Abstract
Step changes in ocular accommodation are controlled by pulse & step signals to the ciliary muscle (agonist) that stretches the passive choroid (antagonist) (Schor & Bharadwaj, 2004). During disaccommodation (near-to-far focusing), the roles of the ciliary muscle & choroid are reversed: the ciliary muscle is the antagonist. Are pulse & step signals also used to control disaccommodation?
Peak velocity of accommodation step responses increase with response magnitude but peak acceleration is invariant. In contrast, peak velocity & peak acceleration of disaccommodation are invariant of response magnitude for a fixed starting position, but they increase with proximity of the starting position (Bharadwaj & Schor, 2005). This suggests that disaccommodation is initiated by a pulse signal toward a constant primary destination & it is followed by a step signal to achieve a desired final position.
In the pulse-step model of accommodation, pulse width is adjusted independently of pulse height to control velocity independently of acceleration. We used a similar pulse-step model for disaccommodation with two differences. First, instead of increasing the width of a fixed-height pulse with response magnitude, we increased height of a fixed-width pulse. Second, the magnitudes of the pulse & step were made independent. Pulse height was appropriate for a response initiated toward a primary destination & step height was proportional to a desired final position. Primary destination was estimated from the negative X intercept of plots of peak velocity as a function of starting position that correspond to the cycloplegic refraction. Time-to-peak-velocity indicated when the step occurred & this did not change with either response magnitude or starting position. The pulse-step model of disaccommodation predicts that when the discrepancy between final position & primary destination was large, mismatched amplitudes between a larger pulse and a smaller step cause overshoots of the step response.