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Y. Chui, L. Thibos, A. Bradley, I. Zakaim; Psychophysical Analysis of an Axonally–Induced Scotoma . Invest. Ophthalmol. Vis. Sci. 2005;46(13):4319.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: On Sept 19, 2004 one of the authors (LNT) suffered a focal retinal lesion subsequently identified as a "cotton wool spot" located 10 degrees from the fovea in the superior nasal retina of his right eye. This report describes the subjective appearance of the lesion plus the results of quantitative, psychophysical tests that reveal its spatial extent, severity, and nature. Methods: Quantitative entoptic mapping was achieved by illuminating the sclera with a moving point of light. Performance deficits were mapped using customized detection and resolution perimetry, and clinical evaluation was obtained using angiography and retinal imaging. Results: (a) Mapping: The initial sign of damage was the entoptic visualization of a narrow, arcuate region of the visual field starting on the horizontal nasal meridian and sweeping below the fixation point, ending near the blind spot. The entoptic disturbance ended abruptly at the horizontal midline (raphe'), and the arc terminated in a hard scotoma about 3 degrees short of the optic disk at a location subsequently identified by ophthalmoscopy and entoptoscopy as the location of the cotton wool spot. This is consistent with a disruption of nerve conduction through the cotton wool spot lesion. Two weeks after the initial event, the border of the lesion was mapped manually with a low–contrast circular target (5%, 0.3deg) and found to agree closely with the entoptic disturbance. (b) Function: The entoptic visualization appeared bright on a dark background and dark on a bright background, which is consistent with a partial blockage of nerve conduction by ganglion cell axons passing through the lesion causing reduced firing in both on and off center axons. However, conduction was evidently not blocked completely since small objects located inside the arcuate disturbance remained visible, although contrast sensitivity was reduced. When contrast was increased to a supratheshold levels, targets appeared distorted and fragmented, as if obscured by a perforated screen. This is consistent with a conduction blockage in a subset of axons, effectively reducing the sampling density of retinal ganglion cells in that area and lowering the neural Nyquist limit. This hypothesis was confirmed by resolution perimetry that revealed a fourfold loss of sampling–limited grating acuity relative to control areas just outside the lesion and in the fellow eye. A two–month follow up indicated a slightly improvement. Conclusions: These results suggest that acute conduction blockage can precipitate induced brightness anomalies and reduced spatial resolution, which may allow inferences to be draw about the type and proportion of axon damage.
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