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PubMed2001

Optic neuritis: differential diagnosis.

Optic neuritis can be mimicked by other optic neuropathies and by anterior segment, choroidal or retinal diseases. Retinal diseases may cause central visual loss when they involve the macular or peripapillary area. Central serous retinopathy, hereditary retinal diseases, white dots syndromes and autoimmune retinopathies may present a clinical picture similar to that of optic neuritis. Complete neuro-ophthalmological examination must be performed to differentiate optic nerve damage from other ocular structures involvement. As in optic neuritis, optic disc and macula appearance may be completely normal in several retinal diseases. Fluorescein angiography and electrophysiological testing are relevant for the differential diagnosis in many challenging cases.

Color Perception↗
PubMed1991

The origin of pain in optic neuritis. Determinants of pain in 101 eyes with optic neuritis.

In 101 eyes with either anterior or retrobulbar optic neuropathy of ischemic or inflammatory origin, ocular pain occurred significantly more often with retrobulbar optic neuropathy. The association of pain with posterior optic nerve lesions supports Whitnall's hypothesis that the pain of optic nerve inflammation is caused by traction of the origins of the superior and medial recti on the optic nerve sheath at the orbital apex. Eye pain reflected neither severity nor origin of optic neuropathy.

Adult↗
PubMed1987

Visual evoked blink reflex in optic neuritis.

The optically evoked blink reflex (BR) was recorded in 30 patients (20 females, 10 males) with primary acute optic neuritis (ON) unassociated with other CNS disorders. The reflex was studied in the acute stage between the 1st and 6th day after onset, during the 1st month following the acute stage once a week, and then 2 and 6 months later. In patients in whom a relapse occurred, the programme was restarted from the beginning. Control values were taken from prior investigations in 50 healthy subjects. In the acute stage differences in the amplitudes were present in 26 patients, but the latencies remained within normal limits. Six patients (20%) developed multiple sclerosis during the 5-year follow-up until December 1985. In these cases the optic BR showed increased latencies and decreased amplitudes. In patients without manifestation of multiple sclerosis the BR remained normal. In 7 patients cranial magnetic resonance imaging (MRI) was done. All patients with some abnormalities in the visual BR also had an abnormal MRI. The pattern-shift visual evoked potentials were abnormal in the acute stage of ON in 90%, and CSF abnormalities were found in 56.6%. In 4 patients (13%) the visual BR could not be evoked at all.

Adolescent↗
PubMed2004

The natural history of recurrent optic neuritis.

BACKGROUND: Optic neuritis (ON) may occur in isolation or may herald multiple sclerosis (MS) or neuromyelitis optica (NMO). Occasionally, ON may recur many times without intervening evidence of dissemination in space. OBJECTIVE: To define the clinical course and prognosis of patients with recurrent ON. DESIGN: Retrospective medical record review and telephone follow-up survey. SETTING: Clinic-based practice in a large tertiary referral institution. MAIN OUTCOME MEASURES: Survival analysis of conversion to MS and NMO and final visual impairment. We studied the association of clinical and demographic factors, the presence of brain lesions on magnetic resonance images, and the use of corticosteroid treatment at the time of the first ON occurrence with conversion to MS and NMO. RESULTS: We identified 1274 patients with ON between 1994 and 2000 and selected 72 (5.7%) with recurrent ON without intervening symptoms of a disseminated demyelinating condition for further analysis. The 5-year conversion rate to NMO was 12.5% and to MS, 14.4%. Among 5 patients with 2 or more lesions consistent with MS on brain magnetic resonance images, 2 (40.0%) converted to MS and none to NMO, while among 11 patients without such lesions, none converted to MS and 2 (18.2%) converted to NMO (P =.16). Conversion to MS occurred in 7 (19.4%) of 36 individuals treated for their first ON episode with corticosteroids vs 4 (44.4%) of 9 untreated individuals (P =.19). There was no difference in the conversion rate to MS between those treated with intravenous steroids (4 [16.7%] of 24) vs oral steroids (3 [25.0%] of 12) (P =.33). Conversion to NMO occurred earlier than conversion to MS (2.3 +/- 1.6 vs 5.3 +/- 4.3 years, respectively; P =.01). Women tended to convert to NMO more frequently than men (female-male ratio for NMO converters, 7:1; MS converters, 2:1; nonconverters, 2:1; P =.56), as did those with a higher annual frequency of ON episodes (NMO converters, 2.0 +/- 1.3; MS converters, 1.0 +/- 1.0; nonconverters, 0.6 +/- 0.5; P =.04). The number of ON events in the first 2 years following the first ON episode was higher in the NMO group (NMO converters, 2.4 +/- 0.9; MS converters, 1.9 +/- 1.1; nonconverters, 1.7 +/- 0.7; P =.04). The final visual impairment was greatest in the NMO group (P =.02). CONCLUSIONS: Patients with rapid succession of severe ON events are more likely to develop a generalized demyelinating disease. Patients with NMO had a worse visual outcome.

Administration, Oral↗
PubMed1998

Visual field defects in optic neuritis and anterior ischemic optic neuropathy: distinctive features.

BACKGROUND: We analyzed the value of visual-field defects in the differential diagnosis of optic neuritis (ON) and non-arteritic anterior ischemic optic neuropathy (AION). METHODS: Ninety-nine consecutive patients with acute-onset optic neuropathy formed the basis for this study. Compressive and vasculitic neuropathies were excluded. Eighty-six patients fulfilled the criteria for either ON (50 patients): < or = 35 years, normal disk, recovery of visual function, or AION (36 patients): > or = 60 years, swelling of the disk, no recovery of visual function. Without knowledge of other clinical data, visual fields obtained by Gold-mann perimetry were classified into five types of defects (forced choice). With the correct diagnosis at hand, fields were reviewed for characteristic features. RESULTS: Forced-choice classification into defect types [%]: Central scotoma ON 68, AION 18; superior altitudinal defect ON 13 AION 7; inferior altitudinal defect ON 8, AION 52; peripheral defect ON 1, AION 5; diffuse defect ON 10, AION 18. Search for pathognomonic defects: a scotoma centered on the fixation point with a sloping border occurred exclusively in ON (25 of 50 patients). An inferior altitudinal defect with a sharp border along the horizontal meridian, particularly in the nasal periphery, occurred only in AION (10 of 36 patients). A steep centrocecal scotoma occurred in 3 of the 36 AION cases and not at all in the ON cases. Scotomas in the center breaking through to the periphery, superior altitudinal defects (with a sloping border along the horizontal meridian) and diffuse depressions verging on blindness occurred in both ON and AION. CONCLUSION: A sctoma centered on the fixation point with a sloping border is highly characteristic of ON, while an inferior altitudinal defect with a sharp border along the horizontal meridian, particularly in the nasal periphery, is highly characteristic of AION. To identify these diagnostic criteria, it can be necessary to examine full fields. With restriction of perimetry to 30 degrees a large central scotoma can be mistaken for a diffuse defect and the border in the nasal periphery can be missed.

Acute Disease↗
PubMed1996

Neural network differentiation of optic neuritis and anterior ischaemic optic neuropathy.

AIMS: The efficacy of an artificial intelligence technique, neural network analysis, was examined in differentiating two optic neuropathies with overlapping clinical profiles-idiopathic optic neuritis (ON) and non-arteritic anterior ischaemic optic neuropathy (AION). METHODS: A neural network was trained with data from 116 patients with 'gold standard' diagnoses of ON or AION. It was then tested with data from 128 patients with presumed ON or AION, and the correlation of the network's diagnosis with that of expert clinicians tabulated. RESULTS: The network agreed with the clinicians on 97.8% (88 of 90) of the patients with presumed ON and 94.7% (36 of 38) of the patients with presumed AION. Youth, female sex, better initial acuity, a central scotoma, subsequent improvement in acuity, or progressive disease biased the network towards a diagnosis of ON, while advanced age, male sex, presence of hypertension, poor initial acuity, an altitudinal field defect, disc oedema, or less improvement in acuity biased the network towards a diagnosis of AION. CONCLUSION: Neural network analysis is a useful technique for classification of optic neuropathies, particularly where there is overlap of clinical findings.

Adult↗
PubMed2002

Acute demyelinating optic neuritis.

Acute demyelinating optic neuritis associated with multiple sclerosis (MS) is the most common cause of inflammation of the optic nerve. The Optic Neuritis Treatment Trial (ONTT) has provided important clinical data on the use of corticosteroids, and demonstrated that patients with characteristic inflammatory lesions within the brain on magnetic resonance imaging had a greater chance of developing clinically definite MS (CDMS). The current approach to patients with optic neuritis has been modified by the results of the Controlled High-Risk Subjects Avonex Multiple Sclerosis Prevention Study (CHAMPS). Patients with an initial clinical episode of demyelination (optic neuritis, incomplete transverse myelitis, or brain-stem/cerebellar syndrome) and at least two characteristic demyelinating lesions within the brain were randomized to receive interferon beta-1a or placebo after initial treatment with intravenous corticosteroids. At the 3-year point patients treated with interferon beta-1a showed a 50% less risk of CDMS. The results of this study have set the standard for patients with a first bout of demyelinating optic neuritis.

Acute Disease↗
PubMed2001

Optic neuritis: historical aspects.

Optic nerve disorders were not reliably diagnosed until the late nineteenth century when ophthalmoscopy became part of the ophthalmic examination. By the early 1900's, all of the salient clinical features of optic neuritis and its relationship to "systemic sclerosis" were recognized, but there was much controversy and misunderstanding about its differential diagnosis, pathogenesis, and possible treatment. During the twentieth century, physicians began to distinguish optic neuritis from infectious, hereditary, toxic, nutritional, and ischemic optic neuropathies. The development of magnetic resonance imaging and the results from recent clinical trials have enhanced our understanding of the relationship between optic neuritis and multiple sclerosis. The next decade holds the promise of further elaborating the pathogenesis and treatment of optic neuritis.

History, 19th Century↗
PubMed1994

Use of pattern electroretinography to differentiate acute optic neuritis from acute anterior ischemic optic neuropathy.

The transient pattern electroretinogram (PERG) was recorded from 16 patients with acute optic neuritis and from 13 patients with acute non-arteritic anterior ischemic optic neuropathy (AION). All patients were tested within 35 days from the the onset of visual symptoms and all had significant central visual field abnormalities in their affected eyes as quantified by automated perimetry. Analysis of the PERGs showed that the amplitude of the N95 peak was abnormally reduced for each eye affected with AION while it remained normal in optic neuritis. No significant alteration in P50 amplitude was observed in either condition. The loss of N95 amplitude in AION was highly correlated with the average depth of visual field loss (in decibels) within a radius of 10 degrees of fixation. These results suggest that PERG could be used early in the course of optic neuropathy to distinguish optic neuritis from AION in those cases for which the diagnosis is still uncertain after the clinical examination.

Adult↗