Neuropsychiatric, perceptual and cognitive deficits are increasingly recognized as non-motor manifestations of Parkinson's Disease (PD).The premorbid personality profile of PD patients is characterized by a number of traits which figure prominently after the disease becomes manifest. In particular, less novelty seeking is one premorbid trait providing an understanding of later cognitive deficits. Anxiety and depression have been shown to precede in some patients motor manifestations and cannot be attributed to anti-parkinsonian therapy. Some neuropsychiatric manifestations and in particular hallucinosis are linked to select perceptual and cognitive changes. Cognitive deficits are common in PD, in particular in younger onset patients. Current animal studies link genetic differences in the dopamine transporter and dopamine catabolic enzyme system to select cognitive impairments attributed to frontal lobe dysfunction.Visuo-cognitive impairment is prevalent in PD. Retinal dopaminergic deficiency has been shown in patients and in the animal model of PD. Visuo-spatial deficits, however, are not simply passive reflections of retinal deficiency. In addition to vision, saccadic eye movements are affected in PD whether they contribute to visuo-spatial dysfunction is unknown. However, recent functional Magnetic Resonance Imaging (fMRI) and electroencephalogram (EEG) studies show an essential role of the occipital cortex in saccadic eye movements and positron emission tomography (PET) studies show occipital hypometabolism in PD. Visual and eye movement studies suggest that certain neuropsychiatric and cognitive deficits in PD are linked to the visual system. Synchrony of signals are essential for the co-operation of distributed neuronal network engaged in sensory-motor coordination. Local, dopaminergic neuronal groups in the retina, basal ganglia and frontal cortical memory system are affected in PD. These connections may not primarily rely on dopamine as a neurotransmitter. It is suggested that to understand visuocognitive changes we should consider pathology affecting neuronal connections, necessary for binding parallel distributed networks.