Treatment of Parkinsonism With Levodopa

Yahr, Melvin D.; Duvoisin, Roger C.; Schear, Myrna; Barrett, Robert E.; Hoehn, Margaret M.

doi:10.1001/archneur.1969.00480160015001

Cited by 556 publications

(234 citation statements)

References 16 publications

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“…Few cases of acute overdose with levodopa or levodopa conjugated with carbidopa have been reported (1)(2)(3), though levodopa has been used for more than 35 years in the treatment of Parkinson's disease (4)(5)(6). This is the first report of an acute overdose of a controlled-release formulation of levodopa with serial measurements of dopamine, adrenalin and noradrenalin plasma concentrations.…”

Section: Introductionmentioning

confidence: 92%

Acute overdose with controlled-release levodopa-carbidopa

Delmas¹,

Rothmann²,

Flesch

2008

Clinical Toxicology

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Introduction. Reports of acute levodopa-carbidopa overdose are rare and no case of an acute overdose with a controlled-release formulation has been described. We describe such a case in which serial concentrations of catecholamines were measured. Case Report. A 55-year-old man ingested 89 tablets of Sinemet ® 50/200 (17.8 g of levodopa, 4.45 g of carbidopa). Clinical effects and plasma concentrations of dopamine, noradrenalin and adrenalin were assessed over 66 hours. On admission 2.5 hours after the ingestion, his physical examination was normal except for mydriasis and urine retention. Five hours post-ingestion he had psychomotor agitation, delirium with logorrhea, joviality, visual hallucinations, regular sinus tachycardia and xerostomia. The clinical course included two episodes hypotension and four of transient tachycardia. Treatment was symptomatic and supportive. Clinical toxicity reappeared 48 hours after the intoxication. The patient was discharged at the end of the fourth day with amnesia for the event. Discussion. Dopamine showed an initial plasma concentration peak 14 hours after the toxic ingestion, followed by a second peak 38 hours after the ingestion. The initial peak of noradrenalin occurred 20 hours post-ingestion with a second lower peak at 38 hours. There were no elevations in adrenalin concentrations. Conclusion. There appeared to be no correlation between the intensity of the clinical signs and the blood concentrations of dopamine and noradrenalin, although the resolution of the clinical signs did correspond to these catecholamines return to normal values. Patients who ingest controlled-release formulations need to be observed until after the second catecholamine peak.

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Section: Introductionmentioning

confidence: 92%

Acute overdose with controlled-release levodopa-carbidopa

Delmas¹,

Rothmann²,

Flesch

2008

Clinical Toxicology

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“…Subsequent open-label levodopa trials with oral preparations confirmed both short and longterm benefits, and a double-blind placebo controlled trial followed (Barbeau 1969;Cotzias et al 1969;Yahr et al 1969). These reports launched levodopa's establishment as the premier agent to treat Parkinson's disease symptoms and signs.…”

Section: Levodopa and Dopamine-based Therapiesmentioning

confidence: 99%

The History of Parkinson's Disease: Early Clinical Descriptions and Neurological Therapies

Goetz

2011

Cold Spring Harbor Perspectives in Medicine

325

193

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“…The plasma half-life of levodopa in the carbidopa-levodopa immediate-release formulation is approximately 90 min [13], while all oral dopamine agonists have half-lives greater than 6 h [11]. Laboratory studies in MPTP-lesioned primate models of PD have consistently shown that development of dyskinesia phenotypes is closely linked to intermittent levodopa administration (relative to dopamine agonists); and that once present, such dyskinesias are significantly reduced by switching from levodopa to dopamine agonists [14][15][16][17][18].…”

Section: Cds and The Transition To Cddmentioning

confidence: 99%