Detection Of Epileptiform Activity Research Articles

Electroencephalographic monitoring in detection and prediction of delayed cerebral ischemia due to non-traumatic subarachnoid hemorrhage

Intensive care of patients with acute non-traumatic subarachnoid hemorrhage primarily relies on diagnostics of delayed cerebral ischemia (DCI). The major difficulty in detecting DCI emerges upon suppression of wakefulness, when clinical assessment of growing neurological deficit becomes complicated. Widely used transcranial dopplerography allows solely to verify a vasospasm development not always leading to DCI exhibiting a multifactorial underlying mechanism. Electroencephalography (EEG) is the only broadly available instrumental tool ensuring a continuous monitoring of cerebral functional status including in subjects at intensive care unit. To date, non-specific EEG parameters pointing at development of acute cerebral injury were identified that provide varying diagnostic and predictive informative value in DCI. We reviewed publications aimed at assessing the data on visual and quantitative EEG parameters such as regional slowing, alpha rhythm spectral power and relative variability, alpha-to-delta power ratio, and detection of epileptiform activity. Having searched international and Russia-wide medical databases, we found only 7 publications quantitatively assessing diagnostic value of EEG monitoring, which showed that for DCI diagnosis its sensitivity ranged from 76% to 100%, and specificity – from 54% to 100%. We also present a clinical case with a 70-year-old female patient who underwent surgery for non-traumatic subarachnoid hemorrhage due to a ruptured aneurysm of the communicating segment of the right internal carotid artery. During the continuous videoEEG monitoring 2 days before clinical deterioration and appearance of ischemic changes in the right cerebral hemisphere on computed tomography scans, an ictal-interictal continuum pattern was noted to emerge. Future studies should be aimed at clarifying and validating the most informative DCI biomarkers including while recording EEG with intracranial electrodes that may contribute to development of automated algorithms for DCI detection.

Epilepsy and epileptiform activity in late-onset Alzheimer disease: clinical and pathophysiological advances, gaps and conundrums.

A growing body of evidence has demonstrated a link between Alzheimer disease (AD) and epilepsy. Late-onset epilepsy and epileptiform activity can precede cognitive deterioration in AD by years, and its presence has been shown to predict a faster disease course. In animal models of AD, amyloid and tau pathology are linked to cortical network hyperexcitability that precedes the first signs of memory decline. Thus, detection of epileptiform activity in AD has substantial clinical importance as a potential novel modifiable risk factor for dementia. In this Review, we summarize the epidemiological evidence for the complex bidirectional relationship between AD and epilepsy, examine the effect of epileptiform activity and seizures on cognition in people with AD, and discuss the precision medicine treatment strategies based on the latest research in human and animal models. Finally, we outline some of the unresolved questions of the field that should be addressed by rigorous research, including whether particular clinicopathological subtypes of AD have a stronger association with epilepsy, and the sequence of events between epileptiform activity and amyloid and tau pathology.

Effective connectivity relates seizure outcome to electrode placement in responsive neurostimulation.

Responsive neurostimulation is a closed-loop neuromodulation therapy for drug resistant focal epilepsy. Responsive neurostimulation electrodes are placed near ictal onset zones so as to enable detection of epileptiform activity and deliver electrical stimulation. There is no standard approach for determining the optimal placement of responsive neurostimulation electrodes. Clinicians make this determination based on presurgical tests, such as MRI, EEG, magnetoencephalography, ictal single-photon emission computed tomography and intracranial EEG. Currently functional connectivity measures are not being used in determining the placement of responsive neurostimulation electrodes. Cortico-cortical evoked potentials are a measure of effective functional connectivity. Cortico-cortical evoked potentials are generated by direct single-pulse electrical stimulation and can be used to investigate cortico-cortical connections in vivo. We hypothesized that the presence of high amplitude cortico-cortical evoked potentials, recorded during intracranial EEG monitoring, near the eventual responsive neurostimulation contact sites is predictive of better outcomes from its therapy. We retrospectively reviewed 12 patients in whom cortico-cortical evoked potentials were obtained during stereoelectroencephalography evaluation and subsequently underwent responsive neurostimulation therapy. We studied the relationship between cortico-cortical evoked potentials, the eventual responsive neurostimulation electrode locations and seizure reduction. Directional connectivity indicated by cortico-cortical evoked potentials can categorize stereoelectroencephalography electrodes as either receiver nodes/in-degree (an area of greater inward connectivity) or projection nodes/out-degree (greater outward connectivity). The follow-up period for seizure reduction ranged from 1.3-4.8 years (median 2.7) after responsive neurostimulation therapy started. Stereoelectroencephalography electrodes closest to the eventual responsive neurostimulation contact site tended to show larger in-degree cortico-cortical evoked potentials, especially for the early latency cortico-cortical evoked potentials period (10-60 ms period) in six out of 12 patients. Stereoelectroencephalography electrodes closest to the responsive neurostimulation contacts (≤5 mm) also had greater significant out-degree in the early cortico-cortical evoked potentials latency period than those further away (≥10 mm) (P < 0.05). Additionally, significant correlation was noted between in-degree cortico-cortical evoked potentials and greater seizure reduction with responsive neurostimulation therapy at its most effective period (P < 0.05). These findings suggest that functional connectivity determined by cortico-cortical evoked potentials may provide additional information that could help guide the optimal placement of responsive neurostimulation electrodes.

Алгоритм детектирования эпилептиформной активности ЭЭГ при отсроченной ишемии головного мозга

An algorithm for automatic detection of epileptiform activity in EEG monitoring data with delayed ischemia after hemorrhage in the subarachnoid space of the brain is proposed and described. The algorithm is based on the formalization of the visual characteristics of epileptiform activity in the form of a peak-wave discharge pattern and analysis of the mutual correlation of multichannel EEG signals with the selected pattern. Fragments of epileptiform activity in each pair of bipolar electrodes were determined from three conditions according to the description of peak-wave discharges of epileptiform activity: 1) the value of positive mutual correlation at the peak of the correlation function should be greater than 0.4; 2) a positive peak of mutual correlation should be followed by a peak with a negative correlation; 3) the width of the peak of negative mutual correlation at half-altitude should be at least 2 times greater than that of the previous positive peak of positive mutual correlation. As with the visual detection of epileptiform activity, the neurophysiologist selected simultaneous peak-wave discharges in several bipolar electrodes. The results of testing the algorithm on an hour-long EEG recording of a patient with delayed ischemia are presented. Fragments with epileptiform activity during the hour under review were identified 17 in the right hemisphere and 2 in the left. Interhemispheric asymmetry is caused by a right-sided aneurysm in patient. The operating time of the algorithm on a modern personal computer is no more than 5 minutes to process 16 bipolar signals, so it can be used to calculate the hourly amount of epileptiform activity in almost real time of the manifestation of this indicator of delayed ischemia after aneurysmal subarachnoid hemorrhage.

Quantitative artifact reduction and pharmacologic paralysis improve detection of EEG epileptiform activity in critically ill patients

ObjectiveEpileptiform activity is common in critically ill patients, but movement-related artifacts—including electromyography (EMG) and myoclonus—can obscure EEG, limiting detection of epileptiform activity. We sought to determine the ability of pharmacologic paralysis and quantitative artifact reduction (AR) to improve epileptiform discharge detection. MethodsRetrospective analysis of patients who underwent continuous EEG monitoring with pharmacologic paralysis. Four reviewers read each patient’s EEG pre- and post- both paralysis and AR, and indicated the presence of epileptiform discharges. We compared the interrater reliability (IRR) of identifying discharges at baseline, post-AR, and post-paralysis, and compared the performance of AR and paralysis according to artifact type. ResultsIRR of identifying epileptiform discharges at baseline was slight (N = 30; κ = 0.10) with a trend toward increase post-AR (κ = 0.26, p = 0.053) and a significant increase post-paralysis (κ = 0.51, p = 0.001). AR was as effective as paralysis at improving IRR of identifying discharges in those with high EMG artifact (N = 15; post-AR κ = 0.63, p = 0.009; post-paralysis κ = 0.62, p = 0.006) but not with primarily myoclonus artifact (N = 15). ConclusionsParalysis improves detection of epileptiform activity in critically ill patients when movement-related artifact obscures EEG features. AR improves detection as much as paralysis when EMG artifact is high, but is ineffective when the primary source of artifact is myoclonus. SignificanceIn the appropriate setting, both AR and paralysis facilitate identification of epileptiform activity in critically ill patients.

Automatic Detection of EEG Epileptiform Abnormalities in Traumatic Brain Injury using Deep Learning.

Traumatic brain injury (TBI) is a sudden injury that causes damage to the brain. TBI can have wide-ranging physical, psychological, and cognitive effects. TBI outcomes include acute injuries, such as contusion or hematoma, as well as chronic sequelae that emerge days to years later, including cognitive decline and seizures. Some TBI patients develop posttraumatic epilepsy (PTE), or recurrent and unprovoked seizures following TBI. In recent years, significant efforts have been made to identify biomarkers of epileptogenesis, the process by which a normal brain becomes capable of generating seizures. These biomarkers would allow for a higher standard of care by identifying patients at risk of developing PTE as candidates for antiepileptogenic interventions. In this paper, we use deep neural network architectures to automatically detect potential biomarkers of PTE from electroencephalogram (EEG) data collected between post-injury day 1-7 from patients with moderate-to-severe TBI. Continuous EEG is often part of multimodal monitoring for TBI patients in intensive care units. Clinicians review EEG to identify the presence of epileptiform abnormalities (EAs), such as seizures, periodic discharges, and abnormal rhythmic delta activity, which are potential biomarkers of epileptogenesis. We show that a recurrent neural network trained with continuous EEG data can be used to identify EAs with the highest accuracy of 80.78%, paving the way for robust, automated detection of epileptiform activity in TBI patients.

Improving Detection of Hippocampal Epileptiform Activity Using Magnetoencephalography.

Magnetoencephalography (MEG) defines the spike-generating zone and provides targets for invasive monitoring with stereotactic electroencephalography. This retrospective, blinded, cross-sectional study determined whether MEG virtual sensors could identify hippocampal epileptiform activity. Using MEG beamformer analysis, virtual sensors were manually placed in bilateral hippocampi and corresponding virtual sensor waveforms were analyzed for the presence of epileptiform activity. These findings were compared with hippocampal stereotactic electroencephalography in the same patients. Concordance was determined using sensitivity and specificity. Thirty patients (mean age 12.5 ± 5.9 years) and 35 hippocampi were included. Patients were also placed into subgroups based on conventional MEG analysis: temporal (n = 19), extratemporal (n = 10), and normal (n = 1). Overall, sensitivity and specificity were 57.9% and 50.0%, respectively (n = 35). Patients with temporal sources based on conventional MEG analysis had sensitivity and specificity of 80.0% and 36.4%, respectively (n = 21). Those with extratemporal sources based on conventional MEG had sensitivity and specificity of 42.9% and 80.0%, respectively (n = 12). When grouped by conventional MEG analysis, virtual sensors can be useful to confirm mesial temporal dipoles seen with conventional analysis. This work may help support the use of MEG for the detection of epileptiform activity in the hippocampus and influence the planning of invasive electrode placement.

The clinical value of long - term electroencephalogram (EEG) in seizure - free populations: implications from a cross-sectional study

BackgroudThis study aimed to explore the clinical value of long - term electroencephalogram (LTM EEG) in seizure-free individuals taking antiepileptic drugs (AEDs) for more than 2 years. We try to look for clinical factors associated with epileptiform activity on LTM EEG in seizure free patients. We hope that the detection of epileptiform activity by the LTM EEG recording can develop the better treatment strategy.MethodsThe LTM EEG recordings of 770 individuals with a definite diagnosis of epilepsy were assessed. Two hundred sixty-two individuals accorded with the inclusion criteria and exclusion criteria. We collect the demographic and clinical information and LTM EEG data of these 262 individuals. We analysed the data by one-way analysis of variance and Cox proportional hazards models.ResultsWe found that more epileptiform activity were found with LTM EEG recording than regular EEG recording in seizure-free individuals. We found several clinical factors could be associated with epileptiform activity on LTM EEG in seizure free patients by a one-way analysis: symptomatic or cryptogenic epilepsy [hazard ratio (HR) = 2.6], history of cerebral trauma (HR = 7.5), and abnormal imaging findings (HR = 3.1). The following factors suggested a correlation between history of cerebral trauma (HR = 2.4) and history of cerebral surgery (HR = 3.4) with epileptiform activity on LTM EEG presentation by multivariate logistic regression analysis.ConclusionsThe study indicated a correlation of a number of factors with abnormal LTM EEG presentation: symptomatic or cryptogenic epilepsy, history of cerebral trauma, history of cerebral surgery, and abnormal imaging findings. The LTM EEG recording may help find epileptiform activity in high risk seizure-free individuals. The individuals need be reevaluated the therapeutic strateagies, and increase the hope to reach real seizure-free.

Clinical and electrocorticographic response to antiepileptic drugs in patients treated with responsive stimulation

ObjectiveThe objective of this study was to explore whether chronic electrocorticographic (ECoG) data recorded by a responsive neurostimulation system could be used to assess clinical responses to antiepileptic drugs (AEDs). MethodsAntiepileptic drugs initiated and maintained for ≥3 months by patients participating in clinical trials of the RNS® System were identified. Such “AED Starts” that produced an additional ≥50% reduction in patient-reported clinical seizure frequency were categorized as clinically beneficial, and the remaining as not beneficial. Electrocorticographic features recorded by the RNS® Neurostimulator were analyzed during three periods: 3 months before the AED Start, first month after the AED Start, and the first 3 months after the AED Start. ResultsThe most commonly added medications were clobazam (n = 41), lacosamide (n = 96), levetiracetam (n = 31), and pregabalin (n = 25). Across all four medications, there were sufficient clinical data for 193 AED Starts to be included in the analyses, and 59 AED Starts were considered clinically beneficial. The proportion of AED Starts that qualified as clinically beneficial was higher for clobazam (53.7%) and levetiracetam (51.6%) than for lacosamide (18.8%) and pregabalin (12%). Across all AED Starts for which RNS ECoG detection settings were held constant, the clinically beneficial AED Starts were associated with a significantly greater reduction in the detection of epileptiform activity (p < 0.001) at 1 (n = 33) and 3 months (n = 30) compared with AED Starts that were not beneficial at 1 (n = 71) and 3 months (n = 60). Furthermore, there was a significant reduction in interictal spike rate and spectral power (1–125 Hz) associated with a clinically beneficial response to an AED Start at 1 (n = 32) and 3 months (n = 35) (p < 0.001). These reductions were not observed at either 1 (n = 59) or 3 months (n = 60) for AED Starts that were not clinically beneficial. ConclusionsSignificant quantitative changes in ECoG data recorded by the RNS System were observed in patients who experienced an additional clinical response to a new AED. While there was variability across patients in the changes observed, the results suggest that quantitative ECoG data may provide useful information when assessing whether a patient may have a favorable clinical response to an AED.

SYNDROMES OF BEHAVIORAL AND SPEECH DISORDERS ASSOCIATED WITH BENIGN EPILEPTIFORM DISCHARGES OF CHILDHOOD ON ELECTROENCEPHALOGRAM

Objective : to assess the role and significance of benign epileptiform discharges of childhood (BEDC) on electroencephalogram (EEG) in development of speech and behaviorial disorders in children. Materials and methods. 90 children aged 3–7 years were included in the study: 30 of them were healthy, 30 had attention deficit hyperactivity disorder (ADHD), and 30 had expressive language disorder (ELD). We analyzed the role of persistent epileptiform activity (BEDC type) in EEG as well as frontal intermittent rhythmic delta activity in the development of some neuropsychiatric disorders and speech disorders in children. Results. We suggest to allocate a special variant of ADHD – epileptiform disintegration of behavior; we also propose the strategies for its therapeutic correction. Conclusion . Detection of epileptiform activity (BEDC type) on EEG in children with ELD is a predictor of cognitive disorders development and requires therapeutic correction, which should be aimed at stimulation of brain maturation. Detection of frontal intermittent rhythmic delta activity in children with ELD requires neurovisualization with further determining of treatment strategy.

PREVENTIVE ANTIEPILEPTIC THERAPY IN PATIENTS WITH TUBEROUS SCLEROSIS

Background . Early detection of epileptiform activity on the electroencephalogram (EEG) and preventive antiepileptic therapy in patients with tuberous sclerosis (TS) help to avoid the development of severe forms of epilepsy as well as cognitive disorders associated with it. Materials and methods . Seventeen patients with TS underwent preventive antiepileptic treatment in the Research and Clinical Institute for Pediatrics named after Y.E Vel’tishev. All patients were diagnosed with TS during their first months of life. The diagnosed was based on the detection of cardiac rhabdomyomas and hypopigmentation spots and then confirmed by a genetic test. Antiepileptic drugs (AED) (vigabatrin in 7 patients, valproic acid in 7 patients and levetiracetam in 2 patients) were administered after detection of epileptiform activity in the routine EEG (EEG was performed monthly). Results . Preventive therapy with valproic acid and levetiracetam was found to be ineffective: 4 out of 7 patients on valproic acid and 1 out of 2 patients on levetiracetam developed epilepsy. All of them were later diagnosed with delayed psychological development and delayed speech development. Among 7 patients receiving vigabatrin, only 1 patient developed epilepsy, but did not have any developmental disorders later. Conclusion . Despite vigabatrin is not registered in the Russian Federation, it should be used as an agent for preventive antiepileptic therapy in patients with TS. This approach ensures more favorable long-term results in terms of cognitive functions and psychological development, thus, providing a better quality of life.

Neuromodulation in the Treatment of Epilepsy.

Neuromodulation devices are used in the treatment of medically refractory epilepsy. This has been defined as epilepsy with persistent seizures despite adequate trials of at least two anti-epileptic drugs (AEDs). In most cases of medically refractory partial epilepsy, the first choice of treatment is resective surgery if the seizure focus can be definitively localized and if surgery can be safely performed without causing intolerable neurologic deficits. Patients with medically refractory epilepsy who are not candidates for potentially curative surgery may benefit from the implantation of a neuromodulation device. While most of these devices require surgical implantation, they provide a significant added seizure reduction without typical medication side effects. Furthermore, the efficacy of these devices continues to improve over years. There are currently no head-to-head trials comparing the different neuromodulation devices but efficacy appears to be roughly similar. The choice of device therefore depends on the type of epilepsy, whether the seizure focus can be identified, and other clinical factors. Vagal Nerve Stimulation (VNS) does not require identification of the seizure focus and also carries an FDA indication for depression. While in the United States VNS is only approved for use in partial epilepsy, it is commonly used off-label to treat generalized seizures as well. VNS delivers stimulation on a scheduled basis, in response to patient activation, or in response to heart rate increases serving as a proxy for seizures. Responsive Neurostimulation (RNS) requires the identification of up to two seizure foci and delivers stimulation only in response to the detection of epileptiform activity. While it requires intracranial placement of electrodes, it allows for long-term monitoring of electrographic seizures and may be effective where VNS has not produced an optimal response. Deep brain stimulation of the anterior nucleus of the thalamus is not FDA approved at this time but is available in Europe and many other parts of the world. While it also carries an indication only for partial epilepsy, it does not require identification of the seizure focus and may be particularly helpful for temporal lobe epilepsy. It also appears effective in cases where VNS has not been sufficiently helpful. The Trigeminal Nerve Stimulation (TNS) system is another treatment modality which is not yet FDA approved but is available in Europe and other countries. Its mechanism of action is similar to the VNS system and it also appears to have anti-depression effects in addition to anti-epileptic benefits. However, the most compelling feature of TNS is that it is not implanted but rather applied to the skin with transdermal electrodes, typically at night.

Detection of epileptiform activity in EEG signals based on time-frequency and non-linear analysis.

We present a new technique for detection of epileptiform activity in EEG signals. After preprocessing of EEG signals we extract representative features in time, frequency and time-frequency domain as well as using non-linear analysis. The features are extracted in a few frequency sub-bands of clinical interest since these sub-bands showed much better discriminatory characteristics compared with the whole frequency band. Then we optimally reduce the dimension of feature space to two using scatter matrices. A decision about the presence of epileptiform activity in EEG signals is made by quadratic classifiers designed in the reduced two-dimensional feature space. The accuracy of the technique was tested on three sets of electroencephalographic (EEG) signals recorded at the University Hospital Bonn: surface EEG signals from healthy volunteers, intracranial EEG signals from the epilepsy patients during the seizure free interval from within the seizure focus and intracranial EEG signals of epileptic seizures also from within the seizure focus. An overall detection accuracy of 98.7% was achieved.

Traumatic brain injury induces rapid enhancement of cortical excitability in juvenile rats.

Following a traumatic brain injury (TBI), 5-50% of patients will develop posttraumatic epilepsy (PTE) with children being particularly susceptible. Currently, PTE cannot be prevented and there is limited understanding of the underlying epileptogenic mechanisms. We hypothesize that early after TBI the brain undergoes distinct cellular and synaptic reorganization that facilitates cortical excitability and promotes the development of epilepsy. To examine the effect of pediatric TBI on cortical excitability, we performed controlled cortical impact (CCI) on juvenile rats (postnatal day 17). Following CCI, animals were monitored for the presence of epileptiform activity by continuous in vivo electroencephalography (EEG) and/or sacrificed for in vitro whole-cell patch-clamp recordings. Following a short latent period, all animals subjected to CCI developed spontaneous recurrent epileptiform activity within 14 days. Whole-cell patch-clamp recordings of layer V pyramidal neurons showed no changes in intrinsic excitability or spontaneous excitatory postsynaptic currents (sEPSCs) properties. However, the decay of spontaneous inhibitory postsynaptic currents (sIPSCs) was significantly increased. In addition, CCI induced over a 300% increase in excitatory and inhibitory synaptic bursting. Synaptic bursting was prevented by blockade of Na(+)-dependent action potentials or select antagonism of glutamate or GABA-A receptors, respectively. Our results demonstrate that CCI in juvenile rats rapidly induces epileptiform activity and enhanced cortical synaptic bursting. Detection of epileptiform activity early after injury suggests it may be an important pathophysiological component and potential indicator of developing PTE.

O16: Detection of epileptiform activity using multi-channel linear prediction coefficients and localization of epileptic foci based on EEG-fMRI data

O16: Detection of epileptiform activity using multi-channel linear prediction coefficients and localization of epileptic foci based on EEG-fMRI data

O17: A novel method to induce human cortical plasticity using cortical disinhibition

O17: A novel method to induce human cortical plasticity using cortical disinhibition

Evaluating accuracy of diagnostic tests with intermediate results in the absence of a gold standard

Intermediate test results often occur with diagnostic tests. When assessing diagnostic accuracy, it is important to properly report and account for these results. In the literature, these results are commonly discarded prior to analysis or treated as either a positive or a negative result. Although such adjustments allow sensitivity and specificity to be computed in the standard way, these forced decisions limit the interpretability and usefulness of the results. Estimation of diagnostic accuracy is further complicated when tests are evaluated without a gold standard. Although traditional latent class modeling can be readily applied to analyze these data and account for intermediate results, these models assume that tests are independent conditional on the true disease status, which is rarely valid in practice. We extend both the log-linear latent class model and the probit latent class model to accommodate the conditional dependence among tests while taking the intermediate results into consideration. We illustrate our methods using a simulation study and a published medical study on the detection of epileptiform activity in the brain.

Brain stimulation for the treatment of epilepsy

Direct brain stimulation is an emerging treatment of epilepsy. Scheduled or responsive stimulation has been applied. The most explored targets for scheduled stimulation are the anterior nucleus of the thalamus and the hippocampus. The anterior nucleus of the thalamus was studied in a large multicenter trial. There was a significant seizure reduction with the stimulator "on" versus "off" during several months after stimulator implantation. The hippocampus as stimulation target has not yet been studied in a large randomized trial. Responsive stimulation applies a stimulus whenever epileptiform activity occurs. It requires on-line detection of epileptiform activity. This concept is based on the observation that epileptiform activity during functional mapping can be aborted by brief pulses of cortical stimulation. Current technology is able to detect seizure activity intracranially on-line and delivers a high frequency stimulus if epileptiform activity is detected. A large randomized multicenter trial has been conducted testing this system for focal epilepsy.

Intracranial Stimulation Therapy for Epilepsy

Epilepsy is a common chronic neurological disorder effecting 1 to 2% of the population. Despite advances in anti-epileptic drug therapy, epilepsy surgery, and vagus nerve stimulation, approximately 30% of patients continue to have seizures. Intracranial stimulation is currently under investigation as an adjunctive treatment to anti-epileptic medications in adults with medically intractable epilepsy. Several different approaches are now being investigated. Specifically, acute and long-term clinical studies have delivered stimulation either to inhibitory regions outside the seizure focus or directly to the seizure focus. These studies have demonstrated the safety of intracranial stimulation and proof of principle in epilepsy patients. In addition to the different locations tested, clinical studies have also used different temporal patterns of stimulation. The majority of studies have used open-loop or scheduled stimulation, in which, stimulation is delivered on a fixed schedule and is independent of electrographic activity. In contrast, a number of recent investigations have demonstrated the feasibility of closed-loop or responsive stimulation, which is stimulation that is contingent upon the detection of epileptiform activity. This chapter will review the acute and long-term clinical studies of intracranial stimulation, including focal, and nonfocal, and open-loop and responsive stimulation. We will also discuss the optimization and safety of therapeutic parameters used in neurostimulation for epilepsy.

Prevalence of epileptiform activity in healthy children during sleep

Background The term epileptiform discharge typically refers to interictal paroxysmal activity that occurs more commonly during sleep. This type of paroxysmal activity does not include the electroencephalographic (EEG) activity observed during a seizure. The prevalence of epileptiform activity in the general pediatric population is unknown. Methods Polysomnographic (PSG) studies were conducted in otherwise healthy children recruited from the general population and with no previous history of seizures or any other medical conditions. All sleep studies included an eight-lead EEG montage. Spike and sharp waves, either alone or accompanied by slow waves, occurring singly or in bursts lasting <5 s were considered as representing epileptiform activity. Results Nine hundred seventy children underwent overnight PSG. In 14 children, evidence of epileptiform activity, in the absence of any additional abnormality in the PSG, occurred. Thus, the prevalence of epileptiform activity was 1.45%. Epileptiform patterns found were either spike or spike and wave and were more prominent during non-rapid eye movement (NREM) sleep, with 11 patients presenting spike and spike and wave patterns in the centro-temporal regions. Four of the six children who underwent neurocognitive tests exhibited abnormal findings in areas of behavior, attention, hyperactivity, and learning. Conclusion Epileptiform activity in otherwise healthy children from the community is relatively frequent and, if confirmed by prospective studies, could be associated with suboptimal cognitive and behavioral functions. Increased awareness by sleep professionals and use of PSG montage that includes temporal leads and >2 standard EEG leads should facilitate the detection of epileptiform activity in children.