Carbidopa/levodopa/entacapone: the evidence for its place in the treatment of Parkinson's disease

The loss of dopamine due to the degeneration of neurons in the substantia nigra pars compacta is the classical pathology in Parkinson’s disease and underlies observed motor defects. Replacement of dopamine by levodopa ameliorates motor symptoms but is also a major cause of motor complications such as the “wearing off” effect and dyskinesia. Agents that prolong the half-life of levodopa have been employed, including carbidopa, an aromatic amino acid decarboxylase inhibitors, and entacapone, a catechol-O-methyltransferase inhibitor. In the current study, the authors assess the evidence for the place of combined carbidopa/levodopa/entacapone (CLE) in the treatment of Parkinson’s disease. CLE has good efficacy, safety and tolerability, similar to entacapone taken separately with carbidopa/levodopa (CL). Compared to CL alone, CLE prolongs levodopa’s benefit and improves the quality of life but not the motor performance of patients with non-debilitating wearing-off or dyskinesia. Dyskinesia rate is increased in early stage Parkinson’s patients and has adverse effects in advanced patients with significant motor complications. CLE is therefore an attractive option for patients with non-disabling wearing off or dyskinesia, and is better suited to patients with advanced rather than early Parkinson’s disease, except for those with severe motor complications.