[Cognitive functions and the basal ganglia: the model of Parkinson disease]

Cognitive changes have long been observed in patients with degenerative diseases or focal lesions that involve primarily subcortical structures. Generally speaking, the deficits that have been reported in these diseases are similar and include: slowing of central processing; defective use of memory stores; impaired behavioural regulation in sorting tasks; disorders of plaining in tower-related tasks; and impaired manipulation of internal representation of visuo-spatial stimuli. Given the modulatory role of the basal ganglia and related structures, these disorders might result from more fundamental deficits concerning the allocation of attentional resources, the temporal organization of behaviour, the maintenance of representations in working memory or the self-elaboration of internal strategy, all of which resemble dysfunctions of processes that are commonly considered to be controlled by the frontal lobes. 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-defined subregions of the basal ganglia to discrete areas of the prefrontal cortex via the thalamus may give some support to this hypothesis.