Targeting errors and reduced oculomotor range following ablations of the superior colliculus or pretectum/thalamus

The physiology of the superior colliculus (SC) implicates it in the visual control of eye movements. In the primate, acute inactivation of the superior colliculus delays the onset of a visually guided saccade, slows its velocity, and shortens its amplitude. Previous research leaves uncertain whether other oculomotor disorders which sometimes follow ablation of this structure are due to tectal pathology, to neural damage surrounding the tectum, or to both causes. In this study, 7 cynomolgus monkeys received SC ablations. In 3 others, control lesions were placed in the pretectal/posterior thalamic region. Both procedures produced a qualitatively similar syndrome of 4 oculomotor changes. Reaction time to initiate saccades to visual targets was slowed. Secondly, the surgery constricted the normal ocular range. At the worst, movement was confined to a radius of 10-12 degrees of primary gaze. The monkeys displayed two kinds of inaccuracies when attempting to foveate stationary visual targets within their surviving ocular range. Saccadic amplitude was reduced, causing the monkeys' initial attempt to fall short of foveating the target. If the target remained lighted there then ensued a series of stepwise corrective saccades toward it. The corrective saccades ceased with the eyes still at a position short of the target. Eye position remained in error for the duration of the trial. The final position was independent of the target's retinal position or the vector of the motor command needed to acquire the target. Rather, the error was related to the angular position of the target about the head ( = desired eye position). The syndrome appeared qualitatively similar whether resulting from tectal or the more rostral pretectal/diencephalic ablation. When occurring along the horizontal axis, the deficits appeared to require damage to the superior colliculus, perhaps combined with pathology of some other structure. The same syndrome along the vertical axis was better correlated with pretectal/diencephalic pathology. Invasion of these areas together with invasion of the transthalamic axons from the frontal eye fields is interpreted as the critical pathology responsible for the syndrome. A similar oculomotor trajectory can be modelled by supposing a loss in the gain of the signal which conveys the target's retinal position, combined with one other fault in the circuit: either a loss in gain of the eye position signal, or the signal representing the target's position in craniocentric coordinates.