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Results for “Peripheral Nerves”

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PubMed1989

[Review of the morphological changes in peripheral nerves in experimental diabetes mellitus].

A survey of morphological changes of myelinated nerve fibers of peripheral nerves recorded in experimental streptozotocin induced diabetes mellitus in rats is presented. Causes of discordant interpretations of findings are considered and pathogenetic mechanisms involved in morphological changes of myelinated nerve fibers of peripheral nerves observed in this model of diabetes mellitus are discussed. (Ref. 41.)

Animals↗
PubMed1998

Chronic inflammatory demyelinating polyradiculoneuropathy with diffuse and massive peripheral nerve hypertrophy: distinctive clinical and magnetic resonance imaging features.

We present 3 patients with chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) with extensive and diffuse hypertrophy of the nerve roots and peripheral nerves. They exhibited slowly progressive sensory impairment and distally predominant limb weakness and muscular atrophy, and markedly enlarged palpable nerve trunks. They responded beneficially to corticosteroid. Magnetic resonance imaging demonstrated diffuse and extensive hypertrophy of the peripheral nerves in the four limbs and the spinal nerve roots, with gadolinium enhancement in the nerve roots but not in the peripheral nerves. These patients were considered to have a hypertrophic variant of CIDP.

Aged↗
PubMed1982

Peripheral nerve phospholipid composition: development in normal nerve and age-dependent changes in Wallerian degenerated nerve.

The phospholipid composition of normal peripheral nerve as a function of developmental age as well as that of Wallerian-degenerated nerve as a function of age at nerve transection and duration of Wallerian degeneration have been quantitated in rabbit sciatic nerve. During development, increases in the proportions of ethanolamine plasmalogen, sphingomyelin, and combined phosphatidyl serine plus phosphatidyl inositol and decreases in the proportions of phosphatidyl choline and phosphatidyl ethanolamine correlated well with the concurrent myelin accretion. During Wallerian degeneration, age-dependent changes in phospholipid composition were observed. The large and statistically significant increase in the proportion of phosphatidyl choline and decrease in the proportion of ethanolamine plasmalogen were manifest promptly in nerves transected at 2 weeks of age but in a delayed manner in nerves transected at 8, 12, and 20 weeks of age. The rate of loss of individual phospholipids was greater in nerves transected at younger ages. The findings from normal developing peripheral nerve may well serve as baseline data for subsequent studies of phospholipid composition in pathological peripheral nerve. The findings from Wallerian-degenerated peripheral nerve provide additional evidence for age-dependent chemical changes occurring in Wallerian-degenerated peripheral nerve that may be of significance in explaining the superior functional recovery from peripheral nerve injury observed in younger compared with older subjects.

Aging↗
PubMed2002

Low-level exposures to organophosphorus esters and peripheral nerve function.

This review evaluates the epidemiological and clinical evidence linking low-level and prolonged exposures to organophosphorus esters, used as insecticides or nerve agents, to peripheral nerve dysfunction. The clinical effects of large doses of these chemicals-including the cholinergic syndrome, the intermediate syndrome, and the delayed polyneuropathy-are all well established and are summarized. Based on these clinical observations and experimental studies, dose-effect relationships indicate that peripheral neuropathy always develops after cholinergic toxicity. However, several studies have suggested that this relationship may be different after low-level prolonged exposures, as, for instance, those experienced by Gulf War veterans and British sheep farmers, thereby leading to the development of peripheral neuropathy without preceding cholinergic toxicity. A critical assessment of these studies, involving subjects with either current or past exposures, indicates that changes in peripheral nerve function were mild, inconsistent, and unexplained and that most studies lack exposure data. Suggestions made about individual hypersusceptibility to delayed polyneuropathy lack support. It is concluded that there is no evidence of peripheral nerve dysfunction caused by low-level prolonged exposures to organophosphate insecticides or nerve agents.

Animals↗
PubMed1992

The distribution of neural crest-derived Schwann cells from subsets of brachial spinal segments into the peripheral nerves innervating the chick forelimb.

Neural crest cells from brachial levels of the neural tube populate the ventral roots, spinal nerves, and peripheral nerves of the chick forelimb where they give rise to Schwann cells. The distribution of neural crest cells in the developing forelimb was examined using homotopic and heterotopic chick-quail chimeras to label neural crest cells from subsets of the brachial spinal segments. Neural crest cells from particular regions of the spinal cord populated ventral roots and spinal nerves adjacent to or immediately posterior to the graft. Crest cells also populated the brachial plexus in accord with their segmental origins. In the forelimb, neural crest cells populated muscle nerves with anterior brachial spinal segments populating nerves to anterior musculature of the forelimb and posterior brachial spinal segments populating nerves to posterior musculature. Similar patterns were seen following both homotopic and heterotopic transplantation. In both types of grafts, the distribution of neural crest cells largely matched the sensory and motor projection pattern from the same spinal segmental level. This suggests that neural crest-derived Schwann cells from a particular spinal segment may use sensory and motor fibers emerging from the same segmental level as substrates to guide their migration into the periphery.

Animals↗
PubMed1984

[Antigens of human peripheral nerves].

The antigens of the peripheral nerves in man were studied by immuno and physicochemical methods. The composition of the peripheral nerves was shown to include antigens of wide specificity which can be found in many organs and tissues of the body. Moreover, antigens of narrow specificity (of the peripheral and the central nervous system) and a specific antigen of the peripheral nerves were identified. Separate peripheral nerves do not differ from each other according to the specific antigens. The specific antigen is thermostable, resistant to the acids and urea and does not fall into sedimentation at 100% saturation with ammonium sulphite. By electrophoretic mobility (similar to serum gamma-globulins) it belongs to cathode proteins. In accordance to its properties, it is designated as a gamma-neurospecific antigen (gamma-NSA).

Adolescent↗
PubMed1994

Magnetic resonance imaging signal changes in denervated muscles after peripheral nerve injury.

The evaluation of peripheral nerve disorders has traditionally relied on a clinical history, physical examination, and electrodiagnostic studies. Recent studies have used magnetic resonance imaging (MRI) to evaluate a variety of both nerve and muscle disorders. In this article, we describe the use of MRI, using short-tau inversion recovery (STIR) sequences, to evaluate muscle signal characteristics in a variety of peripheral nerve disorders. A total of 32 patients were studied, and 12 representative cases are discussed in detail. Increased STIR signal in muscle was seen in cases of severe axonotmetic injuries involving the transection of axons producing severe denervation changes on electromyography. The increased STIR signal in denervated muscles was seen as early as 4 days after the onset of clinical symptoms, which is significantly earlier than changes detected on electromyography. The MRI signal changes were reversible when the recovery of motor function occurred as a result of further muscle innervation. In cases of neurapraxic nerve injuries, characterized by conduction block without axonal loss, the STIR signal in muscle was normal. These findings show that MRI using STIR sequences provides a panoramic visual representation of denervated muscles useful in localizing and grading the severity of peripheral nerve injury secondary to either disease or trauma. MRI using STIR sequences may therefore play an important role in the prediction of clinical outcome and the formulation of appropriate therapy early after peripheral nerve injury.

Adolescent↗
PubMed1991

A case for transmitter plasticity at the molecular level: axotomy-induced VIP increase in the upper spinal dorsal horn is related to blockade of retrograde axoplasmic transport of nerve growth factor in the peripheral nerve.

Blockade of retrograde axoplasmic transport in peripheral nerves, by means of perineurally applied microtubule inhibitors, results in an increased vasoactive intestinal polypeptide (VIP) reaction of the segmentally related, ipsilateral upper dorsal horn. Similar effect is elicited by the perineural application of an anti-Nerve Growth Factor (anti-NGF) serum. At the same time, both treatments result in depletion of Substance P from the same region of the spinal cord. It is assumed that this striking example of transmitter plasticity, obviously taking place at the molecular level, is due to a stimulating effect of NGF upon the perikaryal Substance P-synthesizing mechanism in dorsal root ganglion cells, and the inhibitory effect of NGF upon the VIP synthesizing machinery in these same nerve cells.

Animals↗
PubMed1991

A monoclonal antibody against HSV type 1 ribonucleotide reductase cross-reacts with the P0 protein of peripheral nerve myelin.

An epitope on peripheral nerve myelin was detected by the use of a mouse monoclonal antibody directed against the 38 kDa subunit of herpes simplex virus (HSV) type 1 ribonucleotide reductase. Immunohistochemistry showed reactivity solely in PNS myelin. In nerve roots there was a sharp border in transitional zones to the negative CNS myelin. The immunoreactivity was found in rat, guinea pig, bovine and human peripheral nerves. Western blot analysis of peripheral nerve myelin as well as purified P0 revealed a distinctly stained band corresponding to a molecular weight of approximately 29 kDa. The present finding of a shared antigenic determinant between HSV ribonucleotide reductase and peripheral nerve P0 may be of pathogenetic relevance in virus induced demyelinating diseases in the peripheral nervous system.

Animals↗
PubMed2003

Oxidized galectin-1 stimulates the migration of Schwann cells from both proximal and distal stumps of transected nerves and promotes axonal regeneration after peripheral nerve injury.

Oxidized galectin-1 has recently been identified as a key factor that plays important roles in initial axonal growth in injured peripheral nerves. The aim of this study was to investigate the effects of oxidized galectin-1 on regeneration of rat spinal nerves using acellular autografts (containing no viable cells) and allografts (containing no cell membranes) with special attention to the relationship between axonal regeneration and Schwann cell migration. Immunohistochemically, endogenous galectin-1 was expressed in dorsal root ganglion (DRG) neurons, spinal cord motoneurons, and axons and Schwann cells in normal sciatic nerves. Administration of oxidized recombinant human galectin-1 (rh-gal-lox, 5 ng/ml) in autograft model promoted axonal regeneration from motoneurons as well as from DRG neurons; this was confirmed by a fluorogold tracer study (p < 0.05). Anti-rh-gal-1 antibody (30 microg/ml) strongly inhibited axonal regrowth (p < 0.05). Pretreatment of allografts with rh-gal-lox stimulated the migration of Schwann cells not only from proximal stumps but also from distal stumps into the grafts, resulting in accelerated axonal regeneration (p < 0.05). Moreover, Schwann cell migration preceded the axonal growth in the presence of exogenous rh-gal-lox in the grafts. These results strongly suggest that local administration of exogenous rh-gal-lox promotes the migration of Schwann cells followed by axonal regeneration from both motor and sensory neurons, resulting in acceleration of neuronal repair. This technique may also be of value in the repair of human nerves.

Animals↗
PubMed1996

The influence of predegenerated nerve grafts on axonal regeneration from prelesioned peripheral nerves.

Recent in vitro work has indicated that predegenerated segments of peripheral nerve are more capable of supporting neurite growth from adult neurons than fresh segments of nerve, whereas previous in vivo studies which investigated whether predegenerated nerve segments used as grafts are capable of enhancing axonal regeneration produced conflicting results. We have reinvestigated this question by using predegenerated nerve grafts in combination with conditioning lesions of the host nerve to determine the optimal conditions for obtaining the maximal degree of regeneration of myelinated axons. The sciatic nerve of adult Dark Agouti rats were sectioned at midthigh level, and the distal portion was allowed to predegenerate for 0, 6 or 12 d in situ. 10-15 mm lengths of these distal nerve segments were then syngenically grafted onto the central stumps of sciatic nerves which had themselves received a conditioning lesion 0, 6, and 12 d previously, making a total of 9 different donor-host combinations. The grafts were assessed histologically 3 or 8 wk after grafting. Axonal regeneration in the 9 different donor-host combinations was determined by counting the numbers of myelinated axons in transverse sections through the grafts. All grafts examined contained regenerating myelinated axons. The rats given a 3 wk postgrafting survival period had an average of between 1400 and 5300 such axons. The rats given an 8 wk postgrafting survival period had between about 13,000 and 25,000 regenerating myelinated axons. Analysis of variance revealed significant main effects for both the Donor and Host conditions as well as Weeks (i.e. survival period after grafting). These results indicate that both a conditioning lesion of the host neurons and the degree of predegeneration of peripheral nerve segments to be used as grafts are of importance in influencing the degree of axonal regeneration. Of these 2 factors the conditioning lesion of the host appears to have the greater effect on the final number of regenerating myelinated axons.

Animals↗
PubMed2004

Beneficial effect of nerve growth factor-7S on peripheral nerve regeneration through inside-out vein grafts: an experimental study.

This study investigated the effect of local administration of nerve growth factor-7S (NGF-7S) on the axonal regrowth of mixed peripheral nerves through inside-out vein grafts. Sixty male Wistar rats were randomized into two groups (n = 30). A defect 12 mm long in the right sciatic nerve was created and repaired with an inside-out vein graft from the right jugular vein. NGF-7S (group A) or phosphate-buffered saline (group B; control) was locally administered daily during the first 3 weeks. Walking-track analysis and electrophysiological and histological-morphometric studies were carried out 4, 6, 8, 10, and 12 weeks postoperatively (subgroups a, b, c, d, and e, respectively, n = 6 each). Data analysis showed that 1) the recovery of motor function, as measured by walk pattern analysis and evoked muscle action potential, and 2) the orientation, number, myelin thickness, and diameter of myelinated fibers were better in the NGF-7S than in the control group. These findings present strong evidence of the beneficial effect of NGF-7S on peripheral nerve regeneration through inside-out vein grafts.

Analysis of Variance↗
PubMed2002

Metalloproteinase-dependent predegeneration in vitro enhances axonal regeneration within acellular peripheral nerve grafts.

Injury to peripheral nerve initiates a degenerative process that converts the denervated nerve from a suppressive environment to one that promotes axonal regeneration. We investigated the role of matrix metalloproteinases (MMPs) in this degenerative process and whether effective predegenerated nerve grafts could be produced in vitro. Rat peripheral nerve explants were cultured for 1-7 d in various media, and their neurite-promoting activity was assessed by cryoculture assay, in which neurons are grown directly on nerve sections. The neurite-promoting activity of cultured nerves increased rapidly and, compared with uncultured nerve, a maximum increase of 72% resulted by 2 d of culture in the presence of serum. Remarkably, the neurite-promoting activity of short-term cultured nerves was also significantly better than nerves degenerated in vivo. We examined whether in vitro degeneration is MMP dependent and found that the MMP inhibitor N-[(2R)-2(hydroxamidocarbonylmethyl)-4-methylpantanoyl]-l-tryptophan methylamide primarily blocked the degenerative increase in neurite-promoting activity. In the absence of hematogenic macrophages, MMP-9 was trivial, whereas elevated MMP-2 expression and activation paralleled the increase in neurite-promoting activity. MMP-2 immunoreactivity localized to Schwann cells and the endoneurium and colocalized with gelatinolytic activity as demonstrated by in situ zymography. Finally, in vitro predegenerated nerves were tested as acellular grafts and, compared with normal acellular nerve grafts, axonal ingress in vivo was approximately doubled. We conclude that Schwann cell expression of MMP-2 plays a principal role in the degenerative process that enhances the regeneration-promoting properties of denervated nerve. Combined with their low immunogenicity, acellular nerve grafts activated by in vitro predegeneration may be a significant advancement for clinical nerve allografting.

Animals↗
PubMedDate not supplied

[Possibility of nerve lesions related to peripheral nerve blocks. A study of the human sciatic nerve using different needles].

UNLABELLED: When a needle tip comes too close to a nerve axon, the mechanical effect over the nerve membrane produces paresthesia. We examined the hypothetical mechanical damage of short bevel and long bevel needles over sciatic nerve bundles under scanning electron microscopy. METHODS: We obtained samples of sciatic nerve from three patients of 68, 74 and 76 years old. These samples were fixed, dehydrated and coated with gold microfilm for their observation under scanning electron microscopy. Ten short bevel needles and ten long bevel needles were studied under the same microscopic technique. We interpolated microscopic images from sciatic nerve samples and different needle bevels at various angles to study the mechanical damage of these needles to nerve axons. RESULTS: Sciatic nerve bundles were found 0.1 to 0.2 mm deep in the samples; information was given about the bevel length and angle of needles. The damage is perceptible under scanning electron microscopy, when the needle bevel is introduced 0.3-0.4 mm deep into the nerve bundle; here, the needle tip cuts through the perineurum, piercing the nerve bundle. At a depth of 1 mm, the lesion caused by short bevel needles is greater than that caused by long bevel needles. The type of epineural lesions caused by short bevel needles is also different from the ones caused by long bevel needles. CONCLUSIONS: Lesions that affect superficially the epineurum can cause paresthesia by compression of nerve fascicles without damaging the axons. If the perineurm is damaged, the lession will also affect the blood-nerve barrier, leading probably to posterior sequels.

Aged↗
PubMed1997

Loss of primary afferent nerve terminals in the brainstem after peripheral nerve transection: an anatomical study in monkeys.

In order to investigate the changes in the somatosensory organization that occur after a peripheral nerve injury, a purely sensory nerve (radial nerve - superficial branch) was divided in adult monkeys (Macaca fascicularis). The nerve ends were immediately rejoined by an epineural suturing technique. After 6-21 months the nerve investigated was exposed to an intra-axonal nerve tracer (horseradish peroxidase conjugate) in order to label the primary afferent terminals within the cuneate nucleus of the brainstem. The non-transected nerve on the contralateral side was similarly exposed and served as a control. Terminal labelling was seen throughout the cuneate nucleus, mainly in the middle of its rostro-caudal extension, and in this part it showed a patchy appearance superimposed on cell clusters within the pars rotunda. This pattern of distribution was seen both on the experimental and control sides. On the experimental side there was an obvious loss of terminal labelling within the terminal field as estimated using an image-analysing system: Compared with the contralateral side the median loss (peroxidase activity) was 83% and between 6 and 21 months only minor restoration of the terminal intensity was observed. These results in the primate confirm earlier results in the cat that transection and microsurgical repair of a sensory nerve causes a considerable loss of neurons capable of intraaxonal transport.

Animals↗
PubMed1991

Do neuropeptides in the dorsal horn change if the dorsal root ganglion cell death that normally accompanies peripheral nerve transection is prevented?

Peripheral nerve section causes the death of dorsal root ganglion cells and changes in neuroactive peptides in the dorsal horn of the spinal cord. The relationship between these 2 events has not been previously studied, however. One approach would be to prevent sensory cell death and then determine changes in peptide immunoreactivity. To do this, transected rat sciatic nerve stumps were placed in an impermeable silicone tube for one month. The tube was then removed and after 30 additional days the cells were counted. The data indicate that no cell death occurred. We conclude that the sensory cells are first saved due to some factor present in the tube, and then after 30 days, the cells become independent of the tube and its contents. In these same animals, all of the peptides we examined were significantly changed. Four of the peptides, calcitonin gene-related peptide (CGRP), substance P (SP), cholecystokinin octapeptide (CCK) and galanin (GAL) were significantly depleted in the medial L4-L5 superficial dorsal horn, and vasoactive intestinal polypeptide (VIP) was significantly increased. We conclude that there are major changes in spinal peptide systems following peripheral nerve transection even if there is no accompanying death of sensory neurons. Thus we suggest that dramatic central changes in peptide immunoreactivity following peripheral nerve transection are independent of the sensory cell death that usually occurs in response to this injury.

Animals↗