A volumetric study of parietal lobe subregions in Turner syndrome

Brown, Wendy E.; Kesler, Shelli R.; Eliez, Stéphan; Warsofsky, Ilana S.; Haberecht, Michael F.; Reiss, Allan L.

doi:10.1111/j.1469-8749.2004.tb01024.x

Cited by 46 publications

(17 citation statements)

References 23 publications

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“…Data regarding dosages, prior GH therapy, and age at GH/estrogen therapy initiation were unavailable. There was no union of subjects between the two cohorts; however, previous studies from our colleagues have reported findings using subjects from the secondary cohort (Brown et al, 2002; Brown et al, 2004; Kesler et al, 2003; Kesler et al, 2004). Additionally, seven subjects overlapped in age between the two cohorts (3.0T: 1 TS, 1 TD; 1.5T: 2 TS, 3 TD).…”

Section: Methodsmentioning

confidence: 63%

“…Using univariate structural analyses of brain MRI (e.g., volumetric and voxel-based morphometry [VBM]), the most consistent findings in these TS populations include reduction in parieto-occipital gray matter volume (GMV) (Brown et al, 2004; Cutter et al, 2006; Molko et al, 2004; Reiss et al, 1995) and enlargement of the amygdala (Good et al, 2003; Kesler et al, 2004). Structural and functional abnormalities have also been reported in the hippocampus, caudate, orbitofrontal cortex, and superior temporal gyrus (Cutter et al, 2006; Haberecht et al, 2001; Kesler et al, 2003; Tamm et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

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Neuroanatomical spatial patterns in Turner syndrome

et al. 2011

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Turner syndrome (TS) is a highly prevalent genetic condition caused by partial or complete absence of one X-chromosome in a female and is associated with a lack of endogenous estrogen during development secondary to gonadal dysgenesis. Prominent cognitive weaknesses in executive and visuospatial function in the context of normal overall IQ also occur in affected individuals. Previous neuroimaging studies of TS point to a profile of neuroanatomical variation relative to age and sex matched controls. However, there are no neuroimaging studies focusing on young girls with TS before they receive exogenous estrogen treatment to induce puberty. Information obtained from young girls with TS may help to establish an early neural correlate of the cognitive phenotype associated with the disorder. Further, univariate analysis has predominantly been the method of choice in prior neuroimaging studies of TS. Univariate approaches examine between-group differences on the basis of individual image elements (i.e., a single voxel's intensity or the volume of an a priori defined brain region). This is in contrast to multivariate methods that can elucidate complex neuroanatomical profiles in a clinical population by determining the pattern of between-group differences from many image elements evaluated simultaneously. In this case, individual image elements might not be significantly different between groups but can still contribute to a significantly different overall spatial pattern. In this study, voxel-based morphometry (VBM) of high-resolution magnetic resonance images was used to investigate differences in brain morphology between 13 pediatric, pre-estrogen girls with monosomic TS and 13 age-matched typically developing controls (3.0T imaging: mean age 9.1 ± 2.1). A similar analysis was performed with an older cohort of 13 girls with monosomic TS and 13 age-matched typically developing controls (1.5T imaging: mean age 15.8 ± 4.5). A multivariate, linear support vector machine analysis using leave-one-out cross-validation was then employed to discriminate girls with TS from typically developing controls based on differences in neuroanatomical spatial patterns and to assess how accurately such patterns translate across heterogeneous cohorts. VBM indicated that both TS cohorts had significantly reduced gray matter volume in the precentral, postcentral, and supramarginal gyri and enlargement of the left middle and superior temporal gyri. Support vector machine (SVM) classifiers achieved high accuracy for discriminating brain morphology patterns in TS from typically developing controls and also displayed spatial patterns consistent with VBM results. Furthermore, the SVM classifiers identified additional neuroanatomical variations in individuals with TS, localized in the hippocampus, orbitofrontal cortex, insula, caudate, and cuneus. Our results demonstrate robust spatial patterns of altered brain morphology in developmentally dynamic populations with TS,

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Section: Methodsmentioning

confidence: 63%

Section: Introductionmentioning

confidence: 99%

Neuroanatomical spatial patterns in Turner syndrome

et al. 2011

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“…Genetic and hormonal factors may exert considerable effects on the VSC processing network. For example, females with Turner syndrome (X-chromosome deficiency) are impaired in visuospatial information processing and have structural anomalies in the parietal lobes (Brown et al, 2004;Molko et al, 2003Molko et al, , 2004, therefore, X-chromosome-linked influences on parietal structures have to be assumed, and might help to further elucidate the observed sex-specific pattern of structures correlated with VSC (i.e., GM in females vs. WM in males). Besides genetic factors, sexual hormones exert a considerable effect on cognitive performance, at least in females (Bayer, Kessler, Güntürkün, & Hausmann, 2008;Sherwin, 2003;Rode et al, 1995), and might modulate GM and WM volumes even in the parietal lobes (Goldstein et al, 2001).…”

Section: Possible Mechanisms Mediating a Sex-specific Implementation mentioning

confidence: 98%

Sexual Dimorphism in the Parietal Substrate Associated with Visuospatial Cognition Independent of General Intelligence

Hänggi

Buchmann

Mondadori

et al. 2010

Journal of Cognitive Neuroscience

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Sex differences in visuospatial cognition (VSC) with male advantage are frequently reported in the literature. There is evidence for sexual dimorphisms in the human brain, one of which postulates more gray matter (GM) in females and more white matter (WM) in males relative to total intracranial volume. We investigated the neuroanatomy of VSC independent of general intelligence (g) in sex-separated populations, homogenous in age, education, memory performance, a memory- and brain morphology-related gene, and g. VSC and g were assessed with the Wechsler adult intelligence scale. The influence of g on VSC was removed using a hierarchical factor analysis and the Schmid-Leiman solution. Structural high-resolution magnetic resonance images were acquired and analyzed with voxel-based morphometry. As hypothesized, the clusters of positive correlations between local volumes and VSC performance independent of g were found mainly in parietal areas, but also in pre- and postcentral regions, predominantly in the WM in males, whereas in females these correlations were located in parietal and superior temporal areas, predominantly in the GM. Our results suggest that VSC depends more strongly on parietal WM structures in males and on parietal GM structures in females. This sex difference might have to do with the increased axonal and decreased somatodendritic tissue in males relative to females. Whether such sex-specific implementations of the VSC network can be explained genetically as suggested in investigations into the Turner syndrome or as a result of structural neural plasticity upon different experience and usage remains to be shown.

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“…Meyer-Lindenberg et al, 2004; Reiss, Eckert, Rose, Karchemskiy, Kesler, Chang, Reynolds, Kwon and Galaburda, 2004; Kogan, Bertone, Cornish, Boutet, Der Kaloustian, Anderman, Faubert and Chaudhuri, 2004; Kogan, Boutet, Cornish, Zangenehpour, Mullen, Holden, Der Kaloustian, Andermann and Chaudhuri, 2004). In further support of this hypothesis is the finding of structural and connectivity (WS: Hoeft, Barnea-Goraly, et al, 2007; Eckert et al, 2005; Meyer-Lindenberg et al, 2004; FXS: Barnea-Goraly et al, 2003; TS: Murphy et al, 1993; Brown et al, 2004; Molko et al, 2004; Holzapful et al, 2006; VCFS: Barnea-Goraly et al, 2005) as well as functional (WS: Meyer-Lindenberg et al, 2004; Atkinson, Braddick, Anker, Curran, Andrew, Wattern-Bell and Braddick, 2003; Atkinson, King, Braddick, Nokese, Anker, and Braddick, 1997; FXS: Kwon et al, 2001; Rivera et al, 2002; TS: Kesler et al, 2004; Hart et al, 2004; VCFS: Eliez et al, 2001) abnormalities in the parietal lobe and superior longitudinal fasciculus (the primary white matter pathway running from occipital towards parietal cortex) across all four syndromes (see Table 1). …”

Section: Converging Evidence Across Syndromesmentioning

confidence: 79%

“…The most affected brain areas in TS include decreases in volume in the occipital and parietal cortices, specifically in superior parietal lobe (SPL) and postcentral gyri (Murphy, DeCarli, Daly, Haxby, Allen, White, McIntosh, Powell, Horwitz, Rapoport, et al, 1993; Brown, Kesler, Eliez, Warsofsky, Haberecht and Reiss, 2004), suggesting that parietal cortex abnormalities may be related to the visuospatial deficits seen in TS. Other brain differences include increases in the volume of the superior temporal gyrus (Kesler et al, 2003), enlarged amygdala (Good, Lawrence, Thomas, Price, Ashburner, Friston, Frackowiak, Oreland and Skuse, 2003; Kesler, Garrett, Bender, Yankowitz, Zeng and Reiss, 2004), and reduced hippocampal volume (Kesler et al, 2004).…”

Section: Neurogenetic Syndromes: Genetics Behavior and Imagingmentioning

confidence: 99%

Insights into brain development from neurogenetic syndromes: evidence from fragile X syndrome, Williams syndrome, Turner syndrome and velocardiofacial syndrome

2009

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Over the past few decades, behavioral, neuroimaging and molecular studies of neurogenetic conditions, such as Williams, fragile X, Turner and velocardiofacial (22q11.2 deletion) syndromes, have led to important insights regarding brain development. These investigations allow researchers to examine “experiments of nature” in which the deletion or alteration of one gene or a contiguous set of genes can be linked to aberrant brain structure or function. Converging evidence across multiple imaging modalities has now begun to highlight the abnormal neural circuitry characterizing many individual neurogenetic syndromes. Furthermore, there has been renewed interest in combining analyses across neurogenetic conditions in order to search for common organizing principles in development. In this review, we highlight converging evidence across syndromes from multiple neuroimaging modalities, with a particular emphasis on functional imaging. In addition, we discuss the commonalities and differences pertaining to selective deficits in visuospatial processing that occur across four neurogenetic syndromes. We suggest avenues for future exploration, with the goal of achieving a deeper understanding of the neural abnormalities in these affected populations.

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A volumetric study of parietal lobe subregions in Turner syndrome

Cited by 46 publications

References 23 publications

Neuroanatomical spatial patterns in Turner syndrome

Neuroanatomical spatial patterns in Turner syndrome

Sexual Dimorphism in the Parietal Substrate Associated with Visuospatial Cognition Independent of General Intelligence

Insights into brain development from neurogenetic syndromes: evidence from fragile X syndrome, Williams syndrome, Turner syndrome and velocardiofacial syndrome

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