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PubMed1991

Optic neuritis and ischemic optic neuropathy. Overlapping clinical profiles.

A retrospective analysis of the clinical features of 81 patients with acute idiopathic optic neuritis and 58 patients with nonarteritic anterior ischemic optic neuropathy revealed a surprising overlap of manifestations. The rate of visual decline and the range of visual acuities were the same for both. Central scotomas and improvement in acuity were more common in optic neuritis, but occurred often enough in nonarteritic anterior ischemic optic neuropathy to limit their value as single diagnostic criteria. The similarities observed in this study suggest that it may be difficult to differentiate between optic neuritis and nonarteritic anterior ischemic optic neuropathy solely on nosologic grounds in some instances of acute, unilateral optic neuropathy.

Adult↗
PubMed1995

The dyschromatopsia of optic neuritis: a descriptive analysis of data from the optic neuritis treatment trial.

PURPOSE: We sought to characterize the dyschromatopsia of optic neuritis, to determine the type and severity of color defect present and its relation to central vision and spatial acuity, to examine changes in this dyschromatopsia over time, and to determine the applicability of Köllner's rule to patients with optic neuritis. METHODS: We analyzed the raw data on color vision performance as assembled within the Optic Neuritis Treatment Trial (ONTT). The ONTT was designed to evaluate corticosteroids as a treatment for acute demyelinating optic neuritis and to allow long-term outcome and natural history analyses. Between July 1, 1988 and June 30, 1991, 488 patients were enrolled in this trial. All patients underwent extensive neurologic and ophthalmologic examinations including standardized testing of visual function that included testing of color vision. The ONTT population thus afforded a unique opportunity to characterize acquired dyschromatopsias in a large, homogenous, well-characterized cohort of patients with optic neuritis. We used quantitative analysis of FM-100 scores from this patient cohort to determine the severity of the dyschromatopsia, the selectivity of the dyschromatopsia (polarity of errors) and the type of dyschromatopsia (axis of confusion) by employing quadrant analysis of FM-100 scores. RESULTS: The results of high-and low-selectivity analyses of the FM-100 data showed that during the acute phase of optic neuritis, blue/yellow, red/ green, and non-selective color defects occurred; among patients with pure defects, blue/yellow defects were more frequent than red/green defects. At 6 months after the acute event, however, analyses showed that red/green defects were more common than blue/yellow defects. Among patients with selective color defects both acutely and at 6 months, the defect was as likely to change over time as remain the same. The likelihood of persistent dyschromatopsia at 6 months was related to the severity of initial central acuity loss, but the type of dyschromatopsia present (red/green versus blue/yellow) was not. CONCLUSIONS: Our results suggest that at the time of the acute attack of optic neuritis, the majority of selective color defects were blue/yellow defects, whereas at 6 months, more of the selective defects were red/green defects, though both types of defects (as well as nonselective defects) were seen acutely and at 6 months. Despite the rigorous inclusion criteria of the ONTT, the large number of patients we studied, correlation of color vision with visual acuity, and longitudinal follow up, this study showed that no single type of color defect was consistently associated with optic neuritis. Demyelinating optic neuritis does not obey Köllner's rule. Moreover, the type of defect present changed in some patients over the course of recovery. Thus, the type of defect may not even be consistent in individual patients as they recover. The type of defect appeared to be related to spatial vision at the time of the test, but the type of defect present at 6 months was not related to the severity of the initial visual loss. Therefore, in evaluating color defects associated with optic neuritis, the level of central visual function must be considered.

Acute Disease↗
PubMed1995

[Incidence of acute idiopathic optic neuritis and its therapy in Japan. Optic Neuritis Treatment Trial Multicenter Cooperative Research Group (ONMRG)].

Data on the incidence of and treatment for acute idiopathic optic neuritis were obtained by questionnaire sent to departments of ophthalmology, university hospitals, and general hospitals throughout Japan. Inquiry was made as to the number of cases which developed idiopathic optic neuritis from April 1992 to March 1993 along with their clinical features. The response rate was 53.6%. There were a total of 550 cases, and the male to female ratio was 1:1.22. Patients 14 to 55 years old were 65.9%; bilateral involvement: 28.2%; recurrence: 18.6%; positive past history of the other eye; 7.5%. Assuming the answering rate to be 100% and two thirds of the patients to be included, annual incidence of this disease (the annual number of patients) was determined to be 1.62 for an adult population of 100,000 (1.03 cases/100,000 people). Tochigi, Tokyo, Kanagawa, Hyogo, Wakayama, Okayama, Yamaguchi, Tottori, Shimane, Ehime, and Fukuoka showed an annual incidence exceeding 2.0/100,000 adults. At more than 95% of all medical institutions questioned, patients with optic neuritis were usually treated with systemic corticosteroids. Oral corticosteroid therapy, which was shown in a recent study in USA to be contraindicated, was still being used at 15% of the institutions.

Acute Disease↗
PubMed1999

Is sphenoid sinus opacity significant in patients with optic neuritis?

PURPOSE: Optic neuritis secondary to sinus disease is an infrequent but well-documented association. When a patient presents with signs of optic nerve dysfunction and orbital inflammation the significance of widespread sinus disease on radiology is clear and the management is straightforward. We present a group of patients with isolated optic neuritis and radiological evidence of spheno-ethmoiditis and discuss the clinical relevance of this finding. METHODS: We reviewed the notes of 11 patients with optic neuritis who, because of atypical headache, underwent neuroimaging revealing sphenoid sinus opacity. Six patients had endoscopic drainage of the sphenoid sinus; 4 were treated medically. RESULTS: Sinus contents included fungal infection (2), mucopurulent material (5), polyps (1) and necrotic tumour (1). Narrowing of the optic canal due to chronic osteomyelitis was found in 1 patient with irreversible optic atrophy. Visual loss was reversible in 6 patients. Four patients had normal radiological findings after treatment. Two patients had recurrent optic neuritis with sphenoid sinusitis on MRI scan, resolving on treatment, during the 4 year follow-up period. CONCLUSIONS: Possible mechanisms of nerve damage in this situation include direct spread of infection, occlusive vasculitis and bony deficiency in the wall of the sinus. Patients presenting with isolated optic neuritis and atypical headache should be scanned; an opaque sphenoid sinus in the context of visual loss should not be dismissed as coincidental but assumed to be pathological and the patient referred for drainage. Sphenoid sinusitis is an uncommon but treatable cause of optic neuritis.

Adult↗
PubMed1993

The effect of corticosteroids for acute optic neuritis on the subsequent development of multiple sclerosis. The Optic Neuritis Study Group.

BACKGROUND: Optic neuritis is often the first clinical manifestation of multiple sclerosis, but little is known about the effect of corticosteroid treatment for optic neuritis on the subsequent risk of multiple sclerosis. METHODS: We conducted a multicenter study in which 389 patients with acute optic neuritis (and without known multiple sclerosis) were randomly assigned to receive intravenous methylprednisolone (250 mg every six hours) for 3 days followed by oral prednisone (1 mg per kilogram of body weight) for 11 days, oral prednisone (1 mg per kilogram) alone for 14 days, or placebo for 14 days. Neurologic status was assessed over a period of two to four years. The patients in the first group were hospitalized for three days; the others were treated as outpatients. RESULTS: Definite multiple sclerosis developed within the first two years in 7.5 percent of the intravenous-methyl-prednisolone group (134 patients), 14.7 percent of the oral-prednisone group (129 patients), and 16.7 percent of the placebo group (126 patients). The adjusted rate ratio for the development of definite multiple sclerosis within two years in the intravenous-methylprednisolone group was 0.34 (95 percent confidence interval, 0.16 to 0.74) as compared with the placebo group and 0.38 (95 percent confidence interval, 0.17 to 0.83) as compared with the oral-prednisone group. The beneficial effect of the intravenous-steroid regimen appeared to lessen after the first two years of follow-up. Signal abnormalities on magnetic resonance imaging (MRI) of the brain were a strong indication of risk for the development of definite multiple sclerosis (adjusted rate ratio in patients with three or more lesions, 5.53; 95 percent confidence interval, 2.41 to 12.66). The beneficial effect of treatment was most apparent in patients with abnormal MRI scans at entry. CONCLUSIONS: In patients with acute optic neuritis, treatment with a three-day course of high-dose intravenous methylprednisolone (followed by a short course of prednisone) reduces the rate of development of multiple sclerosis over a two-year period.

Acute Disease↗
PubMed2000

[Optic neuritis--from diagnosis to optic nerve transplantation].

Optic neuritis is a clinical syndrome resulting from inflammation, demyelination, or infection of the optic nerve. Its diagnosis and treatment are complicated. In 1884, Nettleship first reported 28 cases of optic neuritis whose clinical symptoms have been accepted up to the present without any change. On the other hand, the development of diagnostic procedures and steroid therapy have also altered the clinical features of optic neuritis. Among several developed diagnostic procedures, the visually evoked cortical potential (VECP) has become a good tool to prove the impairment of the optic nerve. In 1971, we reported a decrease of threshold intensity required to evoke VECPs in optic neuritis patients whose visual acuity was relatively well preserved. In the same year, Halliday et al. reported that pattern VECP (PVECP) was delayed in 93% of patients with multiple sclerosis (MS) without optic neuritis. Stimulated by this report, a great number of studies appeared to show the usefulness of PVECP in the diagnosis of MS. However, few of these studies gave descriptions of ophthalmic findings. PVECP later become known to be closely related with ophthalmic conditions. In the ophthalmological field, we reported the influence of pupillary size, accommodation power, refractive powers, eccentricity of stimulated retinal area, retinal luminance, contrast, wavelengths, spatial and temporal frequencies, stimulus field etc. On the basis of our results, we developed a television display system in 1975 and applied it clinically. In the present study, we reviewed the medical records of a total of 272 cases of optic neuritis who presented in our clinic between 1978 and 1999. In the diagnostic, therapeutic point of view in relation with the data of other countries, the study was important regarding the racial differences and recent conceptions of optic neuritis. The results showed that there were no racial difference in optic neuritis as had been thought. The development from optic neuritis to multiple sclerosis was not less than in Caucasian patients. Regarding steroid therapy, we found that the most effective method was sub-Tenon injection. For cases which recur and progress to optic atrophy, optic nerve transplantation will be needed. Therefore, we have been studying the reconstruction of the optic nerve in Wister rats. We experimentally damaged the ganglion cells by causing ischemic retina with ligation of the ophthalmic artery and cutting the optic nerve just behind the eyeball. To prevent the apoptosis of ganglion cells, we injected various neurotrophic factors such as BDNF, GDNF, and HSP 27 into the vitreous. For effective injection of DNA, electropolation was applied and the best condition for avoiding apoptosis was chosen. Further, in Mx-c-fos transgenic mice, we found that regeneration of ganglion cells was inhibited. Based on the rescue study of the ganglion cells, optic nerve transplantation was performed using an artificial graft in which cultured Schwann cells from the ischiatic nerve, BDNF, CNTF, insulin, and forscolin were compound and bridged to the superior colliculus. The results showed a regeneration rate of the optic nerve axon of 15%. This rate was much higher than in other reports. Keratoplasty and intraocular lens implantation had a relatively long history of research before achieving clinical success. We believe that optic nerve transplantation will one day be successful in clinical treatment in the same way.

Adult↗
PubMed1976

Measles-virus-specific IgG in optic neuritis and in multiple sclerosis after optic neuritis.

Measles-virus-specific IgG was measured in the serum of 100 patients who had presented with optic neuritis (ON) during 1960-74. When reviewed 41 of them were found to have developed definite symptoms and signs of multiple sclerosis (MS), their serum containing significantly higher titres of the antibody than sera from either the rest of the patients or a group of normal healthy controls. In a few patients from whom cerebrospinal fluid (CSF) was obtained in the acute phase of ON, titres of measles IgG in the serum was higher in those in whom the antibody was detected in the CSF than the serum of patients without CSF antibody.

Age Factors↗
PubMedDate not supplied

Baseline features of idiopathic optic neuritis as determined by a multicenter treatment trial in Japan. Optic Neuritis Treatment Trial Multicenter Cooperative Research Group (ONMRG).

BACKGROUND: An optic neuritis treatment trial was conducted at 30 clinical centers in Japan using the same protocol. Patient participation was based on: age range of 14-55 years; acute symptoms indicative of unilateral optic neuritis of unknown or demyelinating origin; visual symptoms of 14-day duration or less; relative afferent pupillary defect in affected eye; and normal or swollen optic disc of affected eye. CASES: Initially, 102 patients qualified for participation; baseline data were obtained for analysis from 70 of these patients. Demographic characteristics of Japanese patients with optic neuritis were clarified and compared with those in a US study. OBSERVATIONS: The incidence of ocular or periocular pain and the presence of periventricular plaques were noted to be lower, and the incidence of disc swelling higher, in the Japanese patients, suggesting racial differences in the characteristics of the disease. Such differences may possibly be related to the lower incidence of multiple sclerosis in Japanese patients. The results of visual function tests were virtually the same in both studies. The nonaffected eyes of more than half the patients showed abnormal mean deviation in Humphrey field analysis, as also noted in the US study. CONCLUSIONS: The baseline clinical features of optic neuritis in the Japanese patients have been defined. Some racial differences in the characteristics of the disease may exist.

Adolescent↗
PubMed1994

Visual field profile of optic neuritis. One-year follow-up in the Optic Neuritis Treatment Trial.

PURPOSE: The purpose of this present study was to evaluate longitudinal visual field information for 448 patients over their first year of follow-up in the Optic Neuritis Treatment Trial. METHODS: We reviewed 6536 automated static visual fields performed on a visual field analyzer (Humphrey Visual Field Analyzer) at nine visits within the 1-year period for each of the patients. RESULTS: The median values of the mean deviations for affected eyes were as follows: -22.88 dB at baseline, -1.94 dB at 6 months, and -1.62 dB at 1 year. At 6 months, 51% of affected eye visual fields were normal, and at 1 year 55.9% were normal. Approximately two thirds (68.8%) of the fellow eyes were classified as abnormal at baseline, although the defects were generally slight. One third (33.2%) were abnormal at 6 months, and approximately one third were still abnormal at 1 year. More than 87% of those abnormal at 6 months and at 1 year had been abnormal at baseline. Binocular analysis revealed that 13.2% of patients showed a chiasmal or retrochiasmal type of field defect at least once during the year (5.1% bitemporal; 8.9% homonymous). Of the patients who showed a retrochiasmal visual field defect, 75.7% had an abnormal magnetic resonance imaging scan at baseline compared with 46% of the rest of the patients in the Optic Neuritis Treatment Trial (chi 2 = 10.73, df = 1, P < .002). CONCLUSION: Over the first year of follow-up, the majority of patients with visual field defects from acute optic neuritis returned to normal, as measured by automated static perimetry. Many fields showed variation in the pattern and location of the sensitivity loss. Chiasmal and retrochiasmal defects occurred more commonly than previously reported.

Acute Disease↗
PubMed2006

Immunohistochemical evidence of inducible nitric oxide synthase and nitrotyrosine in a case of clinically isolated optic neuritis.

BACKGROUND: Optic neuritis (ON) is a demyelinating inflammation of the optic nerve that may occur as an isolated disease or related to multiple sclerosis (MS). There is little evidence of whether the immunohistochemistry of ON resembles that of typical cerebral MS lesions. METHODS: Pathologic optic nerves were obtained from a patient who died of causes unrelated to ON after clinical recovery from clinically isolated ON. Normal control optic nerves were obtained from an eye bank. Normal and pathologic tissues were probed with antibodies to pathologic proteins including myelin basic protein (MBP) fragment, the inducible form of nitric oxide synthase (iNOS), macrophage markers CD14 and CD64, nitrotyrosine, and cyclooxygenase (COX-2). We also examined MBP, the oligodendrocyte marker cyclic nucleotide phosphodiesterase (CNPase), and glial fibrillary acidic protein. RESULTS: In the affected pathologic nerve, iNOS-positive macrophages/microglia, iNOS-positive astrocytes, COX-2, and nitrotyrosine were observed. iNOS and COX-2 were occasionally observed in the unaffected nerve. Decreased expression of MBP and CNPase was seen in the pathologic optic nerves, along with evidence of gliosis and ongoing myelin degradation indicated by the presence of MBP fragment. CONCLUSIONS: The immunohistochemistry of clinically isolated optic neuritis, as judged by this single case, resembles that of cerebral lesions of MS in showing abnormally high levels of iNOS and nitrotyrosine as well as other mediators of immune damage.

Astrocytes↗
PubMedDate not supplied

[Response to high dose corticosteroids in a girl with bilateral optic neuritis].

INTRODUCTION: Optic neuritis is rare in childhood. Frequently (35-52% of all cases depending on the series) they have, during their clinical course, foci of demyelination leading to the clinical picture of multiple sclerosis (MS). Since 1993, the optic neuritis study group has recommended treatment with high doses of corticosteroids, since this seemed to stop progression, improve long-term results and delay the appearance of MS. The course of our patient was better than we expected. CLINICAL CASE: A 10 year old prepubertal girl complained of progressive loss of vision and slight pain in the right eye for 26 days before admission to hospital. On examination there was obvious papillitis of the right ocular fundus with total loss of the pupillary light reflex, together with consensual hyporeflexia of the left eye. Study of the visual evoked potentials (VEP) showed that there was marked delay of the P-100 wave, and a lower amplitude in the right eye. Magnetic resonance imaging did not show any demyelinated focus. Serological testing for neurotropic viruses was negative. CONCLUSIONS: After the initial phase of intravenous treatment (third day) there was subjective recovery of vision and the pupillary light reflex returned. VEP studies showed marked recovery. Thirty days after treatment was started there was almost complete subjective and VEP recovery. This rapid progress, as compared to that of other paediatric cases published, suggests a mechanism involving decompression of the optic nerve.

Anti-Inflammatory Agents↗