Levodopa only works after it is changed into dopamine inside the brain. The snag is that the converting enzyme, dopa decarboxylase, is everywhere in the body, so a large share of an oral dose becomes dopamine in the bloodstream and never reaches the brain. That wasted peripheral dopamine also triggers nausea and cardiovascular upset.
Carbidopa solves this neatly. It blocks dopa decarboxylase but is unable to cross into the brain, so its enzyme blockade is confined to the periphery. With peripheral conversion shut down, much more intact levodopa crosses the blood brain barrier and is converted to dopamine where it is actually needed. The practical results are a smaller required levodopa dose and far fewer systemic side effects.
The remaining options describe the opposite of reality: efficacy goes up not down, the needed dose falls not rises, and carbidopa never touches central conversion because it stays outside the brain. The intended purpose is to block peripheral decarboxylation.
\[\boxed{\text{Inhibit peripheral decarboxylation of levodopa}}\]