Abstract
PurposeBackground and Purpose: Diabetic retinal neuropathy refers to retinal neural tissue damage occurring before diabetic retinopathy and fulfils many of the criteria for causality for the subsequent vasculopathy. Developing reliable means of measuring neuronal damage in diabetes may be important in efforts to prevent retinopathy. This study aimed to systematically assess current clinical measurements of diabetic retinal neuropathy.MethodsA systematic search of the medical literature since 1984 was performed on PUBMED and EMBASE and the evidence supporting each identified method as an indicator for clinically important diabetic retinal neuropathy was graded relatively as strong, medium or weak according to criteria assessing its relationship to subsequent diabetic retinopathy, quality of supporting studies and published reproducibility.ResultsThe systematic search yielded 6,421 results. Subsequent assessment by two independent investigators identified 601 multiple subject studies in humans assessing clinical aspects of retinal structure, function or psychophysics in the pre‐diabetic retina. Clinical methods assessed as being supported by relatively ‘strong’ evidence included FM‐100 hue colour vision changes, flash ERG b‐wave latency, flash multifocal b‐wave latency, scotopic flash ERG oscillatory potential amplitude and contrast sensitivity.ConclusionsConclusions/Discussions: The results showed moderately poor quality of extant evidence and indicate the best clinical methods for assessing diabetic retinal neuropathy remain to be confirmed. This is the first systematic assessment of the medical literature aiming to assess the breadth and validity of these methods and represents an early step in identifying and developing endpoints for use in trials designed to identify at risk patients or prevent diabetic retinopathy.
Highlights
Diabetic retinopathy is a significant and progressive cause of blindness and visual impairment worldwide [1]
Studies which did not distinguish between patients with diabetes graded as nonretinopathic and early retinopathic grades were included. e evidence supporting each tested method likely to be clinically relevant for identifying diabetic retinal neuropathy was graded relatively as compelling, moderate, medium, or weak according to the GRADE criteria-based table (Table 1). e grade of evidence broadly assessed a positive clinical test’s correlation with the development of subsequent diabetic retinopathy, quality of the study, and published reproducibility across studies; 6432 studies were identified, and 601 of these studies yielded 933 examples of metrics of assessing preclinical or clinical diabetic retinal changes
Retinopathy detection software and digital fundus photography are relevant for identifying the state of a diabetic retinopathy in the period at or after clinical detection of retinal retinopathy but are included where they have developed either proprietary or nonproprietary measures of early diabetic retinal changes which are reported as preceding standard grades of diabetic retinopathy, such as vessel calibre changes, capillary density in perifoveal intercapillary space, and optic nerve head contour or shape
Summary
Diabetic retinopathy is a significant and progressive cause of blindness and visual impairment worldwide [1]. Diabetes causes panretinal damage over time via vasculopathic [2] and neuropathic [3] processes, eventually and progressively resulting in retinal ischaemia, haemorrhages, fibrosis, and irreversible blindness. Preceding clinically detectable retinopathy is a gradually progressive, not fully characterised, pre-retinopathic disease process described as diabetic retinal neuropathy [4,5,6,7]. Irreversible cumulative damage has been described in both the inner and outer retina [10], together with changes in glial cell morphology [9]; interruptions to the phototransduction cascade linked to early pericyte death [11, 12]; overproduction (or impaired removal) of lactate from a superfluity of glucose [5]; increased apoptosis and necrosis, possibly as a result of microglia-induced inflammation [6]; and retinal ischaemia [13].
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