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At least 127 records · Page 7Linked to original sources
PubMed2005

The optic nerve sheath on MRI in acute optic neuritis.

Optic nerve sheath dilatation or gadolinium-enhancement on magnetic resonance imaging in acute optic neuritis have been previously reported but have been thought to be rare occurrences. This study recruited 33 patients with acute unilateral optic neuritis. All had their optic nerves imaged with fat-saturated fast spin-echo (FSE) imaging, and 28 had imaging before and after triple-dose gadolinium-enhanced fat-saturated T(1)-weighted imaging. Follow-up imaging was performed on 20 patients (15 following gadolinium). A dilated subarachnoid space at the anterior end of the symptomatic optic nerve on FSE imaging was seen in 15/33 cases. In three of these cases, dilatation was visible on short-term follow-up. Optic nerve sheath enhancement was seen in 21/28 cases acutely: seven at the anterior end of the lesion only, five at the posterior end only and nine at both ends. Optic sheath enhancement was seen in 13 patients on follow-up. This study suggests that optic nerve sheath dilatation on FSE images and optic nerve sheath enhancement on triple-dose gadolinium-enhanced images are common findings in acute optic neuritis. Optic nerve sheath dilatation may be due to inflammation of the optic nerve, with its associated swelling, interrupting the communication between the subarachnoid space of the diseased optic nerve and the chiasmal cistern. Optic nerve sheath enhancement suggests that meningeal inflammation occurs in optic neuritis, in agreement with pathological studies of both optic neuritis and multiple sclerosis.

Acute Disease↗
PubMed2000

Steroids for multiple sclerosis and optic neuritis: a meta-analysis of randomized controlled clinical trials.

We conducted a meta-analysis of randomized controlled clinical trials on steroid treatment for multiple sclerosis and optic neuritis. Of the 25 trials comparing steroids and controls without steroid treatment that we identified 12 were selected for this review. A meta-analysis was conducted to calculate the overall odds ratio across the studies for the numbers of patients without functional improvement and with new relapses. The trials included a total of 1714 patients: 998 with multiple sclerosis and 716 with optic neuritis. Any type of corticosteroids or adrenocorticotropic hormone (ACTH) treatment was considered, as was any dosage, route of administration, and length of treatment. Main outcome measures were: (a) number of multiple sclerosis patients who did not improve by at least one point on the EDSS or equivalent scale, or number of optic neuritis patients without complete recovery of visual acuity at 8 or 30 days and at longer follow-up; (b) number of multiple sclerosis patients with at least one new relapse, or number of optic neuritis patients in whom definite multiple sclerosis was diagnosed at longer follow-up. We found that corticosteroids or ACTH produced a significant improvement in disability or visual acuity at 30 days (odds ratio 0.49; 95% CI 0.37-0.64). The improvement was not statistically significant at longer follow-up (0.85; 95% CI 0.67-1.09). The treatment did not significantly reduce the number of patients with relapses (0.74; 95% CI 0.54-1.01). Both low and high doses were effective for 30-day improvement, but only high-dose and short-term therapy were factors that identified subgroups with some reduction in the risk of new relapse. However, the power of the statistical analysis to detect a reliable difference in the subgroups was low. Steroid treatment is therefore effective in accelerating short-term recovery in patients with multiple sclerosis or optic neuritis. Whether steroids are also effective in reducing the risk of relapse, and the optimal dose and length of treatment must still be determined.

Disability Evaluation↗
PubMed1995

Optic neuritis in children: recurrence and subsequent development of multiple sclerosis.

Recurrent optic neuritis and the subsequent development of multiple sclerosis in children, particularly in Asian countries, are not well known. We report on recurrent optic neuritis and subsequent multiple sclerosis in 22 Thai children who were younger than 15 years of age at the onset of optic neuritis, had no previous neurologic illness, and were monitored for 6-20 years. Improvement of vision was observed in 8, 10, and 2 patients after the first, second, and third week of onset, respectively. Two patients had recurrent optic neuritis and the other 2 patients subsequently developed clinical definite multiple sclerosis characterized by hemiparesis at 6 months and myelopathy at 2 years later in 1 patient and myelopathy and brainstem dysfunction in the other at 4 and 6 years later. The frequency of subsequent development of multiple sclerosis after optic neuritis may be similar to that reported from the United States and European countries.

Age of Onset↗
PubMed2006

Optic nerve atrophy and retinal nerve fibre layer thinning following optic neuritis: evidence that axonal loss is a substrate of MRI-detected atrophy.

Magnetic resonance imaging (MRI) measures of brain atrophy are often considered to be a marker of axonal loss in multiple sclerosis (MS) but evidence is limited. Optic neuritis is a common manifestation of MS and results in optic nerve atrophy. Retinal nerve fibre layer (RNFL) imaging is a non-invasive way of detecting axonal loss following optic neuritis. We hypothesise that if the optic nerve atrophy that develops following optic neuritis is contributed to by axonal loss, it will correlate with thinning of the RNFL. Twenty-five patients were studied at least 1 year after a single unilateral attack of optic neuritis without recurrence, with a selection bias towards incomplete recovery. They had MR quantification of optic nerve cross-sectional area and optic nerve lesion length, as well as optical coherence tomography (OCT) measurement of mean RNFL thickness and macular volume, quantitative visual testing, and visual evoked potentials (VEPs). Fifteen controls were also studied. Significant optic nerve atrophy (mean decrease 30% versus controls), RNFL thinning (mean decrease 33% versus controls), and macular volume loss occurred in patients' affected eyes when compared with patients' unaffected eyes and healthy controls. The optic nerve atrophy was correlated with the RNFL thinning, macular volume loss, visual acuity, visual field mean deviation, and whole field VEP amplitude but not latency. These findings suggest that axonal loss contributes to optic nerve atrophy following a single attack of optic neuritis. By inference, axonal loss due to other post-inflammatory brain lesions is likely to contribute to the global MRI measure of brain atrophy in multiple sclerosis.

Adult↗
PubMed2003

Ehrlichiosis optic neuritis.

PURPOSE: To describe a case of ehrlichiosis optic neuritis. DESIGN: Single observational case report. METHODS: A 41-year-old woman with symptoms and clinical and imaging signs consistent with optic neuritis presented to a tertiary care academic center for comprehensive neuro-ophthalmic evaluation. Main outcome measures included preoptic and postoptic neuritis polyvalent ehrlichiosis titers and magnetic resonance imaging (MRI) of orbits with gadolinium. RESULTS: Ehrlichiosis titers drawn 11 days before onset of eye symptoms were negative. Titers drawn 7 days after symptoms began were positive. The optic nerve enhanced with gadolinium on MRI. CONCLUSIONS: Ehrlichiosis can cause optic neuritis and should be considered in patients with optic neuritis after a febrile, flu-like illness in an endemic area.

Adult↗
PubMedDate not supplied

Optic neuritis in herpes zoster ophthalmicus.

BACKGROUND: Optic neuritis in herpes zoster ophthalmicus (HZO) has been reported rarely. We report two cases of HZO optic neuritis with detailed magnetic resonance imaging study and treatment responses. CASES: One patient presented with anterior optic nerve involvement, and the second presented with retrobulbar optic neuritis. Contrast enhanced T(1)-weighted images were obtained in these 2 patients. Intravenous acyclovir and oral prednisolone were given simultaneously. OBSERVATIONS: Magnetic resonance imaging revealed peripheral enhancement of the optic nerve sheath complex on T(1)-weighted scan. Both patients recovered their vision within 3 months following the start of treatment. CONCLUSIONS: Magnetic resonance imaging is helpful for the diagnosis of HZO optic neuritis. Systemic acyclovir and steroid are effective in the treatment of HZO optic neuritis.

Acyclovir↗
PubMed1989

T-lymphocyte subpopulations in acute unilateral optic neuritis.

The authors prospectively analyzed T-lymphocyte subpopulations in the peripheral blood of nine patients with acute unilateral optic neuritis and compared them with 25 controls without neurologic disease. The presence or absence of alterations in circulating T-cell subsets has not been examined previously in patients with isolated optic neuritis. The authors found the mean ratio of inducer (CD4) to suppressor (CD8) T-lymphocytes was 2.07 +/- 0.51 for the group with optic neuritis, statistically indistinguishable from a value of 1.78 +/- 1.04 for the control group. Multiple sclerosis (MS) subsequently developed in one patient. Her inducer/suppressor T-cell ratio was initially 2.66, but progressively increased to 3.68 concomitant with the clinical manifestation of focal neurologic signs. Although optic neuritis may be the initial clinical sign of MS, the periodic alteration of circulating T-lymphocytes increasing the inducer/suppressor T-cell ratio in MS was not observed in those with isolated optic neuritis.

Adult↗
PubMed1986

Optic neuritis and myelopathy in systemic lupus erythematosus.

The optic neuritis of systemic lupus erythematosus (S.L.E.) more frequently results in the persistence of a central scotoma or complete blindness after a single attack than demyelinating optic neuritis, although the initial clinical presentations may be identical. A significant number of patients, however, recover normal vision. Optic neuritis may be the presenting symptom of S.L.E. and as myelopathy may also occur in the course of the disease, confusion with multiple sclerosis may result, especially if there are no arthritic, cutaneous nor visceral manifestations. We report a case of lupus optic neuritis associated with anticardiolipin antibodies and a circulating lupus anticoagulant and suggest these may be a marker for vasculitic optic neuritis and play a role in its aetiology.

Antibodies↗
PubMed2005

[Recurrence of a retrobulbar neuritis? Classic VEP and missing periocular pain].

BACKGROUND: In young patients with the clinical symptoms of a neuritis neuroradiological imaging is not always necessary. This case report describes a young patient who suffered from a recurrence after 5 years. Since all findings, particularly visual evoked potentials, were classic for neuritis, the patient was treated for neuritis although periocular pain was not present. CASE REPORT: Five years after a neuritis of the left eye (OS), the patient was again referred with a visual loss (VA 0.3 OS). In addition to an afferent pupillary defect OS and a constricted visual field OS, an inter-eye latency difference was demonstrated in the visually evoked potentials. The patient was treated with megadose steroid therapy. Although periocular pain as a classic symptom was absent, no neuroradiological imaging was performed. Six weeks later visual acuity and visual fields further worsened, such that a nuclear magnetic resonance imaging was indicated revealing a meningioma fronto-basally compressing the optic nerve. After neurosurgical intervention visual acuity and field stabilized. CONCLUSIONS: In rare cases, meningioma may mimic the symptoms of neuritis. Therefore, neuroradiological imaging is indicated in recurrences or complicated disease courses, particularly if classic symptoms such as periocular pain are missing.

Administration, Oral↗
PubMed1984

Bilateral optic neuritis. A long-term follow-up.

We have endeavoured to determine the fate of the adults and children presenting with bilateral optic neuritis who were reported by Hierons and Lyle (1959) and Meadows (1969). We have follow-up information from a variety of sources on 31 of the 34 adults for up to thirty-seven years, and on 17 of 19 children after up to thirty-two years. Three adult cases were excluded after review. The visual prognosis was variable in the adults but excellent in the children. None of the children has developed clinically definite multiple sclerosis. Two of the 11 adults with simultaneous bilateral optic neuritis developed multiple sclerosis, compared with 8 of 20 with sequential optic neuritis. We conclude that the risk of developing multiple sclerosis after simultaneous bilateral optic neurities in childhood is low; in adult life it is probably higher, but some patients even after more than two decades have no clinical evidence of the disseminated disease. Bilateral optic neuritis is aetiologically and prognostically diverse.

Adolescent↗
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↗
PubMed1992

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↗
PubMed1983

Contrast vision and optic neuritis: neural blurring.

In order to understand the vision of patients with long standing optic neuritis, contrast perception was analysed in some detail for three patients with uniocular anomalies. Contrast detection and contrast matching experiments each demonstrate anomalies in contrast processing for eyes with optic neuritis. In this regard, optic neuritis differs from all other visual anomalies so far investigated where the suprathreshold deficits (from matching experiments) are slight compared with those measured under threshold conditions (from detection experiments). Contrast discrimination is also impaired to a mild degree in optic neuritis but this cannot be predicted on the basis of the matching results. These results bear upon the currently proposed models for contrast coding in the normal visual system as well as the nature of the underlying pathology in optic neuritis.

Adult↗
PubMed1985

A comparison of the changes in suprathreshold apparent contrast in acute and simulated optic neuritis.

A thin PVC film was used as a diffusion filter together with glass lenses in order to induce a unilateral artificial contrast sensitivity depression in controls. These artificially depressed contrast sensitivity functions were made comparable to those assessed in patients during the recovery phase of their acute unilateral optic neuritis. A technique of subjective suprathreshold contrast matching was used to determine the suprathreshold apparent contrast in patients and controls with acute and simulated optic neuritis respectively. The results showed that differences in apparent contrast between the eyes is proportional to the discrepancy in threshold contrast for high and intermediate spatial frequencies in patients with optic neuritis. For low frequencies the apparent contrast difference was independent of threshold differences. Contrast vision of controls with simulated optic neuritis did not show this frequency dependency. There was also a discrepancy in visual acuity between the two groups. Generally the control with artificially depressed contrast sensitivity functions has a letter acuity value lower than that of the optic neuritis patient with a corresponding CSF depression.

Adult↗
PubMed1999

Lack of restriction of T cell receptor beta variable gene usage in cerebrospinal fluid lymphocytes in acute optic neuritis.

OBJECTIVES: There have been many studies reporting restricted patterns of T cell receptor usage in established multiple sclerosis and these have led to clinical trials of immunomodulation directed at deleting clonal T cell populations. The present study aims to test the hypothesis that highly restricted T cell populations are also present in the CSF in the earliest clinical stages of acute demyelinating disease of the CNS. METHODS: T cell receptor Vbeta (TCRBV) gene expression was studied in CSF and blood in nine patients with acute optic neuritis within 7 days of onset of symptoms, six patients with an acute relapse of multiple sclerosis, and 13 control subjects. RNA was extracted and cDNA synthesised from unstimulated CSF and blood lymphocytes, and TCRBV gene segments were amplified from the cDNA by polymerase chain reaction (PCR) using 21 family specific primers. PCR products were separated by polyacrylamide gel electrophoresis and detected via a labelled oligonucleotide probe. A semiquantitative analysis of band intensity was performed by laser densitometry. RESULTS: TCRBV mRNA was detected in the CSF of eight of nine patients with optic neuritis, six of six patients with multiple sclerosis, and five of 13 controls, and was closely correlated with the presence of oligoclonal IgG. Usage of a single TCRBV family was demonstrated in two of nine patients with optic neuritis and two of six patients with multiple sclerosis. The number of TCRBV families expressed in the other patients ranged between 5 and 15 (optic neuritis) and 4 and 17 (multiple sclerosis). CONCLUSIONS: There is a relative lack of restriction of TCRBV usage by CSF lymphocytes in the very earliest stages (<7 days) of acute optic neuritis. This may imply either that multiple sclerosis is not a monoclonal disease even at onset, or that the autoimmune response has widened before the disease becomes clinically evident. This may have important consequences for the design of immune therapies in multiple sclerosis. Further studies are required to determine whether the CSF T cell repertoire at presentation has prognostic importance. Longitudinal studies are required to follow the CSF T cell repertoire from the time of presentation and to determine whether it may have prognostic significance.

Acute Disease↗
PubMed1997

MRI of optic nerve enlargement in optic neuritis.

We report two cases of optic neuritis with optic nerve enlargement on MRI. Both had a clinical course typical for optic neuritis but also had a neuroradiologic finding most commonly seen with optic nerve glioma or meningioma, which initially led to an incorrect diagnosis. We review the six previous reported cases of optic nerve enlargement in optic neuritis. Including our cases, six of eight reported cases were in children with severe initial visual loss. Optic nerve enlargement is a rare finding in optic neuritis that might be a subtype of optic neuritis.

Child↗
PubMed2006

Optic neuritis with visual field defect--possible Ibuprofen-related toxicity.

OBJECTIVE: To report a case of optic neuritis with visual field defect associated with ibuprofen. CASE SUMMARY: A 41-year-old white man developed blurred vision in his right eye and pain with eye and head movements that lasted 2 days after use of ibuprofen 400 mg 3 times daily during the preceding 3 weeks. Medical and family histories were negative for significant related disease. Ophthalmologic examination revealed a marked decrease in visual acuity to 20/200 in the right eye with quadrant visual field loss and absent responses in visual evoked potential (VEP). After discontinuation of the drug and treatment with high-dose intravenous methylprednisolone and subcutaneous low-molecular-weight heparin, the patient's vision improved to 20/70, the visual field defect vanished, and the VEP returned to almost normal values during a 1 year follow-up period. An objective causality assessment revealed that the adverse reaction was possibly related to ibuprofen. DISCUSSION: Ocular toxicity with blurred vision and centrocecal visual field defects have been rarely associated with long-term ibuprofen intake. We report a case of retrobulbar optic neuritis with quadrant visual field defect following short-term but regular ibuprofen intake. Although idiopathic optic neuritis cannot be completely ruled out, the absence of other risk factors and additional findings plus the improvement after discontinuation of the drug speak for isolated toxic optic neuritis of the right eye. CONCLUSIONS: Drug toxicity is an important differential diagnosis in retrobulbar optic neuritis. Clinicians should be aware of the potential optic toxicity, even with short-term use of a drug, and perform a thorough medication history in every patient with visual disturbances without a clear cause.

Adult↗
PubMed1999

A putative role for calpain in demyelination associated with optic neuritis.

Calcium activated neutral proteinase (calpain) is an endopeptidase present in the central nervous system which degrades myelin proteins. To examine the role of calpain in demyelination associated with optic neuritis, immunocytochemical expression of calpain was evaluated in Lewis rats with experimental optic neuritis. Calpain expression was increased in activated microglia, infiltrating macrophages, activated T cells, and reactive astrocytes in experimental optic neuritis compared to controls. Calpain activity and translational expression were also examined by Western blotting studies measuring the extent of myelin protein degradation, calpain-specific fodrin proteolysis, axonal neurofilament degradation, and calpain proenzyme content. Results showed myelin associated glycoprotein and 68 kD neurofilament protein levels were significantly decreased while calpain translational expression and calpain-autolyzed fodrin levels were significantly increased in experimental optic neuritis compared to controls. Thus, increased activity and translational expression of calpain in optic neuritis may be integral to the pathogenesis of this disorder.

Animals↗