Exploring the relationship between dystonia and STN-DBS in Parkinson's disease: insights from a single-centre cohort.

INTRODUCTION

Motor side effects may emerge after deep brain stimulation (DBS) of the subthalamic nucleus (STN) in Parkinson's disease (PD) patients. Out of 60 PD patients, we observed 16 patients displaying de novo dystonic symptoms after the implantation and 11 dystonic PD patients without benefit from the stimulation. We hypothesized that a common neural pathway may cause dystonia in both conditions. Our study aims to investigate the clinical and connectivity substrates of dystonia after STN-DBS.

METHODS

We divided our cohort into four groups: 16 patients displaying dystonia after STN-DBS, 11 patients with previously known dystonia not improving after surgery, 14 patients with dystonic symptoms relieved by the stimulation and 19 controls who never experienced dystonia. MANOVA was used to compare clinical data and the distance of the active contact center from the STN border among the four groups. Finally, we reconstructed the "sour" spots for dystonic symptoms and the associated structural and functional connectivity using a Parkinsonian normative connectome.

RESULTS

De novo dystonic and not-improved dystonic patients had a statistically significant longer PD duration before surgery (p = 0.001) and a greater active contact-STN distance (p < 0.001). Moreover, the "sour" spots were similar in both groups and structural and functional connectivity profiles were associated with brain areas correlated with dystonia pathophysiology (cerebellum, midbrain, parietal and temporal cortices).

CONCLUSIONS

We formulated a two-hit model for dystonia after STN-DBS: a clinical feature of Parkinsonian patients causes predisposing altered plasticity contributing to dystonic symptoms development when coupled with the stimulation of dystonia-related subcortical and cortical structures.