Abstract

BackgroundMacular degeneration (MD) is one of the most frequent causes of visual deficit, resulting in alterations affecting not only the retina but also the entire visual pathway up to the brain areas. This would seem related not just to signal deprivation but also to a compensatory neuronal reorganization, having significant implications in terms of potential rehabilitation of the patient and therapeutic perspectives.ObjectiveThis paper aimed to outline, by analyzing the existing literature, the current understanding of brain structural and functional changes detected with neuroimaging techniques in subjects affected by juvenile and age-related maculopathy.MethodsArticles using various typologies of central nervous system (CNS) imaging in at least six patients affected by juvenile or age-related maculopathy were considered. A total of 142 were initially screened. Non-pertinent articles and duplicates were rejected. Finally, 19 articles, including 649 patients, were identified.ResultsIn these sources, both structural and functional modifications were found in MD subjects’ CNS. Changes in visual cortex gray matter volume were observed in both age-related MD (AMD) and juvenile MD (JMD); in particular, an involvement of not only its posterior part but also the anterior one suggests further causes besides an input-deprivation mechanism only. White matter degeneration was also found, more severe in JMD than in AMD. Moreover, functional analysis revealed differences in cortical activation patterns between MD and controls, suggesting neuronal circuit reorganization. Interestingly, attention and oculomotor training allowed better visual performances and correlated to a stronger cortical activation, even of the area normally receiving inputs from lesioned macula.ConclusionIn MD, structural and functional changes in cerebral circuits and visual pathway can happen, involving both cerebral volume and activation patterns. These modifications, possibly due to neuronal plasticity (already observed and described for several brain areas), can allow patients to compensate for macular damage and gives therapeutic perspectives which could be achievable through an association between oculomotor training and biochemical stimulation of neuronal plasticity.

Highlights

  • RationaleMacular degeneration (MD) is one of the most common causes of visual deficit (Pascolini and Mariotti, 2012)

  • It is interesting to look for evidences in the current literature regarding modifications that have occurred in the cerebral volume and cortical activation in patients suffering from these conditions: this review aims to summarize current findings in patients suffering from maculopathy in terms of structural and functional brain changes, detected with the modern techniques of neuroimaging, wondering whether such modifications may imply neuronal plasticity and whether this could have implications in current therapeutic practice

  • Since activity in cortical areas corresponding to central scotoma projection is considered an evidence of functional reorganization, these results suggested a certain degree of remodeling in the early visual cortex in both juvenile MD (JMD) and age-related MD (AMD), even if not complete and apparently more prominent in JMD

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Summary

Introduction

RationaleMacular degeneration (MD) is one of the most common causes of visual deficit (Pascolini and Mariotti, 2012). The damage in visual function due to MD can be very debilitating for daily activities (Scilley et al, 2002; Knudtson et al, 2005) and has a significant social impact It is remarkable how some patients, in order to overcome losing central visual acuity as the result of MD, develop eccentric vision using a different point in the more peripheral retina, the so-called “preferred retinal locus” (PRL) (Vingolo et al, 2007; Verdina et al, 2013). Macular degeneration (MD) is one of the most frequent causes of visual deficit, resulting in alterations affecting the retina and the entire visual pathway up to the brain areas This would seem related not just to signal deprivation and to a compensatory neuronal reorganization, having significant implications in terms of potential rehabilitation of the patient and therapeutic perspectives

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