Individual differences in cognitive planning on the Tower of Hanoi task: neuropsychological maturity or measurement error?

The Tower of Hanoi (ToH) task was given to 238 children aged from 7 to 15 years, and 20 adults. Individual variation within an age band was substantial. ToH score did not correlate significantly with Verbal IQ, nor with ability to inhibit a prepotent response. We readministered the ToH to 45 children after 30 to 40 days. The test-retest correlation of .5 is low in relation to accepted psychometric standards, though at least as high as reliability of the related Tower of London (ToL) in adults. The reasons for low reliability remain unclear: task novelty did not seem to be involved, as children did not improve on retest. We conclude that it is not safe to use this test to index integrity or maturation of underlying neurological systems in children. We compared our results with three published studies using the ToL with children, and found similar levels of performance on problems involving the same number of moves. Another study using automated ToL obtained much poorer scores, suggesting that computerised presentation may impair children's performance.

Evidence from Turner's syndrome of an imprinted X-linked locus affecting cognitive function.

Turner's syndrome is a sporadic disorder of human females in which all or part of one X chromosome is deleted. Intelligence is usually normal but social adjustment problems are common. Here we report a study of 80 females with Turner's syndrome and a single X chromosome, in 55 of which the X was maternally derived (45,X[m]) and in 25 it was of paternal origin (45,X[p]). Members of the 45,X[p] group were significantly better adjusted, with superior verbal and higher-order executive function skills, which mediate social interactions. Our observations suggest that there is a genetic locus for social cognition, which is imprinted and is not expressed from the maternally derived X chromosome. Neuropsychological and molecular investigations of eight females with partial deletions of the short arm of the X chromosome indicate that the putative imprinted locus escapes X-inactivation, and probably lies on Xq or close to the centromere on Xp. If expressed only from the X chromosome of paternal origin, the existence of this locus could explain why 46,XY males (whose single X chromosome is maternal) are more vulnerable to developmental disorders of language and social cognition, such as autism, than are 46,XX females.