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At least 217 records · Page 12Linked to original sources
PubMed1995

Lymphocyte proliferation response to S antigen in patients with uveitis and optic neuritis.

PURPOSE: To evaluate the autoimmunity which may play a major role in the etiology of certain forms of uveitis and optic neuritis. METHODS: Lymphocyte proliferation response to retinal soluble antigen in vitro by incorporation 3H-thymidine with DNA was tested in 115 patients with anterior uveitis, posterior/pan-uveitis, optic neuritis, and 50 volunteers with unrelated diseases such as congenital ptosis, strabismus, or completely healthy persons as control. RESULTS: The positive rate of lymphocyte stimulation was 34% (18/53) in anterior uveitis, 41.5% (17/41) in posterior/pan-uveitis, and 57.1% (12/21) in optic neuritis. The results in the experimental groups were significantly different from those of the control group (X2 = 14.76, P < 0.05, x2 = 19.14, P < 0.005, x2 = 26.38, P < 0.005, respectively). CONCLUSION: The autoimmunity plays a role in the pathogenesis in certain forms of uveitis and optic neuritis. Such immune responses may be secondary to the exposition or release of retinal antigens by various causes, leading to activation or augmentation of meager or low-affinity S antigen specific lymphocytes which may pre-exist in the circulation and starting the pathogenic autoimmune process.

Adolescent↗
PubMed1996

Optic neuritis.

Optic neuritis is an acute inflammation of the optic nerve. It is a common manifestation of multiple sclerosis; it may be the initial expression or occur later in the course of the disease. Approximately 15-20% of cases of definite multiple sclerosis present with optic neuritis; another 40% will suffer an attack at some point. When optic neuritis occurs without antecedent signs of multiple sclerosis, magnetic resonance imaging (MRI) of the brain frequently reveals characteristic signal abnormalities of white matter, and analysis of cerebrospinal fluid often shows oligoclonal bands. Optic neuritis has been considered a forme fruste of multiple sclerosis.

Adrenal Cortex Hormones↗
PubMed1997

[Diagnostic studies of optic neuritis in children and adolescents].

PURPOSE: To evaluate the sensitivity of various diagnostic methods in the optic neuritis. MATERIAL AND METHODS: 15 patients, 10 boys and 5 girls, aged 6-18 years, with optic neuritis have been examined. Multiple sclerosis was diagnosed in 12 cases, the etiology of 3 was unknown. The full ophthalmological examination, including static perimetry and visual evoked potentials (VEP) as well as brain computed tomography (CT) and magnetic resonance imaging (MRI) were performed. RESULTS: MRI revealed plaques of demyelination in 11 patients; no pathological changes were observed in cases of idiopathic neuritis. In CT plaques of demyelination were found in 2 patients only. In most cases VEPs were abnormal, mainly there was prolonged latency of deflection, decreased amplitude and more rarely changes of the shape of the record. Static perimetry, with white and blue target, revealed multiple scattered absolute and relative scotoma in the 30 degrees central area. CONCLUSIONS: MRI and static perimetry were the most sensitive methods for detection of the changes in optic neuritis and these methods are also useful in cases with asymptomatic involvement of visual pathway, especially in multiple sclerosis.

Adolescent↗
PubMed2001

Caloric and search-coil head-impulse testing in patients after vestibular neuritis.

The objective of this study was to compare results of quantitative head-impulse testing using search coils with eye-movement responses to caloric irrigation in patients with unilateral vestibular hypofunction after vestibular neuritis. The study population consisted of an acute group (<3 days; N = 10; 5 male, 5 female; 26-89 years old) and a chronic group (>2 months; N = 14; 8 male, 6 female; 26-78 years old) of patients with unilateral vestibular hypofunction after vestibular neuritis. The testing battery included: (1) simultaneous measurement of eye and head rotations with search coils in a magnetic coil frame during passive Halmagyi-Curthoys head-impulse testing and (2) electronystagmography during bilateral monaural 44 degrees C-warm and 30 degrees C-cold caloric irrigation. The main outcome measures were (1) the gain of the horizontal vestibulo-ocular reflex during search-coil head-impulse testing and (2) the amount of canal paresis during caloric irrigation. All acute and chronic patients had a unilateral gain reduction during search-coil head-impulse testing. A pathological canal paresis factor was present in 100% of the acute patients but in only 64% of the chronic patients. The clinically suspected unilateral vestibular hypofunction resulting from vestibular neuritis was validated in all acute patients by both search-coil head-impulse and caloric testing. Hence, either of these tests is sufficient for diagnosis in the acute phase of vestibular neuritis. Chronic patients, however, were reliably identified only by search-coil head-impulse testing, which suggests that the low-frequency function of the labyrinths often becomes symmetrical, leading to a normal canal paresis factor.

Acute Disease↗
PubMed2001

Optic Neuritis.

Patients with signs and symptoms consistent with acute monosymptomatic optic neuritis should undergo evaluation with gadolinium-enhanced MRI of the brain and orbits to determine whether or not they are at high risk for the development of clinically definite multiple sclerosis (CDMS). The presence of two or more white matter lesions (3 mm or larger in diameter, at least one lesion periventricular or ovoid) suggests high risk for CDMS, and should prompt immediate treatment as follows: Intravenous methylprednisolone sodium succinate (1 g intravenously per day for 3 days) followed by oral prednisone (1 mg/kg per day for 11 days) with a 4-day taper (20 mg on day 1, 10 mg on days 2 and 4). Interferon beta 1-a, which has been demonstrated to significantly reduce the 3-year probability of the development of CDMS and the development of clinically silent MRI lesions in high-risk patients with acute optic neuritis, should be considered following IV methylprednisolone treatment (30 &mgr;g intramuscularly weekly). In monosymptomatic patients with fewer than two white matter lesions by MRI, and in patients for whom a diagnosis of CDMS has been established, treatment with IV methylprednisolone followed by oral prednisone (as outlined), should be considered on an individual basis and may hasten visual recovery, but has not been demonstrated to affect long-term visual outcome. In all cases of typical acute monosymptomatic demyelinating optic neuritis, oral prednisone alone at a dose of 1 mg/kg per day, without prior treatment with IV methylprednisolone (1 g per day for 3 days), may increase the risk for recurrent optic neuritis, and should be avoided.

Journal Article↗
PubMed2006

Clonidine reduces hypersensitivity and alters the balance of pro- and anti-inflammatory leukocytes after local injection at the site of inflammatory neuritis.

Perineural alpha2-adrenoceptor activation relieves hypersensitivity induced by peripheral nerve injury or sciatic inflammatory neuritis. This effect is associated with a reduction in pro-inflammatory cytokines, as well as a reduction in local leukocyte number and their capacity to produce pro-inflammatory cytokines. Curiously, clonidine's antinociceptive effect appears with a 2-3-day delay after injection. Previous observations have shown that alpha-adrenoceptor activation induces apoptosis in leukocytes, which would reduce leukocyte number. Additionally, macrophage scavenging of apoptotic cells results in a shift to an anti-inflammatory phenotype, with expression of transforming growth factor (TGF)-beta1. We therefore examined the effects of perineural clonidine 24 h and 3 days after its injection on apoptosis, TGF-beta1 expression and lymphocyte and macrophage phenotype in acute sciatic inflammatory neuritis. Perineural clonidine reduced ipsilateral neuritis-induced hypersensitivity in a delayed manner (3 days after treatment), along with a reduction at this time in lymphocyte number and an increase in caspase-3 and TGF-beta1 expressing cells and macrophages co-expressing TGF-beta1 in the sciatic nerve. One day after injection clonidine treatment was associated with a reduction in lymphocytes and pro-inflammatory Th-1 cells as well as increased numbers of caspase-3 and TGF-beta1 expressing cells and macrophages co-expressing TGF-beta1 in sciatic nerve. Clonidine's effects were prevented by co-administration of an alpha2-adrenoceptor antagonist. These data suggest that alpha2-adrenoceptor activation in sciatic inflammatory neuritis increases local apoptosis and anti-inflammatory products early after treatment. This early effect likely underlies the delayed anti-inflammatory and anti-hypersensitivity effects of perineural clonidine in this setting.

Adrenergic alpha-Agonists↗
PubMed2004

Methylprednisolone, valacyclovir, or the combination for vestibular neuritis.

BACKGROUND: Vestibular neuritis is the second most common cause of peripheral vestibular vertigo. Its assumed cause is a reactivation of herpes simplex virus type 1 infection. Therefore, corticosteroids, antiviral agents, or a combination of the two might improve the outcome in patients with vestibular neuritis. METHODS: We performed a prospective, randomized, double-blind, two-by-two factorial trial in which patients with acute vestibular neuritis were randomly assigned to treatment with placebo, methylprednisolone, valacyclovir, or methylprednisolone plus valacyclovir. Vestibular function was determined by caloric irrigation, with the use of the vestibular paresis formula (to measure the extent of unilateral caloric paresis) within 3 days after the onset of symptoms and 12 months afterward. RESULTS: Of a total of 141 patients who underwent randomization, 38 received placebo, 35 methylprednisolone, 33 valacyclovir, and 35 methylprednisolone plus valacyclovir. At the onset of symptoms there was no difference among the groups in the severity of vestibular paresis. The mean (+/-SD) improvement in peripheral vestibular function at the 12-month follow-up was 39.6+/-28.1 percentage points in the placebo group, 62.4+/-16.9 percentage points in the methylprednisolone group, 36.0+/-26.7 percentage points in the valacyclovir group, and 59.2+/-24.1 percentage points in the methylprednisolone-plus-valacyclovir group. Analysis of variance showed a significant effect of methylprednisolone (P<0.001) but not of valacyclovir (P=0.43). The combination of methylprednisolone and valacyclovir was not superior to corticosteroid monotherapy. CONCLUSIONS: Methylprednisolone significantly improves the recovery of peripheral vestibular function in patients with vestibular neuritis, whereas valacyclovir does not.

Acyclovir↗
PubMed2001

Individual semicircular canal function in superior and inferior vestibular neuritis.

OBJECTIVE: To examine the concept of selective superior and inferior vestibular nerve involvement in vestibular neuritis by studying the distribution of semicircular canal (SCC) involvement in such patients. BACKGROUND: Vestibular neuritis was traditionally thought to involve the superior and inferior vestibular nerves. Recent work suggests that in some patients, only the superior nerve is involved. So far there are no reported cases of selective involvement of the inferior vestibular nerve. METHODS: The authors measured the vestibuloocular reflex from individual SCC at natural head accelerations using the head impulse test. The authors studied 33 patients with acute unilateral peripheral vestibulopathy, including 29 with classic vestibular neuritis and 4 with simultaneous ipsilateral hearing loss, 18 healthy subjects and 15 surgical unilateral vestibular deafferented patients. RESULTS: In patients with preserved hearing, eight had deficits in all three SCC, suggesting involvement of the superior and inferior vestibular nerves. Twenty-one had a lateral SCC deficit or a combined lateral and anterior SCC deficit consistent with selective involvement of the superior vestibular nerve. Two patients with ipsilateral hearing loss had normal caloric responses and an isolated posterior SCC deficit on impulsive testing. The authors propose that these two patients had a selective loss of inferior vestibular nerve function. CONCLUSION: Vestibular neuritis can affect the superior and inferior vestibular nerves together or can selectively affect the superior vestibular nerve.

Adult↗
PubMed1991

Optic neuritis and ischemic optic neuropathy. Overlapping clinical profiles.

A retrospective analysis of the clinical features of 81 patients with acute idiopathic optic neuritis and 58 patients with nonarteritic anterior ischemic optic neuropathy revealed a surprising overlap of manifestations. The rate of visual decline and the range of visual acuities were the same for both. Central scotomas and improvement in acuity were more common in optic neuritis, but occurred often enough in nonarteritic anterior ischemic optic neuropathy to limit their value as single diagnostic criteria. The similarities observed in this study suggest that it may be difficult to differentiate between optic neuritis and nonarteritic anterior ischemic optic neuropathy solely on nosologic grounds in some instances of acute, unilateral optic neuropathy.

Adult↗
PubMed1997

Does optic disc appearance distinguish ischemic optic neuropathy from optic neuritis?

OBJECTIVE: To determine whether characteristics of optic nerve swelling assist in distinguishing between optic neuritis and anterior ischemic optic neuropathy. METHOD: Optic nerve stereophotograph review by masked observers. RESULTS: Altitudinal swelling, pallor, arterial attenuation, and hemorrhage are found more commonly in anterior ischemic optic neuropathy than in optic neuritis. CONCLUSION: Optic disc appearance does help to distinguish anterior ischemic optic neuropathy from optic neuritis, although there are overlapping features.

Acute Disease↗
PubMed2003

Paraneoplastic autoimmune optic neuritis with retinitis defined by CRMP-5-IgG.

Autoantibodies have defined two paraneoplastic visual disorders related to small-cell lung carcinoma: retinopathy ("CAR"-IgG [23kDa, recoverin]) and optic neuritis collapsin response-mediated protein 5 (CRMP-5-IgG [62kDa]). Among 16 patients with CRMP-5-IgG and optic neuritis (aged 52-74 years; all smokers, 9 women), we documented coexisting retinitis in 5. None had CAR-IgG. Fifteen had subacute vision loss, swollen optic discs, and field defects. Vascular leakage was evident at and remote from the disc; 5/5 tested had abnormal electroretinograms. Nine had striking vitreous cells. Vitrectomy showed reactive lymphocytosis (4/4), predominantly CD4(+) (1/1). Most patients had multifocal neurological accompaniments. Cerebrospinal fluid contained lymphocytes (7-32), elevated protein, multiple oligoclonal immunoglobulin bands, and CRMP-5-IgG. Three patients superficially resembled Devic's disease at presentation. One autopsied patient had predominantly CD8(+) T lymphocytes infiltrating optic nerve and spinal cord. Eleven patients had confirmed small-cell carcinoma; 1 had imaging evidence of lung cancer; 3 had renal or thyroid carcinoma. Full-length CRMP-5 protein was identified in normal retina and optic nerve by Western blot analyses. Photoreceptor cells, retinal ganglion cells, and nerve fibers exhibited CRMP-5-specific immunoreactivity. In summary, CRMP-5-IgG defines a paraneoplastic ophthalmological entity of combined optic neuritis and retinitis with vitreous inflammatory cells. Positive serology obviates the need for vitreous biopsy and expedites the search for cancer.

Aged↗
PubMed2005

Retinal nerve fiber layer axonal loss and visual dysfunction in optic neuritis.

Axonal loss is thought to be a likely cause of persistent disability after a multiple sclerosis relapse; therefore, noninvasive in vivo markers specific for axonal loss are needed. We used optic neuritis as a model of multiple sclerosis relapse to quantify axonal loss of the retinal nerve fiber layer (RNFL) and secondary retinal ganglion cell loss in the macula with optical coherence tomography. We studied 25 patients who had a previous single episode of optic neuritis with a recruitment bias to those with incomplete recovery and 15 control subjects. Optical coherence tomography measurement of RNFL thickness and macular volume, quantitative visual testing, and electrophysiological examination were performed. There were highly significant reductions (p < 0.001) of RNFL thickness and macular volume in affected patient eyes compared with control eyes and clinically unaffected fellow eyes. There were significant relationships among RNFL thickness and visual acuity, visual field, color vision, and visual-evoked potential amplitude. This study has demonstrated functionally relevant changes indicative of axonal loss and retinal ganglion cell loss in the RNFL and macula, respectively, after optic neuritis. This noninvasive RNFL imaging technique could be used in trials of experimental treatments that aim to protect optic nerves from axonal loss.

Adult↗
PubMed1988

Cerebrospinal fluid antibodies to myelin basic protein in acute idiopathic optic neuritis.

Free and bound levels of anti-myelin basic protein (anti-MBP) antibodies were measured by radioimmunoassay in the cerebrospinal fluid of 20 patients with acute idiopathic optic neuritis, 133 patients with multiple sclerosis (MS) divided into three clinical subgroups, and 76 normal control subjects. Patients with idiopathic optic neuritis had elevated levels of anti-MBP predominantly in free form, resulting in an elevated (above unity) free/bound anti-MBP ratio similar to that of MS patients with acute relapses. These data suggest that acute idiopathic optic neuritis, like active MS, is associated with anti-MBP.

Autoantibodies↗
PubMed1990

Macrophages but not Schwann cells express Ia antigen in experimental autoimmune neuritis.

This study was designed to identify which cells express major histocompatibility complex class II (Ia) antigen in experimental autoimmune neuritis and may therefore be antigen presenters. Serial 1-micron-thick cryosections of ventral roots of animals with experimental autoimmune neuritis were labeled with Ox6 antibody against rat Ia, the ED1 antibody to identify monocytes/macrophages and an antiserum against S100, a marker for Schwann cells. Ia-positive cells were predominantly present before overt clinical signs and demyelination (day 12). At later stages when many axons were demyelinated, their number was markedly reduced. Few Ia-positive cells that had extending long processes, which over some distance were in immediate contact with several myelin sheaths, were scattered in normal-appearing nerve roots at these later time points. Most of the Ia-positive cells could be identified as ED1-positive lean monocytes/macrophages, but in contrast most phagocytic macrophages in advanced stages of myelin degradation no longer expressed Ia. Ia-positive structures were invariably negative for S100 at early and late stages of experimental autoimmune neuritis, indicating that Schwann cells did not express identifiable Ia antigen. These findings contrast with reports of expression of major histocompatibility complex class II antigens by Schwann cells in human neuropathies. Furthermore they do not support the notion that aberrant Ia expression by Schwann cells plays a major pathogenic role in experimental autoimmune disease of the peripheral nervous system.

Animals↗
PubMed1991

Uhthoff's symptom in optic neuritis: relationship to magnetic resonance imaging and development of multiple sclerosis.

Eighty-one patients with a first attack of isolated optic neuritis, 40 with Uhthoff's symptom (Group 1) and 41 without (Group 2), were studied. All had a neurovisual examination, 74 of 81 patients had the pattern visual evoked potential recorded at rest, and 43 had magnetic resonance imaging brain scans. The pattern visual evoked potential P100 latency was prolonged, Group 1 with a mean of 136 +/- 19 msec. Group 2 with a mean of 131 +/- 19 msec (control subjects, 102 +/- 5 msec; n = 84), and the P100 amplitude was reduced, without significant difference between the groups. Abnormal magnetic resonance imaging scans were present in significantly more patients in Group 1 (p less than 0.025). Treatment of optic neuritis with corticosteroids had no effect on the evolution or duration of Uhthoff's symptom. Overall, 35 of 81 (43%) patients, followed for a mean of 3.5 years, developed multiple sclerosis. The incidence was significantly greater in Group 1 (p less than 0.01). Uhthoff's symptom also correlated with a higher incidence of recurrent optic neuritis. We conclude that Uhthoff's symptom is a prognostic indicator for the early development of multiple sclerosis.

Acute Disease↗
PubMed2005

Optic radiation changes after optic neuritis detected by tractography-based group mapping.

Postmortem data suggest that trans-synaptic degeneration occurs in the lateral geniculate nucleus after optic nerve injury. This study investigated in vivo the optic radiations in patients affected by optic neuritis using fast marching tractography (FMT), a diffusion magnetic resonance imaging (MRI) fiber tracking method, and group mapping techniques, which allow statistical comparisons between subjects. Seven patients, 1 year after isolated unilateral optic neuritis, and ten age and gender-matched controls underwent whole-brain diffusion tensor MR imaging. The FMT algorithm was used to generate voxel-scale connectivity (VSC) maps in the optic radiations in each subject in native space. Group maps of the left and right optic radiations were created in the patient and control group in a standardized reference frame using statistical parametric mapping (SPM99). The reconstructed optic radiations in the patient group were localized more laterally in the posterior part of the tracts and more inferiorly than in the control group. Patients showed reduced VSC values in both tracts compared with controls. These findings suggest that the group mapping techniques might be used to assess changes in the optic radiations in patients after an episode of optic neuritis. The changes we have observed may be secondary to the optic nerve damage.

Adult↗
PubMed1992

Pattern electroretinogram as a function of spatial frequency after retrobulbar optic neuritis.

Steady-state (8-Hz) pattern electroretinograms in response to counterphased sinusoidal gratings of variable spatial frequency (0.6-4.8 c/deg) were recorded in 17 patients who had had retrobulbar optic neuritis in one or both eyes (23 eyes with a clinical history of optic neuritis) and in 21 age-matched normal subjects. Amplitude and phase of the Fourier-analyzed pattern electroretinogram second harmonic were measured. The mean pattern electroretinogram amplitude of patients was significantly reduced compared with that of controls. Amplitude reductions were more marked at intermediate (1-1.4 c/deg) than at lower or higher spatial frequencies. Therefore, the average amplitude versus spatial frequency response function differed significantly in patients compared with controls, displaying a lowpass instead of a band-pass shape. No significant differences in the mean pattern electroretinogram phase were observed between groups at any spatial frequency. These results indicate spatial frequency-dependent abnormalities in the pattern electroretinogram amplitude after optic neuritis, suggesting a specific loss of retinal neurons sensitive to stimuli of intermediate spatial frequencies.

Adult↗
PubMed1986

Optic neuritis following chickenpox in adults.

Three cases of bilateral optic neuritis, one of which also had transverse myelitis, are described in young adults following chickenpox. Severe bilateral loss of vision developed in all cases and was followed by good visual recovery in the two with isolated optic neuritis, but poor recovery in the patient with concomitant transverse myelitis. The interval between the initial rash and subsequent optic neuritis suggests an immunological pathogenesis for this complication.

Acyclovir↗