Editors' note: Beware of deep water after subthalamic deep brain stimulation

Abstract

In the article “Beware of deep water after subthalamic deep brain stimulation,” Drs. Waldvogel et al. reported 9 patients who lost their ability to swim after a surgery for deep brain stimulation of the subthalamic nucleus for Parkinson disease (PD). The patients had all been proficient swimmers despite their PD but experienced deterioration of their swimming skills after deep brain stimulation (DBS). In response, Drs. Bouça-Machado et al. contend that such swimming difficulties are seen not only in patients with DBS but also in patients with long-standing PD, citing 2 previous studies—a survey in which most patients noticed a decline in swimming after disease onset with close to half having a drowning/near-drowning episode and a study of swimming styles that found that almost three-quarters of patients could not swim, with most having difficulties with movement, breathing, and positioning during the attempt. In another response, Dr. Sidiropoulos cites a previous case report by Drs. Bangash et al. of profound swimming difficulties in a patient who received DBS in the zona incerta noting that a similar risk may exist with other targets and that the difficulty may be a task-specific dystonia. Dr. Sidiropoulos inquires whether the authors considered DBS reprogramming strategies and requested details about the stimulation parameters, DBS brand, the axial Unified PD Rating Scale (UPDRS) subscores, and PD subtypes for these patients and wonders whether the robust reduction in levodopa dose post-DBS may have related to their worsened swimming abilities. Responding to these comments, the authors note that the patients reported in their study had in fact remained good swimmers despite their PD and only lost their swimming ability after DBS initiation. They report that inter-limb coordination—not dystonia—seemed to be the prominent problem in their patients. They clarify that the swimming difficulties could not be mitigated by reprogramming and do not name the DBS brand, deeming the procedure to be the key factor. They contend that if the swimming difficulties were related to the reduced dopaminergic medications, other motor tasks should also have deteriorated and that their patients showed improvement post-DBS including on axial UPDRS subscores. This exchange highlights the need for continued systematic study of swimming safety in patients with PD—both with and without DBS—and of the underlying pathophysiology of post-DBS swimming difficulties. In the article “Beware of deep water after subthalamic deep brain stimulation,” Drs. Waldvogel et al. reported 9 patients who lost their ability to swim after a surgery for deep brain stimulation of the subthalamic nucleus for Parkinson disease (PD). The patients had all been proficient swimmers despite their PD but experienced deterioration of their swimming skills after deep brain stimulation (DBS). In response, Drs. Bouça-Machado et al. contend that such swimming difficulties are seen not only in patients with DBS but also in patients with long-standing PD, citing 2 previous studies—a survey in which most patients noticed a decline in swimming after disease onset with close to half having a drowning/near-drowning episode and a study of swimming styles that found that almost three-quarters of patients could not swim, with most having difficulties with movement, breathing, and positioning during the attempt. In another response, Dr. Sidiropoulos cites a previous case report by Drs. Bangash et al. of profound swimming difficulties in a patient who received DBS in the zona incerta noting that a similar risk may exist with other targets and that the difficulty may be a task-specific dystonia. Dr. Sidiropoulos inquires whether the authors considered DBS reprogramming strategies and requested details about the stimulation parameters, DBS brand, the axial Unified PD Rating Scale (UPDRS) subscores, and PD subtypes for these patients and wonders whether the robust reduction in levodopa dose post-DBS may have related to their worsened swimming abilities. Responding to these comments, the authors note that the patients reported in their study had in fact remained good swimmers despite their PD and only lost their swimming ability after DBS initiation. They report that inter-limb coordination—not dystonia—seemed to be the prominent problem in their patients. They clarify that the swimming difficulties could not be mitigated by reprogramming and do not name the DBS brand, deeming the procedure to be the key factor. They contend that if the swimming difficulties were related to the reduced dopaminergic medications, other motor tasks should also have deteriorated and that their patients showed improvement post-DBS including on axial UPDRS subscores. This exchange highlights the need for continued systematic study of swimming safety in patients with PD—both with and without DBS—and of the underlying pathophysiology of post-DBS swimming difficulties.