The initial treatment of Parkinson's disease should begin with levodopa

Weiner, William J.

doi:10.1002/1531-8257(199909)14:5<716::aid-mds1002>3.0.co;2-q

Cited by 48 publications

(15 citation statements)

References 46 publications

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“…Decades of debate concerning this issue did not clarify the choice because the clinical trials conducted in those years were inadequate to answer the question. 28,29 In this evidenced based-review, only one article provided class I evidence comparing levodopa against pramipexole, 7 while two articles providing class II evidence compared a dopamine agonist (cabergoline 1, ropinirole 1) 5,6 versus levodopa as early monotherapy. All three of these studies compared the effect of a single agonist versus levodopa in the treatment of PD patients who were not receiving dopamine agonist or levodopa therapy.…”

Section: Initiating Dopaminergic Treatment When Symptomatic Therapy mentioning

confidence: 99%

Practice parameter: Initiation of treatment for Parkinson’s disease: An evidence-based review [RETIRED]

Miyasaki¹,

Martin²,

Suchowersky³

et al. 2002

Neurology

346

185

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Abstract-In 1993, the last AAN Practice Parameter on medical treatment of Parkinson's disease (PD) concluded that levodopa was the most effective drug for management of this disorder. Since then, a number of new compounds including non-ergot dopamine agonists (DA) and sustained-release levodopa have been released and studied. Thus, the issue of treatment in de novo PD patients warrants reexamination. Specific questions include: 1) does selegiline offer neuroprotection; 2) what is the best agent with which to initiate symptomatic treatment in de novo PD; and 3) is there a benefit of sustained release levodopa over immediate-release levodopa? Using evidence-based principles, a literature review using MEDLINE, EMBASE, and the Cochrane Library was performed to identify all human trials in de novo PD between 1966 and 1999. Only articles that fulfilled class I or class II evidence were included. Based on this review, the authors conclude: 1) Selegiline has very mild symptomatic benefit (level A, class II evidence) with no evidence for neuroprotective benefit (level U, class II evidence). 2) For PD patients requiring initiation of symptomatic therapy, either levodopa or a DA can be used (level A, class I and class II evidence). Levodopa provides superior motor benefit but is associated with a higher risk of dyskinesia. 3) No evidence was found that initiating treatment with sustained-release levodopa provides an advantage over immediate-release levodopa (level B, class II evidence).

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Section: Initiating Dopaminergic Treatment When Symptomatic Therapy mentioning

confidence: 99%

Practice parameter: Initiation of treatment for Parkinson’s disease: An evidence-based review [RETIRED]

Miyasaki¹,

Martin²,

Suchowersky³

et al. 2002

Neurology

346

185

View full text Add to dashboard Cite

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“…Accordingly, some physicians and patients have opted to defer the use of levodopa for as long as possible [8]. Others physicians support using levodopa as first-line therapy, arguing that it is inappropriate to withhold the most potent symptomatic treatment for PD in the absence of clinical evidence of toxicity [11][12][13].…”

mentioning

confidence: 99%

Does levodopa slow or hasten the rate of progression of Parkinson’s disease?

2005

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The clinical outcomes not only indicate that levodopa is effective in a dose-dependent manner in overcoming the signs and symptoms of PD, they also support the concept that the drug does not hasten the disease progression, but rather may slow down the rate of the disease. The clinical study failed to demonstrate any evidence of levodopa worsening early PD. However, the beta-CIT SPECT substudy indicates the opposite effect, namely that levodopa causes a more rapid decline in the integrity of the dopamine transporter located in the nigrostriatal nerve terminals in the striatum. These contradictory findings warrant further investigation into the effect of levodopa on PD. OTHER OBSERVATIONS: The ELLDOPA study was the first levodopa dose-response study ever conducted. It showed that dose is a factor in the cause of producing motor complications of dyskinesias and wearing-off, and that these can develop as early as 5 to 6 months. On the other hand, freezing of gait could be delayed or its occurrence reduced by high dosage levodopa, compared to placebo or low-dose levodopa. Withdrawal of levodopa over a 3-day step-down can be safely carried out without inducing the neuroleptic-like syndrome. The UPDRS was shown to be a reliable linear marker for disease progression. The ELLDOPA study also called into question the interpretation of beta-CIT SPECT in the presence of dopaminergic agents. Neuroimaging in ELLDOPA also showed that some people diagnosed with early PD do not have a dopaminergic deficit, calling into question how difficult the correct diagnosis may be in people with early symptoms of PD.

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“…There have been numerous editorials, reviews, viewpoints, controversy and consensus publications, and letters to the editor addressing this issue published in journals [3][4][5][6][7][8][9][10][11][12][13][14][15]Class III], and it has been a central theme in many of our national and international meetings. Although this appears to represent an attempt to improve on current therapy, vigilance is needed.…”

Section: Opinion Statementmentioning

confidence: 99%

Parkinson’s disease: Initial treatment with levodopa or dopamine agonists

Factor

2001

Curr Treat Options Neurol

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The question of whether to use levodopa (LD) or dopamine agonists as initial therapy in Parkinson's disease has been a controversy for nearly 20 years. There are several issues relating to this treatment regimen that may effect ones decision. Review of them results in the following conclusions: LD does not cause the onset of motor fluctuations and dyskinesia; it probably relates to disease progression. Tolerance does not develop with long-term LD therapy. LD is not toxic. LD decreases mortality in Parkinson's disease. Motor fluctuations can occur with dopamine-agonist monotherapy, but the actual frequency is as yet unknown. Dopamine agonists are not neuroprotective. Clinical trials have indicated that LD remains the most potent symptomatic therapeutic agent available. Dopamine agonists do provide some symptomatic relief when used alone in early Parkinson's disease. Standard preparations of LD have the same effect on early disease as controlled release preparations. Dopamine agonists cause less dyskinesia and fluctuations. These conclusions indicate that both drugs are effective symptomatic agents with their own positive and negative aspects. There is no incorrect choice. It is reasonable to start young onset patients (younger than 50 years of age) with an agonist, because they seem to be more prone to develop motor fluctuations and dyskinesia. However, if employment is in jeopardy then LD may be needed. Because agonists cause more hallucinations, freezing, and somnolence, problems of particular relevance to the elderly (older than 70 years), then LD would be the best agent for older onset patients. In general, but particularly for those falling in between these age groups, treatment should be individualized. In this time of cost effectiveness, LD remains the least expensive of these agents.

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The initial treatment of Parkinson's disease should begin with levodopa

Cited by 48 publications

References 46 publications

Practice parameter: Initiation of treatment for Parkinson’s disease: An evidence-based review [RETIRED]

Practice parameter: Initiation of treatment for Parkinson’s disease: An evidence-based review [RETIRED]

Does levodopa slow or hasten the rate of progression of Parkinson’s disease?

Parkinson’s disease: Initial treatment with levodopa or dopamine agonists

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