Frontostriatal contributions to reward processing

Dopaminergic projections to striatum and prefrontal cortex are thought to signal rewards, thereby energising movement, facilitating learning, and motivating effort. Extensive evidence links reward to attention and to dopamine. However a direct characterisation of how dopamine influences reward sensitivity in humans is lacking. This thesis examines the effects of dopamine and reward on eye movements. First, I introduced incentive manipulations into an “oculomotor capture” task, in which involuntary saccades are generated towards salient distractors. Whereas rewards increased both speed and accuracy, penalties slowed responses while increasing accuracy. A previously unreported effect is described, in which missed rewards capture attention. Subsequently, I developed a new paradigm that manipulates incentives trial-to-trial, during a speeded saccadic distraction task. In healthy volunteers, reward reduced distractibility and increased vigour (in terms of reaction time and velocity), and pupillary dilatation reflected reward expectation. This new task was then employed in a pharmacological study, in which I found that the dopaminergic D2-selective agonist cabergoline increased reward sensitivity in healthy volunteers. Parkinson's disease (PD) results in dopamine deficiency. PD patients performing my task had reduced reward sensitivity in saccade velocity and distractibility, as well as pupil dilatation. Patients were compared on versus off their dopaminergic medication, and although oculomotor vigour did not improve, medication normalised their blunted autonomic responses. Finally, 20 patients with medial prefrontal damage following subarachnoid haemorrhage performed the oculomotor task. Using lesion mapping, I found specific medial orbitofrontal regions in which damage correlated with reduced reward sensitivity. The results demonstrate that the extent to which reward invigorates behaviour is influenced by dopamine. Importantly, reward improves both speed and accuracy, contravening the theoretically predicted trade-off. To resolve this paradox, I develop an extension of optimal control theory that includes a costly precision signal. This model helps conceptualise reward's power to improve both speed and accuracy

Subthalamic nucleus local field potentials recordings reveal subtle effects of promised reward during conflict resolution in Parkinson's disease

Cognitive action control depends on cortical-subcortical circuits, involving notably the subthalamic nucleus (STN), as evidenced by local field potentials recordings (LFPs) studies. The STN consistently shows an increase in theta oscillations power during conflict resolution. Some studies have shown that cognitive action control in Parkinson's disease (PD) could be influenced by the occurrence of monetary reward. In this study, we investigated whether incentive motivation could modulate STN activity, and notably STN theta activity, during response conflict resolution. To achieve this objective, we recorded STN LFPs during a motivated Simon task in PD patients who had undergone deep brain stimulation surgery. Behavioral results revealed that promised rewards increased the difficulty in resolving conflict situations, thus replicating previous findings. Signal analyses locked on the imperative stimulus onset revealed the typical pattern of increased theta power in a conflict situation. However, this conflict-related modulation of theta power was not influenced by the size of the reward cued. We nonetheless identified a significant effect of the reward size on local functional organization (indexed by inter-trial phase clustering) of theta oscillations, with higher organization associated with high rewards while resolving conflict. When focusing on the period following the onset of the reward cue, we unveiled a stronger beta power decrease in higher reward conditions. However, these LFPs results were not correlated to behavioral results. Our study suggests that the STN is involved in how reward information can influence computations during conflict reso- lution. However, considering recent studies as well as the present results, we suspect that these effects are subtle

Programming the cerebellum

It is argued that large-scale neural network simulations of cerebellar cortex and nuclei, based on realistic compartmental models of me major cell populations, are necessary before the problem of motor learning in the cerebellum can be solved, [HOUK et al.; SIMPSON et al.

Medical-Data-Models.org:A collection of freely available forms (September 2016)

MDM-Portal (Medical Data-Models) is a meta-data repository for creating, analysing, sharing and reusing medical forms, developed by the Institute of Medical Informatics, University of Muenster in Germany. Electronic forms for documentation of patient data are an integral part within the workflow of physicians. A huge amount of data is collected either through routine documentation forms (EHRs) for electronic health records or as case report forms (CRFs) for clinical trials. This raises major scientific challenges for health care, since different health information systems are not necessarily compatible with each other and thus information exchange of structured data is hampered. Software vendors provide a variety of individual documentation forms according to their standard contracts, which function as isolated applications. Furthermore, free availability of those forms is rarely the case. Currently less than 5 % of medical forms are freely accessible. Based on this lack of transparency harmonization of data models in health care is extremely cumbersome, thus work and know-how of completed clinical trials and routine documentation in hospitals are hard to be re-used. The MDM-Portal serves as an infrastructure for academic (non-commercial) medical research to contribute a solution to this problem. It already contains more than 4,000 system-independent forms (CDISC ODM Format, www.cdisc.org, Operational Data Model) with more than 380,000 dataelements. This enables researchers to view, discuss, download and export forms in most common technical formats such as PDF, CSV, Excel, SQL, SPSS, R, etc. A growing user community will lead to a growing database of medical forms. In this matter, we would like to encourage all medical researchers to register and add forms and discuss existing forms