Myopie-Update 2011

 

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Zusammenfassung

Dieser Übersichtsartikel fasst einige neuere Aspekte der Myopieforschung zusammen. Folgende Schlussfolgerungen werden gezogen: Solange die Myopieprogression visuell geregelt ist, kann sie über mindestens drei Wege beeinflusst werden: 1. Brillengläser/Kontaktlinsen, die nur das Zentrum des Gesichtsfelds voll korrigieren und die Peripherie etwas myop belassen, 2. Aufenthalt im Freien oder zeitweilige äquivalente Erhöhung der Beleuchtungsstärke, 3. pharmakologische Beeinflussung der retinalen Wachstumssignale, die an die Sklera weitergeleitet werden. Optionen 1. und 2. können risikofrei angewendet werden, aber es gibt noch Raum für Optimierung. Projekte in Option 3. sind gegenwärtig „wieder” in einer „Orientierungsphase”, in der nach neuen Kandidaten gesucht wird, nachdem Tests mit muskarinischen Antagonisten (Pirenzipin) bei Kindern nicht in eine Phase-III-Studie überführt werden konnten. Liegt die Stärke der Myopie außerhalb des durch die Emmetropisierung geregelten Bereichs (im Falle hoher und pathologische Myopien, die nicht durch Seherfahrung beeinflussbar sind), besteht prinzipiell die Möglichkeit, der mechanischen Schwäche der Sklera pharmakologisch entgegenzuwirken. Besonders hier besteht aber noch Forschungsbedarf. Bisher wurden stattdessen operative Verfahren zur Verstärkung der Sklera eingesetzt, die aber nur beschränkte Verbreitung gefunden haben, da die Wirkung nicht sehr überzeugend war. In 40 – 50 % der hohen Myopien zeigen sich degenerative Prozesse in der Retina, die als Folge der Überdehnung der Fundusschichten gesehen werden können, aber davon unabhängig sein können (es gibt keine signifikante Korrelation mit der Achsenlänge!). Sie können z. T. durch intravitreale anti-VEGF-Therapie verlangsamt werden. Wie eine Langzeitstudie in Dänemark gezeigt hat, erreichen Patienten mit Myopien von 6 – 9 dpt in der Pubertät meist ohne Einschränkungen des Sehvermögens das Pensionsalter.

Abstract

This review summarises some recent aspects of myopia research. The following conclusions have been drawn. As long as myopia progression is visually controlled, at least three different interventions are possible: (i) spectacles/contact lenses which correct only the centre of the visual field and leave the periphery somewhat myopic, (ii) outdoor activity or equivalent temporary increase in illuminance, (iii) pharmacological intervention of retinal growth signals that are transmitted to the underlying sclera. Options (i) and (ii) can be used without risks although there is still room for improvement of the variables. Option (iii) has re-entered a new phase of orientation with new searches for candidate targets after previous testing with muskarinic antagonists (pirenzepine) in children did not enter phase 3 level. If myopia is outside the range over which it is visually controlled by emmetropisation (in the case of high and pathological myopias), in principle the possibility exists to improve the mechanical stability of the sclera pharmacologically. However, there is still a need for more research. Up to now, the mechanical weakness of the sclera in highly mopyic eyes is surgically stabilised by ”scleral buckling”. However, these procedures have found limited acceptance since the effects were not very reliable. In 40 – 50 % of the cases of high myopia, degenerative processes are found in the retina which can be seen as consequence of the mechanical tension in the fundus, but may also be indepedent of this factor (no significant correlation with axial length!). In part they can be slowed down by intravitreal anti-VEGF therapy. A long-term study from Denmark has shown that most patients with myopia of between 6 – 9 dpt during puberty reach retirement age without disabling visual loss.

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Prof. Dr. Frank Schaeffel

Sektion für Neurobiologie des Auges, Forschungsinstitut für Augenheilkunde, Eberhard Karls Universität Tübingen, Tübingen

Calwerstraße 7 / 1

72076 Tübingen

Phone:  ++ 49/70 71/2 98 07 39

Fax:  ++ 49/70 71/29 51 96

Email: frank.schaeffel@uni-tuebingen.de