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At least 19 recordsLinked to original sources

Visual-evoked response differentiation of ischemic optic neuritis from the optic neuritis of multiple sclerosis.

Fifteen patients with ischemic optic neuritis studied electrophysiologically had a characteristic change of marked reduction in the amplitude of the visual-evoked response even when loss of vision was moderate. The optic neuritis of multiple sclerosis rarely produced this change. Occasionally, small increases in the latent period of the visual-evoked response were recorded from the patients with ischemic optic neuritis. The optic neuritis of multiple sclerosis usually produced significant increases in the latent period. When the normal nerve was tested in patients with ischemic optic neuritis, the visual evoked response was normal. In patients with optic neuritis of multiple sclerosis, stimulation of the "normal" nerve usually produced an increase in the latent period similar to that seen when the involved nerve was stimulated.

Aged

A randomized, controlled trial of corticosteroids in the treatment of acute optic neuritis. The Optic Neuritis Study Group.

BACKGROUND AND METHODS: The use of corticosteroids to treat optic neuritis is controversial. At 15 clinical centers, we randomly assigned 457 patients with acute optic neuritis to receive oral prednisone (1 mg per kilogram of body weight per day) for 14 days; intravenous methylprednisolone (1 g per day) for 3 days, followed by oral prednisone (1 mg per kilogram per day) for 11 days; or oral placebo for 14 days. Visual function was assessed over a six-month follow-up period. RESULTS: Visual function recovered faster in the group receiving intravenous methylprednisolone than in the placebo group; this was particularly true for the reversal of visual-field defects (P = 0.0001). Although the differences between the groups decreased with time, at six months the group that received intravenous methylprednisolone still had slightly better visual fields (P = 0.054), contrast sensitivity (P = 0.026), and color vision (P = 0.033) but not better visual acuity (P = 0.66). The outcome in the oral-prednisone group did not differ from that in the placebo group. In addition, the rate of new episodes of optic neuritis in either eye was higher in the group receiving oral prednisone, but not the group receiving intravenous methylprednisolone, than in the placebo group (relative risk for oral prednisone vs. placebo, 1.79; 95 percent confidence interval, 1.08 to 2.95). CONCLUSIONS: Intravenous methylprednisolone followed by oral prednisone speeds the recovery of visual loss due to optic neuritis and results in slightly better vision at six months. Oral prednisone alone, as prescribed in this study, is an ineffective treatment and increases the risk of new episodes of optic neuritis.

Acute Disease

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

Optic neuritis in relation to multiple sclerosis.

Available estimates of the frequency with which a patient with optic neuritis develops multiple sclerosis range from as low as 13% to as high as 87%. In an effort to obtain a better estimate, a nation-wide study of optic neuritis was carried out in Israel. Patients who fulfilled strict diagnostic criteria of optic neuritis were identified and examined periodically. Between 1955 and 1964, 105 patients were found and on the basis of these, the average annual age-adjusted incidence of optic neuritis in Israel was 0.56 per 10(5) population compared to 1.2 per 10(5) cases of multiple sclerosis per year, i.e. optic neuritis was about half as frequent as multiple sclerosis each year. As with multiple sclerosis, optic neuritis was more common in European immigrants to Israel than Afro-Asian immigrants. During a follow-up interval which ranged from 3.3 to 15.6 years (mean 9.5 years), at least 27 of the 105 patients developed multiple sclerosis (28%). A life-table analysis showed that after 10 years 32.3 +/- 5.6% of patients with optic neuritis would develop multiple sclerosis and, after 14 years, about half would develop multiple sclerosis. Risk of dissemination was highest in those who were youngest when optic neuritis developed. Neither sex nor ethnic background influenced risk significantly. Results of the present study support earlier work using life-table methods carried out in Hawaii which also showed that between 29 and 39% of patients with optic neuritis will develop multiple sclerosis within 10 years of onset. The life-table method is a better predictor of prognosis than newer laboratory techniques such as spinal fluid studies of IgG, kappa-lambda light chain ratios and serum/CSF IgG ratios.

Adolescent

[Short-term effect of megadose steroid therapy in optic neuritis].

15 patients with unilateral optic neuritis and 2 patients with bilateral optic neuritis were treated with 1000 mg methylprednisolone i.v. per day for 5 days. In the cases of unilateral optic neuritis, visual acuity was reduced to < or = 0.1, in those with bilateral optic neuritis to < or = 0.6 in the better eye. The treatment was started one to 70 days after the onset of the neuritis. We examined whether vision recovered rapidly during the treatment. As a rapid recovery we defined a fourfold improvement on a logarithmic scale during the 5 days of methylprednisolone medication. Such a rapid recovery was found in 11 of the 15 patients with unilateral and in 1 of the 2 patients with bilateral optic neuritis. A similar recovery was not found before and after the treatment interval. Although we did not have a control group, the correlation in time between the therapy and the rapid recovery suggests that the megadose steroids were effective in our patients. This interpretation is compatible with the results of the randomized controlled multicenter trial of Beck et al. (New Engl. J. Med. 326:81, 1992): However, the beneficial effect was seen up to 6 months only; one year after treatment, visual functions did no longer differ between the megadose and the placebo groups. Low-dose oral steroids did not improve visual function at any time and carried a higher risk for new episodes of neuritis, compared to placebo. Therefore, the "traditional" low-dose steroid therapy for optic neuritis has become obsolete.

Adolescent

Virus antibody levels in the cerebrospinal fluid from patients with optic neuritis.

Virus antibody levels were studied in the cerebrospinal fluid (CSF) of 58 patients with optic neuritis and 58 control patients with no indication of multiple sclerosis (MS) or infectious disorders of the central nervous system (CNS). The specimens were tested against three different structural components of measles virus with measles hemagglutination inhibition (HI), measles hemolysis inhibition (HLI) and gel precipitation (GP) tests. Measles antibodies occurred in 62 per cent of CSF specimens from patients with optic neuritis, and 21 per cent of the controls. In the specimens from patients with optic neuritis, the positive rate figures were: for rubella HI test 35, parainfluenza-1 HI 16, and Epstein-Barr virus immunofuorescence (IF) 53 per cent. The frequencies in the control group were 10, 10 and 26 per cent, respectively. Serum/CSF antibody ratios below 80 occurred in measles tests in 45 per cent of patients with optic neuritis and 16 per cent of the control group. Some patients with optic neuritis (but none from the control group) had a reduced serum/CSF antibody ratio in more than one measles antibody test, The patients with optic neuritis had a higher frequency of low serum/CSF albumin ratios indicating blood brain barrier damage, There were, however, several patients with a normal serum/CSF albumin ratio but low serum/CSF immunoglobulin G and measles antibody ratios. This supports the hypothesis that local production of measles antibodies takes place in CNS in some patients with optic neuritis as well as in MS patients. The CSF specimens were further tested against 12 other viruses and mycoplasma pneumoniae complement fixation, but there were no positive specimens. New CSF specimens were taken from five patients during optic neuritis, and from seven patients later on during the follow-up because of the appearance of new neurological symptoms. There were no changes in virus antibody levels, except for two patients with an increase of measles virus antibody titres.

Adolescent

Factors influencing the risk of multiple sclerosis developing in patients with optic neuritis.

One-hundred and forty-six patients who had presented with optic neuritis but without evidence of demyelination elsewhere in the nervous system, and in whom no specific cause could be identified, were reassessed clinically between one month and twenty-three years after the onset. Fifty-eight patients (40 per cent) had developed MS. All 146 patients were HLA-typed. Three factors were identified which were significantly associated with the development of MS: positive typing for the HLA antigen BT 101, winter onset of the initial attack of optic neuritis in BT 101-positive patients only, and recurrent attacks of optic neuritis. The application of these results to the individual patient is of limited use. However, recurrent attacks of optic neuritis should be given the same significance in the clinical classification of MS as episodes of demyelination occurring elsewhere in the central nervous system in a patient with a previous attack of optic neuritis. The results suggest that optic neuritis is caused by two different environmental agents or groups of agents and that the agent which is most common in the winter leads to the development of MS in the genetically susceptible individual. The agent more common in the summer is much less likely to cause MS in either suscetible or non-susceptible individuals. The biological role of the HLA system in the handling of foreign antigens is discussed and it is suggested that the presence of the HLA antigens associated with MS confers a specific disadvantage on individuals in the ability to handle infection by the MS causative agent and that this allows damaging immunological processes to develop.

Diagnosis, Differential

Delayed visual perception and delayed visual evoked potentials in the spinal form of multiple sclerosis and in retrobulbar neuritis.

(1) We have used both subjective and evoked potential tests to study cases of multiple sclerosis with no history of retrobulbar neuritis (spinal patients) and compared them with patients with multiple sclerosis who had experienced an attack of retrobulbar neuritis (RBN). We measured the delay of steady-state evoked potentials (EPs) elicited by flicker in the medium-frequency (13-25 c/s) range, by flicker in the high-frequency (30-60 c/s) range, and by pattern-reversal. We also measured the delay in seeing (perceiving) both an increase of light intensity and a decrease of light intensity. (2) The difference between perceptual delays for the left and right eyes (D s) was abnormal when retrobulbar neuritis affected only one eye (22/22 patients) even when acuity and discs were normal. It might be supposed that this perceptual test would be ineffective when both eyes were affected by retrobulbar neuritis. However, the value of D was abnormal in cases of bilateral retrobulbar neuritis (5/5 patients). Probably the principal reason is that demyelination was patchy in the patients studied. For this same reason the difference between perceptual delays for two sites in the visual field (T s) may also be abnormal. In principle the perceptual delay test can be effective even when both eyes are similarly delayed: abnormal values of T were recorded in 5 spinal patients for whom D was normal. (3) Perceptual delays were measured for an extended group of 19 patients suffering from spinal multiple sclerosis. Taking both D and T into account, the perceptual delay test alone picked out 12/19 spinal patients. The perceptual delay test has the advantage over EP tests that it can detect islands of demyelination as small as 3 degrees diameter, and the apparatus is cheap and straightforward to use. (4) Thirteen patients with spinal multiple sclerosis, including 6 with no ocular signs or symptoms, were examined with a battery of two evoked potential and one perceptual test. Ten patients had clearly abnormal visual delays. Results for the remaining 3 were equivocal. Delay tests can reveal visual damage in most patients who have not experienced an attack of RBN as well as in practically all patients who have experienced an attack. (5) Correlations between the results of the various tests were different in spinal patients and in multiple sclerosis patients who had experienced an attack of retrobulbar neuritis. Flicker EPs, pattern EPs and visual perception were all delayed in every RBN patient, whereas for spinal patients different tests could pick up different patients. Flicker EPs picked up 5/13 spinal patients, pattern EPs 6/13, perceptual delay (D) picked up 4/13 and perceptual delay T picked up 7/13. (6) Delay tests divided spinal multiple sclerosis patients into two fairly distinct groups. In one group pattern EPs and perception were delayed; in the other group flicker EPs were delayed. This grouping corresponded to a clinical distinction between long-standing patients with visual signs and recent patients without visual signs...

Adult

The epidemiology of optic neuritis in Finland.

Evidence has been presented that optic neuritis partially reflects benign cases of MS which are lost in the epidemiological investigation of the disease. As part of a large epidemiological investigation of MS, 221 patients with pure optic neuritis were identified during the period from January 1, 1967 to December 31, 1971. The mean annual incidence for the whole of Finland was 0.94 per 100,000 population. The female to male ratio was 1.7. The mean age at onset was 31.2 years. The distribution of optic neuritis by counties showed the highest mean annual incidence in the southwestern county of Turku and Pori (1.69) and in the western county of Vaasa (1.68). The prevalence data for MS were highest in these counties. A highly significant deviation from a random distribution according to place at onset and place of birth was obtained. Even the geographical distribution by smaller units, i.e. the combined clerical districts, revealed a firm accumulation to the western districts in the county of Vaasa and to the southwestern districts in the county of Turku and Pori. Thus, optic neuritis showed a similar geographical distribution of Jalasjärvi with several familial cases of MS did not increase the familial percentage when both conditions were considered as a single group. The risk of getting optic neuritis seems to depend on the influence of factors present during childhood. The epidemiological data point to a common factor in the aetiology of optic neuritis and MS.

Adolescent

Later course and prognosis of optic neuritis.

The study was a re-examination of 176 patients with optic neuritis. The follow-up period was for 38 patients, 6-12 months, for 52 patients, 1-5 years and for 86 patients, 6-24 years from the initial attack of optic neuritis. In 66% of the involved eyes visual acuity had again become good or excellent, but in 25% it was poor. The visual field was normal in only 38%, in 30% there was an absolute or relative central defect and in 31% a paracentral or peripheral defect. Recurrent attacks of optic neuritis occurred in one fourth of the patients and was a common finding in MS patients. Nineteen per cent of the eyes had suffered from more than one attack. Visual acuity was good or excellent in more than half, but the visual field was normal in only 29% of the eyes with more than one attack of optic neuritis. The frequency of bilateral involvement was high at the end of the follow-up period, 44% of patients had both eyes involved by optic neuritis. In 47 patients the initial attack was bilateral optic neuritis and 34% of these patient had permanently poor vision in both eyes. The initial attack was unilateral in 30 patients but the other eye became involved later. In 26% of all patients with bilateral involvement, visual acuity was permanently poor in both eyes. Bilateral papillitis was a common manifestation in young patients and in this age group the disease had a tendency towards good recovery.

Adolescent

Retrobulbar neuritis. In vitro evidence of sensitization to myelin basic protein in patients without multiple sclerosis.

Thirty-six normal subjects and 34 patients with retrobulbar neuritis were studied with use of the technique of macrophage migration inhibition factor assay and myelin basic protein as antigen. Serial studies were carried out when possible. Normal subjects gave a mean migration index of 100.9+/-9. Eleven patients with retrobulbar neuritis alone gave a mean migration index of 55+/-16 in the first 3 weeks of illness, 89+/-17.3 during the fourth to the twenty-fourth weeks, and 100.9+/-9.0 after the twenty-fourth week. Ten multiple sclerosis patients with retrobulbar neuritis gave values of 61+/-21 in the first 3 weeks of an attack and 92+/-22.8 during the fourth to the twenty-fourth weeks, and 12 other multiple sclerosis patients 24 weeks or longer after an attack gave a value of 101.9+/-12.6. In a mean follow-up period of 1.9 years, only two patients presenting with retrobulbar neuritis alone have had a diagnosis of multiple sclerosis established; three others have weakness and reflex change in one limb only; and four have minor psychiatric problems. One retrobulbar neuritis patient has a family history of multiple sclerosis, but has no neurologic abnormalities. Comparison of these studies in both groups shows no statistical differences and supports the concept that cell-mediated hypersensitization to central nervous system myelin basic protein, however initiated, is a factor in the pathogenesis of retrobulbar neuritis.

Cell Migration Inhibition

[Recovery of visual field defects in ischemic optic neuropathy and idiopathic optic neuritis].

Fifty-four eyes of 41 patients with optic nerve disease demonstrating acute visual field defects without any traumatic, compressive, or other known etiology were classified into four categories. Those showing poor recovery of visual field defects were ischemic optic neuropathy which was subclassified into either anterior ischemic optic neuropathy (AION) or posterior ischemic optic neuropathy (PION) according to the ophthalmoscopic changes in the optic nerve head. Those showing good recovery of visual field defects were idiopathic optic neuritis which was subclassified into either papillitis or retrobulbar neuritis according to the ophthalmoscopic pathology of the optic disc. Patients with ischemic optic neuropathy were significantly older than those with optic neuritis. All eyes with optic neuritis showed good recovery of vision, whereas those with ischemic optic neuropathy showed varying outcomes of vision. With regard to the pattern of field defect, central or paracentral scotoma was predominant in all but eyes with AION in which altitude defect predominated. Pale swelling of the optic nerve head and angiographic evidence of circulatory disturbance in the optic disc or adjacent choroid were common findings in eyes with AION, whereas such findings were never observed in eyes with papillitis. The amplitude of pattern visual evoked potential was significantly lower in eyes with PION than in those with retrobulbar optic neuritis. Four patients classified as optic neuritis developed into multiple sclerosis in the follow-up study. It was concluded that poor recovery of visual field defect is one of the most convincing evidences for the diagnosis of ischemic optic neuropathy.

Adult

Optic neuritis in children with poor recovery of vision.

We reviewed the records of 10 children with optic neuritis in whom recovery of vision was poor or incomplete. Our cases were otherwise similar to those described in previous studies in that they were always bilateral, often accompanied by a viral prodrome (seven of 10), and usually associated with disc oedema (seven of 10). Seven of twenty eyes had a final visual acuity of 6/60 or worse and only one patient regained 6/6 vision in either eye. In three patients the best vision in either eye was 6/60 or worse. Recovery of vision was often slow, taking up to six years. Five of 10 patients have developed multiple sclerosis (MS), and one child had acute disseminated encephalomyelitis (ADEM) with optic neuritis. Optic neuritis in children does not always carry a good prognosis for recovery of vision; however, the failure of vision recovery in a short period of time does not necessarily indicate a poor outcome. Some children with optic neuritis develop MS, which can develop even when optic neuritis follows a viral illness.

Adolescent

Quantitative perimetry in compressive optic neuropathy and optic neuritis.

The Goldmann perimetric defects in 20 cases of compressive optic neuropathy and 54 cases of optic neuritis were analyzed. While defects involving the papillomacular bundle were the rule in both compressive and neuritis cases, sparing of the fixational area occurred in 24% of neuritis eyes but in none of the eyes with compressive neuropathy. The most reliable differential perimetric sign was the presence of a hemianopic defect; at least one eye of 15 (75%) cases of compression showed such a defect, which was not found in any neuritis cases. The I2e was the largest kinetic isopter to demonstrate the hemianopic defect in a substantial proportion of cases. These defects were corroborated with sequential static presentation of the I2e to I4e stimuli to either side of the vertical meridan, and with similar techniques using 18/1,000 red test objects at the tangent screen.

Adolescent

Management of optic neuritis.

To improve understanding and effectiveness of therapy in optic nerve disease, various causes of so-called optic neuritis should be identified when possible. The clinical characteristics of demyelinating optic neuropathy can be contrasted with those of ischemic optic neuropathy, nutritional optic neuropathy, true optic nerve inflammation (e.g., luetic), optic nerve infiltration with tumor, and compression neuropathy caused by adjacent tumor. Radiologic studies and other means of investigating patients with optic neuritis are reviewed. Arguments in favor of, and against, treatment of presumed demyelinating optic neuritis are presented along with representative corticosteroid treatment regimens. The natural tendency toward spontaneous improvement of optic neuritis makes the effect of treatment difficult to assess.

Adrenocorticotropic Hormone

Virus antibody levels in serum specimens from patients with optic neuritis and from matched controls;.

Virus antibody levels in serum specimens taken in acute and convalescent phases from 77 patients with optic neuritits were tested by measles hamagglutination inhibition (HI), measles hemolysis inhibition (HLI), rubella HI, parainfluenza-1 HI, Epstein-Barr immunofluorescence (IF), and against 11 other viruses and mycoplasma pneumoniae with the complement fixation (CF) technique. The virus antibody levels were indicated to be usually very stable, and a fourfold change in virus antibody levels was demonstrated in only eight patients. The virus antibody levels were compared with specimens from two carefully selected control groups. The first control group consisted of 71 healthy persons matched in age, sex and place of residence with the patients with optic neuritis. The other control group consisted of 58 patients with various neurological diseases other than multiple sclerosis (MS) or infectious diseases of the central nervous system. The patients with optic neuritis had significantly higher measles antibody titres than the two control groups in both measles HI and measles HLI tests. Also in 33 patients with optic neuritis of unknown cause, the measles antibody levels were higher than in the control groups. On the other hand, various other antibody tests showed no statistically significant differences between patients with optic neuritis and the control group.

Acute Disease