Electrical Stimulation as a Means for Improving Vision

Abstract

Evolving research has provided evidence that noninvasive electrical stimulation (ES) of the eye may be a promising therapy for either preserving or restoring vision in several retinal and optic nerve diseases. In this review, we focus on minimally invasive strategies for the delivery of ES and accordingly summarize the current literature on transcorneal, transorbital, and transpalpebral ES in both animal experiments and clinical studies. Various mechanisms are believed to underlie the effects of ES, including increased production of neurotrophic agents, improved chorioretinal blood circulation, and inhibition of proinflammatory cytokines. Different animal models have demonstrated favorable effects of ES on both the retina and the optic nerve. Promising effects of ES have also been demonstrated in clinical studies; however, all current studies have a lack of randomization and/or a control group (sham). There is thus a pressing need for a deeper understanding of the underlying mechanisms that govern clinical success and optimization of stimulation parameters in animal studies. In addition, such research should be followed by large, prospective, clinical studies to explore the full potential of ES. Through this review, we aim to provide insight to guide future research on ES as a potential therapy for improving vision.

Figure 1

Different routes of electrical stimulation of the eye. The red circle represents choroidea, except for the anterior part of the eye. The gray semicircle represents the retinal pigment epithelial cells, and the yellow semicircle illustrates the retina. Image is courtesy of Håkon Raanes (Norway).

Figure 2

Possible neuroprotective mechanisms underlying the effects of transcorneal electrical stimulation. The cellular structure in the figure represents an enlarged image of the retina. BDNF, brain-derived neurotrophic factor; CNTF, ciliary nerve trophic factor; FGF, fibroblast growth factor; GS, glutamine synthetase; IGF-1, insulin-like growth factor 1; MCs, Müller cells; PG, primary microglia; RGCs, retinal ganglion cells; TNF-α, tumor necrosis factor-α.