Abstract

ObjectiveThe restoration of visual functional loss that results from optic nerve lesions is still considered an unsolved problem. Despite the large number of the optic nerve fibers, their capacity of plasticity to achieve recovery is rather limited. In these conditions, it seems appropriate to activate intact visual cortex of blind or partial sight patients to rehabilitate vision. MethodsWe applied impulse modulating therapeutic electrical stimulation (IMTES) to activate visual pathway structure and striate cortex, where small electrical currents are applied to the eye ball non-invasively. Efficacy of this treatment was studied clinically with perimetry and physiologically using EEG, VEP and PET data. The recordings were compared between different etiologies, degrees of initial vision loss and the type of visual field (VF) defects. SubjectsWe analyzed the outcomes of 874 patients, which has sustained either severe or partial optic nerve lesion of traumatic, inflammatory and post-tumour origin. ResultsBefore treatment, most patients had severe vision loss ranging from to total blindness to severe or mild VF defects. The best clinical effect was seen in the group of patients with severe visual impairment. Here, 62.6% of the cases responded positively to IMTES as evidence by perimetric and/or physiological recordings. Repeated perimetry revealed enlargement of peripheral visual field (mean 27.5% from background), visible as contraction or decreased absolute scotoma size. Of the patients with legal blindness (visual acuity not exceed sense of light or small remnant of residual vision was still), 16% showed benefits. In groups of the patients with blindness or slight vision, the recovery of visual function was achieved in 49.7% and 58.2% of the cases, respectively. In some cases, striate cortex activation as documented with EEG and PET confirmed these observations. ConclusionsWe propose that IMTES-induced restoration of vision is not only mediated by improved optic nerve function but it also activates striate and extrastriate cortex in which plasticity is physiologically induced.

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