By Desiderio Pozo Lauzán Albia Josefina Pozo Alonso

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Esta manifestación es el elemento más típico de esta entidad. Este trastorno puede manifestarse en la etapa fetal en forma de movimientos uterinos anormales. La hiperecplexia es por lo general familiar. Se expresa con mayor frecuencia en forma autosómica dominante, con penetrancia completa y expresión variable. También existen formas esporádicas. En algunos pacientes se han identificado mutaciones a nivel 5q. El electroencefalograma realizado durante los espasmos tónicos puede mostrar puntas rápidas, seguidas de una actividad de base lenta.

Pueden ocurrir con predominio en las horas de conciliar el sueño o de despertar, así como, ser exacerbadas por movimientos voluntarios. La duración es breve, menos que 350 ms. El electroencefalograma ictal muestra descargas de polipuntaonda o a veces punta y onda u onda aguda y onda lenta. El interictal muestra descargas iguales que las del ictal. 3. Crisis clónica. Se caracteriza por contracciones clónicas repetitivas, cuya amplitud no disminuye a medida que decrece su frecuencia. La fase posictal habitualmente es breve.

5. Errores innatos del metabolismo: a) Hiperglucinemia no cetósica. 37 b) Acidemia propiónica. c) Deficiencia de sulfito oxidasa. d) Deficiencia de piridoxina. e) Trastornos en el metabolismo de los aminoácidos. f) Trastornos en el ciclo de la urea. g) Otros. 6. Infecciones prenatales: a) Toxoplasmosis. b) Citomegalovirus. c) Rubéola. d) Herpes simple. 7. Insulto hipóxico-isquémico: a) Poroencefalia. b) Leucomalacia periventricular. B. Factores causales perinatales: 1. Encefalopatía hipóxico-isquémica: a) Leucomalacia periventricular.

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