September 13, 2026

@michaelokun

What resonates with me about this important 15-year follow-up is the reminder that when parkinsonism emerges years after GPi DBS for dystonia, we should be cautious about automatically blaming the stimulation. Among 17 patients with isolated generalized dystonia, only 41% maintained a clinically meaningful motor benefit at 15 years, yet disability remained improved, while 94% had parkinsonian signs, predominantly affecting gait, posture and speech, and 67% reported freezing of gait. The particularly provocative finding for me was that greater dystonia severity before DBS strongly predicted later axial parkinsonism, whereas stimulation pulse width showed only a nonsignificant association and total electrical energy delivered was not significantly associated. Parkinsonian features have also been described in people with longstanding dystonia who never received DBS, raising the possibility that what we are seeing may, at least in part, represent the natural evolution or progression of the underlying disease rather than simply an adverse effect of GPi stimulation. At the same time, we cannot completely exonerate DBS: prior reports suggest GPi stimulation can contribute to hypokinetic gait, and pulse-width reduction deserves further study as a programming strategy. Importantly, this study had no preoperative parkinsonism assessment and no OFF-stimulation evaluation, so it cannot establish causality. For me, the message is that long-term DBS care should extend well beyond asking whether the dystonia remains controlled: we need to systematically watch for gait dysfunction, freezing, speech and postural changes, and recognize that disease progression, aging, underlying vulnerability and stimulation may all be contributing to the phenotype we see 15 years later. https://movementdisorders.onlinelibrary.wiley.com/doi/10.1002/mds.70504