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Clinical and pathophysiologic aspects of late levodopa failure.
Neurology. 1993 Dec; 43(12 Suppl 6):S28-30.Neur

Abstract

More than 50% of all patients with Parkinson's disease who initially receive treatment with conventional levodopa will develop late complications, although the underlying mechanisms are not completely understood. Some aspects of levodopa peripheral pharmacokinetic handling contribute to response fluctuations, such as its short half-life and the variations of gastrointestinal absorption and blood-brain barrier transport caused by competition with neutral amino acids. In themselves, however, these are insufficient to explain the late occurrence of "on-off" oscillations. Disease-related central changes in presynaptic handling of levodopa are likely to play a role, as are postsynaptic pharmacodynamic receptor changes, possibly induced by chronic, nonphysiologic, pulsatile stimulation. Pharmacodynamic alterations of dopaminergic receptors have also been implicated in the pathogenesis of levodopa-induced dyskinesias. Recent experimental findings suggest a possible role of downstream functional changes in pallidosubthalamo-thalamic projections.

Authors+Show Affiliations

Department of Neurology, Universitätsklinikum Rudolf-Virchow, Berlin, Germany.

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

8264908

Citation

Poewe, W. "Clinical and Pathophysiologic Aspects of Late Levodopa Failure." Neurology, vol. 43, no. 12 Suppl 6, 1993, pp. S28-30.
Poewe W. Clinical and pathophysiologic aspects of late levodopa failure. Neurology. 1993;43(12 Suppl 6):S28-30.
Poewe, W. (1993). Clinical and pathophysiologic aspects of late levodopa failure. Neurology, 43(12 Suppl 6), S28-30.
Poewe W. Clinical and Pathophysiologic Aspects of Late Levodopa Failure. Neurology. 1993;43(12 Suppl 6):S28-30. PubMed PMID: 8264908.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Clinical and pathophysiologic aspects of late levodopa failure. A1 - Poewe,W, PY - 1993/12/1/pubmed PY - 1993/12/1/medline PY - 1993/12/1/entrez SP - S28 EP - 30 JF - Neurology JO - Neurology VL - 43 IS - 12 Suppl 6 N2 - More than 50% of all patients with Parkinson's disease who initially receive treatment with conventional levodopa will develop late complications, although the underlying mechanisms are not completely understood. Some aspects of levodopa peripheral pharmacokinetic handling contribute to response fluctuations, such as its short half-life and the variations of gastrointestinal absorption and blood-brain barrier transport caused by competition with neutral amino acids. In themselves, however, these are insufficient to explain the late occurrence of "on-off" oscillations. Disease-related central changes in presynaptic handling of levodopa are likely to play a role, as are postsynaptic pharmacodynamic receptor changes, possibly induced by chronic, nonphysiologic, pulsatile stimulation. Pharmacodynamic alterations of dopaminergic receptors have also been implicated in the pathogenesis of levodopa-induced dyskinesias. Recent experimental findings suggest a possible role of downstream functional changes in pallidosubthalamo-thalamic projections. SN - 0028-3878 UR - https://www.unboundmedicine.com/medline/citation/8264908/Clinical_and_pathophysiologic_aspects_of_late_levodopa_failure_ L2 - http://ovidsp.ovid.com/ovidweb.cgi?T=JS&PAGE=linkout&SEARCH=8264908.ui DB - PRIME DP - Unbound Medicine ER -