Historically, dystonia has always been considered a disorder of the basal ganglia. But recent evidence has pointed towards cerebellar circuits as well. Many researchers now believe that dystonia is caused by a disruption of a motor network that involves both the basal ganglia and cerebellum, rather than an isolated dysfunction of only one motor system. But how the motor network relates to the genes and proteins that are thought to be involved in the development of dystonia is a fertile area of research.
The Bachmann-Strauss Foundation’s annual Think Tank has provided a valuable forum for researchers to exchange ideas about where future research should be directed. Promising areas of inquiry have included:
- Understanding the cascade of chemical and electrophysiologic changes that occur as a consequence of loss of striatal dopamine in parkinsonism that can then be translated into new and more effective therapies for both Parkinson's disease and dystonia.
- Demonstrating that fast-spiking interneurons (FSIs) can exert powerful control over striatal output and may be a novel therapeutic target for the treatment of hyperkinetic movement disorders.
- Explaining how plasticity may be a driver of long-term therapeutic effects of deep brain stimulation in dystonia.
- Investigating why dysfunctional interactions between the cerebellum and the basal ganglia are a key factor in the underlying pathophysiology of rapid-onset dystonia-parkinsonism.