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M.B.: En esta última década, las investigaciones sobre el autismo (y de manera especial, las investigaciones biomédicas) han aumentado tanto y tan rápidamente que sería imposible dar cuenta de todos los hallazgos recientes. No obstante, puestos a seleccionar, considero especialmente interesantes cuatro grupos o clases de datos: 1) los que confirman que el autismo es el resultado de procesos atípicos de neurogénesis o maduración cerebral tanto pre- como postnatal (lo que tira por tierra hipótesis explicativas sólo «psicógenas» como las que durante un tiempo ligaron el origen de este trastorno a la personalidad de los padres o los estilos de crianza, o como las que, todavía hoy, prefieren tratar el autismo sólo como un síndrome conductual o un simple problema de «aprendizajes»); 2) los que demuestran que la causación o etiología del autismo implica una interacción extraordinariamente compleja de susceptibilidad genética, con marcadores en varios cromosomas -2q, 7q, 13q, 16p, 17q, X y otros-, y de factores medioambientales diversos, como complicaciones obstétricas, infecciones víricas pre o postnatales, alteraciones gastrointestinales, vacunas, exposición a distintas sustancias tóxicas y otros agentes (lo que abre la puerta al desarrollo de políticas no sólo terapéuticas sino también preventivas –como, por ejemplo, el consejo genético a familias que ya tienen un hijo o hija afectado); 3) los que confirman que hay muchas rutas biológicas posibles para el autismo (esto es, que situaciones y procesos biológicos muy dispares pueden desembocar en ese patrón concreto de afectación del desarrollo y el comportamiento que se sintetiza en la «tríada de Wing»), y, 4) que son las «conexiones a larga distancia» entre diversas estructuras corticales y subcorticales más que la disfunción de regiones o estructuras cerebrales individuales las que están sobre todo afectadas en las personas con autismo (lo que exige modelos explicativos muy globales e integrados tanto a nivel neurobiológico como psicológico).
A la luz de estas consideraciones, quizá alguien podría estar tentado a considerar que, efectivamente, el autismo es un trastorno «incurable» porque nadie puede «dejar de tener autismo» por efecto de algún tratamiento, pero, sinceramente, y como ya apunté en mi respuesta a la anterior pregunta, no creo que el modelo médico de enfermedad resulte adecuado o suficiente aquí. Los hallazgos científicos a lo que nos abocan es a entender que el autismo es una condición neuroevolutiva particular, un modo peculiar de organización y funcionamiento del cerebro y la mente que resulta de procesos ontogenéticos parcialmente deficitarios y/o desviados desde momentos muy tempranos del desarrollo, y del que se derivan dificultades y limitaciones psicológicas para los individuos en unos ámbitos (como el ámbito socioemocional), pero también capacidades en otros ámbitos (por ejemplo, en el dominio de la percepción visual o auditiva) que pueden incluso superar las que habitualmente desarrollan las personas sin autismo (las personas «neurotípicas»). a
Por tanto, quienes han recibido un diagnóstico de autismo no deberían considerarse «enfermos que deban esperar curarse», sino «personas con un modo de funcionar diferente pero no necesariamente deficiente o patológico» que deben entender cuáles son sus capacidades y sus dificultades, y deben saber que con tratamientos adecuados y apoyos suficientes en su entorno, podrán mejorar sus síntomas, podrán desarrollar sus habilidades y hacer muchos y buenos aprendizajes, podrán disfrutar de una buena calidad de vida y podrán llegar, en muchos casos, a hacer aportaciones muy útiles a la sociedad.
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