For many years pathophysiological studies on patients with movement disorders were viewed as inferior to those in animal models because, given the complexity of dealing with the complete interconnected CNS, it was difficult to assign any particular physiological abnormality exclusively to the site of a known lesion. More recently this has come to be seen as an advantage. All the articles reviewed below focus on how healthy parts of the CNS react to damage at a distance, with the result that we are now beginning to have much more insight into how these reactions both compensate and exacerbate the primary deficit.