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Related Experiment Video

Updated: Nov 10, 2025

Induction and Assessment of Levodopa-induced Dyskinesias in a Rat Model of Parkinson's Disease
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Time Distortion in Parkinsonism.

Yasuo Terao1, Motoyasu Honma2, Yuki Asahara3

  • 1Department of Medical Physiology, School of Medicine, Kyorin University, Tokyo, Japan.

Frontiers in Neuroscience
|April 5, 2021
PubMed
Summary

Timing deficits in Parkinson's disease (PD) and progressive supranuclear palsy (PSP) patients were studied using perceptual and motor tasks. Findings suggest complex timing alterations beyond simple dopamine deficiency, involving memory and sensory-motor interactions.

Keywords:
Parkinson’s diseasebasal gangliadopamineprogressive supranuclear palsytime perception

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Dynamic Digital Biomarkers of Motor and Cognitive Function in Parkinson's Disease
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Area of Science:

  • Neuroscience
  • Neurology
  • Chronobiology

Background:

  • Dopamine deficiency in Parkinson's disease (PD) is hypothesized to slow internal clock pace.
  • Existing research shows diverse and complex timing deficits in parkinsonism.
  • Characterizing timing impairments in PD and progressive supranuclear palsy (PSP) is crucial.

Purpose of the Study:

  • To investigate perceptual and motor timing deficits in PD and PSP patients.
  • To contrast timing performance in supra- and sub-second domains.
  • To explore the role of dopamine deficiency and short-term memory in timing impairments.

Main Methods:

  • Evaluated temporal bisection, duration comparison, and time production/reproduction tasks.
  • Studied patients with PD and PSP, 3-4 hours post-medication, alongside age-matched controls.
  • Analyzed performance across supra- and sub-second time scales, considering automatic vs. cognitive tasks.

Main Results:

  • PD and PSP patients showed altered subjective time perception (1s duration) compared to controls.
  • Perceptual timing tasks revealed underestimation of shorter and overestimation of longer durations.
  • Motor timing tasks showed opposite patterns; short-term memory correlated with some PD timing deficits.

Conclusions:

  • Timing deficits in PD and PSP are complex, not solely explained by a slowed internal clock due to dopamine deficiency.
  • Discrepancies between perceptual and motor timing suggest distinct neural processing.
  • Memory distortions and interactions between sensory and motor timing scales likely contribute to observed deficits.