COGNITIVE FUNCTIONS AND THE BASAL GANGLIA - THE MODEL OF PARKINSONS-DISEASE

Cognitive changes have long been observed in patients with degenerativ e diseases or focal lesions that involve primarily subcortical structu res. Generally speaking, the deficits that have been reported in these diseases are similar and include: slowing of central processing; defe ctive use of memory stores; impaired behavioural regulation in sorting tasks; disorders of plaining in tower-related tasks; and impaired man ipulation of internal representation of visuo-spatial stimuli. Given t he modulatory role of the basal ganglia and related structures, these disorders might result from more fundamental deficits concerning the a llocation of attentional resources, the temporal organization of behav iour, the maintenance of representations in working memory or the lobe s. This suggests a functional continuity between the basal ganglia and association areas of the prefrontal cortex. The recent description in primates of parallel, segregated loops that interconnect well - defin ed subregions of the basal ganglia to discrete areas of the prefrontal cortex via the thalamus may give some support to this hypothesis.