title: [Myopia update 2011].
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.
authors.affiliation: Sektion für Neurobiologie des Auges, Forschungsinstitut für Augenheilkunde, Eberhard Karls Universität Tübingen, Tübingen. frank.schaeffel@uni-tuebingen.de
authors.forename: F
authors.initials: F
authors.lastname: Schaeffel
mesh_terms: D000368:Aged; D001285:Atropine / Q000009:adverse effects / Q000627:therapeutic use; D058452:Axial Length, Eye / Q000187:drug effects / Q000502:physiology; D003261:Contact Lenses; D018450:Disease Progression; D005139:Eyeglasses; D005500:Follow-Up Studies; D006801:Humans; D058449:Intravitreal Injections; D018727:Muscarinic Antagonists / Q000009:adverse effects / Q000627:therapeutic use; D009216:Myopia / Q000150:complications / Q000503:physiopathology / Q000628:therapy*; D011379:Prognosis; D012160:Retina / Q000187:drug effects / Q000503:physiopathology; D012162:Retinal Degeneration / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control; D012590:Sclera / Q000503:physiopathology; D012591:Scleral Buckling; D019716:Tissue Inhibitor of Metalloproteinase-2 / Q000009:adverse effects / Q000627:therapeutic use; D042461:Vascular Endothelial Growth Factor A / Q000037:antagonists & inhibitors / Q000502:physiology; D014792:Visual Acuity / Q000502:physiology; D014794:Visual Fields / Q000502:physiology
chemical_list: D018727:Muscarinic Antagonists; C560823:TIMP2 protein, human; C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A; D019716:Tissue Inhibitor of Metalloproteinase-2; D001285:Atropine