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PubMed1985

Retrograde effect of muscle on forms of acetylcholinesterase in peripheral nerves.

In the peripheral nerves of birds and mammals, acetylcholinesterase (AChE) exists in four main molecular forms (G1, G2, G4, and A12). The two heaviest forms (G4 and A12) are carried by rapid axoplasmic transport, whereas the two lightest forms (G1 and G2) are probably much more slowly transported. Here we report that nerves innervating fast-twitch (F nerves) and slow-twitch (S nerves) muscles of the rabbit differ both in their AChE molecular form patterns and in their anterograde and retrograde axonal transport parameters. Since we had previously shown a selective regulation of this enzyme in fast and slow parts of rabbit semimembranosus muscle, we wondered whether the differences observed in the nerve could be affected by the twitch properties of muscle. The results reported here show that in F nerves that reinnervate slow-twitch muscles, both the AChE molecular form patterns and axonal transport parameters turn into those of the S nerve. These data suggest the existence of a retrograde specific effect exerted by the muscles on their respective motoneurons.

Acetylcholinesterase↗
PubMedDate not supplied

Peripheral nerve injury and repair.

Peripheral nerve injuries are common, and there is no easily available formula for successful treatment. Incomplete injuries are most frequent. Seddon classified nerve injuries into three categories: neurapraxia, axonotmesis, and neurotmesis. After complete axonal transection, the neuron undergoes a number of degenerative processes, followed by attempts at regeneration. A distal growth cone seeks out connections with the degenerated distal fiber. The current surgical standard is epineurial repair with nylon suture. To span gaps that primary repair cannot bridge without excessive tension, nerve-cable interfascicular auto-grafts are employed. Unfortunately, results of nerve repair to date have been no better than fair, with only 50% of patients regaining useful function. There is much ongoing research regarding pharmacologic agents, immune system modulators, enhancing factors, and entubulation chambers. Clinically applicable developments from these investigations will continue to improve the results of treatment of nerve injuries.

Humans↗
PubMed2004

Successful removal of a knotted fascia iliaca catheter: principles of patient positioning for peripheral nerve catheter extraction.

Peripheral nerve catheters are typically advanced a substantial distance into a perineural sheath, theoretically increasing the risk of catheter knotting and kinking. In this case report, we describe successful removal of a knotted fascia iliaca catheter and discuss principles of nonsurgical catheter extraction. A 64-yr-old woman with bilateral coxarthrosis presented for total hip arthroplasty under combined general/regional anesthesia. A 20-gauge fascia iliaca catheter was inserted before surgery by using a loss-of-resistance "double pop" technique. The catheter was uneventfully advanced 10 cm past the needle tip. After injection of 30 mL of 0.5% bupivacaine with 1:200,000 epinephrine and 100 microg of clonidine, general anesthesia was induced. An infusion of 0.1% bupivacaine at 20 mL/h was initiated in the recovery room for postoperative analgesia. Approximately 48 h later, resistance was encountered during catheter removal. Catheter extraction was attempted by altering patient positioning, including the supine position during which the catheter placement had occurred. Successful catheter removal was achieved by decreasing tension on the fascia lata and fascia iliaca through flexion of the hip joint and by applying firm, steady traction. The catheter was removed intact with a knot approximately 2 cm from the distal tip. We conclude that the principles for removal of entrapped peripheral catheters are not well known and may differ from those for neuraxial catheters. Patient positioning to minimize pressure and tension on the perineural soft tissues may facilitate catheter removal.

Arthroplasty, Replacement, Hip↗
PubMed1990

Maturation of peripheral nerves in preterm infants. Motor and proprioceptive nerve conduction.

The peripheral nerve maturation (proprioceptive and motor nerve conduction velocities (PNCV and MNCV] was studied in 3 groups of newborn babies. Two groups of premature babies (PT), studied when they reached the expected date of birth (group I, gestational age (GA) at birth 27-31 weeks, n = 13, group II, GA at birth 32-35 weeks, n = 9), were compared to 10 normal full-term newborns (FT). The MNCV of PT babies was similar to that of FT babies: group I 22.8 +/- 3.3 m/sec (X +/- S.D.), group II 24.9 +/- 4.3 m/sec, FT 25.7 +/- 3.9 m/sec. PNCV was significantly lower in group I (18.1 +/- 5.9 m/sec) than in group II (28.3 +/- 6.4 m/sec) and in FT babies (32.0 +/- 7.4 m/sec) (P less than 0.001). Such a delay in maturation could be partly responsible for the neurological impairment often observed in PT babies.

H-Reflex↗
PubMedDate not supplied

A rodent model of organophosphorus-induced delayed neuropathy: distribution of central (spinal cord) and peripheral nerve damage.

Central and peripheral nerve fibre damage has been produced in Long-Evans hooded male rats with tri-ortho-cresyl phosphate. Animals were dosed by gavage with intermittent or daily amounts of the organophosphate and examined after 2, 6, 12, 18 and 24 weeks. The distribution of central nervous system (spinal cord) damage and the differential vulnerability among various peripheral nerves supported a "dying-back' classification for the neuropathy. Giant axonal swellings, containing massive accumulations of smooth endoplasmic reticulum, hallmarked the neuropathy. In spite of severe neurological damage the animals displayed only moderate functional disturbances. These findings have shown that the rat is highly sensitive to the structural damage caused by organo-phosphates, although resistant to the ataxia.

Animals↗
PubMed1989

Suppression by cyclosporine of cellular and humoral reactivity after peripheral nerve allografts in mice.

Peripheral nerve allografting has been the subject of many experimental and clinical studies. As yet, however, no successful method has been established. One reason is the lack of detailed studies on the immune response under different conditions. We examined both the cellular and humoral immune responses in fresh sciatic nerve allografts in inbred mice, using a mixed lymphocyte culture reaction and a lymphocyte-mediated cytotoxicity to examine cellular immunity and a complement-dependent cytotoxicity test to examine humoral immunity. Enhanced MLC activity against donor allogenic major histocompatibility complex antigens was demonstrated, and specific cytotoxic T cell activity and the production of specific antigens in serum also were observed. Thus peripheral nerve tissue exhibited potent immunogenicity. We used cyclosporine, an immunosuppressive agent, to suppress the immune response and obtain favorable nerve regeneration. We performed immunologic and histologic studies to establish a causal relationship. Administration of 20 mg of CsA suppressed both the cellular and humoral immune response to levels comparable to those seen in isografting. Histologic examination disclosed favorable regeneration of axons, also comparable to that seen in isografts.

Animals↗
PubMed1996

Nerve-regenerating effect of 15-deoxyspergualin. Peripheral nerve allotransplants in the rat.

We studied the effect of two immunosuppressive agents, 15-deoxyspergualin and cyclosporine A, on various nerve allografts in inbred rats whose major histocompatibility complex was mismatched. As allografts, we used the sciatic nerve (20 mm) and the saphenous nerve (20 mm). We found that 1) fresh peripheral nerve allografts with a short course of 15-deoxyspergualin and cyclosporine A therapy induced more regenerated axons than autografts did, 2) a short course of 15-deoxyspergualin therapy provided better nerve regeneration than cyclosporine A therapy in all forms of nerve allografts and large caliber nerve allografts induced more regenerated axons.

Animals↗
PubMed1996

Nerve regeneration and origin of Schwann cells in peripheral nerve allografts in immunologically pretreated rats.

For peripheral nerve allografts, the conditions for successful nerve regeneration and the possibility of transplanting Schwann cells were examined using a model of pretreated rats. Incomplete immunosuppression was achieved in recipient rats with donor red blood cell infusions given before allogeneic nerve grafting (RBC group). The origin of Schwann cells in the grafts was assessed by immunohistochemical staining from 1 week to 12 weeks after transplantation. In the RBC group, the replacement of donor Schwann cells by recipient cells was detected at 3-8 weeks, with the graft being filled with many of these cells at all times, and successful nerve regeneration was seen after 12 weeks on morphometric and electrophysiologic evaluations. In peripheral nerve allografts, pretreatment with donor-specific blood transfusion did not induce significant immunosuppression compared with allotransplantations of some tissues and organs. Clinically, if the state of immunosuppression can be controlled by RBC transfusion, it is possible that donor tissues may be replaced by recipient tissues and that nerves will regenerate successfully.

Animals↗
PubMedDate not supplied

Age-dependent VEGF expression and intraneural neovascularization during regeneration of peripheral nerves.

The physiologic ability of peripheral nerves to regenerate after injury is impaired with aging. However, the mechanisms responsible for this phenomenon are still incompletely characterized. In this study, we investigated whether aging influences the intraneural angiogenic response that occurs after injury and during regeneration of peripheral nerves. We performed a crush injury of the sciatic nerve in old and senescence accelerated mice and found that the peripheral nerves of these animals are unable to locally upregulate vascular endothelial growth factor (VEGF), a prototypical angiogenic cytokine, after injury and have substantial deficits in mounting an appropriate intraneural angiogenic response during nerve regeneration. Our findings provide new evidence of possible interdependent relationships between aging, VEGF, angiogenesis, and nerve regeneration and suggest that vascular abnormalities might play a role in aging-associated neurological dysfunction, with potentially important fundamental and clinical implications.

Aging↗
PubMed1989

Regrowth of retinal ganglion cell axons into a peripheral nerve graft in the adult hamster is enhanced by a concurrent optic nerve crush.

Transplantation of a segment of peripheral nerve to the retina of the adult hamster resulted in regrowth of damaged ganglion cell axons into the graft, with the fastest regenerating axons extending at 2 mm/day after an initial delay of 4.5 days (Cho and So 1987b). In this study, the effect of making 2 lesions on the same axon (the conditioning lesion effect) on the regrowth of ganglion cell axons into the peripheral nerve graft was examined. When a conditioning lesion (first lesion) was made by crushing the optic nerve 7 or 14 days before the peripheral nerve grafting (the second lesion) to the retina, the distance of regrowth achieved by the fastest regenerating axons in the graft, measured at the 7th post-grafting day, was lower than in animals with a peripheral nerve grafted to a normal eye. This indicated that in contrast to the situation in peripheral nerve axons (Forman et al. 1980) and goldfish optic axons (Edwards et al. 1981), the conditioning lesion was unable to enhance the regrowth of mammalian retinal ganglion cell axons. However, when crushing of the optic nerve was followed immediately by peripheral nerve grafting, an enhancement in axonal regrowth could be observed. The initial delay time before the axons extended into the peripheral nerve graft was reduced by 1 day while the rate of elongation of the fastest regrowing axons in the graft apparently remained unchanged. Moreover, the shortening of the initial delay could still be observed even when the sequence of performing the 2 lesions was reversed.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2005

Regulation of cholesterol/lipid biosynthetic genes by Egr2/Krox20 during peripheral nerve myelination.

Myelination of peripheral nerves by Schwann cells requires a large amount of lipid and cholesterol biosynthesis. To understand the transcriptional coordination of the myelination process, we have investigated the developmental relationship between early growth response 2 (Egr2)/Krox20--a pivotal regulator of peripheral nerve myelination--and the sterol regulatory element binding protein (SREBP) pathway, which controls expression of cholesterol/lipid biosynthetic genes. During myelination of sciatic nerve, there is a very significant induction of SREBP1 and SREBP2, as well as their target genes, suggesting that the SREBP transactivators are important regulators in the myelination process. Egr2/Krox20 does not appear to directly regulate the levels of SREBP pathway components, but rather, we found that Egr2/Krox20 and SREBP transactivators can synergistically activate promoters of several SREBP target genes, indicating that direct induction of cholesterol/lipid biosynthetic genes by Egr2/Krox20 is a part of the myelination program regulated by this transactivator.

Animals↗
PubMed2005

Different expressions of BDNF, NT3, and NT4 in muscle and nerve after various types of peripheral nerve injuries.

The changes in the expression of brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), and neurotrophin-4 (NT-4) in the rat neuromuscular system as a result of three different types of sciatic nerve injuries have been evaluated. The changes in mRNA and protein levels for BDNF, NT-3, and NT-4 in the soleus muscle and sciatic nerve were assessed 4-28 days after sciatic nerve transection (neurotmesis), sciatic nerve crush (axonotmesis), and mild acute compression (neurapraxia). BDNF mRNA levels increased dramatically with nerve transection in the soleus muscle and the sciatic nerve 7-14 days after injury, whereas the changes were low in other types of injury. The changes of protein levels for BDNF were also similar. The mRNA and the protein levels of NT-3 in the soleus muscle did not show any significant difference. The mRNA for NT-4 in the soleus muscle decreased from 4 to 14 days after sciatic nerve transection, and the protein level was also minimum 14 days after sciatic nerve transection. Our results indicate that the neurotrophic factors in the neuromuscular system could play a role in differentiating peripheral nerve injury.

Analysis of Variance↗
PubMed1988

Occurrence and isotype of antibodies against peripheral nerve myelin in serum from patients with peripheral neuropathy and healthy controls.

Antibodies against peripheral nerve myelin have previously been demonstrated in serum from patients with peripheral neuropathy and IgM paraproteinaemia, and a causal relationship has been suggested. Using enzyme-linked immunosorbent assay (ELISA), anti-myelin antibodies were found in sera from eight of 16 patients with polyneuropathy and paraproteinaemia, but also in 17% of 109 patients with peripheral neuropathy lacking monoclonal immunoglobulin, including five of 10 patients with Charcot-Marie-Tooth disease, and in 16% of 142 blood donors. The antibodies were mostly of IgM class in the two neuropathy groups, while blood donors had mostly IgA antibodies, and a few subjects of each group had antimyelin antibodies of two different isotypes. Western blot confirmed the ELISA results in a majority of antibody positive sera and revealed a 25-30 kD myelin target antigen for sera from the three groups, and for some of the non-paraproteinaemic sera also a 100 kD myelin target antigen. Our results demonstrate that the presence of serum autoantibodies against peripheral nerve myelin does not necessarily indicate a pathological event.

Adult↗
PubMed1986

Electrodiagnostic evaluation of peripheral nerve injuries.

Electrodiagnostic studies of peripheral nerve function remain a valuable adjunct to a thorough clinical examination. The electromyogram and sensory evoked response of the peripheral nerve aid in determining the diagnosis and severity of some neuropathies. The use of signal averaging microprocessors to enhance small evoked responses is adding another dimension in electrodiagnostic studies. This tool provides evaluation of the peripheral nervous system in conjunction with the central nervous system. The intraoperative use of electrodiagnostic studies is readily performed using widely available equipment, but does require a thorough understanding of the equipment used. The equipment, principles, and helpful hints in applying electrodiagnostic techniques to the evaluation of peripheral nerves is reviewed.

Action Potentials↗
PubMed2005

An experimental model of an electrical injury to the peripheral nerve.

OBJECTIVE: Injury to the peripheral nerves is a common complication found in patients suffering from electrical burns. At present, there are many kinds of experimental models for electrical injury, but no report describes an animal-based experimental model for a relatively simple electrical injury to the peripheral nerves. We have designed and constructed a specific device to generate increasingly severe electrical shocks of a known voltage for the experiment. This device can simulate injuries of different degrees (minor, medium and severe) caused by shock to the right sciatic nerve of rats. METHOD: Thirty Sprague-Dawley rats were randomly divided into Group I (3600 V, n=10), Group II (1000 V, n=10) and Group III (500 V, n=10). The voltage required for the electrical shock was generated by the above-mentioned device and was adjusted to deliver 3600, 1000 and 500 V, respectively. The specific voltage, as mentioned above, was delivered three times to the right sciatic nerve of the rats. The shock duration was set to last for 10 ms. The time interval between the shocks was 3 min. Three rats were randomly selected from each group to observe changes in the morphology, electric physiology of the nerve and their histology the first, second and fourth week after injury. RESULTS: All rats survived the injuries. Leg function was partially impaired and swellings occurred on the injured extremity. However, by the second week after the injury the rats had recovered. Digit ulcers were observed by the fourth week after injury in Groups I and II. Neural electric physiology showed that the recovery rate of the neural conduction velocity (RNCV) disappeared in part or in whole immediately after the injury in experimental rats. RNCV recovered up to 65% in Group III and to 7% in Group II by the fourth week after injury, however, RNCV did not recover in Group I at all. Histology showed that blood vessel embolism occurred within the injured nerve. A large number of nerve fibres experienced Waller degeneration while the myelin sheath was vacuolated. The neural plate disintegrated largely by the first week after injury and the myelin sheath disintegrated into a loose structure by the second week after injury in Group I. Group II displayed a similar situation as Group I, wherein some nerve fibres experienced Waller degeneration and disintegration. Regenerative myelin appeared in some rats at about the fourth week after injury. The following changes were seen in Group III: The degree of neural injuries was different. The point of entry of the electric currents showed obvious Waller degeneration and disintegration of the myelin sheath, while some nerves showed a regenerated myelin sheath by the second week after injury. The morphology (such as quantity and diameter) of the injured myelin was basically normal by the fourth week after injury. CONCLUSION: This device can produce controlled injuries to the sciatic nerve giving different degrees of severity (minor, medium and severe), by means of varying the electrical shock voltage and shock duration on the rats. It is a useful model for experimental studies of injuries to peripheral nerves.

Animals↗