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Peter K. Kofoed, Stig K. Holfort, Inger C. Munch, Birgit Sander, Henrik Sillesen, Leif P. Jensen, Helle Iversen, Michael Larsen; Impaired Multifocal Electroretinogram Implicit Times and Amplitudes in Symptomatic Carotid Artery Disease. Invest. Ophthalmol. Vis. Sci. 2011;52(14):3520.
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Oxygen supply is fundamental for retinal function; and ischemia is considered an essential part of the pathogenesis of many eye diseases. Hypoxia has been shown to impair dark adaptation in ophthalmologically healthy patients and ischemia is known to delay multifocal electroretinographic (mfERG) implicit times in ocular ischemic syndrome eyes in patients with occlusive carotid artery disease. It has also been shown that lesser degrees of carotid artery occlusion are associated with functional abnormalities of the visual apparatus. In this study, we examined mfERG in patients with carotid artery disease without the ocular ischemic syndrome or other ocular disease.
Retinal function in twelve patients with carotid artery disease and a history of stroke or transitory ischemic attack was assessed by mfERG ipsilateral and contralateral of the carotid artery with the highest degree of ultrasonographic stenosis. Further assessments included ophthalmic systolic blood pressure measurement by ocular pneumoplethysmography, carotid artery ultrasonography, applanation tonometry, and fundus fluorescein angiography. None of the patients had any demonstrable sequelae of retinal artery occlusion.
Compared with the fellow eye, the eye on the side of the higher degree of carotid artery occlusion demonstrated delayed N1 implicit times (-3.7 %, p=0.12), delayed P1 implicit times (-1.8%, p=0.039), reduced N1 amplitudes (-18.1%, p=0.0080), and reduced P1 amplitudes (-16.1%, p=0.037).
Suppression of retinal cone-driven function in proportion to the degree of carotid artery occlusion in eyes without the ocular ischemic syndrome or other ocular disease are detectable with mfERG. These results are novel and corroborate previous studies of dark adaptation showing suppression of retinal rod function.
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