First Author: S.Antonakis UK
Co Author(s): L. Drayer Turner G. Almeida
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The finding of a solitary torpedo-shaped hypopigmented lesion in the macula proximal and pointing to the fovea has confused researchers about the underlying pathology for many years. Current thinking traces its origins to developmental defects in the RPE. Our cases highlight an essential question regarding the basic pathophysiology: Is torpedo maculopathy static and non-progressive with a dysgenetic RPE and a cleft, or is it progressive, with accumulation of fluid throughout life?
Medical Retina Service, Maidstone and Tunbridge Wells NHS Trust, UK
Our case series reports five cases with varied clinical presentations and torpedo lesions that referred to our clinic. Patients were evaluated for lesion features and course on follow-up, visual acuity and OCT findings. Case-1: 57-year-old Caucasian female was referred for right macular lesion with floaters. Case-2: 26-year-old Caucasian male was referred for a macular lesion in his right eye. History of Type I Diabetes Mellitus but no associated retinopathy. Case-3: 41-year-old Caucasian male was referred to us for an asymptomatic right eye macular lesion. Case-4: 37-year old Caucasian male presented complaining of left eye blurred vision. His presentation was preceded by a short period of high stress. He was diagnosed with OU CSR, with an incidental finding of OD Torpedo Maculopathy. Case-5: 33-year old Caucasian female was referred for exclusion of melanoma.
These five cases challenge some of the suggested theories, specifically with regards to accumulation of subretinal fluid and inner retinal dysfunction. There is no accumulation of fluid in Cases 2, 3 and 5. BCVAs were 6/7.5 , 6/6 and 6/6 respectively. In Case 1 (older patient) there is sub- and intraretinal fluid accumulation. BCVA 6/6 In Case 4, CSR fluid pools over the RPE, which might suggest dysfunction of the RPE on the torpedo lesion. BCVA 6/5
The accumulation of subretinal and intraretinal fluid and associated retinal thinning on the older patient, and the contrast between him and the other cases, suggest an initial structurally normal retina, with primary changes in the RPE causing secondary accumulation of fluid and atrophy throughout life. Early changes might not include accumulation of subretinal fluid. We therefore hypothesize that the RPE dysgenesis leads to a slow secondary accumulation of fluid throughout life. What is certain is that these lesions do not affect vision; despite these large RPE lesions, and varied OCT images.