bluuebunny/crossref_metadata_2025 huggingface dataset:
Oculoclonic Status Epilepticus
Authors: Kanazawa Osamu , Sengoku Akira , Kawai Itsuo
Published: November 2007

Summary: Continuous oculoclonic status epilepticus occurred for 90 min in a 4‐year‐old girl. The seizure consisted of continuous contralateral horizontal nystagmus concurrent with left occipital spike discharges, occasional vomiting and no loss of consciousness. Oculoclonic status epilepticus may be a variant form of versive status epilepticus.

Un état de mal oculoclonique de 90 minutes a été constaté chez une fillette de 4 ans.épisode critique a été représenté par un nystagmus horizontal contralatéral continu associéà des décharges de pointes occipitales gauches, quelques vomisse‐ments, alors qu'il n'y avait pas de perte de connaissance. état de mal oculochlonique peut représenter une variante de état de mal versif.

Una niña de 4 anos presentó un status epilepticus oculoclónico durante 90 minutos. El ataque consistió en nistagmus horizontal contralateral contínuo coincidente con descargas de puntas occipitales izquierdas y vómitos ocasionales sin pérdida de conocimiento. El status epilepticus oculoc16nico puede ser una variante del status epilepticus versivo.

Bei einem 4‐jährigen Mädchen trat ein 90 Minuten langer kontinuierlicher okuloklonischer Status epilepticus auf. Der Anfall bestand aus: kontralateralem, horizontalen Nystagmus, begleitet von linksseitigen spike‐Entladungen, gelegentlichem Erbrechen ohne Bewußtseinsverlust. Der okuloklonische Status epilepticus könnte als Variante des versiven Status epilepticus gedeutet wer‐den.
Tolerance to Anticonvulsant Effects of Diazepam, Clonazepam, and Clobazam in Amygdala‐Kindled Rats
Authors: Rosenberg Howard C. , Tietz Elizabeth I. , Chiu Ted H.
Published: November 2007

Summary: Benzodiazepines are effective anticonvulsants, but long‐term clinical usefulness is limited by development of tolerance. Tolerance to the actions of three prototype anticonvulsant benzodiazepines (BZDs)– diazepam (DZP), clonazepam (CZP), and clobazam (CLB)–was studied in amygdala‐kindled rats. Fully kindled rats were dosed three times daily for 2 or 4 weeks. Amygdala stimulation was given 30 min after drug administration on days 1,2, 3,5, and 7 of chronic treatment and then three times weekly. During treatment, tolerance was observed as a loss of drug effect to suppress behavioral and EEG manifestations of seizure activity. Seizure activity remained stable in rats treated with vehicle. Tolerance to the anticonvulsant effects developed most rapidly during CLB treatment and most slowly during CZP treatment. Tolerance to the motor impairment caused by the drugs developed more rapidly. Assay of the amount of drug in brain extracts, using a BZD receptor assay, showed that tolerance was functional, not metabolic. Doubling the dose did not readily restore full anticonvulsant activity. The response to amygdala stimulation 24 h after treatment was stopped showed no residual BZD effect, but there was a rebound in duration of some seizure measures in rats that had been treated with CLB or DZP. Retesting 48 h after treatment was stopped showed that rats were still tolerant. The amygdala‐kindled rat is a reliable and sensitive model for studying long‐term actions of anticonvulsant BZDs.
Neonatal Sleep Myoclonus Followed by Myoclonic‐Astatic Epilepsy: A Case Report
Authors: Nolte Renate
Published: November 2007

Summary: Neonatal sleep myoclonus documented poly‐graphically during the second month of life and subsequent development of a seizure disorder are reported in a 3‐year‐old boy. Several generalized tonic‐clonic seizures associated with febrile illnesses occurred during the first year of life; astatic and myoclonic attacks began at age 13 months. A complex partial seizure occurred for the first time at age 3 years. Differential diagnosis of age‐related generalized myoclonic epileptic syndromes and various forms of neonatal myoclonus were considered in this unusual case.
Benign Partial Epilepsy with Centrotemporal (or Rolandic) Spikes and Brain Lesion
Authors: Santanelli P. , Bureau M. , Magaudda A. , Gobbi G. , Roger J.
Published: November 2007

We describe three patients with benign partial epilepsy with centrotemporal spikes (BECT) in association with proven brain lesion (agenesis of the corpus cal‐losum, lipoma of the corpus callosum, and congenital toxoplasmosis, respectively). The age of onset, the ictal signs, the interictal electroencephalographic findings and the favorable outcome of epilepsy even after withdrawal of drug therapy led to the diagnosis of BECT although organic brain lesions were present. In such cases, the epilepsy should not be ascribed to the lesions but should be considered benign even though fortuitiously associated with brain lesions.

Les auteurs rapportent les observations de trois enfants présentant une épilepsie partielle bénigne à pointes centrotemporales (EPCT), (ou rolandiques) assoctée à une lésion cérébrale: agénésie du corps calleux, lipome du corps calleux et toxoplasmose conge'nitale respectivement. L'âge de début, la séméologie des crises, les caractéres électroenc éphalo‐graphiques, la bonne évolution de l'épilepsie même après arrêt du traitement permettent de poser le diagnostic d'EPCT malgré la présence d'une lésion cértérale à laquelle l'épilepsie ne doit pas étre attributé. Dans ces trois observations, l'épilepsie doit être considérée comme bénigne et fortuitement associée à une lésion céirébrale.

Die Autoren berichten über 3 Patienten mit benigner Partial‐Epilepsie mit zentro‐temporalen Spikes (BECT) und gleichzei‐tigem Vorkommen einer erwiesenen Himläsion (Corpus callosum‐Agenesie, Lipom des Corpus callosum und congenitale Toxoplasmose). Anfallsbeginn, Anfallsbild, interiktaler EEG‐Befund und der günstige Verlauf der Epilepsie nach Absetzen des Medikamentes führten zur Diagnose BECT trotz vorliegen‐der Himläsion. In diesem Fall soUte die Epilepsie nicht ätiolo‐gisch der Läsion zugeschrieben werden, sondem soUte als zu‐fällig mit der Läsion gemeinsam auftretend interpretiert werden.
Electrophysiologic Effects of γ‐Vinyl GABA and Carbamazepine
Authors: Mervaala Esa , Partanen Juhani , Nousiainen Unto , Sivenius Juhani , Riekkinen Paavo
Published: November 2007

Summary: The effects of ‐γ‐vinyl GABA (GVG) and carbamazepine (CBZ) monotherapy on somatosensory (SEP) and visual (VEP) evoked potentials and spectral quantitative EEG (QEEG) were studied in 17 patients with complex partial seizures using a cross‐over double‐blind study design. CBZ was associated with statistically significant prolongation of SEP latencies. When the drug was switched to GVG, shortening of the peak latencies was observed. Prolonged pattern‐VEP peaks were observed both during CBZ and GVG monotherapies. A similar but more subtle tendency of the peaks was observed in P100 latencies. Spectral EEG revealed a slowing of the occipital rhythm with CBZ. No QEEG changes related to GVG were found. The use of multimodal evoked potentials and QEEG should be considered in studying the effects of new antiepileptic drugs (AEDs). Key Words: An‐tiepileptic drugs–γ‐Vinyl GABA–Carbamazepine– Electroencephalography–Evoked potentials–Spectral EEG.

Les effets du Gamma‐vinyl‐GABA (GVG) et de la carbamazépine (CBZ) sur les potentiels évoqués somesthésiques (PES) et visuels (PEV) ainsi que sur l'EEG quantifé par analyse spec‐trale ont étéétudiés chez 17 patients présentant des crises partielles complexes dans une protocole croisé en double aveugle. La CBZ a été associée à un allongement significatif des latences des PES. Lorsque la CBZ était remplacés par le GVG, une di minution des latences du pic était observed. Un retard au pic des PEV par damiers a été observé sous monothérapie par CBZ et par GVG. Une tendance similaire, mais moins prononcée, a été constatée dans l'éude des latences P100. L'EEG spectral a mis en évidence un ralentissement du rythme occipital sous CBZ; il n'a pas été constaté de modification de l'EEG quantifé sous GVG. Les potentiels évoqués multimodalitaires et l'EEG quantifié devraient être utilisés dans l'évaluation des nouveaux medicaments anti‐épileptiques.

En 17 enfermos con ataques parciales complejos y utilizando un estudio cruzado doble ciego, se nan valorado los efectos del Gamma‐vini] GABA (GVG) y de la Carbamazepina (CBZ) como monoterapias, sobre los potenciales evocados somatosensoriales (SEP) y visuales (VEP) y sobre el estudio espectral cuantitativo del EEG (QEEG). Se observó que la CBZ mostraba una prolon‐gación estadisticamente significativa de las latencias de los SEP. Cuando la medicación se cambio a GVG se observó un acor‐tamiento de los picos de las latencias. El patrón de alargamiento de los picos de los VEP se observó tanto durante la monoterapia con CBZ como con la GVG. Una tendencia similar pero mis sutil de los picos se observd en las latencias P100. El EEG espectral revelo una lentificación de los ritmos occipitales con CBZ. No se encontraron cambios del QEEG relacionables al tratamiento con GVG. La utilización de potenciales evocados multimodales y el QEEG debería ser considerada en el estudio de los efectos de las drogas antiepilépticas.
Prolonged Spontaneous Complex Visual Hallucinations and Illusions as Ictal Phenomena
Authors: Sowa Marian V. , Pituck Stephen
Published: November 2007

Summary: A patient without a previous history of seizures had a generalized tonic‐clonic seizure followed by multiple complex visual hallucinations and illusions (CVHIs) lasting weeks. The patient reported a total of 19 different CVHIs. EEGs performed revealed rhythmic right temporal activity occurring only during the CVHIs. Treatment with antiepileptic drugs (AEDs) resolved the CVHIs and normalized the EEG. An attempt at discontinuation of one AED resulted in a resurgence of the CVHIs and EEG abnormality.

Les auteurs rapportent une observation dans laquelle, en l'absence d'antécédents épileptiques, est survenue une cris généralisée tonico‐clonique qui a été suivie par des hallucinations et illusions visuelles complexes multiples qui ont duré des se‐maines. 19 épisodes différents sont survenus. Les EEG ont révélé l' existence d' une activité rythmique temporale droite qui n'était présente que pendant les épisodes. Le traitement par médicaments antiepiléptiques a interrompu la survenue de ces épisodes et a normalisé l'EEG. Un essai d'arrêt de l' un des médicaments antiépileptiques a été suivi d'une récidive des episodes et des anomalies EEG.

Un enfermo sin historia previa de ataques presentó ataques generalizados tónico‐clónicos seguidos de múltiples alucina‐ciones e ilusiones visuales complejas (CVHI) que persistieron durante semanas. El paciente describfa un total de 19 CVHI diferentes. Los EEGs mostraron una actividad rítmica temporal derecha sólamente durante las CVHI. El tratamiento con medicaciones anti‐epilepticas eliminó las CVHI y normalizeó el EEG. Un intento de interruptión de este tratamiento produjo la reaparición de las CVHI y de las anomalías en el EEG.

Ein Patient ohne Anfallsvorgeschichte bot nach dem ersten generalisierten großen Anfall multiple komplexe visuelle Halluz‐inationen und Illusionen (CVHI) für einige Wochen. Der Patient berichtete über insgesamt 9 verschiedene CVHI. Im EEG zeigte sich rhythmische rechts‐temporale Aktivität, ausschleißlich beim Auftreten der CVHI. Behandlung mit Antiepileptika ließ die CVHI aufhören und normalisierte das EEG. Ein Versuch, die Antiepileptika abzusetzen, führte zum Wiederauftreten der CVHI und der EEG‐Veränderungen.
Acquired Epileptic Aphasia (the Landau‐Kleffner Syndrome) Due to Neurocysticercosis
Authors: Otero Enrique , Cordova Sergio , Diaz Fabian , Garcia‐Teruel Imelda , Brutto Oscar H. Del
Published: November 2007

Summary: A healthy 7‐year‐old boy developed a language disorder associated with clinical seizures and a paroxysmal EEC Computed tomography and magnetic resonance imaging revealed a small cysticercus deep in the left Sylvian fissure. We postulate a cause and effect relationship between the parasitic cyst and the clinical manifestations supported by the strategic location of the cyst and the critical age at which this lesion developed. This case provides evidence that the syndrome of acquired epileptic aphasia may be explained in terms of an unilateral structural brain lesion.

Un petit garcon de 7 ans, en bonne santé, a préterité un trouble du langage associéà des crises cliniques et à des paroxysmes EEG. La scanographie et 1'IRM ont mis en évidence un petit kyste de cysticercose dans la profondeur de la scissure sylvienne gauche. Les auteurs pensent qu'il existe une relation de cause à effet entre le kyste parasitaire et les manifestations cliniques, en se fondant sur la localisation significative du kyste et sur l'âge critique auquel cette lésion s'est développée. Ce cas fournit la preuve qu'un syndrome d'aphasie épileptique acquise peut‐être expliqué par l'existence d'une lésion cérébrale structurale uni‐latérale.

Un niño sano de 7 años de edad desarrolló un trastorno del lenguaje asociado a ataques clinicos y a un EEG paroxístico. Una tomografia Computarizada y una Resonancia Magnética revelaron un pequeño cisticerco localizado en las profundidades de la cisura de Silvio izquierda. Se postula una relación causa‐efecto entre el quiste parasítico y las manifestaciones clínicas debido a la localización estratégica del quiste y a la edad crítica en la que esta lesión se produjo. Este caso aporta evidencia de que el síndrome de afasia epiléptica adquirida puede ser expli‐cado en terminos de una lesión cerebral estructural unilateral.

Ein bis dahin gesunder Junge von 7 Jahren entwickelte eine Sprachstörung, welche mit klinischen Anfällen und paroxys‐malen EEG‐Veränderungen einherging. CT und NMR entdeck‐ten eine kleine Cystizercus‐Zyste tief in der Linken Sylvischen Furche. Wir postulieren einen kausalen Zusammenhang zwis‐chen klinischem Bild und Zyste aufgrund ihrer Lage und des kritischen Erkrankungsalters. Dieser Fall unterstiitzt die An‐sicht, das erworbene Aphasie‐Epilepsie‐Syndrom beruhe auf einer strukturellen Hirnlaesion.
Clonazepam in Juvenile Myoclonic Epilepsy
Authors: Obeid T. , Panayiotopoulos C. P.
Published: November 2007

Summary: We studied the efficacy of clonazepam (CZP) in control of juvenile myoclonic epilepsy (JME) in 17 patients. CZP was very effective in controlling myoclonic jerks in all patients but did not suppress generalized tonic‐clonic seizures (GTCS). A disadvantage occurs because the patient is deprived of the warning jerks which presage the onset of GTCS. The circadian rhythm of the GTCS was also changed in two patients.

Les auteurs ont étudie l'efficacité du clonazépam (CZP), present pour contrôler une épilepsie myoclonique juvénile (EMJ) chez 17 patients. Le clonazépam a été tres efficace dans le contrôle des secousses myocloniques chez tous les patients, mais il n'a pas permis de supprimer les crises généralisées tonico‐cloniques. Ce traitement représente un inconvénient, car il supprime les secousses qui pennettent de prédire l'arriveée d'une crise généralisée tonico‐clonique. Le rythme circadien des crises gdneralisees tonico‐cloniques a étéégalement modifyé chez deux patients.

Hemos estudiado la eficacia del Clonazepan (CZP) como control de la epilepsyía mioclónica juvenil (JME) en 17 pacientes. El CZP fue muy eficaz en el control de los movimientos mioclónicos en todos los pacientes pero no suprimió los ataques tónico‐clónicos generalizados (GTCS). Se constató la desventaja que tienen estos enfermos al estar deprivados del aviso de los movimientos mioclónicos que anteceden al comienzo de los GTCS. El ritmo circadiano de los GTCS también se modifico en dos enfermos.

Bei 17 Patienten untersuchten wir den Effekt von Clonazepam auf die juvenile myoklonische Epilepsie. CZP wirkte bei alien Patienten sehr gut auf die impulsiven Myoklonien, nicht aber auf die großen Anfälle. Als zu‐dem unvorteilhaft erwies sich das alleinige Ausschalten der Myoklonien, weil die Patienten dadurch die warnenden Vorboten von generalisierten Anfällen nicht mehr wahmahmen. Der circadiane Rhythmus der generalisierten Anfälle änderte sich bei 2 Patienten.
Development of New Pharmacological Agents for Epilepsy: Lessons from the Kindling Model
Authors: McNamara James O.
Published: November 2007

Summary: The greatest value of the kindling model for new therapy of epilepsy almost certainly lies in elucidating the molecular basis of its development and persistence. Such an understanding may provide a foundation for therapies aimed at prevention or perhaps even cure of some forms of human epilepsy.
Mechanisms of Action of New Antiepileptic Drugs
Authors: Porter Roger J.
Published: November 2007

Summary: Our understanding of how new antiepileptic drugs work mirrors what we know about how currently marketed antiepileptic compounds exert their action–that information is scarce and elusive. The mechanism of action of antiepileptic drugs is nevertheless inextricably linked to epileptogenesis itself, and investigations of several promising new compounds are underway to establish the levels at which these drugs act. Compounds act on synapses and membranes as well as affecting receptors, neurotransmitters, and peptides. The most extensive data are available on drugs that inhibit the action of GABA or its receptors, including new benzodiazepine‐like agents and barbituric‐acid derivatives. The few drugs that act by inhibiting the effects of excitatory amino acids are reviewed. Finally, the maximal electroshock test is an empirical method to determine the antiepileptic properties of a drug; several agents under development have been effective in this screening technique.
Pharmacology of ACC‐9653 (Phenytoin Prodrug)
Authors: Smith Ronald D. , Brown Barry S. , Maher Robert W. , Matier W. Les
Published: November 2007

Summary: ACC‐9653, the disodium phosphate ester of 3‐hydroxymethyl‐5,5‐diphenylhydantoin, is a prodrug of phenytoin with advantageous physicochemical properties. ACC‐9653 is rapidly converted enzymatically to phenytoin in vivo. ACC‐9653 and phenytoin sodium have equivalent anticonvulsant activity against seizures induced by maximal electroshock (MES) in mice following i.p., oral, or i.v. administration. The ED50 doses were 16 mg/kg for i.v. ACC‐9653 and 8 mg/kg for i.v. phenytoin sodium. ACC‐9653 and phenytoin sodium have similar antiarrhythmic activity against ouabain‐induced ventricular tachycardia in anesthetized dogs. The total doses of ACC‐9653 or phenytoin sodium necessary to convert the arrhythmia to a normal sinus rhythm were 24 ± 6 and 14 ± 3 mg/kg, respectively. Only phenytoin sodium displayed in vitro antiarrhythmic activity against strophanthidin‐induced arrhythmias in guinea pig right atria. In anesthetized dogs, a high dose of ACC‐9653 (31 mg/kg) was infused over 15, 20, and 30 min and the responses were compared to an equimolar dose of phenytoin sodium (21 mg/kg). The ACC‐9653 and phenytoin sodium treatments produced similar marked reductions in diastolic blood pressure and contractile force (UVdP/dt). The maximum effects of each treatment occurred at the time of maximum phenytoin sodium levels. Acute toxicity studies of ACC‐9653 and phenytoin sodium were carried out in mice, rats, rabbits, and dogs by i.v., i.m., and i.p. routes of administration. The systemic toxic signs of both agents were similar and occurred at approximately equivalent doses. Importantly, the local irritation of ACC‐9653 was markedly less than phenytoin sodium following i.m. administration. Thus, ACC‐9653 and phenytoin sodium have similar anticonvulsant, antiarrhythmic, hemodynamic, and acute systemic toxicity effects in experimental animals. The enhanced solubility and nonirritating qualities of ACC‐9653 support its clinical development.
GABA in Epilepsy: The Pharmacologic Basis
Authors: Gale Karen
Published: November 2007

Summary: GABA transmission plays a key role in controlling seizure activity. The precise nature of its effect depends on the particular location in the brain and the pathway involved. Animal studies have helped to define specific brain regions such as the substantia nigra and area tempestas that are critical in controlling seizure activity. Antiepileptic drugs such as vigabatrin [gamma vinyl GABA (GVG)], a drug rationally developed to treat resistant epilepsy, can enhance GABA transmission in these regions and may thereby afford seizure protection.
The Neuropathology of Vigabatrin
Authors: Butler William H.
Published: November 2007

Summary: Vigabatrin (gamma vinyl GABA, GVG), an enzyme‐activated, irreversible inhibitor of GABA transaminase, was administered orally to rats, dogs, and monkeys to observe toxicologic reactions. Myelin vacuolation of the brain was observed. The vacuolation was limited to myelinated tracts and resulted from separation of the myelin sheath at the interperiod line. There was no evidence of demyelination, axonal degeneration, or damage uolation was histologically similar to that observed in association with other drugs such as triethyltin, isoniazid, or hexachlorophene. However, the distribution is limited to the brain and is reversible upon discontinuation of therapy. Two postmortem and three operative specimens from humans have revealed no evidence of vacuolation of myelin.
Long‐Term Evaluation of Vigabatrin (Gamma Vinyl GABA) in Epilepsy
Authors: Dam Mogens
Published: November 2007

Summary: In studies spanning more than 5 years, more than 1,100 patients with epilepsy have been treated with vigabatrin (gamma vinyl GABA, GVG). Sixty‐two patients with partial seizures with secondary generalization took part in this trial: 41 patients continued in the trial after 19 months of treatment. After 36 months, the median percentage of baseline seizures was <20%. GVG is a very potent antiepileptic drug. It is well tolerated in humans. The side effects are few. Skin rash and other allergic reactions have rarely been seen. Tolerance to the sedative effect is in contrast to the lack of tolerance to the anti‐epileptic effect.
Gamma Vinyl GABA: Current Role in the Management of Drug‐Resistant Epilepsy
Authors: Treiman David M.
Published: November 2007

Summary: The goal of management in epilepsy is to make patients completely seizure‐free without side effects. Currently, this goal can be achieved fully in only about one‐half of the 50,000,000 people in the world with epilepsy. Epilepsy is not a benign condition. Uncontrolled epilepsy produces significant morbidity and mortality. Even infrequent seizures put a patient at risk of sudden death and compromise employability and other social functions. The potential risk of a new antiepileptic drug has to be weighed against the potential risk of continuing seizures and the potential for the new drug to control those seizures. Vigabatrin (gamma vinyl GABA, GVG) is one of the promising new antiepileptic drugs now under development. In four large clinical trials half of the patients in each trial had a ≥ 50% reduction in seizure frequency when GVG was added to existing antiepileptic drug. This represents a significant response rate in add‐on trials, which are a severe test of a new antiepileptic drug. Although microvacuoles have been seen in the white matter of the brains of rats and dogs treated with GVG, such pathological changes have not yet been observed in humans. Evoked potential studies have failed to reveal any evidence of microvacuolization in humans. Because of the potential efficacy of GVG in controlling previously therapeutic‐resistant seizures and of the absence of evidence of significant toxicity in humans, carefully monitored clinical trials of GVG in therapy‐resistant patients with epilepsy should continue.
Juvenile Myoclonic Epilepsy: Characteristics of a Primary Generalized Epilepsy
Authors: Dreifuss Fritz E.
Published: November 2007

Summary: Juvenile myoclonic epilepsy (JME) is a primary generalized epilepsy that affects approximately 7% of adolescent and adult epilepsy patients. JME is characterized by myoclonic seizures alone or combined with generalized tonic‐clonic seizures or absence seizures. Seizures are precipitated by sudden awakening, sleep deprivation, photic stimulation, and alcohol consumption. The ictal electroencephalogram (EEG) shows a typical 4‐ to 6‐Hz polyspike and wave pattern; the interictal EEG may be normal. Valproate controls seizures in approximately 80% of JME patients and is recommended for successful management of this disorder.
Toxocara Infection and Epilepsy in Children: A Case‐Control Study
Authors: Arpino Carta , Gattinara Guido Castelli , Piergili Daniela , Curatolo Paolo
Published: November 2007

Summary: A case‐control study of 305 children was done to evaluate the relationship between toxocariasis and seizures and risk factors associated with toxocariasis transmission and seizure onset. A significant association existed between seropositivity for mti‐Toxocara canis and seizures (p < 0.05); the correlation was closest in children aged <5 years of age. Among risk factors, pica was more common in children with seizures than in controls but was not associated with toxocariasis. The association between dog ownership and toxocariasis was highly significant (p < .000001). Our findings suggest that toxocariasis may be involved as a cofactor in the pathogenesis of seizures.

Para valorar la relación existente entre toxocariasis y ataques se ha realizado un estudio de caso‐control en 305 niños. También se han estudiado los factores de riesgo asociados a la transmi‐sidn de toxocariasis y el comienzo de los ataques. Se ha encon‐trado una asociación significativa (p < 0.05) entre las seroposi‐tividad anti‐toxocaracasis y los ataques. La correlación fue más notable en niños menores de 5 años de edad. Entre los factores de riesgo, la pica fue más frecuente en niños con ataques que en los control pero no se asoció a la toxocariasis. Se encontró una alta y significativa associación entre la posessión de un perro y la toxocariasis (p < 10‐6). Nuestros hallazgos sugieren que la toxocariasis puede actuar como un co‐factor en la patogenesis de ataques.

Eine Fall‐Kontroll‐Studie wurde an 305 Kindern durchgeführt, urn die Beziehung zwischen Toxocariasis (T) and Angällen sowie Risikofaktoren die mit der T‐Transmission und dem Anfallsbe‐ginn zusammenhängen zu klären. Es fand sich eine signifikante Assozation zwischen Seropositivität für T und Anfällen (p 0.05). Bei Kindern unter 5 Jahren war diese Korrelation am engsten. Als Risikofaktr o fiel das Pica‐Syndrom öfters bei Anfallskindern als bei Kontrollen auf ‐war aber nicht an T. gebunden. Zwischen Hundehaltung und T. wurde eine hochsignifikante Korrelation gefunden (p < 10‐6). Unsere Ergebnisse lassen vermuten, daß T. als Co‐Faktor in der Pathogenese von Anfällen wirksam sein könnte.
Absolute Bioavailability of Carbamazepine After Oral Administration of a 2% Syrup
Authors: Gérardin A. , Dubois J. P. , Moppert J. , Geller L.
Published: November 2007

Summary: Two healthy male volunteers received 10 mg carbamazepine (CBZ) as a 2‐h constant‐rate intravenous (i.v.) infusion and 100 mg 15N‐labeled CBZ as a 2% oral suspension, concomitantly. The two compounds have identical pharmacokinetics. Their respective concentrations in plasma were determined by gas chromatography‐mass spectrometry (GC‐MS) for 168 h. The comparison of the areas under the plasma curves (AUC) obtained by the two routes of administration, showed the systemic availability of CBZ given as an oral suspension to be equal to its availability when given intravenously. A two‐compartment model was estimated: The apparent volume of distribution of CBZ at the steady‐state (Vss) was ˜1 L/kg.

Deux volontaires sains ont recu simultanément 10 mg de carbamazepine (CBZ) en perfusion intraveineuse à vitesse con‐stante pendant 2 h et, par voie orale, une suspension à 2% contenant 100 g de CBZ marquéà l'azote 15. Les deux produits ont des propriéités pharmacocinétiques identiques. Leurs concentrations respectives dans le plasma ont été mésurées par GC‐MS pendant 168 h. Les résultats, obtenus en comparant les aires sous les courbes correspondant aux deux voies d'administration, démontrent que la biodisponibilité de CBZ administeré sous la forme d'une suspension orale est lot ale. Un modèléà 2 compar‐timents a étea défini: le volume apparent de distribution de CBZ à l'équilibre (VS5) est voisin de 1 L/kg.

A dos varones sanos, voluntarios, se les administeró de modo simultáneo 10 mgrs de Carbamacepina (CBZ) en infuseón intra‐venosa a un ritmo constante durante dos horas y 100 mgrs de 15N‐CBZ marcada en suspensión oral al 2%. Los dos compues‐tos tienen una farmacocinética id éntica. Las concentraciones respectivas en plasma se determinaron mediante GC‐MS en un periodo de 168 horas. La comparación de las áreas bajo las cur‐vas de plasma que se obtuvieron mediante las dos rutas de ad‐ministración, mostraron que la disponibilidad sistémica de CBZ por via oral fue igual. Un modelo de dos compartimentos también fue estimado: el volumen aparente de distribución de la CBZ durante el estado estable (Vss) due alrededor de 1 l/kg.

An zwei gesunden Probanden wurde die gleichzeitige Verab‐reichung von 10 mg Carbamazepin als intravenöse Infusion über 2 Stunden und von 100 mg Carbamazepin als orale 2% Suspension untersucht. Zur Unterscheidung der beiden Verab‐reichungen wurde die Suspension mit 15N‐markiertem Carbamazepin hergestellt. Carbamazepin und 15N‐markiertes Carbamazepin haben identische pharmakokinetische Eigenschaften. Ihre Konzentrationen im Plasma wurden mit einer GC‐MS Kopplung im Zeitintervall von 0 bis 168 Stunden nach Verab‐reichung gemessen. Durch Vergleich der Flächen unter den Kur‐ven und unter Berücksichtigung der verabreichten Dosis konnte die vollständige Bioverfügbarkeit von Carbamazepin aus der oralen Suspension gezeigt werden. Durch Anpassung eines Zweikammermodells wurde ein Verteilungsvolumen von Carbamazepin im Steady State von 1 L/kg errechnet.
Feasibility and Safety of Vagal Stimulation In Monkey Model
Authors: Lockard Joan S. , Congdon William C. , DuCharme Larry L.
Published: November 2007

Summary: The feasibility, safety, and preliminary effects of chronic vagal stimulation were studied in an alumina‐gel monkey model. Pilot studies to perfect the equipment, determine stimulation thresholds, and insure the comfort and safety of the animals preceded this study. Four monkeys were equipped with an indwelling, 2‐electrode cuff (titanium bands spaced 7 mm apart; silicone encased; 1.5 cm total length) in contact around the right vagus nerve; avoidance of the cardiac branch was confirmed by electrocardiograms. After postsurgical recovery, the intact and awake animals received constant‐current stimulation (5 mA; 83 Hz, 143 Hz, or 50–250 Hz randomly; 0.5‐ms pulse width) at the onset of every spontaneous seizure for the duration of the seizure or every 3 h for 40 s if stimulation had not occurred in the preceding hour. Stimulation periods of 2–6 weeks, with differing levels of stimulation, were preceded and followed by at least a 2‐week baseline period of no stimulation. During the stimulation periods, the seizure rate decreased to zero in two monkeys and the interseizure intervals became invariable in the remaining two monkeys. These effects carried over temporarily into the poststimulation baseline periods. Vagal stimulation had no consistent effects on seizure severity or EEG interictal spikes. Histological studies of six vagus nerves were unable to separate electrode cuff damage from any direct effects stimulation may have had on the nerves. Although it appears that chronic vagal stimulation is feasible and that epileptogenic processes are influenced, the safety and efficacy of the procedure are still in question.
An Implantable Neurocybernetic Prosthesis System
Authors: Terry Reese , Tarver W. Brent , Zabara Jacob
Published: November 2007

Summary: The neurocybernetic prosthesis (Cyberonics, Inc.) is an implantable, multiprogrammable pulse generator that delivers constant current electrical signals to the vagus nerve for the purpose of reducing the frequency and/or severity of epileptic seizures. The device is implanted in a subcutaneous chest pocket just below the clavicle, similar to cardiac pacemaker placement. The stimulation signal is transmitted from the prosthesis to the vagus nerve through a stimulation lead. The prosthesis can be programmed using any IBM‐compatible personal computer with programming software and a programming wand. The electrodes used in the first group of patients were found to break at an unacceptable rate. Design modifications appear to have resolved this problem.
Effects of Vagal Stimulation on Experimentally Induced Seizures in Rats
Authors: Woodbury Dixon M. , Woodbury J. Walter
Published: November 2007

Summary: Repetitive stimulation of the vagus nerve inhibits chemically induced seizures in dogs. We report here the results and conclusions from studies designed to answer some of the immediate questions raised by this finding. (1) Maximal stimulation of vagal C fibers at frequencies greater than 4 Hz prevents or reduces chemically and electrically induced seizures in young male rats. (2) Antiepileptic potency is directly related to the fraction of vagal C fibers stimulated. (3) Vagal stimulation shortens but does not shut down a chemical seizure once it has begun. (4) In rats, optimal stimulus frequency is approximately 10–20 Hz; duration of stimulus, 0.5‐1 ms; and stimulus strength, 0.2‐0.5 mA/mm2 of nerve cross‐section. These results, when taken together with similar results obtained from dogs, monkeys, and humans, strongly suggest that periodic stimulation of the vagus nerve using appropriate stimulation parameters is a powerful method for preventing seizures. The data from the literature suggest that the antiepileptic actions of vagal stimulation are largely mediated by widespread release of GAB A and glycine in the brainstem and cerebral cortex. The probable pathway is via projections from the nucleus of the solitary tract to the reticular formation and thence by diffuse projections to the cortex and other areas. Intermittent vagal stimulation has the potentiality of reducing the number and/or the intensity of seizures in patients with intractable epilepsy. These results indicate that feasibility studies in humans should be continued and expanded.
Post‐Traumatic Epilepsy: Cellular Mechanisms and Implications for Treatment
Authors: Willmore L. James
Published: November 2007

Summary: Epilepsy complicates severe head trauma. Development of persistent seizures appears to correlate with the extent of trauma. Although early reports suggested that prophylactic administration of antiepileptic drugs would prevent epileptogenesis, controlled studies have failed to corroborate this assumption. Head trauma initiates a sequence of responses that includes altered blood flow and vasoregulation, disruption of the blood‐brain barrier, increases in intracranial pressure, focal or diffuse ischemia, hemorrhage, inflammation, necrosis, and disruption of fiber tracts. The presence of an intracranial hematoma has a robust association with the development of post‐traumatic epilepsy. Extravasation of blood is followed by hemolysis and deposition of heme‐containing compounds into the neuropil, initiating a sequence of univalent redox reactions and generating various free radical species, including superoxides, hydroxyl radicals, peroxides, and perferryl ions. Free radicals initiate peroxidation reactions by hydrogen abstraction from methylene groups adjacent to double bonds of fatty acids and lipids within cellular membranes. Intrinsic enzymatic mechanisms for control of free radical reactions include activation of catalase, peroxidase, and superoxide dismutase. Steroids, proteins, and tocopherol also terminate per‐oxidative reactions. Tocopherol and selenium are effective in preventing tissue injury initiated by ferrous chloride and heme compounds. Treatment strategies for prevention or prophylaxis of post‐traumatic epilepsy must await absolute knowledge of mechanisms. Antioxidants and chelators may be useful, given the speculation that peroxidative reactions may be an important component of brain injury responses. However, potential treatment strategies involving ‐y‐aminobutyric acid (GABA) agonists, NMDA receptor antagonists, and barbiturates need further scientific assessment.
Education and Epilepsy: Assessment and Remediation
Authors: Henriksen O.
Published: November 2007

Summary: Learning difficulties in children with epilepsy may be caused by brain damage and should be investigated. In many cases, however, seizures and/or electroencephalographic (EEG) findings are the only signs of pathology. Frequency and type of seizures may be determining factors that should, if necessary, be evaluated by long‐term EEG monitoring, preferably during school performance or in conjunction with neuropsychological assessment. This may prove that subclinical epileptiform discharges in the EEG can adversely affect the child's performance. Secondary psychological problems in epilepsy patients, combined with side effects of antiepileptic drugs, may cause or heighten learning problems. Prophylactic control of seizures with one appropriate drug may alleviate learning problems. Computerized neuropsychological testing with simultaneous EEG recording may reveal the influence of epileptiform discharges on cognitive function and also help to evaluate the effects of antiepileptic drugs. Objective assessment of subclinical epileptiform activity makes it easier to treat the pathology identified by the EEG with optimal dosage of the most appropriate drug. A balance is required because epileptiform discharges and even occasional seizures may be less disabling than side effects from large doses of several drugs. Information to the school and the parents concerning the patient's abilities and limitations may be as important as seizure control. Specialized teaching should be started early, when necessary, with the patient integrated into a normal school if possible. However, good functioning in a special school is preferable to marginal functioning in a normal school.
Neuropsychological Assessment of Cognitive Functioning in Children with Epilepsy
Authors: Rugland A.‐L.
Published: November 2007

Summary: The variety of cognitive dysfunctions related to learning disabilities in children with epilepsy have been studied by linking electroencephalogram (EEG) and computerized neuropsychological testing. This showed that “subclinical” discharges impaired performance in 61% of the patients on a simple and a choice reaction time test, although some discharges lasted 1 s only. Neuropsychological investigation of subclinical EEG discharges may help to determine their adverse effect on learning.
Nocturnal Paroxysmal Dystonia with Short‐Lasting Attacks: Three Cases with Evidence for an Epileptic Frontal Lobe Origin of Seizures
Authors: Tinuper Paolo , Cerullo Angelina , Cirignotta Fabio , Cortelli Pietro , Lugaresi Elio , Montagna Pasquale
Published: November 2007

The epileptic or nonepileptic origin of noctur‐ nal paroxysmal dystonia (NPD) has been debated. We studied three patients with frequent attacks during non‐REM sleep. During prolonged video‐EEG monitoring, two patients had a convulsive seizure after a typical NPD episode and on these occasions EEG showed epileptiform discharge. In the three patients, attacks occurred repeatedly with different intensity, representing “fragments” of the same seizure. These fragments of the attack could occur periodically every 20–40 s. We postulate that short NPD attacks are actually epileptic seizures originating from the frontal lobes. The rhythmicity of the episodes may be due to rhythmic oscillation of cortical function during non‐REM sleep.

L'origine épileptique ou non épileptique de la dystonie paroxystique nocturne (DPN) est controversy. Les auteurs ont étudié trois patients présentant des crises fréquentes pendant le sommeil lent. Pendant une surveillance vidéo‐EEG prolongée, deux d'entre eux ont présenté une crise convulsive suivie d'un épisode typique de DPN; à cette occasion, l'EEG a montré une décharge épileptique. Chez trois patients, les attaques survenaient de façon répétée, avec une intensité variable, et représentaient des fragments de la même crise. Ces fragments d'une crise pouvaient survenir périodiquement toutes les 20 à 40 secondes. Les auteurs postulent que des crises brèves de DPN sont en fait des crises épileptiques dont l'origine est au niveau du lobe frontal. La rythmicité des épisodes peut être due à l'oscillation rythmique des fonctions corticales pendant le sommeil lent.

El origen epiléptico o no epiléptico de la distonía paroxistica nocturna (NPD) ha sido muy debatido. Hemos estudiado 3 enfermos con frecuentes ataques durante la fase no‐REM del sueño. Durante la monitorización prolongada con “video‐ EEG's” dos enfermos tuvieron un ataque convulsivo que siguió a un episodio típico de NPD y, en estas circunstancias, los EEG's mostraron descargas epileptiformes. En los tres pacientes los ataques ocurrieron de modo repetido, con diferente intensidad, representando “fragmentos” del mismo ataque convulsivo. Estos fragmentos del ataque podfan ocurrir periódicamente cada 20–40 segundos. Postulamos que los ataques de corta duración de NPD son, de hecho, ataques epilépticos que se originan en los lóbulos temporales. La ritmicidad de estos episodios puede ser debida a las oscilaciones rítmicas de la función cortical durante el sueño no‐REM.
Classification of Epilepsies and Epileptic Syndromes in Two Different Samples of Patients
Authors: Loiseau Pierre , Duché Bernard , Loiseau Jérome
Published: November 2007

Summary: We attempted to classify, according to the International Classification of Epilepsies and Epileptic Syndromes, 986 patients consecutively examined during a 13‐month period either in a specialized private practice (n = 642) or in an adult neurology unit in a university hospital (n = 344). Without major difficulty, we classified 97% of patients in more or less clearly defined syndromes. Benign frontal and benign psychomotor epilepsies of childhood were represented in this sample of patients. In either partial or generalized idiopathic epilepsies, a diagnosis of epilepsy appears justified even after a single epileptic event when sufficient electroclinical characteristics are present. Patients with symptomatic generalized epilepsies often have to be classified under two or three headings. Many children with a symptomatic generalized epilepsy also experience partial seizures. Alcoholic epilepsy is described as a veritable epileptic syndrome. The distribution of epileptic syndromes was clearly different in the two samples, casting doubt on the value of some epidemiologic surveys based on selected groups of patients.

On a essayé de classer selon la classification Internationale des Epilepsies et des Syndromes Epileptiques 986 patients vus de facon consécutive, pendant 13 mois, soit à une consultation spécialisée privée (n = 642) soit dans le service de neurologie ďadultes ďun hôpital universitaire (n = 344) 97% des patients ont pu être classés sans difficultés majeures, dans des syndromes précis ou définis de façon plus vague. Des épilepsies frontales bénignes et psychomotrices bénignes de ľenfance ont été diagnostiquées. Dans les épilepsies idiopathiques, partielles ou généralisées, un diagnostic ďépilepsie parait justifié même après une seule crise, lorsqu'existent des arguments électrocliniques suffisants. Les patients ayant une épilepsie généralisée symptomatique doivent souvent être classés dans deux ou trois rubriques. Un nombre non négligeable ďenfants présentant une épilepsie symptomatique dite géneralisee a aussi des crises partielles. Ľépilepsie alcoolique est présentée comme un authentique syndrome épileptique. La distribution des syndromes épileptiques dans les deux groupes était nettement différente, ce qui jette un doute sur la valeur de certaines études épidémiologiques, fondées sur des groupes sélectionnés de sujets.
Electroencephalographic Correlations of Extracranial and Epidural Electrodes in Temporal Lobe Epilepsy
Authors: Kuzniecky Ruben , Faught Edward , Morawetz Richard
Published: November 2007

Summary: Thirty patients with medically intractable complex partial seizures of temporal lobe origin, but no structural abnormalities on neuroradiologic investigations, had both extracranial (scalp) and epidural EEG recordings. Fifteen patients (50%) had localized, unilateral, ictal, scalp EEGs, but one of these had bilateral independent temporal seizure onset according to epidural recordings. Of the 15 patients in whom scalp EEGs were non‐localizing, 12 had well‐localized epidural ictal EEGs, and 3 had multifocal or bilateral independent temporal ictal recordings. Epidural recordings provide information for determination of site of onset of temporal lobe seizures in selected patients.

Chez Trente patients présentant des crises partielles complexes rebelles ďorigine temporale, sans anomalie sur les investigations neuroradiologiques, ont bénéficiéà la fois ďenregistrements EEG extracrâniens et épiduraux. 15 ďentre eux (50%) présentaient des anomalies paroxystiques localisées, unilatérales, mais ľun de ceux‐ci avait sur les enregistrements épiduraux des crises de début temporal bilatéral indépendant. Chez les 15 patients pour lesquels ľEEG de surface n'était pas localisateur, 12 présentaient des EEG critiques épiduraux bien localisateurs, et 3 des enregistrements critiques multifocaux ou temporaux bilatéraux et indépendants. Les enregistrements épiduraux fournissent des informations sur la détermination du site de début des crises temporales chez des patients sélectionnés.

30 Patienten mit therapieresistenten, komplex‐partiellen Anfällen temporalen Ursprungs ohne strukturelle Abnormalitäten bei der neuroradiologischen Untersuchung wurden einer extra‐kraniellen (Skalp) und epiduralen Elektroenzephalographie un‐terzogen. 15 Patienten (50%) hatten lokalisierende, unilaterale, iktale Skalp‐EEGs, einer davon einen bilateral unabhängige temporalen Anfallsbeginn bei der epiduralen Aufzeichnung. Von den 15 Patienten, bei denen die Skalp‐EEGs nicht lokalisierend waren, hatten 12 Patienten gut lokalisierende epidurale iktale EEGs und 3 multifokale oder bilateral unabhängige temporale iktale Aufzeichnungen. Die epiduralen Aufzeichnungen liefern bei ausgewählten Patienten Informationen zur Bestimmung der Seite des Beginns von TemporallappenAnfällen.
Aggravation of Penicillin‐Induced Epilepsy in Rats with Locus Ceruleus Lesions
Authors: Sullivan Herman C. , Osorio Ivan
Published: November 2007

Summary: The rate and pattern of development of seizures induced by penicillin injected intraperitoneally were determined in rats that had been depleted of brain norepinephrine (NE) by bilateral injections of the neurotoxin 6‐OH dopamine into the locus ceruleus. Behavioral observations and scalp electrographic recordings were made after injection and the efficacy of NE depletion was determined by high performance liquid chromatography measurement of cortical levels of NE and its metabolites. We found that in comparison to sham‐operated control rats, NE‐depleted rats had a significantly shorter latency to first observable myoclonic jerk, the first epileptic discharge, the first convulsion with sustained epileptic discharges, and a longer duration of convulsions. We observed a similar electrographic pattern of multifocal spikes with bilateral synchrony in both groups. However, more of the control rats (six of 12) had convulsions as compared to the lesioned rats (four of 12). These findings are consistent with previous evidence that depletion of neocortical NE facilitates the development of epileptiform activity in the CNS; however, a convulsive state was not induced by NE depletion.