To our knowledge, no study has investigated smooth pursuit initiation latencies in anisometropic amblyopia. It is known that the visually-related reaction times in individuals with amblyopia are prolonged during both manual button-press
37 and saccadic movement
22,23,38–40 tasks. These latter studies tested mostly reflexive
22,23,38,39 or overlap
40 saccades, and have shown that when viewing with the amblyopic eye, the mean saccadic latencies are delayed by 27 to 57 ms compared with the nondominant eye viewing in controls; specifically, in participants with anisometropic amblyopia, the mean saccadic latency delay during amblyopic eye viewing ranges from 32 to 44 ms
22,23,38,40 In this study, we found that the smooth pursuit initiation latencies were 23 ms longer on average during amblyopic eye viewing compared with nondominant eye viewing in controls. This increased delay with amblyopic eye viewing is consistent with the results reported in the aforementioned studies on saccades, but the magnitude of the delay is smaller (∼23 ms compared with 32–44 ms).
The smooth pursuit and saccadic brain circuitry share several cortico-ponto-cerebellar structures; however, there are notable differences between the two.
27 For both smooth pursuit/saccades, the respective visual velocity/position signals are processed first in the primary visual cortex (V1).
27 The difference between the pursuit and saccadic processing pathways arises from the extent of contributions from the frontal lobe, parietal lobe, and superior colliculus. Pharmacologic inactivation of the smooth eye movement subregion in the frontal eye fields reduces the steady state pursuit velocities, but has negligible impact on pursuit initiation latencies.
41 The pursuit region of the posterior parietal cortex (or lateral intraparietal area in monkeys) monitors the extraretinal pursuit signals
42 but does not play a major role in determining pursuit initiation latencies.
43 The superior colliculus, which contains a spatial retinotopic map, plays a limited role in smooth pursuit movements: it may be involved in goal selection for eye movements in general
44 and in modifying pursuit metrics,
45 but it has been speculated that it does not play a direct role in initiating pursuit movements (see fig. 2 in Krauzlis
27). In contrast, the frontal/parietal lobes and the superior colliculus play instrumental roles in the initiation of saccadic eye movements. It is known that the lesions of the human posterior parietal cortex delay the initiation of reflexive saccades.
46 Also, the pharmacologic inactivation of superior colliculus in monkeys causes saccadic latencies to increase.
47
We speculate that the longer latency reported previously in participants with anisometropic amblyopia for reflexive and overlap saccades (32–44 ms
22,23,38,40) compared with that observed here for smooth pursuit (∼23 ms) could be attributable to further signal processing delays at the posterior parietal cortex or superior colliculus. Because these two structures are involved marginally in the initiation of smooth pursuit, they are possible loci where the additional temporal delay for saccadic initiation could occur. Alternatively, the difference between the smooth pursuit and saccadic latency delay could reflect a difference in how the retinal velocity and retinal position signals are processed in anisometropic amblyopia. Smooth pursuit is driven by a retinal velocity signal, whereas saccades are driven by a retinal position signal. It is possible that the processing of velocity error signals by the amblyopic visual system is not as delayed as the processing of position error signals, which could explain why the prolonged latency for pursuit initiation is less than that for saccades. For both kinds of eye movements, it is unlikely that a simple visual acuity loss is associated with the prolonged latency we report here for pursuit and previously for saccades
22,23 because the latencies did not correlate with the severity of visual acuity deficit in the amblyopic eye.
It is known that target contrast can also modulate smooth pursuit latencies. Previous studies have shown that reducing the contrast of the visual stimulus increases the smooth pursuit latencies in visually normal observers.
48,49 Individuals with amblyopia have known contrast sensitivity deficits, and their visual cortical areas under-sample high spatial frequency content. It is therefore not surprising that the smooth pursuit latencies in amblyopic participants, who have inherently reduced contrast sensitivity, are prolonged when compared to visually normal observers. Future investigations should test whether modulating the contrast of the visual target has any effect on smooth pursuit latencies in people with amblyopia.