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PubMed2001

Optic neuritis in an urban black African community.

PURPOSE: To describe the clinical profile of idiopathic optic neuritis in South African blacks. METHODS: South African black patients with acute isolated idiopathic optic neuritis, treated and followed for at least 3 months at a large medical centre, were studied. Exclusion criteria were other causes of optic neuropathy (such as ischaemic optic neuropathy, toxins or Leber's hereditary optic neuropathy); all causes of optic neuritis (such as HIV, neurosyphilis, sarcoid or connective tissue disease); neurological disease outside of the optic nerves; and any race other than South African black. Patients underwent extensive ophthalmic, neurological, radiological, cerebrospinal fluid and blood assessment. RESULTS: Eighteen eyes of 10 patients were studied. The mean age was 35.7 years and 9 patients were female. Only 2 patients had truly unilateral optic neuritis, the other 8 having either bilaterally simultaneous or consecutive disease. Presenting visual acuity (VA) was less than 6/60 in 17 of 18 eyes, with severe dyschromatopsia in all eyes. Fifteen eyes had optic disc swelling. All patients were treated with corticosteroids. After at least 3 months follow-up only 6 eyes recovered VA of 6/12 or better, with only 3 eyes recovering colour vision of 10/13 or better on Ishihara plate testing. No patient had multiple sclerosis (MS) on presentation, nor developed MS on follow-up. CONCLUSION: Idiopathic optic neuritis in black South Africans differs from that in whites. The higher prevalence of bilateral cases and of optic disc swelling, the weaker association with MS and the extremely poor visual outcome distinguish optic neuritis in black South Africans.

Acute Disease↗
PubMed2003

Myelin oligodendrocyte glycoprotein-specific T cell receptor transgenic mice develop spontaneous autoimmune optic neuritis.

Multiple sclerosis (MS) is considered to be an autoimmune disease of the central nervous system (CNS) that in many patients first presents clinically as optic neuritis. The relationship of optic neuritis to MS is not well understood. We have generated novel T cell receptor (TCR) transgenic mice specific for myelin oligodendrocyte glycoprotein (MOG). MOG-specific transgenic T cells are not deleted nor tolerized and are functionally competent. A large proportion (>30%) of MOG-specific TCR transgenic mice spontaneously develop isolated optic neuritis without any clinical nor histological evidence of experimental autoimmune encephalomyelitis (EAE). Optic neuritis without EAE could also be induced in these mice by sensitization with suboptimal doses of MOG. The predilection of these mice to develop optic neuritis is associated with higher expression of MOG in the optic nerve than in the spinal cord. These results demonstrate that clinical manifestations of CNS autoimmune disease will vary depending on the identity of the target autoantigen and that MOG-specific T cell responses are involved in the genesis of isolated optic neuritis.

Amino Acid Sequence↗
PubMed1978

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↗
PubMed1976

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↗
PubMed1975

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↗
PubMed2002

Inferior vestibular neuritis.

Sudden, spontaneous, unilateral loss of vestibular function without simultaneous hearing loss or brain stem signs is generally attributed to a viral infection involving the vestibular nerve and is called acute vestibular neuritis. The clinical hallmarks of acute vestibular neuritis are vertigo, spontaneous nystagmus, and unilateral loss of lateral semicircular function as shown by impulsive and caloric testing. In some patients with vestibular neuritis the process appears to involve only anterior and lateral semicircular function, and these patients are considered to have selective superior vestibular neuritis. Here we report on two patients with acute vertigo, normal lateral semicircular canal function as shown by both impulsive and caloric testing, but selective loss of posterior semicircular canal function as shown by impulsive testing and of saccular function as shown by vestibular evoked myogenic potential testing. We suggest that these patients had selective inferior vestibular neuritis and that contrary to conventional teaching, in a patient with acute spontaneous vertigo, unilateral loss of lateral semicircular canal function is not essential for a diagnosis of acute vestibular neuritis.

Adult↗
PubMed1975

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↗
PubMed1995

Cytomegalovirus optic neuritis: characteristics, therapy and survival.

Little is known about the natural history of cytomegalovirus (CMV) optic neuritis in the acquired immunodeficiency syndrome. We analyzed the clinical course of CMV optic neuritis in 30 consecutive subjects (35 eyes), and compared the survival of patients with CMV optic neuritis to that of a group having CMV retinitis alone, with both groups matched for ganciclovir therapy. Four untreated eyes had a median final visual acuity of no light perception. The median final visual acuity was 20/100 in treated subjects with a mean follow-up of 6.6 months. Following ganciclovir treatment, 2 eyes showed visual improvement, 17 eyes had unchanged visual acuity, and 12 eyes had marked drop in acuity. Relapse occurred in 4 subjects maintained on single-dose ganciclovir, and was controlled on double-dose ganciclovir. Survival was similar in the group of CMV retinitis alone versus the group of CMV optic neuritis with retinitis. Early recognition and therapy of CMV optic neuritis protects against irreversible visual loss. CMV optic neuritis does not carry a worse prognosis for survival than CMV retinitis alone.

AIDS-Related Opportunistic Infections↗
PubMed2006

Retinal ganglion cell loss induced by acute optic neuritis in a relapsing model of multiple sclerosis.

Multiple sclerosis (MS) and its animal model experimental autoimmune encephalomyelitis (EAE) are marked by inflammatory demyelinating lesions throughout the central nervous system, including optic nerve. Neuronal loss also occurs in MS and EAE lesions, but it is not known whether neuronal loss occurs secondary to inflammation, or as a primary process. In the current study, the relationship of inflammation to retinal ganglion cell (RGC) loss during acute optic neuritis is examined. RGCs were labelled with Flourogold, and EAE was induced in SJL/J mice by immunization with proteolipid protein peptide 139-151 (PLP). At various time points, RGCs were counted and optic nerves were examined for inflammatory cell infiltrates. No optic neuritis was detected prior to day 9 following immunization. Incidence of optic neuritis was 30% at day 9 and increased to over 70% by day 11, remaining high through day 18. In contrast, no RGC loss was detected in eyes with optic neuritis until day 14. A 43.1% reduction in RGC numbers at day 14 increased to 50.8% by day 18. No RGC loss occurred in eyes without optic neuritis. The fact that inflammation precedes RGC loss suggests that neuronal loss during optic neuritis occurs secondary to the inflammatory process.

Animals↗
PubMed1977

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↗
PubMed1991

[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↗
PubMed1984

Relationship of optic neuritis to disease of the paranasal sinuses.

The relationship of paranasal sinusitis to optic neuritis remains an intriguing curiosity to both the otolaryngologist and the ophthalmologist. The literature is replete with anecdotal case reports of patients whose sinusitis appears to have caused optic neuritis. There is much speculation about the pathophysiological mechanisms which relate these two distinct disease entities. Five new cases are described which highlight distinct pathophysiologic routes through which paranasal sinus disease has caused optic neuritis. These include compressive optic neuropathy secondary to mucoceles and/or pyoceles; direct extension of sinus infection to the optic nerve from suppurative paranasal sinusitis; and, in one case, from osteomyelitis of the ethmoid and sphenoid sinuses. The usefulness of computerized axial tomography of the orbits and paranasal sinuses to evaluate optic neuritis and to elucidate in detail the pathophysiology of its relationship to disease of the paranasal sinuses is emphasized. Currently, optic neuritis is felt to be a rare complication of paranasal sinusitis. Paranasal sinus surgery is advocated in those cases where sinus suppuration is suspected, or when a compressive optic neuropathy is caused by a sinus mucocele or pyocele. Since in most cases, however, optic neuritis is self-limited, it is difficult to evaluate the results of surgery in circumstances other than those mentioned already. Continued careful evaluation, management, and documentation of this group of patients is necessary to help better define the relationship between these two disease entities.

Adult↗
PubMed1994

[Rhinogenous retrobulbar optic neuritis: a case report].

Rhinogenous retrobulbar optic neuritis is characterized by neuritis secondary to paranasal sinusitis. A case of rhinogenous retrobulbar optic neuritis that was successfully treated by surgery is reported. A 40-year-old man complained of progressive right visual disturbance. The clinical course and neurological examination suggested right retrobulbar optic neuritis. CT and MRI scans demonstrated a massive tumor-like lesion near the right optic canal. Fifteen days after the onset, decompression of the right optic nerve was performed using a right pterional approach. After surgery, visual disturbance improved, and after about 1 month, the symptom had disappeared. Operative findings, histological examination and the postoperative course were consistent with the characteristics of rhinogenous retrobulbar optic neuritis. We consider decompression of the optic nerve to be effective for the treatment of rhinogenous retrobulbar optic neuritis.

Adult↗
PubMed1998

Measurement of the retinal nerve fibre layer with scanning laser polarimetry in patients with previous demyelinating optic neuritis.

OBJECTIVES: Subjective visual deficits are common after demyelinating optic neuritis despite the frequent return of normal visual acuity. Visual and electrodiagnostic tests have demonstrated evidence of these persisting functional abnormalities, which are thought to be secondary to demyelination and variable axonal loss in the optic nerve. Scanning laser polarimetry (SLP) is a new image analysis technique which uses the polarising properties of the retinal nerve fibre layer (RNFL) to produce a quantitative measure of its thickness. This study was carried out to assess the prevalence, extent, and pattern of RNFL loss after demyelinating optic neuritis using SLP. METHODS: Twenty four patients with a history of previous demyelinating optic neuritis were re-examined. Examination included measurement of logmar visual acuity, Pelli-Robson contrast sensitivity, and the presence of a relative afferent pupil defect and optic atrophy. SLP was performed and a mean RNFL profile from a series of three images from each eye was constructed. This was compared with normative data from 20 age matched normal subjects. The lower 99.9% confidence limit of the normal data was calculated and used as the cut off criterion for abnormality. RESULTS: There were a total of 31 eyes with a history of demyelinating optic neuritis and SLP disclosed an abnormality in 29 (94%) of these. Twenty three eyes recovered an acuity of 0.0 or better, 21 of which had evidence of RNFL loss on polarimetry. Scanning laser polarimetry was the only abnormality found in nine of the 31 eyes (29%). The pattern and extent of RNFL loss was very variable and there was no significant difference in these indices between patients with multiple sclerosis compared with those with isolated demyelinating optic neuritis. CONCLUSION: Scanning laser polarimetry can provide a quantitative measure of RNFL loss after demyelinating optic neuritis, demonstrating its occurrence in a high percentage of patients recovering normal visual acuity.

Adult↗
PubMed2004

Neurologic impairment 10 years after optic neuritis.

BACKGROUND: Participants enrolled in the Optic Neuritis Treatment Trial have been observed for more than a decade to assess the relationship between optic neuritis and the development of clinically definite multiple sclerosis. OBJECTIVE: To assess neurologic disability 10 to 12 years after an initial episode of optic neuritis. DESIGN: Longitudinal follow-up of a clinical trial. SETTING: Fourteen Optic Neuritis Treatment Trial clinical centers performed standardized neurologic examinations, including an assessment of neurologic disability. PARTICIPANTS: One hundred twenty-seven patients who had developed clinically definite multiple sclerosis. MAIN OUTCOME MEASURES: Functional Systems Scale and Expanded Disability Status Scale. RESULTS: The disability of most patients was mild, with 65% of patients having an Expanded Disability Status Scale score lower than 3.0. The degree of disability appeared to be unrelated to whether the baseline magnetic resonance imaging scan was lesion-free or showed lesions (P =.51). Among patients with baseline lesions, the degree of disability was unrelated to the number of lesions that were present on the scan (P =.14). Two patients died owing to severe multiple sclerosis, one of whom had no lesions revealed on the baseline scan. CONCLUSION: Most patients who develop clinically definite multiple sclerosis following an initial episode of optic neuritis will have a relatively benign course for at least 10 years.

Adult↗
PubMed2005

Is optic neuritis more benign than other first attacks in multiple sclerosis?

Optic neuritis presentations are thought to have a better prognosis. The aim of our study was to compare conversion to multiple sclerosis on the different topographies of CISs. We prospectively evaluated 320 patients with CISs (123 with optic neuritis, 78 with brainstem syndromes, 89 with spinal cord syndromes, and 30 with other topographies) who were observed for a median of 39 months. Patients underwent brain MRI within 3 months of their first attack and again 12 months later. Conversion to multiple sclerosis determined either clinically or by MRI was evaluated according to topography. Baseline MRI was normal in 49.2% of patients with optic neuritis compared with 24% in brainstem syndromes, 24% in spinal cord syndromes, and 18.5% in other syndromes. Optic neuritis behaved differently from the other CISs for lower conversion to clinically definite multiple sclerosis and smaller proportion of patients fulfilling MRI dissemination in space, time, or both. Nevertheless, when only patients with abnormal cranial MRI results at baseline were selected, no differences for clinical or MRI conversion were found. Optic neuritis has a smaller risk for conversion to multiple sclerosis. Nevertheless, MRI at baseline, not CIS topography, appears to be the crucial issue at multiple sclerosis presentation.

Adult↗
PubMed1987

Alteration of the visual evoked potential by macular holes: comparison with optic neuritis.

Nine patients with maculopathy (macular holes, macular cysts, and lamellar holes) and ten patients with optic neuritis were examined in order to determine changes in the visual evoked potential (VEP) in response to pattern-reversal stimulation. Eyes with lamellar holes had normal P100 latency, but eyes with macular cysts and macular holes had prolonged P100 latency. Eyes with optic neuritis exhibited greater prolongation of the P100 latency than eyes with macular holes. In contrast, eyes with macular holes had a greater reduction in the steady-state VEP amplitude than eyes with optic neuritis. The prolonged latency occurring in maculopathy may be due to a peculiar amplitude summation noted with half-field VEP, rather than to a true conduction delay like that seen in eyes with optic neuritis. The amplitude slope, which is usually positive in normal controls, was negative for 85.7% of eyes with macular holes and 69.2% of eyes with optic neuritis. The negative amplitude slope may represent a subtle defect in retinal ganglion X cells. Eyes with significantly lower values for four or more of the nine central test points on quantitative automated perimetry had negative amplitude slopes and prolonged P100 latency.

Adult↗
PubMed1985

Optic neuritis during lactation.

The condition called "lactation optic neuritis" has been previously considered a clinical entity of its own. Four women, who developed optic neuritis within 1-12 months while breast-feeding their infants, were investigated ophthalmologically and neurologically in order, to find specific clinical features for this condition. The course of the disorder was similar to classic optic neuritis without lactation. The clinical history and laboratory findings in three of the four patients suggested a demyelinating disorder. It is possible that the decreased immunosuppressive activity just after pregnancy induces the manifestation of an underlying demyelinating disease. The existence of "lactation optic neuritis," however, is questioned as a separate entity of its own. Lactation together with decreased immunosuppression may merely act as a provocateur in the onset of optic neuritis, which in many cases is the first clinical manifestation of incipient multiple sclerosis.

Adult↗