title: Bilateral stimulation of nucleus subthalamicus in advanced Parkinson's disease: no effects on, and of, autonomic dysfunction.
abstract: It is not known whether bilateral stimulation of the subthalamic nucleus, performed to improve skeletal motor control in advanced Parkinson's disease, also affects central autonomic regulation of cardiovascular motor function. Furthermore, reduced treatment with dopaminergic and other drugs after bilateral stimulation of the subthalamic nucleus could affect cardiovascular autonomic reflexes and/or other factors controlling blood pressure level. The primary aim of this study was to investigate putative effects of bilateral stimulation of the subthalamic nucleus on the autonomic nervous system, using respiratory heart rate variability and blood pressure responses to tilt as indices. Baseline autonomic tests were performed in 19 patients with Parkinson's disease and 10 matched healthy subjects. Patients were divided in two groups and re-investigated after 1 year of optimized pharmacological treatment (n = 8) or 1 year of bilateral subthalamic nucleus stimulation (n = 11). Both skeletal motor dysfunction and dopaminergic drug treatment were significantly reduced after 1 year of bilateral subthalamic nucleus stimulation. However, heart rate variability as well as blood pressure during tilt was reduced compared to baseline to a similar extent in both patient groups. The number of individual patients showing pathological autonomic test results at 1-year follow-up increased only in the subthalamic nucleus stimulation group. Despite reduced pharmacological treatment and reduced motor disability, bilateral subthalamic nucleus stimulation does not improve cardiovascular autonomic reflex function or protect against development of cardiovascular autonomic failure in Parkinson's disease. Preoperative cardiovascular autonomic reflex dysfunction, conversely, does not exclude an excellent stimulation effect.
authors.affiliation: Institute for Clinical Neuroscience, Sahlgrenska Academy, Gothenburg University, Sweden. bjorn.holmberg@neuro.gu.se
authors.forename: Björn
authors.initials: B
authors.lastname: Holmberg
authors.forename: Olle
authors.initials: O
authors.lastname: Corneliusson
authors.forename: Mikael
authors.initials: M
authors.lastname: Elam
mesh_terms: D000368:Aged; D000978:Antiparkinson Agents / Q000627:therapeutic use; D001342:Autonomic Nervous System Diseases / Q000209:etiology / Q000628:therapy*; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology / Q000528:radiation effects; D016022:Case-Control Studies; D016009:Chi-Square Distribution; D003131:Combined Modality Therapy; D004185:Disability Evaluation; D004599:Electric Stimulation Therapy; D005260:Female; D005500:Follow-Up Studies; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology / Q000528:radiation effects; D006801:Humans; D007980:Levodopa / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D010300:Parkinson Disease / Q000150:complications / Q000628:therapy*; D012189:Retrospective Studies; D012720:Severity of Illness Index; D020531:Subthalamic Nucleus / Q000528:radiation effects*; D016896:Treatment Outcome
chemical_list: D000978:Antiparkinson Agents; D007980:Levodopa