Dysfunction of the basal ganglia and the brain nuclei interconnected with them leads to disturbances of movement and cognition exemplified in Parkinson's disease (PD) and Huntington's disease, including disordered timing of movements and impaired time estimation. Previous research has shown that whereas striatal damage in animals can result in the loss of temporal control over behavior, dopaminergic deregulation in the human striatum associated with PD distorts the memory for time. Here we show a dissociation between deficits in storage (writing to) and retrieval (reading from) temporal memory processes. Both are dysfunctional in PD and sensitive to treatment with dopaminergic agents, but produce dissimilar distortions. When time intervals are stored in memory while the subjects are dopamine depleted, the process is slowed, leading to overestimation of two different time intervals. Conversely, when retrieval occurs in a dopamine-depleted state, interference or coupling occurs between two remembered time intervals, producing overestimation of the shorter and underestimation of the longer one. Whether those two separable patterns of dysfunction in storing and retrieving temporal memories rely on distinct neural networks within the basal ganglia and/or their cortical targets remains to be answered by future research.

Dysfunction of the basal ganglia and the brain nuclei interconnected with them leads to disturbances of movement and cognition, including disordered timing of movement and perceptual timing deflcits. Patients with Parkinson's disease (PD) were studied in temporal reproduction tasks. We examined PD patients when brain dopamine (DA) transmission was impaired (OFF state) and when DA transmission was reestablished, at the time of maximal clinical beneflt following administration of levodopa + apomorphine (ON state). Patients reproduced target times of 8 and 21 sec trained in blocked trials with the peak interval procedure, which were veridical in the ON state, comparable to normative performance by healthy young and aged controls (Experiment 1). In the OFF state, temporal reproduction was impaired in both accuracy and precision (variance). The 8-sec signal was reproduced as longer and the 21-sec signal was reproduced as shorter than they actually were (Experiment 1). This fimigrationfl effect was dependent upon training of two different durations. When PD patients were trained on 21 sec only (Experiment 2), they showed a reproduction error in the long direction, opposite to the error produced under the dual training condition of Experiment 1. The results are discussed as a mutual attraction between temporal processing systems, in memory and clock stages, when dopaminergic regulation in the striatum is dysfunctional.