In terms of pathogenesis, two main factors are involved in the development of LID [4–6]. The first is nigral dopaminer- gic denervation of the striatum presynaptically, and the second consists of plastic changes in striatal dopaminergic neuron cell signalling that leads to abnormal basal ganglion firing patterns postsynaptically. Thus, ample evidence suggests that striatal dopaminergic depletion is required for the development of LID [2, 7–10] and predicts LID in patients with PD [11], even though LID has occasionally been observed in normal animals and human subjects [12, 13].