Worsening vision is an almost inevitable consequence of ageing. Agerelated macular degeneration (AMD) in its advanced stage is the major cause of visual deterioration among the elderly of the industrialised world.1,2 Developing countries are rapidly closing the gap, and it is expected that in coming years the burden of AMD will dramatically increase in those countries as well.3 Despite the recent development of efficient therapeutic solutions, early detection of the advanced stage of AMD is still in its infancy. This article describes the benefits of a preferential hyperacuity perimetry (PHP) device in assisting early detection of advanced AMD, thereby possibly improving the outcome of treatment.
Progression of Age-related Macular Degeneration
AMD is a bilateral degenerative disease that affects the macula, the central portion of the retina. AMD occurs in two major patterns, starting with the atrophic non-exudative form (dry AMD) and eventually developing to the neovascular exudative form (wet AMD, or choroidal neovascularisation [CNV]). The non-exudative form is defined by pigmentary changes in the retinal pigment epithelium (RPE) and extracellular accumulation of debris material (drusen) between choroid and RPE. At this stage, these changes have little impact on vision – most patients retain good visual acuity – and the disease is mostly asymptomatic, although some patients report mild changes in visual acuity, blurring, decreased contrast sensitivity and weak adaptation to darkness. Prevalence of these early and intermediate stages of AMD is estimated at 15% among persons above 55 years of age,4,5 increasing from 2% for those 50–59 years of age to above 30% for those over 75 years of age.
Patients at risk are advised to take supplementary vitamins and to quit smoking. However, within five years over 6% of eyes diagnosed with dry AMD will develop a CNV lesion.4 CNV lesions can be classified as occult or classic according to their appearance on fluorescein angiography (FA). Occult lesions are more difficult to detect and develop relatively slowly. In the more aggressive classic lesion, the Bruch’s membrane ruptures and choroidal blood vessels invade the subretinal space. Usually, the CNV lesion erupts at an extrafoveal location, but choroidal blood vessels rapidly proliferate towards the fovea. These de novo blood vessels characteristically leak, leading to haemorrhage and inflammatory processes. A secondary complication is retinal and/or RPE elevation due to the accumulation of subretinal and/or sub-RPE fluid, which can shift photoreceptors from their original position in the retina, resulting in metamorphopsia (perception of distorted lines). In some cases the photoreceptor layer can detach from the RPE layer, triggering the death of photoreceptors and leading to scotoma (loss of vision in defined areas of the visual field). These processes cause irreversible damage that, when reaching subfoveal areas, affects central vision. If untreated, symptoms such as blurring, scotoma (holes in the visual field) and metamorphopsia rapidly worsen
until vision deteriorates to legal blindness within several weeks or months. Although the prevalence of CNV is only 10–15% among patients with dry AMD, it is responsible for over 85% of blindness resulting from this disease.5–7 In some rare cases, a person affected by CNV may find his or her world changed overnight. In a person who loses vision in one eye as a result of CNV, the risk of developing advanced AMD in the second eye is as high as 43% within five years.8