Abstract
The perception of unambiguous depth from motion parallax relies on an extra-retinal signal from the pursuit eye movement system. Consistent with this link between pursuit and motion parallax, observers with abnormal visual pursuit due to ethanol intoxication (Nawrot, Nordenstom & Olson, 2004) and asymmetric smooth pursuit associated with esotropia (Nawrot, Frankl & Stockert, 2004) show elevated thresholds in motion parallax tasks. Are these motion parallax deficits due to a fundamental disruption to the integrity of the pursuit signal, or are they a “secondary” deficit due to retinal slip of the motion parallax stimulus caused by inadequate pursuit velocity? We studied normal observers using a Rogers & Graham (1979) type random-dot motion parallax stimulus in which the fixation point was translated independently from, and more slowly than, the motion parallax stimulus window. This generated increased retinal slip of the motion parallax stimulus, and mimicked the retinal stimulus for an observer with reduced pursuit gain (0.2 −0.25 for ethanol intoxication, and 0.1 for the gain asymmetry between temporalward and nasalward pursuit in esotropia). In one condition the motion parallax stimulus window remained stationary on the monitor while the fixation point translated in proportion (0.05 to 0.35) with the observer's head translation. In another condition the observer's head remained stationary, while the motion parallax stimulus window translated from side-to-side. The fixation point moved in proportion (0.9 to 0.6) to the stimulus window motion. Depth perception thresholds were only minimally affected by the increased retinal slip. Retinal slip of the motion parallax stimulus does not explain the motion parallax deficits found with reduced pursuit gain in ethanol intoxication and asymmetric pursuit with esotropia. Other causes, such as integrity of the pursuit signal, or interruption of the pursuit signal by the saccadic system, could be more direct causes for these motion parallax deficits.