DRCMR Logo 300px Color
 

Cognition in Movement Disorders

The Cognition in Movement Disorders group bridges computational, cognitive and clinical neuroscience to advance the pathophysiological understanding of movement disorders.

We use computational models of learning and decision-making to probe disease-induced changes in brain and behavior. Traditionally, clinical neuroimaging has often taken a predominantly descriptive approach, describing that there is a change in brain or behavior observed in the disorder. Computational neurology takes one step further: Using computer models of behavior allows us to precisely define the mechanism (or possible alternative mechanisms) in which the process under investigation might be solved by the brain. Such models contain “latent variables”, i.e. variables that cannot be directly observed in behavior. Such variables could for example be the certainty of making a correct choice or the surprise about the outcome of an action. If such a model then fits to the observed behavior and neural activity, we can infer that the brain (approximately) uses the kind of algorithm we defined in the model. The precise operational definition of latent variables can thus lead to a mechanistic understanding, explaining not only that there are disease-induced changes, but how the changes occur at the neural and symptomatic level.

md Brain Cover

The figure gives an example about how we use modeling of behavior in cognitive tasks to probe the brain for computations of latent variables. Here, in a risky decision-making task, we modeled each participant’s “Certainty Equivalent” (CE), i.e. the point where the participant was most uncertain about whether to continue gambling under the risk of losing, or whether she felt she had gained enough. A higher CE means that these participants took riskier decisions in the task. We could then see that as subjects took risky decisions, the subthalamic nucleus (STN) was similarly active in Parkinson’s disease patients with impulse control disorder (ICD), irrespective of their CE. In patients without ICD, however, more cautious behavior (lower CE) was associated with stronger STN activity (Haagensen et al., 2020, Neuroimage: Clinical).

Given the group’s position at the interface of cognitive neuroscience and movement disorders, we have strong ties to the “Movement Disorders” and the “Computational Neuroscience of Reward” group at DRCMR.

Selected Publications

Herz, D. M., Meder, D., Camilleri, J. A., Eickhoff, S. B., & Siebner, H. R. (2021). Brain Motor Network Changes in Parkinson’s Disease: Evidence from Meta-Analytic Modeling. Movement Disorders, Early view. https://doi.org/10.1002/mds.28468

Lohse, A., Meder, D., Nielsen, S., Lund, A. E., Herz, D. M., Løkkegaard, A., & Siebner, H. R. (2020). Low-frequency transcranial stimulation of pre-supplementary motor area alleviates levodopa-induced dyskinesia in Parkinson’s disease: A randomized cross-over trial. Brain Communications, 2(fcaa147). https://doi.org/10.1093/braincomms/fcaa147

Haagensen, B. N., Herz, D. M., Meder, D., Madsen, K. H., Løkkegaard, A., & Siebner, H. R. (2020). Linking brain activity during sequential gambling to impulse control in Parkinson’s disease. NeuroImage: Clinical, 27, 102330. https://doi.org/10.1016/j.nicl.2020.102330

Meder, D., Herz, D. M., Rowe, J. B., Lehéricy, S., & Siebner, H. R. (2019). The role of dopamine in the brain—Lessons learned from Parkinson’s disease. NeuroImage, 190, 79–93. https://doi.org/10.1016/j.neuroimage.2018.11.021

Irmen, F., Horn, A., Meder, D., Neumann, W.-J., Plettig, P., Schneider, G.-H., Siebner, H. R., & Kühn, A. A. (2019). Sensorimotor subthalamic stimulation restores risk-reward trade-off in Parkinson’s disease. Movement Disorders, 34(3), 366–376. https://doi.org/10.1002/mds.27576

Meder, D., Kolling, N., Verhagen, L., Wittmann, M. K., Scholl, J., Madsen, K. H., Hulme, O. J., Behrens, T. E. J., & Rushworth, M. F. S. (2017). Simultaneous representation of a spectrum of dynamically changing value estimates during decision making. Nature Communications, 8(1), 1942. https://doi.org/10.1038/s41467-017-02169-w

Group Members

David Meder

Group Leader

Christopher Fugl Madelung

Søren Asp Fuglsang

Anders Elkjær Lund

Show all group members (7)

External Collaborators

Damian M. Herz, MD, PhD

Nuffield Department of Clinical Neurosciences
University of Oxford


Prof. Ray Dolan, MD, MB BCh

Institute of Neurology, UCL, and
Max Planck-UCL Centre for Computational Psychiatry and Ageing


 Prof. Mark Hallett

NINDS, Human Motor Control Section
National Institute of Neurological Disorders and Stroke College of Medicine