View clinical trials related to Neuritis.
Filter by:Optic neuritis (ON) is a common event in Multiple Sclerosis (MS), and causes significant loss of nerve cells in the eye, resulting in poor vision. Optic neuritis also provides a sensitive way of testing the effectiveness of drugs that may help protect from loss of nerve cells in ON and therefore in MS. The investigators have identified through laboratory and early clinical research in humans that amiloride (a water tablet already in use) may be a drug that can be of benefit in optic neuritis by protecting from loss of nerves cells, ie a neuroprotective drug. The purpose of this study is to assess the efficacy of amiloride as a neuroprotective drug in optic neuritis
The primary objective of the study is to evaluate the efficacy of BIIB033 in subjects with their first episode of unilateral Acute Optic Neuritis (AON). The secondary objective of this study in this study population is to assess the safety, tolerability, and pharmacokinetics (PK) of BIIB033.
Patients aged 18-65 with acute demyelinating optic neuritis where treatment with high dose corticosteroids are already been chosen by the patient and the diagnosing physician will be contacted for screening and enrollment. Patients will then be randomized to receive equivalent doses of either intravenous (IV) or oral corticosteroid treatment. Optic nerve function assessments will be compared at baseline, prior to treatment, one and six months post corticosteroid treatment. This will allow for a comparison on whether the route of medication plays a role in the effectiveness of treatment with high dose corticosteroids.
Optic neuritis is caused by inflammation of the optic nerve and causes loss of vision in the affected eye. It is often associated with multiple sclerosis. Loss of vision after an attack of optic neuritis is caused by damage to the nerve fibres in the optic nerve. There are a number of factors that contribute to nerve fibre damage including increased levels of sodium within them, so blocking sodium entry could help to protect them against damage. The purpose of this study is determine whether phenytoin (which blocks sodium entry into cells) can protect against loss of nerve fibres and prevent loss of vision after optic neuritis.
Although idiopathic steroid resistant optic neuritis is very uncommon, there is no established treatment protocol for such patients. Toll like receptors (TLRs) especially TLR-9 has been shown to play a role in the pathogenesis of optic neuritis. This small case series aims to determine whether immunomodulators directed specifically at TLR-9(i.e. TLR-9 antagonism)play any role in improving the visual function in such patients.
Fifty subjects will be enrolled in this Phase II, investigator-initiated, randomized and blinded cross-over trial of dalfampridine of 8 weeks duration The study will test the hypothesis that dalfampridine, when administered to subjects with incomplete visual recovery after optic neuritis from MS, will result in symptomatic improvement in visual function. The study will consist of one screening/baseline visit, one visit during treatment with active drug, and one visit on placebo. After the baseline visit, subjects will be randomly assigned to receive study medication or placebo for the first three weeks, followed by a two week wash-out, and then treatment reallocation for the latter three weeks.
The purpose of this study is to determine if oral lipoic acid can safely help relieve permanent optic nerve injury in patients diagnosed with acute optic neuritis. It will also explore how the body absorbs and breaks down the study drug, and what effects it has on the immune system.
Incomplete remission after an optic neuritis attack is not uncommon. Visual reconstitution therapy is a software-based approach that has been shown to substantially improve residual visual field deficits in patients with pre- and postchiasmatic lesions. The primary hypothesis of this randomized, controlled clinical trial is, that visual reconstitution therapy is superior to active comparator treatment in improving the visual field after optic neuritis.
The main objective of the study is to determine whether glatiramer acetate 20 mg once daily reduces the amount of axonal loss in the optic nerve after a first event of acute optic neuritis compared to placebo patients and to generate data supporting the potential neuroprotective effect of glatiramer acetate in a human in vivo model of axonal loss.
The primary objective of the study was to evaluate the effect of Nerispirdine (50 mg or 400 mg) and placebo given orally as a single dose once a week in crossover design on latency of Visual Evoked Potentials (VEP) P100 in optic nerves. Secondary objectives included evaluation of the effect of Nerispirdine on VEP amplitude and other visual parameters including visual acuity and contrast, as well as evaluation of the safety and tolerability of Nerispirdine in patients with Multiple Sclerosis (MS). Contrast sensitivity and visual acuity examinations (in addition to Optical Coherence Tomography [OCT] and VEPs) were needed during the screening period for defining etiologic relationships (if non-MS related impairment) and for assessing the effect of treatment of age-related eye disease versus the MS-related vision impairment.