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PubMed1996

Changes of Schwann cell antigenic profile after peripheral nerve injury.

Axons and Schwann cells (SC) in the peripheral nerve (PN) are in permanent interaction. Both myelin-forming SC (MSC) and nonmyelin-forming SC (NMSC) have a defined antigenic phenotype. Four weeks after PN transection, the proliferating SC in the distal stump lose some of their antigens, they start to display antigenic profile of NMSC and, in addition, to reexpress nerve growth factor receptor (NGF-rec) and growth associated protein (GAP-43), two antigens of their precursor cells. It can be assumed that migrating SC may differ in their antigenic profile in regard to resident proliferated SC in denervated distal nerve stump. We found that many SC specific antigens (S-100 protein, glial fibrilary acidic protein-GFAP, NGF-rec, GAP-43) are down-regulated in migrating SC as compared to SC proliferating in situ in the absence of axons.

Animals↗
PubMed1988

Collagenosis in wallerian degeneration depends on peripheral nerve type.

In the mature rat we determined the extent of peripheral nerve collagenosis in response to Wallerian degeneration and examined whether or not nonfibroblastic elements such as Schwann cells were important. Collagen was estimated as the hydroxy-proline content of normal and axotomized nerve fascicles after single or double crush lesions of both myelinated and unmyelinated nerves. Crushed unmyelinated nerve produced two to four times more collagen relative to control nerve than did the sciatic nerve. The nature of the interaction between two successive crushes was different in the two nerves. These results suggest that the degree of collagen fibrillogenesis occurring in Wallerian degeneration is dependent on peripheral nerve type and that the presence of myelin is not necessary for collagen fibrillogenesis.

Animals↗
PubMed1999

Spinal nerve ligation-induced neuropathy in the rat: sensory disorders and correlation between histology of the peripheral nerves.

We studied the effect of unilateral ligation of two spinal nerves on behavioral pain responses evoked by various types of cutaneous stimuli in the adult rat. Furthermore, we determined the effect of spinal nerve ligation on morphology of the peripheral nerves. The most consistent behavioral finding (83%) was a marked decrease in monofilament-induced hindlimb withdrawal thresholds (mechanical allodynia) ipsilateral to the spinal nerve ligation. This mechanical allodynia was observed as early as during the 1st post-operative day and it persisted up to 2 months (the maximum length of the observation period). In contrast, hyperalgesia to noxious mechanical stimulation (Randal-Sellitto test) was not observed in allodynic rats until the 3rd post-operative day. In a minority of rats (13%), spinal nerve ligation-induced mechanical hyperalgesia without a concomitant mechanical allodynia. There was no corresponding heat hyperalgesia in the injured hindlimb (hot water immersion-, radiant heat- or hot-plate-induced hindlimb withdrawal tests). In contrast, hypoalgesia to heat was observed on the 1st postoperative day, but not later. Neuropathological analysis of the peripheral nerves revealed a dramatic decrease in the number of myelinated nerve fibers distal to the spinal nerve ligation site. The results support the previous evidence indicating that ligation of spinal nerves induces a marked allodynia to mechanical stimulation. However, this mechanical allodynia may differentially dissociate from mechanical and thermal hyperalgesia at various post-operative time points. The marked mechanical allodynia together with a dramatic decrease in the number of myelinated nerve fibers is paradoxical, since the activation of myelinated nerve fibers by monofilaments produced abnormally strong behavioral responses. This paradox may be explained by spinal nerve ligation-induced amplification or disinhibition of tactile signals at central levels.

Animals↗
PubMed2005

Immunosuppressants: neuroprotection and promoting neurological recovery following peripheral nerve and spinal cord lesions.

No clinical techniques induce restoration of neurological losses following spinal cord trauma. Peripheral nerve damage also leads to permanent neurological deficits, but neurological recovery can be relatively good, especially if the ends of a transected nerve are anastomosed soon after the injury. The time until recovery generally depends on the distance the axons must regenerate to their targets. Neurological recovery following the destruction of a length of a peripheral nerve requires a graft to bridge the gap that is permissive to, and promotes, axon regeneration. But neurological recovery is slow and limited, especially for gaps longer than 1.5 cm, even using autologous peripheral nerve grafts. Without a reliable means of bridging long nerve gaps, such injuries commonly result in amputations. Promoting extensive neurological recovery requires techniques that simultaneously provide protection to injured neurons and increase the numbers of neurons that extend axons, while inducing more rapid and extensive axon regeneration across long nerve gaps. Although conduits filled with various materials enhance axon regeneration across short nerve gaps, pure sensory nerve graft remains the gold standard for use across long nerve gaps, even though they lead to only limited neurological recovery. Consistent results demonstrate that several immunosuppressive agents enhance the number of axons and the rate at which they regenerate. This review examines the roles played by immunosuppressants, especially FK506, with primary focus on its role as a neuroprotectant and neurotrophic agent, and its potential clinical use to promote improved neurological recovery following peripheral nerve and spinal cord injuries.

Animals↗
PubMedDate not supplied

Complement factors in adult peripheral nerve: a potential role in energy metabolism.

Complement cascade factors are known to play a critical role in myelin clearance after peripheral nerve injury. Here we show that components of both the classical (C1qa, C1qb, C1qc, C2 and C4) and alternative (C3, B and adipsin) pathways are expressed by uninjured peripheral nerve as well. mRNAs of components of the alternative pathway were predominantly found in the peri/epineurium, although factor C3 and factor B were also detected in the endoneurial compartment of adult nerve. Interestingly, adipsin mRNA was detected only in peri/epineurium, while adipsin protein was present in both peri/epineurium and endoneurium. This suggests that adipsin is transported to the endoneurium via the circulation from the peri/epineurium or outside of the nerve. Factor 5 and factor 9, necessary for the formation of the membrane-attack complex, were not detected in any part of the healthy peripheral nerve, which together with the observed presence of negative regulators of complement activation, is likely to prevent damage to the healthy nerve caused by complement activation. By analogy with the known role of complement factors in fat, we propose that local expression of these factors plays a role in the regulation of fatty acid homeostasis in the nerve and, thereby, in energy metabolism cross-talk between different compartments of the peripheral nerve.

Adult↗
PubMed2005

Regeneration into protected and chronically denervated peripheral nerve stumps.

OBJECTIVE: Delayed repair of peripheral nerve injuries often results in poor motor functional recovery. This may be a result of the deterioration or loss of endoneurial pathways in the distal nerve stump before motor axons can regenerate into the stump. METHODS: Using the rat femoral nerve, we protected distal endoneurial pathways of the saphenous nerve with either cross-suture of the quadriceps motor nerve (Group A) or resuture of the saphenous nerve (Group B) to compare later motor regeneration into the "protected" saphenous nerve pathway to chronic denervation and "unprotected" saphenous nerve (Group C). A total of 60 rats, 20 per group, were operated on. After this protection (or lack thereof) for 8 weeks, the motor branch of the femoral nerve was cut and sutured to the distal saphenous nerve to allow motor regeneration into protected and unprotected saphenous nerve stumps. The quantitative assessment of axonal regeneration was performed after 6 weeks by use of nerve sampling for axon counts and retrogradely labeled motor neuron counts. RESULTS: Significantly more myelinated axons innervated the motor (A) than the sensory (B) and no-protection (C) groups. There were significantly more retrogradely labeled femoral motor neurons in Group A than in the unprotected group (C). CONCLUSION: We conclude that even 2 months of denervation of the distal nerve pathway is deleterious to regeneration and that protection of the pathway improves subsequent reinnervation and regeneration. Moreover, if the desired regeneration is motor, protection of the distal nerve pathway by a motor nerve conditions is better than a sensory nerve.

Animals↗
PubMed2006

Clinical electrophysiological characterization of the acquired neuromyotonia phenotype of autoimmune peripheral nerve hyperexcitability.

Acquired autoimmune neuromyotonia is regarded as part of the spectrum of peripheral nerve hyperexcitability disorders. We aimed to use clinical neurophysiological measurements to study the extent, distribution, and characteristics of spontaneous motor unit potentials in 11 patients with acquired neuromyotonia. Investigations revealed that most spontaneous discharges recorded were motor unit, or partial motor unit potentials of normal size. Bursts of motor unit potentials arose more commonly from distal portions of the peripheral nerve and had abnormal absolute and relative refractory periods. Spontaneous discharges in some patients occurred in semirhythmic bursts in certain muscles. No patient had neurophysiological abnormalities detectable in first-order neurons of the central nervous system when using transcranial magnetic stimulation to estimate the threshold for corticomotor excitation and determine central motor conduction time. Only patients with coexistent myasthenia gravis had neurophysiologically detectable defects in neuromuscular transmission. The pathogenic region of abnormality in peripheral nerve hyperexcitability disorders therefore seems to lie within the terminal branches of peripheral motor nerves.

Action Potentials↗
PubMed2001

Convection-enhanced delivery in intact and lesioned peripheral nerve.

OBJECT: Although the use of multiple agents is efficacious in animal models of peripheral nerve injury, translation to clinical applications remains wanting. Previous agents used in trials in humans either engendered severe side effects or were ineffective. Because the blood-central nervous system barrier exists in nerves as it does in the brain, limited drug delivery poses a problem for translation of basic science advances into clinical applications. Convection-enhanced delivery (CED) is a promising adjunct to current therapies for peripheral nerve injury. In the present study the authors assessed the capacity of convection to ferry macromolecules across sites of nerve injury in rat and primate models, examined the functional effects of convection on the intact nerve, and investigated the possibility of delivering a macromolecule to the spinal cord via retrograde convection from a peripherally introduced catheter. METHODS: The authors developed a rodent model of convective delivery to lesioned sciatic nerves (injury due to crush or laceration in 76 nerves) and compared the results to a smaller series of five primates with similar injuries. In the intact nerve, convective delivery of vehicle generated only a transient neurapraxic deficit. Early after injury (postinjury Days 1, 3, 7, and 10), infusion failed to cross the site of injury in crushed or lacerated nerves. Fourteen days after crush injury, CED of radioactively-labeled albumin resulted in perfusion through the site of injury to distal growing neurites. In primates, successful convection through the site of crush injury occurred by postinjury Day 28. In contrast, in laceration models there was complete occlusion of the extracellular space to convective distribution at the site of laceration and repair, and convective distribution in the extracellular space crossed the site of injury only after there was histological evidence of completion of nerve regeneration. Finally, in two primates, retrograde infusion into the spinal cord through a peripheral nerve was achieved. CONCLUSIONS: Convection provides a safe and effective means to deliver macromolecules to regenerating neurites in crush-injured peripheral nerves. Convection block in lacerated and suture-repaired nerves indicates a significant intraneural obstruction of the extracellular space. a disruption that suggests an anatomical obstruction to extracellular and, possibly, intraaxonal flow, which may impair nerve regeneration. Through peripheral retrograde infusion, convection can be used for delivery to spinal cord gray matter. Convection-enhanced delivery provides a promising approach to distribute therapeutic agents to targeted sites for treatment of disorders of the nerve and spinal cord.

Albumins↗
PubMed1981

Branching of sensory axons in the peripheral nerve of the rat.

The currently accepted concept of a primary sensory cell is a cell that gives rise to a central process which passes through the dorsal root to the spinal cord and a peripheral process which passes to the periphery via a peripheral nerve. If this is correct, then there should be equal numbers of sensory axons in the dorsal root, dorsal root ganglion cells, and sensory axons in the proximal peripheral nerve. The present study obtains these counts in animals in which extraneous axons have been removed from the peripheral nerve and root. The counts indicate that there are approximately 2.3 sensory axons in the dorsal root and proximal peripheral nerve for each ganglion cell in the sacral segments of the rat. We interpret these data as indicating that there is significant branching of sensory axons in the dorsal root and proximal peripheral nerve and thus the generally accepted picture of a dorsal root ganglion cell is not correct for some, perhaps all, of these cells. We offer the speculation that this peripheral branching may be an indication of single sensory neurons having receptive fields in two separate locations, and thus this may be an anatomical explanation for certain types of referred pain.

Animals↗
PubMed2002

Optical imaging of intrinsic signals induced by peripheral nerve stimulation in the in vivo rat spinal cord.

We examined neural response patterns evoked by peripheral nerve stimulation in in vivo rat spinal cords using an intrinsic optical imaging technique to monitor neural activity. Adult rats were anesthetized by urethane, and laminectomy was performed between C5 and Th1 to expose the dorsal surface of the cervical spinal cord. The median, ulnar, and radial nerves were dissected, and bipolar electrodes were implanted in the forelimb. Changes in optical reflectance were recorded from the dorsal cervical spinal cord in response to simultaneous stimulation of the median and ulnar nerves using a differential video acquisition system. In the region of the cervical spinal cord, intrinsic optical signals were detected between C5 and Th1 at wavelengths of 605, 630, 730, 750, and 850 nm: the image with the largest signal intensity and highest contrast was obtained at 605 nm. The signal intensity and response area expanded with an increase in the stimulation intensity and varied with the depth of the focal plane of the macroscope. The intrinsic optical response was mostly eliminated by Cd(2+), suggesting that the detected signals were mainly mediated by postsynaptic mechanisms activated by sensory nerve fibers. Furthermore, we succeeded in imaging neural activity evoked by individual peripheral nerve stimulation. We found that the response areas related to each peripheral nerve exhibited different spatial distribution patterns and that there were animal-to-animal variations in the evoked neural responses in the spinal cord. The results obtained in this study confirmed that intrinsic optical imaging is a very useful technique for acquiring fine functional maps of the in vivo spinal cord.

Animals↗
PubMed1993

[Peripheral nerve injuries--current treatment standard].

A review of our century's efforts to overcome nerve defects reveals the conclusion that today microsurgical techniques and interfascicular nerve grafting offer the best chances to get success in peripheral nerve repair. There exists a theoretical grading system of Sunderland, which enables us to understand the very different factors which might influence the sprouting of nerve fibers within the damaged or repaired nerve segments. But in practice, the indication to operate always depends on our own decision. The neurological status and electrophysiological tests can only sometimes facilitate our treatment and judgement on peripheral nerve lesions. The basic principles of microsurgical nerve repair are still valid. Modern techniques have resulted in better prognosis. Vast mobilization to achieve neurorrhaphy by force is obsolete today. Epineural trunk-to-trunk-suture is only allowed after clean cut-injuries. In all other cases we have to prefer a repair by autologous grafting. But some factors still remain which limits our efforts, such as muscle degeneration depending on time interval or ischemic fibrosis after the lesion, direct trauma to the muscle substance or a lesion in the region of nerve ramifications.

Humans↗
PubMed1991

Magnetic resonance appearance of peripheral nerve sheath tumors.

Magnetic resonance imaging (MRI) was used to evaluate 22 histologically proven peripheral nerve sheath tumors, approximately two-thirds of which arose in the lower extremity. The histologic distribution was as follows: 12 schwannomas, 7 neurofibromas, and 3 malignant peripheral nerve sheath tumors (2 of which occurred in patients with neurofibromatosis). Most lesions demonstrated an intermediate to moderately bright signal on T1-weighted images and were minimally inhomogeneous. All lesions were moderately bright on proton-density-weighted images and bright on T2-weighted images, again with variable inhomogeneity. The extent of the tumor was best assessed on proton-density- and T2-weighted images. Smooth margins were noted in 19 lesions. Of the 3 remaining lesions, 2 were malignant (but had been subjected to biopsy prior to MRI), and the other lesion was a plexiform neurofibroma. MRI accurately determined the relationship between the lesion and the adjacent neurovascular structures and muscles, thereby assisting surgical management. On MRI, 5 lesions demonstrated coexistent subtle muscle atrophy along the longitudinal axis of surrounding or distally innervated musculature. This latter finding, together with the presence of a tumor in the vicinity of a large nerve trunk, suggests a peripheral nerve sheath neoplasm.

Adult↗
PubMedDate not supplied

[Monoclonal IgM autoantibody activity vis-à-vis glycoconjugates of peripheral nerves: apropos of 112 cases].

Serum IgM and IgG autoantibodies against carbohydrate epitopes on glycolipids and glycoproteins have been determined in a series of 112 neuropathies associated with monoclonal IgM (M-IgM) by different immunological techniques. The M-IgM anti-myelin sheath antibodies were determined by indirect immunofluorescence microscopy, the M-IgM anti-myelin associated glycoprotein (MAG) antibodies by western-blot analysis, the M-IgM anti-SGPG and SGLPG antibodies by immunodetection on thin-layer chromatography, the M-IgM anti-ganglioside GM3, GM2, GD3, GM1, GD1a, GD1b, GT1b, GQ1b and anti-sulfatide antibodies by immunodot-blot assay on membrane. Among the 112 M-IgM, 81 had autoantibody activity against nerve glycolipid antigens concentrated in peripheral nerve (72%). M-IgM bound strongly to myelin sheath in 34,5% of cases, to MAG in 38% of cases, to SGPG/SGLPG in 52% of cases, to gangliosides in 21.5% of cases and to sulfatide in 26 % of cases. Six M-IgM autoantibody activity profiles have been described in correlation with distinct clinical syndromes: - the M-IgM autoantibody activity profile against the carbohydrate epitope common to the glycolipids SGPG and SGLPG and myelin associated glycoprotein (MAG) in chronic demyelinating sensitive and sensorimotor peripheral neuropathies (58 patients, 52%); - the M-IgM autoantibody activity profile against immunodominant GM1 in demyelinating pure motor neuropathies (9 patients, 8%); - the M-IgM autoantibody activity profile against immunodominant disialosylgangliosides in chronic demyelinating sensitive ataxic neuropathies (8 patients, 7%); - the M-IgM autoantibody activity profile against immunodominant GM2 in demyelinating motor polyneuropathies (3 patients, 2.5%); - the M-IgM autoantibody activity profile against immunodominant GD1a in pure motor polyneuropathies (2 patients, 2%); - the M-IgM autoantibody activity profile against immunodominant GT1b and polysialosylgangliosides in one acute polyradiculoneuropathy (1%). The M-IgM recognized all gangliosides except GM1 and GM2. The neuropathies associated with IgM monoclonal gammopathy with autoreactive specificity form distinct syndromes. In 27.5% of cases, M-IgM had no identifiable activity autoantibodies.

Aged↗
PubMed1998

MR neurography. MR imaging of peripheral nerves.

Recent advances in MR imaging coupled with specially designed phased-array surface coils are revolutionizing imaging of the peripheral nervous system. Direct visualization of normal-sized major peripheral nerves within the body is now possible. This article describes the appearance of normal peripheral nerves together with imaging characteristics of various types of nerve pathology including traumatic injury, compressive syndromes, and neural tumors. Imaging of the brachial plexus, lumbosacral plexus, carpal tunnel, cubital tunnel, and cervical nerves is illustrated and discussed. MR neurography techniques permit imaging detection of peripheral nervous system pathology that in some cases allow earlier and more accurate diagnosis. It is believed that this will ultimately lead to improved understanding of peripheral nerve pathophysiology that will, in turn, lead to improved treatment.

Humans↗
PubMed2005

Electrophysiologic evaluation of peripheral nerve injuries in children following the Marmara earthquake.

The aim of this study was to investigate the clinical, demographic, and electromyographic (EMG) characteristics of 12 earthquake victims in the pediatric age group and to compare the findings with those of the adult group. Following the 1999 Marmara earthquake, 75 subjects with suspected peripheral nerve injury were referred to our EMG laboratory for evaluation. In the pediatric age group, five patients had a history of short-term temporary trauma and seven had a history of being trapped under the debris for 4 to 10 hours and sustaining long-term trauma. Five patients had developed compartment syndrome and one had developed crush syndrome. The EMG examinations revealed peripheral nerve injury findings in all patients. The brachial plexus was damaged in 2 patients, and 19 peripheral nerves were damaged in 10 patients. Peroneal and posterior tibial nerves were predominantly affected. Regeneration was detected in all of the patients with brachial plexus damage at a mean follow-up of 3.5 months and in 62.5% of patients with peripheral nerve damage at a mean follow-up of 7.7 months. Being buried under the debris, compartment syndrome, peripheral nerve injuries in the lower extremities, and total axonal damage in the first EMG examinations were found to be higher in the pediatric age group. Regeneration findings were found at similar rates in both groups, with the brachial plexus being the most favorable. When it is considered that the regeneration process lasts 15 to 18 months and EMG findings mostly show pathologies in the form of neuropraxia and axonotmesis, we think that the prognosis of our patients will be good.

Adolescent↗
PubMed1994

Effect of host age upon the degree of nigrostriatal dopaminergic system recovery following cografts of adrenal medulla and pretransected peripheral nerve.

Accumulation of nerve growth factor (NGF) has been reported to occur at the distal stump of pretransected peripheral nerve. We performed adrenal medullary grafts or cografts of adrenal medulla and distal stump of pretransected peripheral nerve into the striatum of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated young or aging mice. We subsequently compared the survivability of chromaffin cells and the degree of host dopaminergic (DA) fiber recovery in relation to host age. In both young and aging hosts, adrenal medullary chromaffin cells cografted with pretransected peripheral nerve survived better than those in adrenal grafts alone. Host DA fiber recovery, however, showed less recovery and more restriction around the grafted site in aging compared with young hosts. We conclude that pretransected peripheral nerve can enhance the survivability of cografted chromaffin cells both in young and in aging hosts, but that DA fiber recovery is more limited in aging hosts compared to young hosts.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed2005

Autologous fibrin glue in peripheral nerve regeneration in vivo.

The activity of several growth factors on peripheral nerve regeneration is reported. Autologous fibrin glue contains a large number of platelets, which release significant quantities of growth factors. In order to understand the role of autologous fibrin glue in peripheral nerve regeneration, a 15-mm rabbit peroneal nerve defect was repaired using a vein graft filled with autologous fibrin glue. Axonal regeneration was examined using histological and electrophysiological methods. The extent of axonal regeneration was superior when treated with autologous fibrin glue. Our data suggest that fibrin nets formed by fibrinogen, in combination with growth factors present in autologous fibrin glue, might effectively promote peripheral nerve regeneration in nerve defects.

Animals↗
PubMed1988

Use of peripheral nerve action potentials for intraoperative monitoring.

Following a physical injury to peripheral nerve, clinical evaluation and the use of conventional EMG/NCS is often unable to determine whether axons are crossing the site of injury before severe changes in distal tissues occur. The INAP recording identifies functional axons within neuromas before other signs of reinnervation have developed. In clinically complete lesions, recording an INAP across the injury indicates the presence of regenerating axons, and neurolysis of the encasing connective tissue is recommended. If an INAP is absent, resection of the dense neuroma is usually undertaken with end-to-end suture or graft. A present INAP indicates clinically significant regenerating axons even with large distances to target tissue. An absent INAP for injuries far from target tissue indicates a poor prognosis. In clinically incomplete lesions, INAP recording is of no value over the clinical examination and EMG/NCS. INAP can aid peripheral nerve tumor resection by identification of intact nerve fascicles. INAP responses are obtained by placing platinum-iridium bipolar stimulating electrodes proximal to the injury. The INAP is then recorded by distal electrodes. A standard EMG/NCS instrument with an isolated stimulation unit can be used with the appropriate gain and time base settings. Stimulus intensity required for a supramaximal response is usually less than 75 V at 0.05 msec duration. Frequency bandpass is similar to that for conventional EMG/NCS studies. Electrodes must elevate the nerve during the recording. Artifact from 60 Hz line frequency and stimulus are common problems.

Humans↗