[Early onset epileptic encephalopathy in a patient with mutation in SCN8A]. / Encefalopatia epileptica de inicio precoz en un paciente con mutacion en SCN8A.

TITLE: Encefalopatia epileptica de inicio precoz en un paciente con mutacion en SCN8A.

Pain management in Guillain-Barre syndrome: a systematic review.

INTRODUCTION: Pain is a common symptom in patients with Guillain-Barre syndrome. Intensity is moderate to severe in most cases and pain may persist after resolution of the disease. OBJECTIVE: Identify the most appropriate analgesic therapy for pain management in patients with Guillain-Barre syndrome. MATERIAL AND METHODS: Systematic review and selection of scientific articles on treatment of pain in Guillain-Barre syndrome patients, published between January 1985 and December 2012. We included only randomised, double-blind, controlled trials assessing the effectiveness of drugs for pain management in these patients. RESULTS: Four articles met the inclusion criteria. One evaluated the use of gabapentin, another evaluated carbamazepine, a third compared gabapentin to carbamazepine, and the last evaluated use of methylprednisolone. Both carbamazepine and gabapentin were useful for pain management. Patients experienced lower-intensity pain with gabapentin treatment in the study comparing that drug to carbamazepine. Methylprednisolone was not shown to be effective for reducing pain. The published data did not permit completion of a meta-analysis. CONCLUSIONS: There is no robust evidence at present that would point to a single treatment option for this disorder. Further clinical studies of larger patient samples and with a longer duration are needed to characterise types of pain for each patient and measure pain intensity in an objective way.

Central neuropathic pain in Parkinson's disease.

INTRODUCTION: Central pain is one type of pain that occurs in patients with Parkinson's disease (PD). Because of its low incidence and prevalence, it often goes unnoticed and affected patients do not therefore receive adequate analgesic therapy, which increases their suffering. It is a burning pain with spontaneous onset and periods of exacerbation; pain is poorly localised and usually more intense on the more affected side. Its pathophysiology on patients with PD is not clearly defined. METHODS: We performed a search and systematic selection of all clinical studies published from January 1986 to September 2010 concerning central neuropathic pain in Parkinson's disease. CONCLUSIONS: Treatment with L-Dopa has not been demonstrated to have an analgesic effect on this type of pain. Future studies are required to improve our understanding of this condition, and to develop interventions for preventing and treating it.

Do your patients suffer from excessive yawning?

OBJECTIVE: Yawning has been described in relation to drugs such as serotonin reuptake inhibitors, levodopa, dopamine agonists, MAO B inhibitor, morphine, methadone, buprenorphine, dextromethorphan, benzodiazepine, lidocaine, and flecaine. This is a report of two patients, on long-term escitalopram therapy (more than 8 weeks) with stable dosing, who presented excessive yawning. Escitalopram is widely used in major depressive disorder and generalized anxiety disorder. METHOD: A clinical description of two cases. RESULTS: Two females (62 and 59 years old, respectively) developed excessive daytime yawning. It was not associated with sedation or a feeling of needing sleep. The dosage was reduced and yawning disappeared some hours later. The patients' depression did not recur. CONCLUSION: Yawning has been described in relation to different selective serotonin reuptake inhibitors and remitted following their discontinuation; it is interesting that the reported yawning in these two cases disappeared with the reduction of dosage, rather than the interruption of treatment.

[Zinc and epilepsy: is there a causal relation between them?]. / Zinc y epilepsia: existe una relación causal?

INTRODUCTION: Zinc is a fundamental trace element for an adequate nervous system function. It has been suggested that in the brain, a zinc homeostasis alteration may be associated with the genesis of epilepsy, although it is not yet determined if concentrations of zinc are a cause or a consequence of seizures. Another poorly studied aspect is the relationship between antiepileptic drugs and the neuronal zinc behaviour. DEVELOPMENT: We perform a systematic review of the literature to evaluate the role that zinc plays in epilepsy as well as the antiepileptic effect of zinc concentrations. Databases such as MEDLINE, EMBASE, SCISEARCH and LILACS were consulted from January 1974 to July 2005. All articles published in English and Spanish were considered. A manual review of the references present in each article was done in order to identify the articles that the electronic search may have not found itself. The title and abstract of the potential articles were analyzed before asking for the complete article. However, articles that seemed ambiguous were completely analyzed later to establish their relevance. CONCLUSIONS: Clinical research in epilepsy presented contradictory results. In fact, the reviewed studies, both animal and human, did not give enough evidence to determine if organic zinc variations are directly related to epilepsy. Most of them gave not statistically significant results.

[The risk of defects in the neural tube caused by valproic acid and carbamazepine]. / Riesgo de defectos del tubo neural con ácido valproico y carbamacepina.

OBJECTIVE: To determine the risk, if any, of carbamazepine and valproic acid use on the foetus with respect to neural tube defects. MATERIALS AND METHODS: Databases such as MEDLINE, EMBASE, SCISEARCH, The Cochrane Library and LILACS were consulted to have access to published literature from January 1966 to September 2004. All articles published in English and Spanish were considered. A manual review of the references presented in each produced article was done in order to identify the articles that the electronic search may have not found itself. However, articles which seemed ambiguous as to the title and/or abstract were completely analyzed to establish their relevance. Studies that examined the effects of systematic exposure to carbamazepine or valproic acid during pregnancy and that assessed neural tube defects in the infants were eligible. The data was extracted in the form of 2 x 2 tables. The odds ratio (OR), relative risk (RR) and 95% confidence interval (CI) was calculated for each of the studies. RESULTS: The pooled relative risk of neural tube defects among the exposed to valproic acid was 0.61 (95% CI: 0.06-6.72). The risk among the exposed to carbamazepine was 1.10 (95% CI: 0.16-7-75). CONCLUSIONS: Due to the methodologic limitations of most of the studies where the data was insufficient, only three studies could be included in the meta-analysis. There is not enough evidence to establish the risk raised in the objective of the study.

Riesgo de defectos del tubo neural con ácido valproico y carbamacepina / The risk of defects in the neural tube caused by valproic acid and carbamazepine

Objetivo. Establecer el riesgo de desarrollar defectos del tubo neural en los expuestos de forma prenatal a carbamacepina y ácido valproico. Materiales y métodos. MEDLINE, EMBASE, SCISEARCH, The Cochrane Library y LILACS se emplearon para acceder a la literatura publicada entre enero de 1966 y septiembre de 2004. Se tomaron todos los artículos publicados en inglés y español. Se hizo una revisión manual de las referencias presentadas con el fin de identificar artículos que la búsqueda electrónica no identificara. El título y el resumen de los potenciales artículos se analizaron primero antes de solicitar el artículo completo. Sin embargo, artículos que en principio eran ambiguos para determinar su pertinencia también se estudiaron en su totalidad. Se incluyeron los estudios observacionales analíticos que buscaran la presencia de defectos del tubo neural en los hijos de madres expuestas a ácido valproico y carbamacepina durante la correspondiente gestación. Se crearon las tablas de 2 × 2. Los riesgos relativos (RR), las razones de disparidad (OR) y los intervalos de confianza (IC) del 95% se calcularon para cada estudio. Resultados. Se encontró un RR = 0,61 (IC 95%: 0,06-6,72) de desarrollar defectos del tubo neural para quienes están expuestos a ácido valproico en monoterapia. En el caso de exposición a carbamacepina se obtuvo un RR = 1,1 (IC 95%: 0,16-7-75). Conclusiones. Debido a las limitaciones metodológicas de la mayoría de los estudios donde los datos son insuficientes, el metaanálisis sólo pudo incluir tres estudios. No hay evidencia suficiente que permita establecer el riesgo planteado en el objetivo del estudio (AU)

Objective. To determine the risk, if any, of carbamazepine and valproic acid use on the foetus with respect to neural tube defects. Materials and methods. Databases such as MEDLINE, EMBASE, SCISEARCH, The Cochrane Library and LILACS were consulted to have access to published literature from January 1966 to September 2004. All articles published in English and Spanish were considered. A manual review of the references presented in each produced article was done in order to identify the articles that the electronic search may have not found itself. However, articles which seemed ambiguous as to the title and/or abstract were completely analyzed to establish their relevance. Studies that examined the effects of systematic exposure to carbamazepine or valproic acid during pregnancy and that assessed neural tube defects in the infants were eligible. The data was extracted in the form of 2 × 2 tables. The odds ratio (OR), relative risk (RR) and 95% confidence interval (CI) was calculated for each of the studies. Results. The pooled relative risk of neural tube defects among the exposed to valproic acid was 0.61 (95% CI: 0.06-6.72). The risk among the exposed to carbamazepine was 1.10 (95% CI: 0.16-7-75). Conclusions. Due to the methodologic limitations of most of the studies where the data was insufficient, only three studies could be included in the meta-analysis. There is not enough evidence to establish the risk raised in the objective of the study (AU)

[Changes in selenium levels in epilepsy]. / Alteración de la concentración de selenio en la epilepsia.

INTRODUCTION: It has been suggested that antiepileptic drug therapies deplete total body selenium stores and failure to give appropriate selenium supplementation, especially to patients receiving valproic acid during pregnancy may increase the risk of neural tube defects or other free radical mediated damage. Selenium is essential for the synthesis of selenoproteins, including glutathione peroxidase. AIMS: To review the present state of knowledge about selenium behaviour in people with epilepsy taking antiepileptic drugs and to develop guidelines for the appropriate use of selenium supplements. DEVELOPMENT: Databases such as Medline, Embase, Scisearch and Lilacs were consulted to have access to literature. A search in said databases was performed in order to find articles published from January 1966 to August 2004. All articles published in English and Spanish were considered. A manual review of the references present in each produced article was done in order to identify the articles that the electronic search may have not found itself. The title and abstract of the potential articles were analyzed before asking for the complete article. However, articles which seemed ambiguous were completely analyzed later to establish their relevance. CONCLUSIONS: There is insufficient evidence to fully evaluate the effect of selenium supplementation. The possible beneficial effects on pregnancy need to be evaluated in further studies.

Alteración de la concentración de selenio en la epilepsia / Changes in selenium levels in epilepsy

Introducción. Se ha sugerido que los tratamientos anticonvulsionantes disminuyen las reservas de selenio en el organismo y que no administrar suplementos de selenio, especialmente a las pacientes que reciben ácido valproico durante el embarazo, puede aumentar el riesgo de desarrollar defectos del tubo neural u otras alteraciones mediadas por radicales libres. El selenio es un oligoelemento esencial para la síntesis de selenoproteínas, incluida la glutatión peroxidasa. Objetivo. Realizar una revisión sistemática de la literatura para poder presentar el estado del conocimiento sobre el comportamiento del selenio en los pacientes con epilepsia en tratamiento anticonvulsionante y desarrollar unas recomendaciones para el uso adecuado de un suplemento de selenio. Desarrollo. Se consultaron las bases de datos Medline, Embase, Scisearch y Lilacs para acceder a la literatura, y se realizó una búsqueda para localizar artículos publicados entre enero de 1966 y agosto de 2004. Se tomaron todos los artículos publicados en inglés y español. Se realizó una revisión manual de las referencias presentadas en cada artículo con el fin de identificar los que no identificó la búsqueda electrónica. El título y el resumen de los artículos potencialmente útiles se analizaban antes de solicitar el artículo completo. Sin embargo, los artículos en los que éstos eran ambiguos para determinar su pertinencia también se analizaron en su totalidad. Conclusiones. No hay suficientes evidencias para evaluar el efecto de administrar un suplemento de selenio. El posible beneficio durante el embarazo requiere estudios más profundos

Introduction. It has been suggested that antiepileptic drug therapies deplete total body selenium stores and failure to give appropriate selenium supplementation, especially to patients receiving valproic acid during pregnancy may increase the risk of neural tube defects or other free radical mediated damage. Selenium is essential for the synthesis of selenoproteins, including glutathione peroxidase. Aims. To review the present state of knowledge about selenium behaviour in people with epilepsy taking antiepileptic drugs and to develop guidelines for the appropriate use of selenium supplements. Development. Databases such as Medline, Embase, Scisearch and Lilacs were consulted to have access to literature. A search in said databases was performed in order to find articles published from January 1966 to August 2004. All articles published in English and Spanish were considered. A manual review of the references present in each produced article was done in order to identify the articles that the electronic search may have not found itself. The title and abstract of the potential articles were analyzed before asking for the complete article. However, articles which seemed ambiguous were completely analyzed later to establish their relevance. Conclusions. There is insufficient evidence to fully evaluate the effect of selenium supplementation. The possible beneficial effects on pregnancy need to be evaluated in further studies

[Use of anticonvulsive drugs during pregnancy and the risk of malformations in the newborn: a meta-analysis]. / Uso de anticonvulsionantes durante el embarazo y el riesgo de malformaciones en el recién nacido: metaanálisis.

OBJECTIVE: To determine the risk, if any, of anticonvulsants use on the foetus with respect to major malformations. MATERIALS AND METHODS: MEDLINE, EMBASE, SCISEARCH and programs as ProQuest, HINARI and Ovid were searched for human studies. Studies that examined the effects of systematic exposure to any anticonvulsant during pregnancy (any dose, any duration, indicated for any type of epilepsy) were eligible. Studies that assessed major malformations in the infants were eligible. Major malformations were defined using the criteria described by Holmes. The number of neonates exposed to anticonvulsants who did and did not exhibit major malformations, and the number of neonates not exposed to anticonvulsants who did and did not exhibit major malformations, were extracted in the form of 2 x 2 tables. The odds ratio (OR), relative risk and 95% confidence interval (CI) was calculated for each of the studies. RESULTS: Ten cohort studies and four case control studies were included. A total of 2,509 cases and 433,890 controls were included. Major malformations were found in 9.8% among the exposed children and 7.4% among the non exposed. (OR: 2.7; CI 95%: 2.062-3.641; p<0.000). There was no evidence of an association between any anticonvulsant and a specific major malformation. CONCLUSIONS: The available epidemiological data support the hypothesis that anticonvulsants increase the risk of major malformations by an order of 2- to 3-fold.