Study to Observe the Effect of Requip PDÂ® Once-daily (QD) Versus Twice-daily (BID)
1. In order to observe the benefit, side effects, and patient preference of Requip PD when used in QD or BID dosing
2. In order to estimate the conversion rate of dopamine agonists into Requip PD
1. Study subjects : Parkinson disease who are on Requip or Mirapex and are considering to change into Requip PD
2. Cross over study design:
- Group 1: once daily dose for 2 month then into BID in divided dose for 2 months
- Group 2: BID in divided dose for 2 months then into QD dose for 2 months
3. Dose adjustment may be done in the first 4 weeks.
4. Compare the benefit,side effects, and patient preference between the QD vs BID dosing.
Allocation: Non-Randomized, Control: Uncontrolled, Endpoint Classification: Safety/Efficacy Study, Intervention Model: Crossover Assignment, Masking: Open Label, Primary Purpose: Treatment
Seoul National University Hospital
Korea, Republic of
Seoul National University Hospital
Results (where available)
- Source: http://clinicaltrials.gov/show/NCT00986245
- Information obtained from ClinicalTrials.gov on July 15, 2010
Medical and Biotech [MESH] Definitions
A condition caused by the neurotoxin MPTP which causes selective destruction of nigrostriatal dopaminergic neurons. Clinical features include irreversible parkinsonian signs including rigidity and bradykinesia (PARKINSON DISEASE, SECONDARY). MPTP toxicity is also used as an animal model for the study of PARKINSON DISEASE. (Adams et al., Principles of Neurology, 6th ed, p1072; Neurology 1986 Feb;36(2):250-8)
A group of disorders which feature impaired motor control characterized by bradykinesia, MUSCLE RIGIDITY; TREMOR; and postural instability. Parkinsonian diseases are generally divided into primary parkinsonism (see PARKINSON DISEASE), secondary parkinsonism (see PARKINSON DISEASE, SECONDARY) and inherited forms. These conditions are associated with dysfunction of dopaminergic or closely related motor integration neuronal pathways in the BASAL GANGLIA.
Parkinson Disease, Postencephalitic
Parkinsonism following encephalitis, historically seen as a sequella of encephalitis lethargica (Von Economo Encephalitis). The early age of onset, the rapid progression of symptoms followed by stabilization, and the presence of a variety of other neurological disorders (e.g., sociopathic behavior; TICS; MUSCLE SPASMS; oculogyric crises; hyperphagia; and bizarre movements) distinguish this condition from primary PARKINSON DISEASE. Pathologic features include neuronal loss and gliosis concentrated in the MESENCEPHALON; SUBTHALAMUS; and HYPOTHALAMUS. (From Adams et al., Principles of Neurology, 6th ed, p754)
Parkinson Disease, Secondary
Conditions which feature clinical manifestations resembling primary Parkinson disease that are caused by a known or suspected condition. Examples include parkinsonism caused by vascular injury, drugs, trauma, toxin exposure, neoplasms, infections and degenerative or hereditary conditions. Clinical features may include bradykinesia, rigidity, parkinsonian gait, and masked facies. In general, tremor is less prominent in secondary parkinsonism than in the primary form. (From Joynt, Clinical Neurology, 1998, Ch38, pp39-42)
A selective, irreversible inhibitor of Type B monoamine oxidase. It is used in newly diagnosed patients with Parkinson's disease. It may slow progression of the clinical disease and delay the requirement for levodopa therapy. It also may be given with levodopa upon onset of disability. (From AMA Drug Evaluations Annual, 1994, p385) The compound without isomeric designation is Deprenyl.
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