title: Clinical features of dystonia: a pathophysiological revisitation.
abstract: OBJECTIVE
  To elucidate the pathophysiology of some clinical features of dystonic patients and to provide some new insight into the mechanisms underlying task-specific dystonia.
  
  
  RESULTS
  There are three general lines of work at the present time that may indicate the physiological substrate for dystonia. All three are persuasive and it is not clear whether they are related to each other or whether one is more important than the others. According to the first line of research, a loss of inhibition at different levels of the central nervous system might contribute for the excessive movement seen in dystonia. Another field of research suggests that dystonic patients may have faulty processing within the lemniscal pathway with abnormalities in the sensory-motor integration. Finally, another convincing line of evidence is that in some susceptible individuals, during the acquisition of new motor skills, the mechanisms of neuroplasticity are subtly abnormal. In the presence of such predisposition, several environmental factors, such as repetitive training or peripheral nervous system injury, can trigger an abnormal maladaptive plasticity, which can lead to an overt dystonia.
  
  
  CONCLUSIONS
  These findings may be relevant in the development of new therapeutic strategies in dystonia.
authors.affiliation: Dipartimento di Neuroscienze, Scienze Psichiatriche ed Anestesiologiche, Università di Messina, Messina, Italy. angelo.quartarone@unime.it
authors.forename: Angelo
authors.initials: A
authors.lastname: Quartarone
authors.forename: Vincenzo
authors.initials: V
authors.lastname: Rizzo
authors.forename: Francesca
authors.initials: F
authors.lastname: Morgante
mesh_terms: D002490:Central Nervous System / Q000502:physiology / Q000503:physiopathology; D004421:Dystonia / Q000503:physiopathology*; D020821:Dystonic Disorders / Q000503:physiopathology*; D004525:Efferent Pathways / Q000502:physiology / Q000503:physiopathology*; D006801:Humans; D008959:Models, Neurological; D009119:Muscle Contraction / Q000502:physiology*; D009433:Neural Inhibition / Q000502:physiology*; D009473:Neuronal Plasticity / Q000502:physiology; D011597:Psychomotor Performance / Q000502:physiology