PubMed · 13025560
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H E HENKES. 1952-10-18. [Electroretinography].. https://pubmed.ncbi.nlm.nih.gov/13025560/
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The mfERG, when first introduced by Erich Sutter used long sequences with short periods (approximately 15 ms) between steps (flashes). Since then a number of studies have introduced slower or modified sequences to emphasise Oscillatory Potentials (OPs), Optic Nerve Head Components (ONHC) or the s-wave. With this reduction in the rate of presentation many of the investigators have reduced the length of the sequence to allow a shorter recording period. This is also desirable for patient comfort and co-operation in diagnostic investigations. When reducing the length of the sequence there is a risk that it will be too short to ensure orthogonality of the first order component and all significant higher order components, particularly when a large number of areas (hexagons) are stimulated. This paper aims to verify that a short sequence (using the sequence used by the Roland Retiscan stimulating 19 hexagons) is capable of keeping responses of both first and higher orders separate for each stimulating area. The sequence was investigated by placing photodiodes connected to a Diagnosys Espion and then exported to Excel and MATLAB for analysis. It was determined that the sequences used were m-sequences length n = 9. The photodiode only responded to flashes of light so was unable to detect a correcting 0 at the end of sequence. The sequences driving each hexagon were then determined and found to be shifted 26 steps from each other. The correlation coefficients between all sequences was found to be -1/(2n -1). The sequences to decode the second order kernels were determined and the correlation coefficients between each of these sequences, and between these and the original sequences, were also -1/(2n -1). This work provides a mathematical validation of the use of short sequences for slow mfERG, and describes an empirical test method.
We review proposed models and psychophysical and electrophysiological tests performed in many studies for early age-related maculopathy (ARM). We suggest that ischaemia is the trigger for impaired retinal pigment epithelium function causing imbalance of secretion of vascular growth factors, reduced disc degradation capability and reduced metabolic activity and possible inflammatory response. This results in increased deposition of cell debris, such as drusen and thickens Bruch's membrane causing even more ischaemia of the overlying neurosensory retina. The photoreceptors are more resistant to ischaemia given their proximity to the choroid. Furthermore, being 'upstream' from the inner retinal layers, they act as an oxygen sink depriving retinal layers further from the choroid. Postreceptoral cell layers and especially parts of the inner nuclear layer that are located in the watershed zone between two sources of blood supply are preferentially vulnerable to ischaemia. Based on psychophysical and electrophysiological findings we propose that most of the function impairment in early ARM starts postreceptorally.
PURPOSE: To describe the association between retinal degeneration and cobalamin C (cblC) disease and to review previously published ophthalmic data regarding cblC disease. METHODS: Descriptive case series of three patients and compilation of all previously reported cases of cblC disease in the ophthalmic literature. RESULTS: All three new cases presented with macular pigmentary changes and showed attenuation of electroretinographic responses. Sequential ERG (electroretinogram) testing in Case 1 demonstrated ERGs that began at the lower limits of normal and became progressively attenuated over time. CONCLUSIONS: Cobalamin C disease results in progressive retinal degeneration with its onset in the first few months of life and progressing rapidly over the first few years of life.