Cerebral Cortex February 2004; 14:156-164
© Oxford University Press 2004
Enlarged Temporal Lobes in Turner Syndrome: An X-chromosome Effect?
1 Discipline of Biochemistry, School of Molecular and Microbial Biosciences, The University of Sydney, Sydney, NSW 2006, Australia, 2 Department of Medical Genetics, The Children’s Hospital at Westmead, Westmead, NSW 2145, Australia, 3 Developmental Cognitive Neuropsychology Research Unit, The Children’s Hospital at Westmead, Westmead, NSW 2145, Australia, 4 Prince of Wales Medical Research Institute, Barker St, Randwick, 2031 NSW, Australia, 5 Department of Radiology, The Children’s Hospital at Westmead, Westmead, NSW 2145, Australia, 6 Macquarie Centre for Cognitive Science, Macquarie University, Epping, NSW 2109, Australia, 7 Western Sydney Genetics Program, The Children’s Hospital at Westmead, Westmead, NSW 2145, Australia, 8 School of Paediatrics and Child Health, The University of Sydney, Sydney, NSW 2006, Australia, 9 Robert Vines Growth Centre, The Children’s Hospital at Westmead, Westmead, NSW2145, Australia
Gender differences in brain morphology have previously been reported in the temporal lobe and an ‘X-chromosome dosage effect’ has been described in Turner syndrome (45,X). To examine this further, we investigated temporal lobe morphology, metabolism and function in nine children with non-mosaic Turner syndrome using magnetic resonance imaging, 1H magnetic resonance spectroscopy and neuropsychological testing and compared outcomes with results from nine age-matched control girls (46,XX). Turner subjects were found to have significantly larger superior temporal lobes (P = 0.004) and middle temporal lobes (P = 0.047) than controls. The size of the temporal lobe was found to correlate negatively with temporal lobe choline-containing compounds suggesting that increased temporal lobe size is associated with larger cells and/or decreased dendrites. This suggests a developmental failure to prune neurons. The degree of enlargement correlates negatively with functional performance on temporal-lobe associated tasks, suggesting that the enlargement may be a compensatory mechanism, or possibly causative in the case of semantic fluency performance. These temporal lobe abnormalities are discussed with reference to genes which are absent in Turner syndrome and to hormonal differences between Turner syndrome subjects and 46,XX controls.
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