Step 1: After a decade of levodopa-carbidopa, the response becomes pulsatile and short, the dose stops covering the full inter-dose interval. The therapeutic goal is to make each levodopa dose last longer rather than to add a fresh dopaminergic mechanism.
Step 2: Levodopa is degraded peripherally by two enzymes: dopa decarboxylase (already blocked by carbidopa) and COMT. Adding a COMT inhibitor closes the second escape route. Tolcapone does this, and because it has a longer half-life and crosses the blood-brain barrier, it improves levodopa bioavailability and reduces its clearance, translating into longer 'on' periods and less 'off' time.
Step 3: The alternatives miss the target: rasagiline blocks MAO-B, amantadine is reserved for dyskinesias, and benzhexol is an antimuscarinic chiefly for tremor. The drug that directly restores and prolongs the failing levodopa effect is the COMT inhibitor.
\[\boxed{\text{Tolcapone}}\]