The Importance of Checking Impedance: Misinterpretation of Deep Brain Stimulation Dysfunction as Epilepsy
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Authors: Marc E. Wolf MD, Christian Blahak MD and Joachim K. Krauss MD
Article first published online: 27 NOV 2015 | DOI: 10.1002/mdc3.12267
DBS of the globus pallidus internus (GPi) has become an accepted treatment for generalized and segmental dystonia.[1-4] Occasionally, side effects such as dysarthria or visual and gait disturbances have been reported, limiting further voltage increase.[2, 5] However, when respecting thresholds, DBS is generally well tolerated. In less than 1%, serious hardware complications, such as lead fractures, may occur.
We report on an 80-year-old woman with tardive segmental dystonia starting at the age of 59 years. After ineffective medical treatment, selective left-sided ramisectomy, and peripheral denervation of the right sternocleidomastoid muscle, dystonia started to involve oromandibular, facial, and periorbital muscles. Therefore, at the age of 76, quadripolar stimulation electrodes (model 3387; Medtronic Inc., Minneapolis, MN) were implanted bilaterally in the posteroventral lateral GPi with CT-guided stereotactic surgery and microelectrode recording and connected to bilateral implantable pulse generators (IPGs) (Soletra model 7426; Medtronic). Stereotactic CT demonstrated appropriate placement of DBS electrodes. Summarized data were reported previously.
The patient was regularly followed postoperatively every 2 months. After several adjustments, stimulation was set to a monopolar mode (second-most distal contacts bilaterally; 130 Hz; 210 μs). The patient experienced sustained clinical benefit with stimulation at 3.2 V (BFM motor score 55 points preoperatively; 16 points 30 months postoperatively). In the further course, voltage was adjusted as needed in order to maintain therapeutic effectiveness. IPG changes resulting from battery depletion were performed after 14 and 35 months, respectively.
After 50 months of chronic and uneventful stimulation, the patient was admitted to a regional hospital with acute tonic spasms of the right face and arm, severe dysarthria, and mild right-sided hemiparesis, interpreted as focal epileptic status with consecutive Todds' hemiparesis. Acute treatment with intravenous phenytoine and levetiracetam resulted in rather little improvement. Logopedic examination revealed difficulties in swallowing requiring adapted alimentation. Acute stroke was ruled out by CT imaging. After 19 days, the patient was discharged with the diagnosis “prolonged focal epileptic status.” At presentation in our DBS outpatient clinic the next day, she still complained about dysarthria and impaired fine motor skills of the right arm. When checking IPG settings, a markedly increased current drain and corresponding drop of therapeutic impedance by 44% were found for the left-sided active electrode contact (Fig. 1A). Electrode impedance revealed reduced impedances on the two distal contacts (0 and 1). After reducing voltage from 4.6 to 2.4 V, symptoms resolved almost completely within minutes. MRI showed correct position of the electrodes (Fig. 1B). Eleven months after the aforementioned event, the IPG device was replaced. Technical evaluation by the manufacturer was unremarkable. We proceeded with asymmetric stimulation intensities permitting balanced effective currents. The patient did well and never reported ictal events or capsular side effects (10-year follow-up).
Figure 1. (A) Voltage, impedance, and current flow over a 13-month period. Voltage was continuously adjusted over time. After the index event (circle), increased current flow/decreased impedance was found for the active left GPi-DBS contact. (B) MRI illustrates correct electrode placement.
Side effects of DBS need to be handled in the daily routine during follow-up of patients with DBS.[2, 6] Symptoms usually do not occur spontaneously, but during adaptation of stimulation parameters with the aim to optimize the treatment effect on dystonia. Epileptic seizures after DBS electrode implantation have been reported infrequently. Most cases were related to intra- and perioperative complications. The risk has been estimated at <2.4% perioperatively and <0.5% during follow-up.
To our best knowledge, a spontaneous acute overstimulation of the GPi mimicking a focal epileptic status has not been reported previously. The acute spasms of the right face/arm associated with typical worsening of articulation were the result of a spontaneous current increase at the contralateral electrode contact with capsular stimulation. This is supported by two clinical aspects: First, the deficit did not improve significantly with a potent antiepileptic treatment; second, the reduction of DBS intensity resulted in acute improvement of symptoms within minutes.
The pitfalls of management in this case are rather instructive: In DBS patients with new/unusual symptoms, stimulation settings should be checked early. Neglect of DBS-related complications resulted in a long hospitalization requiring several therapeutic approaches and had relevant impact on patients' quality of life. Furthermore, when considering epilepsy as differential diagnosis, EEG might have been useful to exclude ictal activity, despite potential DBS-related artefacts.
The cause of the acute spontaneous increase of current remains unclear. Technical evaluation of the IPG after battery change was unremarkable, and with the new device the impedance of the left lead remained reduced compared to the contralateral side. However, the reduced impedance on the two distal contacts is rather suggestive of a short circuit, which would explain the capsular side effect by the extended field, including the additional distal functionally active contact. Acute changes of tissue conductance nearby the electrode are unlikely after >4 years of chronic DBS.
Concluding, in patients with DBS and suspicion of a prolonged focal epileptic seizure, the neurostimulation system should be checked carefully in the acute situation to detect and correct a potential dysfunction and achieve a rapid relief from symptoms caused by capsular stimulation.