Non-motor symptoms of Parkinson's disease (PD) and particularly mood manifestations such as apathy, depression and anxiety have gained attention in the last few decades due to its high frequency and impact in patient's quality of life. In addition, these psychic non-motor features have been shown to fluctuate alike motor symptoms do, concurring to non-motor fluctuations (NMF) that can be more disabling than motor symptoms. The physiopathological basis of psychic NMF is unclear but mesolimbic dopaminergic denervation has been suggested to underlie mood manifestations during off-periods . At the same time, it has been demonstrated that PD patients suffer from abnormal emotional processing deficits in facial expression recognition and emotional prosody especially concerning negative valanced emotions, and that these impairments could also be linked to mesolimbic dopaminergic mechanisms. The mesolimbic pathway is one of the functional cortico-subcortical loops in which basal ganglia are segregated. It lies in the ventral subportion of each nucleus (ventromedial in the case of the subthalamic nucleus) and through the mediodorsal thalamus projects to the orbito-frontal cortex and the anterior cingulate cortex (ACC), limbic cortical areas that robust evidence has involved in the pathophysiology of mood disturbances and emotional processes like facial expression recognition or emotional conflict resolution. In summary, in the same way that dopamine depletion of the nigrostriatal pathway is at the origin of the parkinsonian motor triad, the lack of dopamine in the mesolimbic loop would account for non-motor psychic manifestations including apathy, anxiety, depression and disturbances in emotional decoding. A proper way to explore these phenomena is through tasks that involve exposure to affective stimuli.