Central to the concept of subcortical demenlia is the implication that the increased response latencies, which distinguish the syndrome, are due to a slowing of thought processes. The term ‘bradyphrenia’ has been applied to this presumed slowing of thought in Parkinson's disease and implies (1) that increased response latencies are not strictly motoric but are due to slowed information processing, and (2) that the mental slowing is analogous to the bradykinesia observed in the motor domain and, hence, attributable to dysfunction of doparninergic basal ganglia mechanisms. The current study attempts to validate this definition of bradyphrenia by seeking a slowing of thought in Parkinson's disease which can be linked directly to bradykinesia. Six parkinsonian patients with end-of-dose akinesia were studied in three experiments which allowed separation of the speed of specific cognitive operations from the speed of motor responses. Serving as their own controls, the were tested both during the parkinsonian ‘off’ state, and when bradykinesia was alleviated by drug therapy. Four additional patients with newly diagnosed Parkinson's disease were sludied before and following successful treatment with L-DOPA/carbidopa. The first experiment measured the rate of memory seanning, the second examined orientating of attention in the visual fields, and the third measured the time required to prepare a manual movement. The results show that overall reaction time increased when patients were in the untreated state, but without a concomitant slowing of purely cognitive components. The slowing of thought often reported in Parkinson's disease does not necessarily accompany bradykinesia and thus may not be related to dopaminergic dysfunction. These findings emphasize the need for caution in inferring a slowing of thought from increased response latencies in subcortical disorders.