In vivo identification of alteration of inner neurosensory layers in branch retinal artery occlusion

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Abstract

Background/aims

To characterise the extension and progression of alteration of neurosensory layers following acute and chronic branch retinal artery occlusion (BRAO) in vivo using spectral-domain optical coherence tomography.

Methods

In this observational case series, eight eyes with acute BRAO and nine eyes with chronic BRAO were analysed using a Spectralis Heidelberg Retina Angiograph (HRA)+optical coherence tomography system including eye tracking. Patients with acute BRAO were examined within 36±5 h after primary event and at weekly/monthly intervals thereafter. Segmentation measurements of all individual neurosensory layers were performed on single A-scans at six locations in affected and corresponding non-affected areas. The thickness values of the retinal nerve fibre layer together with the ganglion cell layer (NFL/GCL), inner plexiform layer (IPL), inner nuclear layer together with outer plexiform layer (INL/OPL), outer nuclear layer (ONL), and photoreceptor layers together with the retinal pigment epithelium (PR/RPE) were measured and analysed.

Results

Segmentation evaluation revealed a distinct increase in thickness of inner neurosensory layers including the NFL/GCL (35%), IPL (80%), INL/OPL (48%) and mildly the ONL by 21% in acute ischaemia compared with corresponding layers in non-ischaemic areas. Regression of intraretinal oedema was followed by persistent retinal atrophy with loss of differentiation between IPL and INL/OPL at month 2. In contrast, the ONL and subjacent PR/RPE retained their physiological thickness in patients with chronic BRAO.

Conclusion

In vivo assessment of retinal layer morphology allows a precise identification of the pathophysiology in retinal ischaemia.

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Most cited references 24

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Blood-retinal barrier in hypoxic ischaemic conditions: basic concepts, clinical features and management.

Wallace Foulds, A.-E. Ling, C. Kaur (2008)

The blood-retinal barrier (BRB) plays an important role in the homeostatic regulation of the microenvironment in the retina. It consists of inner and outer components, the inner BRB (iBRB) being formed by the tight junctions between neighbouring retinal capillary endothelial cells and the outer barrier (oBRB) by tight junctions between retinal pigment epithelial cells. Astrocytes, Müller cells and pericytes contribute to the proper functioning of the iBRB. In many clinically important conditions including diabetic retinopathy, ischaemic central retinal vein occlusion, and some respiratory diseases, retinal hypoxia results in a breakdown of the iBRB. Disruption of the iBRB associated with increased vascular permeability, results in vasogenic oedema and tissue damage, with consequent adverse effects upon vision. Factors such as enhanced production of vascular endothelial growth factor (VEGF), NO, oxidative stress and inflammation underlie the increased permeability of the iBRB and inhibition of these factors is beneficial. Experimental studies in our laboratory have shown melatonin to be a protective agent for the iBRB in hypoxic conditions. Although oBRB breakdown can occur in conditions such as accelerated hypertension and the toxaemia of pregnancy, both of which are associated with choroidal ischaemia and in age-related macular degeneration (ARMD), and is a feature of exudative (serous) retinal detachment, our studies have shown that the oBRB remains intact in hypoxic/ischaemic conditions. Clinically, anti-VEGF therapy has been shown to improve vision in diabetic maculopathy and in neovascular ARMD. The visual benefit in both conditions appears to arise from the restoration of BRB integrity with a reduction of retinal oedema.

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Retinal artery occlusion: associated systemic and ophthalmic abnormalities.

Sohan Hayreh, Patricia Podhajsky, M Zimmerman (2009)

To investigate systematically the various associated systemic and ophthalmic abnormalities in different types of retinal artery occlusion (RAO). Cohort study. We included 439 consecutive untreated patients (499 eyes) with RAO first seen in our clinic from 1973 to 2000. At first visit, all patients underwent detailed ophthalmic and medical history, and comprehensive ophthalmic evaluation. Visual evaluation was done by recording visual acuity, using the Snellen visual acuity chart, and visual fields with a Goldmann perimeter. Initially they also had carotid Doppler/angiography and echocardiography. The same ophthalmic evaluation was performed at each follow-up visit. Demographic features, associated systemic and ophthalmic abnormalities, and sources of emboli in various types of RAO. We classified RAO into central (CRAO) and branch (BRAO) artery occlusion. In both nonarteritic (NA) CRAO and BRAO, the prevalence of diabetes mellitus, arterial hypertension, ischemic heart disease, and cerebrovascular accidents were significantly higher compared with the prevalence of these conditions in the matched US population (all P or =50% stenosis in 31% of NA-CRAO patients and 30% of BRAO, and plaques in 71% of NA-CRAO and 66% of BRAO. An abnormal echocardiogram with an embolic source was seen in 52% of NA-CRAO and 42% of BRAO. Neovascular glaucoma developed in only 2.5% of NA-CRAO eyes. This study showed that, in CRAO as well as BRAO, the prevalence of various cardiovascular diseases and smoking was significantly higher compared with the prevalence of these conditions in the matched US population. Embolism is the most common cause of CRAO and BRAO; plaque in the carotid artery is usually the source of embolism and less commonly the aortic and/or mitral valve. The presence of plaques in the carotid artery is generally of much greater importance than the degree of stenosis in the artery. Contrary to the prevalent misconception, we found no cause-and-effect relationship between CRAO and neovascular glaucoma.

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Central retinal artery occlusion. Retinal survival time.

Shawn M. Zimmerman, Ashish Sanon, A Kimura … (2004)

To investigate the retinal survival time following central retinal artery occlusion (CRAO). In 38 elderly, atherosclerotic and hypertensive rhesus monkeys, transient CRAO (varying from 97 to 240 min) was produced by temporarily clamping the CRA at its site of entry into the optic nerve. Stereoscopic color fundus photography, fluorescein fundus angiography, electroretinography (ERG), and visual evoked potential (VEP) recording were performed before and during CRA clamping, after unclamping, and serially thereafter. After unclamping of the CRA, the animals were followed for variable lengths of time (median duration 8.14 weeks). Finally, the eyes and optic nerves were examined histologically. The data on ERG changes were analyzed in the following four time frames: (1) baseline before CRA clamping, (2) during CRA clamping, (3) immediately after unclamping, and (4) at the end of follow-up. Duration of CRAO was divided into four groups: 97, 105-120, 150-165, and > or = 180 min. A 'negative ERG' appeared during CRA clamping. With removal of the CRA clamp, there was b-wave recovery, with differential rates of recovery of ERG-eyes with shorter CRAO recovered sooner than those with longer occlusion. On removal of clamp, recovery was seen in scotopic 24 dB b-wave, photopic 0 dB single flash b-wave and 30 Hz flicker, with the b/a ratio of the combined rod and cone response and selective rod response showing statistically significant differences amongst the shorter and longer periods of CRAO. A delayed normalization of the depressed b/a ratio immediately after CRA reperfusion may indicate high-grade ischemic damage. At the final follow-up test session, no clear-cut derangement of any ERG parameter was seen for any group, with subtotal b-wave amplitude recovery for all groups. Longer CRAO produced incomplete VEP recovery. On histology, in the macular retina, eyes with CRAO for 97 min showed practically no damage, but duration of CRAO was found to be significantly associated with the amount of damage in the ganglion cell layer (p = 0.009) and inner nuclear layer (p = 0.017). Outer nuclear and plexiform layers and photoreceptors showed no damage at all with CRAO. There was no significant association of the ERG measures and histologic changes with any of the residual retinal circulation variables. Our electrophysiologic, histopathologic and morphometric studies showed that the retina of old, atherosclerotic, hypertensive rhesus monkeys suffers no detectable damage with CRAO of 97 min but above that level, the longer the CRAO, the more extensive the irreversible damage. The study suggests that CRAO lasting for about 240 min results in massive irreversible retinal damage.

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Author and article information

Journal

Journal ID (nlm-ta): Br J Ophthalmol

Journal ID (publisher-id): bjo

Journal ID (hwp): bjophthalmol

Title: The British Journal of Ophthalmology

Publisher: BMJ Group (BMA House, Tavistock Square, London, WC1H 9JR )

ISSN (Print): 0007-1161

ISSN (Electronic): 1468-2079

Publication date (Electronic): 22 April 2011

Publication date (Print): February 2012

Publication date PMC-release: 22 April 2011

Volume: 96

Issue: 2

Pages: 201-207

Affiliations

Department of Ophthalmology, Medical University of Vienna, Vienna, Austria

Author notes

Correspondence to Ursula Schmidt-Erfurth, Department of Ophthalmology, Medical University of Vienna, Austria, Waehringer Guertel 18–20, Vienna A-1090, Austria; ursula.schmidt-erfurth@ 123456meduniwien.ac.at

Article

Publisher ID: bjophthalmol198937

DOI: 10.1136/bjo.2010.198937

PMC ID: 3261730

PubMed ID: 21515559

SO-VID: bdb06469-963b-4846-8d35-53aca55c916f

Copyright © © 2012, Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.

License:

This is an open-access article distributed under the terms of the Creative Commons Attribution Non-commercial License, which permits use, distribution, and reproduction in any medium, provided the original work is properly cited, the use is non commercial and is otherwise in compliance with the license. See: http://creativecommons.org/licenses/by-nc/2.0/ and http://creativecommons.org/licenses/by-nc/2.0/legalcode.

In vivo identification of alteration of inner neurosensory layers in branch retinal artery occlusion

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Abstract

Background/aims

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Karger: Ophthalmology

Most cited references 24

Blood-retinal barrier in hypoxic ischaemic conditions: basic concepts, clinical features and management.

Retinal artery occlusion: associated systemic and ophthalmic abnormalities.

Central retinal artery occlusion. Retinal survival time.

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