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

Abstract

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.