Cognitive dysfunction in schizophrenia: a new set of tools for the assessment of cognition and drug effects

Cognitive impairment in schizophrenia must be seen as a disturbance of cort ico-sub-cortical connectivity with a neurotransmitter imbalance in a circui try system, which connects thalamic input with prefrontal processing and su pplementary motor cortex and basal ganglia output. The concept of maze-solv ing behaviour as a continuous cognitive task evoking a conflict between pre frontal cortex and basal ganglia activity is explained and introduced to di stinguish between the effects of D-2 blocking agents and substances with a predominant 5HT(2A) receptor affinity, such as clozapine and risperidone. C omplex mazes show a cognitive deficit in untreated schizophrenic patients t hat are impaired by conventional and improved by atypical antipsychotic sub stances. Processing speed improves most on clozapine, while parallel proces sing is best supported by the non-sedative atypical substance risperidone. Maze paradigms are presented.