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Study on repair of peripheral nerve injury has been proceeding over a long period of time. With the use of microsurgery technique since 1960s the quality of nerve repair has been greatly improved. In the past 40 years, with the continuous increase of surgical repair methods, more progress has been made on the basic research of peripheral nerve repair.
The blockade of peripheral nerves carries a certain risk of unwanted complications, which can follow after unintentional intraneural injection of a local anesthetic. Up till today, the research of measuring injection pressure has been based on animal models, even though the histological structure of periphery nerve is different for animal and human population, so the application pressure which presages intraneural injection in human population is still unknown. As material in performing this study there have been used 12 Wistar rats and 12 delivered stillborns. After bilateral access to the median nerve, we applied 3 ml of 2% lidocaine with epinephrine, with the help of automatic syringe charger. The needle was at first placed perineural on one side, and then intraneural on the other side of both examination groups. During every application the pressure values were monitored using the manometer, and then they were analyzed by special software program BioBench. All perineural injections resulted with the pressure < or = 27.92 kPa, while the majority of intraneural injections were combined with the injection pressure > or = 69.8 kPa. The difference between intraneural and perineural injection pressures for the two different examination groups (rats and delivered stillborns) was not statistically significant (P>0.05). As prevention from intraneural injections today are in use two methods: the method of causing paresthesia or the method of using the peripheral nerve stimulator. However the nerve injury can still occur, independent from the technique used. If our results are used in clinical practice on human population, than the high injection pressure could be the marker of intraneural lodging of a needle.
The management of peripheral nerve injury continues to be a major clinical challenge. Despite advancements in microsurgical technique, results after nerve repair have been unpredictable and dis appointing. The management of these nerve injuries relies on having a thorough understanding of peripheral nerve anatomy. This is the basis of the classification schemes by Seddon and Sunderland, in which the prognosis of nerve injuries varies depending on the degree of injury to their substructures. The most recent advances in the management of peripheral nerve injuries rely on the ability to manipulate the pathophysiologic processes triggered by nerve injuries and regeneration. End-to-end primary repair should be sought whenever a tension-free repair can be attained. If there is a significant nerve gap, use of nerve autograft remains the gold standard. In nerve injuries where a nerve autograft is not possible, the use of nerve allograft, as well as autogenous, biodegradable, and synthetic nerve conduits has shown promising results in experimental studies.
The evaluation of peripheral nerve injuries has traditionally relied primarily on information gained from the clinical history, physical examination, and electrodiagnostic testing. Taken together, all of this clinical and diagnostic information often allows one to determine the location and severity of the underlying peripheral nerve problem. However, it may not be sufficient in diagnosing a focal entrapment neuropathy superimposed upon a more generalized peripheral neuropathy; localizing a focal lesion along a long segment of nerve which may be difficult to assess accurately with electrodiagnostic studies; distinguishing early between an axonotmetic grade of injury, which can recover through axonal regeneration, and a neurotmetic grade which cannot and therefore may benefit from a surgical exploration and repair procedure; and noninvasively diagnosing and determining the surgical resectability of peripheral nerve mass lesions such as tumors. The goal of this review is to illustrate how standard and evolving magnetic resonance imaging techniques can provide additional information in dealing with some of these problems.
Transected peripheral nerve can be protected with different supplementations. One of them is implantation of dead-ended connective tissue chambers filled with fibrin and growth-promoting substances. The aim of this study was to find whether nerve growth factor (NGF) applied by means of such method exerts neuroprotective effect upon transected sciatic nerves. Study was performed on the adult male Wistar C rats. Connective tissue chambers grew around the silicone tubes implanted under their skin. Chambers were then filled with fibrin (control group) or fibrin with NGF solution (NGF group). Right sciatic nerve was cut, its distal stump was removed and its proximal stump was introduced into the chamber. Following 4 weeks DiI was applied to the free end of implant. The labeled motoneurons in the slices obtained from L3-L4 spinal cord segments and the number of myelinated nerve fibers present in the middle part of the chambers were counted. Acetylcholinesterase-positive fiber endings inside the chambers were also visualized. Our data showed that the number of motor neurons and their diameters as well as the number of myelinated fibers were higher in the NGF group when compared to the control group, but these differences were not significant. In both groups parallelly arranged acetylcholinesterase-positive nerve fibers were present. The obtained results show that NGF has no influence on regeneration of the motor component of the rat sciatic nerves in adult animals.
Recent electrophysiological and biochemical evidence implicates altered peripheral nerve Na-K-ATPase activity in the nerve conduction impairment of acute experimental diabetes. Composite in vitro nerve energy utilization is seriously impaired by experimental diabetes, yet is not modulated directly by insulin action on peripheral nerve. Therefore, we hypothesized that the reduction in diabetic nerve energy utilization reflects impaired nerve Na-K-ATPase activity. The reduction in steady-state energy utilization in diabetic peripheral nerve is shown to be quantitatively equal to the ouabain-inhibitable fraction of respiration, a measure of Na-K-ATPase activity in peripheral nerve. Na-K-ATPase activity in diabetic (but not nondiabetic) endoneurial preparations is influenced by medium solute concentration. Furthermore, diabetic nerve Na-K-ATPase activity and sodium-dependent myo-inositol uptake are similarly affected by medium solute changes, suggesting that the nerve sodium gradient may limit intracellular myo-inositol uptake in diabetic nerve. Conversely, because reduced diabetic nerve myo-inositol content impairs nerve Na-K-ATPase, a possible pathophysiological cycle of progressively deranged myo-inositol metabolism and Na-K-ATPase function may exist in diabetic peripheral nerve.
BACKGROUND: Reconstruction of long or multiple peripheral nerve defects with peripheral nerve autografts may not be possible due to insufficient quantities of donor nerve. There are promising preliminary data that nerve allografting has the potential to improve functional outcome and quality of life after devastating nerve injuries or large tumor resections. The authors previously demonstrated that blockade of the CD40/CD40 ligand costimulatory pathway, via anti-CD40 ligand monoclonal antibody (MR1) therapy, induces tolerance to peripheral nerve allografts in mice. In this study, the authors sought to correlate the immunomodulatory effects of MR1 treatment with functional muscle recovery after peripheral nerve allografting in the murine model. METHODS: In the mouse hindlimb model, peroneal nerve isografts (C57BL/6 into C57BL/6) and allografts (BALB/c into C57BL/6) were utilized to reconstruct 0.8-cm peroneal nerve gaps. MR1 versus vehicle was administered on days 0, 1, and 2. At 60 days after transplantation, splenocyte production of interferon-gamma and interleukins 2, 4, and 5 were quantified using ELISPOT analysis, and in vitro maximum tetanic isometric force of the extensor digitorum longus muscle was measured. RESULTS: At 60 days after transplantation, immunomodulation persisted in MR1-treated, allografted animals, as evidenced by significantly muted interferon-gamma, interleukin 4, and interleukin 2 splenocyte production. Functional extensor digitorum longus muscle recovery after nerve allografting and MR1 administration was improved due to the tolerance induced by MR1 compared with untreated allograft recipients. CONCLUSIONS: Three-day inductive therapy with MR1 produces 60-day immunologic tolerance to peripheral nerve allografts, as evidenced by dramatic decreases in interferon-gamma, interleukin 4, and interleukin 2 production, and results in increased muscle force recovery. This work emphasizes the potential promise of CD40-CD40 ligand costimulatory blockade in reducing or eliminating peripheral nerve allograft rejection.
OBJECTIVE: To examine the utility of repetitive nerve stimulation (RNS) in the evaluation of peripheral nerve hyperexcitability (PNH). BACKGROUND: PNH describes a group of disorders characterized by muscle cramps, twitching and stiffness. When severe, PNH may be characterized by the presence of continuous muscle fiber activity on routine needle electromyography (EMG). In milder forms of the disease, nerve hyperexcitability may be evidenced by the presence of after-discharges or cramp potentials following RNS. METHODS: Fifty-four patients were prospectively recruited and classified into one of three groups-PNH, other neuromuscular disease and controls. We recorded and quantified the after-discharges and cramp potentials following RNS at 1, 5, 10 and 30 Hz. RESULTS: The proportion of nerves with after-discharges and/or cramp potentials was significantly greater in the PNH group than the control group at both 5 Hz (p=0.03) and 10 Hz (p=0.01), as well as in the neuromuscular disease group compared to controls at 5 Hz (p=0.02). There was also a significant concordance between complaints of muscle cramps and fasciculations and the finding of after-discharges and/or cramp potentials at both 5 Hz (p=0.005) and 10 Hz (p=0.004). At a stimulation frequency of 10 Hz, the sensitivity of RNS for the diagnosis of PNH (primary or secondary) was 79% and the specificity was 88%. CONCLUSION: Our findings suggest that RNS at or below a stimulation frequency of 10 Hz (when positive) is a useful test for the diagnosis of PNH, whether it is primary or secondary.
A method is described which records efferent motor nerve action potentials (MNAPs), evoked by trans-skull motor area stimulation, directly from a nerve root or peripheral nerve fibres during operation. The records of MNAPs from the root show whether function of the anterior root is intact and its continuity retained. When recorded from the proximal stump of a divided nerve at the wrist the motor funiculus can be identified, enabling funicular nerve suture to be carried out more easily.
PURPOSE: As alternatives to nerve grafts for peripheral nerve repair, we have synthesized 12 mm long poly(2-hydroxyethyl methacrylate-co-methyl methacrylate) (PHEMA-MMA) porous tubes and studied their regenerative capacity for the repair of surgically-created 10 mm rat sciatic nerve gaps. We compared the in vivo regenerative efficacy of these artificial tubes with the gold standard, the nerve autograft. METHODS: Tubes were assessed in vivo for their ability to support nerve regeneration at 4, 8, and 16 weeks post-implantation by histology, electrophysiology, histomorphometry, and reinnervated lateral gastrocnemius (LG) dry muscle mass. RESULTS: Axonal regeneration within the tubes was observed by 8 weeks, with outcome parameters comparable to autografts. This finding was further supported by the electrophysiological and histomorphometric results. The 16 week tube group had a bimodal response, with 60% of the tubes having a similar response to autografts and the other 40% having significantly lower (p < 0.05) outcome measures in several parameters. CONCLUSIONS: Axonal regeneration in artificial tubes was similar to that in autografts at 8 and 16 weeks, however, a bimodal distribution of regeneration was observed in 16 week tubes.
Blockade of the sciatic nerve in the fossa poplitea is a rarely used form of regional anaesthesia. A new method of identification of the tibial and peroneal nerve and their blockade in combination with blockade of the femoral nerve using a peripheral nerve stimulator, is described. Results in 300 patients during a 12 month period are described and discussed.
Growth cones of regenerating nerves, following crush injury to the rat peripheral nerve system, were studied by electron microscopy and synaptophysin. Localization in the growth cones was revealed by immunohistochemistry at the ultrastructural level. Many regenerating growth cones grew along the Schwann-cell basal laminae tubes at the crushed site. These cones revealed an abundance of organelles, such as heterogenous vesicles and many mitochondria, and a scarcity of cytoskeletons, including microtubules and neurofilaments in the cytoplasm. The periphery of the growth cones (corresponding to the lamellipodia or filopodia of cultured neurons) contained rich electron-dense filamentous materials. Cellular protrusions, such as filopodia, were rarely seen. These growth cones exhibited intense immunoreactivity for synaptophysin by light microscopy. Immunoelectron microscopy demonstrated that immunoreactivity was distributed diffusely in the cytoplasm.
One hundred and three benign, and 10 malignant peripheral nerve tumours were examined immunohistochemically for expression of 75 kDa nerve growth factor receptor (NGFR). In benign tumours NGFR was demonstrated at 61% in neurinoma, 71% in neurofibroma, 93% in neurofibromatosis and 90% in traumatic neuroma. Malignant neurogenic tumours were 100% positive for NGFR. Phosphotyrosine-immunoreactivity was detected in 76% of NGFR-positive tumours but the frequency of immunostained tumour cells was low. These results suggest that both benign and malignant peripheral nerve tumours express 75 kDa NGFR. The receptor seems to serve as growth signal transduction of the tumour cells in terms of phosphorylation of the tyrosine residue of the receptor or the target protein of the NGFR protein tyrosine kinase.
Advances in MR imaging have improved the visualization of normal and pathologic peripheral nerve structures in various clinical settings. Peripheral nerve imaging has the potential to dramatically change the diagnosis and treatment of peripheral nerve pathology and lead to an improved understanding of peripheral nerve pathophysiology. Currently, MR imaging serves as a problem-solving tool when additional anatomic information is needed to clarify ambiguous electrodiagnostic and clinical examinations. The next major advance in MR imaging of peripheral nerves will likely be the transition from anatomic to physiologic imaging with higher resolution as better phased-array surface coils and higher-field-strength magnets become available. Finally, MR neurography should remain complementary to the clinical examination and electrodiagnostic studies in the evaluation of peripheral nerve disorders.
Sensory-motor deficit in a peripheral nerve pattern due to brain lesion is rarely documented. We report on seven patients with a clinical manifestation of sensory-motor deficit, imitating peripheral nerve involvement, due to lacunar brain infarcts verified by brain computed tomography scan. Five of the patients had an ulnar nerve-like deficit and two median nerve-like deficits. The infarcts were located in the thalamus and the corona radiata. No clinical or electrophysiological evidence for peripheral nerve involvement was found. The unusual peripheral nerve pattern of lesions caused by lacunar brain infarcts can be defined as an additional lacunar syndrome and must be taken into consideration in the clinical evaluation of peripheral nerve deficits with normal nerve conduction velocity.
Although the use of peripheral nerve stimulators and unsheathed needles in performing nerve blocks has been previously described, there has been a growing emphasis on the use of specific, expensive equipment to ensure success. The availability of equipment designed for use in peripheral nerve blocks, insulated needles and nerve stimulators, will help promote the use of these techniques, but the expense of purchasing this specialized equipment may contribute to a decline in performance of certain types of blocks. This article reviews the use of standard equipment, available in most anesthesia departments, for performing peripheral nerve blocks successfully.
1. After long-term n-hexane exposure (2000 ppm, 12 h d-1, 6 d week-1, for 24 weeks), the content of neuron-specific enolase (gamma-enolase), creatine kinase-B and beta-S100 protein in the cortex, cerebellum, spinal cord and proximal and distal sciatic nerves of rats was determined by enzyme immunoassay. 2. The amounts of the three proteins decreased significantly in the distal segment of sciatic nerve, whereas they remained unchanged in the brain and proximal sciatic nerve. The quantitative decline in these marker proteins in the distal sciatic nerve could be related to neurophysiological deficits in the peripheral nerves. 3. This study indicates that the biochemical changes observed are consistent with the clinical and pathological findings of n-hexane neuropathy. These nerve-specific marker proteins can be used to assess solvent-related peripheral neurotoxicity.
(1) When hindlimb peripheral nerves are cut across in rats and mice, there is a tendency for the animal to attack the anaesthetic limb. We have called this attack "autotomy". In this paper we describe the time course and degree of autotomy following various types of nerve injury. (2) Four different types of lesion were applied to the sciatic nerve of rats. The most serious autotomy was produced by section of the nerve and encapsulation of its cut end in a polythene tube. Section followed by immediate resuturing also produced serious autotomy. Simple ligation of the nerve end was followed by less autotomy than encapsulation or cut and resuture. A crush lesion caused only minimal attack. (3) Section of the saphenous branch of the femoral nerve produced no autotomy. However, if the saphenous and sciatic nerves were ligated at the same time so that the entire foot became anaesthetic there was a great increase of autotomy over that seen when the sciatic nerve alone was ligated. This increase with the double lesion occurred even if the saphenous nerve was ligated more than 100 days after the sciatic nerve had been cut. (4) Mice showed autotomy very similar to that seen in rats but the onset was somewhat faster. (5) Reasons are given to propose that autotomy is triggered by an abnormal afferent barrage generated in the cut end of the nerve. Autotomy from peripheral nerve lesions is a different phenomenon from that seen after dorsal root section. Autotomy occurs under conditions which produce anaesthesia dolorosa in man. This simple model may be suitable for studies of the prevention of irritations originating from chronic lesions of peripheral nerves.