Objective: To evaluate the frequency and predictors of parkinsonism after GPi-DBS in dystonia; to describe the clinical characteristics and stimulation changes performed to improve parkinsonism.

Background: Dystonia is a movement disorder characterized by involuntary movements and postures for which deep brain stimulation (DBS) in the internal Globus pallidus (GPi) is an established treatment. Some patients are known to develop parkinsonism after GPi-DBS for dystonia, but no studies have addressed the baseline clinical and DBS-related features in these patients.

Method: A retrospective longitudinal study was conducted in all adult dystonia patients submitted to bilateral GPi-DBS between 2010 and 2021 at the Neuroscience Department of the Hospital Santa Maria (HSM), Lisbon, if at least 6 months of follow-up after DBS were present. Medical records were review for demographic, clinical and surgical variables. A topographic analysis of the Volume of Tissue Activated (VTA) was performed.

Results: A total of 43 patients were included, 22 (51.2%) females, with a mean age of dystonia onset of 26.33 (±22.29) years old and mean age at DBS of 45.35 (±16.97) years old. 28 (68.1%) had generalized dystonia, most commonly idiopathic sporadic (48.8%). Seven patients (16.28%) developed parkinsonism at a mean of 30.43 (±28.66) months after DBS. When fully-blown, FOG was the most frequent sign. In the parkinsonism group (Park), the ring angle of the right hemisphere and the left lead depth were significantly different from the non-parkinsonism group (NoPark) (median 71.30 vs 77.80, p=.03 and median 42 vs 41.5, p=.04, respectively). Each patient was submitted to a mean of 11.43 (±11.03) stimulation changes to improve parkinsonism, which was achieved in 4. In the PARK group VTA’s were significantly more inferior/ventral in left hemisphere.

Conclusion: We found a higher frequency and later occurrence of parkinsonism after GPi-DBS in dystonia than previously reported. Differences in ring angle and electrode depth may induce a ventral shift of the VTA involving different GPi areas and neighbor structures. More ventral GPi activation is known to worsen akinesia and gait and GPi stimulation can alter pedunculopontine (PPN) function and cause FOG. The recruitment of different circuits and, eventually, networks, may be responsible for this adverse event.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/parkinsonism-after-internal-globus-pallidus-deep-brain-stimulation-in-dystonia/