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PubMed1985

The use of pergolide and lisuride, two experimental dopamine agonists, in patients with advanced Parkinson disease.

Pergolide, an experimental dopamine agonist, was administered to 56 patients with advanced Parkinson disease who were no longer satisfactorily responding to levodopa, including 45 patients with diurnal oscillations in performance: "on-off" phenomena. Lisuride, an experimental dopamine agonist was administered to 63 patients with advanced Parkinson disease. Pergolide or lisuride, when added to levodopa, resulted in a significant decrease in disability in both the "on" and the "off" period, and an increase in the number of hours in which patients were "on". Forty-one of 56 patients (73%) improved on Pergolide. Thirty-seven of 63 patients (59%) improved on lisuride. Mean dose of pergolide was 2.5 mg. (range 0.2 to 10.0 mg.). Mean dose of lisuride was 2.6 mg. (range 0.2 to 5.0 mg.). Pergolide was discontinued in 18 patients because of adverse effects, including an organic confusional syndrome (six patients), dyskinesias (four patients) and cardiovascular abnormalities (three patients). Lisuride was discontinued in 26 patients because of adverse effects, including an organic confusional syndrome (15 patients), dyskinesias (five patients) and vasospasm (two patients). Pergolide was discontinued in nine patients and lisuride in 12 because of a lack of effect or a declining effect. Both drugs are equally useful in patients with advanced Parkinson disease.

Adult↗
PubMedDate not supplied

Pergolide: multiple-dose pharmacokinetics in patients with mild to moderate Parkinson disease.

The primary objective of this study was to describe the pharmacokinetics of oral pergolide in patients with mild to moderate Parkinson disease using a new high-performance liquid chromatography-tandem mass spectrometry assay. A secondary objective was to investigate the relationship between plasma concentrations and efficacy. Fourteen patients with a diagnosis of Parkinson disease completed this multicenter, open-label, dose-escalating study. Pergolide was administered for 58 days, using increasing daily doses from 0.05 mg daily up to 1 mg three times daily and then tapering the dose. The steady-state pharmacokinetic profile and motor score were determined at dose levels of 0.25, 0.5, and 1 mg three times a day and during elimination after the last dose. Pergolide was absorbed with a median time to maximum concentration of 2 to 3 hours across the dose range. Systemic exposure appeared to increase proportionally with dose over the range of 0.25 to 1 mg three times daily within a patient, but there was a large variability in exposures between patients (interpatient coefficients of variation were 56.4% for the area under the curve). Pergolide was widely distributed (volume of distribution, approximately 14,000 L) and was eliminated with a mean half-life of 21 hours. Motor scores improved as both peak plasma pergolide concentrations and exposure increased. No unexpected safety concerns were identified. Pergolide is absorbed relatively quickly into the systemic circulation, has a large apparent volume of distribution, and has a relatively long half-life (mean, 21 hours). This prolonged half-life is of particular interest, given the current hypothesis that more continuous dopaminergic receptor stimulation may reduce motor complications in patients with Parkinson disease.

Aged↗
PubMed1987

Alpha-2-adrenoceptor-mediated effects of pergolide.

The alpha-adrenoceptor-mediated effects of pergolide were investigated in a number of biochemical and pharmacological test systems. In radioligand binding studies, pergolide more effectively competed for alpha 2-adrenoceptors than for alpha 1-adrenoceptors in membranes prepared from rat cerebral cortex. Consistent with this finding was the observation that pergolide was several orders of magnitude more effective in activating presynaptic alpha 2-adrenoceptors in rat vas deferens to inhibit stimulation-evoked [3H]-norepinephrine release than in activating postsynaptic alpha 1-adrenoceptors in the same tissue to produce a contractile response. Pergolide elicited a potent vasopressor response in pithed rats that was highly sensitive to antagonism by the selective alpha 2-adrenoceptor antagonist, yohimbine, and resistant to blockade by the selective alpha 1-adrenoceptor antagonist, prazosin, suggesting that pergolide selectively activates postsynaptic vascular alpha 2-adrenoceptors. The results of the present study indicate that the alpha-adrenoceptor-mediated effects commonly associated with pergolide result from selective stimulation of alpha 2-adrenoceptors.

Animals↗
PubMed1982

Further studies with pergolide in Parkinson disease.

Pergolide was administered to 56 patients with advanced Parkinson disease who were no longer satisfactorily responding to levodopa. The group included 45 patients with on-off phenomena. Pergolide, when combined with levodopa, resulted in a 44% decrease in disability as assessed in the on period, a 15% decrease in disability as assessed in the off period, and a 148% increase in the number of hours in which patients were on (from 4.6 +/- 0.3 hours to 11.4 +/- 0.6 hours). All these changes were significant at 1%. Forty-one of the 56 patients (59%) improved when pergolide was added to levodopa. Mean dose of pergolide was 2.5 mg (range, 0.2 to 10.0 mg). Mean duration of the study was 13 months (range, 1 day to 34 months). Maximum improvement occurred within 2 months and began to decline, usually after 6 months. The major adverse effects necessitating discontinuing pergolide were the occurrence of an organic confusional syndrome (six patients), increased dyskinesias (four patients), and cardiovascular abnormalities (three patients). Nine patients discontinued pergolide because of a lack of effect or declining effect.

Adult↗
PubMed1985

Double-blind trial of pergolide for Parkinson's disease.

Pergolide mesylate, a dopamine agonist, was studied as adjunctive therapy in a 6-month double-blind trial in 20 patients with Parkinson's disease who were achieving less than optimal response from Sinemet. As pergolide or placebo was administered in increasing dosage, Sinemet was reduced if side effects developed. Both the pergolide and placebo groups improved significantly (p less than 0.05). The pergolide group improved 30% at the end of 24 weeks, and the placebo group 23%. There was no significant difference between drug and placebo groups, possibly due to a fortuitous support group and the side effects that may have burdened the pergolide group. Nevertheless, pergolide had a definite antiparkinsonian effect.

Aged↗
PubMed1985

Long-term study of pergolide in Parkinson's disease.

In 18 patients with Parkinson's disease, the effects of pergolide after 28 months of treatment were compared with the response after the initial 10-week therapy. At a mean 3.2-mg daily dose of pergolide, the daily dose of levodopa was still 33% lower than at the onset of pergolide therapy. The mean motor disability score, which decreased by 65% during the first 10 weeks of pergolide, was still decreased by 42% after 28 months. In the 12 patients with on-off effect, the percent time on increased 117% during the first phase of the study and was still increased 63% after more than 2 years of pergolide therapy. Sudden freezing episodes became the most disabling problem in the majority of patients. "Down-regulation" of dopamine receptors may contribute, but it is not the only cause of loss of responsiveness to pergolide.

Adult↗
PubMed1999

A randomized controlled study of pergolide in patients with restless legs syndrome.

BACKGROUND: Open clinical trials indicate that low doses of pergolide, a long-acting D1 and D2 dopamine agonist, lead to a reduction in the symptoms of restless legs syndrome (RLS) with subjective improvement in sleep quality. OBJECTIVE: To assess the therapeutic efficacy of pergolide in improving sleep and subjective measures of well-being in patients with idiopathic RLS using polysomnography and clinical ratings. METHODS: In a randomized, double-blind, placebo-controlled crossover design we enrolled 30 patients with idiopathic RLS according to the criteria of the International RLS Study Group. All patients were free of psychoactive drugs for at least 2 weeks before the study. Patients were monitored using polysomnography, clinical ratings, and sleep diaries at baseline and at the end of a 4-week pergolide or placebo treatment period. The initial dosage of 0.05 mg pergolide was increased to the best subjective improvement paralleled by 20 mg domperidone tid. RESULTS: At a mean dosage of 0.51 mg pergolide as a single daily dose 2 hours before bedtime, there were fewer periodic leg movements per hour of time in bed (5.7 versus 54.9, p < 0.0001), and total sleep time was significantly longer (373 versus 261 minutes, p < 0.0001). Ratings of subjective sleep quality, quality of life, and severity of RLS were improved significantly without relevant adverse events. CONCLUSION: Pergolide given as a single low-to-medium bedtime dose in combination with domperidone provides a well-tolerated and effective treatment of sensorimotor symptoms and sleep disturbances in patients with primary RLS.

Adult↗
PubMed2000

Tourette's syndrome improvement with pergolide in a randomized, double-blind, crossover trial.

OBJECTIVE: To determine whether pergolide, a mixed D1-D2-D3 dopamine agonist, is efficacious and safe in the treatment of children with Tourette's syndrome. BACKGROUND: Neuroleptics, which block dopamine transmission, are currently used for treatment of children with severe tics, but major side effects and limited efficacy reduce clinical utility. Prior open-label reports of pergolide suggest potential benefit. METHODS: The authors enrolled 24 children age 7 to 17 years with Tourette's disorder, chronic motor tic disorder, or chronic vocal tic disorder by Diagnostic and Statistical Manual of Mental Disorders (4th ed.) criteria, plus severity criteria on the Yale Global Tic Severity Scale (YGTSS) of > or =20, in a double-blind, placebo-controlled, crossover study. Children were randomized to receive either placebo or up to 300 microg/day pergolide for the first 6-week treatment period, with a 2-week placebo washout, followed by crossover to the alternate treatment. The primary outcome measure was tic severity assessed by YGTSS. RESULTS: Compared with placebo treatment, pergolide treatment was associated with significantly lower YGTSS scores (42.0 +/- 20.4 versus 23.5 +/- 18.7; F = 12.0, df = 1, 17, p = 0.0011). No patient had a serious adverse event and pergolide was well tolerated. CONCLUSIONS: In this randomized, placebo-controlled, crossover trial, pergolide appeared to be a safe and efficacious treatment for Tourette's syndrome in children.

Adolescent↗
PubMed2001

Adverse outcomes in a controlled trial of pergolide for cocaine dependence.

We conducted a double-blind, multiple dose comparison study of pergolide versus placebo for the treatment of cocaine dependence. In the present study, we examined patients who met criteria for cocaine dependence without comorbid alcohol dependence (N = 255). Study completion rates favored placebo (48.9%) over the low dose (33.3%) and high dose (21.5%) pergolide subjects (chi2(2) = 14.17, p < or = 0.001). Treatment effectiveness scores (TES) were significantly higher for the placebo group (31.7) than the low dose (25.2) and high dose (14.2) pergolide groups (F2,252 = 6.21, p = 0.002). There were no significant differences in side effect profiles after first dose of pergolide or placebo, or at study termination. Results of this study suggest that pergolide was not efficacious in the treatment of cocaine dependence due to reduced study participation. Caution regarding the outpatient use of pergolide in similar populations is warranted.

Adolescent↗
PubMedDate not supplied

Treatment with pergolide or cyproheptadine of pituitary pars intermedia dysfunction (equine Cushing's disease).

Medical records of 27 horses (including 13 ponies) treated with pergolide or cyproheptadine for pituitary pars intermedia dysfunction were reviewed to determine the effect of treatment on plasma ACTH, insulin, and glucose concentrations and clinical signs. Prior to treatment, the most common clinical signs were laminitis, hirsutism, and abnormal body fat distribution. The median pergolide dose was 3.0 microg/kg p.o. q24h (range, 1.7-5.5 microg/kg). All horses treated with cyproheptadine were given 0.25 mg/kg p.o. q24h. After pergolide treatment, ACTH concentrations (n = 20; median = 30.4 pg/ml; range, 4.2-173) were significantly lower (P < .01) than those in horses treated with cyproheptadine (n = 7; median = 141.0 pg/ml: range, 10-1,230). Among horses treated with pergolide, there was a correlation between ACTH concentration after treatment and the duration of treatment (P < .001) and pergolide dose (P = .04). Significantly (P = .02) more owners of horses treated with pergolide (85%, 17/20) reported an improvement in clinical signs compared to owners of horses treated with cyproheptadine (28%, 2/7).

Adrenocorticotropic Hormone↗
PubMed2002

[Pergolide-induced pleural effusion in a patient with juvenile parkinsonism].

A male patient with juvenile parkinsonism having been treated with pergolide developed pleural effusion. Treatment of pergolide started when the patient was 49. And the symptom appeared 11 years later. The patient had no history of heart disease, chronic cough, or lung tuberculosis. His medications included pergolide 1,000 micrograms/day for the past 7 years. Pergolide had been used since 1990 at the maximum dosage of 2,250 micrograms/day. Chest radiogram showed pleural effusion in the right lung. Parenchymal changes and thickened pleura were observed in the left lung. CT scan of the chest showed encapsulated pleural effusion and atelectasis in the mid and lower zones of the right lung. Interstitial fibrosis and pleural thickening were observed in the left lung. Pleuropulmonary changes are rare adverse effects of pergolide treatment, although they were described in other dopamine agonists such as bromocriptine. The author recommends that patients with parkinsonism who receive pergolide treatment should be regularly monitored for the development of pleuropulmonary complications.

Dopamine Agonists↗
PubMed2005

[Severe insuffiency of the aortic and tricuspidal valves associated with pergolide use].

A 58-year-old woman with Parkinson's disease was treated with high-dose pergolide for 10 years. After the addition of citalopram, a selective serotonin reuptake inhibitor, to treat an anxiety disorder, she developed cardiac decompensation that was most likely related to typical pergolide-related fibroproliferative abnormalities of the tricuspidal, aortic and mitral valves, without cardiomyopathy or coronary heart disease. The aortic and tricuspidal valves were replaced with prosthetics and pergolide was switched to ropinirol. At a control visit after one year, patient's heart function was stable. Pergolide is an ergot-derived dopamine agonist used in the treatment of Parkinson's disease and restless-legs syndrome. In 2002, it was first associated with heart-valve defects. Patients treated with pergolide should be monitored for clinical signs of heart-valve failure. If there is no evidence of heart-valve defects, then regular monitoring of cardiac function is indicated. In case of indications of heart-valve failure pergolide should be discontinued. In some cases the heart-valve abnormalitites are reversible.

Antiparkinson Agents↗
PubMed1991

Long-term pergolide treatment of hyperprolactinemic patients previously unsuccessfully treated with dopaminergic drugs.

Nine hyperprolactinemic patients (seven women aged 25-57 and two men aged 23-51 years) were treated with the dopamine agonist drug, pergolide mesylate, for a period ranging from 4 months to 5 years. All patients had previously received different dopamine agonist drugs; additionally two of the group had undergone surgery and radiation therapy. Group 1 comprised five patients who were given pergolide in an attempt to avoid the marked side effects of bromocriptine and lisuride that had been given earlier. Group 2 comprised four patients treated with pergolide following failure to respond to other dopamine agonist drugs (bromocriptine, lisuride). In group 1, pergolide, at a dose of 25-50 micrograms/day, caused a decrease in the prolactin level to the normal value, restored menstruation, and very few side effects were noted. In group 2, pergolide was administered in a gradually increasing dose, the patients receiving a maximum of 200 micrograms/day. At this dose, there was a significant decrease in the prolactin level in two patients compared with only a slight decrease in the remaining two patients. This study illustrates the efficacy of pergolide in treating hyperprolactinemic patients unable to tolerate other dopaminergic agents (bromocriptine, lisuride).

Adult↗
PubMed1988

Dopaminergic effects on kidney function and responsiveness of aldosterone, plasma renin activity, prolactin, catecholamines, and blood pressure to stimulation in patients with prolactinoma. Comparison of the efficacy of pergolide and bromocriptine therapy.

8 beta-[(Methylthio)methyl]-6-propylergoline (pergolide) is a new, potent, long-acting dopaminergic DA2 receptor agonist currently being investigated for therapeutic use in patients with hyperprolactinemia, acromegaly or Parkinsons's disease. Since the influence of bromocriptine, a well-established dopaminomimetic compound, on aldosterone responsiveness and plasma renin activity is still a matter of debate, the efficacies of both compounds on these parameters and on kidney function, blood pressure, catecholamine release and prolactin levels were compared in 16 patients with prolactinoma. Supine and furosemide (40 mg i.v.)-stimulated plasma renin activity and aldosterone levels were similarly decreased by bromocriptine (2.5-30 mg/d) and pergolide (50-500 micrograms/d). Suppression of blood pressure, inhibition of stimulated norepinephrine release, increase in creatinine clearance, and decrease in base-line prolactin levels were similarly pronounced during treatment with both compounds. Metoclopramide (10 mg i.v.)-induced stimulation of aldosterone and prolactin levels, however, were suppressed only by bromocriptine and not by pergolide. It remains to be studied whether this difference between bromocriptine and pergolide is due to a potential agonist effect of pergolide on dopaminergic DA1 receptors which are influenced by bromocriptine in an antagonistic manner, or whether pergolide can be more readily displaced from its receptors than bromocriptine.

Adult↗
PubMed1995

Agonistic actions of pergolide on firing activity of dopamine neurons in substantia nigra compacta area.

AIM: To study the potency of pergolide as a D2 receptor agonist on the firing activity of substantia nigra compacta (SNC) dopamine (DA) neurons compared with that of bromocriptine and to determine whether pergolide has the nature of D1 receptor agonist in vivo. METHODS: Extracellular single unit recording techniques. RESULTS: Both pergolide and bromocriptine decreased the spontaneously firing rate of "sensitive" and "insensitive" DA cells. In regard of ID50 values, pergolide (11.9, 95% fiducial limits, 5.7-25.1 micrograms kg-1) was more potent than bromocriptine (7.8, 95% fiducial limits, 3.3-18.5 mg kg-1). The discharge inhibition of pergolide was attenuated following the injection of selective D2 receptor antagonist spiperone 0.25 mg kg-1 or selective D1 receptor antagonist Sch-23390 1-2 mg kg-1. However, the inhibition caused by bromocriptine was not always attenuated by spiperone. CONCLUSION: Pergolide is 650 times more potent than bromocriptine at D2 receptors, and possesses D1 receptor agonist characteristics in vivo.

Animals↗
PubMed1982

Pergolide in late-stage Parkinson disease.

Twenty-six patients with late-stage Parkinson disease were given 0.4 to 15 mg of pergolide mesylate daily in addition to, or as replacement for, levodopa or bromocriptine therapy. Despite treatment with individually determined optimum doses of levodopa, bromocriptine, and anticholinergics, they had shown response failure or fluctuating response. Forty percent (11 patients) were unable to tolerate pergolide. Nausea and vomiting, somnolence, and psychiatric disturbances were the most frequent side effects. Eleven of the remaining patients improved on pergolide, 2 were unchanged, and 2 were slightly worse. Among the patients who benefited, pergolide improved dose-related response fluctuations more than non-dose-related fluctuations, with a reduction in number and duration of "off" periods and improvement in quality of sleep and early morning akinesia but little change in freezing episodes. Despite treatment failure in many cases, pergolide is at present the best available drug for specific late-stage management problems.

Bromocriptine↗
PubMed2003

Double-blind, single-dose, cross-over study of the effects of pramipexole, pergolide, and placebo on rest tremor and UPDRS part III in Parkinson's disease.

Tremor is one of the cardinal signs of Parkinson's disease (PD) but its response to antiparkinsonian medication is variable. It has been postulated that pramipexole may have a stronger antiparkinsonian tremor effect than pergolide, another direct acting dopamine agonist medication, possibly because the former has preferential affinity for the dopamine D3 receptor. The purpose of this pilot study was to compare the effects of a single oral dose of either pramipexole (Pr) or pergolide (Pe) or placebo (Pl) on parkinsonian tremor and the motor (part III) subsection of the UPDRS. Ten patients (6 men, 4 women), mean age 65.3 years, mean duration from diagnosis of 2.6 years, with tremor dominant PD were recruited. On three separate occasions a single dose of pramipexole (salt) 500 microg, pergolide 500 microg or placebo were administered in random order to each patient, who were pretreated with domperidone and had their antiparkinsonian medication withheld from midnight before study. After each medication patients were assessed at baseline and then every 30 min for 4 hr using a 0 to 10 tremor rating scale and the UPDRS (part III) in a double-blind protocol. Adverse effects were systematically recorded. The results demonstrate that 500 microg of either pramipexole or pergolide reduced PD rest tremor scores to a similar degree, which at peak effect was significantly greater than placebo (respectively Pe v Pl: P < 0.006, Pr v Pl: P < 0.033). The two active drugs also had weaker beneficial effects on the UPDRS part III. Pergolide, however, was significantly more likely than pramipexole to cause nausea (P = 0.005) or vomiting (P = 0.014).

Aged↗
PubMed1982

Depletion of epinephrine in rat hypothalamus by a dopamine agonist, pergolide.

The i.p. injection of pergolide mesylate, a dopamine agonist, at doses of 0.3-0.6 mg/kg led to a decrease in epinephrine concentration in rat hypothalamus. After a 0.6 mg/kg dose of pergolide mesylate, epinephrine concentration in hypothalamus decreased within 2 hr, reached a minimum concentration at about 8 hrs, and then returned toward control values. Norepinephrine N-methyltransferase activity was not decreased after pergolide injection in vivo nor was it inhibited by pergolide added in vitro at concentrations as high as 10(-3) M. Higher i.p. doses of less potent dopamine agonists, apomorphine (10 mg/kg) and lergotrile (3 mg/kg), also decreased epinephrine concentration in hypothalamus. The pergolide-induced decrease in hypothalamic epinephrine concentration was prevented by pretreatment with haloperidol or spiperone, antagonists of dopamine receptors. Activation of dopamine receptors appears to result in a decrease in epinephrine concentration in rat brain, possibly due to enhanced release of epinephrine.

Animals↗