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At least 829 records · Page 46Linked to original sources
PubMed1993

Quality control functions of the Visual Field Reading Center (VFRC) for the Optic Neuritis Treatment Trial (ONTT).

The Visual Field Reading Center (VFRC) was established to assess visual field testing in the Optic Neuritis Treatment Trial (ONTT), to train and certify ONTT technicians, and to monitor the quality of the visual fields through evaluation of the technical aspects of the visual field testing. We describe the functions of the VFRC personnel and the standardized test protocols developed by the VFRC for Humphrey and Goldmann perimetry. We also describe the VFRC procedures for training and certifying visual field technicians, double-checking the eligibility of ONTT patients, assessing the quality of the visual field data, and processing visual field data. In addition, we describe the principles applied by the director and associate director of the VFRC in their clinical classification of the various localized and diffuse visual field defects observed in the Humphrey and Goldmann visual fields. The VFRC has processed more than 14,000 Humphrey and Goldmann visual field tests. The visual field quality control procedures and visual field defect classification process have been shown to be quite reproducible. Through quality control assessment procedures, we have been able to pinpoint a variety of problems at an early stage and promptly implement corrective measures. The standardized test protocols, technician training and certification procedures, and quality control assessment techniques used by the VFRC for the ONTT may serve as a model for future clinical trials employing visual field data as an outcome measure. These procedures can also be used to enhance visual field reliability in ophthalmological practices.

Education↗
PubMed1986

Acute cubital tunnel syndrome from post traumatic calcific neuritis.

The normal ulnar nerve is not visible on radiographs of the elbow. An unusual case is described in which symptoms of ulnar nerve compression with a swollen, tender ulnar nerve at the elbow developed after relatively minor trauma. Radiology suggested "Calcific Neuritis", but this was short lived with complete regression of the symptoms.

Calcinosis↗
PubMed1991

Sciatic neuritis as initial symptom of spontaneous clostridial myonecrosis.

A 21-year-old woman is reported with aplastic anaemia, who presented with pain in the leg. Rapid loss of sciatic nerve function followed. MRI showed irregular streaks of low intensity in the muscles of the pelvic region. A diagnosis of sciatic neuritis as initial symptom of clostridial myonecrosis was made.

Adult↗
PubMed1987

Ciclosporin A prevents P2 T cell line-mediated experimental autoimmune neuritis (AT-EAN) in rat.

Adoptive transfer experimental autoimmune neuritis (AT-EAN) produced in Lewis rats by injection of P2-reactive T lymphocyte line cells offers the unique possibility to study the exclusive contribution of cell-mediated immune responses to the pathogenesis of autoimmune disease of the peripheral nervous system (PNS). It further lends itself to the evaluation of novel therapeutic approaches that may bear relevance to the human acute Guillain-Barré syndrome. The effects of the immunosuppressive agent ciclosporin A on the clinical, electrophysiological and morphological expression of AT-EAN were examined. We found that ciclosporin A suppressed development of the disease. In view of the known actions of ciclosporin A on T cells, these results indicate the requirement of activation and clonal proliferation of T lymphocytes to produce myelin damage in autoimmune diseases of the PNS.

Animals↗
PubMed1989

Induction of experimental allergic neuritis with synthetic peptides from myelin P2 protein.

P2 protein and 4 synthetic peptides were tested for induction of experimental allergic neuritis (EAN). A peptide comprising the residues 62-78 of the bovine P2 protein sequence has been shown to contain an important neuritogenic determinant. A peptide comprising residues 66-78 produced no clinical symptoms of EAN. These results indicate that some or all of the residues 62 65 (Ile-Ser-Phe-Lys), are necessary for EAN induction.

Amino Acid Sequence↗
PubMed1991

Changes of ionic channel distribution in myelinated nerve fibres from rats with experimental allergic neuritis.

Voltage clamp experiments were performed in single myelinated nerve fibres of rats with experimental allergic neuritis (EAN). Nerve fibres from diseased animals showed a varying degree of demyelination. In fibres with extensive demyelination large K+ currents were measured. Analysis of the contribution of slow and fast K+ channels revealed that in these fibres the relative contribution of slow K+ channels was about 50% compared to about 25% in fibres acutely demyelinated as previously reported. This indicates that chronic demyelination changes the distinct distribution of ionic channels in the rat node of Ranvier.

Animals↗
PubMed1994

Apoptotic cell death of T-lymphocytes in experimental autoimmune neuritis of the Lewis rat.

The present study describes apoptosis of T-lymphocytes in the sciatic nerve in experimental autoimmune neuritis (EAN), a T-cell mediated disorder of the peripheral nervous system (PNS). Morphological signs characteristic for apoptotic cell death were found from day 4 onwards, peaking at day 7. Apoptosis of T-cells could be detected throughout the subsequent recovery period. In situ nick translation (ISNT) followed by immunocytochemical analysis confirmed the presence of DNA fragmentation in T-lymphocytes. We thus show for the first time that apoptosis is not a unique elimination mechanism of inflammatory T-cells in the central nervous system (CNS), but is operative in the PNS as well although at a lesser degree. Identifying the underlying mechanisms may provide a basis for the development of new therapeutic strategies in autoimmune disorders.

Animals↗
PubMed1995

Low-affinity nerve growth factor receptor expression in sciatic nerve during P2-peptide induced experimental allergic neuritis.

Northern blot, immunocytochemistry, and single nerve fiber immunostaining were used to determine the expression of low-affinity nerve growth factor (NGF) receptor (p75NGFR) in the peripheral nervous system of Lewis rats during the course of experimental allergic neuritis (EAN) induced with 100 micrograms of 'SP26' synthetic peptide, corresponding to residues 53-78 of bovine P2 myelin protein. This severe reversible polyneuropathy, characterized by extensive multifocal demyelination in nerve roots, and axonal degeneration within sciatic nerve, represents a useful tool to investigate Schwann cell gene expression in these different pathological conditions. Our results showed that both p75NGFR mRNA and protein were induced within sciatic nerve by day 18 and 23 after 'SP26' immunization. By this time, however, p75NGFR was not detectable in roots of cauda equina. These data demonstrate that, during EAN induced by immunization with 100 micrograms of 'SP26', p75NGFR is up-regulated in Schwann cells and in nerve fibers distally along the nerve. This suggests that the induction of the receptor in sciatic nerve during P2-peptide EAN is related to the loss of axonal contact by Schwann cells.

Animals↗
PubMed1995

Soluble complement receptor type 1 inhibits experimental autoimmune neuritis in Lewis rats.

Experimental autoimmune neuritis (EAN) in Lewis rats induced by immunization with bovine peripheral nerve myelin in complete Freund's adjuvant is an animal model of the human Guillain-Barré syndrome. In this study myelin-induced EAN was treated with 30 mg/kg per day human soluble complement receptor type 1 (sCR1) beginning on day 8 post immunization (p.i.). Clinical signs of disease were markedly suppressed by application of sCR1 and none of eight treated animals but seven of nine control rats developed paraparesis. Electrophysiologic examination of sciatic nerve function 13 days p.i. revealed faster nerve conduction velocities and significantly higher compound muscle action potentials in sCR1-injected animals. In sections of sciatic nerves acquired 16 days p.i. extended demyelination and axonal degeneration was prevented by treatment with sCR1 in vivo. Our findings underscore the functional importance of complement during inflammatory demyelination in the peripheral nervous system and suggest sCR1 as a potential therapeutic approach in these diseases.

Animals↗
PubMedDate not supplied

CT findings in acute optic neuritis.

A patient with unilateral optic neuritis with CT evidence of optic nerve enlargement and reduction in nerve size treatment is reported.

Acute Disease↗
PubMed1996

Availability of frequency-selective fat-saturation pulse (Fat-Sat) MRI in childhood optic neuritis.

A 2-year-old boy with acute optic neuritis, confirmed by gadolinium-DTPA enhancement of the optic nerve using frequency-selective fat-saturation pulse magnetic resonance imaging (Fat-Sat MRI), is reported. Because it is difficult in very young children to sufficiently evaluate visual acuity, visual field, and retroocular pain on eye movement, and visual evoked potential during wakefulness, Fat-Sat MRI will be useful for revealing optic nerve inflammation and for monitoring treatment.

Adipose Tissue↗
PubMed2006

Pain hypersensitivity in rats with experimental autoimmune neuritis, an animal model of human inflammatory demyelinating neuropathy.

Experimental autoimmune neuritis (EAN) is a T cell mediated autoimmune disease of the peripheral nervous system that serves as an animal model of the acute inflammatory demyelinating polyradiculoneuropathy in Guillain-Barre syndrome (GBS). Although pain is a common symptom of GBS occurring in 55-85% of cases, it is often overlooked and the underlying mechanisms are poorly understood. Here we examined whether animals with EAN exhibit signs of neuropathic pain including hyperalgesia and allodynia, and assessed their peripheral nerve autoimmune inflammation. We immunized Lewis rats with peripheral myelin P2 peptide (amino acids 57-81) emulsified with complete Freund's adjuvant, or with adjuvant only as control. P2-immunized rats developed mild to modest monophasic EAN with disease onset at day 8, peak at days 15-17, and full recovery by day 28 following immunization. Rats with EAN showed a significant decrease in withdrawal latency to thermal stimuli and withdrawal threshold to mechanical stimuli, in both hindpaws and forepaws, during the course of the disease. We observed a significant infiltration of T cells bearing alphabeta receptors, and a significant increase in antigen-presenting cells expressing MHC class II as well as macrophages, in EAN-affected rats. Our results demonstrate that animals with active EAN develop significant thermal hyperalgesia and mechanical allodynia, accompanied by pronounced autoimmune inflammation in peripheral nerves. These findings suggest that EAN is a useful model for the pain seen in many GBS patients, and may facilitate study of neuroimmune mechanisms underlying pain in autoimmune neuropathies.

Animals↗
PubMed2005

Activation of p38 mitogen-activated protein kinase in the early and peak phases of autoimmune neuritis in rat sciatic nerves.

To examine the involvement of p38 mitogen-activated protein kinase (MAPK) in autoimmune disorders of the peripheral nerve system, we analyzed the phosphorylation of p38 MAPK protein in the sciatic nerves of Lewis rats with experimental autoimmune neuritis (EAN). Western blot analysis showed that phosphorylated p38 (p-p38) MAPK protein was significantly increased in the sciatic nerves of rats in the early and peak phases of EAN, and declined gradually thereafter. Immunohistochemistry showed that p-p38 MAPK levels were increased in the infiltrating inflammatory cells, including T cells and macrophages, as well as in blood vessels and some Schwann cells in EAN-affected sciatic nerves, as compared to the sciatic nerves of controls. Some inflammatory cells and a few Schwann cells were also positive for TUNEL reaction at the peak and recovery phases of EAN. In conclusion, we postulate that the phosphorylation of p38 MAPK is involved in the elimination of infiltrating inflammatory cells during the course of EAN and may possibly modulate recovery in autoimmune disorders of the peripheral nervous system.

Animals↗
PubMed2006

Immunohistochemical study of caveolin-1 in the sciatic nerves of Lewis rats with experimental autoimmune neuritis.

The expression of caveolin-1 and the related molecule endothelial nitric oxide synthase (eNOS) was analyzed in the sciatic nerves of Lewis rats with experimental autoimmune neuritis (EAN). Western blot analysis showed that caveolin-1 significantly increased in the sciatic nerves with EAN upon initiation of cell infiltration during the early and peak stages (days 10 and 14 post-immunization, p.i.) and declined thereafter. The pattern of eNOS expression over the course of EAN largely matched that of caveolin-1. Immunohistochemistry showed that in EAN lesions, intense caveolin-1 immunostaining occurred in ED1-positive macrophages as well as in vessels, while the caveolin-1 immunoreaction was reduced in Schwann cells in the inflammatory lesions. Consequently, we postulated that caveolin-1 expression increased in the sciatic nerves with EAN; this possibly mediated either molecular trafficking or nitric oxide generation partly through the activation of eNOS in vascular endothelial cells, as well as in inflammatory macrophages in EAN and/or cellular apoptosis of inflammatory cells.

Animals↗
PubMed2006

Intermetatarsal compression neuritis.

Intermetatarsal compression neuritis can be a disabling condition. Individuals who don't respond well to initial treatments are left with persistent pain and frustration. The conservative approach to the treatment of neuromas includes shoe modifications, padding, orthotics, cortisone injections, and serial alcohol sclerosing injections. When a person has failed conservative treatment for a forefoot neuroma, surgery can be considered to alleviate pain and treat the condition. This article describes several different surgical approaches such as neurectomy, carbon dioxide laser, and neurolysis. Results to date show that decompression is similar to neurectomy surgery, if not more successful.

Decompression, Surgical↗
PubMed2003

Brachial neuritis following infection with Epstein-Barr virus.

A case of brachial neuritis after infection with Epstein-Barr virus in a 15-year-old girl is presented. A review of the literature contrasts the presenting features in children and adults. Diagnostic tests, treatment and prognosis are discussed.

Adolescent↗
PubMed2004

Anti-cytokine autoantibodies in experimental autoimmune neuritis in Lewis rats.

Experimental autoimmune neuritis (EAN) is a CD4+ T-cell-mediated, inflammatory demyelinating disease of the peripheral nervous system (PNS) that serves as a model for Guillain-Barre syndrome (GBS) in humans. Cytokine production has been suggested to act a pathogenic role for EAN. To study the potential role of cytokines in context with cytokine autoantibodies (Aabs) in EAN, we used in situ hybridization to detect mRNA expression of interferon (IFN)-gamma, tumor necrosis factor (TNF)-alpha, IL-4, IL-10, and transforming growth factor (TGF)-beta in lymph node mononuclear cell (MNC) and in sciatic nerve sections, as well as ELISA for detection of their autoantibodies in sera and cerebrospinal fluid (CSF) over the course of EAN. Increased mRNA expression for IFN-gamma and TNF-alpha was registered correlating with the peak of clinical signs of EAN, and high levels of mRNA expression for IL-4, IL-10, and TGF-beta were associated with EAN recovery. The levels of cytokine mRNAs were generally inversely correlated to their autoantibodies in serum and CSF, whereby the CSF levels were equal to or lower than the serum levels. Autoantibodies to IFN-gamma dose-dependently inhibited IFN-gamma-induced MHC expression by peritoneal macrophages proving a neutralizing biological effect of these autoantibodies. Our data demonstrate the existence of the anti-cytokine autoantibodies in the sera and CSF of rats with EAN; however, the role of anti-cytokine autoantibodies in the disease process of EAN remains to be resolved.

Animals↗
PubMed2005

Assessment of lesion evolution in experimental autoimmune neuritis by gadofluorine M-enhanced MR neurography.

Experimental autoimmune neuritis (EAN) represents an animal model of acute inflammatory nerve injury mirroring pathophysiological aspects of the human Guillain-Barré syndrome. In the present study, we for the first time visualized the spatiotemporal evolution of autoimmune nerve injury and recovery by magnetic resonance imaging (MRI) by use of the novel micellar magnetic resonance (MR) contrast agent gadofluorine M (Gf). EAN was induced in Lewis rats by T-cell transfer (AT-EAN) leading to severe axonal damage, and Gf was applied intravenously at various disease stages mostly 24 h before MRI. In naive rats, Gf enhancement was present solely in the vascular compartment. In AT-EAN, clinically asymptomatic rats already showed consistent Gf uptake in spinal nerves on day 3, while sciatic nerves were spared. The cauda equina correspondingly exhibited massive T-cell infiltration. Gf enhancement further extended to the plexus lumbosacralis on day 4. On days 5 and 6, the entire peripheral neuraxis from the cauda equina, along the sciatic down to the tibial and peroneal nerves, showed strong Gf enhancement. Spinal and peripheral nerves now exhibited massive inflammation and axonal injury on parallel histological analysis. Gf enhancement persisted in the afflicted nerves until complete recovery and disappeared with a proximodistal gradient. In conclusion, Gf-enhanced MR neurography opens a new avenue for monitoring nerve damage in-vivo during an immune attack.

Animals↗