Various hypotheses derived from Annett's (1972; 1985) genetic theory of handedness are experimentally tested. Results from the first investigation show that excessive bias in favour of right handedness is due to a weakness in left rather than superiority of right hand skill, and is associated with poor nonverbal reasoning ability. A second investigation indicated that risks to reading problems were increased in children with either too little or too much bias in favour of dextrality. A further three studies investigated patterns of ability and disability at both laterality extremes. It was found that language deficits were more frequent in children reduced in bias towards the right hand. An attempt to find a task which those at the dextral tail of the laterality distribution were worse at than those at the sinistral tail met with inconclusive results. The experimental findings are, in general compatible with Annett's hypothesis of a human balanced polymorphism with heterozygote advantage for ability.

All the evidence contained in the investigation of 722 junior high school students points to the fact that there is no connection between the speed of writing and handedness; between the amount of written material produced in 5-minute themes and handedness; and between the effects of writing on subjective evaluations of 5-minute written themes and handedness. The figures show that the incidence of handicap in writing is approximately the same for both right- and left-handed groups. / Arts, Faculty of / Psychology, Department of / Graduate

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Functional asymmetries, most commonly associated in humans with population-level hand preference and lateralization in language processing, are complex, heterogeneous traits with poorly understood biological and genetic bases. Notably, functional asymmetries are also associated with familial non-right handedness suggesting that common genetic factors influence both handedness and functional lateralization. This dissertation has two aims. The first is the development of a specific biological hypothesis that may partially account for the consistent co-lateralization of hand preference and prefrontal language function. I argue that asymmetries in local neural properties that affect the excitability and signal-to-noise ratio of neural assemblies can produce a bias in the direction and, to some extent, the degree of functional lateralization for complex functions. At a high level of representation, this hypothesis is similar to long-standing theories of hemispheric differences, but differs from these by providing a single biological difference between hemispheres that influences both motor and prefrontal asymmetries. Specifically, I propose that a hemispheric asymmetry in the ratio of activity at D1 and D2 dopamine receptors can account for both forms of asymmetry. The second aim is to identify novel electrophysiological and behavioral correlates of genetic effects linked to handedness. By applying a standard genetic model to familial handedness data, I obtain an estimate of these genetic effects for individual research participants that may improve sensitivity over previous studies that have primarily used categorical classifications to study familial handedness effects. Two EEG studies of executive function provide evidence for computational changes associated with familial handedness. The first, an auditory oddball paradigm, suggests that cortical noise is increased in conjunction with estimated genetic effects associated with left handedness. In the second study, a go-nogo task, a dissociation between response inhibition and response conflict processing was found with respect to estimated genetic effects associated with left handedness. In addition to bearing on current theories of conflict processing, these results may provide indirect evidence for dopaminergic contributions to neurological and behavioral differences associated with familial sinistrality. Additional studies of resting EEG and behavioral responses to Necker cube viewing provide additional evidence for broad effects of familial sinistrality.

Thesis (B.A. Hons.))--University of Adelaide, Dept. of Psychology, 1978.

Published also as Thesis (Ph. D.)--Johns Hopkins University. / Bibliography: p. 121.

M.A. (Clinical Psychology) / Please refer to full text to view abstract