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[Surgery of therapy-resistant pain due to peripheral nerve injury].

1. The forms of peripherally triggered or localized pains are differentiated: Local pain of a neuromatous character, propagated pain, sympathalgia, phantom pain, causalgia, and combined forms. 2. Surgical operations are performed locally, to the spinal cord, brain, and sympathicus, as well as by neurostimulation on all levels. 3. The areas of indication differ according to the localization of pain and its probable cause. 4. Serving the prevention of pain after peripheral nerve injuries are the particular topical treatment of a fresh injury, psychic guidance, specific aftercare and physiotherapy, elimination of pension payment problems, and optimum reintegration into normal working life]

Cordotomy↗

Perineurioma: a benign peripheral nerve tumor.

A unique benign peripheral nerve tumor, called a perineurioma, is described in this report. Light and electron microscopy and immunohistochemistry indicate that this tumor was derived from the perineurial cell. We discuss the ultrastructure, histogenesis, and management of this neoplasm.

Adult↗

Peripheral nerve stimulator performance: the influence of output polarity and electrode placement.

The median as well as the ulnar nerve may be used effectively in the evaluation of neuromuscular blockade with the peripheral nerve stimulator. Both ulnar and median nerve stimulation produce flexion of the fingers. For maximum neural stimulation either during the routine use of the peripheral nerve stimulator or when it is used as an aid to peripheral nerve block, the negative pole should be attached to the exploring needle or over the nerve to be stimulated.

Anesthesia↗

Relationship between nerve blood flow and intercapillary distance in peripheral nerve edema.

Some human and experimental neuropathies are characterized by endoneurial edema and increased intercapillary distance (ICD). This may potentially produce chronic endoneurial ischemia. To examine the relationship between nerve blood flow (NBF) and ICD we measured NBF in rats with experimental galactose neuropathy (EGN), a model where ICD is known to be increased. Simultaneous measurements of NBF in the center and subperineurial region were made in normal and edematous tibial nerves using hydrogen-sensitive microelectrodes and hydrogen polarography. NBF was significantly reduced in rats with EGN when compared with controls. A second finding was that in half the rats with EGN there was a greater reduction in NBF in the subperineurial region, a site of maximal ICD increase. In contrast, NBF was similar in central and peripheral regions in control rats. These findings support the hypothesis that an increase in ICD produces a reduction in NBF. Further support for the hypothesis is derived from a computer model of the effect of changes in ICD on endoneurial oxygen tension. We conclude that a chronic reduction in NBF may participate in the pathogenesis of edematous neuropathies.

Animals↗

Processed porcine collagen tubulization versus conventional suturing in peripheral nerve reconstruction: an experimental study in rabbits.

In peripheral nerve reconstruction, various procedures are used. One of the procedures that received the most interest in the past decade is the tubulization technique for small nerve gaps. A disadvantage in the use of non-biodegradable tubes is that the material often has to be removed owing to its mechanical properties. Some investigators, in exploring the use of collagen tubes, being a natural biodegradable material, found either allogenicity or xenogenicity and immune responses that may inhibit nerve regeneration. Processed porcine collagen (PPC) is a new inert and biodegradable material that has a favorable effect on wound healing, as demonstrated by experiments on other tissues. The aim of our study was to compare the healing of nerve sutures with PPC tubes with conventional end-to-end sutures. In our experiments, we reconstructed the saphenous nerves of 27 rabbits. In series 1 (n = 12) and 2 (n = 12), PPC tubes were slid over an end-to-end nerve suture without or with a 10-mm nerve gap, respectively. In series 3 (n = 12), conventional suturing was performed in the collateral saphenous nerves of the animals of series 1. Epineurial suturing was performed. Three other non-operated saphenous nerves served as controls. The healing was studied after 3, 6, and 12 months in sections stained by monoclonal antibodies and by conventional histologic staining. Morphometric analysis of the regenerating axons was done by using confocal scanning laser microscopy (CLSM). Data analysis was carried out using a software program especially developed for this purpose. All results were evaluated statistically. Our results showed that during the healing period in the distal nerve stump, the number of axons of the PPC procedure with a 10-mm gap was significantly higher than that in the procedure without a gap. At 12 months, the mean number of axons of all procedures was significantly lower than in the non-operated nerve, and the mean axon diameter in all distal stumps did not differ significantly from that of the non-operated nerve. In the distal nerve stump, the ratio of total axon area to total fascicle area in the PPC procedure with a gap was significantly higher than that in the conventional suturing procedure. After 12 months, there was no significant difference between the percentages of axon outgrowth of the PPC procedure without a gap, the conventional suturing procedure, and the non-operated nerve (100%). The percentage of axon outgrowth in PPC with a gap was significantly higher than in the other procedures.

Animals↗

Impaired peripheral nerve regeneration in diabetes mellitus.

Diabetes mellitus impairs peripheral nerve regeneration. Regenerative failure likely exacerbates deficits from polyneuropathy or focal neuropathies in patients who might otherwise exhibit spontaneous improvement. Some focal neuropathies, like carpal tunnel syndrome, are common, yet render ongoing disability because of their delayed recovery. Why diabetic nerves fail to regenerate is an interesting question to consider because several mechanisms likely contribute. In this review, we examine a number of these causes. These causes include microangiopathy or disease of small blood vessels, failure to provide proper metabolic support for repair, defects in the entry and actions of inflammatory cells within the injury milieu, less robust support of axons by their Schwann cells, and lack of a full repertoire of trophic factors. A number of the mechanisms that generate neuropathy in the first place also likely contribute to failed regenerative programs, but how they do so is not clear.

Animals↗

Rerouting peripheral nerves for spinal cord lesions.

To provide control of paralyzed limb muscles following spinal cord lesions, peripheral nerves containing motor axons from motoneurons located above a spinal cord lesion could potentially be rerouted to nerves containing motor axons located below the spinal cord lesion. To test this hypothesis in rats, the distal end of a cut tibial nerve, innervated by the L4-6 spinal level, was anastomosed or rerouted to the central end of the cut femoral nerve, innervated by the L3-4 spinal level. Appropriate controls were used. Recovery of lower hind limb motor function was followed at regular intervals, measuring the twitch tension of toe flexion (innervated by the tibial nerve) induced by transcutaneous stimulation of nerve rootlets exiting the spinal cord. After 4-6 months, 54% of motor function returned in the experimental group. Retrograde transport of horseradish peroxidase from the gastrocnemius muscles to spinal motoneuron cell bodies confirmed that the innervation of this group was at a higher level. Furthermore, after an L4 spinal transection, twitch tension responses to spinal cord outlet stimulation remained only in the experimental group. Therefore, a peripheral nerve containing motor axons from above the lesion was rerouted to a distal peripheral nerve to control muscles that would have otherwise been denervated.

Animals↗

Recognition and uptake of human diabetic peripheral nerve myelin by macrophages.

Macrophages recognize and ingest several human proteins whose amino groups have been modified in vitro by specific chemical reagents. Because amino groups of human peripheral nerve myelin proteins become covalently modified in vivo by products of nonenzymatic glycosylation, we examined myelin/macrophage interactions using peripheral nerve myelin prepared from diabetic and nondiabetic patients. Intracellular accumulation of diabetic myelin increased with concentration in an apparently saturable fashion, reaching levels 3-4 times higher than those of age-matched nondiabetic samples. Low-temperature inhibition of cellular myelin accumulation further suggested that diabetic myelin uptake was associated with adsorptive endocytosis. Macrophage recognition and accumulation of nondiabetic myelin glycosylated in vitro increased with duration of sugar incubation, to a level nearly nine times that of the same sample incubated in buffer alone. Data from competition experiments with albumin and myelin glycosylated in vitro showed that recognition of human peripheral nerve myelin proteins by macrophages is specific for protein-bound products of nonenzymatic glycosylation. In vivo, such macrophage recognition of and interaction with nonenzymatic glycosylation products on diabetic peripheral nerve myelin could contribute to the pathogenesis of segmental demyelination.

Adult↗

Clinicopathologic analysis of 124 biopsy-proven peripheral nerve diseases.

We reviewed dinical, histological and ultrastructural findings of 124 cases of sural nerve biopsy specimens to delineate the trends of peripheral nerve diseases in our institute. Eighty-one were men and 43 were women. We categorized them into five groups: specific diagnosis (66 cases, 53.2%), axonal degeneration type (47 cases, 37.9%), demyelinating type (4 cases, 3.2%), mixed axonal degeneration-demyelinating type (6 cases, 4.8%) and normal (1 case, 0.9%). Cases with specific diagnosis included 21 inflammatory demyelinating polyneuropathy (15 chronic inflammatory demyelinating polyradiculoneuropathy, 6 Guillain-Barre disease), 13 hereditary motor and sensory neuropathy (7 Charcot-Marie-Tooth type I, 6 Charcot-Marie-Tooth type II), 10 vasculitis, 6 toxic neuropathy, 4 leprosy, 3 diabetic neuropathy, 2 alcoholic neuropathy, 1 Fabry's disease and other specific diseases (5 cases). In our cases, the proportion of specific diagnoses was higher, while the proportion of demyelinating peripheral neuropathies and normal were lower than those of Western series. The results of this study indicate that 1) a dose clinicopathologic correlation is important to make a precise diagnosis of peripheral nerve biopsy, 2) Biopsy under strict indication may reduce unnecessary histologic examination, 3) There is no difference in disease pattern of peripheral neuropathy between Western people and Koreans.

Adult↗

Localization and inhibition of calcium-activated neutral protease (CANP) in primate skeletal muscle and peripheral nerve.

Localization of calcium-activated neutral protease in normal monkey (Cebus apella) skeletal muscle and peripheral nerve was studied by application of the indirect immunofluorescent and peroxidase-antiperoxidase techniques for light and electron microscopy. In muscle, the protease was demonstrated in association with endomysial collagen fibrils, basal lamina, sarcolemma, and Z-bands and also at neuromuscular junctions. In nerve, the enzyme was demonstrated in association with endoneurial collagen fibrils, basal lamina, axolemma, and neurofilaments of both myelinated and unmyelinated axons. Intramuscular injections of the thiol protease inhibitor, leupeptin, abolished Ca-activated neutral protease immunoreactivity in both muscle and peripheral nerve. These data suggest that the protease is localized both intracellularly and extracellularly in normal primate muscle and peripheral nerve. Inhibition of basal lamina associated neutral protease by leupeptin after denervation may hold significance for protecting this structure against degradation and preserving it as a neurotrophic lattice for axon regeneration.

Animals↗

Techniques for diagnosis of peripheral nerve loss.

The diagnosis of a peripheral nerve loss is an exacting clinical procedure. This requires a basic knowledge of anatomy, including the variations and anomalies. This also includes various specific tests, such as testing for vibratory sensibility with tuning forks, the presence or absence of sweating, the evaluation of sensibility with two-point discrimination, and the von Frey pressure test. Motor function should be evaluated as to both quantity and quality of impairment. The indications for blocking adjacent nerves with local anesthetic agent are defined and cannot be overemphasized. Electrodiagnostic studies and vascular testing are important for a complete clinical evaluation. The significance of the interrelationship between the nervous system and the vascular system and their relationship in assessing end results should be considered on an individual basis in every case.

Diagnosis, Differential↗

[Impairment of peripheral nerve excitability].

Functional abnormalities, especially the excitability changes of axon in the peripheral nerve involvement, were reviewed. In GBS and CIDP, the correlation between conduction block and anti-ganglioside antibodies have been discussed. Using anti GM1 antibody positive sera, the suppression of voltage-gated sodium channels (VGSC) has been reported. Although this findings have not been confirmed, the involvement of VGSC may be an important mechanism for eliciting conduction block. In Isaacs' syndrome, voltage-gated potassium channels (VGKC) were suppressed by autoantibodies to VGKC. Furthermore, in generalized myokymia syndrome which shows only myokymia and muscle cramp without grip myotonia, VGKCs are also suppressed in some cases. These findings suggest that some patients with myokymia and neuromyotonia are induced by anti-VGKC antibodies. For evaluating the axonal excitability in vivo, the threshold electrotonus method have been developed and applied for the involvement of peripheral nerves. In ALS, impairment of potassium conductance was shown and was speculated to have the possible rrelation with fasciculation. Thus threshold electrotonus method will be an important method for evaluating axonal excitability in human. The accumulated knowledge about the involvement of axonal ion channels will expand and will be categorized as axonal channelopathies.

Axons↗

Peripheral nerve regeneration through blind-ended semipermeable guidance channels: effect of the molecular weight cutoff.

Synthetic nerve guidance channels are used to better understand the cellular and molecular events controlling peripheral nerve regeneration. In the present study, the contribution of wound-healing molecules to peripheral nerve regeneration was assessed by varying the molecular weight cutoff of the tubular membrane. Nerve regeneration through polysulfone tubular membranes with molecular weight (Mw) cutoffs of 10(5) and 10(6) Da was analyzed in a transected hamster sciatic nerve model. Cohorts of 6 animals received tubes of either type for 4 or 8 weeks with the distal end of the polymer tube capped. Other cohorts of 6 animals received tubes of either type for 4 weeks with the distal nerve stump secured within the guidance channel so as to create a 4 or 8 mm gap between both nerve stumps. Both types of channels contained regenerated tissue cables extending to the distal end of the guidance channel at both 4 and 8 weeks in the absence of a distal nerve stump. The cables regenerated in the 10(5) Da channels were composed of nerve fascicles surrounded by a loose epineurial sheath, whereas those regenerated in the 10(6) Da channels were composed mainly of granulation tissue. The numbers of myelinated and unmyelinated axons were significantly greater in the 10(5) Da than in the 10(6) Da channels at both 4 and 8 weeks. Both types of channel contained regenerated tissue cables with numerous nerve fascicles when the distal nerve stump was present with either gap length. However, when the gap distance was 8 mm, the 10(6) Da channels contained significantly fewer myelinated axons than the 10(5) Da channels. The present study reveals that the Mw cutoff of a semipermeable guidance channel strongly influences the outcome of peripheral nerve regeneration, possibly by controlling the exchange of molecules between the channel's lumen and the external wound-healing environment. These results suggest that the wound-healing environment secretes humoral factors that can either promote or inhibit the nerve-regeneration process.

Animals↗

Axonal regeneration after crush injury of rat central nervous system fibres innervating peripheral nerve grafts.

Recent experimental studies in adult rodents indicate that neurons in many regions of the brain and spinal cord are capable of extensive axonal growth along peripheral nerve grafts inserted into the C.N.S. To explore further the capacity of damaged intrinsic C.N.S. neurons to initiate and sustain fibre growth we have studied the regenerative response of brain stem and spinal neurons to the crushing of their axons after such axons had already grown across peripheral nerve 'bridges' linking both these levels of the neuraxis. In adult rats, an autologous segment of sciatic nerve approximately 4 cm long was used to connect the medulla oblongata and the lower cervical spinal cord. After 6-42 weeks, when C.N.S. axons are known to have regenerated across these 'bridges', the nerve grafts were crushed near both their rostral and caudal insertions into the C.N.S. Axonal regeneration beyond the sites of injury was investigated 4-11 weeks after crush by retrogradely labelling C.N.S. neurons with horseradish peroxidase (HRP) applied 1 cm away from the injured site, along the assumed course of the C.N.S. fibres regrowing across the graft. The number and distribution of HRP-labelled neurons was found to be similar to that in rats with uncrushed grafts. To prove that such axonal regrowth from spinal and brain stem nerve cells did originate from injury of central nerve fibres innervating the graft and not by sprouting from undamaged C.N.S. neurons at both ends of the 'bridge', we first labelled with the fluorescent dye Fast Blue (FB) the cells whose axons were interrupted by the crush and, after two weeks, applied a second dye, Nuclear Yellow (NY) 1 cm beyond the site of injury. The presence of FB and NY double-labelled C.N.S. neurons in these animals, together with the results of the HRP-labelling experiments, suggest that central neurons whose axons innervate peripheral nerve grafts are capable of renewed growth after axonal injury. Under such experimental conditions these intrinsic C.N.S. neurons respond to axonal interruption in a manner that resembles the responses of cells that normally project along peripheral nerves. We believe this to be an additional indication of the powerful role in regeneration of interactions between neurons and the axonal environment.

Animals↗

An analytical model to predict the electric field and excitation zones due to magnetic stimulation of peripheral nerves.

The main unknown factor in understanding magnetic stimulation of peripheral nerves is the distribution of the induced electric field. We have applied the so-called reciprocity theorem and developed an analytical model to compute the electric field and its spatial derivatives inside pseudocylindrical structures. The results can be used to predict the site of excitation in magnetic stimulation of peripheral nerves.

Computer Simulation↗

Pathological findings on peripheral nerves, lymph nodes, and visceral organs of leprosy.

Pathological findings in a) 103 autopsies, b) biopsy material of peripheral nerve tissue from 210 tuberculoid patients, and c) inguinal lymph nodes from 106 leprosy cases are presented. Overall, lesions in peripheral nerves were most common in the ulnar (85.7% in the TT type, 98.3% in LL), peroneal (77.8% in TT, 97.9% in LL), median (80% in TT, 90.2% in LL), radial (66.6% in TT, 82% in LL), and the great auricular, tibial and supraorbital nerves. The ratio of bilateral nerve involvement in the same nerve was higher than unilateral involvement (approximately 5:1). Lesions of the peripheral nerve ganglion were seen in the LL type (22 cases, 61.1%) and the TT type (8 cases, 53.3%). These have seldom been mentioned in past literature. Superficial lymph nodes were most commonly affected in all types of leprosy. Lymph nodes in the hepatic and splenic portal areas were sometimes involved in lepromatous or borderline cases. Between the two polar types of leprosy, the lesions in the lymph nodes showed gradual transitions in a spectrum-like pattern which were similar to the changes in the lesions in the skin. In lepromatous leprosy, lesions could be found in 85.3% of the cases in the liver, 41.1% in the spleen, 86.7% in the testes, approximately 50% in the upper respiratory tract (including 36.4% in the nasopharynx), and 34.4% in the adrenal gland. Three cases had ophthalmologic lesions. In borderline leprosy, biphasic lesions of leprosy were found in various internal organs.(ABSTRACT TRUNCATED AT 250 WORDS)

Humans↗