The increased activity in the pre-SMA is highly correlated with improved motor performance. The pre-SMA is suggested to be critical in planning and decision-making of movements and might play a primary role in the preparation of self-initiated movements [10–12]. The pre-SMA is also one of the main target regions receiving projections from the basal ganglia motor circuit [13]. These results indicate that the dysfunction of pre-SMA, due to a deficit of the nigrostriatal dopamine system, is an important reason contributing to the akinesia in iPD. The hyperactivity in the premotor cortex, parietal cortex, and cerebellum is likely compensatory. iPD patients need recruitment of other motor circuits to compensate for the functional deficits of the striatum in order to overcome their difficulty in performing movements [3, 6, 7, 14–16].

The motor deficits in iPD appear not only during motor execution, but also in the motor learning process. BOLD fMRI studies of motor learning commonly found that iPD patients have dysfunction in frontostriatal motor circuits, especially with decreased activity in the prefrontal cortex, but with compensatory hyperactivation in the parietal and premotor cortices and cerebellum [17–19]. The difficulty of iPD patients in motor learning is made more obvious when they try to shift learned movements to the automatic stage. It has been shown that iPD patients need greater activity in the cerebellum, premotor area, parietal cortex, precuneus, and prefrontal cortex compared with normal subjects while performing automatic movements. They require more brain activity to compensate for basal ganglia dysfunction in order to perform automatic movements [6].

Functional MRI has also been used to investigate the deficits of iPD patients in more complex coordination motor tasks. For example, iPD patients have difficulty in performing bimanual movements, especially antiphase movements [20]. Antiphase bimanual movements are when both hands perform the same movement with a phase shift of 180° between the two hands (i.e., one hand flexes while the other extends). A recent study found that the SMA was more activated during antiphase movement than inphase movement in controls, but not in iPD patients. In performing antiphase movements, iPD patients showed less activity in the basal ganglia and SMA, and had more activation in the M1, premotor cortex, and cerebellum compared with normal subjects. These findings suggest that dysfunction of the SMA and basal ganglia, abnormal interactions of brain networks, and disrupted attentional networks are important reasons contributing to the difficulty in performing bimanual antiphase movements. More brain activity and stronger connectivity are required in some brain regions to compensate for dysfunction of the supplementary motor area and basal ganglia in order to perform bimanual movements correctly [8].

Idiopathic PD patients also have more difficulty in performing two different tasks simultaneously (dual task). Wu and Hallett [21] found that iPD subjects can execute some simple dual motor and cognitive tasks correctly, but needed greater activity in the cerebellum, premotor area, parietal cortex, precuneus, and prefrontal cortex compared with controls. These fMRI findings suggest that the problem in performing dual tasks in iPD is due to limited attentional resources, defective central executive function, and less automaticity in performing the tasks.

More recently, fMRI has been used to investigate the alterations in connectivity of motor circuits. Since iPD affects large-scale brain networks, examination of network interactions may provide more valuable information in understanding pathophysiological changes than simply investigating local brain activity. The method used to explore network integration is analysis of functional or effective connectivity. Functional connectivity is defined as the degree of temporal correlation between spatially remote brain regions, whereby areas having more similar blood flow responses over time are considered to be more “functionally connected.” Effective connectivity expands on this by predicting the direction of information flow between two regions and is defined as the influence one neuronal system exerts over another [22]. These methods are increasingly being used to investigate iPD-induced modifications of brain networks [23–31]. The primary finding of these studies is that in addition to regional activation changes, the connectivity of brain networks also has iPD-related modifications during the performance of various motor tasks. For example, using structural equation modeling (SEM) [23], psychophysiological interaction (PPI) [30, 31], and dynamic causal modeling (DCM) [24], investigators have identified that iPD patients fail to modulate effective connectivity between prefrontal cortex, premotor cortex, and SMA. During the performance of self-initiated movement, the connectivity of striatal motor circuits is weakened, which might contribute to the impairment in performing self-initiated movements in iPD. Meanwhile, the connections between corticocerebellar motor regions are strengthened and may help compensate for basal ganglia dysfunction ([31], Fig. 9.2). While the use of fMRI activation maps to measure the amplitude of blood flow responses may provide valuable information about regional brain changes, connectivity analyses may be a more sensitive method to detect neural changes in iPD [32].