Typical Absence Epilepsy Research Articles

The interictal activities load and cognitive performance of children with typical absence epilepsy

BackgroundThe description of childhood absence epilepsy (CAE) a benign self-limited generalized epilepsy has become a matter of debate. The objectives of this work were to evaluate the existence of psychiatric and cognitive impairments among patients with typical CAE and to correlate their possible relation to seizure frequency, duration of epilepsy, IISL, and valproate therapy.MethodsThe study was conducted on 19 typical CAE patients receiving valproate therapy, 11 newly diagnosed CAE patients not receiving AEDs, and 30 healthy control subjects (HCS). Participants were subjected to medical history taking, EEG monitoring, child behavior checklist (CBCL), Stanford Binet Intelligence Scale 5th edition, and computerized psychometric tests that assess cognitive domains and executive functions.ResultsThe study revealed a high rate of cognitive and psychiatric dysfunctions in CAE patients. 53.3% of patients had psychiatric problems versus 16.6% in HCS. Attention deficit hyperactive disorder (ADHD) (26.6%), anxiety (16.6%), and depression (6.6%) were the most common psychiatric disorders in the patient group. Withdrawn/depressed symptoms, thought problems, social problems, and attention problems in CAE patients were significantly increased compared to HCS. At the same time, CAE patients perform worse in cognitive scales than HCS with comparable intelligent quotient (IQ) scores.ConclusionCognitive and psychiatric impairments in typical CAE patients appear multifactorial in origin with epilepsy-related factors including the duration of epilepsy and interictal spike load (IISL).

Unmasking the entity of 'drug-resistant' perioral myoclonia with absences: the twitches, darts and domes!

Perioral myoclonia with absences (POMA) is not recognized as a unique electro-clinical syndrome and studies suggest its inclusion under the genetic generalized epilepsy (GGE) spectrum. The aim of this study was to explore the prevalence and electro-clinical homogeneity of this disorder in an epilepsy monitoring unit. Between 2013 and 2019, among drug-resistant epilepsy patients who were referred for video-telemetry, those diagnosed with POMA based on the presence of documented absences with prominently observed peri-oral muscular contractions accompanied by generalized EEG features were included. Among 62 patients who were diagnosed with absence epilepsy, five finally met the criteria for POMA (8.1%) with late childhood or adolescent onset of epilepsy. Four (80%) had a referral diagnosis of focal epilepsy based on historical focal features with exacerbation of seizures on oxcarbazepine. All five patients demonstrated brief absences with orbicularis oris muscle contractions accompanied by subtle focal phenomenology. One patient had concurrent axial-appendicular myoclonic jerks precipitated by hyperventilation. While four patients had strikingly identical interictal and ictal characteristics of typical absence epilepsy, one patient demonstrated additional atypical generalized polyspike discharges without a "dart-dome" morphology. Therapeutic response to introduction of sodium valproate was noted in all five patients. Features that were not consistent with the diagnosis were apparent in one patient who was re-classified with combined focal and generalized epilepsy. Differentiating aspects in this patient included multifocal discharges, background slowing, fast-recruiting ictal rhythms and valproate resistance. This is one of the largest case series of POMA. This entity, which falls under the spectrum of GGE, remains under-diagnosed and its distinctive electro-clinical features need to be recorded in order to prevent misclassification as focal epilepsy of probable opercular origin. Background-slowing, atypical ictal rhythms and valproate unresponsiveness are not consistent with the diagnosis of this unique absence epilepsy. [Published with video sequences].

Are Absence and Limbic Seizures Mutually Exclusive?: An Experimental Approach to Enigmatic Clinical Concept

AbstractThe impressive advances in the several disciplines including neurophysiology, molecular biology, neuroimmunology, neurogenetics, neuroimaging, and neuropharmacology of epilepsies have been stimulating a mutual interaction among basic scientists, clinicians, and professionals from other disciplines, leading to the identification of clinical questions and then the design of basic science paradigms to test enigmatic clinical issues. Based on a clinical observation that the coexistence of genetic (idiopathic) generalized typical absence and mesial temporal lobe epilepsy in the same patient is extremely rare and debatable, we addressed the rare coexistence in the same individual, designed an experimental approach to test the validity of this clinical concept and to study the underlying mechanisms involved. Here we presented evidence of a mutual cross-interaction in the circuits involved in typical absence and temporal lobe epilepsy. This article delineates a phenomenological picture and comprehends a theoretical understanding of a mutual cross-interaction in typical absence as a representative of genetic generalized epilepsies and limbic epilepsy in which seizures often start from the mesial temporal lobe.

Current Controversy: Spikes, Bursts, and Synchrony in Generalized Absence Epilepsy: Unresolved Questions Regarding Thalamocortical Synchrony in Absence Epilepsy.

Absence epilepsy is a disorder of thalamocortical networks. Animal models have provided detailed information regarding the core cellular, synaptic, and network features that contribute to the electroencephalogram spike and wave discharge characteristic of typical absence epilepsy. Understanding of seizure networks and dynamics is a critical step toward improving treatments, yet competing conceptual models have evolved to explain seizure initiation and propagation. Recent studies have questioned 2 key model concepts: (1) T-type Ca2+ channel-dependent burst firing in thalamic relay neurons may not be essential for seizure generation, bringing into question the proposed mechanism for the antiepileptic drug ethosuximide in reducing thalamic bursting and (2) widespread synchronized neural activity may not be a core feature of the seizures, indicating that reductions in synchrony would not be a productive therapeutic goal. In this review, I will discuss these current findings, highlight the innovative approaches that have enabled these insights, and provide a unified framework that incorporates these sometimes-conflicting ideas. Finally, I lay out future work that will be necessary to finally resolve the remaining issues.

Prevalence of idiopathic epilepsy among school children in Gharbia Governorate, Egypt

BackgroundEpilepsy is one of the most common neurological disorders among children. Data about its prevalence in Egypt is limited. Our aim was to study the prevalence of idiopathic epilepsy among school children in Gharbia governorate, Egypt. Subjects and MethodsA Cross-sectional school-based survey study was conducted; a validated screening questionnaire was distributed among urban and rural primary and preparatory school children. Students with suspected epilepsy were subjected to clinical evaluation, Electroencephalogram (EEG), and neuroimaging. Results9545 students completed the questionnaire, of whom 69 children proved to have idiopathic epilepsy. The lifetime prevalence of idiopathic epilepsy among school students aged 6–14 years was 7.2/1000. Higher prevalence was reported in males (7.7/1000) and in children from urban areas (8.25/1000). Generalized seizures were observed in 56.5% of the children with epilepsy, whereas focal seizures were present in 43.5%. Thirty-four (49.27%) children were diagnosed with specific childhood epileptic syndrome: 25 children had benign childhood epilepsy with centrotemporal spikes and nine children had typical childhood absence epilepsy. Treatment gap is around 12.5% in the studied children. Family history of epilepsy and parental consanguinity were evident in 73.9% and 21.7% of the epileptic children, respectively. The odds ratio for idiopathic epilepsy in children with family history of epilepsy was 23.9. ConclusionThe prevalence of idiopathic epilepsy among school students aged 6–14 years in Gharbia Governorate was 7.2/1000. The reported prevalence is similar to the prevalence of epilepsy in other Arab countries, but lower than the prevalence in Upper Egypt and in most developing countries.

Effect of the coordinated reset stimulations on controlling absence seizure

Based on a macroscopic mean-field model associating with the thalamus and cerebral cortex, we investigate how the newly proposed coordinated reset stimulation (CRS) strategy controls the absence seizures as some key parameters are changed. Different from the previous stimulation processes, CRS represents the intermittent pulse current administered to different structures including cortex, specific relay nuclei (SRN) and thalamus reticular nucleus (TRN) at different time by using three different micro-electrodes. In particular, we first simulate a typical absence epilepsy activity under the combined effect of the coupling strength between inhibitory interneurons (IIN)-excitatory pyramidal neurons (EPN) and EPN-TRN pathway. And then we explore the control mechanism of different parameters of 3:2 ON-OFF CRS on spike and slow-wave discharges (SWDs) region. Through analyzing the corresponding two-dimensional bifurcation diagrams, we find CRS is effective on controlling absence seizures in proper ranges of stimulation parameters. Especially, the combination of frequency and positive input duration can inhibit the pathological area more effectively. The obtained results might be helpful to study the pathophysiology mechanism of epilepsy, although the CRS’s feasibility still needs further exploration in clinical experiments.

Eliminating Absence Seizures through the Deep Brain Stimulation to Thalamus Reticular Nucleus.

Deep brain stimulation (DBS) can play a crucial role in the modulation of absence seizures, yet relevant biophysical mechanisms are not completely established. In this paper, on the basis of a biophysical mean-field model, we investigate a typical absence epilepsy activity by introducing slow kinetics of GABAB receptors on thalamus reticular nucleus (TRN). We find that the region of spike and slow-wave discharges (SWDs) can be reduced greatly when we add the DBS to TRN. Furthermore, we systematically explore how the corresponding stimulation parameters including frequency, amplitude and positive input duration suppress the SWDs under certain conditions. It is shown that the SWDs can be controlled as key stimulation parameters are suitably chosen. The results in this paper can be helpful for researchers to understand the thalamus stimulation in treating epilepsy patients, and provide theoretical basis for future experimental and clinical studies.

Evaluation of deep gray matter volume, cortical thickness and white matter integrity in patients with typical absence epilepsy: a study using voxelwise-based techniques.

The objective of this study was to evaluate the cortical thickness and the volume of deep gray matter structures, measured from 3D T1-weighted gradient echo imaging, and white matter integrity, by diffusion tensor imaging (DTI) in patients with typical absence epilepsy (AE). Patients (n=19) with typical childhood AE and juvenile AE, currently taking antiepileptic medication, were compared with control subjects (n=19), matched for gender and age. 3D T1 magnetization-prepared rapid gradient echo-weighted imaging and DTI along 30 noncolinear directions were performed using a 1.5-T MR scanner. FreeSurfer was used to perform cortical volumetric reconstruction and segmentation of deep gray matter structures. For tract-based spatial statistics analysis of DTI, a white matter skeleton was created, along with a permutation-based inference with 5000 permutations. A threshold of p<0.05 was used to identify abnormalities in fractional anisotropy (FA). The mean, radial, and axial diffusivities were also projected onto the mean FA skeleton. Patients with AE presented decreased FA and increased mean diffusivity and radial diffusivity values in the genu and the body of the corpus callosum and right anterior corona radiata, as well as decreased axial diffusivity in the left posterior thalamic radiation, inferior cerebellar peduncle, right cerebral peduncle, and right corticospinal tract. However, there were no significant differences in cortical thickness or deep gray matter structure volumes between patients with AE and controls. Abnormalities found in white matter integrity may help to better understand the pathophysiology of AE and optimize diagnosis and treatment strategies.

Impaired consciousness in patients with absence seizures investigated by functional MRI, EEG, and behavioural measures: a cross-sectional study

BackgroundAbsence seizures are brief episodes of impaired consciousness characterized by staring and behavioral arrest. The neural underpinnings of impaired consciousness and of the variable severity of behavioral impairment observed from one absence seizure to the next are not well understood. We therefore compared fMRI and EEG changes in absence seizures with impaired task performance to seizures in which performance was spared.MethodsPatients were recruited from 59 pediatric neurology practices including hospitals and neurology outpatient offices throughout the United States. We performed simultaneous electroencephalography (EEG), fMRI, and behavioral testing in children and adolescents aged 6 to 19 years with typical absence epilepsy. fMRI and EEG were analyzed using data-driven approaches without prior assumptions about signal time courses or spatial distributions. The main outcomes were fMRI and EEG amplitudes in seizures with impaired versus spared behavioral responses analysed by t-test. We also examined the timing of fMRI and EEG changes in seizures with impaired behavioral responses compared to seizures with spared responses.Findings93 patients were enrolled between September 1, 2005 and January 1, 2013, and we captured a total of 1032 seizures in 39 patients. fMRI changes during seizures occurred sequentially in three functional brain networks previously well-validated in studies of normal subjects. Seizures associated with more impaired behavior showed higher fMRI amplitude in all three networks compared to seizures with spared performance. In the default-mode network fMRI, amplitude was 0·57 ± 0·26% for seizures with impaired and 0·40 ± 0·16% for seizures with spared behavioral responses (mean difference 017%; 95% CI: 0·11 to 0·23%; p < 0.0001). In the task-positive network, fMRI amplitude was 0·53 ± 0·29% for impaired and 0·39 ± 0·15% for spared seizures (mean difference 0·14%; 95% CI: 008 to 0·21%; p < 0.0001). In the sensorimotor-thalamic network, fMRI amplitude was 0·41 ± 0·25% for impaired and 0·34 ± 014% for spared seizures (mean difference 0 07%; 95% CI: 001 to 0·13%; p = 0.02). Seizures with impaired behavior also showed greater EEG power in widespread brain regions compared to seizures with spared behavior. Mean fractional EEG power in the frontal leads was 50·4 ± 15·2 for seizures with impaired and 24·8 ± 6·5 for seizures with spared behavior (mean difference 25·6; 95% CI: 210 to 30·3); middle leads 35·4 ± 6·5 for impaired, 13 3 ± 34 for spared seizures (mean difference 22·1; 95% CI: 20.0 to 24·1); posterior leads 41·6 ± 5·3 for impaired, 24·6 ± 86 for spared seizures (mean difference 170; 95% CI: 14·4 to 19·7); p < 00001 for all comparisons. Average seizure duration was longer for seizures with impaired behavior at 79 ± 66 s, compared to 3·8 ± 3.0 s for seizures with spared behavior (mean difference 4.1 s; 95% CI 3.0 to 5.3 s, p < 00001). However, larger amplitude fMRI and EEG signals occurred at the outset or even preceding seizures with impairment.InterpretationImpaired consciousness in absence seizures is related to the intensity of physiological changes in established networks affecting widespread regions of the brain. Increased EEG and fMRI amplitude occurs at the onset of seizures associated with behavioral impairment. These findings suggest that a vulnerable state may exist at the initiation of some seizures leading to greater physiological changes and altered consciousness.

Increased inhibitory synaptic activity in the hippocampus (CA1) of genetic absence epilepsy rats: Relevance of kindling resistance

PurposeGenetic absence epilepsy rats from Strasbourg (GAERS), a well-validated genetic rat model for typical absence epilepsy, are known to manifest a resistance to secondary generalization of abnormal focal electrical activity evoked by kindling. The mechanism of this resistance is still unclear. In order to understand the possible mechanism of kindling resistance, we investigated for the first time, the differences of short-term synaptic plasticity by using a paired-pulse paradigm as an indicator of GABAergic activity in CA1 region of hippocampus in GAERS and non-epileptic Wistar rats in-vivo. MethodsRats were subjected to kindling process, basolateral amygdala was stimulated twice a day, with a supra-threshold current, until they displayed limbic or convulsive seizures. One hour after the last kindling stimulation, evoked field potentials from CA1 pyramidal layer of hippocampus were recorded in-vivo under urethane anesthesia. ResultsIn response to supra-threshold kindling stimulations GAERS showed a significantly delayed kindling progression and displayed a significant increase in hippocampal excitability at early stages of kindling that is the critical for the development of convulsive seizures. In control rats that were not received kindling stimulation, paired-pulse depression (PPD) was significantly pronounced in GAERS with respect to the Wistar group. During the kindling course, PPD was gradually reduced in the Wistar rats as kindling progression was advanced. However in GAERS, PPD ratios were not significantly changed at early stages of kindling. When GAERS reached convulsive stage, their PPD ratios became similar to that of Wistar rats. DiscussionThe increased inhibition in paired-pulse responses at early stages of kindling in GAERS suggests the role of augmented GABAergic activity as one of the underlying mechanisms of kindling resistance observed in genetic rat models of absence epilepsy.

Evaluation of Executive Functions in Patients With Childhood Absence Epilepsy.

The aim of this study was to evaluate the executive function of patients with typical absence epilepsy. Thirty-eight (19 healthy children and 19 patients) individuals were enrolled in this study. Neurocognitive function tests, such as the Serial Digit Learning Test, Wisconsin Card Sorting Test, Visual Aural Digit Span Test-Form B, KAS-Animal Test, Trail Making Test-A Time Test, and STROOP Test, were given to all of the participants. There was a significant difference between the groups on the Serial Digit Learning Test (P = .037) and on a subtest of the Wisconsin Card Sorting Test. As for the Wisconsin Card Sorting Test performance, there were significant differences in perseverative errors and perseverative responses between the patient and control groups (P = .011 and P = .010, respectively). Long-term risk for learning impairments, failure in executive abilities, and short-term memory and attention disorders can occur in children with absence epilepsy.

P48 – 2876: The evaluation of the frontal lobe function in the patients with absence epilepsy

Objective Based on earlier studies, CAE has been considered as a benign disorder with relatively easily attained seizure control and minimal involvement of cognition and behavior. However, more recent outcome studies report a varying rate of seizure control, as well as learning and cognitive difficulties. The aim of this study is the evaluation of neurocognitive function, especially frontal lobe, in the patients with typical absence epilepsy. Methods Thirty-eight (19 healthy children and 19 patients) participants were enrolled. Neurocognitive function tests such as Serial Digit Learning Test, Wisconsin Card Sorting Test, Visual Aural Digit Span Test and STROOP Test were performed to all participants. Results There was a significant difference between the groups according to Serial Digit Learning Test (SDLT) and the subgroup of Wisconsin Card Sorting Test. As for the WCST performance, there was significant difference in categories achieved, difficulty of maintaining set, perseverative errors, and perseverative responses between patient and control groups (p=0.037, p=0.010, p=0.011). In Serial Digit Learning Test and in the non-perseverative error subgroup of WCST performance, there was a significant difference in the patient group whose seizures started before the age 6 (p=0.029, p=0.041). As for the Visual-Aural Digit Span Test performance, there was a significant difference between the groups when compared to the duration response to drug treatment in categories achieved, aural-oral, visual-oral, aural-written, and visual-written. (p=0.010, p=0.025, p=0.012, p=0.034). Conclusion Long-term risk of learning impairments, failure in executive abilities, short-term memory and attention disorders can occur in children with absence epilepsy, especially in patients whose seizure started before the age of 7 years not responding to single drug, and the duration of response to drug was longer than 6 months. Our results highlight potentially detrimental effect of absence seizures on cognition.

Epileptic activity during early postnatal life in the AY-9944 model of atypical absence epilepsy

Atypical absence epilepsy (AAE) is an intractable disorder characterized by slow spike-and-wave discharges in electroencephalograms (EEGs) and accompanied by severe cognitive dysfunction and neurodevelopmental or neurological deficits in humans. Administration of the cholesterol biosynthesis inhibitor AY-9944 (AY) during the postnatal developmental period induces AAE in animals; however, the neural mechanism of seizure development remains largely unknown. In this study, we characterized the cellular manifestations of AY-induced AAE in the mouse. Treatment of brain slices with AY increased membrane excitability of hippocampal CA1 neurons. AY treatment also increased input resistance of CA1 neurons during early postnatal days (PND) 5–10. However, these effects were not observed during late PND (14–21) or in adulthood (7–10 weeks). Notably, AY treatment elicited paroxysmal depolarizing shift (PDS)-like epileptiform discharges during the early postnatal period, but not during late PND or in adults. The PDS-like events were not compromised by application of glutamate or GABA receptor antagonists. However, the PDS-like events were abolished by blockage of voltage-gated Na+ channels. Hippocampal neurons isolated from an in vivo AY model of AAE showed similar PDS-like epileptiform discharges. Further, AY-treated neurons from T-type Ca2+ channel α1G knockout (Cav3.1−/−) mice, which do not exhibit typical absence seizures, showed similar PDS-like epileptiform discharges. These results demonstrate that PDS-like epileptiform discharges during the early postnatal period are dependent upon Na+ channels and are involved in the generation of AY-induced AAE, which is distinct from typical absence epilepsy. Our findings may aid our understanding of the pathophysiological mechanisms of clinical AAE in individuals, such as those with Lennox–Gastaut syndrome.

Role of Laterodorsal Thalamic Nucleus during Absence Seizure Attacks

Introduction: A typical absence epilepsy is a type of nonconvulsive and generalized epilepsy. The main feature of these attacks is a sudden brief impairment of consciousness. The disturbances in thalamocortical loop play an important role in pathogenesis of absence seizures. However, it is not clear that which part of this network triggers the seizure. This study was aimed to investigate the role of latrodorsal (LD) thalamic neurons during spike and wave discharges (SWDs) in WAG/Rij rats, as the most valid animal model of absence epilepsy. Materials and Methods: Single unit activities in the LD thalamic nucleus and electrocorticogram of somatosensory cortex were simultaneously recorded in six-month-old WAG/Rij rats. Results: During SWDs, unit activity in the LD thalamic nucleus showed burstlike discharges, which were started before the peak component of SWDs. In SWD-free periods, burst like activity in the LD was reduced. Conclusion: Our findings suggest that the burst firing of LD may stimulate the neocortex to exhibit SWDs. It can be concluded that inhibition of

Control of absence seizures induced by the pathways connected to SRN in corticothalamic system

The cerebral cortex, thalamus and basal ganglia together form an important network in the brain, which is closely related to several nerve diseases, such as parkinson disease, epilepsy seizure and so on. Absence seizure can be characterized by 2-4 Hz oscillatory activity, and it can be induced by abnormal interactions between the cerebral cortex and thalamus. Many experimental results have also shown that basal ganglia are a key neural structure, which closely links the corticothalamic system in the brain. Presently, we use a corticothalamic-basal ganglia model to study which pathways in corticothalamic system can induce absence seizures and how these oscillatory activities can be controlled by projections from the substantia nigra pars reticulata (SNr) to the thalamic reticular nucleus (TRN) or the specific relay nuclei (SRN) of the thalamus. By tuning the projection strength of the pathway "Excitatory pyramidal cortex-SRN", "SRN-Excitatory pyramidal cortex" and "SRN-TRN" respectively, different firing states including absence seizures can appear. This indicates that absence seizures can be induced by tuning the connection strength of the considered pathway. In addition, typical absence epilepsy seizure state "spike-and-slow wave discharges" can be controlled by adjusting the activation level of the SNr as the pathways SNr-SRN and SNr-TRN open independently or together. Our results emphasize the importance of basal ganglia in controlling absence seizures in the corticothalamic system, and can provide a potential idea for the clinical treatment.

First-drug treatment failures in children with typical absence epilepsy.

Childhood absence epilepsy (CAE) is a well-known syndrome with onset in middle childhood and is characterized by multiple typical absences per day. Pharmacological treatment is specific and usually successful with a single medication. The goal of the study was to assess on risk factors associated with failure to respond to the initial antiepileptic drug (AED). Fifty-two children with CAE were enrolled. Predictive factors were analyzed by survival methods. Among 52 patients, 32 patients (61.5%) were girls and the remaining 20 (38.5%) were boys and the mean age at the seizure onset was 6.5±1.78 years old (3-11.5 years). Of the 52 patients, 42 (80.8%) were treated relatively successfully with the first AED treatment (Group A), and 10 (19.2%) were not responsed (Group B). Age of seizure onset, coexisting other types of seizures, and photoconvulsive EEG response were significantly associated with failure risk according to univariate analysis. In the multivariate analysis, only photoconvulsive EEG response was the risk factor influencing poor response to initial AED treatment. Factors predicting failure to respond to the AED were age of seizure onset, coexisting other types of seizures, and photoconvulsive EEG response in children with CAE.

Is there such a thing as "generalized" epilepsy?

The distinction between generalized and partial epilepsies is probably one, if not the most, pregnant assertions in modern epileptology. Both absence and generalized tonic-clonic seizures, the prototypic seizures found in generalized epilepsies, are classically seen as the result of a rapid, synchronous recruitment of neuronal networks resulting in impairment of consciousness and/or convulsive semiology. The term generalized also refers to electroencephalographic presentation, with bilateral, synchronous activity, such as the classical 3 Hz spike and wave discharges of typical absence epilepsy. However, findings obtained from electrophysiological and functional imaging studies over the last few years, contradict this view, showing a rather focal onset for most of the so-called generalized seizure types. Therefore, we ask here the question whether "generalized epilepsy" does indeed exist.

Assessment of Control in Typical Childhood Absence Epilepsy

We report relevant results of a survey that was aimed at understanding current practice variations in the assessment of control of typical childhood absence epilepsy.

Towards a large-scale model of patient-specific epileptic spike-wave discharges

Clinical electroencephalographic (EEG) recordings of the transition into generalised epileptic seizures show a sudden onset of spike-wave dynamics from a low-amplitude irregular background. In addition, non-trivial and variable spatio-temporal dynamics are widely reported in combined EEG/fMRI studies on the scale of the whole cortex. It is unknown whether these characteristics can be accounted for in a large-scale mathematical model with fixed heterogeneous long-range connectivities. Here, we develop a modelling framework with which to investigate such EEG features. We show that a neural field model composed of a few coupled compartments can serve as a low-dimensional prototype for the transition between irregular background dynamics and spike-wave activity. This prototype then serves as a node in a large-scale network with long-range connectivities derived from human diffusion-tensor imaging data. We examine multivariate properties in 42 clinical EEG seizure recordings from 10 patients diagnosed with typical absence epilepsy and 50 simulated seizures from the large-scale model using 10 DTI connectivity sets from humans. The model can reproduce the clinical feature of stereotypy where seizures are more similar within a patient than between patients, essentially creating a patient-specific fingerprint. We propose the approach as a feasible technique for the investigation of patient-specific large-scale epileptic features in space and time.

Ethosuximide-Induced Conversion of Typical Childhood Absence to Rolandic Spikes

Coexistence of 2 idiopathic epilepsy syndromes (ie, childhood absence and Rolandic epilepsy), as evidenced by electroencephalographic (EEG) findings with or without clinical features of the 2 conditions, is uncommon and remains controversial. Few case reports support this coexistence either as a continuum or drug-induced conversion, whereas a large sample case review did not find such co-occurrence. The authors report a case of conversion of typical absence to Rolandic spikes after treatment with ethosuximide. An 11-year-old girl was diagnosed with typical childhood absence epilepsy at the age of 6 years with classic clinical and EEG features. She became seizure-free on ethosuximide but her follow-up EEGs consistently recorded right centrotemporal and centroparietal spikes without associated clinical seizures. This case may suggest simultaneous presence of these 2 common childhood idiopathic epilepsies either as a continuum or a drug-induced conversion.