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Abnormal plasticity of sensorimotor circuits extends beyond the affected body part in focal dystonia
  1. Angelo Quartarone (angelo.quartarone{at}
  1. Universitá di Messina, Italy
    1. Francesca Morgante (fmorgante{at}
    1. Universitádi Messina, Italy
      1. Antonino Sant'Angelo (ninosantangelo{at}
      1. Universitá di Messina, Italy
        1. Vincenzo Rizzo (vinceriz{at}
        1. Universitá di Messina, Italy
          1. Sergio Bagnato (sergiobagnato{at}
          1. Fondazione Istituto San Raffaele, Cefalú, Italy
            1. Carmen Terranova (carmen.terranova{at}
            1. Universitá di Messina, Italy
              1. Hartwig Siebner (h.siebner{at}
              1. Christian-Albrechts-University, Germany
                1. Alfredo Berardelli (alfredo.berardelli{at}
                1. Universitý di Roma 'La Sapienza', Italy
                  1. Paolo Girlanda (paolo.girlanda{at}
                  1. Universitá di Messina, Italy


                    Objective: To test whether abnormal sensori-motor plasticity in focal hand dystonia is a primary abnormality or is a mere consequence of the dystonic posture.

                    Methods: We used the paired associative stimulation (PAS) paradigm, an experimental intervention, capable of producing long term potentiation (LTP) like changes in the sensori-motor system in humans. PAS involves transcranial magnetic stimulation (TMS) combined with median nerve stimulation. Ten patients with cranial and cervical dystonia, who showed no dystonic symptoms in the hand, and nine patients with hemifacial spasm (HFS), a non dystonic condition, were compared to ten healthy age-matched controls. Motor-evoked potential (MEP) amplitudes and cortical silent period (CSP) duration were measured at baseline before PAS and for up to 60 min (T0, T30 and T60) after PAS in the abductor pollicis brevis (APB) and first dorsal interosseus (FDI) muscles.

                    Results: Dystonic patients showed a stronger increase in corticospinal excitability than healthy controls and patients with HFS. In addition, patients with dystonia showed a loss of topographical specificity of PAS induced effects, with a facilitation both in median and ulnar innervated muscles. While PAS conditioning led to a prolonged CSP in healthy controls and patients with HFS, it had no effect on the duration of the CSP in patients with cranial and cervical dystonia.

                    Conclusion: Our data suggest that excessive motor cortex plasticity is not restricted to the circuits clinically affected by dystonia but generalizes across the entire sensorimotor system, possibly representing an endophenotipic trait of the disease.

                    • TMS
                    • associative plasticity
                    • dystonia
                    • endophenotype
                    • sensorimotor integration

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