Acquired focal dystonia can be precipitated by either extended practice of skilled movements or damage to the neuronal circuits that are implicated in motor learning. From these observations, investigators propose a theory that dystonia results from a failure of adaptive mechanisms that normally support the acquisition of new skills. This theory is supported by the demonstration of abnormalities in motor sequence learning in non-manifesting human carriers of the early-onset torsion dystonia gene (DYT1) mutation. The most common type of early-onset, generalized dystonia is a GAG deletion in the DYT1 (TOR1A) gene encoding torsin A. This mutation results in loss of a glutamic acid residue near the carboxy terminus of torsin A. Thus, it is reasonable to study mice carrying the DYT1 mutation for abnormalities in motor learning. The most widely accepted and validated tool for the study of motor skills in the mouse is the rotarod. Thus, in addition to systematically evaluating posture with an emphasis on detecting abnormal postures similar to those seen in humans with dystonia, investigators can study future generations of DYT1 transgenic mice for their ability to maintain balance and remain coordinated with repeated rotarod testing. © 2005 Elsevier Inc. All rights reserved.