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This study examined whether Parkinson's disease (PD1) and schizophrenia (SCZ2) share a hypo dopaminergic dysfunction of the prefrontal cortex leading to cognitive impairments in decision processing. 24 medicated PD patients and 28 matched controls performed the Eriksen flanker two-choice reaction time (RT3) task while brain activity was measured throughout, using functional Magnetic Resonance Imaging (fMRI4). Results were directly compared to those of 30 SCZ patients and 30 matched controls. Significant differences between SCZ and PD were found, through directly comparing the z-score deviations from healthy controls across all behavioral measures, where only SCZ patients showed deviances from controls. Similarly a direct comparison of z-score activation deviations from controls indicated significant differences in prefrontal and cingulate cortical activation between SCZ and PD, where only SCZ patients showed hypo-activation of these areas compared to controls. The hypoactivation of the dorsolateral prefrontal cortex was related to larger RT variability (ex-Gaussian tau) in SCZ but not PD patients. Overall, the concluding evidence does not support a shared neural substrate of cognitive dysfunction, since the deficit in speeded decision processing and the related cortical hypo-activation observed in SCZ were absent in PD.

This study examined whether Parkinson's disease (PD1) and schizophrenia (SCZ2) share a hypo dopaminergic dysfunction of the prefrontal cortex leading to cognitive impairments in decision processing. 24 medicated PD patients and 28 matched controls performed the Eriksen flanker two-choice reaction time (RT3) task while brain activity was measured throughout, using functional Magnetic Resonance Imaging (fMRI4). Results were directly compared to those of 30 SCZ patients and 30 matched controls. Significant differences between SCZ and PD were found, through directly comparing the z-score deviations from healthy controls across all behavioral measures, where only SCZ patients showed deviances from controls. Similarly a direct comparison of z-score activation deviations from controls indicated significant differences in prefrontal and cingulate cortical activation between SCZ and PD, where only SCZ patients showed hypo-activation of these areas compared to controls. The hypoactivation of the dorsolateral prefrontal cortex was related to larger RT variability (ex-Gaussian tau) in SCZ but not PD patients. Overall, the concluding evidence does not support a shared neural substrate of cognitive dysfunction, since the deficit in speeded decision processing and the related cortical hypo-activation observed in SCZ were absent in PD.