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Parkinson's disease (PD) is traditionally conceptualised as a disorder of movement, but recent data suggest that motivational deficits may be more pervasive than previously thought. Here, we ask whether subclinical deficits in incentivised decision-making are present in PD and, if so, whether dopaminergic therapy ameliorates such deficits. We devised a novel paradigm in which participants decided whether they were willing to squeeze a hand-held dynamometer at varying levels of force for different magnitudes of reward. For each participant, we estimated the effort level at which the probability of accepting a reward was 50% – the effort ‘indifference point’. Patients with PD (N = 26) were tested ON and OFF their usual dopaminergic medication, and their performance compared to those of age-matched controls (N = 26). No participant was clinically apathetic as defined by the Lille Apathy Rating Scale (LARS). Our data show that, regardless of medication status, patients with PD chose to engage less effort than controls for the lowest reward. Overall, however, dopamine had a motivating effect on participants' choice behaviour – patients with PD chose to invest more effort for a given reward when they were in the ON relative to OFF dopamine state. Importantly, this effect could not be attributed to motor facilitation. We conclude that deficits in incentivised decision-making are present in PD even in the absence of a clinical syndrome of apathy when rewards are low, but that dopamine acts to eliminate motivational deficits by promoting the allocation of effort.

Interactions between the Salience Network (SN) and the Default Mode Network (DMN) are thought to be important for cognitive control. However, evidence for a causal relationship between the networks is limited. Previously, we have reported that traumatic damage to white matter tracts within the SN predicts abnormal DMN function. Here we investigate the effect of this damage on network interactions that accompany changing motor control. We initially used fMRI of the Stop Signal Task to study response inhibition in humans. In healthy subjects, functional connectivity (FC) between the right anterior insula (rAI), a key node of the SN, and the DMN transiently increased during stopping. This change in FC was not seen in a group of traumatic brain injury (TBI) patients with impaired cognitive control. Furthermore, the amount of SN tract damage negatively correlated with FC between the networks. We confirmed these findings in a second group of TBI patients. Here, switching rather than inhibiting a motor response: (1) was accompanied by a similar increase in network FC in healthy controls; (2) was not seen in TBI patients; and (3) tract damage after TBI again correlated with FC breakdown. This shows that coupling between the rAI and DMN increases with cognitive control and that damage within the SN impairs this dynamic network interaction. This work provides compelling evidence for a model of cognitive control where the SN is involved in the attentional capture of salient external stimuli and signals the DMN to reduce its activity when attention is externally focused.