Controlled study of the antiparkinsonian activity and tolerability of cabergoline

Hutton, J. Thomas; Morris, Jerry L.; Brewer, Molly

doi:10.1212/wnl.43.3_part_1.613

Cited by 36 publications

(10 citation statements)

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“…In the previous clinical studies (Hutton et al, 1993;Lieberman et al, 1993;Lera et al, 1993;Ahlskog et al, 1994), cabergoline showed the beneficial effects on daily fluctuations in the treatment of advance Parkinson's disease. This drug improved not only "on"-time parkinsonian score but also "off"-time score, and reduced "off"-time period.…”

Section: Discussionmentioning

confidence: 94%

“…Cabergoline, a DA D2 receptor agonist (Benedetti et al, 1990), exerts long-lasting antiparkinsonian effects in animal experiments (Arai et al, 1995) and reduces "Wearing-off" phenomena found in clinical practice (Hutton et al, 1993;Lieberman et al, 1993;Lera et al, 1993;Ahlskog et al, 1994). The combined effects of treatment with cabergoline and L-dopa may be of therapeutic interest in parkinsonian patients, especially in view of the induction of dopaminergic side effects such as psychosis and dyskinesia.…”

Section: Introductionmentioning

confidence: 99%

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Combined effects of cabergoline and L-dopa on parkinsonism in MPTP-treated cynomolgus monkeys

Arai

Isaji

Kojima

et al. 1996

J. Neural Transmission

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The behavioral effects of L-dopa or cabergoline alone were compared with those of the joint administration of the two drugs in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-lesioned parkinsonian cynomolgus monkeys with attention to the induction of hyperactivity and dyskinesia. Cabergoline alone at 0.2 mg/kg or less improved in a dose-dependent fashion the parkinsonism without inducing hyperactivity and dyskinesia following a single subcutaneous injection. L-dopa alone improved the parkinsonism, but induced hyperactivity and dyskinesia, depending on the dose applied. Doses required for 50% amelioration by L-dopa and cabergoline were 10 and 0.038 mg/kg, s.c., respectively. With low doses (50%-amelioration doses), cabergoline or L-dopa alone improved the parkinsonism without induction of hyperactivity and dyskinesia, but the duration of action was brief. Cabergoline in combination with L-dopa was highly effective in improving motor disability without induction of hyperactivity and dyskinesia. Moreover, the duration of action was more prolonged with the coadministration than with the single administration of each drug. These findings suggest that the combined therapy with low doses of L-dopa and cabergoline is beneficial for treating patients with advanced Parkinson's disease.

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Section: Discussionmentioning

confidence: 94%

Section: Introductionmentioning

confidence: 99%

Combined effects of cabergoline and L-dopa on parkinsonism in MPTP-treated cynomolgus monkeys

Arai

Isaji

Kojima

et al. 1996

J. Neural Transmission

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“…308 Similar results have been obtained with lisuride and cabergoline when used as adjuncts to levodopa. 320,321 Double-blind, placebo-controlled studies have similarly demonstrated that pramipexole and ropinirole exert antiparkinsonian effects with levodopa sparing in patients with advanced PD. 322,323 In a 6-month, doubleblind, controlled study, ropinirole treatment was associated with a reduction in "off " time of 3.7 hours, compared with 1.6 hours in the placebo group (p Ͻ 0.001).…”

Section: No Dyskinesias Up To 6 Monthsmentioning

confidence: 99%

The scientific and clinical basis for the treatment of Parkinson disease (2009)

Olanow¹,

Stern²,

Sethi³

2009

Neurology

760

658

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Parkinson disease (PD) is an age-related neurodegenerative disorder that affects as many as 1-2% of persons aged 60 years and older. With the aging of the population, the frequency of PD is expected to increase dramatically in the coming decades. Current therapy is largely based on a dopamine replacement strategy, primarily using the dopamine precursor levodopa. However, chronic treatment is associated with the development of motor complications, and the disease is inexorably progressive. Further, advancing disease is associated with the emergence of features such as freezing, falling, and dementia which are not adequately controlled with dopaminergic therapies. Indeed, it is now appreciated that these nondopaminergic features are common and the major source of disability for patients with advanced disease. Many different therapeutic agents and treatment strategies have been evaluated over the past several years to try and address these unmet medical needs, and many promising approaches are currently being tested in the laboratory and in the clinic. As a result, there are now many new therapies and strategic approaches available for the treatment of the different stages of PD, with which the treating physician must be familiar in order to provide patients with optimal care. This monograph provides an overview of the management of PD patients, with an emphasis on pathophysiology, and the results of recent clinical trials. It is intended to provide physicians with an understanding of the different treatment options that are available for managing the different stages of the disease and the scientific rationale of the different approaches. 1 PD is the second most common neurodegenerative disorder, with an average age at onset of about 60 years. An estimated 5 million people throughout the world have PD, with 1 million individuals each in the United States and in Europe with the disorder. PD affects approximately 0.3% of the population and 1% to 2% of those older than 60 years.2 With the aging of the population and the substantial increase in the number of at-risk individuals older than 60 years, it is anticipated that the prevalence of PD will increase dramatically in the coming decades.

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“…6), is a full agonist at D 2 receptors and a partial agonist at D 3 -and D 4 -receptors, without appreciable activity at D 1 -type receptors [169,170], and a relatively long half-life of approximately 48 h [5]. Cabergoline was superior to placebo for treating motor signs of PD, but its comparative efficacy versus Ldopa is poorly documented [174]. Lisuride (27) (Fig.…”

Section: Drugs Targeting Dopamine Receptorsmentioning

confidence: 99%

Therapeutic and Diagnostic Agents for Parkinson's Disease

Booth

Neumeyer

Baldessarini

2010

Burger's Medicinal Chemistry and Drug Discovery

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This chapter summarizes the neurobiology of Parkinson's disease and medicinal chemistry relevant to treatment of this neurodegenerative disorder with neuropsychiatric complications. The chapter also surveys basic clinical features of Parkinson's disease, its neuropathophysiology and etiology. Considered are genetic, maturational, metabolic, and environmental contributors to risk for the disease. Pharmacotherapy for Parkinson's disease includes l ‐dopa to counter cerebral dopamine deficiency, direct dopaminergic agonists, and agents that prolong the actions of l ‐dopa or dopamine by preventing their metabolism by peripheral aromatic amino acid decarboxylase, catechol‐ O ‐methyltransferase, or monoamine oxidase. Additional drugs acting on nondopaminergic systems include muscarinic acetylcholine, adenosine, and l ‐glutamate antagonists, as well as serotonin (5‐hydroxytryptamine) agonists. Agents used to diagnose Parkinson's disease and monitor its progression, include radioactive compounds used to image brain l ‐dopa and dopamine neurotransporters and dopamine receptors. Finally, potential contributions are considered of medicinal chemistry to improve pharmacotherapy of Parkinson's disease.

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Controlled study of the antiparkinsonian activity and tolerability of cabergoline

Cited by 36 publications

References 0 publications

Combined effects of cabergoline and L-dopa on parkinsonism in MPTP-treated cynomolgus monkeys

Combined effects of cabergoline and L-dopa on parkinsonism in MPTP-treated cynomolgus monkeys

The scientific and clinical basis for the treatment of Parkinson disease (2009)

Therapeutic and Diagnostic Agents for Parkinson's Disease

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