Abstract

Purpose: Previous studies have shown that motion coherence thresholds are elevated in several disorders including dyslexia (Cornelissen et al. 1995), glaucoma (Silverman et al. 1990), Alzheimer's disease (Gilmore et al. 1994) and Parkinson's disease (Trick et al. 1994). This threshold elevation is consistent with a deficit in the functioning of the magnocellular (M) pathway. We compared two psychophysical methods of temporarily disrupting normal M-pathway functioning as indexed by elevated motion coherence thresholds. Methods: 30 normal adults participated in this study. We measured motion coherence thresholds for limited lifetime dots moving left or right at a speed of 0.935 deg/s. Dot density was 1 dot/deg2. Coherence thresholds were determined in 4 conditions: after 2 minutes of adaptation to (i) a uniform field flickering at 9 Hz (experimental 1) (ii) a uniform gray field (control 1) and with dots presented on (iii) a uniform red background (experimental 2) and (iv) a gray background (control 2). Results: Motion coherence thresholds were significantly elevated in both experimental conditions (experimental 1 M = 0.2771, control 1 M = 0.1981, experimental 2 M = 0.2198, control 2 M = 0.1873). In addition, the threshold elevation was significantly greater after flicker adaptation than in the presence of a uniform red background. Conclusions: Either flicker adaptation or a red background can be used to disrupt direction selective global motion perception. Physiological studies have shown that magnocellular layers of the LGN are inhibited by a red background (Wiesel & Hubel, 1966) and are essential for flicker perception in monkeys (Merigan, Byrne & Maunsell, 1991). Therefore our results suggest that interference with processing at this level in the M pathway disrupts global motion perception. These techniques are currently being used to study the relationship between M-pathway functioning and reading in people with dyslexia.

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