Parkinson's Disease (PD) has traditionally been viewed as primarily a disturbance of motor functioning, typically involving tremor, rigidity, hypokinesia, gait disturbance, and postural instability. More recently, decline in cognitive function has been recognized as a feature of PD. One prominent cognitive symptom of PD involves deficits on tasks of spatial ability. However, findings of visual-spatial deficits in individuals with PD have been inconsistent. There are several methodological issues in this area of research that potentially confound the interpretation of data and need to be taken into consideration, including subject characteristics (e.g., age, sex and education), duration of illness, the current level of disability, the presence of emotional depression, the current level of medications, and the presence of dementia. Further, the tests that have shown visual-spatial deficits in PD are often complex, showing sensitivity to other cognitive processes as well. Another problem in this area of research is the lack of a clear understanding of the brain mechanisms that underlie visual-spatial deficits in PD. One theory of cognitive dysfunction in PD suggests that these cognitive deficits are in some way related to disruption of frontal-basal ganglia neural circuits important in executive functions. However, frontal-basal ganglionic dysfunction does not appear to account entirely for the visual-spatial cognitive deficits seen in PD. Subtle differences in performance on executive function measures appear to dissociate individuals with frontal lobe damage from individuals with PD. Findings from two recent studies indicate that PD is indeed associated with deficits in visual-spatial ability. These findings also indicate that the relationship between visual-spatial ability and frontal-executive function in PD is likely complex, and that the visual-spatial deficits in PD may be sensitive to the sex of the individual with PD.