Abstract
It is well known that perception and estimation of time are fundamental for the relationship between humans and their environment. However, this temporal information processing is inefficient in patients with Parkinson’ disease (PD), resulting in temporal judgment deficits. In general, the pathophysiology of PD has been described as a dysfunction in the basal ganglia, which is a multisensory integration station. Thus, a deficit in the sensorimotor integration process could explain many of the Parkinson symptoms, such as changes in time perception. This physiological distortion may be better understood if we analyze the neurobiological model of interval timing, expressed within the conceptual framework of a traditional information-processing model called “Scalar Expectancy Theory”. Therefore, in this review we discuss the pathophysiology and sensorimotor integration process in PD, the theories and neural basic mechanisms involved in temporal processing, and the main clinical findings about the impact of time perception in PD.
Highlights
When individuals observe a slow-motion movement, the central nervous system (CNS) speeds up or reduces the time in order to balance the movement feedback and visual perception [1]
Several areas of the cerebral cortex have been associated with time perception (TP), such as prefrontal cortex (PFC), right postcentral gyrus, inferior parietal lobe (IPL), basal ganglia (BD) and cerebellum [6]
Central processing of temporal information associated with basal ganglia activity
Summary
When individuals observe a slow-motion movement, the central nervous system (CNS) speeds up or reduces the time in order to balance the movement feedback and visual perception [1]. The results showed that individual differences in visuoperceptual processing efficiency occurred in older people without cognitive impairment, and promoted important changes in motor function This may be an early sign of vulnerability in the corticostriatal circuit, which contributes to sensorimotor integration [75]. Some studies investigated the neural response deficits between the BG and both thalamus and supplementary motor area (SMA), which occur because of an unbalance between the direct and indirect circuits, increasing the quantity of the striatum stimuli going to the substantia nigra [80,83] In another experiment using electrical stimulation, the authors analyzed finger movements in order to verify sensorimotor skills in PD patients.
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