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At least 1,009 records · Page 56Linked to original sources
PubMed1996

Anterior clinoid mucocele masquerading as retrobulbar neuritis.

Mucoceles arising from the anterior clinoid is rare. Although intrinsically benign, mucoceles in the sphenoid sinus (anterior clinoid variant) can lead to complications due to their proximity to other structures. We present a case of a young man whose visual complaints were typical for retrobulbar optic neuritis. Results of radiologic tests for diagnosis led us to the early detection of a surgically treatable condition, a sphenoid sinus mucocele (anterior clinoid variant). Early surgery was helpful in ameliorating the symptoms, leading to full recovery of visual function. The clinician should be aware of this rare entity with its presentation in a wide variety of signs and symptoms.

Adult↗
PubMed1992

Lumbosacral fusion in a patient with recurring Guillain-Barré syndrome and acute brachial neuritis.

A lumbar decompression and fusion with instrumentation was successfully completed on a patient with a history of acute brachial neuritis (ABN) and recurring Guillain Barré syndrome (GBS). Three weeks post-surgery there was a mild exacerbation of the GBS, which resolved with plasmapheresis. This case report shows that surgery may be conducted safely on a patient whose history includes GBS and ABN, without devastating neurological consequences.

Acute Disease↗
PubMed1997

Thalidomide suppresses T- and B-cell responses to myelin antigen in experimental allergic neuritis.

The effects of thalidomide and, for reference, dexamethasone on T- and B-cell functions were assayed in vitro in Lewis rats with experimental allergic neuritis induced by active immunization with bovine peripheral nerve myelin (BPM) and complete Freund's adjuvant. Thalidomide and dexamethasone at the concentration ranges 10(-5)-10(-7) g/ml and 4 x 10(-5)-4 x 10(-9) g/ml, respectively, both inhibited phytohemagglutinin (PHA)- and BPM-induced T-cell proliferation as well as levels of PHA- and BPM-reactive interferon (IFN)-gamma-secreting cells, reflecting the suppression of Th1-like cells. The effect of dexamethasone was most pronounced on PHA-induced T-cell proliferation and IFN-gamma secretion, whereas the effect of thalidomide was most pronounced on BPM-induced T-cell proliferation and IFN-gamma secretion. Thalidomide reduced the B-cell responses to both BPM and Mycobacterium tuberculosis purified protein derivative, but to a lesser extent than dexamethasone. The in vitro design described could be useful to evaluate compounds with putative immunomodulatory activities. The inhibitory effects of thalidomide on autoantigen-induced Th1-cell functions may warrant the use of this substance in T-cell-mediated autoimmune diseases.

Animals↗
PubMedDate not supplied

MR fat suppression combined with Gd-DTPA enhancement in optic neuritis and perineuritis.

A fat suppression MR technique used in combination with Gd-DTPA enhancement was investigated to determine its value in cases of inflammatory optic nerve lesions. This technique, the so-called hybrid method, is a derivative of the chopper fat suppression technique and provides water-only images without increasing the imaging or postprocessing time. The study group consisted of four patients with acute visual loss, all of whom received Gd-DTPA. Conventional T2-weighted and fat suppression post-Gd-DTPA T1-weighted images were obtained in all patients; in addition, in one patient a post-Gd-DTPA T1-weighted image without fat suppression was obtained. In three patients, the conventional T2-weighted images failed to reveal any abnormality. In contrast, the enhanced optic nerve and enhanced perineural inflammatory infiltrate were easily identified on T1-weighted images after administration of Gd-DTPA and application of fat suppression technique. The lesions in inflammatory optic neuritis or perineuritis were easily distinguished from the surrounding fat, which had been suppressed. This combined technique resulted in significantly improved definition of normal anatomic structures and made the enhancing lesions more conspicuous, especially in areas with large amounts of fat such as the retrobulbar orbit.

Adipose Tissue↗
PubMed1977

Attempts to induce chronic experimental allergic neuritis in strain 13 and Hartley guinea pigs.

An attempt has been made to develop a model of chronic experimental allergic neuritis (EAN) using juvenile and adult inbred (Strain 13) and Hartley guinea pigs sensitized with peripheral nerve in complete Freund's adjuvant. Animals were followed clinically for periods ranging from 2 to 44 weeks postinoculation and then sacrificed for light and electron microscopy. Out of a total of 39 animals, 16 showed either clinical signs or had histopathologic changes. The remaining 23 guinea pigs were free of any disease. The animals' age at inoculation and strain did not seem to affect either the clinical course or ultimate histopathologic changes. The 7 animals that had clinical EAN displayed signs ranging from weight loss and soiling to quadriparesis (one animal). The histologic changes consisted of meningeal and perivascular inflammation as well as peripheral nervous system (PNS) and central nervous system demyelination and remyelination. An interesting abnormality seen the nerve roots of several animals was the proliferation of Schwann cells around remyelinated PNS fibers reminiscent of the "onion-bulb" formations seen in human hypertrophic neuropathies. Because of the lack of ongoing demyelination, onion-bulb formation appeared in this case to be a secondary proliferation of Schwann cells after a single primary episode of demyelination. It is concluded from the present study that despite some interesting histopathologic changes, the animals studied were largely resistant both to acute as well as chronic EAN.

Age Factors↗
PubMed1984

Delayed onset of experimental allergic neuritis in rats treated with reserpine.

In delayed-type hypersensitivity most of the invading cells are not specifically sensitized against the initiating antigen but are augmenting cells called in by inflammatory mediators. It has been suggested that vasoactive amines, such as the monoamine serotonin, released by the action of sensitized T-cells on mast cells, may participate in the perivascular emigration of these cells that do not normally leave the blood. To test this hypothesis in experimental allergic neuritis (EAN), Lewis rats sensitized on day zero were treated with a single dose of the monoamine-depleting drug reserpine (2.5 mg/kg) immediately before the onset of early clinical signs on day nine (reserpine day 9, Rd9); during the onset of early clinical signs on day ten (Rd10); or immediately after the onset of early clinical signs on day 11 (Rd11). The results showed that the onset of early clinical signs was delayed in the Rd9 treated rats until approximately day thirteen whereas no effect on the course of the disease was observed in the Rd11 rats, and variable results were obtained in the Rd10 animals. Infiltration of mononuclear cells and leakage of 125I-albumin into the peripheral nerve was reduced in the Rd9 rats killed during the suppressed period. The delay in the onset of early clinical signs in the Rd9 rats correlated well with the time-course of serotonin depletion as reflected by levels in the peripheral blood of reserpine-treated normal animals. Although a role for histamine could not be demonstrated, the results suggest that other vasoactive amines are involved in the reaction. These results, therefore, would support the hypothesis that vasoactive amines play a role in the perivascular transit of inflammatory cells in EAN.

Albumins↗
PubMed1985

Quantitation of mast cells in experimental allergic neuritis.

The number and extent of degranulation of mast cells in the sciatic nerve have been determined in Lewis rats inoculated with bovine intradural root myelin to induce experimental allergic neuritis (EAN). No significant change in either the number of mast cells or the percentage of degranulated cells was observed before eight days post-inoculation (dpi). On day eight, however, there was a significant decrease in the number of detectable mast cells, and on day nine there was a significant increase in the percentage of degranulated cells. These changes immediately preceded the onset of clinical signs of EAN that occurred ten dpi. The number of detectable mast cells remained low throughout the acute stage of the disease, but by three weeks post-inoculation (wpi) there was a significant increase in the number of mast cells (or basophils) that persisted through 16 wpi. The increase in the percentage of degranulated mast cells also persisted through 16 wpi. These results suggest that mast cells participate in the development of EAN in the Lewis rat.

Animals↗
PubMed1991

Comparative histology of experimental allergic neuritis induced with minimum length neuritogenic peptides by adoptive transfer with sensitized cells or direct sensitization.

Using synthetic peptides representing specific regions of the bovine myelin protein P2, the minimum peptide length requirement for the T-cell epitope necessary for successful production of experimental allergic neuritis (EAN) has been shown to involve residues 61-70 of the P2 protein. In this study, morphometric analysis was used to compare the histologic changes in sciatic nerves of Lewis rats after disease was induced by P2 specific neuritogenic T-cell lines (P(2)3) or, alternatively, by direct inoculation of synthetic peptides representing residues 60-70 or 61-70 of the P2 protein sequence. Inoculation with cell line P(2)3 stimulated with residue 61-70 failed to elicit demyelination in sciatic nerves. However, cells stimulated with residue 60-70 produced inflammation, endoneurial edema, mild demyelination and axonal degeneration within seven days. In contrast, disease induced with either peptide by direct sensitization was more severe. Morphometric analysis revealed that inflammation was most severe in animals sensitized to the decapeptide. In the sciatic nerve, axonal degeneration was proportional in frequency to the extent of inflammation. Inflammation was especially intense in spinal roots with extensive destruction of axons including unmyelinated fibers. Spinal root changes were associated with Wallerian degeneration in the posterior white matter tracts of the spinal cord and were apparently secondary to endoneurial inflammation. Disruption of the blood-nerve-barrier (BNB), evident as physical separation of endothelial cells in association with severe perivascular inflammation, was observed.

Animals↗
PubMed1994

Phosphatidylserine suppresses myelin-induced experimental allergic neuritis (EAN) in Lewis rats.

Phosphatidylserine administered as an aqueous dispersion to myelin-induced experimental allergic neuritis rats had a significant effect on disease course. Intraperitoneal injections of 30 mg/kg were given daily beginning at the onset of disease and continued for 14 days. Clinical severity and mortality were markedly reduced by this treatment as compared to saline controls. Improved clinical outcome was associated with a reduction in peripheral nerve pathology. A possible mechanism involving tumor necrosis factor is discussed.

Animals↗
PubMed1995

Intravenous glucocorticosteroid treatment augments apoptosis of inflammatory T cells in experimental autoimmune neuritis (EAN) of the Lewis rat.

Apoptosis plays a critical role in natural recovery from experimental autoimmune disorders of the nervous system. Here we investigated in experimental autoimmune neuritis (EAN) whether apoptosis is augmented by high-dose corticosteroids, the mainstay of therapeutically active compounds in this group of disorders. Adoptive transfer EAN was induced by intravenous injection of P2-specific T cell blasts. At disease onset or at the maximum of disease two pulses of steroids were given within 12 hours, and animals were sacrificed 6 hours later. Steroid therapy significantly reduced T cell infiltration in sciatic nerve. Treatment on both day 4 and day 7 caused a significant increase of T cell apoptosis (42% vs 8.4% in placebo-treated animals on day 4, p < 0.05; 22.5% vs 7.0% on day 7, p < 0.05) in sciatic nerve as assessed by molecular labeling techniques. In addition, reduction of body weight and thymus weight and augmentation of thymocyte apoptosis were observed in steroid recipients. Steroid treatment markedly reduced cellular proliferation in lymphoid organs as measured by bromodeoxyuridine incorporation. Glucocorticosteroid treatment augments T cell apoptosis in inflammatory lesions of the peripheral nervous system, and this may add to their anti-inflammatory properties mediated by downregulation of cytokine expression.

Animals↗
PubMed1998

Prevention of experimental autoimmune neuritis by nasal administration of P2 protein peptide 57-81.

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. Both EAN and GBS are associated with upregulated T and B cells responses to PNS myelin proteins including P2 protein, and by changes of the Th1/Th2 cell balance in favor of Th1. Here we report that EAN can be prevented by the dominant neuritogenic peptide 57-81 of the PNS P2 protein when given nasally before immunization of Lewis rats with bovine PNS myelin (BPM) + Freund's complete adjuvant (FCA). P2 peptide-tolerized rats were also resistant to EAN relapse after challenge with BPM. Tolerance to EAN in rats receiving high dose (60 microg/day/rat) P2 peptide nasally was associated with specific T and B cell anergy. This was characterized by the failure of T cells to proliferate in response to PNS myelin antigens, while responsiveness to phytohemagglutinin was retained. Numbers of BPM- and P2 peptide-reactive interferon-gamma mRNA expressing lymph node cells were reduced, while levels of P2 peptide-reactive interleukin 4 and transforming growth factor-beta mRNA-expressing cells were markedly upregulated on day 18 post immunization in the rats receiving high dose P2 peptide nasally. Tolerance to EAN was also associated with lower CD4+ cell infiltration, low-grade inflammation, or the absence of histological evidence of EAN, as well as with low IL-2 receptor and MHC class II molecule expression within the PNS. This is the first study showing that mucosal tolerance is applicable to EAN and, as an extension, could be considered in GBS.

Administration, Intranasal↗
PubMed1996

Cytomegalovirus retinitis and optic neuritis in a child with severe combined immunodeficiency syndrome.

BACKGROUND: Although cytomegalovirus (CMV) infection of the retina and brain is common in patients with acquired immunodeficiency syndrome (AIDS), it is exceedingly rare in patients with immunodeficiencies due to other causes. This is the first report on ocular and cerebral histopathology of disseminated CMV in a child with severe combined immunodeficiency syndrome (SCID). METHODS: The authors examined by routine histopathologic methods the eyes of a 2-year-old white boy with SCID and bilateral CMV retinitis who died after failure of a third attempt at allogeneic bone marrow transplantation (BMT). RESULTS: Cytomegalovirus inclusions were found in the necrotic retinal remnants, in the hyperplastic and scarred retinal pigment epithelium, and bilaterally in the optic nerves. There were infiltrates of macrophages in response to the infection or the infused silicon, but no lymphoid infiltrates. Cytomegalovirus inclusions also were found in brain tissue. CONCLUSION: The histologic features resembled those of CMV retinitis and optic neuritis in AIDS.

Bone Marrow Transplantation↗
PubMed2005

Bilateral optic neuritis in wegener granulomatosis.

A 32-year-old patient with recurrent sinusitis had severe visual loss from optic neuropathy. Imaging revealed severe bone destruction and soft tissue densities of the paranasal sinuses and enhancement of the dura of the frontal sinuses, optic canals, and superior orbital fissures bilaterally. Endoscopic sinusectomy with biopsy showed granulomatous vasculitis compatible with Wegener granulomatosis (WG). The patient was treated with intravenous and oral corticosteroids and oral cyclophosphamide that led to rapid and dramatic visual recovery. This case draws attention to the fact that optic neuritis may be an early inflammatory manifestation of WG and that rapid diagnosis and aggressive anti-inflammatory treatment is critical before inflammation of arteries leads to infarction and irreversible visual loss.

Adult↗
PubMed2006

Contribution of resident endoneurial macrophages to the local cellular response in experimental autoimmune neuritis.

Macrophages are intimately involved in the pathogenesis of inflammatory neuropathies. The contribution of resident endoneurial macrophages is unknown since their differentiation from infiltrating macrophages is difficult due to missing cellular markers. Previous studies demonstrated the participation of resident macrophages in Wallerian degeneration and the pathogenesis of hereditary neuropathies. The question arises whether resident macrophages are involved in experimental autoimmune neuritis (EAN) where they could contribute to immunosurveillance and antigen presentation. To address this question we used bone marrow chimeric rats, allowing the differentiation between resident and hematogenous cells. Immunohistochemistry and in situ hybridization were applied on to identify and characterize resident macrophages in terms of morphological features, expression of activation markers, proliferation, phagocytosis, and MHC-II expression. Endoneurial macrophages of resident origin were detectable at all stages of disease with a contribution of at least 27% of the total macrophages. They appeared activated by morphological and immunohistochemical criteria and proliferated early. MHC-II-positive resident macrophages were observed that had phagocytosed myelin. These results demonstrate that the macrophage response in EAN is partly of intrinsic origin. The rapid activation and proliferation of resident endoneurial macrophages points toward an active role of these cells in inflammatory peripheral nerve disease, especially early in disease.

Animals↗
PubMed2006

Magnetic resonance imaging at 3.0 tesla detects more lesions in acute optic neuritis than at 1.5 tesla.

OBJECTIVE: We sought to assess whether magnetic resonance imaging (MRI) at 3.0 T detects more brain lesions in acute optic neuritis (ON) than MRI at 1.5 T. MATERIALS AND METHODS: Twenty-eight patients with acute ON were scanned at both field-strengths using fast-fluid-attenuated inversion recovery (FLAIR), proton density and T2-weighted turbo spin echo, and T1-weighted spin echo after contrast. In addition, magnetization-prepared rapid acquisition gradient echo (MPRAGE) was obtained after contrast at 3.0 T. Lesion number and volumes were assessed by an observer blind to patient identity and field strength. RESULTS: Scans at 3.0 T showed a significantly increase in number of lesions detected on FLAIR images (P = 0.002) relative to scanning at 1.5 T. MPRAGE proved to be suitable for detecting enhancing lesions in ON. CONCLUSION: The MRI protocol at 3.0 T was more sensitive to hyperintense brain lesions in ON than the standard MRI protocol at 1.5 T.

Adult↗
PubMed1994

Cellular mRNA expression of interferon-gamma, IL-4 and transforming growth factor-beta (TGF-beta) by rat mononuclear cells stimulated with peripheral nerve myelin antigens in experimental allergic neuritis.

Experimental allergic neuritis (EAN) serves as a useful model for inflammation in the peripheral nervous system. To study the potential role of important immunoregulatory and effector cytokines in EAN, we examined the expression of mRNA for interferon-gamma (IFN-gamma), IL-4 and TGF-beta by in situ hybridization in lymph node and splenic cells cultured with bovine peripheral nerve myelin (BPM), P2 and P0 during the course of EAN in Lewis rats. Levels of IFN-gamma mRNA-expressing mononuclear cells (MNC) from lymph nodes and spleens roughly correlated with clinical status, consistent with a disease-promoting role for IFN-gamma. BPM, P0 and P2-reactive IFN-gamma mRNA-expressing T cells appeared in lymph nodes and spleen before onset of the disease, whereas a significant TGF-beta response to BPM, P2 and P0 was observed at lower levels than the IFN-gamma response and at onset of recovery, consistent with a disease down-regulating role of TGF-beta. IL-4 mRNA-expressing cells were found at levels similar to TGF-beta mRNA-expressing cells, and with the latest peak of the three cytokines examined. This result suggests that IL-4 may also suppress IFN-gamma expression at late recovery phase of EAN.

Animals↗
PubMedDate not supplied

Acetylcholinesterase activity and its fast axonal transport in rabbit sciatic nerves during the recovery phase of experimental allergic neuritis.

Acetylcholinesterase (AChE) activity and its fast axonal transport were studied in rabbit sciatic nerves with a double ligature system during the recovery phase of experimental allergic neuritis (EAN), 6-9 days after the maximal symptoms, in order to obtain biochemical evidence of possible axonal damage in this primary demyelinating disease. The stationary AChE activity was significantly decreased, but the amount of the fast transported enzyme activity remained at the level of the controls. The velocity of the orthograde transport of AChE was slowed by about 15%, but this decrease was not statistically significant. Our results lend further support for the suggested neuronal damage in EAN, which can provide an explanation to the finding that the clinical symptoms in demyelinating diseases of the peripheral nervous system do not always correlate with the state of myelin.

Acetylcholinesterase↗
PubMed1992

Neuropathological findings in chronic relapsing experimental allergic neuritis induced in the Lewis rat by inoculation with intradural root myelin and treatment with low dose cyclosporin A.

Experimental allergic neuritis (EAN) was induced in Lewis rats by inoculation with bovine intradural root myelin and adjuvants. Rats treated with subcutaneous cyclosporin A (CsA) (4 mg/kg on 3 days per week from the day of inoculation until day 29) developed a chronic relapsing course. Tissues from the spinal cord, nerve roots, dorsal root ganglia and sciatic nerve of CsA-treated rats sampled during relapses and remissions were studied by light and electron microscopy. Control rats that were not treated with CsA were studied during or after episodes of acute EAN. Both control and CsA-treated animals studied in the first episode of EAN had evidence of inflammation and primary demyelination of the nerve roots and dorsal root ganglia. In control and CsA-treated animals that had recovered from the first episode there was evidence of remyelination. In CsA-treated animals in the second episode there was severe inflammation and demyelination and remyelination of the nerve roots and dorsal root ganglia, and in addition there was significant demyelination and remyelination in the spinal nerves and sciatic nerves and dorsal columns of the spinal cord, particularly in later stages of disease. In later episodes there was less inflammation, but there was continuing demyelination and onion bulbs were present. In animals sampled after recovery from chronic relapsing EAN onion bulbs were present. Occasional small onion bulbs were also observed in control animals that were inoculated with higher doses of myelin. Plasma cells were present in the inflammatory lesions of later episodes. Mast cells were also observed at different stages of the disease. We conclude that the CsA form of chronic relapsing EAN has clinical and pathological similarities with the human disease, chronic inflammatory demyelinating polyradiculoneuropathy.

Anesthesia↗