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On the biological basis of human laterality: I. Evidence for a maturational left–right gradient

  • Michael C. Corballis (a1) and Michael J. Morgan (a2)

In this paper, we consider human handedness and cerebral lateralization in a general biological context, and attempt to arrive at some conclusions common to the growth of human laterality and of other structural asymmetries. We suggest that many asymmetries appear to be under the influence of a left-right maturational gradient, which often seems to favor earlier or more rapid development on the left than on the right. If the leading side is damaged or restricted, this gradient may be reversed so that growth occurs with the opposite polarity. A mechanism of this sort appears to underlie the phenomenon of situs inversus viscerum et cordis, and the same principle may help explain the equipotentiality of the two sides of the human brain with respect to the representation of language in the early years of life. However we must also suppose that the leading side normally exerts an inhibitory influence on the lagging side, for otherwise one would expect language ultimately to develop in both halves of the brain. Examples of an inhibitory influence of this kind can also be found in other biological asymmetries; for instance, in the crab Alpheus heterochelis, one claw is normally greatly enlarged relative to the other, but if the larger claw is removed the smaller one is apparently released from its inhibitory influence and grows larger.

This last example is particularly interesting because it suggests a mechanism comparable to that proposed by Annett to account for the distribution of handedness in the human population. She argued, in effect, that there is a “right shift” factor among the majority of the population, but that among a minority who lack this factor handedness is determined at random. If it is supposed that cerebral lateralization is also determined at random among this recessive minority, the model can be extended to provide a reasonable fit to the data on the correlation between handedness and cerebral lateralization. However this genetic model (or any other) still fails to account for the near-binomial distribution of handedness among twins and among nontwin siblings. We suggest that right-handedness and leftcerebral dominance for language are manifestations of an underlying gradient which is probably coded in the cytoplasm rather than in the genes. We must leave open the question as to whether departures from this pattern are due to a recessive gene which effectively cancels the asymmetry to environmental influences, or to both genetic and cytoplasmic factors.

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