Definition of pathologic myopia (syn. degenerative myopia) is not uniform. From the view­point of the clinician, axial myopia associated with structural changes of the posterior globe describes the condition most properly, as these alterations may threaten visual acuity. Refraction errors greater than 8 diopters are frequently associated with visual dysfunction. The prevalence of high myopia is apparently increasing, particularly in some Asian subareas. A predilection for Chinese, Japanese, Arab and Jewish populations is ascertained, the disease has a high impact on both, the individual and socioeconomics.

The course emphasizes retino-choroidal and vitreo-retinal pathologies in degenerative myopia. Based on own cases, the spectrum of fundus changes will be presented as well as the current treatment options. Other common associated conditions, such as cataract, glaucoma, peripheral retinal degenerations are not specifically addressed.

Developmental and degenerative changes include tigroid fundus appearance, mottling RPE-changes including lacquer cracks, thinning and atrophy of the choroid and retina resulting in atrophic areas, tilted optic disc with myopic conus and posterior ectasia (staphy­loma). Based on these alterations, further complications may occur, such as macular hemorrhage, myopic CNV and Fuchs’ spot as well as macular and posterior holes that lead to staphyloma-associated retinal detachment. Recent imaging techniques have also demon­strated specific vitreoretinal interface changes. Myopia-associated vitreoschisis and epiretinal membrane formation plus myopic foveoschisis contribute to visual impairment and may precede macular hole formation and retinal detachment.

There is no treatment that regresses or arrests progressive pathologic myopia. In other words, degenerative changes are not susceptible to therapy. However, treatment options are available for several additional complications.

1. Myopic CNV often arise from lacquer cracks, but can effectively be treated by PDT and anti-VEGF. Surgical options, such as limited and 360º macular translocation have been largely quitted today.

2. Visual disturbances and metamorphopsia that originate from myopic vitreo- and foveo­schisis are difficult to identify ophthalmoscopically, but OCT-techniques allow different­tiation. Using visualization aids, subtle peeling of tractional vitreoretinal interface changes is technically feasible. In face of the fact that multiple factors contribute to visual deterioration in pathologic myopia, indications of vitrectomy for this condition are not well defined.

3. Staphyloma-associated retinal detachment is either tractional or rhegmatogenous in nature. It is considered an indication for surgery, however, various methods are suggested and range from macular buckling to vitrectomy with long-acting gas or silicone oil tamponade. The rate of anatomic success differs considerably in the literature. Generally, functional outcomes are often modest due to preexisting myopic fundus changes and the fact, that despite of an attached retina, coexisting macular holes are frequently not closed.

Vision in high myopia can be restored using optical devices or surgery. However, long-term prognosis in pathologic myopia is dubious because of the high potential for severe visual loss. Degenerative chorioretinal changes or retinal detachment lead to irreversible photo­receptor cell damage at the posterior pole and most often affect the macula. As long as we lack measures to prevent early onset and rapid progression of myopia in childhood and young adulthood, potentially visually disabling pathologic myopia may occur in later life. Treatment today aims at complications, such as subretinal CNV, epiretinal traction syndromes and retinal detachment.