DISLEXIA E ATENÇÃO

• Autor(a) principal: Luca, Maria Inez Ocanã de
• Data de Publicação: 2009
• Tipo de documento: Dissertação
• Idioma: por
• Título da fonte: Biblioteca Digital de Teses e Dissertações da METODISTA
• Texto Completo: http://tede.metodista.br/jspui/handle/tede/1434
• topic: Dislexia; Atenção e Psicofisiologia; Dyslexia; Attention; Psychophysiology; CNPQ::CIENCIAS HUMANAS::PSICOLOGIA

Dyslexia is a neurological condition associated to impairments in acquisition and processing of language. Varying in degrees of severity, it is manifested by difficulties in receptive and expressive language, including phonological processing, in reading, writing, spelling, handwriting, and sometimes in arithmetic. Dyslexia is an inherited condition associated to several neurologic abnormalities in visual and auditory cortical areas. One of the most influential theories to explain dyslexic symptoms is the so called Magnocellular hypothesis. According to this, dyslexia arises from abnormal processing of visual information of movement mainly due to dysfunction in magnocellular system. This dissertation explores this hypothesis by comparing fifteen individuals with dyslexia and fifteen controls, aged between 18 and 30 years through two visual attention tests. Both experiments evaluated reaction time to stimuli appearing in entire computer screen while individuals remained sited, with head supported by a chin rest, and with the eyes fixed in a central target. The experiment 1 consisted of white punctual stimuli presented in a black background. In the experiment 2, the same target locations were used but now with target in green over a red background. The results were analyzed taking in consideration the visual quadrants were the stimuli were presented. Patients and controls did not differ in relation to a shorter reaction time to stimuli presented in inferior visual field, compared with the superior field of the same individual. Considering all quadrants, dyslexics reacted slower in experiment 1 conditions but performed similar to controls in experiment 2. These results are compatible to abnormalities in magnocelular system. The implications of these findings to the pathophysiology of dyslexia as well as its treatment are discussed.(AU)