Hyperbaric oxygen therapy increases oxygen pressure and the concentration of reactive oxygen species in blood and tissues. Increased oxygen pressure may be beneficial in some diseases, such as in the treatment of diabetic leg ulcers and diabetic retinopathy; however, due to their cytotoxic properties, an excess of reactive oxygen species in tissues and/or deficiencies in antioxidant activity, may contribute to complications of hyperbaric oxygen therapy, such as cataract. This review examines the possibility that increased tissue concentrations of reactive oxygen species may also exacerbate other ocular diseases. For example, reactive oxygen species and deficiencies in antioxidant activities contribute to the pathogenetic processes in keratoconus. Such impact may be exacerbated by exposure to additional reactive oxygen species during hyperbaric oxygen therapy. The senescent eye may be particularly prone to oxidative damage as exemplified by conditions such as macular degeneration and cataract. Because of its high consumption of oxygen, the retina is particularly susceptible to oxidative stress, which plays a major role in retinopathy. For example, under normal conditions age-related macular degeneration involves oxidative stress and death of the retinal pigment epithelial cells. Hyperbaric oxygen therapy may exacerbate these processes. In addition to cataract, age-related macular degeneration and keratoconus, there may be other ocular diseases for which exposure to hyperbaric oxygen therapy-related oxidative stress may be significantly adverse. In all such cases, careful pre-examination and evaluation of the potential risk and benefit from this form of therapy appears to be warranted. Unless it could interfere with the benefits of hyperbaric oxygen therapy, antioxidant dietary supplementation may be indicated in conjunction with any hyperbaric oxygen therapy, when there are co-existing diseases for which oxidative stress could have significantly adverse side effects. Delivery of hyperbaric oxygen therapy may need to be modified or it may even be contraindicated in these cases. © 2014 The Author. Clinical and Experimental Optometry © 2014 Optometry Australia.

This review examines the role of oxidative stress in damage to cells of the trabecular meshwork and associated impaired aqueous drainage as well as damage to retinal ganglion cells and associated visual field losses. Consideration is given to the interaction between vascular and mechanical explanations for pathological changes in glaucoma. For example, elevated intraocular pressure (IOP) forces may contribute to ischaemia but there is increasing evidence that altered blood flow in a wider sense is also involved. Both vascular and mechanical theories are involved through fluctuations in intraocular pressure and dysregulation of blood flow. Retinal function is very sensitive to changes in haemoglobin oxygen concentration and the associated variations in the production of reactive oxygen species. Reperfusion injury and production of reactive oxygen species occurs when IOP is elevated or blood pressure is low and beyond the capacity for blood flow autoregulation to maintain appropriate oxygen concentration. Activities such as those associated with postural changes, muscular effort, eye wiping and rubbing which cause IOP fluctuation, may have significant vascular, mechanical, reperfusion and oxidative stress consequences. Hyperbaric oxygen therapy exposes the eye to increased oxygen concentration and the risk of oxidative damage in susceptible individuals. However, oxygen concentration in aqueous humour, and the risk of damage to trabecular meshwork cells may be greater if hyperbaric oxygen is delivered by a hood which exposes the anterior ocular surface to higher than normal oxygen levels. Oronasal mask delivery of hyperbaric oxygen therapy appears to be indicated in these cases.Copyright © 2017 Spanish General Council of Optometry. Published by Elsevier España, S.L.U. All rights reserved.

Mild cognitive impairment (MCI) is a common disorder affecting as much as 15% of the elderly population. Transcranial direct current stimulation (tDCS) is a non-invasive technique of neuromodulation that has proven to influence performance in different cognitive domains.We investigated the effects on cognition of 20-day anodal tDCS in 17 MCI patients compared with 17 matched MCI patients.Patients underwent neuropsychological evaluation at baseline and then were randomly assigned to the anodal or sham group. The tDCS protocol consisted in 20 min, 5 days per week (up to a total of 20 days), of 2-mA anodal stimulation over the left dorsolateral prefrontal cortex (DLPFC). The location of anodal electrode was chosen in accordance with previous reports which relate anodal stimulation of this site with cognitive enhancement. At the end of the last day of stimulation, a second neuropsychological evaluation was performed. We compared baseline and post-stimulation neuropsychological results in the anodal vs sham group using repeated measures ANOVA as a statistical analysis test.At follow-up, patients exposed to anodal stimulation showed improvement in episodic verbal memory (p < 0.001) and figure naming test (p < 0.01), in a general index of cognitive function (Brief Mental Deterioration Battery) (p < 0.0001) and in a mood measurement test (Beck Depression Inventory) (p < 0.01).Anodal tDCS could be a useful tool to improve cognitive symptoms in MCI although more evidence is needed to understand the exact underlying mechanisms. Confirmation of its potential benefits in MCI would be significant.

Transcranial direct current stimulation (tDCS) has been investigated as a way to improve motor and cognitive functioning, with largely variable results. Currently, relatively little is known about the neurobiological effects, and possible drivers of variability, in either healthy or clinical populations. Therefore, this study aimed to characterise the neurobiological effects to tDCS in younger adults, older adults and adults with mild cognitive impairment (MCI), and their relationship to cognitive performance. 20 healthy younger adults, 20 healthy older adults and 9 individuals with MCI participated in the study. All completed neuropsychological tasks and TMS-EEG, prior to and following delivery of 20 min of anodal tDCS to the left dorsolateral prefrontal cortex (DLPFC). EEG was also recorded during the 2-Back working memory task. Following tDCS, younger adults demonstrated alterations in early TMS-Evoked Potentials (TEPs), namely P30 and P60. Both younger and older adults exhibited a larger task-related N250 amplitude after stimulation, with contrasting relationships to cognitive performance. The MCI group showed no change in TEPs or ERPs over time. Comparisons between the groups revealed differences in the change in amplitude of early TEP (P60) and ERP (N100) peaks between younger and older adults. Our findings indicate that tDCS was able to modulate cortical activity in younger and older healthy adults, but in varying ways. These findings suggest that varied response to tDCS may be related to factors such as age and the presence/absence of cognitive impairment, and these factors should be considered when assessing the effectiveness of tDCS in healthy and pathological aging.Copyright © 2019 Elsevier Ltd. All rights reserved.