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Neuropsychologia. 2009 Jan;47(2):406-14. doi: 10.1016/j.neuropsychologia.2008.09.008. Epub 2008 Sep 18.

Are dopaminergic pathways involved in theory of mind? A study in Parkinson's disease.

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  • 1Hôpital Pontchaillou, CHU de Rennes, Rue Henri Le Guilloux, 35033 Rennes, France.

Abstract

The "orbitofrontal" and "cingulate" frontostriatal loops and the mesolimbic dopaminergic system that modulates their function have been implicated in theory of mind (ToM). Parkinson's disease (PD) provides a model for assessing their role in humans. Results of the handful of previous studies of ToM in PD providing preliminary evidence of impairment remain controversial, mainly because the patients included in these studies were not accurately described, making it difficult to determine whether their ToM deficits were due to general cognitive deterioration or to a more specific dopaminergic deficit. The aim of our study was therefore to re-examine previous results highlighting ToM in PD and to explore the involvement of the dopaminergic pathways in ToM. ToM was investigated in 17 newly diagnosed PD patients (early PD group), 27 PD patients in the advanced stages of the disease (advanced PD group) and 26 healthy matched controls (HC), using two ToM tasks: a visual one, which is thought to reflect the "affective" ToM subcomponent ("Reading the Mind in the Eyes"), and a verbal one, which is thought to reflect both the "affective" and the "cognitive" ToM subcomponents (faux pas recognition). Furthermore, the early PD group was studied in two conditions: with and without dopamine replacement therapy (DRT). We failed to find any significant difference in ToM between the early PD patients and the HC group. Furthermore, there was no difference between the early PD patients in the medicated and unmedicated conditions. Conversely, the advanced PD patients scored poorly on the intention attribution question ("cognitive" ToM score) in the faux pas recognition task. The present results suggest that the deficit in ToM only occurs in the more advanced stages of the disease. In addition, our results would appear to indicate that these advanced PD patients present "cognitive" ToM impairment rather than global ("cognitive" and "affective") ToM impairment. In other words, the ToM deficit would appear to be present in PD patients where the degenerative process has spread beyond the dopaminergic pathways, but not in early PD patients where neuronal loss is thought to be restricted to the nigrostriatal and mesolimbic dopaminergic systems. In conclusion, our results suggest that the dopaminergic pathways are not involved in ToM.

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