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Brain imaging studies on duration perception usually report the activation of a network that includes the frontal and mesiofrontal cortex (supplementary motor area, SMA), parietal cortex, and subcortical areas (basal ganglia, thalamus, and cerebellum). To address the question of the specific involvement of these structures in temporal processing, we contrasted two visual discrimination tasks in which the relevant stimulus dimension was either its intensity or its duration. Eleven adults had to indicate (by pressing one of two keys) whether they thought the duration or the intensity of a light (LED) was equal to (right hand) or different from (left hand) that of a previously presented standard. In a control task, subjects had to press one of the two keys at random. A similar broad network was observed in both the duration-minus-control and intensity-minus-control comparisons. The intensity-minus-duration comparison pointed out activation in areas known to participate in cognitive operations on visual stimuli: right occipital gyrus, fusiform gyri, hippocampus, precuneus, and intraparietal sulcus. In contrast, the duration-minus-intensity comparison indicated activation of a complex network that included the basal ganglia, SMA, ventrolateral prefrontal cortex, inferior parietal cortex, and temporal cortex. These structures form several subnetworks, each possibly in charge of specific time-coding operations in humans. The SMA and basal ganglia may be implicated in the time-keeping mechanism, and the frontal-parietal areas may be involved in the attentional and mnemonic operations required for encoding and retrieving duration information.

The aims of the present study were to analyze how L-Dopa allows parkinsonian patients to increase their gait velocity and to compare these L-Dopa-induced modifications with those achieved by consciously attempting to walk as fast as possible (intentional modulations). The 'intentional modulations' of velocity were also compared with those of healthy elderly subjects. The results showed that parkinsonian patients walked more slowly, with shorter strides and shorter durations of swing phase, and longer durations of stance and double support phases, although no differences were observed for cycle duration. The mechanisms involved in increasing gait velocity were found to differ according to whether this was achieved through the action of L-Dopa, or by intentional increases in velocity. Intentional increases in velocity were greater than those caused by the effect of L-Dopa. The patients, however, used efficient strategies to increase their velocity when under the influence of L-Dopa. As L-Dopa leads to a ceiling effect on stride length, the patients can increase their velocity by modifying the cycle to such an extent that it compensates for the limitation in stride length. This strategy effectively increases velocity, despite the L-Dopa ceiling effect. The effects of L-Dopa on locomotion and, more generally, on motor control aspects are discussed.