Active clinical trials for "Toxic Optic Neuropathy"

The goal of this double-blind prospective randomized clinical trial is to determine if the effect of intravenous erythropoietin is superior to the effect of intravenous methylprednisolone in cases of toxic optic neuropathy 4 weeks after therapeutic intervention. The main question it aims to answer: • Is there a difference in the visual recovery of toxic optic neuropathies treated with intravenous methylprednisolone in comparison with those treated with intravenous erythropoietin?

The aim of the project is to create a new, non-invasive and safe protocol for the early diagnosis of various types of optic neuropathies with the use of diffusion magnetic resonance imaging

This multicenter, randomized, double-blind, placebo-controlled trial with a single arm run-in period is to evaluate the safety and efficacy of sodium thiosulfate (BYON5667) eye drops to reduce ocular toxicity in cancer patients treated with the antibody-drug conjugate (ADC) SYD985

The axons of the retinal ganglion cells combine to form the optic nerve. The optic nerve transmits electrical signals to the visual cortex by various synapses. Optic nerve axons are more sensitive to toxins than retina because they are outside the blood retinal barrier. Methanol, various solvents and heavy metals, carbon dioxide, antiarrhythmic, antiepileptic, antibiotics and some vasoactive drugs can cause toxic optic neuropathy. There is a different pathophysiology for each toxin. Methanol is easily accessible alcohol in all types of disinfectants. Methanol is converted into formaldehyde and formic acid while metabolized in the liver. Formaldehyde disrupts ATP synthesis by blocking mitochondrial function and oxidative phosphorylation. Formic acid causes demyelination as a result of metabolic acidosis. Neuroinflammation occurs when denatured proteins block axoplasmic flow. All these processes can lead to apoptosis and permanent vision loss. Sildenafil is a vasoactive drug used in erectile dysfunction. Sildenafil decreases optic nerve head blood flow. Neuroinflammation develops secondary to the cessation of axoplasmic flow after hypoxia. If hypoxia and neuroinflammatiom persists, apoptosis and permanent vision loss develop. Amiodarone is an ion channel blocker used in the treatment of cardiac arrhythmias. Long-term use may cause disruption of ion channel balance in the optic nerve. This condition leads to asymmetric neuroinflammation and apoptosis. Wharton's jelly derived mesenchymal stem cells (WJ-MSC) can increase mitochondrial ATP synthesis with paracrine effects and suppress neuroinflammation with immunomodulatory effects. Repetitive electromagnetic stimulation (rEMS) can rearrange ion channel balances and axoplasmic flow. The aim of this prospective phase-3 clinical study is to investigate the effect of WJ-MSC and rEMS combination in the therapy of toxic optic neuropathies. This combination is the first study in the literature for the therapy of toxic optic neuropathies.