Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Peripheral Nerves”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 55 records · Page 3Linked to original sources

Median nerve neurotization by peripheral nerve grafts directly implanted into the spinal cord: anatomical, behavioural and electrophysiological evidences of sensorimotor recovery.

Over the years, peripheral nerve grafts, a favorable environment to support axonal elongation, have given rise to increasing interest as a possible solution for promoting spinal cord repair. In the experiments described here, following an avulsion injury of the rat brachial plexus, the median nerve was repaired by a peripheral nerve graft (PN) inserted directly into the dorsal side of the spinal cord. Eight months later the animals were submitted to behavioral tests, electrophysiological and histological studies. Regrowth of axons from both motoneurons and ganglionic neurons was demonstrated following a single superficial dorsal implantation of a PN. Sensorimotor peripheral reinnervation allowed most of the studied animals to recover enough flexor activity for grasping. Reinnervation was achieved even without prior root avulsion suggesting that the presence of a PN is sufficient to induce sprouting in the spinal cord from axotomized and non-axotomized neurons.

Animals↗

Nerve regeneration through a healthy peripheral nerve trunk as a nerve conduit: a preliminary study of a new concept in peripheral nerve surgery.

The popularity of nerve conduits has increased recently due to the need for alternative nerve reconstruction techniques, obviating the harvest of nerve grafts. Based on ideas suggesting nerve tissue itself, which was the most physiologic environment for nerve regeneration, a study using 40 sciatic nerves of 20 rats was performed. The proximal stumps of transected peroneal nerves were sutured to the lateral wall of healthy tibial nerve trunks after removal of the epineurium. Twelve weeks later, tissue samples were taken from the anastomosis sites and from the levels above and below these sites. Configurations of fascicles were evaluated, and numbers of fibers were estimated. It was observed that the fibers of peroneal nerves regenerated into and through the tibial nerve trunk distally. This suggested that active regenerating fibers of a proximal stump of a nerve could regenerate and progress as a fascicular unit in optimum condition at the trunk of another healthy nerve. This preliminary study should stimulate further studies based on this new concept: that a nerve trunk can serve as the host for the regenerating fibers of another nerve.

Animals↗

Vein conduits with interposition of nerve tissue for peripheral nerve defects.

Vein conduits with interposition of autogenous nerve tissue were used in 16 peripheral nerves to reconstruct defects of between 2.0 and 5.8 cm. This technique was applied in nine digital nerves, four ulnar nerves, two median nerves, and one radial sensory nerve. A single vein conduit was used in digital nerve defects and two or three vein segments were used in defects of nerve trunks. Nerve tissue was sectioned from the proximal nerve stump and inserted inside the vein conduits. Follow-up of 2.5 to 3.5 years has revealed motor recovery to M4 in three nerves, M3+ in three, M2 in one nerve, and sensory recovery to S4 in two nerves, S3+ in five, S3 in four, S2+ in three and S0 in two nerves. Signs of muscle reinnervation of the repaired nerves were noted on electromyography. Two digital nerves with defects of over 5.0 cm did not show any signs of sensory recovery. Sectioning and placement of autogenous nerve tissue is thought to create fresh and additional sources for the release of neurotropic factors, and may serve to convey the neurotropic effect over a longer distance. This clinical study suggests that vein conduits with the interposition of nerve tissue is a practical and reliable procedure for nerve defects between 2.0 cm and 4.5 cm.

Adolescent↗

Peripheral nerve entrapments.

Peripheral nerve entrapment is a rare, but important, cause of foot and ankle pain that often is underdiagnosed and mistreated. A peripheral nerve may become entrapped anywhere along its course, but certain anatomic locations are characteristic. Clinically,nerve entrapment is divided into three stages: in stage I patients feel rest pain and intermittent paresthesias which are worse at night; in stage II, continued nerve compression leads to paresthesias, numbness, and, occasionally, muscle weakness that does not disappear during the day, and in stage III, patients describe constant pain, muscle atrophy, and permanent sensory loss. Diagnostic confusion abounds because of the multiple etiologies of peripheral nerve entrapments and their complex physical and temporal relation. A thorough understanding of the causes of peripheral nerve entrapments, the anatomic course and variation of the peripheral nerves, the diagnostic modalities, and the treatment options can simplify this complex problem.

Diagnosis, Differential↗

Case of dementia and myoclonia in an adult associated with anomalies in polyunsaturated fatty acids in leukocytes and peripheral nerve. An ultrastructural study of peripheral nerve.

We report a case of a 66-year-old patient presenting with abnormal movements and associated dementia. Death occurred 4 years after the onset of symptoms. In spite of the lack of autopsy results, the picture was one of late onset neuronal ceroid lipofuscinosis (Kufs' disease). Ultrastructural study of a peripheral nerve biopsy sample indicated a process of demyelination associated with unusual inclusions in Schwann cell cytoplasm. Biochemical analysis of the same sample and leukocytes showed considerable alterations in polyunsaturated fatty acid levels. These findings are discussed in the light of work on cases of infantile neuronal ceroid lipofuscinosis.

Aged↗

Lectin histochemistry of normal and neoplastic peripheral nerve sheath. 1. Lectin binding pattern of normal peripheral nerve in man.

The binding patterns of lectins to normal peripheral nerves were examined. Twelve biotinylated lectins were used in this study; Canavalia ensiformis (Con A), Pisum sativum (PSA), Lens culinaris (LCA), Ricinus communis 1 (RCA-1), Arachis hypogaea (PNA), Glycine max (SBA), Sophora japonica (SJA), Bandeiraea simplicifolia 1 (BSL-1), Triticum vulgaris (WGA), succinylated WGA (s-WGA), Ulex europaeus 1 (UEA-1) and Helix pomatia (HPA). Cytoplasm of Schwann cells and perineurial cells was stained by Con A, PSA, LCA, s-WGA and WGA. PNA showed specific binding to perineurial cells, while after neuraminidase treatment stain with this lectin was demonstrated also in Schwann cells. Myelin sheaths were stained with fewer lectins. SBA and HPA with sialic acid removal rarely showed reactivity to the peripheral nerve structure in surgical specimens, in contrast to clear staining of Schwann cells, perineurial cells and myelin sheaths in autopsy specimens. The present study shows distinct lectin stainings of specific structures of the normal human peripheral nerves, and provides important basic information on the alterations of lectin binding patterns during pathological processes in the peripheral nerves.

Biotin↗

Quantitative analysis of myelinated nerve fibers of peripheral nerve in streptozotocin-induced diabetes mellitus.

The purpose of this study was to examine morphometric changes of myelinated fibers in early stages of experimental diabetes mellitus. Adult male Wistar rats aged 17 wk were used in this study. Diabetes mellitus was induced by streptozotocin. Samples of common peroneal nerve from diabetic rats (4 and 8 wk after induction of diabetes mellitus) and age-matched control animals were removed and processed. The semithin cross sections were stained with toluidine blue and used for myelinated fiber computer-aided morphometric analysis. There were no significant changes in diabetic animals after 4 wk duration of the disease. There was significant reduction in myelinated nerve fiber caliber in diabetic rats 8 wk after induction of diabetes as compared to age-matched controls. There was no significant reduction of axonal area in this group of diabetic rats, so diminution of fiber area was caused predominantly by reduction of myelin sheath area. The study demonstrates that the induction of diabetes mellitus in rat by streptozotocin is accompanied by early changes of the morphometric indices of myelinated nerve fibers of peripheral nerve.

Animals↗

Methodological issues in size estimation of myelinated nerve fibers in peripheral nerves.

Size estimation of myelinated nerve fibers in peripheral nerves is a very common task in neuromorphology and different dedicated morpho-quantitative procedures have been devised and used to date. Unfortunately, many reports on experimental nerve studies lack comprehensive information on the procedures that have been designed and applied for myelinated fiber size estimation. This paper addresses the issue in the light of the recent advances in quantitative morphology that have recognized the concept of unbiased estimates as the key methodological issue to be addressed in morpho-quantitative studies. The potential foundations of bias at various study levels are analysed together with indications on how to cope with them. In addition, the issue of the precision of size estimates is addressed and the various geometrical parameters that can be selected for myelinated nerve fiber size assessment are outlined. Taken together, information provided in this paper is expected to help investigators conduct an appropriate preliminary study design phase, the key step for setting up the most adequate morpho-quantitative procedure for any given research goal.

Animals↗

Epithelioid sarcoma of the median nerve mimicking a peripheral nerve sheath tumour.

We describe a case of epithelioid sarcoma of the median nerve in a 57-year-old woman presenting with symptoms and signs of carpal tunnel syndrome for 2 years. The clinical examination was suggestive of a wrist ganglion compressing the median nerve. Magnetic resonance imaging (MRI) showed a 5 cm x 3 cm mass involving the median nerve in the carpal tunnel and appearances mimicked a benign peripheral nerve sheath tumour. This report illustrates a rare tumour presenting in a rare location and emphasizes the atypical clinical and MRI features that should alert the radiologist to the possibility of a rare sarcoma mimicking a benign peripheral nerve sheath tumour.

Diagnosis, Differential↗

Changes in the spinal terminal pattern of the superficial radial nerve after a peripheral nerve injury. An anatomical study in cats.

The occurrence of changes within the spinal cord over a long period after a peripheral nerve injury was investigated in adult cats. The lateral superficial branch of the radial nerve was exposed and transsected unilaterally. In one group the nerve endings were re-approximated with epineural sutures and in the other group the proximal nerve stump was enclosed to prevent regeneration. After a survival period of 4-17 months the same nerve on both sides was exposed to an intra-axonal nerve tracer, lectin-conjugated horseradish peroxidase, to label the nerve terminals within the spinal gray matter by transganglionic transport. The general distribution of the terminal field was almost the same after suturing as after encapsulation of the transsected nerve, except for a slightly more cranial location of the terminal area after suturing compared with the control side. The terminal area comprised laminae I-IV of the fifth cervical to the first thoracic spinal segment, concentrated towards the sixth to eighth cervical segments. This distribution was the same as on the control side, but the experimental and control sides differed in intensity of terminals. There was a loss of terminals throughout the terminal field in both operated groups, but after nerve suture there was some recovery of terminal intensity between 4 and 17 months after the injury.

Animals↗

Phosphatidylinositol 3-kinase and Akt nonautonomously promote perineurial glial growth in Drosophila peripheral nerves.

Drosophila peripheral nerves, structured similarly to their mammalian counterparts, comprise a layer of motor and sensory axons wrapped by an inner peripheral glia (analogous to the mammalian Schwann cell) and an outer perineurial glia (analogous to the mammalian perineurium). Growth and proliferation within mammalian peripheral nerves are increased by Ras pathway activation: loss-of-function mutations in Nf1, which encodes the Ras inhibitor neurofibromin, cause the human genetic disorder neurofibromatosis, which is characterized by formation of neurofibromas (tumors of peripheral nerves). However, the signaling pathways that control nerve growth downstream of Ras remain incompletely characterized. Here we show that expression specifically within the Drosophila peripheral glia of the constitutively active Ras(V12) increases perineurial glial thickness. Using chromosomal loss-of-function mutations and transgenes encoding dominant-negative and constitutively active proteins, we show that this nonautonomous effect of Ras(V12) is mediated by the Ras effector phosphatidylinositol 3-kinase (PI3K) and its downstream kinase Akt. We also show that the nonautonomous, growth-promoting effects of activated PI3K are suppressed by coexpression within the peripheral glia of FOXO+ (forkhead box O) a transcription factor inhibited by Akt-dependent phosphorylation. We suggest that Ras-PI3K-Akt activity in the peripheral glia promotes growth of the perineurial glia by inhibiting FOXO. In mammalian peripheral nerves, the Schwann cell releases several growth factors that affect the proliferative properties of neighbors. Some of these factors are oversecreted in Nf1 mutants. Our results raise the possibility that neurofibroma formation in individuals with neurofibromatosis might result in part from a Ras-PI3K-Akt-dependent inhibition of FOXO within Schwann cells.

Animals↗

The influence of donor age on cografting of adrenal medulla with pretransected peripheral nerve.

Pretransected peripheral nerve has been demonstrated to enhance the survival of cografted adrenal medullary chromaffin cells and the recovery of host dopaminergic (DA) systems in animal models of Parkinson's disease. In the present study, we examined the effect of donor age on survival of cografted chromaffin cells. Adrenal medulla and pretransected peripheral nerve from young (1-month-old) or aging (12-month-old) donors were cografted into the striatum of MPTP-treated young (2-month-old) C57/BL mice. Although chromaffin cell survivability was increased by cografting with pretransected peripheral nerve despite donor age, survivability of chromaffin cells from aging donors was less than that using young donors. Image analysis of striatal DA fibers and chemical analysis of striatal DA showed that cografting with pretransected peripheral nerve enhanced the recovery of striatal DA systems more prominently than adrenal grafting alone. However, this effect was less in mice receiving aging donor tissues compared with mice receiving young donor tissues.

Adrenal Medulla↗

Peripheral nerve amyloidosis.

Peripheral nerve amyloidosis is the cardinal feature of familial amyloid polyneuropathy (FAP) but can also be seen in primary light chain (AL) amyloidosis and dialysis (beta 2-microglobulin) related amyloidosis. The generalized neuropathy seen in all forms of peripheral nerve amyloidosis is similar, characterized by a severe progressive mixed neuropathy with autonomic dysfunction. Pathologically, amyloid is found in the peripheral nervous system as amorphous, eosinophilic, extracellular deposits. FAP is most commonly associated with variant plasma transthyretin (TTR), although it has also been described in association with mutant apolipoprotein A-1 and gelsolin. There are now at least 36 point mutations in the TTR gene associated with FAP and these continue to be described. Recent studies on the possible role individual point mutations in the TTR gene may play in amyloidosis have helped give us an insight into the mechanisms behind peripheral nerve amyloidosis. This article reviews the clinical and pathological features of the peripheral nerve amyloidosis and discusses theories of amyloidogenesis based on studies of FAP.

Amino Acid Sequence↗

Sports and peripheral nerve injury.

Peripheral nerve injury is one of the serious complications of athletic injuries; however, they have rarely been reported. According to the report by Takazawa et al., there were only 28 cases of peripheral nerve injury among 9,550 cases of sports injuries which had been treated in the previous 5 years at the clinic of the Japanese Athletic Association. The authors have encountered 1,167 cases of peripheral nerve injury during the past 18 years. Sixty-six of these cases were related to sports (5.7%). The nerves most frequently involved were: brachial plexus, radial nerve, ulnar, peroneal, and axillary nerves (in their order of frequency). The most common causes of such injuries were mountain climbing, gymnastics, and baseball. More often, peripheral nerve injury seemed to be caused by continuous compression and repeated trauma to the involved nerve. Usually it appeared as an entrapment neuropathy and the symptoms could be improved by conservative treatment. Some of the cases were complicated by fractures and surgical exploration became necessary. Results of treatment produced excellent to good improvement in 87.9% of the cases. With regard to compartment syndrome, the authors stress the importance of early and precise diagnosis and a fasciotomy.

Adolescent↗

Using intact nerve to bridge peripheral nerve defects: an alternative to the use of nerve grafts.

This preliminary study was conducted to determine whether a regenerating peripheral nerve in a rat model can use the epineurium of an intact nerve to bridge a nerve gap defect. To create the intact nerve bridge a 1-cm segment of the peroneal nerve is resected leaving a gap defect. The proximal and distal peroneal nerve stumps are sutured 1-cm apart, in an end-to-side fashion, to the epineurium of the intact tibial nerve. The following experimental groups were used (n = 12): group A, immediate primary repair of resected segment; group B, intact nerve bridge technique; group C, nerve autograft; and group D, gap in situ control. Evaluation 12 weeks after surgery included measurement of the tibialis anterior muscle contraction force, axonal counting, wet weight of the tibialis anterior muscle, and histologic examination. The results of this animal study support 3 main conclusions: regenerating axons can use the epineurium of an intact nerve to bridge a gap in nerve continuity; when using functional recovery to assess regeneration, there is no significant difference between standard nerve autografts and the intact nerve bridge technique; and based on histologic examination, the intact nerve bridge technique does not injure the intact tibial nerve used to bridge the gap defect. Taken together, the results of this preliminary animal study suggest that the intact nerve bridge technique may be a potential alternative to standard nerve autografts in appropriate circumstances. Further investigation in a higher animal model is warranted before considering clinical application of the intact nerve bridge technique.

Analysis of Variance↗

Altered sodium channel expression in second-order spinal sensory neurons contributes to pain after peripheral nerve injury.

Peripheral nerve injury is known to upregulate the rapidly repriming Na(v)1.3 sodium channel within first-order spinal sensory neurons. In this study, we hypothesized that (1) after peripheral nerve injury, second-order dorsal horn neurons abnormally express Na(v)1.3, which (2) contributes to the responsiveness of these dorsal horn neurons and to pain-related behaviors. To test these hypotheses, adult rats underwent chronic constriction injury (CCI) of the sciatic nerve. Ten days after CCI, allodynia and hyperalgesia were evident. In situ hybridization, quantitative reverse transcription-PCR, and immunocytochemical analysis revealed upregulation of Na(v)1.3 in dorsal horn nociceptive neurons but not in astrocytes or microglia, and unit recordings demonstrated hyperresponsiveness of dorsal horn sensory neurons. Intrathecal antisense oligodeoxynucleotides targeting Na(v)1.3 decreased the expression of Na(v)1.3 mRNA and protein, reduced the hyperresponsiveness of dorsal horn neurons, and attenuated pain-related behaviors after CCI, all of which returned after cessation of antisense delivery. These results demonstrate for the first time that sodium channel expression is altered within higher-order spinal sensory neurons after peripheral nerve injury and suggest a link between misexpression of the Na(v)1.3 sodium channel and central mechanisms that contribute to neuropathic pain after peripheral nerve injury.

Animals↗

[Role of grafted Schwann cells in the regeneration of intraspinal nerve fibers when peripheral nerve, skeletal muscle or submandibular gland fragments are transplanted into the spinal cord of the mouse].

Small pieces of peripheral nerve, skeletal muscle or submandibular gland, taken from young or new-born mice, were grafted into the non-transected spinal cord of young albino mice, at the thoracic level, through a punctiform meningeal opening. Neighbouring intraspinal nerve fibres, severed during the grafting process, regenerate into and eventually throughout the transplants. In this regenerative process, sedentary or migrating Schwann cells of the transplants probably have a prominent influence in guiding the growth of the axonal sprouts they ensheathe and eventually myelinate.

Animals↗