Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Preventing levodopa-induced dyskinesias.

C W Olanow1, J A Obeso

  • 1Department of Neurology, Mount Sinai School of Medicine, New York, NY 10029, USA.

Annals of Neurology
|April 13, 2000
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

The 201 Trial: a placebo-controlled randomized phase 2 study of safety and tolerance of the c-Abl kinase inhibitor risvodetinib in untreated Parkinson's disease.

Nature aging·2026
Same author

Differential pathological dynamics triggered by distinct Parkinson patient-derived α-synuclein extracts in nonhuman primates.

Science advances·2025
Same author

Nigrostriatal iron accumulation in the progression of Parkinson's disease.

NPJ Parkinson's disease·2025
Same author

Dopaminergic denervation and associated MRI microstructural changes in the nigrostriatal projection in early Parkinson's disease patients.

NPJ Parkinson's disease·2023
Same author

Identification of distinct pathological signatures induced by patient-derived α-synuclein structures in nonhuman primates.

Science advances·2020
Same author

Author Correction: Computer keyboard interaction as an indicator of early Parkinson's disease.

Scientific reports·2018
Same journal

AQP4 and MOG Characterize the Autoantibody Landscape of Checkpoint Blockade-Induced Optic Neuritis.

Annals of neurology·2026
Same journal

Five Issues of Artificial Intelligence in Science: Sailing the Ship of Theseus.

Annals of neurology·2026
Same journal

Reply to "Clinical Value of Aneurysm Wall Enhancement in Unruptured Intracranial Aneurysm".

Annals of neurology·2026
Same journal

Clinical Value of Aneurysm Wall Enhancement in Unruptured Intracranial Aneurysm.

Annals of neurology·2026
Same journal

Imaging of Neurovascular Compression in Thoracic Outlet Syndrome.

Annals of neurology·2026
Same journal

Reply to "Methodological Challenges in Interpreting SAA-Defined Imaging Subgroups in Parkinson's Disease".

Annals of neurology·2026
See all related articles

Levodopa-induced dyskinesias may result from pulsatile stimulation of dopamine receptors. Preventing this stimulation through continuous levodopa delivery or other strategies could prevent dyskinesias.

Area of Science:

  • Neuroscience
  • Pharmacology

Background:

  • Levodopa-induced dyskinesias (LIDs) are a common complication of Parkinson's disease treatment.
  • The precise mechanisms underlying LID development remain unclear.

Purpose of the Study:

  • To explore the hypothesis that pulsatile stimulation of striatal dopamine receptors contributes to LID.
  • To identify potential strategies for preventing or mitigating LIDs.

Main Methods:

  • Review of current evidence on the relationship between levodopa delivery, dopamine receptor stimulation, and dyskinesia.
  • Analysis of factors influencing pulsatile stimulation, including drug half-life and disease severity.

Main Results:

  • Pulsatile stimulation, rather than continuous delivery, is linked to the development of dyskinesias.

Related Experiment Videos

  • In advanced Parkinson's disease, reduced dopamine terminals exacerbate fluctuations in dopamine concentration, increasing pulsatile stimulation.
  • Pulsatile stimulation may induce molecular changes in postsynaptic neurons, leading to dyskinetic movements.

    • Conclusions:

    • Preventing pulsatile striatal dopamine receptor stimulation is a potential strategy to avoid LIDs.
    • Therapeutic approaches could involve long-acting dopaminergic agents, neuroprotection, or enhancing dopamine terminal capacity.
    • Interfering with postsynaptic changes may also offer antidyskinetic benefits.