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PubMed2003

[A degradable artificial nerve guide to bridge peripheral nerve defects].

The standard technique for bridging a peripheral nerve defect is an autologous nerve graft if the nerve ends cannot be sutured. Recent evidence indicates that an alternative procedure-application of a degradable nerve guide-may be feasible. Currently the use of such a degradable nerve guide for the recovery of peripheral nerve defects in the hand is being tested in a multicenter trial. Conventional suturing as well as autologous nerve grafting are accepted methods in the control group within the protocol of the multicenter study. In the first two patients to receive the implant, a 28-year-old man and a 50-year-old women with tendon and nerve injury due to glass cuts, the operation was technically successful. Functional nerve recovery will be assessed in due course.

Absorbable Implants↗
PubMed2002

Effect of nondepleting anti-CD4 monoclonal antibody (Rib 5/2) plus donor antigen pretreatment in peripheral nerve allotransplantation.

Peripheral nerve allotransplantation allows the reconstruction of injuries with long nerve gaps that are otherwise unsalvageable. In this study, the efficacy of anti-CD4 monoclonal antibody (mAb) combined with donor antigen pretreatment in prolonging the survival of short peripheral nerve allografts was investigated in a rodent model. Such an approach could potentially avoid the need for systemic immunosuppression and its concomitant morbidities. Buffalo rats received either nerve isografts or nerve allografts from Lewis rats. Untreated isograft and allograft groups were used as controls. Allograft recipients received either a single dose of RIB 5/2, a nondepleting anti-CD4 mAb, a single dose of Lewis splenocytes, or both antigen and RIB 5/2, 7 days prior to transplantation. Flow cytometric analysis verified that the T-lymphocyte population was maintained, while CD4 expression was downregulated by RIB 5/2. Histologic evaluation demonstrated better regeneration in the allograft recipients receiving both donor antigen and antibody, compared to recipients of untreated allografts or treatment with antigen or antibody alone.

Animals↗
PubMed1986

Alpha-melanocyte-stimulating hormone stimulates the outgrowth of myelinated nerve fibers after peripheral nerve crush.

The effect of alpha-melanocyte-stimulating hormone on peripheral nerve regeneration was studied by monitoring functional recovery and quantifying histologic changes that follow crush lesion of the rat sciatic nerve. The results showed that such treatment of rats with a crushed sciatic nerve resulted in a reduction of the recovery period and in an increase in the number of regenerating nerve fibers.

Animals↗
PubMed2006

Luminal fillers in nerve conduits for peripheral nerve repair.

The use of nerve conduits as an alternative for nerve grafting has a long experimental and clinical history. Luminal fillers, factors introduced into these nerve conduits, were later developed to enhance the nerve regeneration through conduits. Though many luminal fillers have been reported to improve nerve regeneration, their use has not been subjected to systematic review. This review categorizes the types of fillers used, the conduits associated with fillers, and the reported performance of luminal fillers in conduits to present a preference list for the most effective fillers to use over specific distances of nerve defect.

Biocompatible Materials↗
PubMed2006

Sodium channel expression in the ventral posterolateral nucleus of the thalamus after peripheral nerve injury.

Peripheral nerve injury is known to up-regulate the expression of rapidly-repriming Nav1.3 sodium channel within first-order dorsal root ganglion neurons and second-order dorsal horn nociceptive neurons, but it is not known if pain-processing neurons higher along the neuraxis also undergo changes in sodium channel expression. In this study, we hypothesized that after peripheral nerve injury, third-order neurons in the ventral posterolateral (VPL) nucleus of the thalamus undergo changes in expression of sodium channels. To test this hypothesis, adult male Sprague-Dawley rats underwent chronic constriction injury (CCI) of the sciatic nerve. Ten days after CCI, when allodynia and hyperalgesia were evident, in situ hybridization and immunocytochemical analysis revealed up-regulation of Nav1.3 mRNA, but no changes in expression of Nav1.1, Nav1.2, or Nav1.6 in VPL neurons, and unit recordings demonstrated increased background firing, which persisted after spinal cord transection, and evoked hyperresponsiveness to peripheral stimuli. These results demonstrate that injury to the peripheral nervous system induces alterations in sodium channel expression within higher-order VPL neurons, and suggest that misexpression of the Nav1.3 sodium channel increases the excitability of VPL neurons injury, contributing to neuropathic pain.

Animals↗
PubMed1990

Inclusion body myositis: peripheral nerve involvement. Combined morphological and electrophysiological studies on peripheral nerves.

The occurrence of neuropathy in 5 cases of inclusion body myositis (IBM) was studied. The intramuscular nerve branches showed variable ultrastructural changes in all cases. The observed changes were loss of axons, wallerian degeneration and axon terminal atrophy. EMG with concentric needles showed myopathic motor unit potentials in all cases. A reduced interference pattern due to loss of motor units was found in all cases. All but one patient showed fibrillation potentials in several muscle groups. Motor nerve conduction velocities and F-wave latencies were pathological in two of the cases, in which there were motor unit potentials with increased amplitude and duration as evidence of reinnervation. Sural nerve biopsy in one of these cases revealed slight neuropathy of the axonal type. These findings support the concept of peripheral nerve involvement in many cases of IBM.

Action Potentials↗
PubMed2002

[Protection effect of nerve implantation after peripheral nerve injury to rats].

OBJECTIVE: To investigate the protection effect of nerve implantation to the neurons after sciatic nerve injury to adult rats. METHODS: Thirty male Sprague-Dawley rats weighing 180 - 220 g (8 - 9 weeks of age) were randomly divided into four groups. Group A consisted of normal rats without operation. In group B, the sciatic nerve of rats was transected, with the proximal stump of the sciatic nerve ligated to inhibit nerve regeneration. In group C, a sciatic nerve crushed model was set up. In group D, a sciatic nerve implantation model was established. The rats were sacrificed on postoperative days 7, 14 and 28 respectively. The L(4)-L(6) segments of the spinal cord were harvested. TUNEL technique was used to detect apoptotic motor neurons. HE and Toluidine Blue staining was used for counting motor neurons. RESULTS: The apoptotic neurons detected on the 28th postoperative day were significantly fewer in the implantation group than in the other groups (P < 0.05). The number of motor neurons was significantly higher in the implantation group than in other two control groups (P < 0.05). CONCLUSIONS: Nerve implantation exerts protective effect on neurons after nerve injury.

Animals↗
PubMed1990

[Dynamic changes in abnormal afferent activities following peripheral nerve injury].

Peripheral nerve injury by chronic compression caused a decrease in conductive velocity or a delay in the transmission of the action potential, later blocking it completely following demyelination of the damaged nerve region. Abnormal firing activities were recorded from the injured peripheral nerve fibers after the 6-7th postoperative day. There were different patterns of abnormal firing from fibers. Regular tonic ectopic firings with high frequency were always recorded from A beta fibers. A delta/C fibers, however, had burst or irregular spikes. A single antidromic shock to the damaged region sometimes induced ectopic spikes following the expected one. The demyelinated region of the damaged nerve was very sensitive to both tetraethylammonium, a K+ channel blocker, and noradrenaline. The authors suggest that new ion channels or receptors, absent in normal, form in the damaged region.

Action Potentials↗
PubMed1993

Drainage of molecules from subarachnoid space to spinal nerve roots and peripheral nerve of the rat. A study based on Evans blue-albumin and lanthanum as tracers.

The purpose of the present investigation was to find out if a compound injected into the spinal subarachnoid space, after having entered ventral and dorsal nerve roots, can be traced to the epineurial-perineurial sheaths and the endoneurium of peripheral nerves. This would indicate a centrifugal movement of substances from the cerebrospinal fluid along nerves; one route of drainage of cerebrospinal fluid which in the past has been widely discussed. In vivo studies were made using Evans blue-albumin and lanthanum chloride as tracers. Evans blue-albumin is macromolecular in size and emits a red fluorescence after exposure to ultraviolet light. Lanthanum ions are small and easily visible in the electron microscope. The tracers were injected into the cervical subarachnoid space and 15 min to 24 h later samples from roots, dorsal root ganglia, proximal part of spinal nerves and the median nerves were taken and further processed for detection of tracers. Fluorescence microscopy from samples removed 15 min and 24 h after the injection of Evans blue-albumin showed a red fluorescence of low intensity in the endoneurium of nerve roots, ganglia and proximal spinal nerve. After 24 h also the median nerve elicited some fluorescence. The sheaths around these structures were also fluorescent. Lanthanum was detected between cell layers of the nerve root sheath as well as inside the nerve root parenchyma. In about 50% of the samples from dorsal root ganglia extracellular lanthanum was found in the capsule. The tracer was also found in the epineurium of 50% of the spinal nerves and occasionally in the perineurium.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1998

NT-3 modulates NPY expression in primary sensory neurons following peripheral nerve injury.

Peripheral nerve transection induces significant changes in neuropeptide expression and content in injured primary sensory neurons, possibly due to loss of target derived neurotrophic support. This study shows that neurotrophin-3 (NT-3) delivery to the injured nerve influences neuropeptide Y (NPY) expression within dorsal root ganglia (DRG) neurons. NT-3 was delivered by grafting impregnated fibronectin (500 ng/ml; NT group) in the axotomised sciatic nerve. Animals grafted with plain fibronectin mats (FN) or nerve grafts (NG) were used as controls. L4 and L5 DRG from operated and contralateral sides were harvested between 5 and 240 d. Using immunohistochemistry and computerised image analysis the percentage, diameter and optical density of neurons expressing calcitonin gene-related peptide (CGRP), substance P (SP), vasoactive intestinal peptide (VIP) and NPY were quantified. Sciatic nerve axotomy resulted in significant reduction in expression of CGRP and SP, and significant upregulation of VIP and NPY (P < 0.05 for ipsilateral vs contralateral DRG). By d 30, exogenous NT-3 and nerve graft attenuated the upregulation of NPY (P < 0.05 for NT and NG vs FN). However, NT-3 administration did not influence the expression of CGRP, SP or VIP. The mean cell diameter of NPY immunoreactive neurons was significantly smaller in the NT-3 group (P < 0.05 for NT vs FN and NG) suggesting a differential influence of NT-3 on larger neurons. The optical densities of NPY immunoreactive neurons of equal size were the same in each group at any time point, indicating that the neurons responding to NT-3 downregulate NPY expression to levels not detectable by immunohistochemistry. These results demonstrate that targeted administration of NT-3 regulates the phenotype of a NPY-immunoreactive neuronal subpopulation in the dorsal root ganglia, a further evidence of the trophic role of neurotrophins on primary sensory neurons.

Analysis of Variance↗
PubMed1994

Immunogenicity and regenerative potential of acellular nerve allografts to repair peripheral nerve in rats and rabbits.

This study describes the ability of acellular nerve allografts (genetically different) to repair injured peripheral nerve in rats and rabbits. We recently reported the regeneration supporting potential and immunogenicity of acellular nerve allografts in rats. The present study extends our previous work and quantitates the extent of axonal regeneration through various nerve grafts in rats. In addition, the use of longer nerve grafts to repair rabbit peripheral nerve is described. Inbred strains of Fischer and Buffalo rats and New Zealand white and Dutch rabbits were used. Acellular grafts were prepared by repeated freezing and thawing of in situ degenerated nerves. Non-frozen predegenerated nerves were used as cellular grafts for comparison. Nerve isografts (genetically identical) were also performed. The graft length was 2.0 cm in rats and 4.0 cm in rabbits. In both rats and rabbits the cellular isografts showed the most rapid regeneration and target muscle innervation. The cellular allografts were invariably rejected and only showed limited regeneration. In contrast, acellular allografts, in spite of their mild immunogenicity, allowed significant regeneration through them. It is concluded that acellular nerve allografts are capable of supporting axonal regeneration because of their reduced immunogenicity, and thus can be used to bridge nerve gaps after nerve injury.

Animals↗
PubMed1985

Morphometric effects of use and disuse on peripheral nerve.

Rat peripheral nerve was evaluated morphometrically following hemicordotomy, tenectomy, or both to assess the effects of disuse and hyperactivity on the peripheral nervous system. Hemicordotomy resulted in an increase in diameter of nerve fibers supplying both "fast" and "slow" skeletal muscles in hypoactive and hyperactive limbs. Nerve fiber atrophy occurred only in nerve to "fast" muscle following disuse induced by hemicordotomy and tenectomy. The possible role of "motor nerve growth factor" or altered axoplasmic flow in bringing about these morphologic changes in peripheral nerve is discussed.

Animals↗
PubMed2007

Ultrasound-guided peripheral nerve blockade.

Peripheral nerve blockade (PNB) for orthopedic surgery is usually performed without visual guidance, relying mainly on surface anatomic landmarks and electrical stimulation to localize nerves. Moreover, multiple trial and error attempts to place a needle can frustrate the operator, cause unwarranted pain to the patient, and waste valuable time in the operating room. Inaccurate needle placement and spread of local anesthetic account for most PNB failures, whereas "trial and error" needle manipulations for nerve localization can cause complications. The recent application of ultrasound (US) to PNB affords real-time imaging of the target nerve, needle, and surrounding vasculature, such that needle proximity to the nerve is ensured and vascular puncture avoided. This article reviews the advantages, principles, and techniques of US for the most common types of PNB.

Brachial Plexus↗
PubMed1996

Peripheral nerve regeneration.

Peripheral nerve regeneration comprises the formation of axonal sprouts, their outgrowth as regenerating axons and the reinnervation of original targets. This review focuses on the morphological features of axonal sprouts at the node of Ranvier and their subsequent outgrowth guided by Schwann cells or by Schwann cell basal laminae. Adhesion molecules such as N-CAM, L1 and N-cadherin are involved in the axon-to-axon and axon-to-Schwann cell attachment, and it is suggested that integrins such as alpha 1 beta 1 and alpha 6 beta 1 mediate the attachment between axons and Schwann cell basal laminae. The presence of synaptic vesicle-associated proteins such as synaptophysin, synaptotagmin and synapsin I in the growth cones of regenerating axons indicates the possibility that exocytotic fusion of vesicles with the surface axolemma supplies the membranous components for the extension of regenerating axons. Almost all the subtypes of protein kinase C have been localized in growth cones both in vivo and in vitro. Protein kinase C and GAP-43 are implicated to be involved in at least some part of the adhesion of growth cones to the substrate and their growth activity. The significance of tyrosine kinase in growth cones is emphasized. Tyrosine kinase plays an important role in intracellular signal transduction of the growth of regenerating axons mediated by both nerve trophic factors and adhesion molecules. Growth factors such as NGF, BDNF, CNTF and bFGF are also discussed mainly in terms of the influence of Schwann cells on regenerating axons.

Animals↗