New hypotheses about postural control support the notion that all dystonias are manifestations of excessive brain postural function.

This paper postulates that all forms of the neurological movement disorder, dystonia, can be argued to reflect excessive function of one or more components of the brain postural system. This is based on four central arguments. First, because some forms of postural control are already known to be dynamic, rather than static, it is suggested that hyperkinetic dystonias reflect excessive function of dynamic postures, rather than abnormal movements. Second, the range of functional roles served by the postural system is hypothesized to include direct control of movement, suggesting a postural basis for task-specific dystonias. Third, by defining posture as a neural system that maintains body stabilization, it can be shown that the range of mechanical means of implementing stabilization, including co-contraction of antagonistic muscles, matches the range of presentations of dystonia. Fourth, it is shown that the above premises are able to account for previously unexplained observations in dystonia. Based on the inhibitory influence that stabilizing mechanisms exert on movement, it is suggested that the broad functional role that is here referred to as posture may be the function served by the indirect pathway of the basal ganglia. Specifically, it is proposed that this pathway centrally coordinates function of the distributed network of brain regions controlling posture and, in conjunction with the direct pathway, coordinates posture and movement.