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At least 865 records · Page 48Linked to original sources
PubMed1978

Acquired color vision defects in retrobulbar neuritis.

We used the Farnsworth-Munsell 100 Hue Test to study the incidence of acquired color vision defects in 16 patients with unilateral and and seven patients with bilateral retrobulbar optic neuritis whose visual acuity had recovered to 6/12 (20/40) or better. We recorded the visual-evoked response to a pattern stimulus on the same day. All 30 affected eyes showed an excessive number of errors on Farnsworth-Munsell 100 Hue testing. The number of errors increased with greater residual optic nerve damage. One false-positive and two false-negative visual-evoked responses were found.

Adult↗
PubMed2000

Seasonal patterns in optic neuritis and multiple sclerosis: a meta-analysis.

To quantify and characterize seasonal variation in monosymptomatic optic neuritis (MON) onsets, multiple sclerosis (MS) onsets and MS exacerbations (MSE), a meta-analysis was performed, using established methods and pooling weighted information obtained from nine reports on MON, six reports on MS onsets and nine reports on MSE, which fulfilled specific criteria for report quality and data homogeneity. The results suggested that MON, MS onsets and MSE in the Northern hemisphere present a similar pattern with highest frequencies in spring and lowest in winter. These differences were highest for MS onsets, 45% with 95% CI 36-55%, and lowest for MSE, 10% with 95% CI 7-13%, statistically significant and robust, insensitive to an alternative seasonal definition, not unduly influenced by any single primary study, and supported by fail-safe N calculations. Random variation, misclassification and publication bias were less likely to account for the reported generalized seasonal patterns.

Data Interpretation, Statistical↗
PubMed2001

Autonomic dysfunction in experimental autoimmune neuritis: heart rate.

Autonomic nervous system (ANS) dysfunction occurs in more than half of Guillain--Barré syndrome (GBS) patients and is an important cause of death in the disease. In this study we examined heart rate (HR) changes in an animal model of GBS, experimental autoimmune neuritis (EAN), induced by immunization with myelin extracted from bovine spinal roots. The animals developed progressive motor weakness accompanied by significant weight loss and hypothermia. HR was measured in 33 EAN rats at rest (rHR) and followings stressful stimulation (sHR). Average pre-immunization rHR was 341+/-28 beats per minute (b.p.m.) and sHR was 486+/-21 bpm. Although the mean rHR in rats with EAN was not significantly different compared to that at baseline, there was a significant increase of variation of rHR with six rats demonstrating bradycardia (<280 b.p.m.) and 10 tachycardia (>400 b.p.m.) (P<0.01, F-test). sHR in EAN rats was significantly lower (P<0.01), suggesting sympathetic system impairment. These findings may serve as a basis for testing treatments of ANS dysfunction in EAN.

Animals↗
PubMed1996

Suppression of experimental autoimmune neuritis by phosphodiesterase inhibitor pentoxifylline.

Phosphodiesterase inhibitor pentoxifylline (POX) has been shown to have multiple immunomodulatory effects in vitro and in vivo. It inhibits T cell proliferation, T helper 1-type cytokines, and tumor necrosis factor. We postulated that POX might have an in vivo immunomodulatory effect on a T-cell-mediated autoimmune peripheral nervous system disease, experimental autoimmune neuritis (EAN). We investigated the effect of POX on EAN in rats immunized with peripheral nerve myelin containing neuritogenic peptide SP26. At 200 mg/kg/day, there was significant suppression of clinical EAN, weight loss, and T cell proliferation to SP26 compared to controls. Proliferation of T cells from immunized rats to SP26 was suppressed by POX in vitro. These studies demonstrate a beneficial role for POX in EAN, with potential applicability to human autoimmune demyelination.

Animals↗
PubMed1998

Nasal administration of multiple antigens suppresses experimental autoimmune myasthenia gravis, encephalomyelitis and neuritis.

Oral tolerization with acetylcholine receptor (AChR) and myelin basic protein (MBP) prior to immunization with AChR+MBP+ complete Freund's adjuvant (CFA) alleviated clinical signs of experimental autoimmune myasthenia gravis (EAMG)+experimental allergic encephalomyelitis (EAE) and AChR- or MBP-specific T and B cell responses. Tolerance induced via the nasal route needs much less tolerogen and may still be as effective as oral tolerance induction. We now immunized Lewis rats with AChR+MBP+bovine peripheral nerve myelin (BPM)+CFA, which resulted in a multiphasic clinical picture with a combination of clinical signs of the EAMG+EAE+experimental allergic neuritis (EAN), accompanied by massive macrophage infiltrations in sections of muscle, spinal cord and sciatic nerve, and strong T and B cell responses to AChR, MBP and BPM in lymphoid organs. Nasal administration of microg doses of AChR+MBP+BPM prior to immunization with a mixture of these antigens+CFA effectively suppressed the incidence and severity of clinical disease, reduced macrophage infiltrations in sections of muscle, spinal cord and sciatic nerve, and down-regulated autoreactive T cell responses to the three antigens in lymphoid organs. Numbers of AChR-, MBP-, BPM-reactive Th1 type of cytokine interferon (IFN)-gamma, tumor necrosis factor (TNF)-alpha mRNA expression in lymph node cells were markedly suppressed, while transforming growth factor-beta (TGF-beta) mRNA expression was upregulated from nasally tolerized rats, suggesting an active suppression mechanism may act partly in the induction of tolerance. The results implicate the possibility to establish multiple autoantigen-based vaccination for the prevention of autoimmune diseases in humans.

Administration, Intranasal↗
PubMed1998

Incidence of optic neuritis in Stockholm, Sweden 1990-1995: I. Age, sex, birth and ethnic-group related patterns.

We studied the incidence of monosymptomatic optic neuritis (MON) in Stockholm county, Sweden and its variation with person-related factors. Patients with suspected or diagnosed MON between January 1, 1990 and December 31, 1995 were referred from ophthalmologists and neurologists to a research registry. The diagnosis was based on accepted clinical criteria only, and verified by an ophthalmologist who examined all the patients. Data were collected by interview using a structured questionnaire. The crude mean annual incidence, based on 147 patients, 118 females and 29 males, diagnosed with MON, was 1.46 per 100,000 person-years, 2.28 for females and 0.59 for males. The corresponding age-adjusted incidences were 1.40, 2.28 and 0.53. The age-specific incidence curve for both sexes suggested a bimodal distribution with peaks at 30-34 years and 45-49 years. The smoothed cumulative incidences in 1 year birth cohorts showed a notchy profile, related to bimodality. The incidence among residents born out of the Nordic countries was low, 0.28 per 100,000. Patients with onset of MON before 40 years of age had a significantly higher frequency of mononuclear pleocytosis in cerebrospinal fluid and shorter duration to conversion to multiple sclerosis. In summary, MON occurred in Stockholm at a relatively low frequency, particularly among males. The presence of particular birth date and birth place related patterns might be etiologically relevant.

Adult↗
PubMed1998

Schwann cell undergoes apoptosis during experimental allergic neuritis (EAN).

Schwann cell apoptosis is not detectable in the normal mature mammalian peripheral nervous system (PNS). However, during PNS cell-mediated demyelination, apoptosis contributes to the elimination of endoneurial T-lymphocytes. We report here that approximately 10% of Schwann cells die by apoptosis during the early phases of recovery from experimental autoimmune neuritis (EAN) in the adult rat, a model for the Guillain-Barrè syndrome. Schwann cell apoptosis, follows endoneurial T-cell clearance, and is prominent in the nerve roots, the site of most severe segmental demyelination, but is rare in the more distal regions of the PNS, where Wallerian degeneration predominates. Further immunological analysis showed that the p75 neurotrophin receptor (p75NTR) is expressed in 2% of both apoptotic and non apoptotic Schwann cells, while Ki-67, a marker of cell proliferation, is expressed in 20% of apoptotic and in 1% of non apoptotic Schwann cells. Our new observations indicate that apoptosis during cell-mediated demyelination can be a phenomenon related either to the development or the recovery of autoimmune cell mediated inflammation.

Animals↗
PubMed1999

The expression of CD59 in experimental allergic neuritis.

Complement is implicated as an effector in inflammatory demyelination occurring in Guillain-Barré syndrome (GBS) and in experimental allergic neuritis (EAN). CD59, a potent complement regulatory protein that inhibits the formation of the terminal cytolytic membrane attack complex (MAC), is expressed on human and rat Schwann cells. In EAN the expression of CD59 was increased on Schwann cells during demyelination and axonal degeneration, evaluated by immunostaining of nerve sections and teased fibres. Mac-1 (CD11b) positive leukocytes were localized close to the Schwann cells showing enhanced CD59 staining. The increased CD59 expression in EAN could therefore be due to the release of cytokines or other immunoregulatory molecules from the inflammatory cells. However, interferon gamma (IFN-gamma) or tumor necrosis factor alfa (TNF-alpha) did not upregulate the expression of CD59 on rat Schwann cells in culture. The increased expression of CD59 in EAN is likely to be important in the protection of Schwann cells from MAC.

Animals↗
PubMed2002

Suppression of experimental autoimmune neuritis by ABR-215062 is associated with altered Th1/Th2 balance and inhibited migration of inflammatory cells into the peripheral nerve tissue.

The therapeutic effects of ABR-215062, which is a new immunoregulator derived from Linomide, have been evaluated in experimental autoimmune neuritis (EAN), a CD4(+) T cell-mediated animal model of Guillain-Barré syndrome in man. In previous studies, we reported that Linomide suppressed the clinical EAN and myelin antigen-reactive T and B cell responses. Here EAN induced in Lewis rats by inoculation with peripheral nerve myelin P0 protein peptide 180-199 and Freund's complete adjuvant was strongly suppressed by ABR-215062 administered daily subcutaneously from the day of inoculation. ABR-215062 dose-dependently reduced the incidence of EAN, ameliorated clinical signs and inhibited P0 peptide 180-199-specific T cell responses as well as also the decreased inflammation and demyelination in the peripheral nerves. The suppression of clinical EAN was associated with inhibition of the inflammatory cytokines IFN-gamma and TNF-alpha, as well as the enhancement of anti-inflammatory cytokine IL-4 in lymph node cells and periphery nerve tissues, respectively, in a dose-dependent manner. These effects indicate that ABR-215062 may mediate its effects by regulation of Th1/Th2 cytokine balance and suggest that ABR-215062 is potentially a new chemical entity for effective treatment of autoimmune diseases.

Adjuvants, Immunologic↗
PubMed2000

Rolipram suppresses experimental autoimmune neuritis and prevents relapses in Lewis rats.

Rolipram, a phosphodiesterase type 4 inhibitor, can markedly down-regulate antigen-driven T cell proliferation and suppress TNF-alpha production in vitro and in vivo. Here we report the effects of Rolipram on experimental autoimmune neuritis (EAN), which can be induced by immunization with myelin components of the peripheral nervous system (PNS) combined with Freund's complete adjuvant (FCA), and which represents a CD4+ T cell-mediated animal model for human Guillain-Barré syndrome. EAN induced in Lewis rats by inoculation with the PNS P2 protein peptide 57-81 and FCA was strongly suppressed by Rolipram administered twice daily intraperitoneally from day 9 post immunization (p.i.), i.e. after onset of clinical EAN. Suppression of EAN was associated with down-regulated myelin antigen-induced T cell responses as well as down-regulated IFN-gamma and TNF-alpha production. A relapse of clinical EAN occurred upon treatment of a short duration (7 days), while prolongation of treatment resulted in the prevention of clinical EAN relapse. There was no relationship between clinical EAN relapse and high levels of TNF-alpha. The immunomodulatory effects of Rolipram call for further research into the potential role of drugs acting on the immune system in the treatment of autoimmune diseases.

Animals↗
PubMed2005

[Optic neuritis in cat scratch disease].

Ocular and neuro-ophthalmic manifestations of cat scratch disease are not uncommon. The association of anterior optic neuritis with retinal lesions suggests neuroretinitis, which is highly suggestive of cat scratch disease. A new case is described.

Adolescent↗
PubMed1994

Intraoperative spinal root stimulation to detect most proximal site of leprous ulnar neuritis.

In 10 patients with leprous ulnar neuritis, we investigated the most proximal site of lesion in the affected nerves. Spinal roots C8 and T1 were stimulated intraoperatively to evoke efferent mixed compound nerve action potentials which were recorded from the exposed ulnar nerves. The site at which amplitudes reached a maximum was considered the most proximal site of lesion. Nerve damage was found far proximally from the thickened segments in otherwise inconspicuous sections. Epineuriotomy within these apparently unaffected segments revealed fibrosis of the interfascicular epineurium in 9 patients, which is an indication for microsurgical interfascicular neurolysis.

Action Potentials↗
PubMed2002

Use of magnetic resonance imaging to differentiate optic neuritis and nonarteritic anterior ischemic optic neuropathy.

OBJECTIVE: To determine if magnetic resonance imaging (MRI) of the optic nerves obtained during the acute phase can distinguish patients with optic neuritis (ON) from those with nonarteritic anterior ischemic optic neuropathy (NAION). DESIGN: Retrospective, neuroradiologic, observational study. PARTICIPANTS: Sixty-four patients diagnosed as having either ON or NAION who were diagnosed by clinical criteria and imaged by MRI. METHODS: Demographic information on the MRI scans was masked and the patients were presented randomly and in a blinded fashion to a neuroradiologist (JDR) for determination of abnormalities. Reproducibility was assessed by presenting 10 of the scans a second time to the same neuroradiologist. MAIN OUTCOME MEASURES: The presence or absence and location of abnormal MRI signals of the optic nerve. RESULTS: Evaluation of reproducibility revealed identical interpretations of the ten scans submitted a second time. The optic nerve was abnormal in the clinically affected eye in 31 of the 32 ON patients but in only 5 of the 32 NAION patients. Thirty of the 31 ON patients who received gadolinium had enhancement, and 27 of the 32 ON patients had increased short T(1) inversion recovery signal in the clinically affected optic nerve. The five NAION patients with abnormal scans in the clinically affected eye had increased short T(1) inversion recovery signal, and in two of these, there also was enhancement of the optic nerve. For the ON patients, enhancement involved the entire length of the intraorbital optic nerve in 18 cases and the intracranial segment of the optic nerve in 19 cases. CONCLUSIONS: Our study shows that MRI scanning of the optic nerve shows significantly different results between patients clinically diagnosed with either ON or NAION.

Acute Disease↗
PubMed1987

Cytomegalovirus retinitis and optic neuritis in acquired immune deficiency syndrome. Report of a case.

A 33-year-old man with acquired immune deficiency syndrome (AIDS) was found to have bilateral cytomegalovirus (CMV) retinitis with concomitant unilateral optic neuritis. The patient died and postmortem examination of both eyes disclosed CMV inclusions in all layers of the involved retinas including the retinal pigment epithelium (RPE). Also found were CMV inclusions in the optic nerve of his left eye. Immunohistochemical stains for glial fibrillary acid protein demonstrated that glial cells were infected in the optic nerve.

Acquired Immunodeficiency Syndrome↗
PubMed1990

Gadolinium-DTPA-enhanced magnetic resonance imaging in experimental optic neuritis.

Magnetic resonance imaging (MRI) with gadolinium-diethylenetriaminepentaacetic acid (Gd-DTPA) was used to investigate disruption of the blood-optic nerve barrier associated with acute autoimmune demyelination. Leakage of Gd-DTPA was seen in the optic nerves and optic chiasm of adult guinea pigs sensitized for acute experimental allergic encephalomyelitis, but not in normal unsensitized animals. This finding occurred as early as 5 to 8 days after antigenic sensitization with the myelin emulsion and before the onset of paralysis or ataxia. Pathologic examination at this early stage of experimental allergic encephalomyelitis showed an absence of demyelination in the optic nerves and optic chiasm, although scant perivascular foci of inflammatory cells were seen. Leakage of Gd-DTPA in the optic nerve before demyelination of this white matter tract illustrates that increased permeability of the blood-optic nerve barrier is an early, if not the initial, event in autoimmune demyelination, and the optic nerve is a common site of central nervous system involvement during the initial phase of acute experimental allergic encephalomyelitis. Findings in this animal model appear comparable with the results of MRI with Gd-DTPA in patients with optic neuritis, and they suggest that disruption of the blood-optic nerve barrier is a common denominator for both disorders of primary demyelination.

Animals↗
PubMed1990

Bilateral postinfectious optic neuritis and intravenous steroid therapy in children.

Six patients presented with acute, simultaneous, bilateral optic neuritis. Five of the six patients admitted to a recent history of a brief upper respiratory or gastrointestinal illness, presumably viral in nature. Visual acuity was severely reduced in all patients. Five of the six patients also demonstrated marked neurologic deficits, including seizure activity and cerebellar dysfunction. Three patients demonstrated enhancing intracranial lesions on magnetic resonance imaging (MRI) consistent with demyelinative plaques, whereas lumbar puncture was abnormal in three patients. HLA tissue typing was performed on five of the six patients. All patients were treated with intravenous methylprednisolone, followed by a 2-month tapering course of oral prednisone. Each patient experienced a rapid and nearly complete recovery of vision during treatment.

Adolescent↗
PubMed1998

Inhibition of experimental autoimmune neuritis by the immunomodulator linomide.

Experimental autoimmune neuritis (EAN) is an animal model that shares clinical, pathological and electrophysiological features with the human disease Guillain-Barre syndrome. The synthetic immunomodulatory substance linomide has been successfully used to prevent the development of several experimental autoimmune models in laboratory animals and has been proved to be beneficial in modulating the course of multiple sclerosis in humans. In the present study we demonstrate that oral administration of linomide prevents the development of clinical and histopathological signs of EAN in Lewis rats, inoculated with the P2 (60-70) synthetic peptide. The immunomodulatory effect of linomide on this experimental model of disease was associated with marked apoptosis of lymphocytes in thymus and spleen early after starting the treatment. Furthermore, a downregulation of the endothelial expression of the adhesion molecules ICAM-1 at the target site and LFA-1 on lymphocytes could also contribute to the absence of inflammatory cells in the neuraxis.

Adjuvants, Immunologic↗
PubMed2000

Experimental allergic neuritis in the SJL/J mouse: induction of severe and reproducible disease with bovine peripheral nerve myelin and pertussis toxin with or without interleukin-12.

We report a reproducible model of experimental allergic neuritis (EAN) with severe clinical signs and consistent pathological features in mice. Pertussis toxin (PT) in the presence or absence of murine recombinant interleukin-12 (mrIL-12) was used as an adjuvant with bovine peripheral nerve myelin (BPNM) to induce clinical EAN in SJL/J mice. After immunization with a combination of BPNM in complete Freund's adjuvant (CFA) and PT, mice developed severe consistent signs of EAN. The additional treatment of immunized mice with mrIL-12 prolonged the course of EAN characterized by earlier clinical signs of the disease and delayed the recovery stage. Mice injected with BPNM and CFA without PT developed mild clinical signs. Histological examination of the caudae equinae and the sciatic nerves taken from mice with clinical signs of EAN during the recovery stage revealed severe demyelination, remyelination and remnants of mononuclear cell infiltration. Moderate to severe EAN can be induced in SJL/J mice by the injection of a combination of BPNM in CFA and PT. This model can provide a better understanding of mechanism of demyelination in infiltrating peripheral neuropathy.

Animals↗