For the past 15 years, measurements of cerebral blood flow as an indicator of neuronal activity have been used to gain a better understanding of the neural basis of motor and cognitive deficits in Parkinson's disease. The initial studies, using positron emission tomography, yielded results in keeping with the hypothesis that symptoms result from excessive cortical inhibition from cortico-striatal loops. However, subsequent studies with functional magnetic resonance imaging (fMRI) have shown that specific aspects of the paradigms used, such as the need to pay attention to one's movements, have a significant impact on activation patterns, which may complicate the interpretation of results. Functional neuroimaging has also been used to investigate the causes of cognitive impairment in Parkinson's disease. While some studies implicate dopamine loss in striatum, more recent investigations using anatomical MRI to measure cortical atrophy suggest that some cognitive deficits are attributable to direct cortical involvement by the disease.