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PubMedDate not supplied

[The effect of cytokines on regeneration results of compressed nerve roots and transsected peripheral nerves].

The possible beneficial effect of Interleukin-1 (IL-1) on nerve regeneration was studied using clinical, neurophysiological and histomorphological methods. The sciatic nerves of Wistar rats were transsected and the severed ends abutted, sewn together and covered with fibrin adhesive. In a second group the lumbar-sacral nerve roots were exposed, IL-1 was injected and compression of the nerve roots was carried out. The region surrounding the lesion was infused with either saline (controls) or IL-1 (treatment group) in both groups. Compared to the controls, the treated animals showed a significant improvement of nerve regeneration as measured by clinical and neurophysiological parameters. After 3 months of observation, the total number of myelinated axons distal to the site of lesion was increased, while the fiber diameter distribution was unchanged. It is likely that cloned IL-1 will soon become available for human treatment. The present results indicate that it may be worthwhile to investigate its usefulness in the treatment of peripheral nerve injury in primates and humans.

Animals↗
PubMed1992

Laminin B1 and collagen type IV gene expression in transected peripheral nerve: reinnervation compared to denervation.

The expression of B1 laminin and type IV collagen was followed in the microsurgically isolated endoneurium of transected rat sciatic nerves from 3 days until 8 weeks. Northern hybridizations revealed that after nerve transection the proximal stumps of denervated, as well as freely regenerating, nerves showed a markedly increased expression of laminin and type IV collagen which lasted from 3 days up to 8 weeks. In the distal stumps, close to the site of transection (2-7 mm), the expression of laminin, and to a certain extent that of type IV collagen, seemed to be enhanced if free axonal reinnervation was allowed. Further distally (10-15 mm), the patterns of B1 laminin and type IV collagen expression were similar in both experimental groups, so that an increased expression was noticed during the first 2 weeks. The present results suggest that laminin and type IV collagen gene expression is markedly different in different parts of transected rat sciatic nerve. During peripheral nerve regeneration, there is a long-lasting basement membrane gene expression in the proximal stump. In the distal part of the transected nerve, the axonal reinnervation possibly up-regulates, but is not essential for, the expression of B1 laminin and type IV collagen.

Animals↗
PubMed1980

Radiation-induced malignant and atypical peripheral nerve sheath tumors.

The reported peripheral nerve complications of therapeutic irradiation in humans include brachial and lumbar plexus fibrosis and cranial and peripheral nerve atrophy. We have encountered 9 patients with malignant (7) and atypical (2) peripheral nerve tumors occurring in an irradiated site suggesting that such tumors represent another delayed effect of radiation treatment on peripheral nerve. The neoplasms appeared 4 to 41 years following radio-therapy, at a time when the patients (6 females and 3 males) were 16 to 70 years old and cured of their original tumors. Eight patients had received irradiation to treat malignant disease; the ninth had a benign condition. The sites of peripheral nerve tumor were the brachial plexus in 5, cervical plexus in 1, lumbar plexus in 2, and retroperitoneum in 1. Eight patients presented with painful masses, and in 6 of the 8 there was a progressive neurological deficit. Seven patients died with metastases within two years of diagnosis. In all instances the radio-therapy was within an acceptable radiation dosage, yet 3 patients developed local radiation-induced skin and bony abnormalities. In 3 patients there were either clinical signs or a family history of von Recklinghausen disease, but the malignant peripheral nerve sheath tumors developed only in the radiation port. Animal studies support the clinical observation that malignant peripheral nerve sheath tumors can occur as a delayed effect of irradiation. Other etiological mechanisms, including an increased risk of second primaries in cancer patients and a genetic predisposition to peripheral nerve tumors, may also play a role.

Adolescent↗
PubMed1991

Nerve growth factor promotes CNS cholinergic axonal regeneration into acellular peripheral nerve grafts.

Peripheral nerve grafts promote vigorous regeneration of adult mammalian CNS axons. Elimination of nerve-associated cells by freeze-thawing abolishes this promoting quality, possibly by creating inhibitory cellular debris and/or destroying the production of stimulatory factors by living Schwann or other cells. Here, debris-free acellular peripheral nerve segments placed between the disconnected septum and the hippocampal formation acquired almost no cholinergic axons after 1 month. However, such acellular nerve grafts treated before implantation with purified beta-nerve growth factor (NGF) contained nearly as many longitudinally oriented cholinergic axons as did fresh cellular nerve grafts. These results suggest that (i) NGF is required for the regeneration of adult CNS cholinergic axons into nerve grafts and (ii) an important function of living cells within peripheral nerve may be the production of neuronotrophic factors such as NGF.

Acetylcholinesterase↗
PubMed1992

Syngeneic Schwann cells derived from adult nerves seeded in semipermeable guidance channels enhance peripheral nerve regeneration.

At present, clinical strategies to repair injured peripheral nerve concentrate on efforts to attain primary suture of the cut nerve ends. If this is not possible, autografts are used to unite the separated nerve segments. Both strategies are based on the recognition that the Schwann cells resident in the peripheral nerve trunk play a crucial role in the regenerative process. Neither strategy may be feasible, however, in extensive or multiple injuries because the amount of autograft material is limited, and allografts are subject to immune rejection. Artificially produced nerve bridges constructed of autologous Schwann cells seeded in guidance channels could be used to overcome these limitations. In the present experiments, the potential of Schwann cells derived from adult nerves and seeded in permselective guidance channels to promote neurite regeneration across an 8 mm nerve gap was evaluated in transected rat sciatic nerves. Immunological sequalae were evaluated by comparing Schwann cells from syngeneic and heterologous rat strains. Schwann cells from either adult outbred (Sprague-Dawley, CD) rats or inbred (Fisher, F) rats were suspended in a Matrigel solution at a density of 80 x 10(6) cells/ml (CD) or 40, 80, or 120 x 10(6) cells/ml (F-40, F-80, and F-120 channels, respectively). Channels containing Schwann cells were compared to sciatic nerve autografts, empty channels, or channels filled with Matrigel alone. One day after seeding permselective synthetic guidance channels with a Schwann cell suspension, a central cable of Schwann cells oriented along the axis of the tube was formed due to syneresis of the hydrogel. By 3 weeks postimplantation, regenerating axons had grown into all channels and autografts. Sciatic nerve autografts supported extensive regeneration, containing 4-5 x 10(4) myelinated axons at the graft midpoint. The ability of channels containing syngeneic Schwann cells to foster regeneration was dependent on the Schwann cell seeding density. At the channel's midpoint, the myelinated axon population in F-120 tubes was intermediate between that in sciatic nerve autografts and F-80 channels, and was significantly higher than in F-40 or control channels. The nerve cable in Schwann cell-containing tubes consisted of larger, more organotypic fascicles than acellular control channels. In contrast, heterologous (CD) Schwann cells elicited a strong immune reaction that impeded nerve regeneration. The present study shows that cultured adult syngeneic Schwann cells seeded in permselective synthetic guidance channels support extensive peripheral nerve regeneration.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1999

End-to-side nerve suture--a technique to repair peripheral nerve injury.

End-to-side nerve suture (ETSNS) has until recently been extensively researched in the laboratory animal (rat and baboon). Lateral sprouting from an intact nerve into an attached nerve does occur, and functional recovery (sensory and motor) has been demonstrated. We have demonstrated conclusively that ETSNS in the human is a viable option in treating peripheral nerve injuries, including injuries to the brachial plexus. Among the many advantages of this new technique are: (i) simple and short operation; (ii) shorter recovery time--suture is done closer to the target organs; (iii) nerve grafts to bridge injured gaps are eliminated, reducing the morbidity of nerve surgery to a minimum; (iv) innervation of paralysed muscles, for which there was previously thought to be no hope of recovery, opens up many new treatment options; and (v) certain aspects of nerve function and regeneration, unknown until recently, open new horizons and understanding. ETSNS has given us new dimensions in the management of peripheral nerve injuries.

Animals↗
PubMed1991

A simple method for reducing autotomy in rats after peripheral nerve lesions.

Experiments using peripheral nerve lesions (crush or transection) in rats to study repair processes are hampered by the tendency for the animals to attack the limb in which the peripheral nerves are damaged (autotomy). In this paper we describe a simple method which significantly reduces the incidence of autotomy after peripheral nerve lesions. The method consists of painting the hind paws of operated rats with a commercially available non-toxic lotion, which is used to discourage nail-biting and thumb-sucking in humans. Although the method is not absolute, it was extremely beneficial in our experiments, since the number of animals that had to be taken out of the experiment due to severe autotomy was greatly reduced. We believe that this method may prove to be as beneficial to other investigators who are using experimental peripheral nerve lesions to study the regenerative aspects of the nervous system.

Animals↗
PubMed1992

Response of the gustatory system to peripheral nerve injury.

Peripheral taste nerve damage occurs as a result of disease and surgery. The response depends on the taste field affected and the species. Nerve regeneration is robust after the nerve is crushed or after it is cut if the severed ends are anastomosed. Taste buds, which appear after nerve regeneration, may be derived from dormant stem cells outside of taste buds or from remnants of taste buds that persist following denervation. Sprouting by intact taste nerves into denervated fields apparently does not occur. Regenerated primary afferents have taste response specificity, but it is unknown if neural response types are retained peripherally or centrally. Recent behavioral studies show specific deficits following loss of restricted taste fields in rodents, but little is known about recovery after nerve regeneration. Specific deficits have not been demonstrated in humans, although taste sensitivity has been correlated with numbers of taste buds. Enigmas such as these may be solved once the response of the central nervous system to gustatory nerve injury is defined.

Animals↗
PubMed1999

Adenoviral vector-mediated expression of a foreign gene in peripheral nerve tissue bridges implanted in the injured peripheral and central nervous system.

Axons of the CNS do normally not regenerate after injury, in contrast to axons of the PNS. This is due to a different microenvironment at the site of the lesion as well as a particular intrinsic program of axonal regrowth. Although transplantation of peripheral nerve tissue bridges is perhaps the most successful approach to promoting regeneration in the CNS, ingrowth of CNS nerve fibers with such transplants is limited. Genetic modification of peripheral nerve bridges to overexpress outgrowth-promoting proteins should, in principle, improve the permissive properties of peripheral nerve transplants. The present study shows that pieces of peripheral intercostal nerve, subjected to ex vivo adenoviral vector-mediated gene transfer and implanted as nerve bridges in transected sciatic nerve, avulsed ventral root, hemi-sected spinal cord and intact brain, are capable of expressing a foreign gene. In vitro studies showed expression of the reporter gene LacZ up to 30 days in Schwann cells. After implantation, LacZ expression could be detected at 7 days postimplantation, but had virtually disappeared at 14 days. Schwann cells of the transduced nerve bridges retained the capacity of guiding regenerative peripheral and central nerve fiber ingrowth. Transduction of intercostal nerve pieces prior to implantation should, in principle, enable enhanced local production of neurotrophic factors within the transplant and has the potential to improve the regeneration of injured axons into the graft.

Adenoviridae↗
PubMed2004

Methylation analysis of the neurofibromatosis type 1 (NF1) promoter in peripheral nerve sheath tumours.

Peripheral nerve sheath tumours are hallmarks of neurofibromatosis type 1 (NF1). Development of plexiform neurofibromas to malignant peripheral nerve sheath tumours (MPNST) is common. The NF1 gene promoter harbours a hypomethylated CpG island. Thus, methylation changes may be involved in the development of different types of neurofibromas and malignant transformation. We investigated NF1-associated dermal (n=9) and plexiform neurofibromas (n=7), MPNST (n=5) and non-NF1 leucocyte samples (n=20) for their methylation pattern by bisulphite genomic sequencing. We could not find global hypermethylation in the NF1 promoter in our series. Nevertheless, site-specific methylation, involving transcription factor binding sites for SP1, CRE (-10), and AP-2, was observed. One region of the 5'-UTR (untranslated region) overlapping with a putative AP-2 binding site was methylated at 30-100% in 4/20 control samples. In conclusion, we did not find hypermethylation in NF1-associated tumours. Instead, low level methylation could parallel a global genomic hypomethylation in malignancy.

Antioxidants↗
PubMed1998

Neurotrophins, neurones and peripheral nerve regeneration.

Successful peripheral nerve regeneration requires optimal conditions both in the macro-environment and micro-environment. Many methods have been used to improve the macro-environment for the regenerating nerve. However, much less is known about the micro-environment, and in particular the complex neurochemical interactions involved. Several neurotrophic factors have been shown to play an essential trophic role in the development, maintenance and regulation of neuronal function. These include nerve growth factor (NGF) and several recently identified members of the NGF family, namely brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), neurotrophin-4/5 (NT-4/5) and neurotrophin-6 (NT-6). In this review we summarize recent studies of the effects of these neurotrophins on neurones, especially their effects on motor neurones and their axonal outgrowth. We discuss prospects for the future and point out what remains to be understood about the role of neurotrophins to enhance peripheral nerve regeneration.

Animals↗
PubMed2005

Promoting neurological recovery following a traumatic peripheral nerve injury.

If a peripheral nerve is crushed, or if the nerve is cut and the ends sutured together soon after the lesion (anastomosed), neurological recovery is good. When a length of a peripheral nerve is destroyed, and anastomosis is not possible, the standard surgical repair technique is to graft a length/s of sensory nerve from the patient, into the gap. For gaps <2 cm neurological recovery is moderate, for gaps 2-4 cm recovery is generally poor, and for gaps >4 cm recovery is limited to non-existent. The limited recovery is because sensory nerves act as passive scaffolds for axon regeneration and do not actively promote axon regeneration. However, such grafts remain the "gold standard" for nerve repairs. New techniques are required that induce improved neurological recovery. This paper reviews current clinical and basic research techniques for inducing neurological recovery following traumatic peripheral nerve injuries.

Humans↗
PubMed1980

Clinical and experimental aspects of injection injuries of peripheral nerves.

Injury to peripheral nerves complicating deep intramuscular injections of antibiotic and other agents is well recognized and can result in significant permanent neurological deficit. The purpose of this paper is to review the subject of nerve injection injuries, and report on a series of recent experimental studies carried out in this laboratory designed to improve our understanding of the pathophysiology of this condition and help provide a rational basis for its treatment. A wide variety of chemotherapeutic, prophylactic, and local anaesthetic agents in common use were injected into the sciatic nerve of the adult Wistar rat. Both intrafascicular and extrafascicular injections were examined. Results revealed that the site of injection was the most crucial factor in determining the degree of nerve fiber injury. Following intrafascicular injection, the degree of injury varied significantly, depending upon the specific agent injected. The most severe injuries were associated with wide-spread axonal and myelin degeneration. Pathological alterations in the nerve were evident as early as 30 minutes following injection injury. Regeneration was a constant finding in nerve damage by injection of the various agents. The mechanism of injury appeared to be a direct toxic effect of the injected compound on neural tissue, with an associated break down of the blood-nerve barrier.

Anesthetics, Local↗
PubMed2000

Axotomized and intact muscle afferents but no skin afferents develop ongoing discharges of dorsal root ganglion origin after peripheral nerve lesion.

After peripheral nerve lesions, some axotomized afferent neurons develop ongoing discharges that originate in the dorsal root ganglion (DRG). We investigated in vivo which functional types of afferent neurons contributed to this ectopic activity. Six to twelve days after the gastrocnemius soleus (GS) nerve supplying skeletal muscle and the sural (SU) nerve supplying skin had been transected (experimental group E1), 20.4% of afferent neurons with myelinated axons projecting into the GS nerve produced ongoing discharges of irregular or bursting pattern. In contrast, all SU neurons were silent. Additional transection of peroneal and tibial nerves (group E2) induced ongoing activity in a similar percentage of GS neurons (22.1%), but their mean discharge frequency was higher (6.0 vs 2.7 Hz), and more of them exhibited bursting discharges (63 vs 17%). When the GS nerve had been left intact while tibial, peroneal, and SU nerve had been transected (group E3), 18.8% of unlesioned GS neurons developed ongoing discharges at a mean frequency of 6.1 Hz; most of them exhibited a bursting pattern. Without a preceding nerve lesion, almost no GS neuron (1.1%) fired spontaneously. Most afferent neurons with ongoing activity had an axonal conduction velocity of 5-30 m/sec indicating that some of these neurons may have had nociceptive function. These findings provide the first evidence that after peripheral nerve injury both axotomized as well as intact afferent neurons supplying skeletal muscle but not skin afferents generate ongoing activity within the DRG, probably because of a yet unknown signal in the DRG triggered by axotomy.

Animals↗
PubMed1969

Internal neurolysis in treatment of traumatic peripheral nerve lesions.

Many peripheral nerve injuries are of a contusing type with resultant intraneural scarring which causes neurologic deficit even though the nerve is still in continuity. Internal neurolysis can relieve pain and restore neurologic function in such lesions. It is important that such lesions be recognized early, fully evaluated and carefully followed so that surgical intervention can be carried out before permanent changes can develop in the denervated muscles, joints and skin. The procedure is frequently rewarded with prompt and gratifying results. The risk is minimal and the patient need spend only a short time in hospital.

Adult↗
PubMed2006

Effects of hyperbaric oxygen on peripheral nerves.

BACKGROUND: Injuries of peripheral nerves are common and usually are part of acute traumatic injuries to the limbs. Damage to peripheral nerves may be extensive. Microsurgery has improved the rate of recovery of these injuries, but some problems remain to be solved. The purpose of this investigation was to study the long-lasting effects of hyperbaric oxygenation on peripheral nerves after transection and repair with microsurgery in the rat sciatic nerve model. METHODS: Forty male Wistar rats were divided randomly into four groups: (1) no hyperbaric oxygen, sectioned and repaired (n = 10), euthanized at 7 weeks; (2) hyperbaric oxygen, sectioned and repaired (n = 10), euthanized at 7 weeks; (3) no hyperbaric oxygen, sectioned and repaired (n = 10), euthanized at 14 weeks; and (4) hyperbaric oxygen, sectioned and repaired (n = 10), euthanized at 14 weeks. Nerve recovery was assessed by neurophysiologic studies at 7 or 14 weeks. Foot-ankle angle response (dorsiflexion) and histopathology with automated morphometry were performed after 7 or 14 weeks. Statistical analysis was performed with the Friedman test and the Mann-Whitney U test. RESULTS: At 7 weeks, motor latency showed statistical significance in both groups, treated and not treated, whereas amplitude, axons, and blood vessel number was higher in the hyperbaric oxygen-treated group. After 14 weeks, electromyography showed no denervation and a better foot-ankle angle response in the hyperbaric oxygen groups. CONCLUSION: These results suggest that functional recovery in transected peripheral nerves may be improved and accelerated by hyperbaric oxygenation following microsurgical repair.

Animals↗
PubMed1995

Relation between functional deficit and intraneural local anesthetic during peripheral nerve block. A study in the rat sciatic nerve.

BACKGROUND: During peripheral nerve block, local anesthetic (LA) penetrates within and along the nerve to produce the observed functional deficits. Although much is known about the kinetics and steady-state relation for LA inhibition of impulse activity in vitro in isolated nerve, little is known about the relation between functional loss and intraneural LA content in vivo. This study was undertaken to investigate the relation of functional change to intraneural LA. METHODS: A sciatic nerve block was performed in rats with 0.1 ml 1% lidocaine radiolabeled with 14C. The total intraneural uptake of LA was determined at different times after injection, and the distribution of lidocaine along the nerve was assayed at different stages of functional block. Drug content was also compared with equilibrium lidocaine uptake in the isolated rat sciatic nerve. RESULTS: Total intraneural lidocaine in vivo increased to near steady-state in about 3 min, stabilizing at approximately 14.3 nmol/mg wet tissue for about 12 min before decreasing to zero at 70 min after injection. Although intraneural lidocaine was 1.6% of the injected dose during full block, only 0.3% was left when deep pain sensation returned and 0.065% was still detected when functions fully recovered. Despite these large differences in total lidocaine content, the longitudinal distribution remained constant. Intraneural lidocaine concentrations obtained at full block and partial recovery could be achieved in vitro by equilibration in 0.7-0.9 and 0.2-0.3 mM lidocaine, respectively. CONCLUSIONS: During peripheral nerve block only a small amount of injected LA penetrates into the nerve. The intraneural content of LA correlates with the depth of functional block.

Animals↗