Research Article No Evidence for Retinal Damage Evolving from Reduced Retinal Blood Flow in Carotid Artery Disease Henning Heßler, 1 Hanna Zimmermann, 1 Timm Oberwahrenbrock, 1 Ella Maria Kadas, 1 Janine Mikolajczak, 1 Alexander U. Brandt, 1 Andreas Kauert, 2 Friedemann Paul, 1,3 and Stephan J. Schreiber 3 1 NeuroCure Clinical Research Center, Charit´ e-Universit¨ atsmedizin Berlin, 10117 Berlin, Germany 2 Department of Neurology, K¨ onigin-Elisabeth-Herzberge Hospital, 10365 Berlin, Germany 3 Department of Neurology, Charit´ e-Universit¨ atsmedizin Berlin, 10117 Berlin, Germany Correspondence should be addressed to Henning Heßler; henning.hessler@charite.de Received 22 May 2015; Revised 24 June 2015; Accepted 25 June 2015 Academic Editor: Goji Tomita Copyright © 2015 Henning Heßler et al. Tis is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Introduction. Carotid artery disease (CAD) comprising high-grade internal carotid artery stenosis (CAS) or carotid artery occlusion (CAO) may lead to ipsilateral impaired cerebral blood fow and reduced retinal blood supply. Objective. To examine the infuence of chronic CAD on retinal blood fow, retinal morphology, and visual function. Methods. Patients with unilateral CAS 50% (ECST criteria) or CAO were grouped according to the grade of the stenosis and to the fow direction of the ophthalmic artery (OA). Retinal perfusion was measured by transorbital duplex ultrasound, assessing central retinal artery (CRA) blood fow velocities. In addition, optic nerve and optic nerve sheath diameter were measured. Optical coherence tomography (OCT) was performed to study retinal morphology. Visual function was assessed using high- and low-contrast visual paradigms. Results. Twenty-seven patients were enrolled. Eyes with CAS 80%/CAO and retrograde OA blood fow showed a signifcant reduction in CRA peak systolic velocity (no-CAD side: 0.130 ± 0.035 m/s, CAS/CAO side: 0.098 ± 0.028;  = 0.005;  = 12). OCT, optic nerve thicknesses, and visual functional parameters did not show a signifcant diference. Conclusion. Despite assessable hemodynamic efects, chronic high-grade CAD does not lead to gaugeable morphological or functional changes of the retina. 1. Introduction Carotid artery disease (CAD) comprising high-grade carotid artery stenosis (CAS) or carotid artery occlusion (CAO) of the internal carotid artery (ICA) was shown to be associated with restricted ocular blood fow as measured by Doppler sonography [15]. Te higher the grade of CAS, the more relevant the impairment of the retinal blood fow, especially if the ophthalmic artery (OA) shows a retrograde blood fow [6]. A common carotid artery occlusion (CCA-O) impedes the blood fow of the ipsilateral internal and external carotid artery (ECA) and is another risk factor for limited orbital perfusion [7, 8]. Ocular manifestations of CAD are a common fnding, for instance, occurring as amaurosis fugax caused by acute embolic central retinal artery occlusion or as a chronic retinal ischemia in the form of ocular ischemic syndrome (OIS). Retinal examination in CAD patients is generally performed in direct time relation to the occurrence of clinical symptoms like sudden or progressive visual loss. However, it remains unclear whether subclinical retinal abnormalities or visual impairment occurs. Ultrasound allows reliable dynamic assessment of orbital blood fow, measured as central retinal artery (CRA) fow velocity. It can also be used for structural analysis of optic nerve sheath diameter (ONSD) and is a proven diagnostic tool to evaluate papilledema in intracranial pressure with comparable results to MRI exam- inations [9]. Optical coherence tomography (OCT) allows reliable quantifcation of retinal layers and is able to detect retinal axonal and neuronal loss even in the absence of clinical visual symptoms in multiple sclerosis and other CNS diseases [1012]. In this pilot study, we analyze the efects of CAD- induced chronic reduced retinal blood fow on optic nerve thickness and retinal morphology and function. Hindawi Publishing Corporation BioMed Research International Volume 2015, Article ID 604028, 8 pages http://dx.doi.org/10.1155/2015/604028