ABSTRACT
The term “dyskinesia” is particularly used for hereditary paroxysmal movement disorders such as dystonia, choreoathetosis, and ballism, and for drug-induced complications such as levodopainduced dyskinesia (LID) or tardive dyskinesia (TD). Dyskinesias represent common and severe movement disorders and are regarded as a basal ganglia disorder, that is, they are based within brain structures that are crucial for the initiation and processing of voluntary and automatic movements. However, the limited knowledge about the pathophysiology of various types of dyskinesias hampers the development of effective therapeutics. Dyskinesias are dif‰cult to treat and often lead to severe disabilities in patients. Although the etiology of different forms (e.g., hereditary and drug-induced) of this disabling condition is heterogeneous, it cannot be excluded that they share, at least in part, common pathophysiological mechanisms and have identical targets for new strategies in prevention and therapy. For example, clinical and epidemiological studies in humans revealed that the severity of dyskinesias and the frequency of paroxysmal forms are altered by factors such as the onset of puberty, pregnancy, cyclical changes, and stress, indicating an underlying hormonal component (Kranick et al. 2010; Soorani-Lunsing et al. 1994; Weber and Lerche 2009). Therefore, this chapter focuses on the possible pathophysiological, preventive, and therapeutic role of the “neuroactive steroid” dehydroepiandrosterone (DHEA) in drug-induced and hereditary paroxysmal dyskinesias.
