation. Results showed higher amplitudes in anterior tibialis muscle, induced by "native" peroneal (vs. tibial) stimulation in four of five animals, and higher amplitudes in interosseous muscles after "native" tibial (vs. peroneal) stimulation in all cases examined. Preparations in which bridges between proximal and distal nerve stumps were bridged with unbranched tubes showed random patterns of muscle innervation. The results suggest that if allowed to express "specificity" at the level of nerve trunk transection, regenerating mammalian peripheral axons can grow into, and form functional connection with, native (vs. foreign) muscle groups. This finding has possible clinical significance.

Action Potentials↗
PubMed2002

Systemic acetyl-L-carnitine eliminates sensory neuronal loss after peripheral axotomy: a new clinical approach in the management of peripheral nerve trauma.

Several hundred thousand peripheral nerve injuries occur each year in Europe alone. Largely due to the death of around 40% of primary sensory neurons, sensory outcome remains disappointingly poor despite considerable advances in surgical technique; yet no clinical therapies currently exist to prevent this neuronal death. Acetyl- L-carnitine (ALCAR) is a physiological peptide with roles in mitochondrial bioenergetic function, which may also increase binding of nerve growth factor by sensory neurons. Following unilateral sciatic nerve transection, adult rats received either one of two doses of ALCAR or sham, or no treatment. Either 2 weeks or 2 months later, L4 and L5 dorsal root ganglia were harvested bilaterally, in accordance with the Animal (Scientific Procedures) Act 1986. Neuronal death was quantified with a combination of TUNEL [TdT (terminal deoxyribonucleotidyl transferase) uptake nick end labelling] and neuron counts obtained using the optical disector technique. Sham treatment had no effect upon neuronal death. ALCAR treatment caused a large reduction in the number of TUNEL-positive neurons 2 weeks after axotomy (sham treatment 33/group; low-dose ALCAR 6/group, P=0.132; high-dose ALCAR 3/group, P<0.05), and almost eliminated neuron loss (sham treatment 21%; low-dose ALCAR 0%, P=0.007; high-dose ALCAR 2%, P<0.013). Two months after axotomy the neuroprotective effect of high-dose ALCAR treatment was preserved for both TUNEL counts (no treatment five/group; high-dose ALCAR one/group) and neuron loss (no treatment 35%; high-dose ALCAR -4%, P<0.001). These results provide further evidence for the role of mitochondrial bioenergetic dysfunction in post-traumatic sensory neuronal death, and also suggest that acetyl- L-carnitine may be the first agent suitable for clinical use in the prevention of neuronal death after peripheral nerve trauma.

Acetylcarnitine↗
PubMed2005

Continuous peripheral nerve blockade in lower extremity surgery.

Peripheral nerve blocks afford numerous benefits for lower extremity surgery. There is growing interest in continuous peripheral nerve blocks, mainly for treatment of postoperative pain, a field that represents a challenge to the anaesthesiologist. This paper seeks to review the efficacy of continuous lower limb blocks for postoperative pain relief. Not only do continuous peripheral nerve blocks afford specificity of analgesic area but current research has shown that they enhance postoperative analgesia and patient satisfaction. New techniques and devices are increasingly appearing, and catheters are constantly being developed and improved; an example being the stimulating catheter, which represents one of the newest advances in this area. The above techniques show that continuous postoperative analgesia with catheters in the lower extremities is not only possible, but indeed provides sustained effective postoperative analgesia, reduces use of opioids, and improves rehabilitation and patient well-being with minimal side-effects. These techniques could prove an alternative to postoperative pain treatment following ambulatory surgery.

Humans↗
PubMedDate not supplied

Use of skeletal muscle tissue in peripheral nerve repair: review of the literature.

The management of peripheral nerve injury continues to be a major clinical challenge. The most widely used technique for bridging defects in peripheral nerves is the use of autologous nerve grafts. This technique, however, necessitates a donor nerve and corresponding deficit. Many alternative techniques have thus been developed. The use of skeletal muscle tissue as graft material for nerve repair is one example. The rationale regarding the use of the skeletal muscle tissue technique is the availability of a longitudinally oriented basal lamina and extracellular matrix components that direct and enhance regenerating nerve fibers. These factors provide superiority over other bridging methods as vein grafts or (non)degradable nerve conduits. The main disadvantages of this technique are the risk that nerve fibers can grow out of the muscle tissue during nerve regeneration, and that a donor site is necessary to harvest the muscle tissue. Despite publications on nerve conduits as an alternative for peripheral nerve repair, autologous nerve grafting is still the standard care for treatment of a nerve gap in the clinical situation; however, the use of the skeletal muscle tissue technique can be added to the surgeon's arsenal of peripheral nerve repair tools, especially for bridging short nerve defects or when traditional nerve autografts cannot be employed. This technique has been investigated both experimentally and clinically and, in this article, an overview of the literature on skeletal muscle grafts for bridging peripheral nerve defects is presented.

Animals↗
PubMed2004

The multifunctional role of IGF-1 in peripheral nerve regeneration.

The elements of peripheral nerve regeneration comprise a complex combination of nerve growth, muscle satellite cells proliferation and differentiation and vessel growth. There is also increasing evidence that growth factors may act at multiple levels in the regenerative response. One such factor affecting multiple cell processes is insulin-like growth factor (IGF-1). As a neurotrophic factor IGF-1 is known to promote nerve elongation and branching. As a myogenic factor, IGF-1 promotes satellite cell proliferation, differentiation and muscle hypertrophy. As an angiogenic factor, IGF-1 is known to promote angiogenesis in regenerating skeletal muscle by activating VEGF and VEGF receptors. Additionally, recent studies show that IGF-1 may also promote the activation of muscle stem cells during the regenerative process. This review will outline the pathways by which IGF-1 affects multiple layers of the regenerative response and how these pathways converge to promote the regeneration of nerves.

Animals↗
PubMed1991

[Therapeutic effect of hyperbaric oxygen on recovery of surgically repaired peripheral nerve injury].

114 patients with peripheral nerve injury were treated microsurgically. 54 patients with 65 nerve injuries were given hyperbaric oxygen as supplementary treatment. The excellent and good results of the 65 nerves accounted for 89.2%, but of those nerves in patients not treated with hyperbaric oxygen for 73.2% (P less than 0.05). The result was better in the hyperbaric oxygen group regardless of the repairing method used, particularly in those nerve grafting had been done (24.9, P less than 0.05). As for the time lapsed from injury to surgery. The results of fresh injuries showed no difference in either group, but hyperbaric oxygen was of much benefit to the old cases: the longer the delay the greater in difference between different groups, but better results were obtained in the hyperbaric oxygen group. The early the operation the better the result in either group.

Adolescent↗
PubMed1997

Advances in peripheral nerve repair.

The basic tenets of peripheral nerve repair as outlined in the introduction remain valid. Advances in the field of peripheral nerve repair have become focused on enhancement of the rate, completeness, and accuracy of neural regeneration on a cellular and molecular level. It is hoped that, within the next decade, techniques that have shown promise experimentally will become mainstays of treatment.

Gap Junctions↗
PubMed2002

Platelet-derived growth factor-b expression induced after rat peripheral nerve injuries.

Schwann cells are crucially important for peripheral nerve regeneration. These cells synthesize several factors that are supposed to enhance axonal regeneration when injured. Platelet-derived growth factor (PDGF) B-chain and its beta-receptor are expressed in Schwann cells in both normal peripheral nerves and culture. To elucidate the role of PDGF-B in peripheral nerve regeneration, we investigated its expression in cut or crush-injured rat sciatic nerves for up to 28 days. Northern blotting identified substantial increase of PDGF B-chain transcripts in injured nerves. Immunohistochemistry demonstrated that protein products of the transcripts were augmented at the distal tip of swollen axons in proximal nerve segments and in regenerating axons. Soon after both types of injury, considerable amounts of PDGF-B accumulated in numerous Schwann cells in distal segments of both models. With restoration of the axon-Schwann cell relationship in the crush model, levels of PDGF-B tended to decrease, eventually returning to normal. In the cut model in which the relationship cannot be restored, the PDGF-B was depleted to a very low level. The spatiotemporal correlation between PDGF-B and cell proliferation was very close throughout the study. These results differed strikingly from those of our previous study of rat optic nerve transection, in which PDGF-B was expressed only in a few recruited macrophages and glial cells. Augmented PDGF-B expression after sciatic nerve injury might contribute to peripheral nerve regeneration because PDGF-B is a mitogen and survival factor for Schwann cells and because it has trophic activity on neurons.

Animals↗
PubMed1995

Digital nerve conduction velocity for evaluation of peripheral nerve impairments in vibration syndrome.

In order to evaluate peripheral nerve impairments in vibration syndrome, sensory nerve conduction velocity (SCV) in the digital segment of the median nerve was measured by applying electrical stimulation to the wrist and recording from two pairs of electrodes attached to the middle finger. Fractionated SCVs were also measured in the palm-to-finger, wrist-to-palm, and elbow-to-wrist segments of the median nerve. Subjects were 65 patients with vibration syndrome and 48 healthy controls of similar age. SCVs in the digital nerve segment were significantly slower in the patients than in the controls. Significant slowing was also found in the wrist-to-palm segment. SCVs in the palm-to-finger and elbow-to-wrist segments did not differ between the two groups. Slowed SCVs were most frequently encountered in the digital segment (38% of the patients). The slowing in the wrist-to-palm segment was found in 20% of the patients. Present findings indicate that the digital segment is most frequently affected in vibration-induced neuropathy, and measurement of SCVs in the digital segment would serve to evaluate the peripheral neuropathy in vibration syndrome.

Case-Control Studies↗
PubMed1994

[Regeneration of peripheral nerves after interposition of acellular muscle into larger defects].

Peripheral nerve grafting is an established procedure in reconstructive surgery. Nerve grafts, however, are only available to a limited extent and patients are faced with neurologic deficits at the donor areas. Pretreated skeletal muscle has been proposed as an alternative grafting material. In nine adult Sprague-Dawley rats, a 2 cm gap of the sciatic nerve is grafted with a M. gracilis segment which has been pretreated through repeated freezing and thawing. Regeneration is evaluated after six weeks postoperatively. The results are compared to nine conventional nerve grafts. Regeneration was evident in all grafts. Histologically, the muscle grafts revealed a high proportion of connective tissue, a good vascularisation but an inferior degree of myelinisation. Morphometrically, the muscle grafts proved to be inferior according to axon counts and myelinisation. Muscle grafts provide a substrate comparable to peripheral nerves regarding the tubular architecture based on laminin. There are however no viable Schwann cells within these substitutes, which makes them inferior compared to conventional nerve grafts for peripheral nerve repair. These results are discussed with respect to further experiments concerning allogeneic nerve grafting and peripheral nerve preservation.

Animals↗
PubMed2001

Magnetic resonance neurography: magnetic resonance imaging of peripheral nerves.

With advances in modern MR imaging, direct MR visualization of many peripheral nerves is now possible. MR nerve imaging can detect and delineate the extent of neural tumors, demonstrate nerve continuity in cases of traumatic injury, and demonstrate abnormal enlargement and abnormal signal in diseased peripheral nerves. This ability to image peripheral nerves has the potential to dramatically change the diagnosis and treatment of peripheral nerve disease. This article describes the techniques for peripheral nerve imaging and provides a brief overview of a broad spectrum of peripheral nerve abnormalities.

Humans↗