bluuebunny/crossref_metadata_2025_split huggingface dataset:
Slow‐Frequency Repetitive Transcranial Magnetic Stimulation in a Patient with Focal Cortical Dysplasia
Authors: Menkes Daniel L. , Gruenthal Michael 
Published: August 2005

Summary: Purpose: To evaluate the effect of slow‐frequency repetitive transcranial magnetic stimulation (SF‐rTMS) on interictal epileptiform activity and seizure frequency in a patient with medically refractory partial seizures due to focal cortical dysplasia. Methods: A 9‐cm circular coil was positioned over the area of cortical dysplasia. One hundred stimuli given at 0.5 Hz at 5% below motor threshold were given biweekly for four consecutive weeks. The EEG was recorded for 30 min before and after the first 100 stimuli. The number of seizures during the month of stimulation was compared with that of the month before stimulation. Results: Stimulation was associated with a 70% reduction in the frequency of seizures and a 77% reduction in the frequency of interictal spikes. No seizures occurred during stimulation. Conclusions: SF‐rTMS was safe and well tolerated in this patient. The reduction in seizures and interictal spikes associated with SF‐rTMS supports the concept of SF‐rTMS‐induced cortical inhibition.
MR Spectroscopy Shows Reduced Frontal Lobe Concentrations of N‐Acetyl Aspartate in Patients with Juvenile Myoclonic Epilepsy
Authors: Savic I. , Lekvall A. , Greitz D. , Helms G. 
Published: August 2005

Summary: Purpose: Neuropsychological studies suggest frontal lobe dysfunctions in patients with juvenile myoclonic epilepsy (JME). In this study we investigated whether an underlying mechanism could be a regional neuronal damage not visible with structural magnetic resonance (MR), but detectable with magnetic resonance spectroscopy (MRS). Methods: The study included 15 patients with JME and 10 matched healthy controls. Quantitative single voxel MRS was conducted at 1.5 Tesla by using a STEAM sequence (TR/TE/TM = 6,000/30/13.7 ms). The voxels were placed over the right cerebellum, right thalamus, and the prefrontal and occipital cortex. The quantitation included fitting of transmitter gain, and correction for partial volume of cerebrovascular fluid. LC‐Model was used for estimation of the absolute concentrations of total N‐acetyl aspartate (NAA), cholines, total creatine, and myoinositol. Results: Patients with JME had significantly reduced prefrontal concentrations of NAA in relation to controls (9.1 ± 1.0 vs. 10.2 ± 0.8 mM; p = 0.031 after Bonferroni correction). The other regions showed normal NAA values, as did the other metabolites. Conclusions: The observed reduction in NAA levels suggests a prefrontal neuronal lesion in patients with JME.
Childhood Epilepsy and Asthma: Changes in Behavior Problems Related to Gender and Change in Condition Severity
Authors: Austin Joan K. , Dunn David W. , Huster Gertrude A. 
Published: August 2005

Summary: Purpose: We conducted a 4‐year follow‐up study of behavior problems in children with either epilepsy (n = 115) or asthma (n = 105) to identify changes in behavior problems as they were related to gender and change in condition severity. All children were between ages 8 and 13 years and had been diagnosed with their respective conditions for 1 year at entry into the study. Methods: Behavior problems were measured by using the mother's rating on the Child Behavior Checklist. Baseline and follow‐up behavior problem scores were examined to see if significant changes occurred over the observation period of the study. To explore change in behavior based on condition severity, each child was placed into “low” and “high” condition severity groups at each time, resulting in four groups: low/low, low/high, high/low, or high/high. There were too few cases in the low/high group to be included in some analyses. Data were analyzed by using analysis of covariance with adjustment for baseline behaviors, age, and age of onset. Results: Within both samples, there was a significant improvement over time for the Total Behavior Problems and Internalizing Problems scores (p 0.006). Improvement in Internalizing Problems was greater for the asthma sample than for the epilepsy sample (p 0.007). Within the epilepsy sample, there was a significant gender‐by‐change in seizure condition interaction for Total Behavior Problems, Internalizing Problems, and Externalizing Problems. The interaction effect indicated that behavior problems in girls with high seizure severity at both baseline and follow‐up became substantially worse over the 4‐year period. Conclusions: It was concluded that adolescent girls, particularly those with high‐severity epilepsy during the transition to adolescence, merit closer clinical supervision for behavior problems.
Acute Encephalopathy Associated with Vigabatrin in a Six‐Month‐Old Girl
Authors: Haas‐Lude K. , Wolff M. , Riethmüller J. , Niemann G. , Krägeloh‐Mann I. 
Published: August 2005

Summary: Purpose: Vigabatrin (VGB) is a new‐generation anticonvulsant used in the treatment of partial seizures and West syndrome. Side effects of VGB treatment in adults and children are well described. Acute encephalopathy with VGB has recently been reported in eight adults. They developed stupor, confusion, and electroencephalographic abnormalities after starting VGB. Does the acute encephalopathy with VGB also occur in childhood? Methods: We describe a 6‐month‐old girl with infantile Alexander disease with hydrocephalus who developed similar clinical symptoms with apathia, somnolence, and sopor, as well as slowing of the background activity in EEG, 3 days after starting VGB. After exclusion of shunt dysfunction, encephalitis, metabolic dysfunction, and renal failure, VGB was discontinued. Results: During the next 2 days, symptoms subsided, and after 10 days, EEG background activity returned to the one before starting VGB. Conclusions: Acute encephalopathy associated with VGB in children seems to be very rare, but should not be ignored.
Effects of Gabapentin on Brain GABA, Homocarnosine, and Pyrrolidinone in Epilepsy Patients
Authors: Petroff Ognen A. C. , Hyder Fahmeed , Rothman Douglas L. , Mattson Richard H. 
Published: August 2005

Summary: Purpose: Gabapentin (GBP) was introduced as an antiepileptic drug (AED) and has been used in the management of neuropathic pain. We reported that daily dosing increased brain γ‐aminobutyric acid (GABA) in patients with epilepsy. This study was designed to determine how rapidly brain GABA and the GABA metabolites, homocarnosine and pyrrolidinone, increase in response to the first dose of GBP. Methods: In vivo measurements of GABA, homocarnosine, and pyrrolidinone were made of a 14‐cc volume in the occipital cortex by using a 1H spectroscopy with a 2.1‐Tesla magnetic resonance spectrometer and an 8‐cm surface coil. Six patients (four women) were studied serially after the first oral dose (1,200 mg) of GBP. Five patients (three women) taking a standard daily dose (range, 1,200–2,000 mg) of GBP were rechal‐lenged with a single high dose (2,400 mg). Results: The first dose of GBP increased median brain GABA by 1.3 mM (range, 0.4–1.8 mM) within 1 h. Homocarnosine and pyrrolidinone did not change significantly by 5 h. Daily GBP therapy increased GABA (0.5 mM;95% CI, 0.2–0.9), homocarnosine (0.3 mM; 95% CI, 0.2–0.4), and pyrrolidinone (0.10 mM; 95% CI, 0.06–0.14). Rechallenging patients taking GBP daily increased median brain GABA by 0.4 mM (range, 0.3–0.5) within 1 h. Conclusions: GBP promptly elevates brain GABA and presumably offers partial protection against further seizures within hours of the first oral dose. Patients may expect to experience the anticonvulsant effects of increased homocarnosine and pyrrolidinone with daily therapy.
Sleep and Epilepsy: A Key Role for Nitric Oxide?
Authors: Faradji H. , Rousset C. , Debilly G. , Vergnes M. , Cespuglio R. 
Published: August 2005

Summary: Purpose: It has been suggested that nitric oxide (NO) is involved in sleep mechanisms and in the pathophysiology of epilepsy. Data are, however, controversial because it is not clear whether NO facilitates sleep or waking, or whether it exerts pro‐ or antiepileptic influences. Methods: The question was considered through NO voltammetric measurements and electroencephalographic recordings performed in GAERS rats (Genetic Absence Epilepsy Rat from Strasbourg): an experimental model of “petit‐mal” human disease. Regulatory processes of sleep and epilepsy were studied after administration of a NO synthase inhibitor [l‐arginine‐p‐nitroanilide (lANA) 100 mg/kg i.p.], a NO donor (SIN‐1 100 ng/2 μl i.c.v.), and the antiepileptic drugs used in clinic [valproate (VPA 200 mg/kg i.p.) and ethosuximide (ESM 100 mg/kg i.p.)]. Results: In GAERS rats, spontaneous circadian organizations of spike‐wave discharges and paradoxical sleep (PS) occur in an opposite way; spontaneous NO concentrations are higher during seizures than during wakefulness, slow‐wave sleep, and PS, respectively. lANA induces a disappearance of NO peak, an epileptic induction, and a loss of PS while SIN‐1 induces opposite effects. Antiepileptic effects of VPA and ESM are associated with a PS increase and a significant release of NO. Conclusions: These results indicate that NO could be, in GAERS rats, a central piece in the reciprocal inhibitory mechanisms regulating the induction of PS and spike‐wave discharges. NO could prevent absence epilepsy and act as an antiepileptic substance in facilitating PS. Antiepileptic efficiency of VPA and ESM may work through their ability to release NO. A track for a new treatment of petit‐mal disease in children can be envisioned.
Body Dimensions of Infants Exposed to Antiepileptic Drugs In Utero: Observations Spanning 25 Years
Authors: Wide K. , Winbladh B. , Tomson T. , Källén B. 
Published: August 2005

Summary: Purpose: To investigate the influence of maternal antiepileptic drug (AED) treatment on pregnancy duration, birth weight, body length, head circumference, and intrauterine growth in infants exposed in utero to antiepileptic drugs in Sweden between 1973–1997, with 963 singleton infants. Methods: Data collected from (a) 1973–1981 (record linkage between a hospital discharge register and a medical birth register); (b) 1984–1995 (prospectively collected information in one defined catchment area with two delivery hospitals); and (c) 1995–1997 (medical birth register data). Observed numbers of infants below a defined size for body measurements compared with expected numbers calculated from all births in Sweden after stratification for year of birth, maternal age, parity, and education or smoking habits in early pregnancy. Standard deviation scores estimated with same stratification procedures. Results: Fraction of monotherapy exposures increased from −40% to −90% from 1973 to 1997. Significantly increased numbers of infants with small body measurements found in exposed group. Negative influence on body dimensions decreased over time. More marked effects found in infants exposed to polytherapy. In monotherapy, only infants exposed to carbamazepine consistently showed reduction in body dimensions. Significant effect on gestational age in girls and on number of small for gestational age (<2 SD) in boys. Conclusions: Polytherapy with antiepileptic drugs and negative influence on body dimensions decreased. In monotherapy, only carbamazepine has a negative influence on body dimensions in this study.
Topiramate in Refractory Epilepsy: A Prospective Observational Study
Authors: Stephen Linda J. , Sills Graeme J. , Brodie Martin J. 
Published: August 2005

Summary: Purpose: This prospective observational study explored the efficacy and tolerability of topiramate (TPM) in patients with refractory epilepsy attending a single outpatient clinic. Methods: One hundred seventy patients (82 men, 88 women, aged 18–75 years) with refractory localization‐related (n = 134) or idiopathic generalized epilepsy (n = 36) were started on adjunctive TPM using a standard titration schedule. TPM was introduced after a 3‐month prospective baseline, and doses were adjusted according to clinical response. End points were seizure freedom for 6 months, 50% seizure reduction for 6 months compared with baseline at the highest tolerated TPM dose (responder), or discontinuation of TPM because of side effects, lack of efficacy, or both. Results: Thirty‐nine (23%) patients were seizure‐free, and 80 (47%) more patients had a useful therapeutic response. Thirteen seizure‐free patients and 16 responders took 100 mg of TPM daily or less. TPM was discontinued in 51 (30%) patients. The most common side effects resulting in withdrawal were fatigue, weight loss, irritability, paresthesia, depression, and headache. Concomitant antiepileptic drugs (AEDs) were stopped in 30 patients. Twelve were established on TPM monotherapy, eight of whom remained seizure‐free. Final TPM doses and concentrations varied widely among the three outcome groups. Conclusions: TPM was efficacious as add‐on and mono‐therapy in patients with refractory partial and generalized seizures in everyday clinical use. A good response was obtained in many patients with TPM doses substantially lower than those studied in regulatory clinical trials. The wide variation in dose‐response and dose‐toxicity relationships may reflect different neurobiologies causing refractory epilepsy and differential efficacy of AED combinations.
Newly Diagnosed Epilepsy: Can Nurse Specialists Help? A Randomized Controlled Trial
Authors: Ridsdale L. , Kwan I. , Cryer C. ,   and the Epilepsy Care Evaluation Group
Published: August 2005

Summary: Purpose: To describe a group of people with newly diagnosed epilepsy and to test the effect of an epilepsy nurse specialist on patients' knowledge of epilepsy, satisfaction with the advice provided, and psychological well‐being. Methods: Neurologists in the United Kingdom (U.K.) recruited adults with newly diagnosed epilepsy. Patients were randomized to receive the offer of two appointments with an epilepsy nurse specialist or usual medical care. The main outcome measures were a questionnaire assessing patients' knowledge of epilepsy, the Hospital Anxiety and Depression Scale, and patients' reported satisfaction with the advice and explanations provided on key epilepsy‐related topics. Results: Ninety people with new epilepsy completed the trial. At baseline, fewer than half the patients reported having been given enough advice on epilepsy, and there were important differences in patients' knowledge of epilepsy. Lack of a U.K. school‐leaving examination pass (General Certificate School Examination) was associated with lower knowledge of epilepsy (p = 0.03). At follow‐up, the patients randomized to see the nurse specialist were significantly more likely to report that enough advice had been provided on most epilepsy‐related topics compared with the control group. There were no significant differences in knowledge of epilepsy scores. However, there were significant differences in the group who, at baseline, had knowledge scores in the lowest quartile; those randomized to the nurse had higher knowledge scores (42.7 vs. 37.2; p < 0.01). Compared with doctors, the nurse was highly rated for providing clear explanations. Conclusions: Patients who have less general education have less knowledge of epilepsy. The introduction of a nurse specialist in epilepsy is associated with a significant increase in patient reports that enough advice has been provided. Nurse intervention appears to help those with the least knowledge of epilepsy improve their knowledge scores.
Early and Late Intracortical Inhibition in Juvenile Myoclonic Epilepsy
Authors: Manganotti Paolo , Bongiovanni Luigi Giuseppe , Zanette Gianpietro , Fiaschi Antonio 
Published: August 2005

Summary: Purpose: We investigated 15 patients with juvenile myoclonic epilepsy (JME) by subjecting them to single and paired transcranial magnetic stimulation to test the hypothesis that motor cortical inhibition may be abnormal in this form of benign epilepsy. Methods: Different conditioning paradigms of paired transcranial magnetic stimulation were used with interstimulus intervals (ISIs) of varying lengths (1 to 400 milliseconds) to investigate changes in balance between excitatory and inhibitory intracortical circuits. Results: Motor evoked potential (MEP) inhibition at ISIs of 1 to 4 milliseconds was significantly lower in JME patients than in age‐matched healthy controls (p < 0.001), whereas no significant differences in MEP inhibition were noted at long ISIs (100 to 150 milliseconds). This pattern was observed in both hemispheres in seven of seven patients studied bilaterally and was present in both treated and untreated patients. There were no group differences between JME patients and controls in intracortical facilitation, motor threshold, MEP amplitude, and cortical silent period. Conclusions: We documented a different pattern of MEP inhibition in JME patients, suggesting impaired functioning of inhibitory interneuronal circuits, which may account for the hyperexcitability of the motor system in this form of epilepsy.
Risk of Epilepsy in Long‐Term Survivors of Surgery for Aneurysmal Subarachnoid Hemorrhage: A Population‐Based Study in Iceland
Authors: Olafsson Elias , Gudmundsson Gunnar , Hauser W. Allen 
Published: August 2005

Summary: Purpose: Epilepsy is known to result from aneurysmal subarachnoid hemorrhage (SAH). There are no population‐based estimates of the absolute risk or the duration for which this risk is elevated. We have conducted a population‐based study in Iceland of the risk of epilepsy after a ruptured cerebral aneurysm to address these questions. Methods: The index patients are all of the patients who presented with SAH caused by ruptured cerebral aneurysm in Iceland during an 11‐year period (1958 to 1968) and survived more than 6 months. We determined the number of index patients who developed epilepsy. The observed number of cases of epilepsy was compared with that expected based on the incidence of epilepsy in Iceland. Results: There were 44 index patients; 11 (25%) developed epilepsy, all within 4 years of the insult. Seven (70%) of 10 patients with acute symptomatic seizures (defined as seizures during the first 2 weeks after the hemorrhage) developed epilepsy (relative risk, 7.0; 95% confidence interval, 2.3–21.6). Epilepsy was more frequent in patients with severe neurological residua (48%) compared with patients without (20%) (relative risk, 2.5; 95% confidence interval, 0.9–6.3). Conclusions: The risk for epilepsy among survivors of SAH caused by ruptured cerebral aneurysm is substantially increased. Both acute symptomatic seizure and persistent neurological impairment are associated with a further increase in the risk of epilepsy.
Glutamate Receptor Activation in the Kindled Dentate Gyrus
Authors: Behr Joachim , Heinemann Uwe , Mody Istvan 
Published: August 2005

Summary: Purpose: The contribution of α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazolepropionic acid (AMPA), N‐methyl‐d‐aspartate (NMDA), and kainate receptor activation to the enhanced seizure susceptibility of the dentate gyrus was investigated in an experimental model of temporal lobe epilepsy. Methods: Using the specific NMDA and AMPA receptor antagonists D‐APV and SYM 2206, we examined alterations in glutamate receptor‐dependent synaptic currents 48 hours and 28 days after kindling in field‐potential and voltage‐clamp recordings. Results: Forty‐eight hours after kindling, the fractions of AMPA and NMDA receptor‐mediated excitatory postsynaptic current components shifted dramatically in favor of the NMDA receptor‐mediated response. Four weeks after kindling, however, AMPA and NMDA receptor‐mediated excitatory postsynaptic currents reverted to control‐like values. Neither single nor repetitive perforant path stimuli evoked kainate receptor‐mediated excitatory postsynaptic currents in dentate gyrus granule cells of control or kindled rats. Conclusion: The enhanced excitability of the kindled dentate gyrus 48 hours after the last seizure most likely results from transiently enhanced NMDA receptor activation. The NMDA receptor seems to play a critical role in the induction of the kindled state rather than in the persistence of the enhanced seizure susceptibility.
Plasticity of Excitatory Amino Acid Transporters in Experimental Epilepsy
Authors: Claudio O. I. , Ferchmin P. , Velíšek L. , Sperber E. F. , Moshé S. L. , Ortiz J. G. 
Published: August 2005

Summary:Purpose: To examine the relationship between seizures and excitatory amino acid transporter (EAAT) activity and whether up‐regulation of EAAT activity alters epileptogenicity.Methods: In this study, we exposed rat hippocampal slices to different convulsants before measuring EAAT activity. Rats were exposed to the EAAT inhibitor pyrrolidine‐2,4‐dicarboxylic acid (PDC) before entorhinal cortex/hippocampal slices were obtained. These slices were exposed to low‐Mg2+buffer while electrophysiological recordings were obtained from the entorhinal cortex. mGluR III acting agents were used to study whether activation of mGluR III could regulate EAAT activity and if this regulation could overcome the effects on EAAT activity induced by the convulsants.Results: Veratridine, kainic acid (KA), and pilocarpine reduced EAAT activity in rat hippocampal slices.l‐2‐Amino‐4‐phosphonobutyric acid (an mGluR III agonist) restored EAAT activity and reduced epileptiform activity to near control levels. The saturation curve for glutamate uptake in slices from KA‐seized rats killed 2 hours after the first forelimb clonus was displaced to the left, suggesting a compensatory change for the enhanced excitation. On the other hand, rats injected with the EAAT inhibitor PDC (by intracerebroventricular injection) had more severe KA‐induced seizures andN‐methyl‐d‐aspartate epileptiform activity than control rats. Furthermore, hippocampal slices from KA‐ or KA+PDC‐treated rats exposed to low Mg2+reduced their firing rate to nearly zero once they returned to normal solution, whereas their control counterparts continued to fire, although at a lower rate.Conclusions: These results suggest a significant contribution of EAATs in some experimental epilepsy models and point to their short‐term regulation by mGluR III as a possible source of their plasticity.
Autosomal Dominant Nocturnal Frontal Lobe Epilepsy in a Japanese Family
Authors: Kobayashi Kenichiro , Ito Maatoshi , Fujii Tatsuya , Miyajima Tomoko , Okuno Takehiko 
Published: August 2005

Purpose: Autosomal dominant nocturnal frontal lobe epilepsy (AD‐ NFLE) is a newly recognized partial epilepsy first reported by Scheffer ct al. Thc aim of our work is to describc the clinical picture of thc disease found for the first time in a Japanese fiunily.Method: Affected members were investigated electroclinically, and thc mutations within ncuronal nicotinic acctylcholinc rcceptor alpha‐4 subunit (CHRNA4) gene were examined. Results: All affccted members presented clusters of brief tonic seizures, secondarily generalized, which occurred exclusively in sleep. The scimrc symptomatology and clcctrocnccphalographic findings were compatible with those of ADNFLE. None of the members had aura prcccding the scizure and nonc was aware of the seizure. They all had the same point mutation in the CHRNA4 gene, although intrafiamilial variations of seizure severity such as onset, frequency, and response to therapy were noted. Conclusions: We described the first instances of ADNFLE in a Japanese family with a novel missense mutation of exon 5 of the CHRNA4 gene. It was a C to T transition and replaces serine in the second mcmbranc‐spanning domain (M2) with lcucine (scr 252 LCU). We suggest that intra‐familial heterogeneity is one of the important aspects or ADNFLE.