Parkinson’s disease (PD) is a neurodegenerative disorder affecting dopaminergic neurons in the substantia nigra leading to dysfunctional cortico-striato-thalamic-cortical loops. In addition to the characteristic motor symptoms, PD patients often show cognitive impairments, affective changes and other non-motor symptoms, suggesting system-wide effects on brain function. Here, we used functional magnetic resonance imaging and graph-theory based analysis methods to investigate altered whole-brain intrinsic functional connectivity in PD patients (n = 37) compared to healthy controls (n = 20). Global network properties indicated less efficient processing in PD. Analysis of brain network modules pointed to increased connectivity within the sensorimotor network, but decreased interaction of the visual network with other brain modules. We found lower connectivity mainly between the cuneus and the ventral caudate, medial orbitofrontal cortex and the temporal lobe. To identify regions of altered connectivity, we mapped the degree of intrinsic functional connectivity both on ROI- and on voxel-level across the brain. Compared to healthy controls, PD patients showed lower connectedness in the medial and middle orbitofrontal cortex. The degree of connectivity was also decreased in the occipital lobe (cuneus and calcarine), but increased in the superior parietal cortex, posterior cingulate gyrus, supramarginal gyrus and supplementary motor area. Our results on global network and module properties indicated that PD manifests as a disconnection syndrome. This was most apparent in the visual network module. The higher connectedness within the sensorimotor module in PD patients may be related to compensation mechanism in order to overcome the functional deficit of the striato-cortical motor loops or to loss of mutual inhibition between brain networks. Abnormal connectivity in the visual network may be related to adaptation and compensation processes as a consequence of altered motor function. Our analysis approach proved sensitive for detecting disease-related localized effects as well as changes in network functions on intermediate and global scale.

The use of D2/D3 dopaminergic agonists in Parkinson's disease (PD) may lead to pathological gambling. In a placebo-controlled double-blind study in healthy volunteers, we observed riskier choices in a lottery task after administration of the D3 receptor-preferring agonist pramipexole thus mimicking risk-taking behavior in PD. Moreover, we demonstrate decreased activation in the rostral basal ganglia and midbrain, key structures of the reward system, following unexpected high gains and therefore propose that pathological gambling in PD results from the need to seek higher rewards to overcome the blunted response in this system.

State effects on frontal alpha electroencephalograph asymmetry (ASY) are thought to reflect approach and withdrawal motivational tendencies. Although this motivational direction model has inspired a large body of research, efforts to disentangle influences of emotion (EMO) and motivational direction (MOT) on ASY are rare. The authors independently manipulated EMO (fear and anger) and MOT (approach and withdrawal) in a between-subjects design. Irrespective of MOT, anger led to greater changes toward relative left frontal activation (LFA) than did fear. Conversely, higher ratings of negative valence were associated with greater changes toward LFA in withdrawal but with greater changes toward relative right frontal activation in approach. Results are discussed within a model based on behavioral inhibition system-behavioral activation system theory.

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We investigated psychophysiological responses to fear and anger inductions during real-life and imagination. Female participants (N = 158) were assigned to a fear-treatment, fear-control, anger-treatment, or anger-control group. Context (real-life, imagination) was varied in two sessions of fixed order. Eleven self-report and 29 somatovisceral variables were registered. Results showed that (a) except during anger imagination, control groups were emotionless; (b) in control groups, contexts prompted diverging somatovisceral responses, but similar emotion self-reports; except during fear imagination, the emotion inductions (c) were successful and (d) produced specific emotion reports; (e) during real-life, somatovisceral fear and anger responses exhibited a marked cardiovascular defense reflex; (f) in addition, real-life fear showed an adrenaline-like specific response pattern, whereas real-life anger showed specific forehead temperature and EMG extensor increases, accompanied by an elevated DBP during imagination. A Component Model of Somatovisceral Response Organization is proposed.