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PubMed2000

Alterations in the distribution of stimulus-evoked c-fos in the spinal cord after neonatal peripheral nerve injury in the rat.

Neonatal peripheral nerve injury results in a significant rearrangement of the central terminals of surviving axotomized and adjacent intact primary afferents in the dorsal horn of the spinal cord. This study investigates the ability of these afferents to make functional contacts with dorsal horn cells, using c-fos expression as a marker of synaptic activation. Graded electrical stimulation at A- or C-fiber strength of either the neonatally axotomized sciatic nerve or the adjacent uninjured saphenous nerve was performed in adult rats. Stimulation of the contralateral uninjured nerve served as a control. Quantitative examination of the number and distribution of c-fos-labeled cells in the spinal cord laminae was performed. Electrical stimulation of the previously axotomized sciatic nerve at A-fiber intensity resulted in many labeled profiles in laminae I-V of the lumbar spinal cord on the experimental as compared to the contralateral side. Electrical stimulation of uninjured saphenous nerve or saphenous-nerve-innervated skin (using pin electrodes) at A-fiber intensity did not evoke c-fos. Stimulation of the saphenous nerve at C-fiber intensity, however, resulted in a significant increase in the number and distribution of c-fos-labeled profiles in laminae I-V on the experimental side as compared to the contralateral control side. The results show that the distribution of c-fos-expressing cells after neonatal nerve injury is compatible with the previously demonstrated distribution of sprouting of primary afferents belonging to an uninjured nerve adjacent to an injured nerve, and that the surviving axotomized afferents are capable of transmitting signals to postsynaptic cells. These findings indicate that Abeta afferent stimulation of injured but not uninjured afferents elicits c-fos expression in postsynaptic cells. This may reflect an injury-induced maintenance of a normal developmental process whereby Abeta stimulation elicits c-fos in dorsal horn neurons.

Animals↗
PubMed2002

Gene transfer with DNA strand technique and peripheral nerve injuries.

Although much progress has been made, current treatments of peripheral nerve injury often result in only partial recovery. Many methods have been used to improve the surgical exploration for injured nerve repair. However, much less is known about the involvement of complex neurochemical interactions. 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. In this article we give an overview of the process of peripheral nerve injury and regeneration, review the roles of Schwann cells and neurotrophic factors, and summarize perspectives on how gene therapy with viral vectors and cell-mediated DNA strand technology may be used to improve treatment of peripheral nerve injuries.

Gene Transfer Techniques↗
PubMed1996

Functional assessment of peripheral nerve injury and repair.

Based on 191 follow-ups of patients with peripheral nerve injury and repair, the authors suggest that a reasonable assessment should consist of motor, sensory, and autonomic nerve indices. It is also suggested that a method of functional assessment about the autonomic nerve should be included. The method of evaluating motor function should be selected according to the site of the nerve injury. Lovett's method was adopted for nerve injury at the wrist and lower third of the forearm, as well as the British Medical Research Council (BMRC) method for nerve injury at the upper forearm or other nerves. Standards and grades of the BMRC should be raised somewhat, in order to compare more consistently with the results obtained using the method of Lovett; then both can be correlated satisfactorily.

Adult↗
PubMed2005

Technology insight: visualizing peripheral nerve injury using MRI.

Currently, the evaluation of peripheral nerve disorders depends on clinical examination, supplemented by electrophysiological studies. These approaches provide general information on the distribution and classification of nerve lesions-for example, axonal versus demyelinative-but nerve biopsies are still required to obtain morphological and pathophysiological details. In this article, we review recent progress in the imaging of peripheral nerve injury by magnetic resonance (MR) neurography. Axonal nerve injury leads to Wallerian degeneration, resulting in a hyperintense nerve signal on T2-weighted MR images of the distal nerve segment. This signal is lost following successful regeneration. Concomitant denervation-induced signal alterations in muscles can further help us to determine whether nerve trunks or roots are affected. These signal changes are caused by various combinations of nonspecific tissue alterations, however, and are not related to particular pathoanatomical findings, such as inflammation, demyelination or axonal injury. New experimental MR contrast agents, such as gadofluorine M and superparamagnetic iron oxide particles, allow visualization of the dynamics of peripheral nerve injury and repair. Further clinical development of these MR contrast agents should allow these functional aspects of nerve injury and repair to be assessed in humans, thereby aiding the differential diagnosis of peripheral nerve disorders.

Animals↗
PubMed2006

Closed fractures complicated by peripheral nerve injury.

Closed fractures may be complicated by associated peripheral nerve injury. However, because clinical information is limited, determining the best course of treatment is difficult. Most patients with closed fractures have a local nerve injury without nerve division; their prognosis for recovery is favorable. In the acute setting, immediate surgery is usually unwarranted because of the difficulty in accurately defining the severity and extent of nerve injury. When débridement of an open fracture or repair is not required, peripheral nerve injuries are best observed and the extremity treated with splinting and exercise to prevent loss of joint motion. Patients who fail to demonstrate signs of recovery at 6 months, either clinically or with electrodiagnostic testing, should undergo exploration to maximize the likelihood for return of function. When, during exploration, the nerve is in continuity, intraoperative measurement of nerve action potentials should be done. Measuring nerve action potentials will determine whether nerve grafting, local neurolysis, or excision of the injured segment, accompanied by primary repair, is the most appropriate treatment.

Algorithms↗
PubMed2003

Sex-related difference in collateral sprouting of nociceptive axons after peripheral nerve injury in the rat.

Possible sex-related differences in the extent of collateral sprouting of noninjured nociceptive axons after peripheral nerve injury were examined. In the first experiment, peroneal, tibial, and saphenous nerves were transected and ligated in female and male rats. Eight weeks after nerve injury, skin pinch tests revealed that the nociceptive area of the noninjured sural nerve in the instep skin expanded faster in females; the final result was a 30% larger increase in females than in males. In the second experiment, the end-to-side nerve anastomosis was used as a model for axon sprouting. In addition to the previous procedure, the end of an excised peroneal nerve segment was sutured to the side of the intact sural nerve. Eight weeks later, collateral sprouting of nociceptive axons into the anastomosed peroneal nerve segment was assessed by the nerve pinch test and axon counting. There was no significant difference with respect to the percentages of male and female rats with a positive nerve pinch test. The number of myelinated axons in the anastomosed nerve segment was significantly larger in female (456 +/- 217) than in male (202 +/- 150) rats, but the numbers of unmyelinated axons were not significantly different. In normal sural nerves, the numbers of either all myelinated axons or thin myelinated axons did not significantly differ between the two sexes. Therefore, the more extensive collateral axon sprouting observed in female than in male rats is probably due to the higher sprouting capacity of thin myelinated sensory axons in females.

Animals↗
PubMed1981

Peripheral nerve injuries of the hand in children. A follow-up study of 38 patients.

Thirty-eight children in whom a peripheral nerve injury of the hand had been repaired from 2 to 18 years earlier (mean 7.5 years) were examined. All repairs had been performed with the conventional technique with epineural sutures, and nearly all were primary neurorrhaphies. Sensory recovery was evaluated by using the two-point discrimination test (2 PD). The results were considered good if the 2 PD value was less than 6 mm and poor if this value was more than 15 mm. Of the 20 repairs of an ulnar or median nerve, or both, results were good in eight (40%), fair in 10 (50%) and poor in two (10%). Of the 18 digital nerve repairs, results were good in 14 (77.8%) and fair in four. The results in this series are better than results reported for adults series.

Adolescent↗
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↗
PubMed1999

[The emergent repair of peripheral nerve injury of the wrist].

OBJECTIVE: To investigate the effect of the emergent repair of peripheral nerve injury of the wrist. METHODS: From July 1993 to December 1997, 17 cases were admitted, which 21 injured peripheral nerves were repaired emergently. Among them, there were 11 cases of median nerve injury, 2 cases of ulnar nerve injury and 4 cases of median and ulnar nerve injury. All the nerves were ruptured completely except one which was partially ruptured. The emergent operation was taken and the injured nerves were repaired by microsurgical technique. RESULTS: Followed up 6 to 18 months after operation, 95.25% injured nerves had good outcome. CONCLUSION: Because of the specific structure of the wrist, nerve injury at this part need to be repaired emergently. It can enhance the regeneration of the injured nerve, preserve the function of the intrinsic muscle of hand, and decrease the local adhesion.

Adolescent↗
PubMed2000

Transient action of the endothelial constitutive nitric oxide synthase (ecNOS) mediates the development of thermal hypersensitivity following peripheral nerve injury.

Neuropathic pain is a disabling feature of peripheral nerve injury. Following injury, local inflammation and the release of mediators may contribute to ectopic mechanosensitivity of the nerve-trunk and pain hypersensitivity. In the present study we investigated whether nitric oxide (NO) action and local nitric oxide synthase (NOS) expression play a role in pain hypersensitivity and A fibre-mediated ectopic hyperexcitability following a chronic constriction injury to a rat sciatic nerve. Using immunohistochemical methods we provide evidence for a unique endothelial constitutive nitric oxide synthase (ecNOS) immunoreactivity localized in early axonal endbulb-like structures of injured peripheral nerve axons. Moreover, we show that following nerve injury there is increased ecNOS-mRNA expression within the lumbar sympathetic ganglia, and that axoplasmic transport in sympathetic and other axons rather than local non-neural synthesis accounts for its accumulation in nerve fibres. We also demonstrate here that local inhibition of NOS action with the broad-spectrum inhibitor NG-nitro-L-arginine-methyl ester (L-NAME), but not more specific inhibitors of other NOS isoforms, has stereospecific, dose- and time-dependent analgesic effects that were reversed by local administration of L-arginine, the natural precursor of NO. In further work, using a teased fibre preparation, we show that administration of L-NAME, but not D-NAME, to the injury site also blocks ectopic mechanosensitivity of injured A-fibres. Our results indicate that an early and transient local ecNOS expression within early axonal endbulb-like structures, some arising from sympathetic axons, plays a critical role in the development of neuropathic pain.

Animals↗
PubMed1982

Experimental studies with clinical application to peripheral nerve injury: a review of the past decade.

A great deal of information concerning nerve regeneration after injury and repair has been developed during the past decade. Technologic advances concerned with the mechanics of repair have probably reached their nadir and other means of promoting more efficient central to peripheral connections will need to be sought. Studies which relate central nervous system regenerative events to those occurring in the periphery should provide additional needed information. At this time research workers must concentrate on control of scar formation at the suture line and the correct orientation of regenerating axons toward their peripheral connections. These goals will most likely be achieved by biochemical manipulations at the cellular level.

Animals↗
PubMed2004

Comparison of five different rat models of peripheral nerve injury.

Described here is a comparison of five peripheral sciatic nerve injury models in rats which all result in various degrees of neuropathic pain symptoms. They are the chronic constriction injury (CCI), the spinal nerve ligation (SNL), the partial sciatic ligation (PSL), the tibial and sural transection (TST), and the complete sciatic transection (CST) model. Behavioral testing was performed on these models over a 56-day period under strict experimental conditions to minimise variability between the surgical models and to allow for an accurate evaluation of the sensory deficits produced by each model. Overall, all five models of neuropathic pain produced signs of allodynia and hyperalgesia to various stimuli. However, the duration and magnitude of the evoked responses varied considerably between the different models.

Animals↗