Functional neuroanatomy of visuo-spatial working memory in turner syndrome
Turner syndrome (TS), a genetic disorder characterized by the absence of an X chromosome in females, has been associated with cognitive and visuo‐spatial processing impairments. We utilized functional MRI (fMRI) to investigate the neural substrates that underlie observed deficits in executive functi...
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Published in | Human brain mapping Vol. 14; no. 2; pp. 96 - 107 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
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New York
John Wiley & Sons, Inc
01.10.2001
Wiley-Liss |
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Online Access | Get full text |
ISSN | 1065-9471 1097-0193 |
DOI | 10.1002/hbm.1044 |
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Abstract | Turner syndrome (TS), a genetic disorder characterized by the absence of an X chromosome in females, has been associated with cognitive and visuo‐spatial processing impairments. We utilized functional MRI (fMRI) to investigate the neural substrates that underlie observed deficits in executive functioning and visuo‐spatial processing. Eleven females with TS and 14 typically developing females (ages 7–20) underwent fMRI scanning while performing 1‐back and 2‐back versions of a standard visuo‐spatial working memory (WM) task. On both tasks, TS subjects performed worse than control subjects. Compared with controls, TS subjects showed increased activation in the left and right supramarginal gyrus (SMG) during the 1‐back task and decreased activation in these regions during the 2‐back task. In addition, decreased activation in the left and right dorsolateral prefrontal cortex (DLPFC) and caudate nucleus was observed during the 2‐back task in TS subjects. Activation differences localized to the SMG, in the inferior parietal lobe, may reflect deficits in visuo‐spatial encoding and WM storage mechanisms in TS. In addition, deficits in the DLPFC and caudate may be related to deficits in executive function during WM performance. Together these findings point to deficits in frontal‐striatal and frontal‐parietal circuits subserving multiple WM functions in TS. Hum. Brain Mapping 14:96–107, 2001. © 2001 Wiley‐Liss, Inc. |
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AbstractList | Turner syndrome (TS), a genetic disorder characterized by the absence of an X chromosome in females, has been associated with cognitive and visuo-spatial processing impairments. We utilized functional MRI (fMRI) to investigate the neural substrates that underlie observed deficits in executive functioning and visuo-spatial processing. Eleven females with TS and 14 typically developing females (ages 7-20) underwent fMRI scanning while performing 1-back and 2-back versions of a standard visuo-spatial working memory (WM) task. On both tasks, TS subjects performed worse than control subjects. Compared with controls, TS subjects showed increased activation in the left and right supramarginal gyrus (SMG) during the 1-back task and decreased activation in these regions during the 2-back task. In addition, decreased activation in the left and right dorsolateral prefrontal cortex (DLPFC) and caudate nucleus was observed during the 2-back task in TS subjects. Activation differences localized to the SMG, in the inferior parietal lobe, may reflect deficits in visuo-spatial encoding and WM storage mechanisms in TS. In addition, deficits in the DLPFC and caudate may be related to deficits in executive function during WM performance. Together these findings point to deficits in frontal-striatal and frontal-parietal circuits subserving multiple WM functions in TS. Turner syndrome (TS), a genetic disorder characterized by the absence of an X chromosome in females, has been associated with cognitive and visuo‐spatial processing impairments. We utilized functional MRI (fMRI) to investigate the neural substrates that underlie observed deficits in executive functioning and visuo‐spatial processing. Eleven females with TS and 14 typically developing females (ages 7–20) underwent fMRI scanning while performing 1‐back and 2‐back versions of a standard visuo‐spatial working memory (WM) task. On both tasks, TS subjects performed worse than control subjects. Compared with controls, TS subjects showed increased activation in the left and right supramarginal gyrus (SMG) during the 1‐back task and decreased activation in these regions during the 2‐back task. In addition, decreased activation in the left and right dorsolateral prefrontal cortex (DLPFC) and caudate nucleus was observed during the 2‐back task in TS subjects. Activation differences localized to the SMG, in the inferior parietal lobe, may reflect deficits in visuo‐spatial encoding and WM storage mechanisms in TS. In addition, deficits in the DLPFC and caudate may be related to deficits in executive function during WM performance. Together these findings point to deficits in frontal‐striatal and frontal‐parietal circuits subserving multiple WM functions in TS. Hum. Brain Mapping 14:96–107, 2001. © 2001 Wiley‐Liss, Inc. Turner syndrome (TS), a genetic disorder characterized by the absence of an X chromosome in females, has been associated with cognitive and visuo-spatial processing impairments. We utilized functional MRI (fMRI) to investigate the neural substrates that underlie observed deficits in executive functioning and visuo-spatial processing. Eleven females with TS and 14 typically developing females (ages 7-20) underwent fMRI scanning while performing 1-back and 2-back versions of a standard visuo-spatial working memory (WM) task. On both tasks, TS subjects performed worse than control subjects. Compared with controls, TS subjects showed increased activation in the left and right supramarginal gyrus (SMG) during the 1-back task and decreased activation in these regions during the 2-back task. In addition, decreased activation in the left and right dorsolateral prefrontal cortex (DLPFC) and caudate nucleus was observed during the 2-back task in TS subjects. Activation differences localized to the SMG, in the inferior parietal lobe, may reflect deficits in visuo-spatial encoding and WM storage mechanisms in TS. In addition, deficits in the DLPFC and caudate may be related to deficits in executive function during WM performance. Together these findings point to deficits in frontal-striatal and frontal-parietal circuits subserving multiple WM functions in TS.Turner syndrome (TS), a genetic disorder characterized by the absence of an X chromosome in females, has been associated with cognitive and visuo-spatial processing impairments. We utilized functional MRI (fMRI) to investigate the neural substrates that underlie observed deficits in executive functioning and visuo-spatial processing. Eleven females with TS and 14 typically developing females (ages 7-20) underwent fMRI scanning while performing 1-back and 2-back versions of a standard visuo-spatial working memory (WM) task. On both tasks, TS subjects performed worse than control subjects. Compared with controls, TS subjects showed increased activation in the left and right supramarginal gyrus (SMG) during the 1-back task and decreased activation in these regions during the 2-back task. In addition, decreased activation in the left and right dorsolateral prefrontal cortex (DLPFC) and caudate nucleus was observed during the 2-back task in TS subjects. Activation differences localized to the SMG, in the inferior parietal lobe, may reflect deficits in visuo-spatial encoding and WM storage mechanisms in TS. In addition, deficits in the DLPFC and caudate may be related to deficits in executive function during WM performance. Together these findings point to deficits in frontal-striatal and frontal-parietal circuits subserving multiple WM functions in TS. |
Author | Reiss, Allan L. White, Christopher D. Neely, E. Kirk Haberecht, Michael F. Menon, Vinod Warsofsky, Ilana S. Glover, Gary H. Dyer-Friedman, Jenny |
AuthorAffiliation | 2 Program in Neuroscience, Stanford University School of Medicine, Stanford, California 5 Department of Pediatrics, Stanford University School of Medicine, Stanford, California 1 Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Stanford, California 4 Department of Radiology, Stanford University School of Medicine, Stanford, California 3 Stanford Brain Research Center, Stanford University School of Medicine, Stanford, California |
AuthorAffiliation_xml | – name: 1 Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Stanford, California – name: 3 Stanford Brain Research Center, Stanford University School of Medicine, Stanford, California – name: 2 Program in Neuroscience, Stanford University School of Medicine, Stanford, California – name: 5 Department of Pediatrics, Stanford University School of Medicine, Stanford, California – name: 4 Department of Radiology, Stanford University School of Medicine, Stanford, California |
Author_xml | – sequence: 1 givenname: Michael F. surname: Haberecht fullname: Haberecht, Michael F. email: mhaber1@leland.stanford.edu organization: Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Stanford, California – sequence: 2 givenname: Vinod surname: Menon fullname: Menon, Vinod organization: Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Stanford, California – sequence: 3 givenname: Ilana S. surname: Warsofsky fullname: Warsofsky, Ilana S. organization: Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Stanford, California – sequence: 4 givenname: Christopher D. surname: White fullname: White, Christopher D. organization: Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Stanford, California – sequence: 5 givenname: Jenny surname: Dyer-Friedman fullname: Dyer-Friedman, Jenny organization: Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Stanford, California – sequence: 6 givenname: Gary H. surname: Glover fullname: Glover, Gary H. organization: Department of Radiology, Stanford University School of Medicine, Stanford, California – sequence: 7 givenname: E. Kirk surname: Neely fullname: Neely, E. Kirk organization: Department of Pediatrics, Stanford University School of Medicine, Stanford, California – sequence: 8 givenname: Allan L. surname: Reiss fullname: Reiss, Allan L. organization: Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Stanford, California |
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Keywords | Chromosomal aberration Human Dysgenesia Image processing Vision disorder Sexual differentiation disorder Cognition Turner syndrome Nuclear magnetic resonance imaging Female genital diseases Eye disease Malformation Gonad Medical imagery Functional imaging |
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Snippet | Turner syndrome (TS), a genetic disorder characterized by the absence of an X chromosome in females, has been associated with cognitive and visuo‐spatial... Turner syndrome (TS), a genetic disorder characterized by the absence of an X chromosome in females, has been associated with cognitive and visuo-spatial... |
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SubjectTerms | Adolescent Biological and medical sciences Brain Mapping caudate Caudate Nucleus - pathology Caudate Nucleus - physiopathology Cerebral Cortex - pathology Cerebral Cortex - physiopathology Child Chromosome aberrations Female Frontal Lobe - pathology Frontal Lobe - physiopathology Functional Laterality - physiology functional MRI Humans Intelligence Tests Learning Disorders - etiology Learning Disorders - pathology Learning Disorders - physiopathology Magnetic Resonance Imaging Medical genetics Medical sciences Memory Disorders - pathology Memory Disorders - physiopathology Memory, Short-Term - physiology neuroimaging Neuropsychological Tests Original parietal cortex Parietal Lobe - pathology Parietal Lobe - physiopathology prefrontal cortex Psychomotor Performance - physiology Space Perception - physiology spatial cognition Turner Syndrome - pathology Turner Syndrome - physiopathology X monosomy |
Title | Functional neuroanatomy of visuo-spatial working memory in turner syndrome |
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