I am particularly interested in the pathophysiology of movement disorders such as Parkinson’s disease and tremor. Especially resting tremor in Parkinson’s disease intrigues me: how does a hyperkinetic symptom arise in a hypokinetic disorder? Notably patients with tremor usually have a better prognosis of their disease progression. Could it be that tremor is somehow a compensation mechanism and if so, how does this work? To investigate this I use techniques such as EMG, accelerometry and functional MRI in order to elucidate underlying cerebral mechansims. I especially like to focus on these mechanisms at a system-level’s perspective, to which extent I use Dynamic Causal Modelling (to model effective connectivity) and seed-based functional connectivity.
Currently I focus on the question how it is possible that especially resting tremor is often hard to treat in patients with Parkinson’s disease. Specifically there is a large group of patients with a remarkable dopamine-resistant tremor, i.e. a tremor that does not respond as well to dopaminergic medication. Thus, I ask myself the question: what are the differences in cerebral mechanisms underlying dopamine-resistant versus dopamine-responsive tremor?