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Objective The epileptic baboon provides an animal model for juvenile myoclonic epilepsy (JME), demonstrating spontaneous generalized tonic‐clonic seizures (GTCS) in addition to generalized myoclonic, absence and multifocal seizures. While photoconvulsive responses have been described in this model, spontaneous GTCS have not been characterized. Methods In this study, we characterized 46 seizures in 7 epileptic baboons (5 females, 12 ± 3 years old) by video recording. While housed in single cages, the baboons were monitored for a median of 2 (range 1‐10) weeks, with high‐resolution, infrared‐capable camera systems. Each GTCS was evaluated for evidence of preconvulsive ictal symptoms, focal convulsive behaviors, duration of the preconvulsive and convulsive periods, postictal immobility, and recovery of an upright posture. The circadian pattern of GTCS was also for each baboon. Results More than half of GTCS occurred in sleep, beginning from an upright position in all but one tethered baboon. Focal semiological findings were noted in 19 (41%) GTCS, and these included preconvulsive focal ictal motor behaviors as well as lateralized motor activity during the convulsions. The convulsive portion lasted 47 ± 10 seconds, whereas the entire seizure lasted 54 ± 21 seconds. Postictally, the baboons remained immobile for a median latency of 40 (range 14‐347) seconds, recovering an upright posture after 173 (range 71‐1980) seconds. GTCS demonstrated circadian patterns in all but one baboon, with 34 (74%) all seizures occurring between 1‐9 am. Significance GTCS in the baboon revealed intersubject variability, but semiology remained stereotyped in a given baboon. Similar to GTCS in people with JME, focal symptoms were also observed in epileptic baboons. The postictal recovery period, characterized by postictal immobility and myoclonus as well as time to recumbency, also varied among baboons.

Objectives Nonhuman primates (NHPs) are model organisms for understanding the pathophysiology and treatment of epilepsy in humans, while data from human patients informs the diagnosis and treatment of NHP with seizures and epilepsy. We reviewed the literature and surveyed veterinarians at zoos and NHP research centers to (a) better define the range of seizures and epilepsy in NHP, (b) understand how NHPs can inform our knowledge of the pathophysiology and treatment of epilepsy in humans, and (c) identify gaps of knowledge and develop more effective guidelines to treat seizures and epilepsy in NHP. Methods We searched PrimateLit, PubMed, and Google Scholar for studies on experimental models of epilepsy in NHPs and on naturally occurring seizures and epilepsy in NHPs in captivity. In addition, we created a survey to assess methods to diagnose and treat epilepsy in NHPs. This survey was sent to 41 veterinarians at major international zoos and research facilities with NHP populations to study seizure phenomenology, diagnostic criteria for seizures and epilepsy, etiology, and antiseizure therapies in NHPs. Results We summarize the data from experimental and natural models of epilepsy in NHPs and case reports of epilepsy of unknown origin in captive primates. In addition, we present survey data collected from veterinarians at eight zoos and one research facility. Experimental data from NHP epilepsy models is abundant, whereas data from primates who develop epilepsy in the wild or in zoos is very limited, constraining our ability to advance evidence-based medicine. Significance Characterization of seizure or epilepsy models in NHPs will provide insights into mechanisms and new therapies that cannot be addressed by other animal models. NHP research will better inform species-specific diagnoses and outcomes.

Before the development of experimental murine and rodent models of epilepsy, photosensitivity provided a promising platform for testing antiepileptic therapies. Animal models, particularly the epileptic baboon and domestic fowl were used to evaluate the efficacy of antiepileptic medications. A more recently characterized natural animal model of photosensitivity, namely the Rhodesian Ridgeback, may offer the most easily available platform for this purpose. While the underlying genotypes may differ among the three models, they share underlying mechanisms and networks. This chapter will provide a comprehensive review of these three natural animal models and their contributions to our understanding of photosensitivity. The chapter will also explore how these models may be best utilized in the future and the potential role for experimental knock-in or knockout experimental genetic models of photosensitivity, including zebra fish and the Mediterranean fruit fly.

Background Tuberous sclerosis complex (TSC) is an autosomal dominant genetic condition that involves abnormalities of the skin, hamartomas in the heart, brain, and kidneys, seizures, as well as TSC‐associated neuropsychiatric disorders (TAND). About 90%–95% of individuals with TSC will have an identifiable pathogenic variant in either TSC1 or TSC2. We present here two family members with clinical diagnoses of TSC that were later determined to be due to two different genetic etiologies. Methods A 2‐year‐old Caucasian female (Patient 1) was born to non‐consanguineous healthy parents and was determined to have a clinical diagnosis of TSC at 2 months old. Her paternal great‐uncle (Patient 2) was also known to have a clinical diagnosis of TSC. Sequencing and deletion/duplication analysis for TSC1 and TSC2 were performed on both individuals. Results Mutation analysis revealed that both Patient 1 and Patient 2 had identifiable pathogenic variants in TSC2. Patient 1 had c.4800_4801delTG (p.Cys1600Trpfs*2), while Patient 2 had c.4470_4471delinsTT (p.Glu1490_Lys1491delinsAsp*). Conclusion To our knowledge, our clinical report is of significance as it is the third kindred to be identified with affected members with two distinct genetic etiologies for TSC. Our case report highlights the importance of incorporating genetic testing into the clinical evaluation for individuals with features suggestive of TSC., Our clinical report is of significance as no other family has been reported in the medical literature with two clinical individuals with tuberous sclerosis complex (TSC) caused by two distinct genetic etiologies. Patient 2 is the paternal great‐uncle to Patient 1, yet they have different pathogenic variants in TSC2. This report highlights the importance of incorporating genetic testing into the clinical evaluation for individuals with features suggestive of TSC.

Epilepsy is a common neurological disorder associated with increased morbidity and mortality, including premature death from different causes. Sudden unexpected death in epilepsy, or SUDEP, is one of the most common causes of death in people with epilepsy and originally brought to light by medical examiners. It accounts for 5% to 30% of all deaths in individuals with epilepsy and up to 50% in individuals with medically refractory epilepsy. It is commonly associated with a history of generalized tonic-clonic seizures and may be mitigated by other electroclinical risk factors, such as postictal electroencephalographic suppression, prone position, altered heart rate variability, conduction abnormalities, gender, or antiepileptic medications, to name a few. More recently, potential neuroimaging biomarkers have also been identified. Still, despite the increased mortality risk in people with epilepsy due to SUDEP, little is known about its underlying pathophysiology. The pathogenesis is likely to be multifactorial, resulting in neurogenic pulmonary edema or, in some cases, fatal cardiac arrhythmias. Medical examiners can provide an important role in our understanding of the magnitude of the problem and ongoing research into the underlying mechanisms. In this review, we discuss diagnostic criteria, incidence, risk factors, and current theories regarding the pathophysiology of SUDEP.

The epileptic baboon provides a natural model of idiopathic generalized epilepsy (IGE) and sudden unexpected death in epilepsy (SUDEP). This retrospective, case-controlled study aims to evaluate cardiac biomarkers of epilepsy, specifically QT-interval prolongation and heart rate variability (HRV), in pedigreed, captive baboons undergoing scalp electroencephalography (EEG). We retrospectively identified 21 epileptic (9 females, mean age 11.4 +/− 5.4 years) and 19 asymptomatic control (12 females, mean age 10.5 +/− 6.3 years) baboons, who had undergone scalp EEG studies with an artifact-free, ten-beat electrocardiogram (ECG) sample. All baboons were sedated with subanesthetic doses of ketamine prior to electrode placement. PR-, QT- and RR-intervals were measured, and QTcF (Fridericia-corrected QT duration) and RMSSD (root mean square of successive differences between RR-intervals, representative of HRV) values were compared between the groups. The epilepsy group had significantly prolonged QT and QTcF intervals (p=0.005) compared to controls. RMSSD values were non-significantly decreased in epileptic baboons compared to the control group. This study demonstrates cardiac repolarization anomalies and reduction of HRV in epileptic baboons, providing new cardiac biomarkers in pedigreed baboons and potential risk factors for SUDEP.

Introduction Epilepsy affects about 1% of the world’s population (over 50 million). Of these, one-third have refractory or medication-resistant epilepsy. This group of people drives the development and testing of new interventions for epilepsy. To better address the needs of people with epilepsy, the characteristics of clinical trials, as well as the gaps in the population of interest, need to be evaluated. Methods We searched the www.ClinicalTrials.gov database using the keywords “seizure” or “epilepsy” between 9/1/2008−9/1/2018 and filtering for Interventional Clinical trials. The data were categorized by three equal time intervals (tertiles), and evaluated by type of intervention (behavioral, diet, device, drug, other), primary purpose (treatment, diagnosis, prevention, or basic science), gender, age, phase (Phase1 to Phase 4 trials), length and status of the study, enrollment/recruitment/randomization, location, blinding status, assignment group (single/parallel/crossover/factorial/sequential), and funding. We focused on drugs and devices and used a binary logistic regression model to analyze the role of time, length of study, funding, location, randomization, and age. Results We found 359 epilepsy clinical trials; of these, 245 (68.2%) clinical trials involved drugs, and 55 (15.3%) were device trials. Over the three tertiles, the percentage of device trials increased while medication trials decreased. Device:drug trial odds ratios increased six times by the third tertile. Also, the results showed that clinical trials for drugs and devices occurred more in adults than children. Industry funding decreased 20% over time. The US contribution to clinical research was stable, but device trials were more likely to occur outside of the US. Conclusion Drugs constitute the substantial fields of interventional trials in epilepsy but decreased in proportion over the last decade, while the presence of the device trials steadily increased. Device trials focused on treatment and diagnosis of seizures and have been more invested in non-US countries.

This article critiques the International League Against Epilepsy (ILAE) 2015-2017 classifications of epilepsy, epileptic seizures, and status epilepticus. It points out the following shortcomings of the ILAE classifications: (1) they mix semiological terms with epileptogenic zone terminology; (2) simple and widely accepted terminology has been replaced by complex terminology containing less information; (3) seizure evolution cannot be described in any detail; (4) in the four-level epilepsy classification, level two (epilepsy category) overlaps almost 100% with diagnostic level one (seizure type); and (5) the design of different classifications with distinct frameworks for newborns, adults, and patients in status epilepticus is confusing. The authors stress the importance of validating the new ILAE classifications and feel that the decision of Epilepsia to accept only manuscripts that use the ILAE classifications is premature and regrettable.

This educational review describes the classification of paroxysmal events and a four-dimensional epilepsy classification system. Paroxysmal events are classified as epileptic and non-epileptic paroxysmal events. Non-epileptic events are, in turn, classified as psychogenic and organic paroxysmal events. The following four dimensions are used to classify epileptic paroxysmal events: ictal semiology, the epileptogenic zone, etiology, and comorbidities. Efforts are made to keep these four dimensions as independent as possible. The review also includes 12 educational vignettes and three more detailed case reports classified using the 2017 classification of the ILAE and the four-dimensional epilepsy classification. In addition, a case is described which is classified using the four-dimensional epilepsy classification with different degrees of precision by an emergency department physician, a neurologist, and an epileptologist. [Published with video sequences on www.epilepticdisorders.com].

Since lacosamide was approved as an adjuvant agent for the treatment of medically refractory focal epilepsy over ten years ago, it is becoming more widely used for the treatment of idiopathic (genetic) generalized epilepsies. Several studies have demonstrated efficacy in reducing primary generalized tonic-clonic seizures (GTCS), but efficacy is less well-characterized for myoclonic and absence seizures. A 29-year-old man with juvenile myoclonic epilepsy and medically refractory GTCS on a combination of levetiracetam and topiramate was started on lacosamide adjunctive therapy with the plan to replace topiramate. While his GTCS became controlled, he was witnessed to have confusional episodes, with waxing and waning responsiveness, lasting a few days, several times a month. After eight months of adjunctive lacosamide therapy, he was admitted to the epilepsy monitoring unit, where paroxysms of generalized spike-and-wave complexes, lasting for 30-90 minutes, were recorded, interrupted only by sleep. During these periods, he demonstrated psychomotor slowing and disorientation on examination. The absence status was successfully broken by lorazepam, and lacosamide was discontinued. The patient had no further confusional episodes at the most recent follow-up visit, four months after discharge.

We evaluated the spatiotemporal distribution of photic driving (PDR), photoparoxysmal (PPR), and photoconvulsive (PCR) responses recorded by intracranial electrodes (ic-EEG) in a patient with generalized photosensitivity and right frontal lobe cortical dysplasia. Intermittent light stimulation (ILS) was performed thirteen times in nine days. Cortical responses to ILS recorded by ic-EEG were reviewed and classified as PDRs, PPRs, and PCRs. Photic driving responses were restricted to the occipital lobe at ILS frequencies below 9Hz, spreading to the parietal and central regions at >9Hz. Photoparoxysmal responses commonly presented as focal, medial occipital, and parietal interictal epileptic discharges (IEDs), the latter propagating to the sensorimotor cortices. Generalized IEDs were also generated in the setting of PPRs. Photoconvulsive responses, characterized by repetitive bilateral upper extremity myoclonus sustained until the end of the stimulus, were associated with propagation of the medial parieto-occipital discharge to the primary sensorimotor and supplementary area cortices, while generalized myoclonic seizures were associated with a generalized spike-and-wave discharge with an interhemispheric posterior cingulate onset sparing the sensorimotor cortices. Both types of PCR could occur during the same stimulus. Regardless of the pathway, PCRs only occurred when PDRs involved the parietal cortices. While there may be more than one pathway underlying PCRs, parietal lobe association cortices appear to be critical to their generation.

Purpose Since the approval of Vagal Nerve Stimulation (VNS) Therapy for medically refractory focal epilepsies in 1997, it has been also reported to be effective for a wide range of generalized seizures types and epilepsy syndromes. Instead of conventional VNS Therapy delivered at 20–30 Hz signal frequencies, this study evaluates efficacy and tolerability of high-frequency burst VNS in a natural animal model for genetic generalized epilepsy (GGE), the epileptic baboon. Methods Two female baboons (B1 P.h. Hamadryas and B2 P.h. Anubis x Cynocephalus) were selected because of frequently witnessed generalized tonic-clonic seizures (GTCS) for VNS implantation. High-frequency burst VNS Therapy was initiated after a 4–5 week baseline; different VNS settings (0.25, 2 or 2.5 mA, 300 Hz, 4 vs 7 pulses, 0.5–2.5 s interburst interval, and intermittent stimulation for 1–2 vs for 24 h per day) were tested over the subsequent 19 weeks, which included a 4–6 week wash-out period. GTCS frequencies were quantified for each setting, while seizure duration and postictal recovery times were compared to baseline. Scalp EEG studies were performed at almost every setting, including intermittent light stimulation (ILS) to evaluate photosensitivity. Pre-ILS ictal and interictal discharge rates, as well as ILS responses were compared between trials. The Novel Object test was used to assess potential treatment effects on behavior. Results High-frequency burst VNS Therapy reduced GTCS frequencies at all treatment settings in both baboons, except when output currents were reduced (0.25 mA) or intermittent stimulation was restricted (to 1–2 h/day). Seizure duration and postictal recovery times were unchanged. Scalp EEG studies did not demonstrate treatment-related decrease of ictal or interictal epileptic discharges or photosensitivity, but continuous treatment for 120–180 s during ILS appeared to reduce photoparoxysmal responses. High-frequency burst VNS Therapy was well-tolerated by both baboons, without cardiac or behavioral changes. Repetitive muscle contractions involving the neck and left shoulder girdle were observed intermittently, most commonly at 0.5 interburst intervals, but these were transient, resolving with a few cycles of stimulation and not noted in wakefulness. Conclusions This preclinical pilot study demonstrates efficacy and tolerability of high-frequency burst VNS Therapy in the baboon model of GGE. The muscle contractions may be due to aberrant propagation of the stimulus along the vagal nerve or to the ansa cervicalis, but can be reduced by minimal adjustment of current output or stimulus duration.

There are at least five types of alterations of consciousness that occur during epileptic seizures: auras with illusions or hallucinations, dyscognitive seizures, epileptic delirium, dialeptic seizures, and epileptic coma. Each of these types of alterations of consciousness has a specific semiology and a distinct pathophysiologic mechanism. In this proposal we emphasize the need to clearly define each of these alterations/loss of consciousness and to apply this terminology in semiologic descriptions and classifications of epileptic seizures. The proposal is a consensus opinion of experienced epileptologists, and it is hoped that it will lead to systematic studies that will allow a scientific characterization of the different types of alterations/loss of consciousness described in this article.

Focal seizures represent aberrant electrical rhythms that originate in a specific cortical region, the seizure onset zone (SOZ), and propagate in a network of anatomically connected regions. MRI has emerged as a leading diagnostic methodology in the field of epilepsy over the last 20 years and has significantly impacted the surgical evaluation of patients with medically refractory focal epilepsy. However, thus far clinical MRI has largely been used as a structural tool, and there is an interest in developing MRI-based measures of seizure propagation and inter-regional connectivity. Resting state functional connectivity MRI (rsfMRI) allows identification of macroscopic brain networks based on functional connectivity, or co-activation, within regions (nodes) comprising the network. Functional connectivity (FC) describes the temporal correlation between spatially remote neurophysiologic events, and has been measured using different modalities including rsfMRI. Given the network characteristics of epilepsy, there has been an interest in applying rsfMRI to examine the seizure-generating regions of the brain and their functional interactions with other parts of the brain. In this review, we have focused on focal epilepsy, one of the two subtypes of epilepsy by physiology. Most studies of focal epilepsy, with notable exceptions, reported reduced functional connectivity of epilepsy producing and propagating regions, as well as associated reduction in functional connectivity of networks performing cognitive functions including memory, attention and language. We also reviewed reports of early applications of rsfMRI to lateralize/localize epileptic activity. Overall, resting state functional connectivity MRI (rsfMRI) has already contributed to a better understanding of epilepsy-related networks and promises to add to the non-invasive evaluation of patients with a non-lesional clinical MRI.

The epileptic baboon, once studied because of its photosensitivity, has regained importance as a model for human genetic generalized epilepsy (GGE). Because of its electroclinical presentation, natural history, and response to antiepileptic medications, the genetic epilepsy closely resembles juvenile myoclonic epilepsy (JME). By combining intracranial EEG, structural, and functional MRI, it is evident that the occipital lobe plays a more central role in the baboon model of epilepsy, not only by mediating the photoepileptic response, but as a generator of ictal and interictal epileptic discharges. In contrast to earlier hypotheses suggesting that GGE in baboons and humans is due to an abnormal frontothalamic network, changes in cortical structure, whether developmental or seizure-induced, and in functional connectivity, indicate a more diffuse, multilobar disease. In this chapter, we will review EEG, neuroimaging findings, and histopathology in the epileptic baboon, exploring new directions of research into epileptogenesis, behavioral complications, and mortality associated with epilepsy, as well as novel therapies for GGE.

Summary Brain MRI studies in people with idiopathic generalized epilepsies demonstrate regional morphometric differences, though variable in magnitude and location. As the baboon provides an excellent electroclinical and neuroimaging model for photosensitive generalized epilepsy in humans, this study evaluated MRI volumetric and morphometric differences between baboons with interictal epileptic discharges (IEDs) on scalp EEG and baboons with normal EEG studies. Seventy-seven baboons underwent high-resolution brain MRI and scalp EEG studies. The scans were acquired using an 8-channel primate head coil (Siemens TRIO 3T scanner, Erlangen, Germany). After spatial normalization, sulcal measurements were obtained by object-based-morphology methods. One-hour scalp EEG studies were performed in animals sedated with ketamine. Thirty-eight (22F/16M) baboons had normal EEGs (IED−), while 39 (22F/17M) had generalized IEDs (IED+). The two groups were compared for age, total brain volume, and sulcal areas (Hotelling's Trace) as well as between-subjects comparison of 11 individual sulcal areas (averaged between left and right hemispheres). There were no differences between IED− and IED+ groups with respect to age or total brain (gray or white matter) volume, and multivariate tests demonstrated a marginally significant decrease of sulcal areas in IED+ baboons ( p =0.075). Tests of between-subjects effects showed statistically significant decreases in the intraparietal ( p =0.002), central ( p =0.03) and cingulate sulci ( p =0.02), and marginal decreases involving the lunate ( p =0.07) and superior temporal sulci ( p =0.08). Differences in sulcal areas in IED+ baboons may reflect global developmental abnormalities, while decreases of areas of specific sulci reflect anatomical markers for potential generators or cortical nodes of the networks underlying spontaneous seizures and photosensitivity in the baboon.

Summary Objective Automatic detection of generalized tonic–clonic seizures (GTCS) will facilitate patient monitoring and early intervention to prevent comorbidities, recurrent seizures, or death. Brain Sentinel (San Antonio, Texas, USA) developed a seizure-detection algorithm evaluating surface electromyography (sEMG) signals during GTCS. This study aims to validate the seizure-detection algorithm using inpatient video–electroencephalography (EEG) monitoring. Methods sEMG was recorded unilaterally from the biceps/triceps muscles in 33 patients (17white/16 male) with a mean age of 40 (range 14–64) years who were admitted for video-EEG monitoring. Maximum voluntary biceps contraction was measured in each patient to set up the baseline physiologic muscle threshold. The raw EMG signal was recorded using conventional amplifiers, sampling at 1,024 Hz and filtered with a 60 Hz noise detection algorithm before it was processed with three band-pass filters at pass frequencies of 3–40, 130–240, and 300–400 Hz. A seizure-detection algorithm utilizing Hotelling's T-squared power analysis of compound muscle action potentials was used to identify GTCS and correlated with video-EEG recordings. Results In 1,399 h of continuous recording, there were 196 epileptic seizures (21 GTCS, 96 myoclonic, 28 tonic, 12 absence, and 42 focal seizures with or without loss of awareness) and 4 nonepileptic spells. During retrospective, offline evaluation of sEMG from the biceps alone, the algorithm detected 20 GTCS (95%) in 11 patients, averaging within 20 s of electroclinical onset of generalized tonic activity, as identified by video-EEG monitoring. Only one false-positive detection occurred during the postictal period following a GTCS, but false alarms were not triggered by other seizure types or spells. Significance Brain Sentinel's seizure detection algorithm demonstrated excellent sensitivity and specificity for identifying GTCS recorded in an epilepsy monitoring unit. Further studies are needed in larger patient groups, including children, especially in the outpatient setting.

Purpose : To study the relationship of complex febrile seizures (CFS) in the evolution of mesial temporal sclerosis. Methods : We studied five children 22–68 (mean 44) months old with MRI volumetry 2 days–46 months after their first CFS, and compared total hippocampal volumes and right to left hippocampal volume ratios to those of 11 controls, 15–83 (mean 55) months old, who had MRI for complaints which turned out to be neurologically insignificant. Results : In control children, total hippocampal volumes increased linearly with age, while right to left hippocampal volume ratios tended to decrease with age. In children with CFS total hippocampal volumes tended to be smaller than in controls. Right to left ratios were greater than 1 in all five children with CFS compared to seven of 11 controls. Hippocampal asymmetry was noted in only one child, with the right to left volume ratio exceeding two standard deviations from the control mean. The MRI of this child also demonstrated a subarachnoid cyst in the left frontocentral region, ipsilateral to the smaller hippocampus. Visual inspection of the remaining patients revealed no definite structural cortical abnormalities. None of the children developed subsequent afebrile seizures during the brief follow-up period. Conclusions : Hippocampal volumetry in controls revealed a linear increase in total hippocampal volumes and a statistically nonsignificant trend toward reduced right larger than left hippocampal ratios between 17 and 83 months old. The tendency for smaller total hippocampal volumes and larger right to left hippocampal volume ratios in children with CFS compared to controls could suggest a developmental abnormality, injury during CFS, or be age-related. The significant hippocampal asymmetry in a single child with CFS suggests that age may not be a factor in every case. Further studies are needed to collect control data in young children as well as prospectively follow children with CFS with serial imaging to better understand the relationship between CFS and the evolution of hippocampal atrophy.

Background Status epilepticus (SE) is a medical emergency, as deleterious long-term effects are well known. Medically induced burst suppression is often required if first-line and second-line treatments fail. Surgical intervention can be considered in some patients after prolonged treatment failure of medically induced coma. Multiple surgical options for terminating SE have been demonstrated in the literature, with only 2 reports including hemispherectomy in adults. Case Description We present 2 cases of adults with refractory SE who failed more conservative medical/surgical treatment but responded to functional hemispherectomy. Pertinent electroencephalography and imaging findings are discussed. In addition, all previously published pediatric and adult cases are briefly reviewed. Conclusions Functional hemispherectomy can be considered in patients, including adults, with super-refractory SE and diffuse hemispheric onset. We report acceptable outcomes and quality of life in our 2 patients.

Epilepsy is a condition of recurrent seizures that are not caused by some other medical condition. Over 1.5 million people in the United States have been diagnosed with epilepsy, with about 150,000 new diagnoses each year. Antiepileptic drugs (AED) are the most common therapy used to treat epilepsy. There are a number of AED. The one chosen by the physician for a particular patient is based on several factors. These include the type of epilepsy the patient has, how likely the medicine is to work for that patient, and the side effects the medication may cause. Another thing to keep in mind is that many other medications, prescription and over the counter, may interfere with how well AED work. They may increase or decrease the amount of AED in the blood and brain, which in turn can lead to more seizures or side effects. More information about epilepsy can be found on the next page. In this issue of Neurology , investigators study the use of complementary or alternative therapies (CAM) by patients with epilepsy. “Complementary” and “alternative” are medications that are available over the counter without a prescription. They are not covered by medical insurance. Many have not been tested in scientific studies for how well they work or how safe they are. One goal of this study was to find out how often people with epilepsy use CAM. Other goals were to find out whether physicians knew whether their patients were using CAM and whether physicians even recognized more commonly used CAM. This study also gathered information about the effects of CAM use on seizure control and quality of life in patients with epilepsy. A 40-question survey was mailed to 3,100 …