SUMMARY The charts of 46 children diagnosed as deaf and autistic were reviewed. Nearly one‐fifth had normal or near‐normal non‐verbal intelligence and only one‐fifth had severe mental deficiency. The severity of the autistic behavior was related to the severity of the mental deficiency, but not to that of the hearing loss. In 11 of the 46 children, autism went unrecognized for over four years after the diagnosis of hearing loss, and in 10 the hearing loss went unrecognized for several years after the diagnosis of autism. The educational experience of some children was generally disastrous because of the frequently late and incorrect diagnoses and the lack of specialized facilities for hearing‐impaired autistic children. RÉSUMÉ Enfants à la fois sourds et autistes Les dossiers de 46 enfants portant à la fois le diagnostic de surdité et celui d'autisme ont été analysés. Près d'un cinquième des enfants avaient une intelligence non verbale normale ou proche de la normale, et seulement un cinquième des enfants avaient une intelligence non‐verbale normale ou proche de la normale, et seulement un cinquième avaient une déficience mentale grave. La sévérité de l'autisme était liée à celle de la déficience mentale mais pas à celle de la surdité. Chez 11 des 46 enfants, l'autisme fut despisté plus de quatre ans après la surdité, tandis que chez 10 enfants c'est la surdité qui resta méconnue plusieurs années après le diagnostic de l'autisme. L'expérience éducative de ces enfants fut généralement désastreuse du fait du dépistage tardif et des erreurs de diagnostic, ainsi qu'à cause du manque presque total de programmes scolaires spécialisés pour enfants à la fois sourds et autistes. ZUSAMMENFASSUNG Hörgestörte autistische Kinder Von 46 tauben und autistischen Kindern wurden die Krankengeschichten kontrolliert. Fast ein Fünftel hatte eine normale oder nahezu normale non‐verbale Intelligenz und nur ein Fünftel hatte eine schwere geistige Behinderung. Der Schweregrad des autistichen Verhaltens stand in Relation zum Schweregrad der geistigen Behinderung, nicht aber zu dem des Hörverlustes. Bei 11 der 46 Kinder wurde der Autismus erst vier Jahre nach der Diagnose des Hörverlustes festgestellt und bei 10 wurde der Hörverlust erst mehrere Jahre nach der Diagnose des Autismus erkannt. Die Schulbildung dieser Kinder war im allgemeinen schlecht wegen der naurig verspäteten und ungenauen Diagnosen und wegen fehlender spezialisierter Ausbildungsmöglichkeiten für hörgeschädigte autistische Kinder. RESUMEN Niños autísticos con alteratión de oído Se revisaron los protocolos de 46 niños diagnosticados como sordos y autísticos. Casi una quinta parte de ellos tenían una inteligencia no verbal normal o casi normal y sólo una quinta parte tenia un deficit mental grave. La gravedad del comportamiento autístico estaba en relación con la gravedad de la deficiencia mental, pero no con la de la pérdida de la audición. En 11 de los 46 niños el autismo no fue diagnosticado en el curso de los cuatro años siguientes al diagnóstico de la pérdida de aud...
Autism spectrum disorders affected 19 of 38 unselected children at a school for the blind in Cordoba, Argentina. Autism was linked to total congenital blindness, not blindness' etiology, acquired or incomplete blindness, sex, overt brain damage, or socioeconomic status. Autism "recovery," had occurred in 4 verbal children. Congenital blindness causes profoundly deviant sensory experience and massive reorganization of brain connectivity. Its ≥ 30 times greater prevalence than in sighted children suggests a distinct pathogenesis. Unawareness of autism's high prevalence in blind individuals includes blindness' rarity, misunderstanding of autism as "disease" rather than dimensional behavioral diagnosis, reluctance to diagnose it in blind children, and ignorance of its potentially more favorable outcome. Future investigation may suggest interventions to prevent or mitigate it.
After been exposed to the visual input, in the first year of life, the brain experiences subtle but massive changes apparently crucial for communicative/emotional and social human development. Its lack could be the explanation of the very high prevalence of autism in children with total congenital blindness. The present theory postulates that the superior colliculus is the key structure for such changes for several reasons: it dominates visual behavior during the first months of life; it is ready at birth for complex visual tasks; it has a significant influence on several hemispheric regions; it is the main brain hub that permanently integrates visual and non-visual, external and internal information (bottom–up and top–down respectively); and it owns the enigmatic ability to take non-conscious decisions about where to focus attention. It is also a sentinel that triggers the subcortical mechanisms which drive social motivation to follow faces from birth and to react automatically to emotional stimuli. Through indirect connections it also activates simultaneously several cortical structures necessary to develop social cognition and to accomplish the multiattentional task required for conscious social interaction in real life settings. Genetic or non-genetic prenatal or early postnatal factors could disrupt the SC functions resulting in autism. The timing of postnatal biological disruption matches the timing of clinical autism manifestations. Astonishing coincidences between etiologies, clinical manifestations, cognitive and pathogenic autism theories on one side and SC functions on the other are disclosed in this review. Although the visual system dependent of the SC is usually considered as accessory of the LGN canonical pathway, its imprinting gives the brain a qualitatively specific functions not supplied by any other brain structure.
A better understanding of the pathogenesis of autism will help clarify our conception of the complexity of normal brain development. The crucial deficit may lie in the postnatal changes that vision produces in the brainstem nuclei during early life. The superior colliculus is the primary brainstem visual center. Although difficult to examine in humans with present techniques, it is known to support behaviors essential for every vertebrate to survive, such as the ability to pay attention to relevant stimuli and to produce automatic motor responses based on sensory input. From birth to death, it acts as a brain sentinel that influences basic aspects of our behavior. It is the main brainstem hub that lies between the environment and the rest of the higher neural system, making continuous, implicit decisions about where to direct our attention. The conserved cortex-like organization of the superior colliculus in all vertebrates allows the early appearance of primitive emotionally-related behaviors essential for survival. It contains first-line specialized neurons enabling the detection and tracking of faces and movements from birth. During development, it also sends the appropriate impulses to help shape brain areas necessary for social-communicative abilities. These abilities require the analysis of numerous variables, such as the simultaneous evaluation of incoming information sustained by separate brain networks (visual, auditory and sensory-motor, social, emotional, etc.), and predictive capabilities which compare present events to previous experiences and possible responses. These critical aspects of decision-making allow us to evaluate the impact that our response or behavior may provoke in others. The purpose of this review is to show that several enigmas about the complexity of autism might be explained by disruptions of collicular and brainstem functions. The results of two separate lines of investigation: 1. the cognitive, etiologic, and pathogenic aspects of autism on one hand, and two. the functional anatomy of the colliculus on the other, are considered in order to bridge the gap between basic brain science and clinical studies and to promote future research in this unexplored area.
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