Prenatal US and MR imaging findings of lissencephaly: Review of fetal cerebral sulcal development

被引:70
作者
Ghai, Sandeep
Fong, Katherine W.
Toi, Ants
Chitayat, David
Pantazi, Sophia
Blaser, Susan
机构
[1] Mt Sinai Hosp, Dept Med Imaging, Toronto, ON M5G 1X5, Canada
[2] Mt Sinai Hosp, Prenatal Diag & Med Genet Program, Toronto, ON M5G 1X5, Canada
[3] Univ Toronto, Toronto, ON M5G 1X5, Canada
[4] Univ Toronto, Hosp Sick Children, Div Clin & Metab Genet, Toronto, ON M5G 1X8, Canada
[5] Univ Toronto, Hosp Sick Children, Dept Diagnost Imaging, Toronto, ON M5G 1X8, Canada
关键词
D O I
10.1148/rg.262055059
中图分类号
R8 [特种医学]; R445 [影像诊断学];
学科分类号
1002 ; 100207 ; 1009 ;
摘要
The cerebral cortex develops in three overlapping stages: cell proliferation, neuronal migration, and cortical organization. Abnormal neuronal migration may result in lissencephaly, which is characterized by either the absence (agyria) or the paucity (pachygyria) of cerebral convolutions. The two main clinicopathologic types of lissencephaly may be differentiated according to their prenatal imaging features. Other cranial and extracranial abnormalities also may occur in association with lissencephaly. The prognosis is often poor, but prenatal diagnosis allows appropriate counseling and optimization of obstetric management. Familiarity with the normal ultrasonographic (US) and magnetic resonance (MR) imaging appearances of the fetal cerebral cortex at various stages of gestation is essential for the early detection of abnormal sulcal development. The primary fissures and sulci that can be examined with prenatal US and MR imaging include the parieto-occipital fissure, calcarine fissure, cingulate sulcus, convexity sulci, and sylvian fissure and insula. (C) RSNA, 2006.
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收藏
页码:389 / U6
页数:18
相关论文
共 39 条
[1]   Classification system for malformations of cortical development - Update 2001 [J].
Barkovich, AJ ;
Kuzniecky, RI ;
Jackson, GD ;
Guerrini, R ;
Dobyns, WB .
NEUROLOGY, 2001, 57 (12) :2168-2178
[2]   Second-trimester diagnosis of fetal cataract in a fetus with Walker-Warburg syndrome [J].
Beinder, EJ ;
Pfeiffer, RA ;
Bornemann, A ;
Wenkel, H .
FETAL DIAGNOSIS AND THERAPY, 1997, 12 (04) :197-199
[3]   Mutations in the O-mannosyltransferase gene POMT1 give rise to the severe neuronal migration disorder Walker-Warburg syndrome [J].
Beltran-Valero de Bernabé, D ;
Currier, S ;
Steinbrecher, A ;
Celli, J ;
van Beusekom, E ;
van der Zwaag, B ;
Kayserili, H ;
Merlini, L ;
Chitayat, D ;
Dobyns, WB ;
Cormand, B ;
Lehesjoki, AE ;
Cruces, J ;
Voit, T ;
Walsh, CA ;
van Bokhoven, H ;
Brunner, HG .
AMERICAN JOURNAL OF HUMAN GENETICS, 2002, 71 (05) :1033-1043
[4]  
BENACERRAF BR, 1998, ULTRASOUND FETAL SYN, P134
[5]  
Benacerraf BR, 1998, ULTRASOUND FETAL SYN, P130
[6]  
BLAAS HG, PUBLICATION FETUS NE
[7]  
BLASER S, 2003, POCKET RADIOLOGISTS, P57
[8]   Refinement of a 400-kb critical region allows genotypic differentiation between isolated lissencephaly, Miller- Dieker syndrome, and other phenotypes secondary to deletions of 17p13.3 [J].
Cardoso, C ;
Leventer, RJ ;
Ward, HL ;
Toyo-oka, K ;
Chung, J ;
Gross, A ;
Martin, CL ;
Allanson, J ;
Pilz, DT ;
Olney, AH ;
Mutchinick, OM ;
Hirotsune, S ;
Wynshaw-Boris, A ;
Dobyns, WB ;
Ledbetter, DH .
AMERICAN JOURNAL OF HUMAN GENETICS, 2003, 72 (04) :918-930
[9]   GYRAL DEVELOPMENT OF HUMAN-BRAIN [J].
CHI, JG ;
DOOLING, EC ;
GILLES, FH .
ANNALS OF NEUROLOGY, 1977, 1 (01) :86-93
[10]  
des Portes V, 1998, CELL, V92, P51