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<p>Pallidal deep brain stimulation (DBS) for dystonia can induce bradykinesia. We analyzed retrospective (<i>n</i> = 55) and prospective (<i>n</i> = 11) cohorts to identify risks and anatomical substrates for this side effect. Bradykinesia was prevalent (60–72%), with female sex, older dystonia onset, shorter disease duration, and crucially, stimulation pulse width identified as key predictive factors. Probabilistic mapping isolated a posterolateral globus pallidus internus “sour spot” for bradykinesia, which was spatially distinct from therapeutic “sweet spots” and demonstrated patient-level predictive power in cross-validation (R² = 0.16, <i>p</i> = 0.0013). Kinematic analysis showed reducing stimulation selectively improved movement frequency without altering amplitude. The effect appears mediated by local grey-matter modulation, not major white matter tracts. These findings suggest programming strategies using shorter pulse widths while avoiding the identified sour spot can mitigate bradykinesia without sacrificing antidystonic benefit.</p>

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Bradykinesia induced by pallidal neurostimulation in dystonia: clinical risk factors and anatomical mapping

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年10月23日

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  • Florian Lange,
  • Diego L. Guarin,
  • Stella Mosert,
  • Berenike Karrasch,
  • Jonas Roothans,
  • Benedikt Weigl,
  • Pavel Navratil,
  • Christine Daniels,
  • Thorsten Odorfer,
  • Gregor Brandt,
  • Philipp Mahlknecht,
  • Joachim K. Krauss,
  • Joachim Runge,
  • Andrea A. Kühn,
  • Günther Deuschl,
  • Jens Volkmann,
  • Robert Peach,
  • Martin M. Reich

摘要

Pallidal deep brain stimulation (DBS) for dystonia can induce bradykinesia. We analyzed retrospective (n = 55) and prospective (n = 11) cohorts to identify risks and anatomical substrates for this side effect. Bradykinesia was prevalent (60–72%), with female sex, older dystonia onset, shorter disease duration, and crucially, stimulation pulse width identified as key predictive factors. Probabilistic mapping isolated a posterolateral globus pallidus internus “sour spot” for bradykinesia, which was spatially distinct from therapeutic “sweet spots” and demonstrated patient-level predictive power in cross-validation (R² = 0.16, p = 0.0013). Kinematic analysis showed reducing stimulation selectively improved movement frequency without altering amplitude. The effect appears mediated by local grey-matter modulation, not major white matter tracts. These findings suggest programming strategies using shorter pulse widths while avoiding the identified sour spot can mitigate bradykinesia without sacrificing antidystonic benefit.