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LA EPILEPSIA DEL LOBULO TEMPORAL PODRIA ESTAR INFLUIDA POR EL PASO DE LA ALBUMINA A TRAVES DE LA BARRERA HEMATOENCEFALICA

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LA EPILEPSIA DEL LOBULO TEMPORAL PODRIA ESTAR INFLUIDA POR EL PASO DE LA ALBUMINA A TRAVES DE LA BARRERA HEMATOENCEFALICA

(especial para SIIC © Derechos reservados)
La rotura de la barrera hematoencefálica permite el paso de la albúmina al espacio extracelular cerebral, activando los astrocitos por medio del receptor TGF-β, que sufren cambios en la expresión genética.
pastorgomez9.jpg Autor:
Jesús Pastor Gómez
Columnista Experto de SIIC

Institución:
Hospital Universitario La Princesa

Artículos publicados por Jesús Pastor Gómez
Recepción del artículo
11 de Agosto, 2008 		Aprobación
1 de Octubre, 2008
Primera edición
29 de Abril, 2009 		Segunda edición, ampliada y corregida
7 de Junio, 2021

LA EPILEPSIA DEL LOBULO TEMPORAL PODRIA ESTAR INFLUIDA POR EL PASO DE LA ALBUMINA A TRAVES DE LA BARRERA HEMATOENCEFALICA

Resumen
Introducción: La epilepsia del lóbulo temporal (ELT) es el tipo más frecuente de epilepsia resistente a los fármacos en humanos. La necesidad de estudios invasivos y la resección de tejido permiten numerosos estudios acerca de su fisiopatología. Objetivos: Se revisan algunos de los datos y teorías más recientes sobre la fisiopatología de la ELT, haciendo especial referencia a la participación de la albúmina en la activación de los astrocitos tras la rotura de la barrera hematoencefálica (BHE). Se observa una remodelación de la excitación glutamatérgica y la inhibición gabaérgica que deriva en hiperexcitabilidad. Aunque se conocía desde hace tiempo la rotura de la BHE en la ELT, no se había asignado un papel a este aumento de permeabilidad. Recientemente, se demostró que dicha rotura permite el paso de la albúmina al espacio extracelular cerebral, activando los astrocitos por medio del receptor TGF-β, que sufren cambios en la expresión genética. Estos cambios podrían condicionar las modificaciones en la respuesta neuronal responsables de la hiperexcitabilidad. Conclusiones: El estudio multidisciplinario de la fisiopatología de la ELT en la última década nos ha permitido aumentar nuestro conocimiento sobre los procesos que subyacen a la génesis de las crisis, su clínica y evolución.

Palabras clave
albúmina, astrocitos, barrera hematoencefálica, EEG, esclerosis mesial, epilepsia del lóbulo temporal


Artículo completo
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Pathophysiological Basis of Temporal Lobe Epilepsy: The Role of Albumin

Abstract
Introduction: Temporal lobe epilepsy (TLE) is the most frequent form of pharmaco-resistant epilepsy in human. The necessity of invasive studies and epileptic tissue resection allow a number of studies pertaining to the pathophysiology. Objectives: Here, we review recent findings and theories pertaining to the pathophysiology of TLE, with special reference to astocyte activation by albumin after blood-brain barrier (BBB) increase in permeability. Data suggest that the common principle that appears to underlie the epileptic condition is the reorganization of excitation and inhibition resulting in hyperexcitability. From a long time, it had been observed an increase in permeability of BBB in epilepsy. However, no definitely role in the epileptogenesis had been ascribed to this disruption. Recently, it has been showed the BBB disruption allows that albumin goes into the extracellular space, activating astrocytes through TGF- receptor and inducing changes in gene expression. These changes can induce alterations in the neuronal response, underling the hyperexcitability. Conclusions: A multidisciplinary approach can help to fill gaps in our knowledge and to provide unique insights into the pathophysiology of TLE.

Key words
albumin, astrocytes, blood-brain barrier, EEG, mesial sclerosis, temporal lobe epilepsy

Clasificación en siicsalud
Artículos originales > Expertos de Iberoamérica >
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Especialidades
Principal: Anatomía Patológica, Neurología
Relacionadas: Diagnóstico por Imágenes, Diagnóstico por Laboratorio, Medicina Interna



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Enviar correspondencia a:
Jesús Pastor Gómez, Hospital Universitario La Princesa Unidad de Cirugía de la Epilepsia Sección de Neurofisiología Clínica, C/Diego de León 62, Madrid, España
Patrocinio y reconocimiento:
Este trabajo ha contado con financiación del Plan Nacional de Investigación Científica, Desarrollo e Innovación Tecnológica (I+D+I), Instituto de Salud Carlos III, Subdirección General de Evaluación y Fomento de la Investigación, PI060349.
Bibliografía del artículo

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