The authors describe a case of very early onset Parkinson’s disease in a 19-year old man reporting previous Ecstasy use. The patient reported having used Ecstasy twice monthly for 6 months (1 tablet per occasion, Kuniyoshi 2003, personal communication)) prior to symptom onset. The patient first reported resting tremor in his right hand approximately 2 months after he last used Ecstasy. The tremor progressed his right leg. He was diagnosed with Parkinson’s disease, and selegiline (deprenyl) was first prescribed, but was switched to trihexyphenidyl. The patient has a family history of young-onset Parkinson’s disease, both in his father (onset at 49, diagnosis at 52) and his uncle (onset at 50). Relying on findings from a study in non-human primates (Ricaurte et al. 2002) that has since been retracted (Ricaurte et al. 2003), the authors suggest that a predisposition to developing Parkinson’s disease made the functional effects of Ecstasy-induced dopamine neurotoxicity appear earlier than usual in their patient. However, since the retraction of Ricaurte et al. 2002, this case probably cannot be treated as a mere acceleration of MDMA effects on dopamine cells. It is still possible that dopamine neurons in people with family histories of early-onset Parkinson’s disease are more sensitive to oxidative stress, including oxidative stress produced after ingesting MDMA (see Zhou et al. 2003A; 2003B), but it seems extremely unlikely that the general population has the same vulnerability. This is the second case of Parkinson’s disease or Parkinsonian symptoms appearing in a person reporting previous Ecstasy use (see Mintzer et al. 1999). Any causal link between Ecstasy use and Parkinson’s disease could more appropriately be established if rates of Parkinson’s disease were compared in people reporting Ecstasy use and people who failed to report Ecstasy use rather than accumulating instances where Ecstasy users later developed Parkinson’s disease.