Budipine Provides Additional Benefit in Patients With Parkinson Disease Receiving a Stable Optimum Dopaminergic Drug Regimen | Movement Disorders | JAMA Neurology | JAMA Network
[Skip to Navigation]
Access to paid content on this site is currently suspended due to excessive activity being detected from your IP address Please contact the publisher to request reinstatement.
[Skip to Navigation Landing]
Original Contribution
May 2002

Budipine Provides Additional Benefit in Patients With Parkinson Disease Receiving a Stable Optimum Dopaminergic Drug Regimen

Author Affiliations

From the Department of Neurology, Ruhr University of Bochum, Bochum, Germany (Drs Przuntek, Kraus, and T. Müller); Byk Gulden Pharmaceuticals, Constance, Germany (Drs Bliesath and Steinijans); the Department of Neurology, Ludwig Maximilian University of Munich, Munich, Germany (Dr Büttner); Parkinson Clinic, Wolfach (Dr Fuchs); the Department of Neurology, University of Bonn, Bonn, Germany (Dr Klockgether); the Department of Neurology, Barmbek General Hospital (Dr Lachenmayer), the Department of Neurosurgery, University of Hamburg (Dr D. Müller), and Lundbeck GmbH & Co (Dr Sgonina), Hamburg, Germany; Paracelsus-Elena Clinic, Kassel, Germany (Dr Ulm); and Josephstadt Neurological Outpatient Clinic, Vienna, Austria (Dr Volc). Drs Bittkau, Glass, Haller, Rathay, and Teshmar are in private practice in Germany.

Arch Neurol. 2002;59(5):803-806. doi:10.1001/archneur.59.5.803

Background  The complex pharmacological profile of the antiparkinsonian drug budipine influences neurotransmission beyond the dopaminergic system. Previous studies have demonstrated the therapeutic efficacy of budipine on motor symptoms in insufficiently treated patients with Parkinson disease.

Objective  To demonstrate the efficacy of 20 mg of budipine, 3 times daily, in addition to a stable, prior, optimum-titrated dopaminergic substitution consisting of a combination of levodopa and a dopa decarboxylase inhibitor, bromocriptine mesylate, and optional selegiline hydrochloride in 99 patients with idiopathic Parkinson disease in a multicenter, double-blind, placebo-controlled trial.

Results  Budipine significantly (P<.001) decreased the Columbia University Rating Scale sum score (median, 15.0; 95% confidence interval, 11.3-17.0) compared with placebo (median, 4.3; 95% confidence interval, 3.0-7.5) at study end point. Budipine reduced Columbia University Rating Scale subscores for tremor, rigidity, and akinesia.

Conclusion  The additional application of budipine provides further therapeutic benefit in subjects with Parkinson disease receiving a stable, prior, optimum-titrated dopaminergic drug regimen because of the hypothetical positive impact of budipine on altered nondopaminergic neurotransmission in patients with Parkinson disease.