LETTER TO THE EDITOR Paroxysmal positive symptoms caused by hardware malfunctioning in deep brain stimulation To the Editor: Hardware complications have been reported since the beginning of deep brain stimulation (DBS) use for Parkinson’s disease. Most reports include infectious complications and disconnections of the DBS system. 1,2 We report an unusual case in which hardware dysfunction was revealed by transient positive symptoms. Its diagnostic, probable cause and management are discussed. A 62-year-old female patient with Parkinson’s disease for 12 years was initially treated by L-dopa leading to good symptomatic control. Motor complications of L-dopa treat- ment started 4 years ago by unpredictable blocks and incapacitating dyskinesia. Bilateral subthalamic nucleus stimulation was proposed after a positive L-dopa test and workup to exclude Parkinson-plus syndromes and associated central nervous system (CNS) diseases. Surgery was per- formed with success (UPDRS III in ‘‘OFF-medication’’ before and in ‘‘OFF-medication-On-stimulation’’ after surgery was 33 and 8, respectively) (Figure 1,A). After 1 year of sustained symptomatic control, she was addressed to the emergency department of our institution with hori- zontal diplopia and paresthesia on the left hand of sudden onset, lasting some seconds, and occurring many times a day. Turning the head to the right side could trigger the symptoms most of the times. A full cardiovascular evaluation excluded cerebrovascular ischemic diseases. The right sub- thalamic nucleus was stimulated monopolarly by using elec- trode 2 as a cathode at 2.7 V, 90 ms, and 130 Hz. Impedance was higher than 4000 U and current bellow 15 mA, whereas during a regular control visit made 1 week earlier, values were 1076 U and of 28 mA, respectively. No trauma or fall was reported. Turning off the stimulation on the right side abolished the paroxystic symptoms but could not be tolerated because of worsening of the parkinsonian symptoms. A decrease in the intensity of stimulation (from 2.7-2.5 V) was then tried. Partial control of parkinsonian symptoms was obtained, with resolution of diplopia and paresthesia. A radiographic study of the system and a computed tomo- graphic (CT)-scan with 3-dimensional reconstruction showed no disconnections or breakages. One week later, an electrode test was performed. Interestingly, stimulation of both lower electrodes (0 and 1) triggered horizontal diplopia and paresthesia of the left hand, even at low current stimula- tions. On this occasion, the impedance and current on elec- trode 2 changed spontaneously from . 4000 U and , 15 mA to 955 U and 28 mA on two consecutive measures on the same week, whereas all other stimulation parameters were unchanged. Considering the strong probability of a hardware malfunctioning, a surgical revision of the system was performed. A breakage proximal to the connection of the DBS electrode with the extension was identified intraopera- tively: the plastic protection was respected, whereas the wire inside was disconnected (Figure 1,B). The DBS elec- trode was replaced and the patient regained symptomatic control after a couple of weeks. Hardware dysfunction is commonly detected after an acute loss of control of parkinsonian symptoms that is not credited to disease evolution or other causes. 2 In most reports, the breakage is present on the extension wires, making the diagnosis straightforward by a radiographic evaluation. 3 The current case is particularly illustrative because the patient presented positive signs in a paroxystic pattern. Interestingly, symptoms could be reproduced when adjacent electrodes were stimulated. This suggests that perhaps the system manifested its defect by an unexpected switch in the stimulating electrodes, leading to intermittent side effects as well as impedance and current changes. It would explain why parkinsonian symptoms were only fairly affected. We conclude from this intermittent side- effect profile that the wire fracture was small enough to allow some current to pass along it, depending on head position. This is supported by the fact that therapy imped- ance and current varied autonomously in the same week. Because radiographic studies did not disclose the discon- nection site, a surgical exploration of the system was necessary. The defect in the DBS wire was located just adjacent to the connection site, which facilitated its detec- tion during surgery. A similar defect located more distally would be more difficult to diagnose. This case underlines that DBS hardware malfunction may manifest itself by intermittent positive symptoms despite the 1935-861X/10/$ -see front matter Ó 2010 Elsevier Inc. All rights reserved. doi:10.1016/j.brs.2009.07.002 Brain Stimulation (2010) 3, 61–2 www.brainstimjrnl.com