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READING disabilities, unless associated with obvious and gross cerebral damage, have come to be regarded as psychological or pedagogical problems apparently unrelated to the functions of the central nervous system. Most writers on the subject have concluded that there is no evi-dence of organic neurological dysfunction in cases of reading disability. However, since 1905 (Fisher, Thomas) many case reports in the literature have suggested a genetic factor in some forms of dyslexia. Hallgren (1950), on the basis of an analysis of 116 cases of dyslexia, was able to conclude that: "The genetic statistical analysis shows that specific dyslexia with a high degree of probability, follows a monohybrid autosomal dominant mode of inheritance." Thus a single gene is involved in a dominant non-sexlinked form of inheritance. Hallgren's work (1950) is the most complete study yet avail-able and tends to confirm the conclusion of earlier workers who made less complete investigations but who for the most part suspected a dominant genetic tendency. If dyslexia is inherited as a dominant trait then either there is a "pure word-letter-blindness " due to failure of formation or maturation of a "reading centre"; or "pure word-letter-blindness " does not exist, and in inherited dyslexia other associated neurological abnormalities can be expected if properly searched for and assessed. The first alternative re-quires a return to the now generally outmoded concept of discrete cerebral localization of function. On the other hand, if associated neurological abnormalities are detected in genetically determined dyslexias, it is necessary to attempt to postulate a unitary defect of cerebral function, which is capable of dominant genetic transmission. Any such formulation must be able to incorporate the many apparently diverse observations into
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Arthur L. Drew (1956) studied this question.
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