Evidence map›Paper›PMID 21881839›Full record

ReviewJournal of neural transmission (Vienna, Austria : 1996)2011

Mechanisms underlying the onset and expression of levodopa-induced dyskinesia and their pharmacological manipulation.

Mahmoud M Iravani, Peter Jenner

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of neural transmission (Vienna, Austria : 1996), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 1 pooled it
8.0field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

43 citing papers in PubMed, 1 synthesis or guideline pooled it, 79 citations in OpenAlex.

  1. Pooled it
  2. Effect of levodopa-carbidopa intestinal gel on dyskinesia in advanced Parkinson's disease patients.Movement disorders : official journal of the Movement Disorder Society · 2016
    Trial
  3. Review
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  7. Article
  8. Article
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  10. Review
  11. Adenosine AFrontiers in neurology · 2017
    Article
  12. Review
  13. Article
  14. Modulation by Trace Amine-Associated Receptor 1 of Experimental Parkinsonism, L-DOPA Responsivity, and Glutamatergic Neurotransmission.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015
    Article
  15. Assessment of Parkinson's disease levodopa-induced dyskinesia: a qualitative research study.Quality of life research : an international journal of quality of life aspects of treatment, care and rehabilitation · 2015
    Article
  16. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 2 countries.

Mahmoud M IravaniNeurodegenerative Disease Research Centre, Institute of Pharmaceutical Sciences, School of Biomedical Sciences, King's College, London, UK. m.iravani@kcl.ac.uk
Peter Jenner
King's College London · GB

Funding

Parkinson's UK G-0804
6 · The paper itself

Abstract

A significant proportion of patients with Parkinson's disease (PD) receiving dopamine replacement therapy in the form of levodopa develop dyskinesia that becomes a major complicating factor in treatment. Dyskinesia can only be effectively treated by a reduction in drug dose, which limits efficacy, by co-administration of the weak NMDA antagonist amantadine or by surgical treatment (pallidotomy, DBS). This raises the important question of why dyskinesia occurs in PD and how it can be avoided or suppressed by pharmacological treatment. This review assesses some of the mechanisms that underlie dyskinesia induction and expression from presynaptic changes in dopaminergic neurones to postsynaptic alterations in basal ganglia function and examines potential approaches to prevention and treatment. These include glutamatergic approaches where agents that directly or indirectly alter glutamatergic neurotransmission modify the intracellular influx of Ca(2+) and reduce the formation of nitric oxide by neuronal nitric oxide synthase that may form an integral component of the complex cascade of events leading to dyskinesia. There is increasing evidence for the role of serotoninergic neurones in dyskinesia induction related to non-physiological formation and release of dopamine and serotoninergic agonists can modify dyskinesia expression. Similarly, noradrenergic receptors may serve to alter dyskinesia intensity and α-2-adrenoceptor antagonists alter the expression of levodopa-induced dyskinesia in both experimental models of PD and in man. Finally, other potential approaches to dyskinesia treatment based on manipulation of opiate, cannabinoid, adenosine and histamine receptors are considered. The conclusion is that the cause of levodopa-induced dyskinesia remains to be fully elucidated and that new approaches to treatment through non-dopaminergic mechanisms are required to control the onset and expression of involuntary movements.

Indexed as

AnimalsAntiparkinson AgentsDopaminergic NeuronsDyskinesia, Drug-InducedHumansLevodopaNeuronal PlasticityNeurotransmitter AgentsParkinson DiseaseSignal TransductionAntiparkinson AgentsLevodopaNeurotransmitter Agents

Identifiers

PMID21881839
OpenAlexW2141698775

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.