bluuebunny/crossref_metadata_2025_split huggingface dataset:
The Effects of Lamotrigine on Sleep in Patients with Epilepsy
Authors: Foldvary Nancy , Perry Michael , Lee Julia , Dinner Dudley , Morris Harold H. 
Published: March 2003

Summary:  Purpose: The older antiepileptic drugs (AEDs) have a variety of effects on sleep, including marked reduction in REM, slow‐wave sleep (SWS) and sleep latency, and increased percentage of light sleep. The effects of the newer AEDs on sleep are unknown. Our purpose was to study the effect of lamotrigine (LTG) on sleep.Methods: Ten adults with focal epilepsy, in whom the decision was made to add LTG to either phenytoin (PHT) or carbamazepine (CBZ) for control of seizures, were the subjects of this study. Patients underwent pre‐ and posttreatment polysomnography (PSG) and completed sleep questionnaires. Polygraphic variables and Epworth Sleepiness Scale (ESS) scores, a subjective measure of sleep propensity, were compared by using the Wilcoxon sign rank test.Results: Seven patients were taking CBZ, and three were treated with PHT. All subjects were titrated to an LTG dose of 400 mg/day. Treatment with LTG produced a significant decrease in SWS and an increase in stage 2 sleep percentage. No significant difference in ESS or any of the other polygraphic variables was observed. However, LTG treatment was associated with a reduction in arousals and stage shifts and an increase in REM periods. No subjects reported insomnia with treatment.Conclusions: LTG appears to be less disruptive to sleep than some of the older AEDs.
Validity of Three Measures of Health‐related Quality of Life in Children with Intractable Epilepsy
Authors: Sherman Elisabeth M. S. , Slick Daniel J. , Connolly Mary B. , Steinbok Paul , Camfield Carol , Eyrl Kim L. , Massey Cathy , Farrell Kevin 
Published: March 2003

Summary:  Purpose: Validity studies on health‐related quality of life (HRQOL) scales for pediatric epilepsy are few, and cross‐validation with other samples has not been reported. This study was designed to assess the validity of three parent‐rated measures of HRQOL in pediatric epilepsy: (a) the Impact of Childhood Illness Scale (ICI), (b) the Impact of Child Neurologic Handicap Scale (ICNH), and (c) the Hague Restrictions in Epilepsy Scale (HARCES).Methods: Retrospective data were examined for 44 children with intractable epilepsy. Validity was assessed by evaluating differences across epilepsy severity groups as well as correlations between HRQOL scales and neurologic variables (seizure severity, epilepsy duration, current/prior antiepileptic medications) and psychosocial measures (emotional functioning, IQ, social skills, adaptive behavior). Scale overlap with a global QOL rating also was assessed.Results: The HRQOL measures were moderately to highly intercorrelated. The scales differed in terms of their associations with criterion measures. The HARCES was related to the highest number of neurologic variables and the ICNH to the fewest. All three scales were related to psychosocial functioning and to global quality of life.Conclusions: The results of this study suggest that the three measures are likely adequate measures of HRQOL for use in intractable childhood epilepsy. The measures were highly intercorrelated, and they were all broadly related to criterion measures reflecting specific domains of HRQOL as well as global QOL. Some differences between scales emerged, however, that suggest care in choosing HRQOL instruments for children with epilepsy.
Calcium‐dependent Epileptogenesis in an In Vitro Model of Stroke‐induced “Epilepsy”
Authors: Sun David A. , Sombati Sompong , Blair Robert E. , DeLorenzo Robert J. 
Published: March 2003

Summary:  Purpose: Stroke is the most common cause of acquired epilepsy. The purpose of this investigation was to characterize the role of calcium in the in vitro, glutamate injury–induced epileptogenesis model of stoke‐induced epilepsy.Methods: Fura‐2 calcium imaging and whole‐cell current clamp electrophysiology techniques were used to measure short‐term changes in neuronal free intracellular calcium concentration and long‐term alterations in neuronal excitability in response to epileptogenic glutamate injury (20 μM, 10 min) under various extracellular calcium conditions and in the presence of different glutamate‐receptor antagonists.Results: Glutamate injury–induced epileptogenesis was associated with prolonged, reversible elevations of free intracellular calcium concentration during and immediately after injury and chronic hyperexcitability manifested as spontaneous recurrent epileptiform discharges for the remaining life of the cultures. Epileptogenic glutamate exposure performed in solutions containing low extracellular calcium, barium substituted for calcium, or N‐methyl‐d‐aspartate (NMDA)‐receptor antagonists reduced the duration of intracellular calcium elevation and inhibited epileptogenesis. Antagonism of non–NMDA‐receptor subtypes had no effect on glutamate injury–induced calcium changes or the induction epileptogenesis. The duration of the calcium elevation and the total calcium load statistically correlated with the development of epileptogenesis. Comparable elevations in neuronal calcium induced by non–glutamate receptor–mediated pathways did not cause epileptogenesis.Conclusions: This investigation indicates that the glutamate injury–induced epileptogenesis model of stroke‐induced epilepsy is calcium dependent and requires NMDA‐receptor activation. Further, these experiments suggest that prolonged, reversible elevations in neuronal free intracellular calcium initiate the long‐term plasticity changes that underlie the development of injury‐induced epilepsy.
The Effectiveness of Cognitive Rehabilitation for Attention Deficits in Focal Seizures: A Randomized Controlled Study
Authors: Engelberts Nadine H. J. , Klein Martin , Adèr Herman J. , Heimans Jan J. , Trenité Dorothée G. A. Kasteleijn‐Nolst , Van der Ploeg Henk M. 
Published: March 2003

Summary:  Purpose: Cognitive deficits are one of the major limiting factors in the everyday life functioning of patients with focal seizures. Although cognitive rehabilitation methods have been successfully applied to patients with other central nervous system (CNS) lesions, these methods have not yet been evaluated in cognitively impaired patients with epilepsy. The present study evaluated the effectiveness of two commonly used methods for attention deficits: (a) the Retraining Method, aimed at retraining impaired cognitive functions; and (b) the Compensation Method, aimed at teaching compensatory strategies while taking neuronal loss for granted.Methods: Fifty adult outpatients with focal seizures and attention impairments receiving carbamazepine (CBZ) monotherapy were randomly assigned to the Retraining Method, the Compensation Method, or to a waiting‐list control group. Established and self‐reported neuropsychological outcomes and self‐reported quality of life of these groups were evaluated at pretraining, posttraining, and at a 6‐month follow‐up measurement point and were completed by 44 patients.Results: Neuropsychological outcomes related to training, self‐reported neuropsychological outcomes, and quality of life at the 6‐month follow‐up measurement point improved both in the Retraining Method group (n = 19) and the Compensation Method group (n = 17) relative to the waiting‐list control group (n = 8). The Compensation Method was more effective in improving self‐reported neuropsychological outcomes and quality of life, especially for patients with less education. The patients with active epilepsy benefited more from both methods than did the seizure‐free patients.Conclusions: These data show that cognitive rehabilitation programs are effective for patients with focal seizures and attention deficits and should, therefore, be incorporated into comprehensive care programs.
Expression of the Multidrug Transporter P‐glycoprotein in Brain Capillary Endothelial Cells and Brain Parenchyma of Amygdala‐kindled Rats
Authors: Seegers Ulrike , Potschka Heidrun , Löscher Wolfgang 
Published: March 2003

Summary:  Purpose: Based on data from brain biopsy samples of patients with pharmacoresistant partial epilepsy, overexpression of the multidrug transporter P‐glycoprotein (PGP) in brain capillary endothelium has recently been proposed as a potential mechanism of resistance to antiepileptic drugs (AEDs). We examined whether PGP is overexpressed in brain regions of amygdala‐kindled rats, a widely used model of temporal lobe epilepsy (TLE), which is often resistant to AEDs.Methods: Rats were kindled by stimulation of the basolateral amygdala (BLA); electrode‐implanted but nonkindled rats and naive (not implanted) rats served as controls. PGP was determined by immunohistochemistry either 1 or 2 weeks after the last kindled seizure, by using a monoclonal anti‐PGP antibody. Six brain regions were examined ipsi‐ and contralateral to the BLA electrode: the BLA, the hippocampal formation, the piriform cortex, the substantia nigra, the frontal and parietal cortex, and the cerebellum.Results: In both kindled rats and controls, PGP staining was observed mainly in microvessel endothelial cells and, to a much lesser extent, in parenchymal cells. The distribution of PGP expression across brain regions was not homogeneous, but significant differences were found in both the endothelial and parenchymal expression of this protein. In kindled rats, ipsilateral PGP expression tended to be higher than contralateral expression in several brain regions, which was statistically significant in the piriform cortex and parietal cortex. However, compared with controls, no significant overexpression of PGP in capillary endothelial cells or brain parenchyma of kindled rats was seen in any ipsilateral brain region, including the BLA. For comparison with kindled rats, kainate‐treated rats were used as positive controls. As reported previously, kainate‐induced seizures significantly increased PGP expression in the hippocampus and other limbic brain regions.Conclusions: Amygdala‐kindling does not induce any lasting overexpression of PGP in several brain regions previously involved in the kindling process. In view of the many pathophysiologic and pharmacologic similarities between the kindling model and TLE, these data may indicate that PGP overexpression in pharmacoresistant patients with TLE is a result of uncontrolled seizures but not of the processes underlying epilepsy. It remains to be determined whether transient PGP overexpression is present in kindled rats shortly after a seizure, and whether pharmacoresistant subgroups of kindled rats exhibit an increased expression of PGP. Furthermore, other multidrug transporters, such as multidrug resistance–associated protein, might be involved in the resistance of kindled rats to AEDs.
Partial Epilepsy Manifesting Atonic Seizure: Report of Two Cases
Authors: Satow Takeshi , Ikeda Akio , Yamamoto Junichi , Takayama Motohiro , Matsuhashi Masao , Ohara Shinji , Matsumoto Riki , Begum Tahamina , Fukuyama Hidenao , Hashimoto Nobuo , Shibasaki Hiroshi 
Published: March 2003

Summary:  Purpose: Atonic seizures are commonly seen in patients with generalized epilepsy but only infrequently in patients with partial epilepsy. Clinically generalized atonic seizures as a partial epilepsy have not been studied in detail with video/EEG monitoring. Here we describe the clinical and physiologic characteristics of atonic seizures due to partial epilepsy and discuss the underlying mechanism.Methods: Two patients with partial epilepsy manifesting atonic seizures, one with frontal lobe epilepsy (FLE) and the other with parietal lobe epilepsy (PLE), were reported. The long‐term video/EEG monitoring, magnetic resonance imaging (MRI), and interictal fluorodeoxyglucose–positron emission tomography (FDG‐PET) were investigated in each patient.Results: Paroxysmal diminution of muscle tone mainly involved the axial muscles in both patients. In contrast with the abrupt falls seen in patients with Lennox–Gastaut syndrome, the falls in these patients were slow, taking 2–5 s to fall down. Ictal EEG records showed low‐voltage fast activity in the frontocentral area followed by repetitive spikes at the midline frontocentral area in the patient with FLE, and rhythmic spikes in the left central area in the patient with PLE. Interictal FDG‐PET disclosed hypometabolic regions consistent with the clinical and EEG findings.Conclusions: Slow falls might be a feature of atonic seizures in partial epilepsy. Long‐lasting atonia in partial epilepsy could be due to either one of the following two possible mechanisms: (a) epileptic activities arising from the negative motor area, of which 50‐Hz electric stimulation causes motor inhibition, or (b) sustained atonia with successive electromyogram (EMG) silent periods caused by epileptic discharges arising from the inhibitory area of the primary sensorimotor area.
Neural Networks Underlying Epileptic Humming
Authors: Bartolomei Fabrice , Wendling Fabrice , Vignal Jean‐Pierre , Chauvel Patrick , Liégeois‐Chauvel Catherine 
Published: March 2003

Summary:  Purpose: Humming is a rare automatism occurring in partial seizures that has received little attention. Its study could shed light on the neural networks underlying melodic expression. In this study, we examined the anatomoelectroclinical correlates of humming during epileptic seizuresMethods: Three patients undergoing presurgical stereoelectroencephalography (SEEG) for medically intractable temporal lobe epilepsy were studied. Coherence analysis of SEEG activity was carried out to study the functional coupling of different regions of the brain, whereas time–frequency (TF) analysis was conducted to assess epileptic discharge patterns. Changes in coherence were studied to identify the neural structures/systems implicated in humming.Results: Humming began after the onset of seizures generated in medial limbic regions of the temporal lobe. At seizure onset, coherence analysis showed an increase in amygdala–hippocampus coupling. Humming began after the onset of a rhythmic discharge over lateral regions of the superior temporal gyrus (STG). A highly significant increase in coherence was observed between prefrontal regions and the STG. TF analysis of the STG discharge showed a reproducible pattern with a single fundamental frequency and associated harmonics. This frequency was ∼6 Hz for two patients and 15 Hz for one patient.Conclusions: These findings suggest that the occurrence of humming during epileptic seizures of the temporal lobe is associated with activity in a neural network involving the STG and the inferior frontal gyrus.
Effects of Fluoxetine and TFMPP on Spontaneous Seizures in Rats with Pilocarpine‐induced Epilepsy
Authors: Hernandez Eric J. , Williams Philip A. , Dudek F. Edward 
Published: March 2003

Summary:  Purpose: Fluoxetine is a selective serotonin [5‐hydroxytryptamine (5‐HT)] reuptake inhibitor (SSRI) commonly used to treat depression. Some uncontrolled clinical studies have reported that SSRIs increase seizures, but animal experiments with evoked‐seizure models have suggested that SSRIs at therapeutic doses decrease seizure susceptibility. We tested the hypothesis that fluoxetine and trifluoromethylphenylpiperazine (TFMPP, a nonselective 5‐HT–receptor agonist) reduce the frequency of spontaneous motor seizures in pilocarpine‐treated rats.Methods: Fluoxetine (20 mg/kg) and TFMPP (5 mg/kg) were administered to rats with pilocarpine‐induced epilepsy. Phenobarbital (PB; 10 mg/kg) was a positive control, and saline (i.e., 0.5 ml) controlled for the injection protocol. Each rat received each treatment (intraperitoneally) once per day for 5 consecutive days with 1 week between treatments. Rats were continuously video‐monitored for the last 72 h of each treatment.Results: When compared with saline over the entire 72‐h observation period, PB and fluoxetine treatment, but not TFMPP, reduced the spontaneous‐seizure rate. Plots of magnitude of the drug effect as a function of seizure frequency after saline treatment revealed larger drug effects for fluoxetine and PB in the rats with the highest control seizure rate. When the data from the five rats with the highest seizure frequency in saline were analyzed for the first 6 h after treatment, TFMPP also significantly reduced seizure frequency.Conclusions: Animal models with spontaneous seizures can be used to screen potential antiepileptic drugs, and fluoxetine and TFMPP reduce spontaneous seizures in the pilocarpine model of temporal lobe epilepsy.
Hippocampal Region Asymmetry Assessed by 1H‐MRS in Rolandic Epilepsy
Authors: Lundberg Staffan , Weis Jan , Eeg‐Olofsson Orvar , Raininko Raili 
Published: March 2003

Summary:  Purpose: In a previous study, we reported hippocampal abnormalities on magnetic resonance imaging (MRI) in six of 18 children with rolandic epilepsy (RE). In this study, metabolic changes were analyzed in the hippocampal region with proton magnetic resonance spectroscopy (1H‐MRS).Methods: In 13 children with electroclinically typical RE and 15 healthy controls, 1H‐MRS results of both hippocampal regions were analyzed. The voxels, 2 × 2 × 4‐cm each, were placed to include the head and body of the hippocampus. A PRESS sequence with TR 2,000 ms and TE 32 ms was used. Total N‐acetylaspartate (tNAA), glutamine and glutamate (Glx), and choline compounds (tCho) were related to total creatine (tCr), and asymmetry indices (AIs) were calculated. MRI was performed in all 13 patients and in 13 controls.Results: The tNAA/tCr AI of the hippocampal region was significantly higher in children with RE than in control children (z = 4.49; p < 0.001). The AIs of Glx/tCr and tCho/tCr did not show a significant difference between the groups. Lateralization of the interictal epileptiform activity corresponded with the lower tNAA/tCr ratio in 10 of 13 patients. MRI revealed a hippocampal asymmetry in four of 13 in the RE group, three of them showed concordance between the lateralization of the lower tNAA/tCr ratio and the smaller hippocampus. In the control group, a subtle asymmetry in four of 13 children was found.Conclusions: A significant asymmetry of the hippocampal regions, measured by tNAA/tCr ratios, indicates an abnormal neuronal function in children with RE.
The Predictive Value of Electroencephalogram during Early Infancy for Later Development of West Syndrome in Infants with Cystic Periventricular Leukomalacia
Authors: Suzuki Motomasa , Okumura Akihisa , Watanabe Kazuyoshi , Negoro Tamiko , Hayakawa Fumio , Kato Toru , Itomi Kazuya , Kubota Tetsuo , Maruyama Koichi 
Published: March 2003

Summary: Purpose:The aim of this study was to elucidate a predictive value of electroencephalogram (EEG) during early infancy for later development of West syndrome (WS) in premature infants with cystic periventricular leukomalacia (PVL).Methods:The subjects of this study were 19 infants with cystic PVL born between 1992 and 1996. EEGs were recorded at 3 months of corrected age (CA) in all of them. We divided these 19 infants into the following two groups; group A (n = 9), no paroxysmal discharge was recognized; and group B (n = 10), paroxysmal discharges were recognized.Results:In none of the infants in group A did WS develop. Subsequent EEGs were normal in all infants in group A. WS developed in seven of 10 infants in group B. The occurrence of WS is significantly higher in group B than in group A. The mean age at the onset of WS was 6 months of CA. Paroxysmal discharges in infants in group B were observed as irregular spikes‐and‐waves and polyspikes‐and‐waves, mainly in bilateral parietooccipital areas. In seven of eight patients with severe MRI findings in group B, WS developed.Conclusions:Paroxysmal discharges during early infancy were correlated with later development of WS in infants with cystic PVL. The possibility of developing WS had increased in the children with the combination with EEG and MRI findings.
Electrocardiographic Changes at the Onset of Epileptic Seizures
Authors: Leutmezer Fritz , Schernthaner Christiana , Lurger Stefanie , Pötzelberger Klaus , Baumgartner Christoph 
Published: March 2003

Summary: Purpose:We studied heart‐rate (HR) changes at the transition from the preictal to the ictal state in patients with focal epilepsies to gain some insight into the mechanisms involved in the neuronal regulation of cardiovascular function.Methods:We assessed ECG changes during 145 seizures recorded with scalp EEG in 58 patients who underwent video‐EEG monitoring. Consecutive RR intervals were analyzed with a newly developed mathematical method for a total of 90 s.Results:Ictal‐onset tachycardia occurred in 86.9% of all seizures, whereas bradycardia was documented only in 1.4%. The incidence as well as the amount of ictal HR increase was significantly more pronounced in patients with mesial temporal lobe epilepsy (TLE) as compared with those with non‐lesional TLE or extratemporal epilepsy. Moreover, right hemispheric seizures were associated with ictal‐onset tachycardia. On average, ictal HR increase preceded EEG seizure onset by 13.7 s in TLE patients and 8.2 s in patients with extratemporal epilepsy. This difference was significant. Ictal HR changes could be classified according to their temporal evolution into two different patterns. These two patterns differed significantly between the temporal lobe and the extratemporal epilepsy patient group.Conclusions:Epileptic discharges directly influence areas of the central autonomic network, thus regulating HR and rhythm. Such changes occur before ictal discharges appear on surface electrodes. Our newly developed method may be of potential use for clinical applications such as automatic seizure‐detection systems. Moreover, our method might help to clarify further the basic mechanisms of interactions between heart and brain.
Epileptogenesis During Development: Injury, Circuit Recruitment, and Plasticity
Authors: Sankar Raman , Shin Don , Liu Hantao , Wasterlain Claude , Mazarati Andrey 
Published: March 2003

Summary:  Purpose: To use animal models of variable seizure induction in rats at different developmental stages to determine contributing factors for spontaneous seizures resulting from status epilepticus (SE) early in life.Methods: Two models of SE with distinct modes of seizure induction, lithium–pilocarpine (LiPC) and perforant path stimulation (PPS), were used at different ages. Multiple methods of determining neurodegeneration during an acute period and plastic changes in those monitored during the chronic phase were used.Results: Different modes of seizure induction lead to varying types and extents of damage, dependent on the age of the animals at the time of insult. LiPC resulted in injury to animals as young as 2 weeks and became widespread in animals 3 weeks old, whereas widespread damage after PPS was not seen until P35. Rats at an age with widespread damage in response to seizures also showed extensive immediate‐early gene activation and often developed spontaneous seizures and features of hippocampal plasticity seen in the epileptic brain.Conclusions: SE early in life results in multiple consequences to the developing brain. These changes, coexisting in the nonepileptic brain, can overlap in a maladaptive combination to result in the diseased state of epilepsy. The consequence of early seizures in immature animals is a function of both the developmental stage and the method of seizure induction.