Abstract
PurposeTo investigate the effect of the combination of Wharton's jelly derived mesenchymal stem cells (WJ-MSC) and high frequency repetitive electromagnetic stimulation (rEMS) in the therapy of toxic optic neuropathies with severe symptoms after the available current therapy modalities which were unsucessful.Material and methodsThis prospective, open-label clinical phase-3 study was conducted at Ankara University Faculty of Medicine, Department of Ophthalmology between April 2019 and April 2021. Thirty-six eyes of 18 patients with toxic optic neuropathy (TON) were included in the study. Within 1–3 months after the emergency interventions, patients with various degrees of sequela visual disturbances were studied in this clinical trial. The cases were divided into three groups according to similar demographic characteristics. Group 1: Consists of 12 eyes of 12 patients treated with the WJ-MSC and rEMS combination in one eye. Group 2: Consists of 12 eyes of 12 patients treated with only rEMS in one eye. Group 3: Consists of 12 eyes of six patients treated with only WJ-MSC in both eyes. The course was evaluated by comparing the quantitive functional and structural assessment parameters measured before and at the fourth month of applications in each group.ResultsThe mean best corrected visual acuity (BCVA) delta change percentages of the groups can be ranked as: Group 1 (47%) > Group 3 (32%) > Group 2 (21%). The mean fundus perimetry deviation index (FPDI) delta change percentages of the groups can be ranked as: Group 1 (95%) > Group 2 (33%) > Group 3 (27%). The mean ganglion cell complex (GCC) thickness delta change (decrease in thickness) percentages can be ranked as: Group 1 (− 21%) > Group 3 (− 15%) > Group 2 (− 13%). The visual evoked potential (VEP) P100 latency delta change percentages of the groups can be ranked as: Group 1 (− 18%) > Group 3 (− 10%) > Group 2 (− 8%). The P100 amplitude delta change percentages of the groups can be ranked as: Group 1 (105%) > Group 3 (83%) > Group 2 (24%).ConclusionToxic optic neuropathies are emergent pathologies that can result in acute and permanent blindness. After poisoning with toxic substances, progressive apoptosis continues in optic nerve axons and ganglion cells. After the proper first systemic intervention in intensive care clinic, the WJ-MSC and rEMS combination seems very effective in the short-term period in cases with TON. To prevent permanent blindness, a combination of WJ-MSC and rEMS application as soon as possible may increase the chance of success in currently untreatable cases.Trial Registration ClinicalTrials.gov ID: NCT04877067.
Highlights
The visual function begins with converting light energy into biochemical, electrical signals in the outer layers of the retina
After poisoning with toxic substances, progressive apoptosis continues in optic nerve axons and ganglion cells
After the proper first systemic intervention in intensive care clinic, the Wharton’s jelly derived mesenchymal stem cells (WJ-MSC) and repetitive electromagnetic stimulation (rEMS) combination seems very effective in the short-term period in cases with toxic optic neuropathy (TON)
Summary
The visual function begins with converting light energy into biochemical, electrical signals in the outer layers of the retina. Electrical signals are transmitted from the photoreceptors (first neuron) to the bipolar cells (second neuron) and to the ganglion cells (third neuron). The axons of the ganglion cells (retinal nerve fibers) form the optic nerve. The number of optic nerve axons from the post-laminar region to the lateral geniculate nucleus is approximately 1,200,000. The optic nerve transmits electrical signals to the visual center located in the brain’s occipital cortex through various synapses, including the lateral geniculate nucleus (fourth neuron) [1,2,3]. Optic nerve fibers are more sensitive to various toxins than the retina because they are outside the protecting feature of the blood-retinal barrier. Metabolites of some toxins disrupt adenosine three phosphate (ATP) synthesis by blocking mitochondrial function and oxidative phosphorylation
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