The motivation to choose one action or another differs between humans, for example in the context of gambling where subjects will display different degrees of risk-aversion. On the other hand, brain disorders such as Parkinson’s disease affect the ability to voluntarily execute movements and to inhibit involuntary movements. This workpackage investigates the neural underpinnings of intentional action control.
Gelskov SV, Henningsson S, Madsen KH, Siebner HR, Ramsøy TZ (2015) Amygdala signals subjective appetitiveness and aversiveness of mixed gambles. Cortex 66:81–90.
People are more sensitive to losses than to equivalent gains when making financial decisions. We used functional magnetic resonance imaging (fMRI) to illuminate how the amygdala contributes to loss aversion. The individual level of loss aversion was expressed by the decision boundary, i.e., the gain-loss ratio at which subjects accepted and rejected gambles with equal probability. Amygdala activity increased the more the gainloss ratio deviated from the individual decision boundary showing that the amygdala codes action value. This response pattern was more strongly expressed in loss aversive individuals, linking amygdala activity with individual differences in loss aversion.
Figure on the right; Activity profile of the amygdala during the decision-making phase. A) Brain responses reflecting distance to the individual decision boundary λ. White circle indicates left amygdala cluster. B) The heat-map illustrates the activation pattern in left amygdala peak shows that amygdala responses are higher for increasing deviations from the decision boundary. C) Response profile of the left amygdala to extreme ratios relative to the intermediate ones around the decision boundary.
Herz DM, Haagensen BN, Christensen MS, Madsen KH, Rowe JB, Løkkegaard A, Siebner HR (2014b) The acute brain response to levodopa heralds dyskinesias in Parkinson disease. Ann Neurol 75:829–836.
Executing a voluntary movement and suppressing unwanted movements is a central aspect of motor control. In Parkinson disease (PD), long-term treatment with the dopamine precursor levodopa gradually induces involuntary “dyskinesia” movements. Immediately before and after levodopa intake, we performed fMRI, while patients produced a mouse click with the right or left hand or no action (No-Go) contingent on 3 arbitrary cues. During No-Go trials, PD patients who would later develop dyskinesias showed an abnormal gradual increase of activity in the presupplementary motor area (preSMA) and the bilateral putamen after levodopoa intake. At the individual level, the excessive No-Go activity in the predyskinesia period predicted whether an individual patient would subsequently develop dyskinesias as well as severity of their day-to-day symptomatic dyskinesia. PD patients with dyskinesias display an immediate hypersensitivity of preSMA and putamen to levodopa, which heralds the failure of neural networks to suppress involuntary dyskinetic movements.
For the above figure; A) A first set of MRI scans was obtained after withdrawal of dopaminergic medication. Patients then received levodopa and the same sequence of fMRI-scans was repeated twice after levodopa intake. If dopaminergic levels reached the threshold for triggering dyskinesias, fMRI measurements were immediately discontinued. At least one post-levodopa-fMRI-scan after intake of levodopa could be acquired for all patients before emergence of dyskinesias.
B) The motor task consisted of three different stimuli indicating participants to press a button with their left index finger, right index finger or to refrain from any motor response (No-Go).
A) Analysis of time-modulation of NoGo after levodopa intake (first post-levodopa-scan) showed a significant stronger increase in activation of preSMA and bilateral putamen in LID patients compared to patients without dyskinesias. This was not observed during right or left button presses.
B) Regression analysis showed that dopaminergic modulation of preSMA activity during No-Go was a strong predictor of severity of emerging dyskinesia.
C) Dopaminergic modulation of preSMA activity did not predict severity of Parkinson symptoms.