Generic Requip is an anti-Pakirson medication. Generic Requip is also used to treat restless legs syndrome (RLS).
Other names for this medication:
Generic Requip is an anti-Pakirson medication. Generic Requip is also used to treat restless legs syndrome (RLS).
Other names for this medication:
Also known as: Ropinirole.
Generic Requip is an anti-Pakirson medication.
Generic Requip is used to treat symptoms of Parkinson's disease such as stiffness, tremors, muscle spasms, poor muscle control.
Requip is also known as Ropinirole, Ropidon, Adartrel, Ropark.
Generic Requip is also used to treat restless legs syndrome (RLS).
Generic Requip has some of the same effects as a chemical called dopamine, which occurs naturally in your body. Low levels of dopamine in the brain are associated with Parkinson's disease.
Generic name of Generic Requip is Ropinirole.
Brand names of Generic Requip are Requip, Requip XL.
Take Generic Requip orally.
Take Generic Requip with or without food.
The dose and timing of Generic Requip in treating Parkinson's disease is different from the dose and timing in treating RLS.
If you want to achieve most effective results do not stop taking Generic Requip suddenly.
If you overdose Generic Requip and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Generic Requip overdosage: nausea, vomiting, weakness, fainting, agitation, confusion, hallucinations, muscle twitching, tingly feeling, chest pain.
Store at room temperature between 20 and 25 degrees C (68 and 77 degrees F) away from moisture, light and heat. Keep container tightly closed. Throw away any unused medicine after the expiration date. Keep out of the reach of children.
The most common side effects associated with Requip are:
Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.
Do not take Generic Requip if you are allergic to Generic Requip components.
Be very careful with Generic Requip if you are pregnant, planning to become pregnant, or are breast-feeding.
Be very careful with Generic Requip if you have heart disease, high or low blood pressure, mental illness or compulsive behaviors, kidney or liver disease.
Be very careful with Generic Requip if you are taking levodopa, ciprofloxacin (Cipro), fluvoxamine (Luvox), metoclopramide (Reglan), omeprazole (Prilosec); medication used to treat nausea and vomiting or mental illness, such as chlorpromazine (Thorazine), fluphenazine (Prolixin), mesoridazine (Serentil), perphenazine (Trilafon), thioridazine (Mellaril), promazine (Sparine), trifluoperazine (Stelazine), thiothixene (Navane), or haloperidol (Haldol); estrogen such as Premarin, Prempro, Estratest, Ogen, Estraderm, Climara, Vivelle, estradiol and others.
Avoid getting up too fast from a sitting or lying position. Get up slowly and steady yourself to prevent a fall.
Avoid alcohol and smoking.
Avoid machine driving.
It can be dangerous to stop Generic Requip taking suddenly.
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Assess the rate of augmentation as it occurs during standard long-term dopaminergic treatment of RLS, potential risk factors or predictors of augmentation, the relationship between treatment duration and augmentation, and the clinical impact of augmentation on subjects' health outcomes.
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NMSs in untreated de novo PD patients were evaluated both quantitatively and qualitatively using the Non-Motor Symptoms Assessment Scale (NMSS); the findings were compared to those of control subjects. The effects of dopaminergic treatment on NMSs were also determined.
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Somnolence and "sleep attacks" have been reported as an adverse effect of several antiparkinsonian drugs. The authors document, in a placebo-controlled, randomized, double-blind, crossover study performed in 20 healthy volunteers, using the Multiple System Latency Test (MSLT) as primary outcome, that ropinirole reduces time to sleep onset in humans. Ropinirole therapy was not associated with daytime episodes of rapid eyes movement (REM) sleep.
To determine whether adding orally disintegrating selegiline (ODS) while decreasing dopamine agonist (DA) dosages would reduce DA-related adverse effects (AEs) of excessive daytime sleepiness (EDS), pedal edema, hallucinations, and impulse control disorders (ICDs) without compromising efficacy in Parkinson disease (PD) patients.
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RLS severity decreased across time in all three groups; however, the ropinirole treatment was better than the bupropion and iron-folate therapy. Moreover, RLS-related quality of life although improved among all groups, it was comparable among three groups.
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The aims of this study were to assess the safety, tolerability, and efficacy of sumanirole, a highly selective D(2) dopamine receptor agonist, versus placebo in subjects with advanced Parkinson's disease (PD), and to demonstrate noninferiority of sumanirole to ropinirole. In this flexible-dose, randomized, double-blind, double-dummy, parallel-group study, 948 subjects were treated with sumanirole 1 to 48 mg/day, ropinirole 0.75 to 24 mg/day, or placebo. Treatment consisted of 13 weeks of dose escalation, 26 weeks of maintenance, and 1 week of tapering. Approximately 70% of subjects treated with either sumanirole or ropinirole completed the study. Statistical significance (P < 0.0001) was achieved when both sumanirole and ropinirole groups were compared with placebo, with mean differences of -7.7 and -8.8 on combined sum of the Unified Parkinson's Disease Rating Scale (UPDRS) part II (average on and off) and part III total scores at the end of maintenance. Noninferiority of sumanirole to ropinirole was also demonstrated, with a sumanirole minus ropinirole difference of 1.17 (90% CI: -0.56 to 2.89). Both dopamine agonists, sumanirole and ropinirole, were statistically superior compared with placebo as adjunctive therapy for patients with advanced Parkinson's disease, based on UPDRS II + III total score. Noninferiority of sumanirole to ropinirole was established, with comparable tolerability profiles.
We analysed electrocardiogram (ECG) abnormalities, cardiovascular reflexes (CVR) and orthostatic hypotension (OH) in 148 patients with idiopathic PD assigned to five different combination therapies of levodopa (LD) plus either bromocriptine (BRO), ropinirole (ROP), selegiline (SEL), anticholinergic (ACH) or amantadine (AMA) or to LD monotherapy before and after a 1-week washout of the add-on drug. Patients were matched for age and disease severity (Hoehn and Yahr stage 2-3). Rater-blinded cardiovascular testing was performed at baseline, and following a 1-week washout period of the add-on drugs.
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It is suggested that dysfunction of the diencephalospinal dopaminergic (DAergic) pathway may cause restless legs syndrome. We examined the mRNA and protein levels as well as DA receptor subtypes function within the lumbar spinal cord of an RLS animal model. C57BL/6 male mice with or without iron deprivation were lesioned with 6-hydroxydopamine (6-OHDA) in the bilateral A11 nuclei. Locomotor behaviors were observed. DA concentration, mRNA, and protein levels of D1, D2, and D3 receptors in the lumbar spinal cords were analyzed, and the specific binding of D1, D2, and D3 receptors was determined using [(3)H]SCH23390, [(3)H]Spiperone, and [(3)H]PD128907 radioligands respectively. The behavioral tests showed that the locomotor activities were increased significantly in the mice treated with iron-deficiency (ID) diet and 6-OHDA lesions, which were reversed by the D2/D3 agonist ropinirole. DA in the spinal cord was decreased significantly by 6-OHDA lesioning in A11. D2/D3 mRNA and protein levels as well as their binding capacity in the spinal cord were decreased significantly by 6-OHDA lesions. ID with 6-OHDA lesions produced a synergistic greater decrease of D2 binding. Although ID increased D1 mRNA and protein expression in the spinal cord, it did not significantly change D1 receptor binding. The present study suggests that ID and 6-OHDA lesions in A11 nuclei differentially altered the D1, D2, and D3 receptors expression and binding capacity in the lumbar spinal cord of RLS animal model, which was accompanied by changes in locomotor activities.
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In order to determine the overall rate of subjective sleep problems in PD and to determine if any factors, including specific medications, correlate with sleep pathology, the authors surveyed consecutive patients with PD seen over a 3-month period in a Movement Disorders Clinic. The authors collected demographic and medication data, and the patients completed the Epworth Sleepiness Scale (ESS), questions assessing the presence of restless legs syndrome (RLS), a modified National Sleep Foundation sleep survey, and specific questions regarding falling asleep while driving.
Effect sizes were calculated from controlled studies. Rates of intolerable side effects and manic switching were estimated by pooled analysis of controlled and uncontrolled studies.
requip 25 mg
Considerable evidence indicates that cholinomimetic-induced tremulous jaw movements in rats share many characteristics with human Parkinsonian tremor, and several antiparkinsonian drugs suppress cholinomimetic-induced tremulous jaw movements. The present study investigated three different types of dopamine agonists, which have known antiparkinsonian characteristics, for their ability to suppress the tremulous jaw movements induced by tacrine (5.0 mg/kg). The non-selective dopamine agonist pergolide, a widely used antiparkinsonian drug, was highly potent at suppressing tacrine-induced jaw movements (e.g. 0.125-1.0 mg/kg). The selective D2 agonist ropinirole, which also is used clinically as an antiparkinsonian drug, suppressed jaw movements in the dose range of 2.5-20.0 mg/kg. The D1 agonist CY 208-243, which has been reported to suppress tremor, also reduced jaw movement activity (4.0 mg/kg). Across several studies, the rank order of potency for suppressing cholinomimetic-induced jaw movements in rats is related to the potency for producing antiparkinsonian effects in humans. Together with previous studies, the present results suggest that cholinomimetic-induced jaw movements in rats can be used to characterize dopaminergic antiparkinsonian agents and to investigate the basal ganglia circuits involved in the generation of tremulous movements.
requip 4 mg
A 54-year-old man with a left leg amputation 22 years ago developed RLS, primarily at night, that met the International RLS Study Group's criteria for RLS. This RLS, however, involved both his real and phantom lower limbs. Movement and phantom movements, as well as treatment with dopamine agonists, relieved this symptom in both the real and amputated limbs. However, creating an image of the limb moving without "moving" the limb did not improve the uncomfortable sensations in either limb.
Pharmacotherapy for Parkinson's disease is focused on dopaminergic drugs, mainly the dopamine precursor levodopa and dopamine receptor agonists. The elimination half-life (t(1/2)) of levodopa from plasma (in combination with a decarboxylase inhibitor) of about 1.5 hours becomes more influential as the disease progresses. The long-duration of response to levodopa, which is evident in early Parkinson's disease, diminishes and after a few years of treatment motor performance is closely correlated to the fluctuating plasma concentrations of levodopa. Absorption of levodopa in the proximal small intestine depends on gastric emptying, which is erratic and may be slowed in Parkinson's disease. The effects of levodopa on motor function are dependent on gastric emptying in patients in the advanced stages of disease. The current treatment concept is continuous dopaminergic stimulation (CDS). Sustained-release formulations of levodopa may provide more stable plasma concentrations. Oral liquid formulations shorten the time to reach peak concentration and onset of effect but do not affect plasma levodopa variability. The t(1/2) of levodopa can be prolonged by adding a catechol-O-methyltransferase inhibitor (entacapone or tolcapone), which may reduce fluctuations in plasma concentrations, although both peak and trough concentrations are increased with frequent administration. Intravenous and enteral (duodenal/jejunal) infusions of levodopa yield stable plasma levodopa concentrations and motor performance. Enteral infusion is feasible on a long-term basis in patients with severe fluctuations. Among the dopamine receptor agonists the ergot derivatives bromocriptine, cabergoline, dihydroergocryptine and pergolide, and the non-ergot derivatives piribedil, pramipexole and ropinirole, have longer t(1/2) compared with levodopa. Thus, they stimulate dopamine receptors in a less pulsatile manner, yet pharmacokinetic studies of repeated doses of dopamine receptor agonists are few. Optimisation of these drugs is often performed with standardised titration schedules. Apomorphine and lisuride have short t(1/2) and are suitable for subcutaneous infusion, with results similar to those of levodopa infusion. Transdermal administration of dopamine receptor agonists such as rotigotine might be an alternative in the future. In general, initial dopamine receptor agonist monotherapy is associated with poorer motor performance and lower incidence of motor complications compared with levodopa. Buccal administration of the monoamine oxidase-B inhibitor selegiline (deprenyl) provides better absorption and less formation of metabolites compared with standard tablets. To conclude, several new drugs, formulations and routes of administration have been introduced in the treatment of Parkinson's disease during the last decade, mainly with CDS as the aim. CDS can be approached by optimising the use of dopaminergic drugs based on pharmacokinetic data.
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To compare the effects of ropinirole with those of placebo on sleep, as evaluated by specific domains of the Medical Outcomes Study (MOS) sleep scale, as well as the Clinical Global Impression-Improvement (CGI-I) scale, in patients with restless legs syndrome (RLS).
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The baseline validation population included 551 subjects on which full longitudinal data are available. Psychometric assessment of four MOS sleep domains revealed satisfactory item convergent validity (r > 0.40) for most items. All domain items in both trials surpassed the standard for item discriminant validity, with no significant floor or ceiling effects. The MOS sleep domain scores showed good internal consistency reliability. Concurrent validity (r = 0.40) was exceeded in correlations between the RLS overall quality-of-life score and sleep problems index II. The clinical validity of the MOS Sleep Scale was demonstrated against self-reported RLS symptoms and clinician-determined severity; changes in MOS Sleep Scale were responsive to improvements in RLS severity, as measured by the Clinical Global Impression-Improvement and Severity-of-Illness scales.
To date, the lack of highly selective antagonists at the dopamine D(3) receptor has hampered clarification of their involvement in the actions of currently used therapies in Parkinson's disease. However, the novel benzopyranopyrrole, S33084, displays greater than 100-fold selectivity as an antagonist for D(3) versus D(2) receptors and all other sites tested. S33084 was administered to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-lesioned marmosets previously primed with levodopa to elicit dyskinesia. Administered alone, S33084 exerted a modest, but significant, anti-parkinsonian effect without provoking dyskinesia. At low D(3)-selective doses (0.16 and 0.64 mg/kg), S33084 potentiated, though to different extents and in qualitatively different ways, the anti-parkinsonian actions of both ropinirole and levodopa. At these doses, S33084 did not significantly modify levodopa-induced or ropinirole-induced dyskinesia. These data suggest that ropinirole and levodopa do not exert their anti-parkinsonian or pro-dyskinetic actions via D(3) receptor stimulation. Indeed, stimulation of D(3) receptors may be detrimental to the anti-parkinsonian properties of D(2)/D(3) agonists. Selectivity for stimulation of D(2), over D(3), receptors may therefore be a beneficial property of dopamine receptor agonists in management of motor symptoms of Parkinson's disease patients with established dyskinesia.
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To generate a discriminative stimulus (DS) with S32504 and undertake substitution/antagonism studies with diverse antiparkinson and antipsychotic agents.
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Dopaminergic agents such as ropinirole are the drugs of first choice in treating restless legs syndrome (RLS). Recently, gabapentin, a structural analogue of gamma-aminobutyric acid, has also been shown to improve sensorimotor symptoms in RLS. Therefore, the tolerability and efficacy of randomized treatment with either gabapentin or ropinirole in patients with idiopathic RLS was evaluated in this 4-week open clinical trial. Patients with idiopathic RLS were treated with either 300 mg of gabapentin (n = 8) or 0.5 mg of ropinirole (n = 8) as the initial dose, and the dose was up-titrated until relief of symptoms was achieved (gabapentin mean dosage 800 +/- 397 mg, range 300-1,200 mg; ropinirole mean dosage 0.78 +/- 0.47 mg, range 0.25-1.50 mg). In both groups, International Restless Legs Syndrome Study Group questionnaire scores improved significantly (p < or = 0.018), whereas the scores of the Epworth sleepiness scale remained unchanged within normal limits. Polysomnographic data showed a reduction of periodic leg movements during sleep (PLMS; p < 0.03) and PLMS index (p < 0.02) in both groups. Side effects were only mild and mostly transient. After 6-10 months of follow-up, in most patients, RLS symptoms were still improved. We conclude that gabapentin and ropinirole provide a similarly well-tolerated and effective treatment of PLMS and sensorimotor symptoms in patients with idiopathic RLS.
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The purpose of this study was to evaluate the incidence of augmentation over 66 weeks of treatment with ropinirole in patients with primary restless legs syndrome (RLS). Augmentation is the main complication of long-term dopaminergic treatment of RLS. Despite widespread use of ropinirole in RLS, no studies have prospectively and systematically assessed the incidence of augmentation with its use. The study consisted of 26 weeks of double-blind flexible-dose treatment with ropinirole or placebo, followed by 40 weeks of open-label ropinirole treatment.. Patients had no previous history of augmentation. Potential cases of augmentation were identified with the Structured Interview for the Diagnosis of Augmentation and the Augmentation Severity Rating Scale and through reporting of adverse events. Cases were blindly evaluated by an expert panel using the NIH diagnostic criteria for augmentation. Four hundred and four patients participated in the double-blind study and 269 in the open-label phase, with a discontinuation rate of 42%. IRLS baseline scores improved at the end of the double-blind (DB) phase (mean ± SE) by -15.9 ± 0.76 for ropinirole, by -13.4 ± 0.77 for placebo (P < .05) and by -20.4 ± 0.55 during the open-label phase. The incidence rates of augmentation were 3.5% for ropinirole and <1% for placebo during the DB phase and 3% during the open-label phase. Clinically significant augmentation occurred in 3%, <1%, and 2%, respectively. Discontinuation of treatment occurred in 50% of all patients (7 of 14) with augmentation. The incidence of augmentation was 3.1% higher with ropinirole than with placebo. New patients with first episodes of augmentation continued to cumulate at a stable rate over the duration of this study.
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Mucoadhesive temperature-mediated in situ gel formulations using chitosan and hydroxyl propyl methyl cellulose were used to enhance intranasal (i.n.) delivery of the dopamine D2 agonist ropinirole to the brain. Formulations were tested for gelation time, thermosensitivity, mucoadhesion, in vitro release and permeation, in vitro cytotoxicity, nasal clearance, in vivo bioavailability and brain uptake. In vivo bioavailability and brain uptake of ropinirole were assessed in albino rats following intranasal administration of 99mTc-ropinirole in situ gel, intranasal ropinirole solution and intravenous (i.v.) ropinirole solution. Radiolabeled ropinirole uptake was calculated as a fraction of administered dose. The absolute bioavailabilty of ropinirole from the temperature-mediated in situ gelling nasal formulation was 82%. The AUC (0-480 min) in brain after nasal administration of ropinirole in situ gel was 8.5 times (869 +/- 250% x min/g versus 102 +/- 20% x min/g) that obtained following i.v. administration, this value was also considerably higher (869 +/- 250% x min/g versus 281 +/- 52% x min/g) than that achieved with intranasal ropinirole solution. High brain direct drug transport percentage (DTP; 90.36%) and drug targeting index (DTI) > 1 confirms direct nose to brain transport of the intranasal in situ gel formulation of ropinirole.
Chronic congestive heart failure is a highly prevalent and progressive disorder associated with excess morbidity and mortality; it has huge economic impact. Left heart failure may be systolic or may occur as isolated diastolic dysfunction. The diastolic form predominates in older people. Sleep disorders are frequent in both types. Most systematic studies have been performed in patients with systolic heart failure. Prospective studies show the presence of obstructive and central sleep apnea, periodic limb movements, and significant alterations in sleep architecture, characterized by poor efficiency, excess stage 1 and arousals, and lack of deep sleep. Both obstructive sleep apnea and central sleep apnea occur in patients with heart failure and have been shown to be associated with excess mortality. Obstructive sleep apnea is best treated with continuous positive airway pressure (CPAP) devices. Central sleep apnea is also best treated with CPAP, but only about 50% of the patients are considered responders. Survival improves when heart failure patients are effectively treated with CPAP for both central and obstructive sleep apnea. A new positive airway pressure device, a pressure support servo-ventilator, is the next best choice for heart failure patients whose central sleep apnea does not respond to CPAP. Nocturnal oxygen should be used for patients whose central sleep apnea does not respond to positive pressure devices. Both periodic limb movements and insomnia could have adverse hemodynamic consequences for the failing heart. There are no guidelines or long-term studies regarding treatment of these conditions in heart failure. For restless legs syndrome with or without periodic limb movements, pramipexole and ropinirole have been approved. Treatment of insomnia comorbid with heart failure depends on the cause. In the absence of any known cause, a trial of ramelteon is the first choice.
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