May 2004
Volume 45, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2004
670 nm LED Treatment of Affected Carriers of the 11778 Leber's Hereditary Optic Neuropathy (LHON) Mutation in Brazil.
Author Affiliations & Notes
  • J.T. Eells
    Health Sciences, UW–Milwaukee, Milwaukee, WI
  • S. Salomao
    Ophthalmology, Sao Paulo Federal University, Sao Paulo, Brazil
  • A. Berezovsky
    Ophthalmology, Sao Paulo Federal University, Sao Paulo, Brazil
  • M. Moraes
    Colatina Ophthalmology Clinic, Colatina, Brazil
  • J.M. Roth
    College of Optometry, SUNY, New York, NY
  • H. Paula
    Colatina Ophthalmology Clinic, Colatina, Brazil
  • J. Sherman
    College of Optometry, SUNY, New York, NY
  • T. Lam
    Ophthalmology, USC, Los Angeles, CA
  • A.A. Sadun
    Ophthalmology, USC, Los Angeles, CA
  • Footnotes
    Commercial Relationships  J.T. Eells, None; S. Salomao, None; A. Berezovsky, None; M. Moraes, None; J.M. Roth, None; H. Paula, None; J. Sherman, None; T. Lam, None; A.A. Sadun, None.
  • Footnotes
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Investigative Ophthalmology & Visual Science May 2004, Vol.45, 828. doi:
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      J.T. Eells, S. Salomao, A. Berezovsky, M. Moraes, J.M. Roth, H. Paula, J. Sherman, T. Lam, A.A. Sadun; 670 nm LED Treatment of Affected Carriers of the 11778 Leber's Hereditary Optic Neuropathy (LHON) Mutation in Brazil. . Invest. Ophthalmol. Vis. Sci. 2004;45(13):828.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Abstract: : Purpose: Near–infrared (NIR) light–emitting diode (LED) arrays have been shown to stimulate mitochondrial respiration and improve functional recovery of the retina and optic nerve after acute toxic injury. The present study tested the hypothesis that a brief course of NIR–LED treatment would reduce serum concentrations of the neuronal stress marker, neuron–specific enolase (NSE), and improve visual function in affected carriers of the 11778 LHON mutation Methods: NIR–LED treatment was investigated in 6 affected 11778 LHON mutation carriers in Colatina, Brazil (protocol approved – Institutional Review Board, Sao Paulo Federal University). Each subject exhibited a profound deficit in central vision. Baseline values for NSE, Humphrey visual fields and nerve fiber analysis were obtained prior to LED treatment. LED treatment consisted of irradiation at 670 nm for 80 seconds delivered to each eye producing an estimated energy density of 4 joules/cm2 at the optic nerve head. LED treatment was administered once per day for 3 days using handheld LED arrays (Quantum Devices, Barneveld, WI.) positioned 1 inch from each closed eye. Treatment response was assessed 1 day following the last LED treatment (dy 4) and again on day 10. Results: Two LED–treated subjects reported a transient (1day) improvement in color vision and visual acuity. In these two subjects, NSE concentrations increased dramatically (0.9 µg/L pre–exposure to 7.6 µg/L; 2.2 µg/L pre–exposure to 5.3 µg/L), in contrast to smaller increases or decreases in NSE measured in the other 4 subjects. Peripheral visual fields showed improvement in 4 of the 6 subjects by 10 days post–treatment. No change was observed in nerve fiber layer measurements. No detrimental effects of NIR–LED treatment were reported or observed in visual function tests. Conclusions: The findings of this pilot study confirm and extend previous studies which have reported that NIR–LED treatment produces no detrimental effects on visual function. They further suggest that NIR–LED treatment may exert a beneficial effect in LHON. However, the transient improvement in color vision and visual acuity and improvement in visual fields should be tempered with the findings of increased NSE concentrations, potentially indicative of an increase in neuronal stress secondary to activation of mitochondrial metabolism

Keywords: neuroprotection • mitochondria • visual impairment: neuro–ophthalmological disease 
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