In patients affected by Parkinson's disease, and in the monkey model of this disease, visual defects have been shown using psychophysical and electrophysiological measures of spatial and temporal contrast sensitivity. These studies imply an essential role for dopamine in primate vision. There is electrophysiological and neurochemical evidence to suggest that at least part of the problem is impaired retinal processing caused by systemic dopaminergic deficiency. Some of the deficits that have been demonstrated, consistent with physiological studies, suggest that center-surround interaction of neurons may suffer as a consequence of dopaminergic deficiency. The role of the regulation of retinal dopamine (D1 and D2) receptors in primate vision and of the balance of these receptors in presynaptic dopaminergic deficiency is not yet determined. Using sinusoidal grating stimuli in cognitively loaded tasks may increase understanding of the behavioral consequences of visual deficits seen in dopamine deficiency syndromes.