The most effective treatment of PD still remains l-dopa. The global antiparkinsonian efficacy of l-dopa is so dramatic and predictable that a positive therapeutic response is used to define the disease itself. The major issue regarding introducing l-dopa is when to start treatment, considering the well-known effects of long-term use [74]. It has been largely reported that the premature therapeutic introduction of l-dopa, especially in young patients, leads to develop long-term side effects such as dyskinesias and motor fluctuations. For this reason, some authors have recommended the l-dopa-sparing strategy, which consists of the use of other antiparkinsonian medication in young PD who are more likely to develop dyskinesias and fluctuations related to long term use of l-dopa. The reason why l-dopa long term use determines the onset of motor dysfunction might be due to the toxicity of l-dopa upon dopaminergic neurons. In an in vitro experimental setting, it has been demonstrated that l-dopa metabolites increase oxidative stress and they are toxic to cultures of mesencephalic neurons [75]. However, there is no in vivo evidence that l-dopa accelerates disease progression and, as it was shown by an ELLDOPA (Early versus Later Levodopa therapy in PD patients) study [76], that patients in l-dopa treatment actually are less impaired even after stopping medication for a few weeks compared to patients who delay l-dopa therapy. Previous studies have also documented that dopaminergic depletion is involved in visual dysfunction in PD patients, therefore l-dopa therapy may improve visual disturbances investigated by electrophysiological tests [77,78].