Authors:

OWEN, A.M. & Doyon, J.

Reference:

Year of publication:

1999

CBU number:

3659

Abstract:

In Parkinson's disease, the characteristic triad of motor deficits, bradykinesia, rigidity and tremor, is accompanied by a progressive pattern of neuropsychological impairment, which, in its earliest stages, resembles that seen after frontal-lobe excisions in patients. These deficits in PD may reflect damage to one or more cortico-striatal circuits that parallel the well described ëmotor loopí, but subserve cognitive, rather than motor, functions. However, since PD is also associated with intrinsic frontal pathology, the ëfrontal-likeí deficits observed may result from either, or both, of these forms of pathology. In this paper we describe a series of positron emission tomography (PET) studies in patients with PD designed specifically to address this issue. The results suggest that striatal dopamine depletion in PD disrupts the normal pattern of basal-ganglia outflow through the globus pallidus and, consequently, affects cognitive functions that are dependent upon components of this circuitry.