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PubMed2004

Transection of peripheral nerves, bridging strategies and effect evaluation.

Disruption of peripheral nerves due to trauma is a frequently occurring clinical problem. Gaps in the nerve are bridged by guiding the regenerating nerves along autologous grafts or artificial guides. This review gives an overview on the different methods of nerve repair techniques. Conventional suturing techniques are discussed as well as the use of e.g. biological, synthetic, non-degradable or degradable nerve guides. Functional assessment showed that repair of a gap with a bio-degradable guide is superior to that with autologous grafts. But still, long lasting changes were observed in the Sciatic Function Index (SFI), abnormal walking patterns, disturbed Electro Myo Graphic (EMG) patterns, next to shifts in the histochemical properties of the muscles and longlasting abnormalities in neuromuscular contacts. These phenomena are explained by an at-random reinnervation. When transecting the nerve at young ages, this did not lead to enhanced recovery. Rearing rats operated at adult age in an enriched environment, also had no beneficial effect. Future research should aim at developing longer guides, possibly lined with Schwann cells, or additives, improving specific reinnervation of the former target areas.

Absorbable Implants↗
PubMed1975

[The technic of "sensorimotor" differentiated fascicular suture of peripheral nerves].

A method for the differentiation of motor and sensory nerve fibres of mixed peripheral nerves is presented. This method is based on the different content of acetylcholinesterase in motor and sensory nerve axons. The median and ulnar nerves of 13 human cadavers were biopsied at the wrist within three hours post mortem. All specimens were stained after the method of KARNOVSKY. The axons of the motor nerve fibres with their high content of acetylcholinesterase thus were marked. In all the examined ulnar nerves the motor fibres were found in the ulnar part. They were different in size and figure. In the median nerves only 1 to 3 motor fascicles were found, which are localized in the palmar and radial section of the nerve. These motor fibres represent only a little part of the whole cross section of the median nerve. As a consequence of this method of differentiation between motor and sensory fibres the surgery of peripheral mixed nerves may be influenced.

Acetylcholinesterase↗
PubMed1984

Malignant peripheral nerve sheath tumors in childhood.

Malignant peripheral nerve sheath tumor (MPNST) is an uncommon sarcoma in the pediatric population; however, its presence should be considered in a child with an enlarging or painful soft-tissue mass. Diagnosis of this neoplasm depends on either the demonstration of its origin within a peripheral nerve or the association with a contiguous neurofibroma. We have identified 16 cases of MPNST involving children 16 years of age or less, which represent 12.8% of the total cases seen at the Mayo Clinic. Most of the lesions arose in children with von Recklinghausen's disease and were associated with a contiguous neurofibromatous component. The mean survival of patients who were known to have died of tumor was only 1.8 years. This sarcoma requires prompt aggressive therapy utilizing wide surgical excision. Because of the association of MPNST with von Recklinghausen's neurofibromatosis, a careful workup and family history should be obtained for the potential prognostic value and for the purpose of genetic counseling.

Adolescent↗
PubMed1999

In vivo predegeneration of peripheral nerves: an effective technique to obtain activated Schwann cells for nerve conduits.

In vivo predegeneration of peripheral nerves is presented as a convenient and effective method to obtain activated Schwann cells and an enhanced cell yield following in vitro cultivation. The experiments conducted in rats were aimed at clinical use in gaining Schwann cell suspensions for filling artificial conduits in order to bridge peripheral nerve gaps. The rat sciatic nerve used as a model was transected distally to the spinal ganglia. Predegeneration in vivo was allowed to take place for 1, 2, 3 and 4 days and up to 1, 2 and 3 weeks. The nerve was then resected and prepared for cell cultivation. Schwann cells cultivated from the contralateral untreated nerve served as control. Immunostaining for S100, nerve growth factor receptor and the adhesion molecules N-cadherin and L1 was used to characterize the general state of the cultures. Viability was assessed by fluorescein fluorescence staining, and the proliferation index was determined by bromodeoxyuridine-DNA incorporation. The Schwann cells from predegenerated nerves revealed an increased proliferation rate compared to the control, whereas fibroblast contamination was decreased. Best results were obtained 1 week after predegeneration.

Animals↗
PubMed1983

Tracing of sensory neurones and spinal motoneurones of the pigeon by injection of fluorescent dyes into peripheral nerves.

The projection of peripheral sensory and motor nerves was investigated in the pigeon (Columba livia) by means of retrogradely transported fluorescent dyes. Two combinations of fluorescent tracers were used that could be identified within the same cell when excited by light of 405 nm: 1) Propidium iodide and Bisbenzimide, which label the cytoplasm orange and the nucleus blue, respectively; 2) Fast Blue, which labels the cytoplasm blue, and Nuclear Yellow, which labels the nucleus (especially the nucleolar ring) yellow. The presence of the tracers in a given cell was confirmed microspectrophotometrically. Following injection of the tracers into peripheral nerves, labelled sensory neurones were seen in the dorsal root ganglia and motoneurones of the spinal cord. The peroneal and tibial nerves projected to L2-L5 and L2-L7, respectively, whereas the median and ulnar nerves projected to C12-Th2 and C13-Th1. Double-labelled sensory neurones were observed when both peroneal and tibial, or median and ulnar nerves were injected with different tracers. This indicates that some sensory neurones possess peripheral processes that dichotomize to pass down two different peripheral nerves. Double labelling was never seen in motoneurones, or in sensory neurones after tracer injection into the sciatic and femoral nerves.

Animals↗
PubMed1988

Evaluation of acellular and cellular nerve grafts in repair of rat peripheral nerve.

Nerve grafts composed of basal lamina scaffolds and lacking viable Schwann cells have recently been shown to be effective in supporting axonal regeneration. As only short grafts were used in those studies, the present investigation was conducted to evaluate the ability of long acellular basal lamina nerve grafts and equivalent cellular grafts to support axonal regeneration for nerve gap repair. Cellular grafts consisted of nerve segments that had degenerated in situ for 4 weeks. Acellular grafting material consisted of similar segments that were repeatedly frozen and thawed to kill all cells prior to grafting. The results show that host axons can regenerate through the entire 4-cm length of cellular grafts but not through acellular basal lamina grafts. However, in the acellular grafts numerous axons were seen in the proximal 2-cm region. It is concluded that basal lamina grafts possess limited ability to support axonal regeneration. As in cellular grafts, viable Schwann cells appear to be important for regeneration to occur over longer distances.

Animals↗
PubMed1988

[Stimulating effect of isolated nerve segments on the regeneration of peripheral nerves].

The present paper concerns observations in two series of experiments in which the effect of isolated nerve segments on nerve regeneration was studied. Bridging of a nerve defect with a tube was used as an experimental model--a model often used in studies on nerve regeneration today. In the first series of experiments performed on rats, 14 mm of the femoral nerve were removed and the gap bridged with the femoral vein. A 2-mm nerve segment was inserted at the center of the vein in one group of the animals. In the second experimental series performed on rabbits, 40-45 mm of the peroneal nerve was resected. Up to three segments were introduced into the lumen of the bridging vein. The experiments demonstrated the promoting effect of nerve segments on nerve regeneration and indicated the probable mode of their action: the nerve segments serve as an additional source of Schwann cells and of neurofibroblasts, contributing substantially to the formation of the guiding structures for the axons. The nerve segments are apparently able to develop a similar nerve structure to that formed by the distal nerve stump. However, this ability also appears to be limited to a distance of 10 mm as is the case with distal nerve stumps. These conclusions do not exclude a possible neurotropic action of the nerve segments.

Animals↗
PubMed2000

Upregulation and interaction of TNFalpha and gelatinases A and B in painful peripheral nerve injury.

Chronic constriction injury (CCI) to peripheral nerve causes a painful neuropathy in association with a process of axonal degeneration and endoneural remodeling that involves macrophage recruitment and local increase in extracellular proteases and tumor necrosis factor alpha (TNF-alpha). Cell surface activation of TNF-alpha from its transmembrane precursor, as well as sequestration of TNF-alpha receptors II and I, is performed by the zinc-dependent endopeptidase family of matrix metalloproteinases (MMPs). Among TNF-alpha-converting MMPs, basal lamina degrading gelatinases are thought to play a role in sciatic nerve injury. In the present study, we determined the forms of TNF-alpha involved in the development of CCI neuropathy in rats, using Western blot analysis, and the temporal correlation of TNF-alpha and TNFRI protein profiles with gelatinases activity at the site of peripheral nerve injury. We observed two peaks in TNF-alpha protein during the first week of CCI that correspond to previously reported peaks in painful behavior. We propose that the first peak at 6 h post-CCI is due to the local expression of the cytotoxic transmembrane 26 kDa TNF-alpha protein released by resident Schwann cells, mast cells and macrophages. This peak in TNF-alpha protein expression corresponds to an increase in gelatinase B (MMP-9) activity, which is greatly upregulated as early as 3 h following CCI to rat sciatic nerve. The second peak occurs at 5 days post-CCI, and may represent TNF-alpha protein released by hematogenously recruited macrophages. This peak is marked by the increase in active soluble 17 kDa TNF-alpha and by gelatinase A (MMP-2) upregulation. These observations suggest that there is a pathogenic role for the TNF-alpha-converting function of MMP-2 in painful CCI neuropathy. We conclude that severe nerve injury induces MMPs, TNF-alpha and TNFRI, which interactively control the privileged endoneurial environment and the pathogenesis of the painful neuropathies associated with the macrophage-dependent processes of Wallerian degeneration.

Animals↗
PubMed1961

The application of x-ray diffraction and electron microscopy to the study of human peripheral nerve obtained by biopsy.

Human peripheral nerves obtained by biopsy from patients suffering from neuromuscular disorders have been studied by x-ray diffraction and electron microscopy. Few abnormal diffraction patterns have yet been recorded and their significance is not yet established. Electron micrographs have revealed wide variations in the numbers of myelinated fibres included in the nerve trunks and have facilitated a detailed study of the Schwann cell-axon relationships in the large numbers of unmyelinated fibres always present. Some indications of demyelination have been encountered.

Axons↗
PubMed1985

Spinal ganglia and peripheral nerves from a patent with Tay-Sachs disease. Morphological and ganglioside studies.

We examined the spinal ganglia and peripheral nerves from a patient with Tay-Sachs disease, comparing the other nervous tissues morphologically and lipid-biochemically. The spinal ganglia and peripheral nerves showed numerous membranous cytoplasmic inclusion bodies (MCBs), which are characteristic of GM2-ganglioside storage in the neuronal cell bodies of the patient brains. In spinal ganglia, all neurons and satellite cells around the neurons contained membrane-bound lipid materials. In peripheral nerves, Schwann cells and myelinated axons except for enlarged axons were devoid of MCBs. Major ganglioside stored in both spinal ganglia and peripheral nerve was also GM2-ganglioside. The contents of ganglioside in the spinal ganglia and peripheral nerves were 50 and 10 times more than those from normal tissues, respectively. The spinal cord contained a slightly higher amount of gangliosides than the normal control. The cerebral white matter totally demyelinated in this patient accumulated a much higher amount of gangliosides than the cerebral gray matter. The retinal tissue showed GM2-ganglioside as the major one also.

Cerebral Cortex↗
PubMed1983

A scanning electron microscopy evaluation of peripheral nerve regeneration.

Regeneration of a transected peripheral nerve following repair is often impeded by scar formation and misdirection of axon sprouts. This paper describes the use of the scanning electron microscope (SEM) in conjunction with other physiologic tests to evaluate nerve regeneration. A central one centimeter segment was removed from the peroneal branch of both sciatic nerves in 37 white New Zealand rabbits. Sectioned nerves were divided into four experimental groups according to type of repair performed: (A) no repair; (B) mobilization and direct epineural repair; (C) interpositional nerve graft repair; (D) polyglycolic acid (PGA) conduit repair. Each animal was reexplored eight months later and nerves examined by electrophysiologic testing and scanning electron microscopy. Unrepaired nerves viewed by SEM showed impaired axonal regeneration and loss of fascicular morphology with increased scar tissue. Nerve sections of direct epineural and interpositional graft repairs showed the best return of axonal morphology. Nerves regenerated across a one centimeter gap through a PGA conduit demonstrated regrowth of small and large myelinated axons grouped into "mini-fascicles" with increased connective tissue. PGA conduit repairs were electrically inferior to graft and direct repairs as measured by conduction velocity and the amplitude of evoked response. These findings correlated well with anatomy seen on scanning electron micrographs. The scanning electron microscope proved an excellent adjunctive tool for the study of peripheral nerve regeneration.

Animals↗
PubMed1992

Adult Retinofugal Axons Regenerating Through Peripheral Nerve Grafts Can Restore the Light-induced Pupilloconstriction Reflex.

To investigate the ability of mature regenerating retinal axons to form functional connections within central targets, severed axons were guided into the primary visual centres which subserve the pupillary constriction reflex in response to light. The ocular stump of the transected optic nerve of adult rats was connected by means of an autologous peripheral nerve graft with the pretectal region which contains the relay nucleus of pupillary constriction, the olivary pretectal nucleus. This nucleus is efferently connected with preganglionic neurons in the oculomotor nuclear complex which innervates parasympathetically the muscle constrictors of the iris. Six to sixteen weeks after optic nerve transection and peripheral nerve transplantation, brisk responses were observed in the pupils upon illumination of the transplanted eye. Recovery of the pupil responses indicated that retinal neurons used the peripheral nerve 'bridge' to access the pretectum, in which they established synaptic contacts in sufficient density and with appropriate specificity to reconstitute the function of the traumatically interrupted neuronal circuitry.

Journal Article↗
PubMedDate not supplied

[The validation of the microsurgical plastic repair of damaged peripheral nerves by using allografts (experimental and clinical research)].

Experimental study of allostatic grafts of peripheral nerves showed that the regeneration of the nerve fibres occurs in a regulated manner with good vascularization. Clinical approbation of allografts in 90 patients in injury to the peripheral nerves with a large diastasis (more than 4 cm) revealed good regeneration of the nerve fibres with subsequent improvement of the function of the extremity. The method of alloplasty is indicated in large defects in injured peripheral nerves which make the performance of neurorrhaphy impossible.

Adolescent↗
PubMed2006

Spinal prostaglandin E receptors of the EP2 subtype and the glycine receptor alpha3 subunit, which mediate central inflammatory hyperalgesia, do not contribute to pain after peripheral nerve injury or formalin injection.

Inflammation, peripheral nerve injury and chemical irritants can cause central sensitization in pain pathways. Prostaglandins produced in the CNS induce central sensitization during inflammation mainly by relieving nociceptive neurons from glycinergic inhibition. We have recently identified spinal prostaglandin E receptors of the EP2 subtype (EP2 receptors) and the glycine receptor alpha3 subunit (GlyR alpha3) as signal transduction elements involved in the generation of central inflammatory hyperalgesia. It is however still unknown to what extent inhibition of glycine receptors by PGE2 contributes to neuropathic or chemically induced pain. To address this question, we have analyzed mice deficient in the EP2 receptor (EP2-/- mice) or in the GlyR alpha3 subunit (GlyR alpha3-/- mice) using the chronic constriction injury (CCI) model of neuropathic pain and the formalin test. We found that EP2-/- mice and GlyR alpha3-/- mice develop thermal and mechanical hyperalgesia in the CCI model indistinguishable from that seen in wild-type mice. In the formalin test, EP2-/- mice, but not GlyR alpha3-/- mice, exhibited reduced nocifensive behavior. The lack of a phenotype in GlyR alpha3-/- mice together with the absence of a facilitating effect of intrathecal PGE2 on formalin-induced nociception in wild-type mice suggests that peripheral rather than spinal EP2 receptors are involved. These results indicate that inhibition of glycinergic neurotransmission by EP2 receptor activation does not contribute to pain following peripheral nerve injury or chemical irritation with formalin. Our results thus provide further evidence that inflammatory hyperalgesia and neuropathic pain involve different mechanisms of central sensitization.

Animals↗
PubMed1993

Long-term effects of cografts of pretransected peripheral nerve with adrenal medulla in animal models of Parkinson's disease.

Trophic factor supplementation has been reported to enhance the survivability of grafted adrenal chromaffin cells. Because the content of nerve growth factor in the distal stump of a pretransected peripheral nerve increases markedly 1 day after transection, we injected cografts of adrenal medulla with pretransected peripheral nerve into the striata of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated mice and performed follow-up histological and neurochemical analyses over a 12-month period. Adrenal medullary chromaffin cells cografted with pretransected peripheral nerve survived better than in adrenal grafts alone at 1, 3, and 12 months after transplantation. Host dopaminergic fiber recovery adjacent to the grafts was more prominent in mice with cografts than in mice with adrenal grafts alone at 1 and 3 months after transplantation. Twelve months after transplantation, however, there was no significant difference between the two groups of animals because of the natural recovery of intrinsic dopaminergic fibers from MPTP toxicity. Dopamine concentration in the striata of cografted mice was higher than in mice with adrenal grafts alone at 1 month after transplantation. At 3 and 12 months after transplantation, the natural recovery of dopamine concentration from MPTP toxicity was apparent in both groups of animals and no significant difference was observed between the groups. We conclude that adrenal medullary chromaffin cells can survive for at least 12 months after grafting when cografted with pretransected peripheral nerve. Cografts enhanced the recovery of the host nigrostriatal dopaminergic system up to 3 months after transplantation, but this enhancement was not apparent at 12 months because of the natural recovery of dopaminergic fibers from MPTP toxicity.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗