Eye movements, visual acuity and spatial constancy

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Abstract
How are eye movements related to acuity or to the lack of spatial constancy, oscillop-sia (OSOP)? How do subjects with congenital nystagmus (CN) suppress OSOP? Can we apply their strategies to cases of acquired nystagmus? In normals, the maintenance of target foveation with low retinal slip is thought to be necessary for good visual acuity. Retinal slip velocities below 1.67-4 deg/sec have been given as upper bounds for good vision. Subjects with CN do not usually have OSOP and can have good (even normal) visual acuity. CN subjects can maintain target position (SD=0.21 deg) and low retinal slip velocities (SD=1.97 deg/sec). Previously, the author identified two possible mechanisms for the suppression of OSOP in subjects with CN: (1) efference copy of the CN waveform to negate the effects of the oscillation or (2) the stable vision available during foveation periods. A 48-year-old man with hereditary CN lost consciousness; when he came to, he had troublesome, intermittent OSOP. Recordings revealed a jerk left with extended foveation (JLef) waveform when OSOP was absent (SD of eye position was 0.24 deg and SD of retinal slip velocity was 1.87 deg/sec). However, with the onset of OSOP, his CN waveform abruptly changed to jerk right (JR) and was biased several degrees to the right of the target. Phase-plane analysis revealed that, during the periods of OSOP, the JR waveform did not enter the foveation window defined by the limits, 0±0.5 deg and 0±4.0 deg/sec. CN direction shifts, common in some CN subjects, do not normally result in loss of foveation periods or OSOP. During electronic retinal image stabilization (RIS), transient OSOP persisted with the same CN waveform changes. RIS usually results in OSOP that can be suppressed by the CN subject. This subject also suppressed OSOP during his normal JLef waveform but was unable to do so when the biased, JR waveform appeared. The efference-copy mechanism is tenable only if the man's pathology occurred at a point beyond where the efference-copy signal is fed back. Stable vision by itself is insufficient since RIS causes OSOP in CN. The author concludes that the mechanism that prevents OSOP requires the motor stability provided by the CN foveation periods. Without them, OSOP is not suppressed even during RIS. If we presume that CN subjects make use of existing mechanisms for preserving the sense of spatial constancy (even allowing that they may have optimized these mechanisms), the suppression of OSOP in cases of acquired nystagmus should be possible if we can provide a foveation window during each nystagmus cycle.