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Deep Brain Stimulation for Seizure Control in Drug-Resistant Epilepsy

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Deep Brain Stimulation for Seizure Control in Drug-Resistant Epilepsy NEUROSURGICAL FOCUS Neurosurg Focus 45 (2):E4, 2018 Deep brain stimulation for seizure control in drug-resistant epilepsy Neil Klinger, MD,1,2 and Sandeep Mittal, MD, FRCSC1,2 1Department of Neurosurgery, Wayne State University; and 2Comprehensive Epilepsy Program, Detroit Medical Center, Wayne State University, Detroit, Michigan Antiepileptic drugs prevent morbidity and death in a large number of patients suffering from epilepsy. However, it is estimated that approximately 30% of epileptic patients will not have adequate seizure control with medication alone. Resection of epileptogenic cortex may be indicated in medically refractory cases with a discrete seizure focus in nonelo- quent cortex. For patients in whom resection is not an option, deep brain stimulation (DBS) may be an effective means of seizure control. Deep brain stimulation targets for treating seizures primarily include the thalamic nuclei, hippocampus, subthalamic nucleus, and cerebellum. A variety of stimulation parameters have been studied, and more recent advances in electrical stimulation to treat epilepsy include responsive neurostimulation. Data suggest that DBS is effective for treat- ing drug-resistant epilepsy. https://thejns.org/doi/abs/10.3171/2018.4.FOCUS1872 KEYWORDS medically refractory epilepsy; catastrophic epilepsy; brain stimulation; seizures; epilepsy surgery; responsive neurostimulation PILEPSY has an estimated lifetime prevalence of 7.6 transporter hypothesis, efflux pumps are thought to restrict cases per 1000 persons and an incidence of 68 cas- AED movement into cells and to be overexpressed in pa- es per 100,000 individuals internationally.19 In the tients resistant to AEDs.61 P-glycoprotein (Pgp) is one such E2010 Global Burden of Disease Study, epilepsy was found multidrug transporter that has been implicated in drug-re- to have a worldwide burden second only to migraine head- sistant epilepsy. Significantly increased levels of Pgp have aches among neurological disorders.48 The International been found in patients with medically refractory epilepsy.18 League Against Epilepsy defines drug-resistant epilepsy Among patients with drug-resistant epilepsy, adding surgi- as a failure to achieve sustained seizure freedom after two cal treatment is four times more likely to result in seizure appropriately chosen, tolerated, and scheduled antiepilep- freedom than medical treatment alone.58 A meta-analysis tic drugs (AEDs), whether they are given as monotherapy of long-term (≥ 5 years) seizure freedom after epilepsy or in combination.35 Estimates of patients with drug-resis- surgery revealed that 66% of patients who underwent tem- tant epilepsy are as high as 30% but vary depending on the poral lobe resections were seizure free, though this figure resistance criteria used and are generally slightly lower in was lower among patients requiring extratemporal resec- more developed countries.53 tion.62 A review of nine systematic reviews and two large The mechanism by which the disorder is resistant to case series of patients with intractable epilepsy revealed a AEDs remains incompletely understood. The most preva- median 62.4% of patients to be seizure free after epilepsy lent explanations include the “target hypothesis” and the surgery; however, surgery was found to be less effective “transporter hypothesis.” In the target hypothesis, it is for epilepsy not associated with structural pathology and/ thought that changes in the AED targets, such as ion chan- or extratemporal lesions.31 Better surgical outcomes were nels, lead to decreased drug efficacy. In contrast, in the reported when seizures were associated with hippocampal ABBREVIATIONS AED = antiepileptic drug; ANT = anterior nucleus of thalamus; CMT = centromedian nucleus of thalamus; DBS = deep brain stimulation; ECoG = electro- corticographic; RNS = responsive neurostimulation; SANTE = Stimulation of the Anterior Nucleus of the Thalamus for Epilepsy; STN = subthalamic nucleus; TLE = temporal lobe epilepsy; VNS = vagus nerve stimulation. SUBMITTED February 9, 2018. ACCEPTED April 16, 2018. INCLUDE WHEN CITING DOI: 10.3171/2018.4.FOCUS1872. ©AANS 2018, except where prohibited by US copyright law Neurosurg Focus Volume 45 • August 2018 1 Unauthenticated | Downloaded 10/01/21 01:58 PM UTC Klinger and Mittal FIG. 1. Common targets for DBS in the treatment of epilepsy: thalamic nuclei (CMT, ANT), STN, hippocampus, and cerebellum. sclerosis and benign tumors. Mortality with epilepsy sur- Some literature suggest that at least part of the efficacy gery was reported to be 0.1%–0.5%, and surgery is effec- of DBS may simply be attributable to the lesional effect tive and safe for correctly selected patients. of electrode placement.5,6, 14, 28, 38,64 However, this notion In general, contraindications to epilepsy surgery in- has been experimentally controlled for and debated by clude the lack of a discrete seizure focus, seizure foci in- other groups.20,32, 37, 50,69 For example, a recent study exam- volving eloquent cortex, or significant comorbidities such ined nine patients with refractory epilepsy treated with that the patient is not medically stable for resective sur- DBS.13 These patients were followed up for changes in gery. For patients whose epilepsy is refractory to medi- seizure rates after their stimulator battery had been de- cal therapy and who are not good candidates for resective pleted. Only two patients did not have changes in their epilepsy surgery, other treatment options are available. seizure frequency, whereas seven (78%) had increased Nonsurgical therapies that may reduce seizures in appro- seizure frequency. Interestingly, five of the seven indi- priately selected patients include the administration of a viduals still reported a seizure frequency less than even ketogenic diet and, to a lesser degree, the use of cannabidi- their baseline before DBS, suggesting that a portion of, ol, although current data are conflicting as to their effica- 17,49,72 but not all, seizure relief is due to the lesional effect. cies. Vagus nerve stimulation is less invasive than re- Many structures have been the target of stimulation in sective surgery and improves seizure control in carefully 16,25,47 human trials to improve seizure control (Fig. 1 and Table selected individuals. Deep brain stimulation (DBS) 1), including the ANT,2,20, 39, 57,66 the centromedian nucleus is another promising treatment modality that has shown of the thalamus (CMT),21,52, 60, 64,67 the cerebellum,4,65, 69,75 efficacy in decreasing seizure frequency in patients with the hippocampus,5,7, 14, 15, 30, 68,73 and the subthalamic nucleus refractory epilepsy. (STN).10,26,36,71 Mechanism of Action and Preclinical Data Common DBS Targets Deep brain stimulation’s mechanism of action in treat- Studies on Targeting the ANT ing epilepsy remains poorly understood. Stimulation may, in fact, disrupt pathological network activity by reducing The ANT is divided into the anterodorsal, anteroven- neuronal activity in the stimulated target.43 However, tral, and anteromedial subnuclei, which all have distinct studies have shown complex patterns of excitation as well patterns of connectivity. These include widespread con- as inhibition with DBS.40 Animal studies have demon- nections to the frontal lobes as well as to other members strated that high-frequency stimulation of the anterior nu- of the Papez circuit. The ANT receives inputs from the subiculum, the mammillary bodies via the mammillo- cleus of the thalamus (ANT) leads to cortical desynchro- 29 nization and may be protective against seizures, whereas thalamic tract, and the retrosplenial cortex. This local low-frequency stimulation provokes seizures.45 Rhythmic network has further diffuse cerebral connectivity, which stimulation from DBS has been likened to a pacemaker likely underlies its therapeutic potential for seizure con- that helps to synchronize thalamocortical networks and trol. Most available data suggest that ANT DBS is most prevent the disorganized cortical spread thought to un- useful for the treatment of partial and secondarily general- derlie seizures.33 The optimal stimulation parameters for ized seizures. any given DBS target are largely based on trial-and-error The highest quality data supporting the use of ANT methodologies or the use of parameters that have been DBS comes from the Stimulation of the Anterior Nucleus successful for other DBS targets. For example, some of the Thalamus for Epilepsy (SANTE) trial. Results of studies have demonstrated that the DBS current is more this landmark multicenter, double-blind randomized study important than the stimulation frequency in pilocarpine- of bilateral ANT stimulation were reported in 2010.20 The induced seizure models.24 However, the efficacy of hip- study population consisted of patients ages 18–65 years pocampal stimulation may be driven by the frequency of with partial seizures, including secondarily generalized stimulation and may be independent of stimulation inten- seizures, in whom at least three AEDs had failed. A crite- sity.1 rion for study inclusion was seizures for at least 6 months, 2 Neurosurg Focus Volume 45 • August 2018 Unauthenticated | Downloaded 10/01/21 01:58 PM UTC Klinger and Mittal TABLE 1. Summary of studies using various targets for deep brain stimulation for intractable epilepsy Authors & Year No. Target Stimulation Seizure Outcomes* Fisher et al., 2010; Sala- 110 Bilat ANT 5 V, 90 µsec, 145 Hz; 1 min on/5 mins off 69% nova et al., 2015 Hodaie et al., 2002 5 Bilat ANT 10 V, 90 µsec, 100
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