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Tratamiento para prevenir daño cerebral tras convulsiones prolongadas
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Tratamiento para prevenir daño cerebral tras convulsiones prolongadas

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Tratamiento para prevenir daño cerebral tras convulsiones prolongadas

Se trata de un compuesto de plomo que puede reducir la mortalidad cuando se administra a ratones después de ataques inducidos.

Investigadores de la Escuela de Medicina de la Universidad de Emory (Estados Unidos) han desarrollado un nuevo tipo de tratamiento profiláctico para la lesión cerebral después de prolongados ataques de epilepsia, según publica la revista Proceedings of the National Academy of  Sciences (doi: 10.1073/pnas.1218498110).

El estado epiléptico, un ataque persistente que puede durar hasta 30 minutos, da lugar a alrededor de 55 000 muertes cada año en Estados Unidos y puede ser causado por apoplejía o infección en el cerebro, así como un control inadecuado de la epilepsia. Actualmente, el estado epiléptico se trata con la administración de una anestesia general o anticonvulsivante, que detiene los ataques.

Los investigadores de Emory han experimentado con antiinflamatorios que pueden ser administrados después de una crisis aguda de epilepsia para reducir el daño al cerebro. Así, han descubierto un compuesto de plomo que puede reducir la mortalidad cuando se administra a ratones después de ataques inducidos.

"El 30% de los adultos que experimentan una crisis de más de una hora muere a las cuatro semanas", señala dice Ray Dingledine, director del Departamento de Farmacología de la Facultad de Medicina de la Universidad de Emory. "Creemos ", afirma, "que tenemos una vía eficaz para reducir al mínimo el daño cerebral causado por el estado epiléptico no controlado".

El equipo de Dingledine identificó compuestos que bloquean los efectos de la prostaglandina E2, una hormona involucrada en procesos como la fiebre, el parto, la digestión y la regulación de la presión arterial. La prostaglandina E2 también está implicado en la inflamación tóxica en el cerebro después de que surja el estado epiléptico.

El primer autor del artículo, el becario postdoctoral Jianxiong Jiang, y el químico medicinal en gran parte responsable del desarrollo de los compuestos, Thota Ganesh, indujeron el estado epiléptico en ratones con el fármaco alcaloide pilocarpina, y les administraron un compuesto, TG6-10-1, cuatro horas más tarde y otra vez a las 21 y 30 horas. TG6-10-1 bloquéo las señales de EP2, uno de los cuatro receptores de prostaglandina E2.

Entre los animales que recibieron el bloqueador EP2, el 90% sobrevivió después de una semana, frente al 60%de un grupo de control que superó con vida el episodio.

Cuatro días después del ataque epiléptico, todos los animales que recibieron TG6-10-1 se mostraron normales en la construcción del nido, pero más de una cuarta parte de los animales de control que viven no fueron capaces de construirlos.

Además, los cerebros de los ratones tratados con TG6-10-1 tenían niveles reducidos de proteínas mensajeras inflamatorias (citoquinas) y menos lesión cerebral en el incumplimiento de la barrera sangre-cerebro. Las consecuencias del estado epiléptico refractario pueden incluir daño cerebral, dificultad para respirar, ritmo cardiaco anormal e insuficiencia cardiaca.

Dingledine sostiene que la primera prueba clínica de un compuesto de bloqueo EP2 sería probablemente como un tratamiento complementario para el estado epiléptico prolongado, varias horas después de haber terminado las convulsiones. También podría ser probado en situaciones similares, como la hemorragia subaracnoidea, convulsiones febriles prolongadas o epilepsia refractaria a la medicación, agrega.

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