Cognitive function in Parkinson's disease: from description to theory.
From the large body of empirical evidence on cognitive function in Parkinson's disease, a number of attempts have been made to describe the characteristics of the deficits and the conditions under which they are observed. This review considers descriptions limited to specific domains of cognition such as visuospatial function, memory and 'frontal' function, and more general descriptions relating to 'set-shifting', sequencing, temporal ordering and recency discrimination, the locus of cognitive control and bradyphrenia. Later in the paper an attempt is made to provide some theoretical framework for the various descriptions. Two theories are discussed representing contrasting, but complementary approaches. The first is a 'psychological' theory in which the concept of depleted processing resources is suggested as a possible mechanism to explain the observable deficits. The second is a neurobiological model that attempts to integrate information from diverse sources to provide a model for the neuroanatomical and neurochemical substrate that may underlie some of the behavioural deficits.
MRC Human Movement, National Hospital, London, UK.
R G
RG
Brown
C D
CD
Marsden
D002421:Caudate Nucleus / Q000503:physiopathology; D003071:Cognition / Q000502:physiology*; D005625:Frontal Lobe / Q000503:physiopathology; D006801:Humans; D008568:Memory / Q000502:physiology; D008954:Models, Biological; D010300:Parkinson Disease / Q000503:physiopathology*; D014796:Visual Perception / Q000502:physiology