Brain stimulation for epilepsy provides an alternative to pharmacotherapy and resective, ablative, or disconnection surgery for patients with medication-resistant epilepsy. Although relatively rarely achieving seizure freedom, these therapies can provide substantial benefits to quality of life, reducing the risk of sudden unexpected death in epilepsy, reducing the burden of common comorbidities, and occasionally reducing antiseizure medication side effects. They also can provide unique insights into epilepsy through ultra-long-term monitoring. Stimulation routes include vagus nerve stimulation, deep brain stimulation, and responsive neurostimulation system, as well as some other novel targets. Due to FDA approval in the United States, this article focuses on vagus nerve stimulation, deep brain stimulation, and responsive neurostimulation system.
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• Responsive neurostimulation system (RNS) provides targeted stimulation to up to 2 locations in the brain.
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• Responsive neurostimulation system can augment typical inpatient telemetry monitoring prior to subsequent neurosurgery.
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• Deep brain stimulation (DBS) requires less precise localization while also providing substantial improvements in seizure frequency and perhaps neurocognitive outcomes.
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• Vagus nerve stimulation (VNS) provides an alternative to intracranial surgery while also providing both seizure frequency improvement and reducing rates of sudden unexpected death in epilepsy (SUDEP).
Historical note and terminology
The first neurostimulation therapy was vagus nerve stimulation in 1988 and it was licensed in 1997. Subsequently, responsive neurostimulation and then deep brain stimulation were shown to be alternatives. Although numerous other targets have been explored, these 3 have earned U.S. Food and Drug Administration (FDA) approval. More recently, other techniques and targets are being explored as adjunctive therapies for epilepsy including focused ultrasound, trigeminal nerve stimulation (TNS), transcranial magnetic stimulation (TMS), transcranial direct current stimulation (TDCS), and chronic subthreshold cortical stimulation.
Each of these technologies share common goals to modify the abnormal network that is associated with epileptic seizures. By stimulating these networks, modulation of the network activity is achieved and, ideally, acute stimulation can stop, shorten, or reduce the spread of epileptic seizures. Chronic stimulation may cause network modification to reduce the propensity for epileptic seizures. In this way, the onset of action can be delayed and maximum efficacy of neurostimulation or neuromodulation technologies can be years after initiation of treatment. The term neuromodulation reflects how the stimulation from these technologies can modify the epileptic network. The unique perspective of each technology also can provide supplemental information about the pathophysiology of epilepsy both on an individual and population level.