bluuebunny/crossref_metadata_2025_split huggingface dataset:
Heart Disease Mortality and Morbidity in Patients with Epilepsy
Authors: Annegers John F. , Hauser W. Allen , Shirts Sally B. 
Published: November 2007

Summary: All‐cause and heart disease mortality and ischemic heart disease incidence among patients with an initial diagnosis of epilepsy while residents of Rochester, MN, from 1935 through 1979 were determined. Death rates from heart disease were slightly elevated for persons with epilepsy. The increased death rate from heart disease was confined to persons <65 years of age. The incidence of ischemic heart disease and of sudden cardiac death as the initial manifestation of ischemic heart disease was significantly increased in persons with epilepsy, but the increase was primarily limited to those with symptomatic epilepsy attributed to cerebrovascular disease. The occurrence of ischemic heart disease and sudden cardiac death was not related to anticonvulsant medication status.RESUMENLa mortalidad de las enfermedades cardiiacas, y de todas las causas, y la incidencia de enfermedades cardiacas isquémicas entre los pacientes con un diagnóstico inicial de epilepsía mientras eran résidentes en Rochester, Minesota, desde 1.935 a 1.979 ha sido determinada. El número de fallecimientos de enferme dades cardiacas fué ligeramente más elevados en las personas que padecían epilepsía. El aumento del número de muertes por enfermedades cardiacas estaba limitado a personas menores de 65 años. La incidencia de enfermedad cardiaca isquémica y de muerte cardiaca repentina, como única manifestatión de enfermedad isquémica cardiaca, estaba aumentada significativamente en personas con epilepsia pero este aumento estaba limitado, primariamente, a los enfermos con epilepsia sintomática atribuída a enfermedades cerebrovasculares. La presencia de enfermedad cardiaca isquémica y muerte cardiaca súbita no estaba relacionada con el estado de la medicación anticonvulsivante.ZUSAMMENFASSUNGAus den Jahren 1935 bis 1979 wurde bei alien Einwohnern von Rochester, Minnesota mitder initialen Diagnose einer Epilepsie Ursache und Mortalität von Herzerkrankungen und Häufigkeit ischämischer Herzerkrankungen bestimmt. Die Todeshäufigkeit an Herzerkrankungen war fiir Patienten mit Epilesie geringfiigig erhöht. Diese erhöhte Todeshäufigkeit an Herzerkrankungen war auf Personen unter 65 Jahren beschränkt. Die Häufigkeit ischämischer Herzerkrankungen und plötzlicher Todesfälle als initi‐aler Manifestation einer ischamischen Herzerkrankung war bei Patienten mit Epilepsie signifikant erhöht; die Zunahme war primär beschränkt auf Patienten mit symptomatischer Epilepsie aufgrund einer cerebrovaskulären Erkrankung. Die Häufigkeit ischämischer Herzerkrankungen und plötzlicher Herztodesfälle zeigte keine Beziehung zur antikonvulsiven Medikation.
Topographical Analysis of the Centrotemporal Discharges in Benign Rolandic Epilepsy of Childhood
Authors: Gregory D. L. , Wong P. K. 
Published: November 2007

Summary: The onset, distribution, and spread of the average of 20 centrotemporal discharges for each of 10 patients with typical benign rolandic epilepsy of childhood (BREC) were examined using a computerized topographical mapping technique. A stereotypic dipole field was present along the rolandic region in all discharges. During its most prominent phase, the negative pole of the dipole was maximum at the centrotemporal region, with the positive pole involving the bifrontal region. A hypothesis is proposed that all discharges arise from a single generator which is oriented tangential to the surface. The generator is most likely situated in the lower rolandic region where the zero potential zone exists, between the frontal positivity and the centrotemporal negativity. Identification of this dipole configuration may be useful for differentiating BREC from focal epilepsy of other etiologies.RÉSUMÉLe début, la distribution, et la propagation de la moyenne de 20 décharges centrotemporales pour chacun de dix patients ayant une épilepsie rolandique bénigne de l'enfant (EPR), ont étéétudiés, en utilisant une technique d'analyse topographique computorisée. Un champ dipole stéréotypéétait présenté sur la région rolandique dans toutes les décharges. Pendant sa phase la plus importante, le pôle négatif du dipole était maximum dans la région centrotemporale, et le pôle positif occupant la région bifrontale. Il est proposé l'hypothèse que toutes les décharges proviennent d'un seul générateur qui est orienté tangentiellement á la surface. Le générateur est le plus probablement situé dans la région rolandique basse ou existe la zone de potentiel zéro, entre la positivité frontale et la négativité centro‐temporale. L'identification de la configuration de ce dipole peut être utile pour différencier l'EPR des epilepsies focales d'autres etiologies.ZUSAMMENFASSUNGDer Beginn, die Verteilung und die Ausbreitung des Mittel‐werts 20 centrotemporaler Entladungen bei jedem der 10 Pa‐tienten mit typischer benigner Rolandischer Epilepsie des Kin‐desalters (B.R.E.C.) wurden mit Hilfe einer komputerisierten topographischen Landkartentechnik untersucht. Ein stereotyp‐isches Dipol‐Feld konnte bei alien Entladungen entlang der Ro‐landischen Region beobachtet werden. Auf seinem Höhepunkt zeigte der negative Pol zur Zentro‐Temporal‐Region, der positive Pol zu beiden Frontalregionen. Als Hypothese wird vorge‐schlagen, daβ alle Entladungen von einem einzigen Generator ihren Ausgang nehmen, der tangential zur Oberfläche orientiert ist. Dieser Generator sitzt am wahrscheinlichsten in der unteren Rolandischen Gegend, in der das Nullpotential zu denken ist zwischen der frontalen Positivität und der zentro‐temporalen Negativität. Die Identifizierung dieser Dipol‐Konfiguration mag nützlich sein für Differenzierung von B.R.E.C. und fokalen Epi‐lepsien anderer Ätiologie.
Some Clinical and EEG Aspects of Benign Juvenile Myoclonic Epilepsy
Authors: Asconapé Jorge , Penry J. Kiffin 
Published: November 2007

Summary: Twelve patients with benign juvenile myoclonic epilepsy (BJME) representing 4% of our population of epileptics (n = 275) are presented. Only two patients (17%) had myoclonic jerks as the only seizure type. Seven (58%) had generalized tonic‐clonic seizures (GTCS) and myoclonus. Three patients (25%) had absence seizures (AS), GTCS, and myoclonic jerks. Electroencephalographic evidence of photosensitivity was found in four (33%). Auditory precipitation of seizures was found in one patient. As is the case with other primary generalized epilepsies, the onset of BJME seems to be age specific. In our series the mean age of onset in years was 4.3 for AS, 14.75 for myoclonic jerks, and 16.4 for GTCS. It took an average of 8.5 years from the onset of BJME (range, 2–20 years) and 6.5 years from the onset of GTCS (range, 2 months‐6 years) until the condition was properly recognized. Five patients experienced at least one episode of myoclonic status epilepticus. Generalized, paroxysmal, symmetric poly spike and slow wave discharges are the typical EEG finding. These complexes, however, showed considerable interpatient variability. Sleep deprivation proved to be the most valuable activating procedure. Valproic acid monotherapy effectively controlled myoclonic jerks as well as associated GTCS in most patients.RESUMENSe presentan los hallazgos clínicos y electroencefalográficos de 12 pacìentes con epilepsia juvenil mioclónica benigna. Dichos individuos representan el 4% de nuestra población de pacientes epilépticos (n = 275). Sólo dos pacientes (17%) presentaron mioclonias exclusivamente, sin otro tipo de crisis epilépticas. Siete pacientes (58%) presentaron la combinación de mioclonias y crisis generalizadas tónico clónicas. Tres pacientes (25%) de‐mostraron mioclonias, ausencias y crisis generalizadas tónico clónicas. Evidencia electroencefalográfica de fotosensibilidad se demostró en cuatro casos (33%). Un paciente presentó precipitación auditiva de crisis epilépticas. En forma similar a otros tipos de epilepsia generalizada, la edad de comienzo de la epilepsia juvenil mioclónica benigna resulto ser específica. La edad de comienzo en años, para los distintos tipos de crisis epilépticas, fue la siguiente: 4,3 en las ausencias; 14,75 en las mioclonias; y 16,4 en las crisis generalizadas tónico clónicas. El diagnóstico correcto de esta forma de epilepsia se demoró un promedio de 8,5 años desde el comienzo de las mioclonias (rango, 2–20 años) y 6,5 años desde el comienzo de las crisis generalizadas tónico clónicas (rango, 2 meses‐6 años). Cinco pacientes demostraron, por lo menos, un episodio de estado epiléptico mioclónico. El hallazgo típico en el EEG es la polipunta onda, generalizada, simétrica. Dichas descargas, sin embargo, demostraron una variabilidad considerable entre los diferentes individuos. La deprivación de sueño demostró ser un valioso método de activación. Monoterapia con ácido valproico controló las mioclonias y las crisis generalizadas tónico clónicas en la mayoria de los casos.
Electroencephalographic Alterations During Intoxication with Sodium Valproate:A Case Report
Authors: Pedersen Birthe , Juul‐Jensen Palle 
Published: November 2007

Summary: A case of severe valproic acid poisoning with coma and insufficient respiration is reported. The clinical condition and EEG changes are presented. The patient recovered completely, and the toxicity of sodium valproate to the brain and the liver in severe intoxication is discussed.RESUMENSe presenta un caso de intoxicación severa por ácido valpróico con coma e insuficiencia respiratoria y, en especial, la situación clínica y los cambios en el EEG. El enfermo se recuperó total‐mente. Se discute la toxicidad cerebral y hepática del valproato sódico en casos severos.ZUSAMMENFASSUNGBericht eines Falles einer schweren Valproinsäurevergiftung mit Koma und Ateminsuffizienz. Das klinische Bild und die EEG‐Veränderungen werden mitgeteilt. Der Patient erholte sich vollständig. Die Toxizität des Natrium Valproat für das Gehirn und die Leber bei schweren Intoxikationen wird diskutiert.
Enhanced Gastrointestinal Excretion of Phenytoin in a Patient with Crohn's Disease
Authors: Lesser Ronald P. , Irace P. , Kutt H. , Pippenger C. E. , Winkelman E. L. , Terrentine S. , Gardner M. 
Published: November 2007

Summary: : A patient with Crohn's disease and generalized seizures who lacked the distal small bowel and ascending colon required 600 mg of intravenous phenytoin daily (11 mg/kg/24 h) to maintain her plasma phenytoin levels in the 12–24 μg/ml range. She received no oral phenytoin. Stool volumes ranged from 1,125 to 1,875 ml/ 24 h, and stool fraction phenytoin levels from 15 to 41 μ.g/ml. Urinary 5‐(p‐hydroxyphenyl)‐5‐phenylhydantoin and phenytoin levels in three 24‐h samples were sufficient to account for 26, 46, and 57% of the administered drug, compared with the expected 70–90%. This was most likely due to an alteration of the normal cycle of absorption and reexcretion between the intestinal lumen and the blood resulting in net excretion of phenytoin into the bowel.RESUMENUna paciente con enfermedad de Crohn y ataques generalizados a quien le faltaba el intestino delgado distal y el cólon ascendente requireó 600 mg diarios de fenitoina intravenosa (11 mg/kg/24 horas) para mantener los niveles plasmáticos de fenitoina en el rango 12–24 μg/ml. No recibió fenitoina oral. Los volúmenes de heces oscilaron entre 1125–1875 ml/24 horas y los niveles de fenitoina en fracciones de heces entre 15–41 mug/ml. Los niveles en orina de HPPH y fenitoina, en 3 muestras de 24 horas, fueron suficientes para corresponder al 26, 46 y 57% de la droga administrada comparados con el calculado de 70–90%. Esto fue, probablemente, debido a una alteración del ciclo normal de absorción y re‐excreción entre la luz del intestino y sangre que conduce a una excreción neta de fenitoina en el intestino.ZUSAMMENFASSUNGEine Patientin mit M. Crohn und generalisierten Anfällen, ohne distalen Dünndarm und Colon aszendenz benötigte täglich 600 mg Phenytoin i.v. (11 mg/kg/die) um Plasmaspiegel zwischen 12 und 24 μg/ml aufrechtzuerhalten. Sie erhielt kein Phenytoin oral. Das Stuhlvolumen schwankte zwischen 1125 bis 1875 ml/ die und die Phenytoinausscheidung im Stuhl betrug 15 bis 41 (xg/ ml. Urin HPPH und Phenytoinspiegel in drei 24‐Stundenproben erreichten 26, 46 and 57% des zugeführten Medikaments verglichen mit dem Erwartungswert von 70 bis 90%. Der Grund hierfür liegt wahrscheinlich in einer Veränderung des normalen Kreislaufs von Absorptionund Wiederausscheidung aus dem Darmlumen bzw. dem Blut, die zu einer Exkretion des Pheny‐toins in den Darminhalt führte.
Non‐Dose‐Related Side Effects of Valproate
Authors: Jeavons P. M. 
Published: November 2007

SUMMARYThe clinical and histological findings in 88 patients in whom hepatotoxicity with valproate has been reported were reviewed.The characteristic lesion is microvesicular steatosis. Hepatotoxicity appears to be an idiosyncratic reaction and is most likely to appear within 6 months from the start of therapy, especially in young patients on comedication. The condition may be reversible if the drug is immediately withdrawn in patients who show acute gastrointestinal symptoms, drowsiness or lethargy, jaundice, or change in seizure pattern. Clinical monitoring is more important than laboratory monitoring.The outcome of pregnancies in 344 women who received valproate in the first trimester was reviewed. There were 225 normal babies and 68 abnormal babies. The role of valproate in the aetiology of neural tube defects remains uncertain, but mothers treated with valproate should receive prenatal counselling.
Sodium Valproate and Cognitive Function
Authors: Trimble Michael R. , Thompson Pamela J. 
Published: November 2007

SUMMARYThe literature concerning the effects of sodium valproate on cognitive function was reviewed, including both volunteer and patient studies. Two were reported from the National Hospital—one a double‐blind crossover investigation against placebo in volunteers, and the other in patients on monotherapy. It was concluded that sodium valproate has minimal adverse effects, although those that are seen are probably dose related. It has less of an effect on cognitive function than some of the other commonly used anticonvulsants.
Amino Acid Neurotransmitters and New Approaches to Anticonvulsant Drug Action
Authors: Meldrum Brian 
Published: November 2007

Summary: Amino acids provide the most universal and important inhibitory (γ‐aminobutyric acid (GABA), glycine) and excitatory (glutamate, aspartate, cysteic acid, cysteine sulphinic acid) neurotransmitters in the brain. An anticonvulsant action may be produced (1) by enhancing inhibitory (GABAergic) processes, and (2) by diminishing excitatory transmission. Possible pharmacological mechanisms for enhancing GABA‐mediated inhibition include (1) GABA agonist action, (2) GABA prodrugs, (3) drugs facilitating GABA release from terminals, (4) inhibition of GABA‐transaminase, (5) allosteric enhancement of the efficacy of GABA at the receptor complex, (6) direction action on the chloride ionophore, and (7) inhibition of GABA reuptake. Examples of these approaches include the use of irreversible GABA‐transaminase inhibitors, such as γ‐vinyl GABA, and the development of anticonvulsant β‐carbolines that interact with the “benzodiazepine receptor.” Pharmacological mechanisms for diminishing excitatory transmission include (1) enzyme inhibitors that decrease the maximal rate of synthesis of glutamate or asparate, (2) drugs that decrease the synaptic release of glutamate or aspartate, and (3) drugs that block the post‐synaptic action of excitatory amino acids. Compounds that selectively antagonise excitation due to dicarboxylic amino acids have recently been developed. Those that selectively block excitation produced by N‐methyl‐D‐aspartate (and aspartate) have proved to be potent anticonvulsants in many animal models of epilepsy. This provides a novel approach to the design of anticonvulsant drugs.Summary: Animal studies show potent anticonvulsant actions of pharmacological agents that either specifically enhance GABAergic inhibition or decrease excitatory transmission by dicarboxylic amino acids. This evidence supports the concept that some established anticonvulsant drugs act on inhibitory and excitatory transmission. It provides a theoretical framework for the search for new anticonvulsant drugs. The optimal anticonvulsant agents are likely to possess a subtle combination of selective actions on both excitation and inhibition.
The Relevance of Secondary Epileptogenesis to the Treatment of Epilepsy: Kindling and the Mirror Focus
Authors: Goldensohn Eli S. 
Published: November 2007

Summary: Human beings with partial epilepsy and demonstrable cerebral lesions show, in addition to ipsilateral epileptiform EEG discharges, apparently independent epileptiform discharges from the opposite hemisphere. Patients with apparent unilateral focal onset of their partial seizures but without demonstrable lesions also frequently display what appear to be bilaterally independent EEG foci. When surgical treatment or medical prognosis is considered and there is no demonstrable lesion, the decision of which of the two apparent foci is primarily responsible for the seizures is often difficult.Even with a known structural lesion the question arises whether, following its removal, the contralateral focus will persist and will be epileptogenic. Two related experimental phenomena bear directly on these questions—kindling and the mirror focus. This presentation looks critically at existing evidence and finds that it fails to support the idea that kindling and the mirror focus have roles in human epilepsy that currently should influence clinical decisions.
Bicuculline Methiodide in the Blood‐Brain Barrier‐Epileptogen Model of Epilepsy
Authors: Remler Michael P. , Marcussen William H. 
Published: November 2007

Summary: Focal epilepsy can be produced by a blood‐brain barrier (BBB)‐excluded systemic convulsant (penicillin, folic acid, etc.) in the presence of a focal BBB lesion. Bicuculline methiodide, a γ‐aminobutyric acid blocking epileptogen, crosses the normal BBB of rats poorly and produces no consistent abnormality behaviorally or on EEG at 36 mg/kg. When the BBB is opened in 0.25 ml of cortex by 6,000 rad of α particles, by a pin trauma lesion, or by a heat lesion, the rats are normal clinically and on EEG. When these lesioned rats are challenged with bicuculline methiodide, 36 mg/kg, an intense, highly localized epileptiform discharge results that begins ˜ 20 min after injection and lasts 30–90 min. The plausibility and experimental utility of the BBB‐epileptogen model of epilepsy are enhanced by these observations.RÉSUMÉOn peut provoquer une épilepsie focale avec un convulsivant systémique exclu par la barrière hémo‐cérébrale (BBB) si on crée une lésion dans cette barrière. La bicuculline methiodide (Bm), 4Apileptogène bloquant l'acide gamma aminobutyrique (GABA), traverse peu la BBB des rats et n'entraîne pas d'anomalie du comportement ou de l'EEG à la dose de 36 mg/kg. Quand la BBB est ouverte sur 0,25 cc de cortex, par 6 000 r de particules alpha, par lésion traumatique ou par le chaleur, les rats sont chiniquement normaux et ont un EEG normal. Quand on administre à ces rats porteurs d'une lésion 36, mg/kg de Bmon provoque une décharge éjpileptiforme intense, très localisée, qui commence environ 20 minute ajprés l'injection et dure 30 à 90 minutes. Ces observations mettent en évidence l'intérêt du modèle d'épilepsie BBB‐épileptogène.
Spread of Epileptic Seizure Activity in Humans
Authors: Mars Nicolaas J. I. , Thompson Paul M. , Wilkus Robert J. 
Published: November 2007

Summary: A computer‐augmented approach to ictal EEG analysis has been developed. A method for determining both the predictability of one signal from another and the time delay between those two signals—the average amount of mutual information (AAMI) method—has been applied to representative seizures of two patients with focal‐onset seizures and one patient with generalized seizures. High AAMI values characterized the EEG derived from the sites of the epileptic foci. AAMI values were high in all sampled brain areas in the patient with generalized seizures. Time delays were not consistent in any subject. The results indicate that the AAMI technique can differentiate focal from generalized seizures and identify the site of seizure onset.RÉSUMÉUne analyse par ordinateur de l'activité EEG critique a été entreprise. Une technique permettant de déterminer à la fois la prédictibilité d'un signal par rapport aG l'autre et le délai de temps entre ces deux signaux (la méthode de la quantité moyenne d'information mutuelle (AAMI)) a été appliquée à des crises représentatives à 2patients ayants des crises à début focal et un patient ayant des crises généralisées. Les EEG provenant du siège des foyers épileptiques avgaient des valeurs AAMI élevées. Les valeurs AAMI étaient élevées dans tous les échantillions EEG de toutes les aires cérébrales homologues dans le cas ayant des crises généralisées. Il n'y avait de délai de temps significatif chez aucun sujet. Ces résultats indiquent que la meathode AAMI peut différencier les crises focales des crises généralisées et identifier le siège du début des crises.RESEUMENSe ha desarrollado una neueva lécnica para anàlisis del EEG ictal mediante un sistema de computerización—aumentada. Un método para determinar la predictibilidad de una señal partiendo de otra y la latencia temporal entre estas dos señales—método de Cantidad de Promedio de Información Mutua (AAMI)—ha sido aplicado a lso ataques representativos de dos enfermos con ataques de comienzo focal y u paciente con cirisis generalizadas. Valores altos de AAMI caracterizaron el EEG que se derivaba de los lugares de los focos epilépticos. Los valores del AAMI estaban elevados en todas las muestras de las áreas cerabrales estudiadas en el caso de crisis generalizadas. Las latencias temporales no fueron consisentes en ningún sujeto. Estos resultados indican que la técnica de AAMI puede diferenciar los ataques focales de los generalizados en identifar el lugar de origen de origen de las crisis.
Developmental Hyperthermic Seizures Alter Adult Hippocampal Benzodiazepine Binding and Morphology
Authors: Chisholm Jane , Kellogg Carol , Franck J. E. 
Published: November 2007

Summary: Experimental hyperthermic seizures in 15‐day‐old rats resulted in both an alteration in the benzodiazepine (BDZ) binding site in the hippocampal region and morphologic changes in hippocampal neurons. These alterations were not apparent until adulthood. Experimental adult animals also showed a reduced anticonvulsant response to a selective BDZ ligand when challenged with pentylenetetrazol. Developmental hyperthermic seizures may initiate dynamic changes in the hippocampus that contribute to adult functional impairment.RÉSUMÉDes crises hyperthermiques, créées expérimentalement chez des rats âgés de 15 jours ont entrainéà la fois des altérations des sites de liaison des benzodiazepines au niveau de l'hippocampe et des modifications morphologiques des neurones hippocampiques. ces altérations n'ont étéévidentes qu'ag l'âge adulte. chez les animaux d'expérience adultes on trouvait aussi une réonse anticonvulsivante diminuée à un ligand benzodiazepinique sélectif testé avec le pentylenetetrazol. les crises hyperthermiques au cours du développement peuvent donc être le point de départ de modifications hippocampiques qui contribuent à son dysfonctionnement à l'âge adulte.RESUMENLas crisis hipertérmicas experirnentales en ratas de 15 días de edad producen una alteratión en el lugar de unión de la benzodiazepinaen la región del hipocampo y cambios morfológicos en las neuronas del hipocampo. Estas alteraciones no fueron aparentes hasta la edad adulta. Los animales adultos también mostraron una respuesta anticonvulsiva reducida a1 ligando selectivo de la carbamazepina cuando fué comparada con pentylentetrazol. El desarrollo de crisis hipertérmicas puede iniciar cambios dinámicos en el hipocampo que pueden contribuir a un deterioro funcional en el adulto.