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Abstract
Patients with psychiatric symptoms, such as depression, anxiety, and visual hallucinations, may be at increased risk for adverse effects following deep brain stimulation of the subthalamic nucleus for Parkinson’s disease, but there have been relatively few studies of associations between locations of chronic stimulation and neuropsychological outcomes. We sought to determine whether psychiatric history modulates associations between stimulation location within the subthalamic nucleus and postoperative affective and cognitive changes. We retrospectively identified 42 patients with Parkinson’s disease who received bilateral subthalamic nucleus deep brain stimulation and who completed both pre- and postoperative neuropsychological testing. Active stimulation contacts were localized in MNI space using Lead-DBS software. Linear discriminant analysis identified vectors maximizing variance in postoperative neuropsychological changes, and Pearson’s correlations were used to assess for linear relationships. Stimulation location was associated with postoperative change for only 3 of the 18 neuropsychological measures. Variation along the superioinferior (z) axis was most influential. Constraining the analysis to patients with a history of depression revealed 10 measures significantly associated with active contact location, primarily related to location along the anterioposterior (y) axis and with worse outcomes associated with more anterior stimulation. Analysis of patients with a history of anxiety revealed 5 measures with location-associated changes without a predominant axis. History of visual hallucinations was not associated with significant findings. Our results suggest that a history of depression may influence the relationship between active contact location and neuropsychological outcomes following subthalamic nucleus deep brain stimulation. These patients may be more sensitive to off-target (nonmotor) stimulation.
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1 University of Pittsburgh School of Medicine, Department of Psychiatry, Pittsburgh, USA (GRID:grid.21925.3d) (ISNI:0000 0004 1936 9000); University of Pittsburgh School of Medicine, Brain Modulation Laboratory, Department of Neurological Surgery, Pittsburgh, USA (GRID:grid.21925.3d) (ISNI:0000 0004 1936 9000); Stanford University School of Medicine, Department of Psychiatry and Behavioral Sciences, Stanford, USA (GRID:grid.168010.e) (ISNI:0000000419368956)
2 University of Pittsburgh School of Medicine, Brain Modulation Laboratory, Department of Neurological Surgery, Pittsburgh, USA (GRID:grid.21925.3d) (ISNI:0000 0004 1936 9000); University of Pittsburgh School of Medicine, Pittsburgh, USA (GRID:grid.21925.3d) (ISNI:0000 0004 1936 9000)
3 University of Pittsburgh School of Medicine, Brain Modulation Laboratory, Department of Neurological Surgery, Pittsburgh, USA (GRID:grid.21925.3d) (ISNI:0000 0004 1936 9000)
4 College of Medicine, University of Arizona, Department of Psychiatry, Tucson, USA (GRID:grid.134563.6) (ISNI:0000 0001 2168 186X)
5 Massachusetts General Hospital, Department of Neurosurgery, Boston, USA (GRID:grid.32224.35) (ISNI:0000 0004 0386 9924); Harvard Medical School, Boston, USA (GRID:grid.38142.3c) (ISNI:000000041936754X)