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      Coenzyme Q10 treatment improved visual field after homonymous quadrantanopia caused by occipital lobe infarction


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          To report the clinical findings and management of a case of occipital lobe infarction with homonymous quadrantanopia in a patient treated with vitamins and coenzyme Q10.


          A currently 69-years-old patient presenting in 2007 left inferior quadrantanopia following a right occipital lobe stroke with initial visual field index of 82% and 79% in the right and left eyes, respectively. From 2007 to 2010 was treated with vitamin and antioxidant complexes, without specific signs of changes observed in the visual field (81% right eye, 79% left eye). In 2011 was treated for the first time with coenzyme Q10 (Active complex ® Q10 Gold 100 mg) in addition to the vitamin and antioxidant supplementation. A promptly slight improvement of the visual field in both eyes was observed. In 2013, a remarkable improvement was noticed observing a slight scotoma where previously presented the quadrantanopia. Thereafter, in the successive one-year follow-up examinations the patient experienced an exponential improvement in the visual field with gradually fading of the scotoma. Currently the patient no longer presents any sign of quadrantanopia, with normal visual field in both eyes (99% right eye, 98% left eye).

          Conclusion and importance

          Spontaneous improvement more than 6 months after stroke is thought to be unlikely. However, we observed, for the first time, an amelioration of the visual field after 10 years of an occipital lobe stroke. The combination of vitamins and coenzyme Q10 (100 mg) improved the prognosis with significant recovery of the visual field, which is impossible to recover under current knowledge.

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          Most cited references26

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          Coenzyme Q 10 Supplementation in Aging and Disease

          Coenzyme Q (CoQ) is an essential component of the mitochondrial electron transport chain and an antioxidant in plasma membranes and lipoproteins. It is endogenously produced in all cells by a highly regulated pathway that involves a mitochondrial multiprotein complex. Defects in either the structural and/or regulatory components of CoQ complex or in non-CoQ biosynthetic mitochondrial proteins can result in a decrease in CoQ concentration and/or an increase in oxidative stress. Besides CoQ10 deficiency syndrome and aging, there are chronic diseases in which lower levels of CoQ10 are detected in tissues and organs providing the hypothesis that CoQ10 supplementation could alleviate aging symptoms and/or retard the onset of these diseases. Here, we review the current knowledge of CoQ10 biosynthesis and primary CoQ10 deficiency syndrome, and have collected published results from clinical trials based on CoQ10 supplementation. There is evidence that supplementation positively affects mitochondrial deficiency syndrome and the symptoms of aging based mainly on improvements in bioenergetics. Cardiovascular disease and inflammation are alleviated by the antioxidant effect of CoQ10. There is a need for further studies and clinical trials involving a greater number of participants undergoing longer treatments in order to assess the benefits of CoQ10 treatment in metabolic syndrome and diabetes, neurodegenerative disorders, kidney diseases, and human fertility.
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            Bioenergetic and antioxidant properties of coenzyme Q10: recent developments.

            For a number of years, coenzyme Q (CoQ10 in humans) was known for its key role in mitochondrial bioenergetics; later studies demonstrated its presence in other subcellular fractions and in plasma, and extensively investigated its antioxidant role. These two functions constitute the basis on which research supporting the clinical use of CoQ10 is founded. Also at the inner mitochondrial membrane level, coenzyme Q is recognized as an obligatory co-factor for the function of uncoupling proteins and a modulator of the transition pore. Furthermore, recent data reveal that CoQ10 affects expression of genes involved in human cell signalling, metabolism, and transport and some of the effects of exogenously administered CoQ10 may be due to this property. Coenzyme Q is the only lipid soluble antioxidant synthesized endogenously. In its reduced form, CoQH2, ubiquinol, inhibits protein and DNA oxidation but it is the effect on lipid peroxidation that has been most deeply studied. Ubiquinol inhibits the peroxidation of cell membrane lipids and also that of lipoprotein lipids present in the circulation. Dietary supplementation with CoQ10 results in increased levels of ubiquinol-10 within circulating lipoproteins and increased resistance of human low-density lipoproteins to the initiation of lipid peroxidation. Moreover, CoQ10 has a direct anti-atherogenic effect, which has been demonstrated in apolipoprotein E-deficient mice fed with a high-fat diet. In this model, supplementation with CoQ10 at pharmacological doses was capable of decreasing the absolute concentration of lipid hydroperoxides in atherosclerotic lesions and of minimizing the size of atherosclerotic lesions in the whole aorta. Whether these protective effects are only due to the antioxidant properties of coenzyme Q remains to be established; recent data point out that CoQ10 could have a direct effect on endothelial function. In patients with stable moderate CHF, oral CoQ10 supplementation was shown to ameliorate cardiac contractility and endothelial dysfunction. Recent data from our laboratory showed a strong correlation between endothelium bound extra cellular SOD (ecSOD) and flow-dependent endothelial-mediated dilation, a functional parameter commonly used as a biomarker of vascular function. The study also highlighted that supplementation with CoQ10 that significantly affects endothelium-bound ecSOD activity. Furthermore, we showed a significant correlation between increase in endothelial bound ecSOD activity and improvement in FMD after CoQ10 supplementation. The effect was more pronounced in patients with low basal values of ecSOD. Finally, we summarize the findings, also from our laboratory, on the implications of CoQ10 in seminal fluid integrity and sperm cell motility.
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              Natural history of homonymous hemianopia.

              To describe the characteristics of spontaneous recovery of homonymous hemianopia (HH). The authors reviewed medical records of all patients with HH confirmed by formal visual field testing and seen in follow-up in their service between 1989 and 2004. Clinical characteristics, causes, neuroradiologic definition of lesion location, final outcome, and evolution of the visual field defects were recorded. The associations among final visual field defect outcome, time from injury, and clinical features were analyzed. A total of 254 patients with 263 HH were included in this study. Spontaneous visual field defect recovery was observed in 101 HH (38.4%). The likelihood of spontaneous recovery decreased with increasing time from injury to initial visual field testing (p = 0.0003). The probability of improvement was related to the time since injury (p = 0.0003) with a 50 to 60% chance of improvement for cases tested within 1 month after injury that decreased to about 20% for cases tested at 6 months after surgery. No other factor was found to correlate with the final outcome of the visual field defects. Improvement after 6 months from injury was mild and usually related to improvement of the underlying disease. Spontaneous improvement of homonymous hemianopia is seen in at least 50% of patients first seen within 1 month of injury. In most cases, the improvement occurs within the first 3 months from injury. Spontaneous improvement after 6 months postinjury should be interpreted with caution as it is most likely related to improvement of the underlying disease or to improvement in the patient's ability to perform visual field testing reliably.

                Author and article information

                Am J Ophthalmol Case Rep
                Am J Ophthalmol Case Rep
                American Journal of Ophthalmology Case Reports
                09 December 2018
                March 2019
                09 December 2018
                : 13
                : 70-75
                [a ]Instituto Oftalmológico Fernández-Vega, Avenida Doctores Fernández-Vega, 34, 33012, Oviedo, Spain
                [b ]Instituto Universitario Fernández-Vega, Fundación de Investigación Oftalmológica, Universidad de Oviedo, Spain
                [c ]Departamento de Morfología y Biología Celular, Universidad de Oviedo, Spain
                [d ]Hospital de Cabueñes, Gijón, Spain
                [e ]Facultad de Ciencias de la Salud, Universidad Autónoma de Chile, Temuco, Chile
                Author notes
                []Corresponding author. Instituto Oftalmológico Fernández-Vega, Avda. Dres. Fernández-Vega, 34, 33012, Oviedo, Spain. beatriz@ 123456fernandez-vega.com
                [∗∗ ]Corresponding author. Instituto Oftalmológico Fernández-Vega, Avda. Dres. Fernández-Vega, 34, 33012, Oviedo, Spain. h.gonzalez@ 123456fio.as
                © 2018 The Authors

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                : 26 June 2018
                : 15 November 2018
                : 7 December 2018
                Case report

                stroke,occipital lobe,homonymous quadrantanopia,vitamins,coenzyme q10


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