The differential modulation of the ventral premotor–motor interaction during movement initiation is deficient in patients with focal hand dystonia

Authors

  • Elise Houdayer,

    1. Human Motor Control Section, Medical Neurology Branch, National Institute of Neurological Disorders and Stroke, NIH, 10 Center Drive MSC 1428, Building 10, Room 7D37, Bethesda, MD 20892-1428, USA
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  • Sandra Beck,

    1. Human Motor Control Section, Medical Neurology Branch, National Institute of Neurological Disorders and Stroke, NIH, 10 Center Drive MSC 1428, Building 10, Room 7D37, Bethesda, MD 20892-1428, USA
    2. Department of Neurology and Clinical Neurophysiology, University of Freiburg, Freiburg im Breisgau, Germany
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  • Anke Karabanov,

    1. Human Motor Control Section, Medical Neurology Branch, National Institute of Neurological Disorders and Stroke, NIH, 10 Center Drive MSC 1428, Building 10, Room 7D37, Bethesda, MD 20892-1428, USA
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  • Brach Poston,

    1. Human Motor Control Section, Medical Neurology Branch, National Institute of Neurological Disorders and Stroke, NIH, 10 Center Drive MSC 1428, Building 10, Room 7D37, Bethesda, MD 20892-1428, USA
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  • Mark Hallett

    1. Human Motor Control Section, Medical Neurology Branch, National Institute of Neurological Disorders and Stroke, NIH, 10 Center Drive MSC 1428, Building 10, Room 7D37, Bethesda, MD 20892-1428, USA
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M. Hallett, as above.
E-mail: hallettm@ninds.nih.gov

Abstract

A major feature of focal hand dystonia (FHD) pathophysiology is the loss of inhibition. One inhibitory process, surround inhibition, for which the cortical mechanisms are still unknown, is abnormal in FHD. As the ventral premotor cortex (PMv) plays a key role in the sensorimotor processing involved in shaping finger movements and has many projections onto the primary motor cortex (M1), we hypothesized that the PMv–M1 connections might play a role in surround inhibition. A paired-pulse transcranial magnetic stimulation paradigm was used in order to evaluate and compare the PMv–M1 interactions during different phases (rest, preparation and execution) of an index finger movement in patients with FHD and controls. A sub-threshold conditioning pulse (80% resting motor threshold) was applied to the PMv at 6 ms before M1 stimulation. The right abductor pollicis brevis, a surround muscle, was the target muscle. In healthy controls, the results showed that PMv stimulation induced an ipsilateral ventral premotor–motor inhibition at rest. This cortico-cortical interaction changed into an early facilitation (100 ms before movement onset) and turned back to inhibition 50 ms later. In patients with FHD, this PMv–M1 interaction and its modulation were absent. Our results show that, although the ipsilateral ventral premotor–motor inhibition does not play a key role in the genesis of surround inhibition, PMv has a dynamic influence on M1 excitability during the early steps of motor execution. The impaired cortico-cortical interactions observed in patients with FHD might contribute, at least in part, to the abnormal motor command.

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