Summary
Synopsis
When used to treat patients with Parkinson’s disease pergolide acts at dopamine receptors in the corpus striatum to improve locomotor activity, reducing the tremor, gait disturbances, bradykinesia or akinesia and rigidity experienced by such patients. Treatment with pergolide often allows substantial reductions in concomitant levodopa dosage, and occasionally levodopa can be completely replaced by pergolide therapy in short term use. Pergolide has a long duration of action, thus reducing the wearing-off and end-of-dose phenomena frequently seen with long term levodopa therapy, suppressing fluctuations in levodopa response, and increasing total ‘on’ time. Despite a lack of well controlled studies comparing this drug with other dopamine agonist agents, pergolide appears to result in adverse effects and anti-Parkinson responses similar to those of bromocriptine and lisuride.
Thus, pergolide would appear to be at least as useful as other dopamine agonists such as bromocriptine or lisuride for the management of patients with Parkinson’s disease when administered in combination with levodopa. Future research should be directed towards establishing which patients are most likely to benefit from pergolide therapy, and clarifying the relative efficacy and safety of the anti-Parkinsonian drugs available to the clinician. If pergolide does provide clinical benefit when substituted for levodopa-adjunct drugs that are producing less than optimal control, this will be an advantage in a disease area which at present has few therapeutic options.
Pharmacological and Pharmacokinetic Properties
Pergolide is a dopamine receptor agonist which acts at both D1 and D2 receptors in the nigrostriatal regions of the brain where it affects locomotor activity, exemplified by circling behaviour in lesioned rats. It stimulates adenylate cyclase activity via D1 receptors in the corpus striatum in a manner similar to dopamine and has minor α2-stimulating activity which may cause a vasopressor response at high doses.
Pergolide initially increases serum corticosterone levels in rats, possibly via central dopamine receptors, but tolerance to this effect develops after as little as 5 days of continuous administration. Pergolide 0.0075 mg/kg reduces blood pressure in normotensive dogs by 17% although 0.03 mg/kg caused an initial 25% increase in pressure; larger reductions of blood pressure occur in hypertensive animals. Similarly, heart rate, blood pressure and plasma dopamine, norepinephrine (noradrenaline) and lactic acid levels are reduced at rest and/or during exercise when pergolide 0.05 mg/day is administered to healthy volunteers. The hypotensive effects of the drug are dose proportionate and tend to diminish with continued treatment of patients. Pergolide appears devoid of effects on glucose metabolism in either animals or patients with Parkinson’s disease. Furthermore, pergolide reduces intraocular pressure in healthy volunteers and causes significant reductions in prolactin levels at rest and during exercise. In animal models of Parkinson’s disease, pergolide has induced Stereotypic behaviour in rats and guinea-pigs by direct stimulation of striatal dopamine receptors. In rats, pre- and postsynaptic dopamine receptors may play a part in decreases and increases in locomotor activity, respectively. Increased locomotion is accompanied by stereotypy and could be sustained for long periods. Effects of the drug on prolactin levels appear to last 24 hours or more and although its duration of activity in Parkinson’s disease is shorter, it still exceeds that of levodopa. The onset of action against Parkinson’s disease symptoms in 8 patients occurred in 80 minutes and effects lasted a mean of 5.5 hours.
Pergolide is rapidly absorbed from the gastrointestinal tract, reaching peak plasma concentrations within 1 to 2 hours. Complete elimination of a single radiolabelled dose from the body is achieved within 4 to 5 days, with a mean elimination half-life of 27 hours. Pergolide is 90% bound to plasma proteins. 55% of a radioactive dose is eliminated via the kidneys, 5% via the lungs and the remainder by the liver. Pergolide appears to concentrate in dopamine-rich areas of the brain such as the corpus striatum.
Therapeutic Trials
In short term noncomparative studies (less than 3 months) in Parkinson’s disease, administration of pergolide frequently results in reduced levodopa requirements (complete withdrawal has occasionally been possible), reduced disability and decreased ‘off’ time in patients who no longer respond reliably to bromocriptine and/or levodopa. Placebo-controlled studies demonstrate that mean daily dosages of pergolide 2.5 to 4.6mg result in a 33 to 78% reduction in the requirement for levodopa while improving the duration and extent of response to the latter and reducing the total duration of ‘off’ time by 1.4 to 2.8 hours per day. However, switching from pergolide to placebo results in deterioration of symptoms in all patients. Sleep disturbances tend to be suppressed by pergolide in some patients with Parkinson’s disease.
Long term (6 months to 7 years) studies of pergolide show that both disability and levodopa dosage tend to be reduced and mobility improved, with the most persistent responses seen in patients who achieved the greatest initial benefit. Peak clinical improvement appears to occur after 2 to 12 months and results may diminish slowly thereafter, although some patients continue to respond for up to 7 years without increasing pergolide or levodopa dosages. Previous response to bromocriptine is not predictive of likely outcome with pergolide since, in a small study involving 25 patients, 50% of individuals who did not improve on bromocriptine gained significant benefit when switched to pergolide.
When compared with bromocriptine in a double-blind crossover study, pergolide induced similar improvements in gait, tremor, rigidity and dyskinesia, with slightly more patients preferring to continue pergolide at the end of 14 to 20 weeks of study. If efficacy with bromocriptine or pergolide decreases, the substitution of pergolide for bromocriptine appears more likely to be clinically beneficial than the switch to bromocriptine after pergolide therapy. Comparisons of pergolide with lergotrile, lisuride, and mesulergine have usually been of one-way crossover design, and while similar responses have been seen in a small number of patients, some studies show marginally more favourable responses to pergolide. However, given the limited nature of these clinical trials any conclusions regarding relative efficacy must remain tentative. De novo monotherapy with pergolide has shown limited promise. However, use of pergolide combined with levodopa in the early therapy of Parkinson’s disease may yet prove to delay the onset of levodopa related adverse effects.
Adverse Effects
Overall, pergolide appears to be relatively well-tolerated in patients with Parkinson’s disease, although adverse effects have resulted in discontinuation of therapy in 27% of patients in clinical trials. The most frequently reported adverse effects during pergolide treatment have been dyskinesias, nausea, dizziness, hallucinations, rhinitis and other CNS or gastrointestinal symptoms.
ECG changes and other cardiac effects have been noted infrequently, but close observation may be required in patients with prior heart disease. Occasional first-dose postural hypotension makes gradual introduction and increments of pergolide dosage advisable. Rarely, abrupt withdrawal of the drug has resulted in confusion or hallucinations, so if pergolide therapy needs to be stopped it is prudent to discontinue the drug gradually if at all possible. In general, long term use of the drug does not adversely alter neuro-psychological parameters.
Dosage and Administration
When used to treat Parkinson’s disease, slow incremental increases in oral dosage of pergolide are recommended, beginning with 0.05 mg/day and increasing by 0.05 to 0.15 mg/day every third day for 2 weeks, then by 0.25 mg/day every third day until an optimum dosage is reached. Reductions in concomitant levodopa dosages may be required. Dosages of 2 to 4 mg/day are most common, administered in 3 to 4 divided oral doses. The effects of dosages above 5 mg/day have not been fully examined.
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Various sections of the manuscript reviewed by: J.E. Ahlskog, Department of Neurology, Mayo Clinic, Rochester, Minnesota, USA; J. Arnt, Psychopharmacological Section, Pharmacological Research, H. Lundbeck A/S, Copenhagen-Valby, Denmark; K. De Meirleir, Vrije Universiteit Brussel, Brussels, Belgium; S.G. Diamond, Reed Neurological Research Center, UCLA School of Medicine, Center for Health Sciences, Los Angeles, California, USA; E. Jungmann, Zentrum der Inneren Medizin, Abteilung fur Endokrinologie, Johann Wolfgang-Goethe-Universitat, Frankfurt Main, West Germany; A. Lieberman, Barrow Neurological Institute, Phoenix, Arizona, USA; C.D. Marsden, University Department of Clinical Neurology, Institute of Neurology, University of London, London, England; N.P. Quinn, University Department of Clinical Neurology, Institute of Neurology, University of London, London, England; C.M. Tanner, Department of Neurological Sciences, Rush-Presbyterian-St Luke’s Medical Center, Chicago, Illinois, USA.
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Langtry, H.D., Clissold, S.P. Pergolide. Drugs 39, 491–506 (1990). https://doi.org/10.2165/00003495-199039030-00009
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DOI: https://doi.org/10.2165/00003495-199039030-00009