Tags

Type your tag names separated by a space and hit enter

Aberrant Cortical Morphometry in the 22q11.2 Deletion Syndrome.
Biol Psychiatry 2015; 78(2):135-43BP

Abstract

BACKGROUND

There is increased risk of developing psychosis in 22q11.2 deletion syndrome (22q11DS). Although this condition is associated with morphologic brain abnormalities, simultaneous examination of multiple high-resolution measures of cortical structure has not been performed.

METHODS

Fifty-three patients with 22q11DS, 30 with psychotic symptoms, were compared with demographically matched nondeleted youths: 53 typically developing and 53 with psychotic symptoms. High-resolution magnetic resonance imaging measures of cerebral volume, cortical thickness, surface area, and an index of local gyrification were obtained and compared between groups.

RESULTS

Patients with 22q11DS demonstrated global increases in cortical thickness associated with reductions in surface area, reduced index of local gyrification, and lower cerebral volumes relative to typically developing controls. Findings were principally in the frontal lobe, superior parietal lobes, and in the paramedian cerebral cortex. Focally decreased thickness was seen in the superior temporal gyrus and posterior cingulate cortex in 22q11DS relative to nondeleted groups. Patterns between nondeleted participants with psychotic symptoms and 22q11DS were similar but with important differences in several regions implicated in schizophrenia. Post hoc analysis suggested that like the 22q11DS group, cortical thickness in nondeleted individuals with psychotic symptoms differed from typically developing controls in the superior frontal gyrus and superior temporal gyrus, regions previously linked to schizophrenia.

CONCLUSIONS

Simultaneous examination of multiple measures of cerebral architecture demonstrates that differences in 22q11DS localize to regions of the frontal, superior parietal, superior temporal, and paramidline cerebral cortex. The overlapping patterns between nondeleted participants with psychotic symptoms and 22q11DS suggest partially shared neuroanatomic substrates.

Authors+Show Affiliations

Brain Behavior Laboratory, Department of Psychiatry, Neuropsychiatry Section, University of Pennsylvania; Department of Radiology, Hospital of the University of Pennsylvania.Brain Behavior Laboratory, Department of Psychiatry, Neuropsychiatry Section, University of Pennsylvania.Brain Behavior Laboratory, Department of Psychiatry, Neuropsychiatry Section, University of Pennsylvania; Department of Child and Adolescent Psychiatry.Brain Behavior Laboratory, Department of Psychiatry, Neuropsychiatry Section, University of Pennsylvania.Brain Behavior Laboratory, Department of Psychiatry, Neuropsychiatry Section, University of Pennsylvania.Brain Behavior Laboratory, Department of Psychiatry, Neuropsychiatry Section, University of Pennsylvania.Brain Behavior Laboratory, Department of Psychiatry, Neuropsychiatry Section, University of Pennsylvania.Division of Human Genetics, Children's Hospital of Philadelphia.Brain Behavior Laboratory, Department of Psychiatry, Neuropsychiatry Section, University of Pennsylvania.Brain Behavior Laboratory, Department of Psychiatry, Neuropsychiatry Section, University of Pennsylvania.Division of Human Genetics, Children's Hospital of Philadelphia; Department of Pediatrics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.Division of Human Genetics, Children's Hospital of Philadelphia; Department of Pediatrics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.Brain Behavior Laboratory, Department of Psychiatry, Neuropsychiatry Section, University of Pennsylvania; Department of Radiology, Hospital of the University of Pennsylvania.Division of Human Genetics, Children's Hospital of Philadelphia; Department of Pediatrics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.Brain Behavior Laboratory, Department of Psychiatry, Neuropsychiatry Section, University of Pennsylvania; Department of Radiology, Hospital of the University of Pennsylvania. Electronic address: raquel@upenn.edu.

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

25555483

Citation

Schmitt, J Eric, et al. "Aberrant Cortical Morphometry in the 22q11.2 Deletion Syndrome." Biological Psychiatry, vol. 78, no. 2, 2015, pp. 135-43.
Schmitt JE, Vandekar S, Yi J, et al. Aberrant Cortical Morphometry in the 22q11.2 Deletion Syndrome. Biol Psychiatry. 2015;78(2):135-43.
Schmitt, J. E., Vandekar, S., Yi, J., Calkins, M. E., Ruparel, K., Roalf, D. R., ... Gur, R. E. (2015). Aberrant Cortical Morphometry in the 22q11.2 Deletion Syndrome. Biological Psychiatry, 78(2), pp. 135-43. doi:10.1016/j.biopsych.2014.10.025.
Schmitt JE, et al. Aberrant Cortical Morphometry in the 22q11.2 Deletion Syndrome. Biol Psychiatry. 2015 Jul 15;78(2):135-43. PubMed PMID: 25555483.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Aberrant Cortical Morphometry in the 22q11.2 Deletion Syndrome. AU - Schmitt,J Eric, AU - Vandekar,Simon, AU - Yi,James, AU - Calkins,Monica E, AU - Ruparel,Kosha, AU - Roalf,David R, AU - Whinna,Daneen, AU - Souders,Margaret C, AU - Satterwaite,Theodore D, AU - Prabhakaran,Karthik, AU - McDonald-McGinn,Donna M, AU - Zackai,Elaine H, AU - Gur,Ruben C, AU - Emanuel,Beverly S, AU - Gur,Raquel E, Y1 - 2014/11/21/ PY - 2014/03/25/received PY - 2014/10/23/revised PY - 2014/10/24/accepted PY - 2015/1/4/entrez PY - 2015/1/4/pubmed PY - 2016/3/10/medline KW - 22q11 Deletion syndrome KW - Cortical thickness KW - Genetics KW - Gyrification index KW - MRI KW - Psychosis SP - 135 EP - 43 JF - Biological psychiatry JO - Biol. Psychiatry VL - 78 IS - 2 N2 - BACKGROUND: There is increased risk of developing psychosis in 22q11.2 deletion syndrome (22q11DS). Although this condition is associated with morphologic brain abnormalities, simultaneous examination of multiple high-resolution measures of cortical structure has not been performed. METHODS: Fifty-three patients with 22q11DS, 30 with psychotic symptoms, were compared with demographically matched nondeleted youths: 53 typically developing and 53 with psychotic symptoms. High-resolution magnetic resonance imaging measures of cerebral volume, cortical thickness, surface area, and an index of local gyrification were obtained and compared between groups. RESULTS: Patients with 22q11DS demonstrated global increases in cortical thickness associated with reductions in surface area, reduced index of local gyrification, and lower cerebral volumes relative to typically developing controls. Findings were principally in the frontal lobe, superior parietal lobes, and in the paramedian cerebral cortex. Focally decreased thickness was seen in the superior temporal gyrus and posterior cingulate cortex in 22q11DS relative to nondeleted groups. Patterns between nondeleted participants with psychotic symptoms and 22q11DS were similar but with important differences in several regions implicated in schizophrenia. Post hoc analysis suggested that like the 22q11DS group, cortical thickness in nondeleted individuals with psychotic symptoms differed from typically developing controls in the superior frontal gyrus and superior temporal gyrus, regions previously linked to schizophrenia. CONCLUSIONS: Simultaneous examination of multiple measures of cerebral architecture demonstrates that differences in 22q11DS localize to regions of the frontal, superior parietal, superior temporal, and paramidline cerebral cortex. The overlapping patterns between nondeleted participants with psychotic symptoms and 22q11DS suggest partially shared neuroanatomic substrates. SN - 1873-2402 UR - https://www.unboundmedicine.com/medline/citation/25555483/Aberrant_Cortical_Morphometry_in_the_22q11_2_Deletion_Syndrome_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0006-3223(14)00890-7 DB - PRIME DP - Unbound Medicine ER -