SEARCH · Search PubMed

Results for “Neuritis”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

SourceResearch connectionFrom yearThrough year

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 91 records · Page 5Linked to original sources

PubMed1981

Diagnosing acute retrobulbar neuritis by vitreous fluorophotometry.

We studied six patients with acute retrobulbar neuritis (including two with definite multiple sclerosis) during acute episodes and in convalescence, clinically and with fluorescein angiography and vitreous fluorophotometry. We compared vitreous fluorophotometric readings with visual-evoked responses. In seven of ten eyes with abnormal visual-evoked responses, there was an acute increase in posterior vitreous fluorophotometric readings. Vitreous fluorophotometry may be useful as objective evidence of (1) acute retrobulbar neuritis, (2) involvement of the asymptomatic eye in acute retrobulbar neuritis, (3) the duration of neuritic inflammation in acute retrobulbar neuritis, (4) a recurrence of acute retrobulbar neuritis, (5) alterations in the blood-ocular barrier in patients with acute retrobulbar neuritis in multiple sclerosis, and (6) the effects of corticosteroids and other therapeutic agents in the treatment of acute retrobulbar neuritis.

Acute Disease↗

PubMed2005

Evolving management of optic neuritis and multiple sclerosis.

PURPOSE: To review the relation of optic neuritis to multiple sclerosis (MS) and the indications, modalities, and results of therapy for optic neuritis, for both visual and general neurologic function. DESIGN: Literature review and author's experience. METHODS: Analysis of both laboratory and clinical evidence supporting the use of corticosteroids, immunomodulation agents, and other modalities in the treatment of optic neuritis and MS. RESULTS: Although treatment of optic neuritis with corticosteroids may hasten visual recovery to a minor degree, it has no long-term beneficial effect on visual outcome. Optic neuritis is frequently the initial manifestation of multiple sclerosis. The risk of later development of clinically definite MS (CDMS) correlates with white matter demyelinative lesions on magnetic resonance imaging (MRI). The role of corticosteroid therapy alone in reducing the risk of subsequent MS is unclear, but recent studies suggest that the combination of immunomodulation agents (IMAs) and corticosteroids significantly reduces the later development of MS. Current research indicates that, contrary to previous doctrine, axonal damage is an early finding in MS. CONCLUSIONS: The risk of MS after optic neuritis may be predicted. The use of corticosteroids and IMAs, particularly in those at substantial risk, reduces the frequency and severity of developing CDMS. Earlier, more aggressive therapy in optic neuritis may be proven to reduce permanent axonal injury and progressive disability in MS.

Adjuvants, Immunologic↗

PubMed2003

Correlation between optic disc atrophy and aetiology: anterior ischaemic optic neuropathy vs optic neuritis.

BACKGROUND: The morphologic features of swollen disc in the acute stage of optic neuritis and anterior ischaemic optic neuropathy (AION) have been extensively investigated in contrast to the morphologic features of optic disc atrophy after these events. OBJECTIVE: : A prospective study to evaluate the morphologic features of optic disc atrophy 6 months or more after optic neuritis and nonarteritic AION. PATIENTS AND METHODS: A total of 35 optic discs after nonarteritic AION (n=27) and 24 after optic neuritis (n=19) in otherwise healthy subjects have been evaluated by direct fundoscopic examination with a +90 diopters lens and optic disc photography. The average age of patients at the onset of AION was 57.8 years (range: 38-80) and at the onset of optic neuritis was 32.6 (range: 19-46). The female:male ratio was 18 : 17 in the former and 15 : 9 in the latter. The evaluated parameters included: degree of rim pallor (0 to +3), location of rim pallor, height of rim above the retina, depth and width of cup, peripapillary retinal artery to vein (A : V) ratio, and peripapillary pigment epithelial atrophy. A comparison was made also with 17 age-matched normal discs of 17 patients. Statistical significance was calculated with chi(2) and Fisher's exact test. RESULTS: Most of the discs after AION were paler (+2: 70%, +3: 26%) than after optic neuritis (normal colour: 8%, +1: 58%, P< or =0.007). Rim segmental involvement after AION was usually either superior 'altitudinal' (53%) or inferior 'altitudinal' (29%), whereas after optic neuritis, it was usually either temporal-central (papillomacular) (42%) or diffuse temporal (42%, P<0.0001). Discs had lower A : V ratio (1 : 3, 40%) after AION compared with optic neuritis (1 : 3, 8%) (P=0.007). There were no significant differences between the two groups in height of the rim, cupping, and peripapillary atrophy. CONCLUSIONS: : A combination of the degree of rim pallor, location of rim pallor, and A : V ratio may be of value in assessing the aetiology of optic disc atrophy when no previous clinical data are available and a compressive lesion has been ruled out.

Acute Disease↗

PubMed1994

Autoimmune T cell repertoire in optic neuritis and multiple sclerosis: T cells recognising multiple myelin proteins are accumulated in cerebrospinal fluid.

Monosymptomatic unilateral optic neuritis is a common first manifestation of multiple sclerosis. Abnormal T cell responses to myelin components including myelin basic protein (MBP), proteolipid protein (PLP), and myelin-associated glycoprotein (MAG) have been implicated in the pathogenesis of multiple sclerosis. Antigen-reactive T helper type 1 (Th1)-like cells that responded by interferon gamma (IFN-gamma) secretion on antigen stimulation in vitro were counted. Untreated patients with optic neuritis and multiple sclerosis had similarly raised levels of T cells recognising MBP, PLP, and MAG in peripheral blood. Such T cells were strongly enriched in CSF. None of these myelin antigens functioned as immunodominant T cell antigen characteristic for optic neuritis or multiple sclerosis. The autoimmune T cell repertoire was not more restricted in optic neuritis (as an example of early multiple sclerosis). The autoreactive T cell repertoires differed in blood compared with CSF in individual patients with optic neuritis and multiple sclerosis. No relations were found between specificity or quantity of autoreactive T cells in blood or CSF, and clinical variables of optic neuritis or multiple sclerosis, or occurrence of oligoclonal IgG bands in CSF. The role of raised MBP, PLP, and MAG reactive Th1-like cells found in optic neuritis and multiple sclerosis remains unexplained.

Adolescent↗

PubMed2005

Optic neuritis with concurrent etanercept and isoniazid therapy.

OBJECTIVE: To report a case of optic neuritis associated with concurrent etanercept and isoniazid therapy. CASE SUMMARY: A 55-year-old man diagnosed as having rheumatoid arthritis had received treatment with nonsteroidal antiinflammatory drugs, sulfasalazine, oral methotrexate, leflunomide, and deflazacort. Four months prior to admission, he had a Disease Activity Score of 6.06; treatment with etanercept was considered. Three months prior to admission, because of evidence of latent tuberculosis, isoniazid 300 mg once daily and pyridoxine 50 mg once daily were prescribed. Treatment with subcutaneous etanercept 25 mg twice weekly was started 5 days after isoniazid was initiated. Two weeks prior to admission, the patient developed blurred vision in his left eye. Ten days later, his vision worsened and he was hospitalized. The visual acuity in both eyes was 0.7, and a campimetric examination was compatible with optic neuritis. Magnetic resonance imaging of the brain revealed lesions suggesting demyelinating lesions. The clinical course was consistent with bilateral optic neuritis. Etanercept was stopped, and isoniazid was replaced with rifampin 600 mg once daily. The patient was treated with intravenous methylprednisolone hemisuccinate 1 g/day for 5 days followed by oral prednisolone, resulting in a minor subjective improvement in left eye visual acuity. He then received oral prednisone for 3 weeks, slowly tapering to discontinuation. DISCUSSION: No physiologic factors could have predisposed this patient to develop optic neuritis. He was not diagnosed with a demyelinating disease or underlying systemic condition. The optic neuritis was unlikely to be an early manifestation of multiple sclerosis based on the clinical course and the negative results of the imaging tests. Furthermore, there was a close temporal correlation between the drug exposure and the onset of symptoms. After discontinuation of etanercept and isoniazid therapy, the patient's general condition improved. Use of the Naranjo probability scale indicated a possible relationship between optic neuritis and combined etanercept-isoniazid therapy. CONCLUSIONS: Patients initiated on etanercept and isoniazid should be closely monitored for the development of adverse neurologic signs and effects. If optic neuritis is determined, etanercept and isoniazid should be discontinued immediately.

Antitubercular Agents↗

PubMed2006

[Clinical characteristic of optic neuritis and its relevancy with human leukocyte antigen].

OBJECTIVE: To investigate clinical characteristics of optic neuritis and its association with HLA (human leukocyte antigen). METHOD: The clinical data of 42 patients with optic neuritis were collected and flow polymerase chain reaction-reverse sequence specific oligonucleotide probe (PCR-rSSOP) was used to determine the genotype of HLA-DRB1. RESULTS: Two patients confirmed as Leber hereditary optic neuropathy by gene sequencing were excluded from the study. The complaint of pain was found in the patients (31/40) of optic neuritis. The visual field defect varied with patients and central and pericentral scotoma were demonstrated in 7 patients of 17. Of 40 patients with optic neuritis, 20 (50.0%) showed multifocal brain lesions in white matter by MR scanning. 26 of 38 patients had increased STIR signals. Inflammatory demyelinating changes were found in cerebral spinal fluid in 21 patients (80.8%). Out of demonstrated brain abnormal was revealed in 29 (72.5%) patients using MRI and/or CSF examination. The rate of HLA-DRB1(*)15 in the patients (35.0%) was much higher than control (19.4%), (chi(2) = 4.2328, P = 0.0397). Frequencies of HLA-DRB1(*)15 increased significantly in 26 female patients. The increased frequencies of HLA-DRB1(*)15 were associated with CSF abnormality and no relevancy was found with onset times, brain MR changes and increase of optic nerve signals. Acute optic neuritis responded well to intravenous megadose of methylprednisolone or immunoglobulin. CONCLUSIONS: Most of optic neuritis was characterized as clinical inflammatory demyelinating disease. HLA-DRB1(*)15 might correlated with genetic susceptibility of female patients with optic neuritis.

Adolescent↗

PubMedDate not supplied

[Surgical decompression of neuritis of Hansen's disease].

The recent progress were focused on: the identification of the general immunological mechanism of the hansenian neuritis, demonstrated by endoneural biopsies; the different pathology of the two categories of neuritis; the pathophysiologic derangements, inducing hypoxia or anoxia in the truncular involved segment. The adjuvant role of the canals is important; the clinical differences of the two categories of neuritis and the cases we shall treat by emergency; the importance of antireactionnal treatment and of the notation by tests for the study of the results. The goals are the hemodynamic decompression, useful in the first stage of ENL neuritis, the mechanical decompression of neural fasciculus and the urgent exeresis of necroses or evacuation of febrile abscess. Three technics a re studied: Extraneural and epineural decompression fascicular endoneural necrosis, neurolysis and complex neurolysis for evaluated ENL neuritis and for endoneural necrosis. The different indication according to the two categories: medico-surgical treatment for ENL neuritis, and according the precocity and the delay of the antireactional treatment, and also the absolute emergency of the necrosis and febrile abscess. The results of the treatment of 258 cases of recent neuritis are presented.

Acute Disease↗

PubMed1998

Optic neuritis in African Americans.

OBJECTIVE: To describe the clinical profile of demyelinating optic neuritis in African Americans. METHODS: The medical records of all patients with a diagnosis of optic neuritis examined at the Neuro-Ophthalmology Unit at the Emory University Eye Center (Emory) and at the Grady Memorial Hospital Eye Clinic (Grady), Atlanta, Ga, between 1989 and 1996 were retrospectively reviewed. PATIENTS: African American and white patients, aged 15 through 55 years, with a single initial episode of acute optic neuritis of unknown or demyelinative origin were included in the study. Study patients included 23 African American patients and 56 white patients examined at Emory as well as 10 African American patients examined at Grady. RESULTS: There were no significant differences among the African American study patients, the white study patients, and patients from the Optic Neuritis Treatment Trial (ONTT) regarding sex (P=.36), age (P=.73), or the presence of disc edema (P=.40), lesions found on magnetic resonance imaging (P=.43), or multiple sclerosis (P=.54) at the onset of an initial episode of optic neuritis. The Emory African American patients presented with more frequent severe visual loss (13 [93%] of 14 patients with a visual acuity < or =20/200) compared with Emory white patients (12 [39%] of 31 patients; P=.002) and with ONTT patients (161 [36%] of 448 patients; P<.001). At follow-up examination of at least 1 year, Emory African American patients had worse vision (9 [39%] of 23 patients <20/40, and 4 [17%] of 23 patients < or =20/200) compared with Emory white patients (5 [8%] of 63 patients <20/40, P=.001; 3 [5%] of 63 patients < or =20/200, P=.08), and with ONTT patients (29 [7%] of 409 patients <20/ 40, P=.0001; 12 [3%] of 409 patients < or =20/200, P=.01). Compared with ONTT patients, the Emory African American patients combined with the Grady African American patients had more frequent severe visual loss (visual acuity < or =20/200) at presentation (18 [90%] of 20 patients vs 161 [36%] of 448 patients; P<.001) and at follow-up examination of at least 1 year (6 [18%] of 33 patients vs 12 [3%] of 409 patients; P=.002). Seven (58%) of 12 African American patients with multiple sclerosis had a "neuromyelitis optica" presentation defined by the presence of neurological deficits limited to the optic nerves and spinal cord. CONCLUSIONS: The African American study patients with a single episode of demyelinating optic neuritis had visual acuities more severely affected at onset and after 1 year of follow-up compared with the white study patients and with patients in the ONTT. In the African American patients, multiple sclerosis occurred most frequently in a "neuromyelitis optica" form.

Acute Disease↗

PubMed1999

Adenoviral gene therapy with catalase suppresses experimental optic neuritis.

OBJECTIVE: To determine if adenoviral-mediated transfer of the gene for catalase (CAT), the reactive oxygen species scavenger, suppresses experimental optic neuritis. CLINICAL RELEVANCE: Gene therapy with CAT delivered by an adeno-associated viral vector was previously shown to suppress experimental optic neuritis. Because the transduction of protein expression with recombinant adeno-associated viral vector is relatively slow, taking weeks to reach full levels, we studied the effects of replication-deficient adenovirus containing CAT in suppressing experimental optic neuritis. Transduction with adenovirus occurs within days of inoculation, thus, it may be more applicable for the treatment of patients with acute optic neuritis. MATERIALS AND METHODS: Replication-deficient adenovirus containing CAT was injected above the right optic nerve heads of SJL/J mice that were simultaneously sensitized for experimental allergic encephalomyelitis. For controls, the left eyes were injected with the replication-deficient adenovirus without CAT or no virus. The histological effects of CAT on the lesions of experimental allergic encephalomyelitis were measured by computerized analysis of the myelin sheath area (for demyelination), optic disc area (for optic nerve head swelling), the extent of the cellular infiltrate, extravasated serum albumin labeled with immunogold (for disruption of the blood-brain barrier), and the in vivo hydrogen peroxide reaction product. RESULTS: After 1 month, cell-specific catalase activity, evaluated by the quantitation of catalase immunogold, was increased about 2-fold each in endothelia, oligodendroglia, astrocytes, and axons of the CAT-inoculated right optic nerves compared with the control left optic nerves. The increased cellular levels of catalase reduced demyelination by 30%, optic nerve head swelling by 25%, cellular infiltration by 26%, disruption of the blood-brain barrier by 61%, and in vivo levels of hydrogen peroxide by 81%. CONCLUSIONS: Adenoviral-mediated gene transfer increased catalase levels in all optic nerve cell types, and it persisted for 1 month after inoculation. The increased cellular levels of catalase suppressed demyelination and blood-brain barrier disruption at the foci in the optic nerve where prior magnetic resonance imaging and histopathologic studies have demonstrated the demyelinating inflammation of experimental and human optic neuritis. Together, they suggest that gene therapy with CAT may be helpful in the treatment of patients with optic neuritis.

Adenoviridae↗

PubMed1995

Acute optic neuritis: myelin basic protein and proteolipid protein antibodies, affinity, and the HLA system.

Anti-myelin basic protein, anti-proteolipid protein, and anti-myelin basic protein peptide (amino acid residues 1-20, 63-88, and 89-101) antibody-secreting cells were studied in 20 patients with idiopathic optic neuritis, 20 with optic neuritis as part of multiple sclerosis, and 20 neurological control subjects. Antibody-secreting cells were enumerated with an immunospot assay; the relative binding affinity of the antibodies was estimated by elution with thiocyanate. Patients with optic neuritis had more anti-myelin basic protein and anti-proteolipid protein antibodies than did control subjects (both p < 0.05); there was no difference between idiopathic optic neuritis and optic neuritis as a symptom of multiple sclerosis. Presence of the multiple sclerosis-associated DRB1*1501 gene was not associated with preferential synthesis of high-affinity antibodies reactive with a single myelin basic protein peptide or with preferential synthesis of either anti-myelin basic protein or anti-proteolipid protein antibodies. The results demonstrate a potential for intrathecal synthesis of both anti-myelin basic protein and anti-proteolipid protein antibodies of high apparent affinity in patients with optic neuritis.

Adolescent↗

PubMed2006

Imaging of the optic disc and retinal nerve fiber layer in acute optic neuritis.

PURPOSE: To demonstrate whether optical coherence tomography (OCT-3) and scanning laser ophthalmoscopy (HRT-2) can be used to measure changes of the optic disc and peripapillary retinal nerve fiber layer (RNFL) in eyes with acute retrobulbar optic neuritis that have no clinically apparent optic disc swelling. To correlate these findings with presentation magnetic resonance imaging (MRI) of the affected optic nerve. METHODS: Eight consecutive patients with acute retrobulbar optic neuritis, who had no prior optic neuritis in either eye, were prospectively investigated at presentation and at between 1 and 3 months with clinical examination, OCT-3, HRT-2. At presentation, MRI of the optic nerves were performed in 7/8 patients. RESULTS: Compared to unaffected eyes, affected eyes without clinically seen optic disc swelling at baseline, there was a non-significant trend to increased thickness in the total RNFL, superior and nasal measurements. Baseline HRT in affected eyes showed smaller mean cup to disc ratio (p=0.003) and a smaller cup area (p=0.002) compared with the unaffected eye. The MRI-demonstrated optic nerve lesion did not correlate with OCT RNFL thickening or HRT decrease of the physiological cup. Follow-up imaging of the affected eyes showed normalization of HRT cup size parameters and OCT RNFL thickness (p<0.04). At follow-up, the temporal RNFL had thinning in 7/8 affected eyes (46.8 mum, p=0.021) compared with fellow unaffected eyes (57.8 mum), which did not change. CONCLUSION: OCT-3 and HRT demonstrate mild RNFL thickening or optic disc swelling in acute optic neuritis, even when swelling is not seen clinically. OCT-3 appears to reveal measurable RNFL thinning in the temporal quadrant after retrobulbar optic neuritis, even though vision improves. RNFL imaging may be useful in future studies of residual injury after optic neuritis.

Acute Disease↗

PubMed2004

Clinical characteristics of Japanese children with optic neuritis.

The clinical characteristics of children with optic neuritis have been reported to be different from that of adults and to vary among different races. To determine the clinical characteristics of Japanese children with optic neuritis, we examined the medical records of 41 children who were diagnosed with optic neuritis at the Department of Ophthalmology of Chiba University Hospital between January 1979 and December 2001. Information on the sex, age of onset, laterality, initial visual acuity, final visual acuity, recent infections and immunizations, and presence of systemic neurologic diseases, such as multiple sclerosis or acute disseminated encephalomyelitis, was obtained. These findings revealed that the clinical features of optic neuritis in children were similar to those reported earlier. The percentage of optic neuritis cases that developed multiple sclerosis in children was similar to that for children in Europe and North America, and this percentage was not lower than that in adults in our clinic. These findings can be taken as the characteristics of optic neuritis of children in Japan.

Adolescent↗

PubMed1999

Comparison of central and peripheral visual field properties in the optic neuritis treatment trial.

PURPOSE: To compare the results of peripheral kinetic visual field testing and central static perimetry for patients enrolled in the Optic Neuritis Treatment Trial to determine (1) whether loss and recovery of visual field sensitivity in the far periphery was different from that observed in the central visual field and (2) whether the far peripheral visual field provided additional useful information that was not available in the central visual field results. METHODS: Both affected and fellow eyes of 448 patients with optic neuritis in the Optic Neuritis Treatment Trial were evaluated according to the trial protocol during the patients' first 3 years in the study. Central static visual field tests were performed with program 30-2 on the Humphrey Field Analyzer, and peripheral kinetic testing consisted of plotting the I3e and II4e isopters on the Goldmann perimeter. Both test procedures were conducted according to the trial protocols, and quality control assessments and clinical evaluations were performed on all the visual fields. RESULTS: For both affected and fellow eyes at all 11 visits, there was a greater number of abnormal visual fields in the central static perimetry results than in the peripheral kinetic data. Only 2.9% of affected eyes had an abnormal peripheral visual field with a normal Humphrey mean deviation during year 1. At baseline, 97.1% of affected eyes had an abnormal Humphrey mean deviation on central static testing, whereas only 69.9% had abnormal peripheral kinetic visual fields. Approximately 80% of the I3e and II4e isopters for affected eyes that were abnormal at baseline were within normal limits at 30 days, but it took until week 19 for even 70% of the Humphrey mean deviations to return to normal. In addition, the II4e isopters (more peripheral than the I3e isopters) that were abnormal at baseline showed a somewhat greater percentage of improvement from baseline through day 30 than the abnormal I3e isopters. Although this difference is statistically significant, it is probably not clinically significant. For visits after week 19, approximately 25% to 30% of affected eyes had an abnormal Humphrey mean deviation, whereas only 10% to 15% of peripheral kinetic fields were abnormal. CONCLUSIONS: For the affected eye in optic neuritis, the central visual field shows greater abnormalities than the far peripheral visual field. When the results obtained through Humphrey automated central static visual fields and Goldmann peripheral kinetic isopters are compared, the far periphery appears to recover more rapidly and more completely than the central field, at least in more severe cases of optic neuritis. In most cases, recovery in optic neuritis can probably be monitored effectively with automated perimetry of the central visual field alone. However, in cases of severe loss of the central visual field, a peripheral kinetic visual field obtained with a Goldmann perimeter may provide additional information about the patient's vision in the far periphery.

Adolescent↗

PubMed2000

Ophthalmology update for primary practitioners. Part I. Update on optic neuritis.

Optic neuritis is a common cause of acute visual loss. It is typified by sudden onset of visual impairment and pain with eye movements, followed by spontaneous recovery of vision over several months. Pathologically, optic neuritis is an acute demyelinating event affecting the optic nerve. Objective physical findings are typically few, including an afferent pupillary defect or Marcus-Gunn pupil, whereas subjective psychophysical findings abound (ie, diminished central visual acuity, color vision, decreased contrast sensitivity, and visual field abnormalities). These characteristics have made the diagnosis of optic neuritis based solely on clinical grounds disquieting to practitioner and patient alike. In addition, the fact that optic neuritis is often associated with multiple sclerosis as the first clinical manifestation of disease gives further reason for both patient and physician anxiety. The serious nature of visual loss and the consequences of making the diagnosis of optic neuritis has given rise to extensive testing and expensive treatments. This review is intended to explore our current state of knowledge with regard to (1) clinical presentation, (2) ancillary testing, (3) therapeutic intervention, and (4) associated disease, specifically the risk for multiple sclerosis in the patient who presents with an acute optic neuritis. Finally, a suggestion guide for informing the patient and addressing his or her concerns will be presented.

Humans↗

PubMed2002

Optic neuritis after anthrax vaccination.

OBJECTIVE: To report the occurrence of optic neuritis after anthrax vaccination in two patients. DESIGN: Observational case reports, review of literature. METHODS: Description of clinical history, examination, neuroimaging, and further studies in two patients experiencing optic neuritis in temporal association with anthrax vaccination. MAIN OUTCOME MEASURES: Visual acuity, visual fields. RESULTS: Two patients, 39 and 23 years of age, were seen with acute optic neuritis 1 month and 2 weeks, respectively, after anthrax booster vaccination and successfully treated with intravenous methylprednisolone. The first patient had a typical presentation and course of unilateral retrobulbar optic neuritis with excellent visual recovery. The second patient had a bilateral anterior optic neuritis and has required chronic immunosuppression to maintain his vision. Retinal and optic nerve autoantibodies were present in the second patient. No cross-reactive epitopes between anthrax vaccine and retina/optic nerve were identified. CONCLUSION: Optic neuritis is a potential adverse reaction of anthrax vaccination.

Acute Disease↗

PubMed1990

Retrobulbar optic neuritis in a two-year-old boy.

We report a 2-year-4-month-old boy with retrobulbar optic neuritis. He had a sudden onset of impaired vision, which progressed to total blindness within a day. The visual evoked potential (VEP) showed no activity, but the electroretinogram was normal. Computed tomography (CT) and magnetic resonance imaging (MRI) showed no abnormal findings in the visual tract. The cerebrospinal fluid (CSF) myelin basic protein (MBP) level was elevated and serum anti-myelin antibody was positive. These findings suggested that optic neuritis in our patient was induced by retrobulbar demyelination, perhaps as a result of an autoimmune process. His visual impairment recovered gradually, but not completely, following oral prednisolone therapy. We have followed him for one year since discharge and have found neither recurrence of optic neuritis nor any other neurological disorders. Optic neuritis in children is rare and, to our knowledge, this patient is one of the youngest to be reported. This case suggests that autoimmune mechanisms may induce optic neuritis even in early childhood. In addition to VEP and MRI studies, the CSF MBP and serum anti-myelin antibody can be useful in the diagnosis and follow-up the patients with optic neuritis.

Child, Preschool↗

PubMed1994

Ivermectin and onchocercal optic neuritis: short-term effects.

In 1982 the macrocyclic lactone, ivermectin, was first tested in human patients with onchocerciasis. It has since undergone phase I to IV trials and is now being widely distributed in onchocercal areas. The previous microfilaricide, diethylcarbamazine citrate (DEC), is known to precipitate or exacerbate active optic neuritis in some onchocercal patients, as part of a wider inflammatory response (the Mazzotti reaction). Ivermectin may also cause a mild reaction, especially in people with high microfilarial loads. Few data are available concerning the effect of ivermectin on active optic neuritis. A large, randomised, double-masked, phase IV trial is reported. Individuals were screened for evidence of optic nerve disease (OND), and those identified as possible cases of OND underwent detailed ophthalmic examination, including fluorescein angiography, before being dosed with ivermectin or placebo. A total of 6831 persons were screened of whom 856 (13%) underwent angiography prior to dosing. At 7-14 days after dosing an attempt was made to re-examine 50% of adults over the age of 20 years, including all those with OND. Six hundred and eighty-eight repeat or new angiograms were performed. During this period, 5 new cases of active optic neuritis and one case of exacerbation of existing optic neuritis were identified. Five of these individuals had received placebo and one ivermectin. Two individuals with optic neuritis before dosing had improved after 7-14 days. One had received placebo, the other ivermectin. Ivermectin does not appear to precipitate or exacerbate optic neuritis at a period of 7-14 days.

Adolescent↗

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↗