We have studied the neural mechanisms of visual spatial attention in humans and monkeys. Both species fixated on a spot of light and responded with their hands to peripheral visual targets. Reaction times were faster for targets preceded by a light (cue) on the same side (validly cued) than when the curing light was on the opposite side (invalidity cued). The performance of the monkeys was selectively altered by injection of transmitter-related drugs into the superior colliculus. Neurons recorded from the colliculus while monkey performed this task responded well to both the cue and target when they were in the visual receptive field. For some cells when the cue was placed outside of the visual receptive field, the neuron still discharged (weakly) as if it were influenced by the movement of attention through its receptive field. We tested a population of males treated for Kallmann's syndrome. All responded faster than did age-matched control subjects. The controls were only able to equal the patient's performance when highly motivated. A subset of patients have synkinesis. This group performs the task as do subjects with lesions of parietal cortex. They are very slow responding to invalidly cued targets to one side and responding to any targets after diffuse cues. Such data suggest that these patient have an undiagnosed dysfunction of the parietal cortex. When patients with progressive supranuclear palsy are tested, they are substantially slower in all respects compared to control subjects. They have significantly increased differences between valid and invalid reaction times suggesting a slowing of the movement of attention. They are able to move their attention vertically as well as horizontally, even though they cannot make vertical eye movements. Treatment with physostigmine, a cholinesterase inhibitor, reduces the differences in reaction times suggesting an improvement in the ability to move attention. The therapy had no effect on the oculomotor capacity of the patients.
