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Harrison, J.E., Stow, I. & Owen, A.M.
In J. E. Harrison & A. M. Owen (Eds), Cognitive Deficits in Brain Disorders. London: Martin Dunitz Ltd, 197-215
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At first look, Parkinson’s disease appears to offer a par excellence model of basal ganglia dysfunction since the best evidence supports the view that the disease is caused by damage to the pars reticulata/compacta of the substantia nigra. It seems that not only is the disorder homogeneous with regard to its signs and symptoms, but also that the focussed pathology is responsible for the cardinal signs of tremor, rigidity, bradykinesia and postural instability. Add in the fact that a ready supply of study subjects is available from any neurologists’ outpatient clinic and one ostensibly has an excellent model with which to investigate basal ganglia function. On paper, then, it seems that the neuropsychological study of PD provides the opportunity to establish both the changes in cognition caused by the disorder and to determine the role of the basal ganglia in normal subjects. In spite of all this, it is a surprise to discover that identifying a single, indisputable fact about cognition in PD is virtually impossible. In this chapter we consider the reasons for this state of affairs and illustrate some of the difficulties attached to determining the cognitive changes associated with PD.