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1.
An Pediatr (Barc) ; 69(3): 227-31, 2008 Sep.
Artículo en Español | MEDLINE | ID: mdl-18775267

RESUMEN

INTRODUCTION: There are very few studies on the aetiology of temporal lobe epilepsy (TLE) in childhood. The purpose of the present study is to analyse the data of 61 children diagnosed with TLE, in order to describe the aetiology of TLE in children seen in a neuropaedriatic clinic. We also discuss the currently proposed classification. PATIENTS AND METHODS: A retrospective analysis was carried out on patients diagnosed with TLE. Patients consisted of 61 children less than 15 years old. RESULTS: Patients were classified into three groups: Group 1 (symptomatic temporal lobe epilepsy) consisted of 25 patients (40.98 %) with any temporal lesion on neuroimaging (tumours, malformations or infections) or significant history; Group 2 (Mesial temporal sclerosis) consisted of 17 patients (27.86 %), a history of simple and complex febrile seizure were common in this group; and Group 3 (Cryptogenic epilepsy) consisted of 19 patients (31.15 %) with no abnormalities on neuroimaging or significant history. CONCLUSION: To our knowledge, this is the largest paediatric series of childhood new-onset TLE assessed only by MRI in the literature. We have modified the previous aetiological classification in order to make the groups more realistic.


Asunto(s)
Epilepsia del Lóbulo Temporal/clasificación , Epilepsia del Lóbulo Temporal/etiología , Adolescente , Niño , Preescolar , Femenino , Humanos , Lactante , Masculino , Estudios Retrospectivos
2.
An. pediatr. (2003, Ed. impr.) ; 69(3): 227-231, sept. 2008. tab
Artículo en Es | IBECS | ID: ibc-67454

RESUMEN

Introducción. La etiología de la epilepsia del lóbulo temporal (ELT) en la edad pediátrica se ha descrito en escasas ocasiones. El propósito de este estudio es analizar el diagnóstico etiológico de 61 pacientes con ELT atendidos en una consulta de neurología infantil. Analizamos y comentamos la clasificación actual. Pacientes y métodos. Se trata de un estudio de carácter retrospectivo, en el que se incluyó a 61 pacientes con ELT. Resultados. Los pacientes fueron clasificados en tres grupos en función del diagnóstico etiológico: grupo 1 (ELT sintomática), incluye a 25 pacientes (40,98 %) con lesiones en el lóbulo temporal (malformación, tumor o infección) o antecedentes significativos para presentar epilepsia; grupo 2 (esclerosis mesial temporal [EMT]), incluye a 17 pacientes (27,86 %), el antecedente de crisis febriles (tanto simples como complejas) se encontraba presente en un porcentaje elevado de pacientes con EMT; grupo 3 (ELT criptogénica), incluye a 19 pacientes (31,15 %), sin hallazgos patológicos en la resonancia magnética (RM) craneal o antecedentes significativos. Conclusión. Hasta la fecha, es la mayor serie que analiza, mediante RM, la etiología de la ELT de comienzo en la edad pediátrica. Hemos pretendido matizar la clasificación etiológica más aceptada, con el propósito de hacer grupos más flexibles y realistas


Introduction. There are very few studies on the aetiology of temporal lobe epilepsy (TLE) in childhood. The purpose of the present study is to analyse the data of 61 children diagnosed with TLE, in order to describe the aetiology of TLE in children seen in a neuropaedriatic clinic. We also discuss the currently proposed classification. Patients and methods. A retrospective analysis was carried out on patients diagnosed with TLE. Patients consisted of 61 children less than 15 years old. Results. Patients were classified into three groups: Group 1 (symptomatic temporal lobe epilepsy) consisted of 25 patients (40.98 %) with any temporal lesion on neuroimaging (tumours, malformations or infections) or significant history; Group 2 (Mesial temporal sclerosis) consisted of 17 patients (27.86 %), a history of simple and complex febrile seizure were common in this group; and Group 3 (Cryptogenic epilepsy) consisted of 19 patients (31.15 %) with no abnormalities on neuroimaging or significant history. Conclusion. To our knowledge, this is the largest paediatric series of childhood new-onset TLE assessed only by MRI in the literature. We have modified the previous aetiological classification in order to make the groups more realistic


Asunto(s)
Humanos , Masculino , Femenino , Lactante , Preescolar , Niño , Adolescente , Epilepsia del Lóbulo Temporal/diagnóstico , Epilepsia del Lóbulo Temporal/etiología , Estudios Retrospectivos , Hospitales Universitarios , España
3.
Rev Neurol ; 43(8): 481-8, 2006.
Artículo en Español | MEDLINE | ID: mdl-17033982

RESUMEN

INTRODUCTION AND DEVELOPMENT: Migraine is an episodic primary headache defined by its clinical characteristics. Several pathophysiological hypotheses have been put forward in an attempt to explain the mechanism by which headaches develop in patients suffering from migraine. We believe that there are enough data available to consider that in the cerebral cortex, and in certain situations, there may be either an alteration in the balance of glutamate in the extracellular space or generation of excitatory post-synaptic potentials at rest based on the activation of slightly increased AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) and kainate receptors, which would account for the cortical hyperexcitability and the interictal changes observed in patients with migraine. CONCLUSIONS: Further knowledge about the mechanisms that start and trigger migraines is essential for the development of new therapeutic approaches.


Asunto(s)
Ácido Glutámico/fisiología , Trastornos Migrañosos/fisiopatología , Depresión de Propagación Cortical , Humanos , Trastornos Migrañosos/etiología , Nervio Trigémino/irrigación sanguínea
4.
Rev. neurol. (Ed. impr.) ; 43(8): 481-488, 16 oct., 2006. ilus
Artículo en Es | IBECS | ID: ibc-049864

RESUMEN

Introducción y desarrollo. La migraña es una cefaleaprimaria episódica definida por sus características clínicas. Variashan sido las hipótesis fisiopatológicas que han intentado explicarel mecanismo por el cual se desarrolla la cefalea en los pacientesmigrañosos. Creemos que existen datos suficientes como para considerarque en la corteza cerebral, y ante determinadas situaciones,puede existir o bien una alteración en el balance de glutamatoen el espacio extracelular, o bien una generación de potencialespostsinápticos excitatorios en reposo, a partir de la activación dereceptores AMPA (ácido alfa-amino-3-hidroxi-5-metil-4-isoxazolpropiónico)y kainato, ligeramente aumentados, que explicarían lahiperexcitabilidad cortical y los cambios interictales observadosen los pacientes migrañosos. Conclusión. El conocimiento de losmecanismos por los que se inicia y desencadena la migraña resultafundamental para desarrollar nuevos abordajes terapéuticos


Introduction and development. Migraine is an episodic primary headache defined by its clinical characteristics.Several pathophysiological hypotheses have been put forward in an attempt to explain the mechanism by which headachesdevelop in patients suffering from migraine. We believe that there are enough data available to consider that in the cerebralcortex, and in certain situations, there may be either an alteration in the balance of glutamate in the extracellular space orgeneration of excitatory post-synaptic potentials at rest based on the activation of slightly increased AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) and kainate receptors, which would account for the cortical hyperexcitabilityand the interictal changes observed in patients with migraine. Conclusions. Further knowledge about the mechanisms thatstart and trigger migraines is essential for the development of new therapeutic approaches


Asunto(s)
Humanos , Receptores AMPA/fisiología , Receptores de Glutamato/metabolismo , Excitación Neurológica , Migraña con Aura/etiología , Migraña con Aura/fisiopatología , Corteza Cerebral/patología , Transmisión Sináptica/fisiología
5.
Rev Neurol ; 38(4): 347-58, 2004.
Artículo en Español | MEDLINE | ID: mdl-14997460

RESUMEN

AIMS: In the search for new, potentially treatable, vascular risk factors, one of the most recent to be put forward is the presence of increased total homocysteine (tHc) levels in blood plasma and this has also given rise to a large amount of literature and controversy. The origin of this hypothesis lies in the observation that patients with congenital disorders affecting homocysteine (Hc) metabolism suffered from early atherosclerosis. In this paper we analyse the studies that have been published about Hc and cerebrovascular disease (CVD). DEVELOPMENT: An important number of retrospective case control studies have found a strong dose dependent link between levels of Hc in plasma and cerebrovascular, heart and peripheral thromboembolic disease. Yet the prospective studies that have been published to date note only a weak or inexistent link between homocysteine and CVD. Moreover, some observations question the causal relationship between hyperhomocysteinemia and atherothrombosis and account for the findings in the retrospective studies as being a result of the rise in Hc following a stroke or its increasing because of classical vascular risk factors. In any case, knowing that the ingestion of folic acid, vitamin B12 and pyridoxine lowers tHc levels in plasma has led to clinical trails being set up that evaluate the effects of this treatment on vascular risk. CONCLUSION: The relation between Hc levels in plasma and CVD is open to controversy. New studies and the findings of clinical studies with vitamin therapy will allow this relation to be fully explained in coming years.


Asunto(s)
Trastornos Cerebrovasculares/sangre , Homocisteína/sangre , Hiperhomocisteinemia/metabolismo , Arteriosclerosis/sangre , Arteriosclerosis/tratamiento farmacológico , Enfermedades Cardiovasculares/sangre , Enfermedades Cardiovasculares/tratamiento farmacológico , Estudios de Casos y Controles , Trastornos Cerebrovasculares/tratamiento farmacológico , Humanos , Metilenotetrahidrofolato Reductasa (NADPH2)/genética , Metilenotetrahidrofolato Reductasa (NADPH2)/metabolismo , Estudios Retrospectivos , Factores de Riesgo , Trombosis/sangre , Trombosis/tratamiento farmacológico , Vitaminas/uso terapéutico
6.
Rev. neurol. (Ed. impr.) ; 38(4): 347-358, 16 feb., 2004. graf, tab
Artículo en Es | IBECS | ID: ibc-30897

RESUMEN

Objetivo. En la búsqueda de nuevos factores de riesgo vascular potencialmente tratables, la presencia de una elevación de los niveles plasmáticos de homocisteína total (tHc) en sangre se ha postulado como uno de ellos en los últimos años, y ha generado numerosa bibliografía y controversia. El origen de esta hipótesis se basa en la observación de que los pacientes con trastornos congénitos del metabolismo de la homocisteína (Hc) padecían aterosclerosis precoz. En la presente revisión se analizan los estudios publicados sobre Hc y enfermedad cerebrovascular (ECV). Desarrollo. Un importante número de estudios retrospectivos, casos-control, han encontrado una asociación fuerte y dosis dependiente entre los niveles plasmáticos de Hc y ECV, coronaria y tromboembólica periférica. Sin embargo, los estudios prospectivos publicados observan una asociación entre homocisteinemia y ECV débil o inexistente. Además, algunas observaciones cuestionan la relación de causalidad entre hiperhomocisteinemia y aterotrombosis, que explican los hallazgos de los estudios retrospectivos como resultado de la elevación de la Hc tras un ictus o su incremento por factores de riesgo vascular clásicos. A pesar de todo, el conocimiento de que la ingesta de ácido fólico, vitamina B12 y piridoxina disminuyen los niveles plasmáticos de tHc, ha llevado a iniciar ensayos clínicos que evalúan los efectos de este tratamiento sobre el riesgo vascular. Conclusión. La relación entre los niveles plasmáticos de Hc y la ECV es controvertida. Nuevos estudios y el resultado de los ensayos clínicos con tratamiento vitamínico aclararán en los próximos años esta relación (AU)


Aims. In the search for new, potentially treatable, vascular risk factors, one of the most recent to be put forward is the presence of increased total homocysteine (tHc) levels in blood plasma and this has also given rise to a large amount of literature and controversy. The origin of this hypothesis lies in the observation that patients with congenital disorders affecting homocysteine (Hc) metabolism suffered from early atherosclerosis. In this paper we analyse the studies that have been published about Hc and cerebrovascular disease (CVD). Development. An important number of retrospective case-control studies have found a strong dose-dependent link between levels of Hc in plasma and cerebrovascular, heart and peripheral thromboembolic disease. Yet the prospective studies that have been published to date note only a weak or inexistent link between homocysteine and CVD. Moreover, some observations question the causal relationship between hyperhomocysteinemia and atherothrombosis and account for the findings in the retrospective studies as being a result of the rise in Hc following a stroke or its increasing because of classical vascular risk factors. In any case, knowing that the ingestion of folic acid, vitamin B12 and pyridoxine lowers tHc levels in plasma has led to clinical trails being set up that evaluate the effects of this treatment on vascular risk. Conclusion. The relation between Hc levels in plasma and CVD is open to controversy. New studies and the findings of clinical studies with vitamin therapy will allow this relation to be fully explained in coming years (AU)


Asunto(s)
Femenino , Humanos , Adulto , Hiperhomocisteinemia , Vitaminas , Trombosis , Factores de Riesgo , Estudios de Casos y Controles , Metilenotetrahidrofolato Reductasa (NADPH2) , Homocisteína , Trastornos Cerebrovasculares , Enfermedades Cardiovasculares , Hipotensión Intracraneal , Estudios Retrospectivos , Radiofármacos , Pentetato de Tecnecio Tc 99m , Arteriosclerosis
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