I read the article, “New drug options for neurologic disorders” (May 2010) with considerable interest because the problems these medications are designed to treat are of growing concern. However, I wonder about the rationale used for the inclusion of carbidopa along with levodopa. More important than minimizing nausea (the rationale given in the article), this combination allows increased amounts of levodopa to be available for entry into the central nervous system (CNS). Thus, although dopamine does not cross the blood-brain barrier, levodopa (its immediate precursor) does. Once in the brain, levodopa can be decarboxylated to dopamine. As noted, however, it can also be decarboxylated peripherally. When levodopa is given with a dopa decarboxylase inhibitor, such as carbidopa, which does not penetrate the blood-brain barrier, the peripheral metabolism is minimized, thus increasing the plasma levels of levodopa and allowing more to enter the CNS where it can be used therapeutically.—MARGARET WALLHAGEN, PhD, APRN, San Francisco

It is true that carbidopa blocks the peripheral conversion of levodopa to dopamine. From a practical standpoint, that peripheral conversion is responsible for nausea, vomiting, and cardiac arrhythmias. Without the carbidopa component, the dosing of levodopa would be limited by the side-effect profile, thus the rationale. After a range of 50-75 mg of carbidopa daily, most of that blockade has taken place. Additional same-dose carbidopa is unnecessary if the patient is able to understand and effectively use different-strength tablets (DiPiro JT, Schwinghammer TL. Pharmacotherapy: A Pathophysiologic Approach. New York, N.Y.: McGraw-Hill Medical; 1993:1243-1255).—Deborah Downey, CNRN, CNS, ANP (141-14) 

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