Botulinum toxin modulates cortical maladaptation in post-stroke spasticity

Authors

  • William Huynh MBBS,

    1. Neuroscience Research Australia and Prince of Wales Clinical School, University of New South Wales, Randwick, New South Wales 2031, Australia
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  • Arun V. Krishnan PhD,

    1. School of Medical Sciences, University of New South Wales, Randwick, New South Wales, Australia
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  • Cindy S.-Y. Lin PhD,

    1. School of Medical Sciences, University of New South Wales, Randwick, New South Wales, Australia
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  • Steve Vucic PhD,

    1. Neuroscience Research Australia and Prince of Wales Clinical School, University of New South Wales, Randwick, New South Wales 2031, Australia
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  • Pesi Katrak MBBS,

    1. Rehabilitation Medicine, Prince of Wales Hospital and School of Public Health & Community Medicine, University of New South Wales, Randwick, New South Wales, Australia
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  • Michael Hornberger PhD,

    1. Neuroscience Research Australia and Prince of Wales Clinical School, University of New South Wales, Randwick, New South Wales 2031, Australia
    2. School of Medical Sciences, University of New South Wales, Randwick, New South Wales, Australia
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  • Matthew C. Kiernan DSc

    Corresponding author
    • Neuroscience Research Australia and Prince of Wales Clinical School, University of New South Wales, Randwick, New South Wales 2031, Australia
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  • W.H. is receiving the NHMRC postgraduate medical scholarship (630766).

Correspondence to: M. C. Kiernan; e-mail: m.kiernan@unsw.edu.au

Abstract

Introduction: Maladaptive plasticity involving the unaffected hemisphere (UH) in stroke patients may contribute to post-stroke deficits, including spasticity. We investigated the central and peripheral effects of botulinum toxin in post-stroke spasticity to determine whether there is modulation of cortical processes in the UH. Methods: Transcranial magnetic stimulation and peripheral nerve excitability studies were undertaken in 5 stroke patients with upper limb spasticity before (T1) and 6 weeks after (T2) botulinum injection. Results: Transcranial magnetic stimulation demonstrated inexcitable motor cortices of the affected hemisphere at T1 and T2, and short-interval intracortical inhibition (SICI) in the UH was significantly reduced at T1. At T2, SICI in the UH increased significantly compared with T1, normalizing to controls, and was found to be associated with clinical improvements in spasticity. Peripheral excitability parameters were unchanged after injection. Conclusion: Cortical excitability changes were demonstrated in UH, suggesting that the clinical benefits of botulinum toxin relate to modulation of abnormal central reorganization (maladaptive plasticity) in post-stroke spasticity. Muscle Nerve, 2013

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