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H. Zwick, P. Edsall, D. J. Lund, R. Cunningham, B. E. Stuck; Evidence of NHP Spectral Sensitivity Deficits Associated With Retinal Nerve Fiber Layer (RNFL) Damage Derived From a Pursuit Motor Tracking Task at Suprathreshold Exposure Levels Temporal to the Macula. Invest. Ophthalmol. Vis. Sci. 2008;49(13):3828.
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© ARVO (1962-2015); The Authors (2016-present)
Intact retinal visual function provides the visual guidance component for the highly integrated visual motor interaction required for a visual motor performance task (VPMT). In complex visual motor tasks, capability to differentiate retinal dysfunction from neural motor performance components provides visual function metric for direct assessment of retinal photoreceptor dysfunction. A metric for separating the sensory component from the motor component was employed to assess retinal function in visual pursuit motor performance.
A spectral sensitivity metric was derived from the visual pursuit motor task (VPMT) to separate laser induced retinal dysfunction. Laser induced retinal function was separated from the VPMT by deriving spectral sensitivity functions from the NHP (non-human primate) VPMT using an up and down threshold technique ranging from 50 to 70 percent time on target criteria. Spectral sensitivity functions were plotted for an equal energy spectrum normalized at 580 nm.
VPMT derived spectral sensitivity measurements for both CW (543 nm, 250 msec) and Q-switched (532 nm, 7 nsec) at and above threshold damage levels required at least 8 weeks of post exposure recovery. Laser induced retinal damage to the Papillary Macular Bundle (PMB) required about a week prior to visible retinal evidence of retinal nerve fiber layer loss, indicated functionally by neurally opponent variations in spectral sensitivity measurements of cone photoreceptor systems.
A greater loss in visual function was obtained with the spectral sensitivity metric in revealing longer periods of retinal photoreceptor damage recovery as well as a 5 day delay of inner retinal damage damage to occur in the ganglion cell layer and associated disruption of complex neurally opponent systems resident in this region of the retina.
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