Adult: As monotherapy: Initially, 50 mcg in the evening on day 1, then increased to 50 mcg bid on days 2-4. Then, increased by 100-250 mcg every 3-4 days, given in 3 divided doses, up to a daily dose of 1.5 mg at day 28. Then, after day 30, dose is increased by a max of 250 mcg twice wkly, until optimum response is attained. Maintenance dose: 2.1-2.5 mg daily, given in 3 divided doses. Max: 3 mg daily. As adjunct to levodopa: Initially, 50 mcg daily for 2 days, then increased by 100-150 mcg, given in 3 divided doses every 3 days over the next for 12 days. Then, increased by 250 mcg every 3 days, concurrently decrease levodopa dose until an optimum response is attained. Max: 3 mg daily.
History of cardiac valvulopathy and fibrotic disorders.
Patient w/ history of psychosis, confusional states, hallucination, somnolence; risk factor for cardiac dysrhythmias; sleep disorders. Pregnancy and lactation. Avoid abrupt withdrawal.
This drug may cause somnolence and sudden sleep onset, if affected, do not drive or operate machinery.
Assess CV status including ECG before initiation of treatment and periodically thereafter. Perform baseline evaluation of ESR, other inflammatory markers, lung function/chest X-ray, serum creatine, renal function and monitor thereafter. Monitor for signs and symptoms of valvulopathy (e.g. dyspnoea, oedema, CHF, cardiac murmurs), fibrotic disorders (e.g. cough, dyspnoea, oedema, CHF, cardiac rub, urinary tract obstruction), development of impulse control disorders.
Symptoms: Vomiting, hypotension, agitation, severe hallucinations, severe involuntary movements, tingling in arms and legs, palpitations, ventricular extrasystoles. Management: Symptomatic and supportive treatment. Maintain arterial BP. May give antiarrhythmic agent if necessary. Give phenothiazine or butyrophenone neuroleptic agent for CNS stimulation. Establish patient’s airway and support ventilation and perfusion. May employ activated charcoal instead of or in addition to gastric emptying to hasten elimination of absorbed drug.
Increased risk of sudden sleep onset w/ sedating agents. May increase risk of hypotension w/ antihypertensive agents. Exacerbation of confusion, hallucination and dyskinesia w/ levodopa. Decreased effectiveness w/ dopamine antagonists (e.g. metoclopramide, neuroleptics).
Description: Pergolide, an ergot derivative, is a potent dopamine agonist at D1, D2 and D3 receptor sites. In Parkinson’s disease, it directly stimulates postsynaptic dopamine receptors in the nigrostriatal system. Pharmacokinetics: Absorption: Absorbed from the GI tract. Distribution: Plasma protein binding: Approx 90%. Metabolism: Extensively metabolised into at least 10 metabolites including N-despropylpergolide, pergolide sulfone and pergolide sulfoxide. Excretion: Mainly via urine (approx 55%, as metabolites); faeces (40%, as metabolites); expired CO2 (5%, as metabolites).