Implantation of an Endovenous Pacemaker in a Patient with Parkinson's Disease and Bilateral Deep Brain Stimulators
Author(s) -
Maxime De Guillebon,
Pierre Bordachar,
Jacques Clémenty
Publication year - 2007
Publication title -
clinical medicine cardiology
Language(s) - English
Resource type - Journals
ISSN - 1178-1165
DOI - 10.4137/cmc.s286
Subject(s) - medicine , parkinson's disease , deep brain stimulation , cardiology , disease , anesthesia
Deep brain stimulation (DBS) has recently been introduced as a new surgical option for patients with advanced Parkinson’s disease and drug-refractory disabling motor complications.1 In this procedure, an electrode is implanted in the brain target and connected to a subcutaneous pacemaker. Stimulating the spine at the thoracic or cervical level of the dorsal column has been reported to reduce pain effectively in hitherto untreatable patients.2 With an extended clinical spectrum for neurostimulation therapy, coincidence with an indication for a cardiac pacemaker will potentially increase and raises concerns about possible interactions between the implanted electrical devices. The authors report the case of a 65 year old man with severe Parkinson’s disease who had disabling tremor despite optimal drug therapy. Therefore, he was implanted 10 years ago with a thalamic deep brain stimulator (Medtronic) in both sub-clavicular regions. Stimulation parameters were selected that led to best tremor reduction without side effects (amplitude of 3 V under bipolar stimulation, pulse duration of 90 μsec, and frequency of 140 Hz). The tremor was successfully controlled after 10 years of effective bilateral thalamic deep brain stimulation. He was referred to our centre for repeated syncope. The ECG monitoring revealed episodes of high degree atrioventricular block. There was therefore no alternative to cardiac pacing. A VDD pacemaker was implanted under local anaesthesia in the left subclavicular region on the inside of the DBS device. There were no adverse events during surgery and no evidence of inappropriate sensing through the lead at the atrial or ventricular levels. With programming of bipolar sensing (atrial sensitivity level: 0.4 mV, ventricular sensitivity level: 3.5 mV), we did not
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