The Normal and Pathological Fetal Brain - Ultrasonographic Features

The Normal
and Pathological
Fetal Brain
Ultrasonographic
Features
Jean-Philippe Bault
Laurence Loeuillet
123
The Normal and Pathological Fetal Brain
Jean-Philippe Bault • Laurence Loeuillet
The Normal and

Pathological Fetal Brain
Ultrasonographic Features
Jean-Philippe Bault Laurence Loeuillet
Centre d'échographie Ambroise Paré Hôpital Cochin
Les Mureaux Paris
France France
ISBN 978-3-319-19970-2 ISBN 978-3-319-19971-9 (eBook)

DOI 10.1007/978-3-319-19971-9
Library of Congress Control Number: 2015947148
Springer Cham Heidelberg New York Dordrecht London

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Foreword
Nothing could interest me more than this new Atlas of normal and pathological
fetal brain ultrasound images prepared by Jean-Philippe Bault and Laurence
Loeuillet with assistance from Guillaume Benoist. Its high-resolution images pro-
vide not only a “map” of the developing brain but also close-ups of its various
“territories.”
In my younger days as a pediatrician and embryologist, focused on the problems
of developmental anomalies, the fetal brain was terra incognita! Prenatal brain
imaging was in its infancy, and neuropathological examinations were conducted
only rarely, for research purposes only.
With guidance from Claudie Larroche, who was educated in neuropathology at
Harvard, and inspired by her comprehensive knowledge of premature infants, we
endeavored to undertake a systematic analysis of the fetal brain. Thousands of
examinations later, we collated the results of this pioneering work on the dynamics
of brain development and the significance of its malformations – including a special
focus on anatomical pathology-ultrasonic correlations – in what today have become
a number of classic books: The Pathology of the Developing Human Nervous
System, S Duckett (ed) Lea & Febiger, 1994; Textbook of fetal and perinatal pathol-
ogy, Vol. 2, Wigglesworth JS and Singer DB (eds), Blackwell Scientific Publications,
Oxford 1995. Central Nervous System Malformations. Potter’s Pathology of the
Fetus and Infant, Vol 2, Gilbert-Barness E (ed), Mosby, St Louis 1997, 2009.
Because the fetal brain changes over time, its evaluation requires a comprehen-
sive knowledge of brain development, which begins in the middle of the 3rd week
of gestation and continues well after birth. The cerebral hemispheres and the cere-
bellum emerge very rapidly at the end of the 4th week, while their synaptic connec-
tions are slowly forged. The imaging of this origami-like art as practiced by nature
requires patience and pertinence, akin to the special qualities of the great photogra-
pher. The authors have met this challenge with talent! They have captured the
dynamics of brain development every 2 weeks from the 8th to the 34th week of
gestation. Each ultrasound image shown is accompanied by carefully selected
pathology specimens and histology preparations, and this superimposition provides
a clear picture of the architecture of the normal brain and of deformations in its
shape and structure. Generous practical advice is given on how to acquire high-
quality images and avoid pitfalls and, along with the precious guidelines provided,
make this atlas immensely useful for those interested in the developing brain,
v
vi Foreword
particularly trainee sonographers and those who already have some experience and
are seeking to perfect their technique.
In vivo observation of the fetal brain is an ancient dream that has come true! The
increasingly early acquisition of ever more high-resolution images has made ultra-
sonography the tool of choice for the diagnosis of brain anomalies.
After devoting the first part of my life to a gross and microscopic analysis of the
developing brain, I should now switch to evaluating its image, which is far more
elegant.
Férechté Encha-Razavi, MD
President of the Société Française de Foetopathologie, 2005–2009
Unité de Génétique Embryo-Foetale, Necker-Enfants-Malades, Paris
Contents
Part I The Normal Brain
1 Brief Review of Embryology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3

2 Ultrasound Images of the Normal Brain . . . . . . . . . . . . . . . . . . . . . . . . 7
From 8 to 10 GW: Early Morphological Examination . . . . . . . . . . . . . . . . 7
Anatomical Landmarks . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8
From 11 to 13 GW: Early Morphological Examination . . . . . . . . . . . . . . . 9
From 14 to 16 GW: Morphological Examination . . . . . . . . . . . . . . . . . . . . 13
Midline . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 29
3 Detailled Study of Certain Brain Structures . . . . . . . . . . . . . . . . . . . . . 63
Corpus Callosum. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 63
Anatomy of the Corpus Callosum. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 63
Development of the Corpus Callosum . . . . . . . . . . . . . . . . . . . . . . . . . . 64
Ultrasonographic Features of the Corpus Callosum . . . . . . . . . . . . . . . . 65
vii
viii Contents
Lateral Ventricles . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 73
Lateral Ventricles: Biometrics and Images . . . . . . . . . . . . . . . . . . . . . . . 73
Morphology. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 76
Sylvian Fissure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 78
Sylvian Fissure and Study of the Gyration . . . . . . . . . . . . . . . . . . . . . . . 78
Sylvian Fissure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 78
Other Anatomical Landmarks . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 88
Posterior Fossa . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 91
Changes in the Cerebellum Over Time . . . . . . . . . . . . . . . . . . . . . . . . . . 92
Normal Ultrasound Images of the Posterior Fossa . . . . . . . . . . . . . . . . . 97
Cerebral Circulation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 104
Pericallosal Circulation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 105
Arteries of Central Gray Nuclei . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 110
Willis’ Circle . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 111
Venous Circulation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 115
Sutures and Fontanels . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 116
4 Brain Biometrics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 123
Biparietal Diameter (BPD) and Head Circumference (HC) . . . . . . . . . . . . 123
Atrial Diameter . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 125
Cisterna Magna . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 125
Corpus Callosum. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 126
Cerebellum and Brainstem . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 127
Transverse Diameter . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 127
Cerebellar Vermis and Brainstem . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 128
Interorbital Distance . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 130
5 Tips and Traps . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 131
Choosing the Right Route of Approach . . . . . . . . . . . . . . . . . . . . . . . . . . . 131
Use of the Transvaginal Approach . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 132
Moving the Fetus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 133
Use of 3D Ultrasound . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 134
Part II The Pathological Brain
6 First-Trimester Pathologies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 137

Acrania . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 137
Holoprosencephaly . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 141
Opacities in Skull Images . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 145
Brain Anomalies Related to Neural Tube Closure Anomalies . . . . . . . . . . 148
Anomalies of the Posterior Fossa . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 151
7 Second- and Third-Trimester Pathologies . . . . . . . . . . . . . . . . . . . . . . . 153
Skull Contour Anomalies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 153
Acrania . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 153
Opacities in Skull Images . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 154
Other Examples of Skull Deformations Related to Craniosynostosis . . 161
Contents ix
Midline Anomalies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 163

Holoprosencephaly . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 163
Corpus Callosum Anomalies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 167
Ventriculomegaly . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 181
Definitions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 181
Etiologies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 181
Anomalies of the Posterior Fossa . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 195
Anomalies of the Gyration . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 197
Ultrasound Images . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 206
Intracranial Expansive Processes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 223
Brain Tumors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 223
Tuberous Sclerosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 227
Corpus Callosum Lipomas . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 228
Arachnoid Cysts . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 231
Hematomas . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 234
Cysts of the Germinal Zone . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 235
Hemimegalencephaly . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 236
Infectious Pathologies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 237
Cytomegalovirus (CMV) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 237
Toxoplasmosis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 252
Hemorrhagic and Ischemic Pathologies . . . . . . . . . . . . . . . . . . . . . . . . . . . 258
Hemorrhagic Pathologies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 258
Ischemic Pathologies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 262
Vascular Pathologies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 266
Vein of Galen Aneurysms . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 266
Thrombosis of the Dural Sinuses . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 268
Other Vascular Lesions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 269
Biometric Anomalies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 271
Microcephaly . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 271
Major Hydrocephalus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 276
Gyration Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 279
Three Groups: Lissencephaly Type I (LIS I), II (LIS II),
and III (LIS III) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 279
Heterotopia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 283
Polymicrogyria . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 284
Part III Biometric Tables
8 Biometric Tables . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 289

Biparietal Diameter (Snidjers) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 290
Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 301
Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 311
Part I
The Normal Brain
Brief Review of Embryology
1
This brief review aims simply to describe the main steps in the development of the
fetal brain and should allow ultrasonographers to familiarize themselves with the
structures they will see during an early dating or first-trimester ultrasound.
The brain starts to form from the neural tube at the end of the 1st month of
pregnancy. The appearance of folds and vesicles segments the neural tube into the
forebrain or prosencephalon, midbrain or mesencephalon, and hindbrain or
rhombencephalon.
Secondarily (around the 5th week of pregnancy), the prosencephalon itself sub-
divides into the telencephalon and the diencephalon, whereas the rhombencephalon
divides into the metencephalon and the myelencephalon.
The optic stems and cups form from the diencephalon.
The cortex forms from the telencephalon, the cerebellum and the brainstem from
the metencephalon, and the medulla oblongata from the myelencephalon.
The cerebral vesicles later form the ventricular system.
© Springer International Publishing Switzerland 2015 3

J.-P. Bault, L. Loeuillet, The Normal and Pathological Fetal Brain:
Ultrasonographic Features, DOI 10.1007/978-3-319-19971-9_1
4 1 Brief Review of Embryology
Prosencéphale Télencéphale
Diencéphale
Mésencéphale
Mésencéphale
Métencéphale
Rhombencéphale
Myélencéphale
Fig. 1.1 Segmentation of the neural tube
Rhombencéphale
Mésencéphale
Prosencéphale
Fig. 1.2 Bending of the neural tube

1 Brief Review of Embryology 5
Fig. 1.3 (a) Ultrasound images and corresponding 7-week embryo. (b) Anatomic and histological
correlation (7-week embryo)
Fig. 1.4 (a) Ultrasound images and corresponding 9-week embryo. (b) Corresponding fetal
pathology specimens: a 8-week embryo, b 9-week embryo
6 1 Brief Review of Embryology
Fig. 1.5 Cerebral vesicles “inversion mode”
Fig. 1.6 Cerebral vesicles:

Sono AVC (9 gw)
Ultrasound Images of the Normal Brain
2
From 8 to 10 GW: Early Morphological Examination
From 8 to 10 gw
8 gw
9 gw

8 2 Ultrasound Images of the Normal Brain
10 gw
a b c
d e f
Fig. 2.1 Corresponding histology from 8 to 10 gw: (a) 8 gw, (b) 9 gw, (c) 9 gw1/2, (d–f) 10 gw
Anatomical Landmarks
From 8 gw, the falx cerebri is visible (* telencephalic vesicles), and the
rhombencephalic vesicle (°) is easily identifiable.
The cranial contours are visible from 9 gw.
The cerebral aqueduct becomes visible (arrow).
From 11 to 13 GW: Early Morphological Examination 9
From 11 to 13 GW: Early Morphological Examination
11 gw
a b
c d
Fig. 2.2 Corresponding histology at 11 gw. (a–c) Coronal sections, (d) axial section
12 gw
a b
c d
Fig. 2.3 Corresponding histology at 12 gw. (a, b) Coronal sections, (c, d) axial sections
From 11 to 13 GW: Early Morphological Examination 11
13 gw
a b c
Fig. 2.4 Corresponding histology at 13 gw. (a, b) Coronal sections, (c) pathology specimen
Fig. 2.5 Fourth ventricle: histology at 13 gw (coronal sections) V4 intracerebral transluscency,

CN cisterna magna
The fourth ventricle (yellow arrows) is bordered by closure of the edges of the
rhomboencephalic vesicles.
The third ventricle is clearly visible (turquoise arrows).
The upper part of the diencephalon (blue arrow) is visualized between the
choroid plexuses of the lateral ventricles.
From week 12, the cerebral cortex can be visualized, and the orientation of
Bichat’s fissures is clearly visible (dotted arrow). These fissures are oblique
and form an acute angle with a posterior point. No Sylvian fissures are
present (pink arrow).
An intracerebral transluscency is visible in the first trimester (Chaoui et al.
2009; Chaoui and Nicolaides 2010): it corresponds to the fourth ventricle;
we will see later that its disappearance is suggestive of open spina bifida.
From 14 to 16 GW: Morphological Examination 13
From 14 to 16 GW: Morphological Examination
Fig. 2.6 16w: (a) Triplane, (b) Axial TIU, (c) Coronal TIU, (d) Sagittal TIU
Fig. 2.6 (continued)
Fig. 2.7 Corresponding specimens and histology at 15 gw

14 gw
14 gw
14 gw
At 14 gw, the cerebellar vermis (green arrow) can be seen behind the fourth
ventricle (yellow arrows); the cisterna magna (yellow dotted arrow) can be
distinguished behind the cerebellum.
The third ventricle (turquoise arrow) and the upper part of the diencephalon
or roof of the third ventricle (blue arrow) are visible.
16 gw
16 gw
16 gw
a b c d
e f g
Fig. 2.8 Corresponding specimens and histology at 16 gw: brain (a–d), cerebellum (e dorsal view),
(f, g) Sagittal sections
At 14 weeks, the fourth ventricle is clearly visible (yellow arrow).

The third ventricle (turquoise arrow) and the upper part of the diencephalon
or roof of the third ventricle (blue arrow) are visible.
At 16 gw, the anterior part of the corpus callosum may be visible (orange arrow).
Fig. 2.9 18 gw: (a) Triplane, (b) Axial TIU, (c) Coronal TIU, (d) Sagittal TIU
a b
c d e
Fig. 2.10 Brain at 18 gw: (a) ventral view, (b) lateral view, (c) axial section, (d) sagittal section,
(e) coronal section
18 gw
Fig. 2.12 Corresponding ultrasound images and fetal pathology specimens at 18 gw

18 gw
20 gw
Fig. 2.13 Fetal pathology specimen at 18 gw
At 18 gw, the corpus callosum (red arrows) is already well developed and is
visible in sagittal and coronal images. The Sylvian fissures (yellow arrows)
are almost invisible.
At 20 gw, the corpus callosum is clearly visible and can be measured for
thickness, length, and echogenicity (red arrows). The large commissures
are recognizable by their upward scalloping and their marked echogenicity
(green arrows). The Sylvian fissures are still discrete (yellow arrows) (see
changes in Sylvian fissures).
20 gw
Fig. 2.14 Fetal pathology specimen at 20 gw: coronal section
20 gw
a b
Fig. 2.15 Crura of fornix at 20 gw: (a) ultrasound images, (b) fetal pathology specimen

a
Fig. 2.17 Fetal pathology specimen: axial section at 21 gw
Fig. 2.18 Fetal pathology specimen: coronal section

Fig. 2.19 Fetal pathology specimen: sagittal section at 22 gw
In its recommendations, the Comité National Technique de l’Echographie (French

National Ultrasonography Technical Committee) recommends visualization of the
following during screening:
• Skull contours
• Lateral ventricles
• Midline
• Cavum of the septum pellucidum
• Posterior fossa and cerebellum
Let us remember that “normal appearance” means that the structure has been
identified and recognized as being normal.
Skull Contours
These should be identified in all three axial, sagittal, and coronal planes and must be
regular and equilibrated. The sutures should be visible, and no areas of deformation
should be apparent.
Lateral Ventricles
In addition to biometrics, the appearance and content of the ventricles must also be
evaluated. Particular attention should be paid to the frontal and temporal horns (see
chapter 3 on lateral ventricles).
Midline
This must be studied in all three planes (Fig. 2.22). It should be noted here that the
transfrontal approach is most useful (Fig. 2.23) (Viñals et al. 2007; Vinals et al.
2008) since in a single sagittal image it provides a view of the corpus callosum,
cerebellar tentorium, and cerebellar vermis.
Figs. 2.20 and 2.21 Skull contours (yellow arrows): sutures
The corpus callosum and visualization of the posterior fossa are studied in sepa-
rate chapters.
For many years, any visualization of a cavity of the septum pellucidum was con-
sidered to testify to the presence of a corpus callosum (a “sentinel” of the corpus
callosum). This is in fact untrue; the axial image should show the “anterior com-
plex” described by Laurent Guibaud (Figs. 2.24 and 2.25): in front of the cavity of
the septum pellucidum should be located the genu of the corpus callosum and the
Fig. 2.22 Triplane of the midline (yellow arrows falx cerebri, turquoise dotted arrow cavum
of the septum pellucidum, yellow dotted arrow third ventricle, dotted pink arrow cisterna
ambiens)
Fig. 2.23 Transfrontal

approach
precallosal fissure, which, with the falx cerebri, produces an image resembling a
“small anchor.” If sonographers are able to recognize this “anterior complex,” they
can reject a false septal cavity (Fig. 2.27).
Figs. 2.24 and 2.25 Anterior complex (red arrow falx cerebri, dotted turquoise arrow precallosal
fissure, pink genu of the corpus callosum, green frontal horns, black cavity of the septum pellu-
cidum, CS cavity of septum pellucidum)
Fig. 2.26 Fetal pathology specimen: anterior complex

Fig. 2.27 False septal cavity

(yellow arrow) in agenesis of
the corpus callosum
Fig. 2.28 Cavum of the septum pellucidum in three planes (*)
Cavum of the Septum Pellucidum

Special attention should be paid to the study of the lateral walls and the content,
which normally is anechoic (Fig. 2.28).
The axial study plane must be precisely chosen: if it is too low, it will show the
crura of the fornix; if too rearward, it will show the cavum vergae, which is the
posterior extension of the cavum of septi pellucidi (Fig. 2.29).
Cavum of the septum pellucidum at 22 and 23 gw: axial and coronal sections
Fig. 2.29 Lef excessively low plane showing the crura of the fornix; righ plane excessively rear-
ward plane showing the cavum vergae as the posterior extension of the cavum of septi pellucidi
Posterior Fossa and Cerebellum

These structures will be described in a separate chapter.
The new recommendations for diagnosis published in 2010 by the French
National Ultrasonography Technical Committee include
• Visualization of the choroid plexuses and the third ventricle

• Visualization of at least one Sylvian fissure
• Study of brain parenchyma
• Visualization of the corpus callosum
• Visualization – in the posterior fossa – of the cerebral vermis, cerebral hemi-
spheres, and cisterna magna
Studies of the Sylvian fissure, corpus callosum, and posterior fossa will be
described in specific chapters.
• Choroid plexuses, third ventricle:
The plexuses should be visualized in three planes, and particularly their posterior
region (glomus) in the axial plane. If the choroid plexus occupies the entirety of the
posterior horn, then ventriculomegaly may be ruled out (Fig. 2.30a).
The third ventricle is visible at 22 gw as a fine ellipsoid structure on the axial and
coronal images (Fig. 2.30). At 32 gw, it appears to be more rectangular and above
all is visible on the sagittal image with its recesses (Fig. 2.30c, d).
Brain parenchyma should be homogeneous and free from hyper- or hypoechoic
foci. Echogenic trabecula are visible on the coronal image as extensions of the fron-
tal horns toward the parenchymal periphery, corresponding to the paths of neuronal
migration (Fig. 2.32)
The area of central gray nuclei requires particularly attentive study: infectious
diseases may generate hyperechoic foci in this area or linear calcifications along
thalamic vessels. A sagittal section can be used to visualize the head of the caudate
nucleus, the lentiform nucleus, and the thalami (Fig. 2.34).
An attentive study, particularly using high-frequency transducers (vaginal probe
if cephalic presentation), should be used to visualize fine structures such as the
cerebral aqueduct (Fig. 2.36).
Let us remember that in the second trimester, and if in particular no screen for
chromosomal anomalies has previously been conducted, it is possible to measure
neck soft tissues using the technique described by B. Benacerraf (Shipp, 202).
These measurements were initially made at 18 gw, and an overview of published
studies by K. Nicolaides (2003) gave a likelihood ratio (LHR) of +9.8 for the risk of
aneuploidy. These measurements should be made on a cavum septum pellucidum-
cerebellar section as illustrated in Fig. 2.37.
Fig. 2.30 (a) Choroid plexus (*) occupying the whole posterior horn of the lateral ventricle.
(b) Third ventricle at 22 gw (green arrows). (c) Third ventricle at 32 gw: upper axial images, lower
left sagittal image, lower right coronal image (green arrows). (d) Third ventricle at 32 gw sagittal
image (yellow arrow supraoptic recess, turquoise arrow pineal recess)

Fig. 2.31 Fetal pathology

specimen: choroid plexuses
Fig. 2.32 Brain parenchyma (white and black arrows echogenic trabecula)

specimen
Fig. 2.34 Central gray

nuclei: full arrow head of the
caudate nucleus, dotted arrow
lentiform nucleus, (*)
thalamus
Fig. 2.35 Histology at

21 gw
Fig. 2.36 Cerebral aqueduct (white arrows)

Fig. 2.37 Measurement of

soft tissues (1)

Fig. 2.39 Macroscopic appearance at 24 gw

Fig. 2.41 Fetal pathology specimens: coronal sections at 26 gw
Fig. 2.42 Sylvian fissure operculization (dotted green arrows)

Fig. 2.43 Sylvian fissure operculization (dotted green arrows). The intraparenchymatous trabec-
ula (white arrow) are more clearly visible. Coronal images can be used to visualize the temporal
lobes (dotted white arrows) that are often overlooked during this examination and the central gray
nuclei (blue arrows)
Fig. 2.44 Coronal images can be used to visualize the temporal lobes (dotted white arrows) that
are often overlooked during this examination and the choroid plexus of the third ventricle located
at its roof (black arrow)
Fig. 2.45 Fetal pathology specimens at 26 gw
Fig. 2.46 The third ventricle is clearly visible (yellow arrows), as is its choroid plexus located at
the roof of the third ventricle
Sylvian fissure operculization (Figs. 2.42 and 2.43).

Intraparenchymatous trabecula (Fig. 2.43) are more clearly visible.
Coronal images (Figs. 2.43 and 2.44) can be used to visualize the temporal
lobes (dotted white arrows) that are often overlooked during this examina-
tion and the central gray nuclei (blue arrows).
The third ventricle is clearly visible (Fig. 2.46), as is its choroid plexus located
at the roof of the third ventricle (Fig. 2.44).

specimens at 28 gw

Fig. 2.50 Fetal pathology specimens at 30 gw

Fig. 2.51 Developmen of the
gyration: the superior frontal
sulcus (pink arrow) and the
cingulate sulcus (yellow
arrow) are visible. The
fissure is operculized (dotted
green arrow). (*) cavity of
septum pellucidum, (°)
frontal horns of lateral
ventricles

specimen
Fig. 2.53 Development of

the gyration: the cingulate
sulcus is visible (yellow
arrow) above the cingulate
cortex (*)
Fig. 2.54 The olfactory sulci on the lower side of the frontal lobes are clearly visible in the
coronal image (dotted white arrows)
Fig. 2.55 Olfactory sulci

(dotted white arrow) are
visible in their entirety in the
axial plane.Volumetric
reconstruction in rendering
mode further clarifies their
appearance

specimen
The morphology of the brainstem can be visualized using axial images at different
levels (Fig. 2.57).
Fig. 2.57 Brainstem (°)
Development of the gyration:
• The superior frontal sulcus is visible (Fig. 2.51),

• The cingulate sulcus is visible (Figs. 2.53 and 2.54) with the cingulate
cortex located above it (Fig. 2.53).
• The olfactory sulci on the lower side of the frontal lobes are clearly visible
in the coronal image (Fig. 2.54). The medulla oblongatas are visible in
their entirety in the axial plane. Volumetric reconstruction in rendering
mode further clarifies their appearance (Fig. 2.55).


specimen at 31 gw
Fig. 2.60 Fetal pathology specimen at 32 gw


specimen at 31 gw
34 sa
Fig. 2.62 Sagittal plane


specimen at 31 gw
Fig. 2.64 Interventricular

foramens on the coronal
plane: foramina of Monro
(white arrows) link the lateral
ventricles (°) and the third
ventricle (v3)
Fig. 2.65 Fetal pathology specimens
The third ventricle and its connections may easily be studied at this point:
this ventricle is identifiable in the sagittal image (Fig. 2.62) and in the
coronal image. Its supraoptic recess (green arrow Fig. 2.62) is visible in
its anterior part.
The sagittal image (Fig. 2.62) can also be used to visualize the cerebral aque-
duct that links the third and fourth ventricles (pink arrows), the corpus
callosum (yellow arrows), the cavum of the septum pellucidum (*), and the
brainstem (+).
Detailled Study of Certain Brain
Structures 3
Corpus Callosum
Anatomy of the Corpus Callosum
The corpus callosum is the main commissure (bundle of neural fibers crossing the
midline and connecting the two cerebral hemispheres). It is made up of four parts,
from front to back: rostrum, genu, body, and splenium.

64 3 Detailled Study of Certain Brain Structures
Development of the Corpus Callosum
The corpus callosum develops from front to back in a rotating movement.

Corpus Callosum 65
Ultrasonographic Features of the Corpus Callosum
16 gw
It is possible to visualize the genu of the corpus callosum from 16 gw (yellow

arrows).
17 gw
Fetal pathology specimen at 18 gw

19 gw
Corpus Callosum 67
21 gw
Fetal pathology specimens at 20–21 gw

23 gw
Fetal pathology specimens at 22, 23, and 24 gw

Corpus Callosum 69
23 gw Omniview
25 gw

27 gw

Corpus Callosum 71
29 gw 30 gw
32 gw
32 gw 34 gw
Ideally, the corpus callosum should be visualized in a sagittal image by conven-

tional 2D or 3D ultrasound.
Volume reconstruction from an axial plane (figure below) provides an indirect
indication as to the presence of the corpus callosum: the echoic formation (yellow
arrows) corresponds to the interface between the septum pellucidum and underlying
tissues and vessels such as the pericallosal artery (Pilu et al. 2006; Malinger et al.
2007, 2009; Plasencia et al. 2007). This interface must not be confused with a
lipoma of the corpus callosum.
The corpus callosum may nevertheless sometimes be visualized as a finely
echoic band located beneath this interface (green arrow).
Coronal images are particularly useful, in particular for detecting indirect signs:
abnormal orientation of the frontal horns (see agenesis of the corpus callosum). The
pathway of the pericallosal artery (which is seen in a sagittal plane) will be dis-
cussed in the section on “Cerebral circulation”.
Lateral Ventricles 73
Lateral Ventricles
Lateral Ventricles: Biometrics and Images
Biometrics
The size of the lateral ventricles should be determined by measuring atrial
diameter.
In order to guarantee the quality and reproducibility of such measurements, the
method employed must be perfectly standardized.
Two proposals have so far been issued concerning the standardization of such
measurements:
• ISUOG’s guidelines (ISUOG 2007)

• Laurent Guibaud’s score (Guibaud 2009)
ISUOG’s guidelines (Fig. 3.1)

Measurements must be made at the glomus of the choroid plexus, perpendicu-
larly to the cavity, with the calipers places “on to on.” This method calls for a few
comments: the axial measurement plane would not appear to be perfectly defined as
the position of the glomus may vary as it is affected by gravity.
Fig. 3.1 Localisation of the calipers according to ISUOG Guidelines
Fig. 3.2 Landmarks for

Laurent Guibaud’s score
Laurent Guibaud’s Score (Fig. 3.2)

This method has the advantage of strictly defining the plane and point at which the
measurement is made. The author also provides a scoring system that can be used
for quality control.
The midline must be placed horizontally with a perfectly symmetrical plane. The
anterior anatomical landmark is the lower part of the septal cavity or, even better,
the point at which the crura of the fornix join together (green square), i.e., very
slightly below the septum. The posterior anatomical landmark is the cisterna
ambiens: triangular formation with a posterior peak located slightly rearward of the
thalami (pink figure). The measurement is made perpendicularly to the walls of the
ventricles at the internal occipital sulcus (white arrow) (Figs. 3.2 and 3.3).
Using 3D ultrasound and splitting into three planes (Fig. 3.4) can best locate the
anterior anatomical landmarks on the anterior part of the crura of the fornix.
Fig. 3.3 Calipers at the

appropriate localisation
Fig. 3.4 Using 3D ultra-

sound and splitting into
3 planes
A score may be established using a model similar to that published by Herman

to assess the quality of nuchal translucency measurements.
Criteria Score Technical requirements
Axial plane only 0–2 Midline perpendicular to the transducer, equivalent
distances from the cranial walls
Appropriate section 0–1 Anterior anatomical landmark: crura of fornix
position Posterior anatomical landmark: cisterna ambiens
Measurement point 0–1 At the internal occipital sulcus
Caliper position 0–2 Measurement made perpendicularly to the walls of the
ventricles
Calipers “on to on”
Image size 0–1 Image of the cranium filling the entire screen with the
contours of the cranium visible
The maximum score possible is 7 (the primary criteria are underlined in red, the
secondary criteria in blue). A score of more than 5 is considered to be acceptable.
It should be noted that these measurements are made only on the ventricles that
are distal to the transducer. It is therefore important to check the appearance of the
anterior horns. If the proximal anterior horn seems to be unusually broad, the atrial
diameter of the ventricle must be measured after changing fetal position either by
spontaneous movements of the fetus, gently moving the fetus, or seeing the patient
again some time later.
Morphology
This diagram illustrates the connections between the cerebral ventricles: the two
lateral ventricles communicate with the third ventricle via the foramina of Monro.
The third ventricle in turn communicates with the fourth ventricle via the cerebral
aqueduct. Finally, the fourth ventricle communicates with the arachnoid spaces via
the median aperture on the midline and via the paired lateral aperture.
Lateral ventricle
CP
CF
V3
Cerebral
aqueduct CT
Fig. 3.5 Diagram of the

ventricular system.
V4
CP posterior horn,
CF frontal horn, CT tempo-
ral horn, V3 third ventricle,
V4 fourth ventricle
Fig. 3.6 Ventricle walls and

content
Ventricular system at 40 gw (V4 °, V3 *)

It is important to assess not only the size of the ventricles but also visualize their
walls while examining for any hyperechoic areas and their contents while examin-
ing for echogenic structures suggestive of clots that could indicate intraventricular
hemorrhage (Fig. 3.6).
Sylvian Fissure
Sylvian Fissure and Study of the Gyration
Development of the cerebral cortex is divided into three phases:
• Proliferation and differentiation of neuronal precursor cells

• Neuronal migration to the surface along migratory tracts to create cerebral lami-
nation up to 20 gw (Fig. 3.7c) (Pugash 2012)
• Rapid development of the superficial layer but without development of the deep
layers, accompanied by synapse creation and apoptosis
Although any study of the gyration is the prerogative of MRI, which, by its tech-
nical aspects, can be used to assess the cerebral cortex in its entirety, the sonogra-
pher may, particularly by studying the Sylvian fissure and some of the main sulci,
provide a useful and informative assessment of the gyration.
Sylvian Fissure
This may be studied in the axial plane, but the coronal plane is more appropriate.
Fig. 3.7 (a) Sylvian fissure in a coronal image at 22 gw, (b) shape of the Sylvian fissure at 27 gw
in parasagittal images (TUI volume mode), (c) cerebral lamination: green arrows, white arrows:
migratory tracts (TUI volume mode)
Sylvian Fissure 79

Fetal pathology specimens at 22 gw
Fig. 3.8 Sylvian fissure at 25

gw axial image
Sylvian Fissure 81
Fig. 3.9 Standardized method for assessing Sylvian fissure operculization in axial plane using the
following anatomical landmarks. (a) cisterna ambiens, (b) third ventricle, (c) lower part of the
cavum at the crura of the fornix

Sylvian fissure operculization may be assessed by calculating a score (Quarello
et al. 2008) that includes the angle formed by the base of the Sylvian fissure and the
anterior edge of the insular lobe and the extent to which this edge is curved. This
measurement should be made in the axial plane from the crura of the fornix at the
front to the cisterna ambiens at the rear (passing through the third ventricle). The
score ranges from 1 to 10. In the example below (Fig. 3.9), the score is 3, corre-
sponding to the 50th percentile at 25 gw.
Scores for various time points are shown below:
The score ranges from 1 to 10 and can be used to describe the degree to which
the cortex is covered by the temporal lobe, with the horizontal line representing the
base of the Sylvian fissure.
Score 0 to 2: the angle between the temporal lobe and the cortex is indicated.
Score 3 to 10: the curve represents the extent to which the temporal lobe is covered
(Score 4: 1/4 covered, Score 6: 1/2 covered, Score 8: 3/4 covered, Score 10: fully
covered).
Sylvian Fissure 83
10
6
SFO score
22 23 24 25 26 27 28 29 30 31 32
Gestational age (weeks)
Reference values for Sylvian fissure operculization between 22 and 32 gw. The
solid line represents the 5th percentile and the dotted line the 95th percentile. Dates
are based on measurements of CRL in the first trimester.
Assessment of fetal Sylvian fissure operculization between 22 and 32 weeks: a
subjective approach. Ultrasound Obstet Gynecol 2008; 32: 44–49.
E. Quarello*, J. Stirnemann*, Y. Ville* and L. Guibaud† *Department of
Obstetrics and Gynecology, Centre Hospitalier Intercommunal de Poissy, Poissy
and †Department of Pediatric Fetal Imaging, Hopital Femme-Mère-Enfant,
Université Claude Bernard Lyon I, Lyon-Bron, France. With permission
b c
Fig. 3.10 (a) Sylvian fissure at 26 gw in coronal and axial images, (b) shape of the Sylvian fissure
in parasagittal images (TUI volume mode), (c) fetal pathology specimens at 26 gw
Sylvian Fissure 85
Fig. 3.11 Sylvian fissure in

a coronal image at 28 gw. At
28 gw, the superior frontal
sulcus is present (pink
arrow), as is the cingulate
sulcus (yellow arrow). The
temporal lobe is causing
partial operculization of the
Sylvian fissure (dotted green
arrow). Asterisk cavity
of septum pellucidum,
Circles frontal horns of
lateral ventricles
Fig. 3.12 Sylvian fissure at

28 gw in an axial image
Fig. 3.13 Sylvian fissure

(arrow) coronal image
at 32 gw

It is also possible to measure the distance between (1) the base of the Sylvian fis-
sure and the midline and (2) the base of the Sylvian fissure and the parietal bone and
measure the depth of the parieto-occipital sulcus. In the example at 28 gw, the mea-
surements correspond to the fifth percentile at that time point (Alonso et al. 2010).
Sylvian Fissure 87
Fig. 3.14 Sylvian fissure

coronal image at 34 gw

Other Anatomical Landmarks
Calcarine Fissure
This runs horizontally on the inner surface of the occipital horn. It is readily visual-
ized in the posterior coronal image and becomes visible from 22 gw but is clearer at
24 gw.
Fig. 3.15 Path of the sulci

on the inner surface of the
occipital horn: blue line
calcarine fissure, red line
internal occipital fissure
Sylvian Fissure 89
Calcarine fissure at 23 gw, posterior coronal image
a b
Fig. 3.16 Calcarine fissure (white arrows): (a) 22 gw, (b) 24 gw
This runs obliquely upward and backward on the inner surface of the occipital
hemisphere. It is most clearly visualized in the axial plane (it should be noted that it
corresponds to the point at which atrial diameter is measured, see section “Lateral
ventricles” on page 73). At 22 gw, it has a foam-like appearance but is far clearer at
24 gw.
Internal occipital sulcus at 22 gw
Fig. 3.17 Internal occipital

sulcus (white arrow):
(a) 22 gw, (b) 24 gw
Posterior Fossa 91
Cingulate Sulcus
This is visible on the inner surface of the frontal part of the hemispheres. It is clearly
visible from 24 gw in a coronal image. Figure 3.11 illustrates its appearance at 28
gw (yellow arrow).
Superior Frontal Sulcus

This is visible at 28 gw in an anterior coronal image, as illustrated in Fig. 3.11 (pink
arrow).
It is therefore possible for a sonographer to assess the gyration in an already
satisfactory manner by studying the different anatomical landmarks described
above.
Fig. 3.18 Temporal sulcus:

white arrow
Temporal Sulcus
This is visible in an axial image from 26 gw.
Posterior Fossa
Located in the lower posterior part of the intracranial cavity, the posterior cranial
fossa is bounded posteriorly and inferiorly by the occipital squama, anteriorly by
the apex of the petrous temporal, and superiorly by the cerebellar tentorium, the
posterior median insertion point of which into the occipital squama is the torcular.
It communicates with the spinal canal through the foramen magna and with the
supratentorial space through the indented anterior part of the cerebellar tentorium.
Anteriorly, it contains the brainstem and posteriorly the cerebellum and the cisterna
magna (posterior cerebellomedullary cistern of CSF) between the brainstem and the
cerebral vermis: superiorly, it contains the cerebral aqueduct and in its median part
the fourth ventricle (V4) with its characteristic rhomboid shape. V4 itself
communicates in its inferior and median part with the arachnoid spaces through the
median aperture and laterally through the lateral aperture (Fig. 3.19).
Fig. 3.19 Diagram of the posterior

fossa (arrow median aperture) 40 gw.
TC brain-stem, V4 fourth ventricle,
VC vermian cerebellum, GC citerna
magna TC V4 VC
GC
40 gw
Changes in the Cerebellum Over Time
It is important for ultrasonographers to be aware that the cerebellum may appear not
to be “closed” in its posterior part until 16 gw and that it is also necessary for the
superior part of Blake’s pouch to undergo normal fenestration in order to disappear
as noted, in principle, during the morphological ultrasound scan at 22 gw.
The appearance of the posterior fossa and formation of the cerebellum up to 14
gw are illustrated and described in the first part of this atlas. The images below
illustrate the development of the posterior fossa and in particular show Blake’s
pouch from 16 to 20 gw. (Zalel 2002)
Posterior Fossa 93
Fig. 3.20 (a) Posterior fossa at 16 gw: the yellow arrows indicate Blake’s pouch. Below corre-
sponding anatomic pathology specimens. (b) Posterior fossa at 18 gw: the yellow arrows indicate
Blake’s pouch. Below corresponding anatomic pathology specimens. (c) Posterior fossa at 20 gw:
the yellow arrows indicate Blake’s pouch. Below corresponding anatomic pathology specimens

Posterior Fossa 95
Fig. 3.21 Fetal pathology specimens at 18 gw. Macroscopic and histological sagittal sections
(upper line). Macroscopic and histological axial sections (lower line)
Fig. 3.22 Fetal pathology specimens at 20 gw. Macroscopic and histological axial sections (upper
line). Macroscopic and histological sagittal sections (lower line)
Posterior Fossa 97
Normal Ultrasound Images of the Posterior Fossa
The posterior cranial fossa should mainly be studied in the axial and sagittal planes.
The most appropriate axial plane is from the cavum to the cerebellum, ideally
passing through the fourth ventricle. This plane provides the best visualization of
the cerebral vermis, which is more echogenic than the hemispheres, which appear
to be clearly outwardly scalloped posteriorly. The fourth ventricle, on the other
hand, is inwardly scalloped posteriorly (Fig. 3.22).
Fig. 3.23 Axial plane of the posterior fossa (* V4, ° vermis). gc citerna magna, vs sylvian fissure,
Sep cavity of septum pellucidum
The anechoic cisterna magna is visible posteriorly. Generally, the cisterna magna
is seen to contain septa that take the form of fine, lateral, anterior-posterior trabecula
corresponding to vestigial remnants of Blake’s pouch (Fig. 3.24) (Robinson and
Goldstein 2007). It is in this plane that the cisterna magna should be measured (see
Chap. 8).
Fig. 3.24 Cisterna magna:

vestigial remnants of Blake’s
pouch (yellow arrows)
It should be noted that it is difficult to visualize the cerebellum in an axial image

due to interpositioning of the petrous pyramids. Appropriate reconstruction of the
cerebral vermis may be achieved by 3D ultrasound with acquisition through the
mastoid fontanel (Figs. 3.25a–c) (Shen et al. 2011). The use of VCI in the C-plane
or “Omniview” mode may provide a precise visualization of the cerebral vermis
(Fig. 3.25d) (Viñals et al. 2005).
Fig. 3.25 (a–c)

Posterior fossa in 3D
ultrasound (d) Right
sinus (yellow arrows) at
the ridge of the
cerebellar tentorium.
(e) Fissures in the
vermis at 26 gw (dotted
white line primary
fissure, dotted yellow
line secondary fissure)
Posterior Fossa 99

A sagittal image can be used to determine
• The position of the cerebellar tentorium and torcular. If difficulties are encoun-
tered when visualizing the cerebellar tentorium, a Doppler ultrasound scan may
be used to visualize the right sinus that proceeds to the ridge of the cerebellar
tentorium (Fig. 3.25d)
• The morphology of the cerebral vermis with a special focus on its inferior part
and the presence of primary and secondary fissures (Fig. 3.25e) which may be
visualized from 22 gw
• The morphology of the brainstem with its reliefs
• The appearance of the fourth ventricle which is triangular in shape with the peak
(fastigium) posteriorly
• The appearance of the cisterna magna
Appearance over time
a b
Fig. 3.26 Cerebellum at 21 gw (a) axial, (b) triplane
Fig. 3.27 Cerebellum at 23 gw (sagittal section)

Posterior Fossa 101
Fig. 3.28 Cerebellum at 25 gw (sagittal section). Red arrow sagittal plane obtained from an axial
aquisition
Fig. 3.29 Cerebellum at 28 gw (a) axial image, (b) sagittal image

Posterior Fossa 103
Fig. 3.30 Cerebellum at 32 gw (a) sagittal image, (b) axial image (a) the brainstem appears to be
made up of two shades, with the anterior part more echogenic (yellow arrow pons, dotted yellow
arrow pontobulbar sulcus), fetal pathology specimens at 31 gw
Cerebral Circulation
The brain is supplied with blood through three main arteries: the two internal carotid
arteries and the basilar artery which arises from the confluence of the vertebral
arteries (see figure below).
Internal carotid arteries
a b
Fig. 3.31 Basilar artery (a), vertebral arteries (b)

Cerebral Circulation 105
Pericallosal Circulation
The pericallosal artery and the callosomarginal artery arise from the posterior com-
municating part (A2) of the anterior cerebral arteries and run to the upper edge of
the corpus callosum
16 gw
18 gw
23 gw
27 gw
29 gw
32 gw
Basilar artery, vein of Galen, callosomarginal artery

25 gw
Green arrow basilar artery, Yellow arrow vein of Galen, Red arrow callosomar-
ginal artery
28 gw
Green arrow basilar artery

33 gw
Basilar artery coronal image

33 gw
Basilar artery at 33 gw: ventral view

Arteries of Central Gray Nuclei
23 gw
28 gw
Willis’ Circle
a b
Ant. cerebral A.
Ant. communicating A.
middle cerebral A.
Carotid A.
Post communicating A.
Post cerebral A.
Basilar A.
Fig. 3.32 Willis’ Circle (a), correlation at 40 gw (b)
12 gw
22 gw
32 gw
When seeking to detect possible fetal anemia, the site at which peak blood flow
velocity is measured in the middle cerebral artery is crucial.
Measurement of middle cerebral artery peak systolic velocity

Venous Circulation
Main Venous Sinuses

Blood is drained from the central part of the brain through the internal cerebral
veins (white arrows in the figure below), which themselves drain into the vein of
Galen, which is extended by the right sinus. Blood from the peripheral parts of the
brain is drained through the sinuses: the main sinuses (see the figure below) are the
right sinus (green arrows), which drains the vein of Galen (yellow arrow), and the
superior sagittal sinus (white arrow), which runs beneath the superior sagittal suture
and anteriorly beneath the metopic suture. It is readily visualized by Doppler ultra-
sound scan in a strictly sagittal plane.
These right and sagittal sinuses join at the torcular.
Blood drainage then continues through the transverse sinuses, the sigmoid
sinuses, and the internal jugular veins (see figure below).
Internal cerebral veins (white arrows)
a b
Fig. 3.33 Transverse sinuses with the following legend: (a) Transverse sinus (white arrows),
(b) sigmoid sinuses (green arrows)
Sutures and Fontanels
As it is difficult to visualize sutures and fontanels using conventional ultrasound

scans, a tangential scanning technique should be preferred. 3D ultrasound has
proven to be the technique of choice. It may use thin slices with volume contrast
imaging (VCI) (Fig. 3.34) or rendering in “maximum” mode. These techniques
provide a “facial image” (Fig. 3.35).
Fig. 3.34 Anterior fontanel in VCI mode

Sutures and Fontanels 117
Fig. 3.35 Volume acquisition and rendering: “facial image” bony structures, fontanel, and sutures
a b
c d
Fig. 3.36 Fontanels and sutures during the morphological examination: (a) anterior fontanel (yel-
low arrow), superior sagittal suture (blue arrow), posterior fontanel (green arrow). (b) metopic
suture (white arrow). (c) Posterior fontanel (green arrow), lamboid sutures (yellow arrows), mas-
toid fontanels (turquoise arrows). (d) Coronal suture (white arrow), squamous suture (pink arrow),
mastoid fontanel (turquoise arrow)
Fig. 3.37 Fontanels

The images below illustrate the changes undergone by the metopic suture and the
coronal sutures over the course of pregnancy (Figs. 3.38 and 3.39).
13gw 16gw 21gw
22gw 27gw 33gw
Fig. 3.38 Changes in the metopic suture during pregnancy

13gw 19gw
22gw 28gw 32gw
Fig. 3.39 Changes in coronal sutures during pregnancy

It is by no means rare to discover ossicles called wormian bones (Fig. 3.40) in the
sutures or fontanels. Their significance is still unknown, but their discovery should
prompt a very careful examination of cerebral structures and the entire skeleton in
order not to overlook defective osteogenesis.
Fig. 3.40 Wormian bones: left in the superior sagittal suture, right in the posterior fontanel
Brain Biometrics
4
Brain biometrics is a vital part of the examination of the fetal brain. Many parameters
can be measured by examining the brain. In addition to discussing the conventional
measurement of biparietal diameter and head circumference, this chapter will
address the biometrics of atrial diameter, cisterna magna, corpus callosum, brain-
stem, and cerebral vermis. It will also address the measurement of interorbital dis-
tance, anomalies of which may be indicative of fetal brain anomalies.
In order to be reproducible and relevant, biometric measurements require rigor in
terms of the planes and sections used and compliance with certain quality criteria.
A number of tables are provided at the end of this book for purposes of
consultation.
Biparietal Diameter (BPD) and Head Circumference (HC)
Solid quality criteria have been established for the measurement of biparietal diam-
eter and head circumference (Salomon et al. 2006):
• The measurement plane must be symmetrical.

• The plane must pass through the thalami, the cavum of the septum pellucidum,
and the posterior part, and the cerebellum must not be visible.
• The image of the brain must make up more than half the ultrasound image.
• The calipers must be correctly positioned.
Figure 4.1 illustrates these different requirements.

124 4 Brain Biometrics
Fig. 4.1 Quality criteria for

the measurement of BPD
and HC: Green rectangle
cavum of the septum
pellucidum, pink triangle
thalami, red circle cerebel-
lum not visible, yellow line
symmetry, turquoise circle
calipers, BIP biparietal
diameter
Regarding the calipers, their position depends on the methodology used to con-
struct the standard plot off which the measurements are read. For instance, if Collège
Français d’Echographie Foetale (CFEF) standard plots are used, the calipers should
be placed in the middle of the skull’s proximal and distal bones. If the plots used are
those prepared by Snijdjers and Nicolaides (1994), the calipers should be placed at
the external interface of the skull. This remark is, of course, also valid when posi-
tioning the ellipse used to measure head circumference (Fig. 4.2).
Fig. 4.2 Positioning the

ellipse when measuring HC
Cisterna Magna 125
Atrial Diameter
Readers should refer to the Chap. 3 devoted to the lateral ventricles.
Cisterna Magna
An axial plane passing through the cavum of the septum pellucidum and the cere-
bellum is used to measure the cisterna magna. The actual measurement is made on
the midline between the posterior surface of the cerebellar vermis and the internal
surface of the occipital squama (Snijders and Nicolaides 1994; Steiger et al. 1995).
Fig. 4.3 Biometrics of the

cisterna magna
Corpus Callosum
The corpus callosum may be measured for both its length and thickness (Achiron
and Achiron 2001). Its length should be measured in a strict sagittal plane from the
most anterior part of the genu to the most posterior part of the splenium. Its thick-
ness should be measured in a median coronal plane bounded downward by the
cavum of the septum pellucidum, upward by the echogenic line between the two
hemispheres, and laterally by the frontal horns (Fig. 4.4).
Fig. 4.4 Measuring the corpus callosum: left length, right thickness
Its thickness may also be measured at the genu, the truncus, or the splenium in a
sagittal plane (Lerman-Sagie et al. 2009), which may also be used to measure its
length.
Fig. 4.5 Measuring the

thickness of the corpus
callosum (yellow arrows)
Cerebellum and Brainstem 127
Cerebellum and Brainstem
Transverse Diameter
This measurement is made in the same plane as that used to measure the cisterna
magna, from one lateral edge of the cerebellum to the opposite edge (Snijders and
Nicolaides 1994; Vinkesteijn et al. 2000).
Fig. 4.6 Measuring

transverse cerebellar
diameter. 2 measurement
of cisterna magna
Cerebellar Vermis and Brainstem
The following measurements may be made:
• Vermis height (Achiron 2001; Achiron et al. 2004; Mirlesse et al. 2010) in a
parallel plane to that of the brainstem and using a strictly sagittal plane (includ-
ing the corpus callosum, septum pellucidum, fourth ventricle, vermis, and pons)
by a posterior approach at the sagittal suture slightly above the posterior fontanel
(Fig. 4.7).
Fig. 4.7 Height of vermian

Cerebellum and Brainstem 129
• Vermis circumference or surface area (Fig. 4.8) (Malinger et al. 2001): surface
area is 1 ± 0.2 cm2 at 22 gw and 2.8 ± 0.3 cm2 at 32 gw.
Fig. 4.8 Circumference of

vermian
• Anterior diameter of the brainstem in the sagittal plane perpendicular to the mea-
surement of vermis height (Achiron et al. 2004; Mirlesse et al. 2010).
Interorbital Distance
Interorbital distance may be modified by certain brain pathologies; for example,

hypotelorism is often seen in cases of holoprosencephaly.
In France, it is customary to measure the distance from the middle of one orbit to
the middle of the other (Fig. 4.9).
Fig. 4.9 Inter-orbital

diameter (middle to middle)
Tips and Traps

Normal values according to studies by J.M. Levaillant are as follows:
• 22 gw: 25.2 ± 1.3 mm
• 32 gw: 34.8 ± 2.5 mm
It is above all useful to calculate the ratio between IOD value and BPD
value. Normal values for this ratio are as follows:
• 22 gw: 0.47 ± 0.5
• 32 gw: 0.42 ± 0.5
Tips and Traps
5
Choosing the Right Route of Approach
It is important for sonographers to be familiar with the anatomic structures they are
imaging, as this allows them to choose the best route of approach. For instance, as
the skull constitutes a barrier to ultrasounds, the transducer must be positioned in
such a manner that it emits ultrasound through an acoustic window, i.e., a suture or
a fontanel. The figure below gives a few examples of best routes of approach and
indications for their use.
Fig. 5.1 Routes of approach from left to right: lateral approach through the sphenoid fontanel (red
arrow) for axial planes, median sagittal through the anterior fontanel (green arrow) and superior
sagittal suture for the midline, posterolateral approach through the mastoid fontanel (purple arrow)
for the cerebellum

132 5 Tips and Traps
It should be underlined here that serious errors may arise from choosing the
incorrect route of approach as illustrated in the example below, where schizenceph-
aly was unrecognized because of a shadow area made up of the proximal bone.
Fig. 5.2 Acoustic shadow created by the proximal bone and hiding major schizencephaly-type
lesions of the cerebral parenchyma
Use of the Transvaginal Approach
It should be recalled that use of the transvaginal approach may be of precious assis-
tance when the fetus is in cephalic presentation.
Moving the Fetus 133
Moving the Fetus
In a number of cases, it may be advantageous to move the fetus gently in order for
it to be oriented in such a manner that the usual route of approach can be used.
Before pressure With pressure
Fig. 5.3 (a) Gentle pressure allowing the midline to be visualized by a transfrontal approach
(Images Ph. Bouhanna). (b) Moving the transducer allows the sonographer to “unroll cerebral
structures in coronal planes” (Images Ph. Bouhanna)
134 5 Tips and Traps
Use of 3D Ultrasound
As we have seen throughout this book, 3D ultrasound, and particularly multiplane

sections and tomographic ultrasound imaging (TUI), is of precious assistance in
understanding the disposition of cerebral structures in space. In a number of cases,
3D ultrasound can also be used to visualize structures that the fetus’ position would
render impossible to see (example below) (Fig. 5.4). For more details, readers may
refer to the book Pratique de l’échographie volumique en Obstétrique by the same
publisher.
Finally, familiarity with anatomy, patience, pugnacity, and the use of many cross
sections (without forgetting the coronal plane) will allow the sonographer to better
illustrate cerebral structures and progress both with screening and diagnosis.
Midline turned
horizonally
Centering of point at
which the axes cross
Quality of the image

improved: VCI 1 mm Z-axis c-plane
80 % x-rays / 20 % max rotation
Fig. 5.4 Visualization of the corpus callosum in an axial image. Red circle cerebellum, Green
circle rotation point
Part II
The Pathological Brain
First-Trimester Pathologies
6
The Comité National Technique de l’Echographie de Dépistage Prénatal (French

National Committee on Prenatal Ultrasound Screening) indicated in its report pub-
lished in 2005 that the ultrasound scan performed during the first trimester of preg-
nancy must check that the fetus does not present any cranial or midline anomalies.
These recommendations aim to ensure that sonographers check that no acrania or
holoprosencephaly is present. However, this first-trimester ultrasound scan may
also be employed to screen for other anomalies of the cephalic extremity.
Acrania
The appearance of this anomaly will vary depending on the stage at which the fetus
is examined. The brain will vary in appearance in relation to the extent to which
brain tissue has disappeared. These malformations have been grouped together
under the umbrella term “acrania,” and all, as common denominator, feature the
absence of the bony dome of the skull.
It should be noted that amniotic fluid is often echogenic in acrania (Fig. 6.3b).
The discovery of acrania must prompt the sonographer to undertake a careful
examination for amniotic band syndrome (Fig. 6.3c).

138 6 First-Trimester Pathologies
a b
Figs. 6.1 (a, b) Acrania: (a) dome of the skull absent in maximum mode and (b) in sagittal image.
(c) Exencephaly 10 gw + 6 days (3D ultrasound: HD live rendering method)
Acrania 139
Fig. 6.2 (a, b) Acrania: images of exencephaly
Fig. 6.3 (a) Anencephaly: corresponding ultrasound image – pathology specimen. (b) Acrania:
echogenic amniotic fluid. (c) Acrania: amniotic band syndrome (white arrow)

Holoprosencephaly 141
Holoprosencephaly
These midline anomalies share the common feature of showing merged midline
structures. This may be more or less severe and produce a picture of holoproscen-
cephaly ranging from the alobar form, where merger is almost total, to the lobar
form, where only slight merger is seen. The alobar form is that most commonly
detected in the first trimester, but semilobar forms may also be encountered at this
point.
In alobar holoproscencephaly, the cerebral masses are completely merged
(Fig. 6.4a), as are the lateral ventricles, giving the appearance of a single ventricle
(Fig. 6.4b). These cephalic signs are often associated with facial anomalies such as
the absence of nasal structures, marked hypotelorism or cyclopia, and possibly the
presence of a proboscis (Fig. 6.4c).
a b
Fig. 6.4 (a, b) Alobar holoproscencephaly: (a) cerebral masses merged, (b) single ventricle. (c)
Alobar holoproscencephaly at 14 gw: anterior and posterior views of the brain, hypotelorism, and
cleft (trisomy 13), fetal pathology specimens. (d) Proboscis. (e) Alobar holoproscencephaly:
single ventricle (white arrow middle upper picture), cyclopia (white arrow middle picture median
line) with two crystalline lenses, proboscis and absence of nasal structures, median cleft of palate
(white arrow lower left picture). BIP Biparietal diameter

Holoprosencephaly 143
In the semilobar forms, the merger of the cerebral masses and lateral ventricles
is incomplete, affecting only the anterior part of the brain.
Fig. 6.5 (a) Semilobar holoproscencephaly. (b) Semilobar holoproscencephaly at 15 gw, fetal
pathology specimens: merger of the frontal lobes and arrrhinencephaly (a), single ventricular cav-
ity to the front (c, d) separate hemispheres to the rear (b, e)
a b
c d e

Opacities in Skull Images 145
Opacities in Skull Images
Besides these major, conventional anomalies, the first-trimester ultrasound scan may
also show skull anomalies: meningocele or meningoencephalocele (Figs. 6.6a, b),
which are visible in the axial and sagittal planes. But as shown in Fig. 6.6a, special
care is required to visualize meningoencephalocele.
Fig. 6.6 Meningoencephalocele: (a) axial image. (b) TUI in the sagittal plane, (c) fetal pathology
specimens
Discovery of posterior meningocele (Fig. 6.7b) should prompt investigations for

possible kidney anomalies (Fig. 6.7a) and hexadactyly (Fig. 6.7c) suggestive of
Meckel-Gruber syndrome (Ickowicz et al. 2006; Shin et al. 2007; Roszkowski et al.
2009).
Fig. 6.7 Meckel-Gruber syndrome: (a) cystic renal dysplasia. (b) Meningoencephalocele. (c)
Hexadactyly. (d) Fetal pathology specimens: a gross appearance, b gross appearance of kidneys, c
histology of kidneys
Opacities in Skull Images 147
b c

Brain Anomalies Related to Neural Tube Closure Anomalies
Several signs of open spina bifida may be identified during the first-trimester ultra-
sound examination:
• The parallelism of Bichat’s fissures (Fig. 6.8) (Bernard et al. 1997; Buisson et al.
2002) corresponds to the rearward attraction of cerebral structures caused by
leakage of CSF.
Fig. 6.8 Bichat’s fissures: left normal appearance (yellow dotted line), right fissures are parallel
related to open spina bifida (green dotted line)
• Changes in skull shape:
As in the second trimester, the skull may be deformed and the occipital bone may
be concave (Fig. 6.9a) with a flattening of the occipital region causing the usual
“lemon” sign which becomes visualizable toward 14 gw (Fig. 6.9b) (Sebire et al.
1997).
a b
Fig. 6.9 (a) Concave occipital bone. (b) “Lemon” signs. (c) Decreased biparietal diameter
Brain Anomalies Related to Neural Tube Closure Anomalies 149

c
• Shortening of biparietal diameter:
A shortening of biparietal diameter is a very reliable indirect sign of a neural tube

closure anomaly (Bernard et al. 2013).
• Intracranial translucency:
More precisely, R. Chaoui reported that intracranial translucency disappeared in

open spina bifida (Chaoui et al. 2009; Chaoui and Nicolaides 2010). Intracranial
translucency corresponds to the presence of the fourth ventricle in the sagittal image
of the fetal cephalic extremity (Fig. 6.10a).
V4 : Intra cranial
translucency
Nuchal translucency
Cisterna magna
Fig. 6.10 (a) Intracranial translucency: left correspondance between axial plane and sagittal
plane showing the level of intracranial translucency, right comparison between sagittal and axial
images. (b) Absence of intracranial translucency culminating in a broadening of the pons (double
arrow: brain stem). (c) Sacral spina bifida (yellow arrow): sagittal image and surface rendering of
3D ultrasound images
The disappearance of intracranial translucency culminates in a broadening of the

pons (Fig. 6.10b).
Examining for the disappearance of intracranial translucency would appear to be
a significant step forward in screening for open spina bifida in the first trimester
(Chaoui and Nicolaides 2011), particularly given that screening by the assay of
maternal plasma alpha-fetoprotein was abandoned with the generalization of tests
for first-trimester markers in connection with screening for Down syndrome.
But specific training is indispensable if screening using this technique is to be
reliable (Fong et al. 2011; Mangione et al. 2011).
An axial image of the posterior fossa may prove to be an extremely useful sup-
plement by visualizing the fourth ventricle and the posterior edges of the rhomben-
cephalon (Fig. 6.10a).
Obviously, examinations for these indirect signs do not release the sonographer
from the obligation to examine directly the spine and the membranes that cover it,
particularly in the lumbar and sacral regions. This examination of the spinal cord is
best performed using the sagittal approach route with the transducer facing the back
of the fetus (Fig. 6.10c).
Anomalies of the Posterior Fossa 151
Anomalies of the Posterior Fossa
Anomalies such as arachnoid cyst (Fig. 6.11a) or cerebellar agenesis (Fig. 6.11b)
may be discovered in the first trimester.
a b
Fig. 6.11 (a) Arachnoid cyst of the posterior fossa. (b) Cerebellar agenesis
Many anomalies may thus be evidenced in the first trimester of pregnancy. Their
association with chromosomal anomalies, e.g., holoencephaly and trisomy 13, cer-
ebellar agenesis and triploidy, requires recourse to karyotyping.
Second- and Third-Trimester Pathologies
7
Skull Contour Anomalies
Acrania
As we have already seen, acrania is generally diagnosed in the first trimester, but
should no ultrasound examination have been performed in the first trimester, the
sonographer may be faced with the classic image of the “reptilian” face (Fig. 7.1).
Fig. 7.1 Anencephaly

154 7 Second- and Third-Trimester Pathologies
Opacities in Skull Images
Meningocele and Meningoencephalocele

Meningocele yields a poorly echogenic image of the skull (Fig. 7.2).
Fig. 7.2 Meningocele
The meningoencephalocele is made up of meninges and brain tissue that yield

images of mixed echogenic structure. The underlying brain structures are
disorganized.
It should be noted that the size of the meningoencephalocele is not necessarily
related to the extent of the brain lesions (Fig. 7.3a) (Kesrouani 2010).
Fig. 7.3 (a) Meningoencephalocele at 16 gw (triplane image and surface rendering).

(b) Meningoencephalocele: fetal pathology specimens at 20 gw. (c) Small meningoencephalocele
accompanying major hydrocephalus. (d) Meningoencephalocele: fetal pathology specimens.
(e) Meningoencephalocele and cystic dysplasia at 22 gw in connection with Meckel-Gruber syn-
drome. (f) Meckel-Gruber syndrome: fetal pathology specimens: a encephalocele, b hexadactyly,
c cystic renal dysplasia
Skull Contour Anomalies 155
a b c

Obviously, in the same manner as in the first trimester, rigorous investigations

should be conducted to detect associated signs. The discovery of kidney lesions
should in particular be suggestive of Meckel-Gruber syndrome (Fig. 7.3e, f) (Hartge
et al. 2010).
Hemangioma of the Scalp

These vascular malformations appear as opacities, particularly at the level of the
skull. Doppler ultrasound can be used to confirm the vascular nature of the lesion
(Fig. 7.4) (Okaro et al. 1998; Buckmiller et al. 2010).
Fig. 7.4 Hemangioma of the scalp
Skull Contour Anomalies Related to Neural Tube Closure Anomalies

Open spina bifida, and particularly that with myelomeningocele, is accompanied by
cerebral signs: the frontal bones of the skull are deformed by inward scalloping,
giving the classic “lemon” sign reported by K. Nicolaides et al. (1986). This defor-
mation of the frontal bones may be more or less pronounced (Fig. 7.5a, b).
a b
Fig. 7.5 (a, b) Deformation of the cranium related to neural tube closure anomalies. (Yellow
arrows) deformation of frontal bones (convex to interior)
The fact that no cerebral signs are present should not lead the sonographer to rule
out neural tube closure anomalies as these signs are absent in some 10 % of cases,
particularly in cases of closed spina bifida or spina bifida with lipoma (Ghi et al.
2006).
Skull Contour Anomalies Related to Aneuploidy

In a number of cases, chromosomal anomalies are accompanied by particular skull
shapes: bracycephaly in cases of trisomy 21 (Fig. 7.6a) and, “strawberry” sign in
cases of trisomy 18 (Fig. 7.6b), mentioned here simply as a reminder. These cases
of aneuploidy can be detected by careful screening in the first trimester and detailed
morphological examinations conducted early.
a b
Fig. 7.6 (a) Bracycephaly in trisomy 21, (b) “strawberry” sign in trisomy 18
Craniosynostoses
The premature fusion of one or several sutures of the skull results in deformation of
the fetal cranium. A classification of these deformations may be established depend-
ing on the sutures seen to fuse prematurely (Fig. 7.7).
Metopic suture: trigonocephaly
Coronal suture (unilateral): Coronal suture (bilateral):

anterior plagiocephaly brachycephaly
Lamboid suture (unilateral): Sagittal suture: scaphocephaly

posterior plagiocephaly
Fig. 7.7 Classification of cranial deformations in cases of craniosynostosis

Conventional ultrasound provides only a limited visualization of the cranial

sutures and fontanels. 3D ultrasound provides an “in front” view (Fig. 7.8)
(Dikkeboom et al. 2004) of these structures and thereby provides for a more precise
diagnosis.
Fig. 7.8 3D ultrasound with “in front” view technique

The example below shows premature fusion of the sagittal suture at 24 gw causing
scaphocephaly and clearly illustrates the advantages of 3D ultrasound (Fig. 7.9a, b).
Fig. 7.9 (a) Scaphocephaly. (b) (Left) premature fusion of the sagittal suture at 24 gw, (right)
normal appearance at the same term
Other Examples of Skull Deformations Related

to Craniosynostosis
a b
Fig. 7.10 (a) “Cloverleaf” skull (left) caused by fusion of the coronal sutures, (right) images of
the interior of the skull showing imprints of bony “fingers”. (b) “Cloverleaf” skull: a fetal pathol-
ogy specimen, b X-ray image. (c) “Cloverleaf” skull: fetal pathology specimen, (c) bony “fingers”
imprint inside the skull
Fig. 7.11 (a) left, tower skull (fusion of the coronal sutures), right, trigonocephaly (fusion of the
metopic suture). (b) craniosynostosis at 30 gw, fetal pathology specimens: fusion of the coronal
sutures and protrusion of the metopic suture
It should also be noted that craniosynostosis may initially be detected as a com-

pensatory widening of one or several other sutures.
The discovery of such a skull contour anomaly caused by craniosynostosis
should prompt a full examination and in particular genetic testing (Delahaye et al.
2003).
Midline Anomalies 163
Midline Anomalies
Holoprosencephaly
Alobar holoprosencephaly should have been diagnosed in the first trimester.

However, and in particular if no ultrasound scan was performed in the first trimester,
the diagnosis may only be suggested during the second-trimester morphological
examination.
The sonographic signs are of course identical to those described for the first tri-
mester, particularly a single ventricle, hypotelorism or cyclopia, or a proboscis; the
nose may be absent or reduced to a single nostril. 3D ultrasound in maximum mode
may show fusion of the frontal bones.
a b
c d
a b c
Fig. 7.12 (a) Alobar holoprosencephaly in the second trimester, a single ventricle, b single nos-
tril, c proboscis, d fusion of the frontal bone plates. (b) Alobar holoprosencephaly at 22 gw: fetal
pathology specimens, a dorsal vein in situ, b posterior coronal image, c single nostril and premaxil-
lary agenesis
Semilobar holoprosencephaly: the fusion in general involves only the anterior

part of the brain causing less marked fusion of the ventricles than in the alobar form.
The thalami are only partly merged; the posterior part of the midline is present; the
corpus callosum may in part be present (mainly at the level of the splenium)
(Fig. 7.13a, b).
Fig. 7.13 (a) Semilobar holoprosencephaly at 23 gw (the posterior fossa here is abnormal). (b)
Semilobar holoprosencephaly: fetal pathology specimens
Lobar holoprosencephaly (Fig. 7.14) is the most difficult to diagnose: fusion

concerns only a small part of the brain: the corpus callosum is present and often
dysmorphic. A rupture may be seen in the continuity between the frontal horns of
the lateral ventricles. Sometimes, only the frontal lobes are merged. In such cases,
it is particularly interesting to visualize the paths of the anterior cerebral arteries for
if the frontal hemispheres are merged, the cerebral arteries cannot follow their usual
pathways. They pass beneath and in front of the merged frontal lobes and run
beneath the table of the bone, giving the appearance of the “cerebral artery crawling
under the skull” (Fig. 7.15) (Bernard et al. 2002; Blin et al. 2004).
Fig. 7.14 Lobar holoprosencephaly at 23 gw, (a) minimal fusion of the anterior part of the lateral
ventricles, (b) 3D “reverse face” view
Fig. 7.15 “Cerebral artery crawling under the skull” at 22 gw: the green arrows indicate the path
of the anterior cerebral arteries that run beneath the frontal bones. Right control image: normal
path of the cerebral arteries
Finally, it should be noted that it is possible to detect an anomaly of the upper

maxilla such as solitary median maxillary central incisor, which constitutes a mid-
line anomaly (Fig. 7.16) (Johnson et al. 2008).
Fig. 7.16 Right solitary median maxillary central incisor at 24 gw. Left control
Corpus Callosum Anomalies
Agenesis of the Corpus Callosum

This may be complete or partial.
Complete Agenesis
In most cases, the diagnosis is made on the basis of indirect signs:
• In a coronal image: the frontal horns of the lateral ventricles show the character-
istic feature of being indented, giving the characteristic so-called bulls horn”
appearance (Fig. 7.17a, b).
Fig. 7.17 (a) Complete corpus callosum agenesis: indented frontal horns. (b) Complete corpus
callosum agenesis at 35 gw, fetal pathology specimens: frontal horns drawn out to form “bull’s
horns” and cavum septum pellucidum absent
• The axial image shows ventriculomegaly, which is often moderate, but here, the
posterior horns are globular, constituting the “tear drop” sign (Fig. 7.18) (Pilu
et al. 1993).
Fig. 7.18 Complete corpus

callosum agenesis: “tear
drop” configuration of the
posterior horn
• The coronal image shows the characteristic “triple leaf” appearance due to absent
corpus callosum. The cerebral hemispheres are separated; the falx cerebri is vis-
ible between them and extends downward to the third ventricle that shows ascent
(Fig. 7.19) (Pilu et al. 1993).

callosum agenesis: “triple
leaf” (green arrow), absent
corpus callosum (yellow
arrow), V3 in ascent (blue
arrow) (Fig. 7.20a, b)
(Pilu et al. 1993)
Fig. 7.20 (a) Complete

corpus callosum agenesis.
a
Radial folds (third trimester).
(b) Complete corpus
callosum agenesis at 32 gw:
fetal pathology specimens:
radial folds
b
• Cavum septum pellucidum absent and ascent of V3: absent corpus callosum
accompanied by absent cavum septum pellucidum allowing ascent of the V3
(Fig. 7.21a). Triplane 3D ultrasound can be used to clearly visualize this anom-
aly in all three planes (Fig. 7.21b) (Pilu et al. 2006, 2007; Plasencia et al. 2007).
• In the sagittal image, Omniview 3D thin slice technology provides a clear view
of the ascending V3 (Fig. 7.22) (Rizzo et al. 2011).
Fig. 7.21 (a) Anterior part of the ascending V3 (yellow arrow). (b) Complete corpus callosum
agenesis, triplane ultrasound images: ascending V3 and cavum septum pellucidum absent

callosum agenesis: ascending
V3 (green outline)
• In the axial image, the ascent of the V3 may simulate a false cavum septum pel-
lucidum (Fig. 7.23) (see anterior complex in the Chap. 3 on the normal brain).

callosum agenesis: false
cavum septum pellucidum
• In the sagittal image provided by Doppler ultrasound, cerebral vascularization

appears to be disorganized, and in particular, it is impossible to follow the usual
path of the pericallosal artery (Figs. 7.24 and 7.25).
Fig. 7.24 Complete corpus callosum agenesis: abnormal vascularization by TUI

a b
Fig. 7.25 (a) Complete corpus callosum agenesis: abnormal vascularization (glass body mode).
(b) Complete corpus callosum agenesis and abnormal vascularization (fetal pathology specimens),
a at 36 gw, b corpus callosum and normal vascularization at 32 gw
Direct signs are visible on the sagittal image: the structure corresponding to the
corpus callosum cannot be found (Figs. 7.26 and 7.27).
Fig. 7.26 Complete corpus callosum agenesis in fetus A, normal corpus callosum in fetus JB
(Dichorionic-diamniotic twin pregnancy at 22 gw)

callosum agenesis at 32 gw
Partial Agenesis
Given the development of the corpus callosum (see Chap. 3 on the normal corpus
callosum), this generally concerns the most posterior part of the corpus callosum
(Fig. 7.28) (the splenium). But partial agenesis of the anterior part may also be
encountered (Fig. 7.29). Partial agenesis is clearly visible in the strict sagittal image.
Indirect signs are often seen, in particular indenting of the frontal horns and
above all colpocephaly (Volpe et al. 2006).
28 gw
Fig. 7.28 (a) Partial agenesis of the posterior part of the corpus callosum. (b) Agenesis of the
posterior part of the corpus callosum at 34 gw (fetal pathology specimens)
Fig. 7.29 Partial agenesis of

the anterior part of the corpus
callosum. (Yellow arrows)
deformation of frontal bones
(convex to interior)
23 gw
Short, Thick Corpus Callosum

In a number of cases, the corpus callosum may appear to be short and thick (see
Chap. 8 for length and thickness of the corpus callosum) (Fig. 7.30).
Fig. 7.30 (a) Short, thick

corpus callosum. (b) Short,
a
thick corpus callosum at
35 gw (fetal pathology
specimens)
35 gw
b
Should complete or partial agenesis be detected or the corpus callosum have a

dysmorphic appearance, a full examination is required combining tests for genetic
anomalies with a full morphological examination (Volpe et al. 2006; Ghi et al. 2010;
Lerman-Sagie et al. 2009; Fong et al. 2004; Godard et al. 2005), with a special focus
on detecting associated cerebral signs such as those illustrated in the two examples
below (Figs. 7.31 and 7.32).
Fig. 7.31 Short, dysmorphic corpus callosum at 24 gw in connection with Miller-Dieker

lissencephaly
Fig. 7.32 Dysmorphic corpus callosum and facial dysmorphy in trisomy 8
Lipomas of the corpus callosum will be addressed in the section on intracranial

expansive processes.
Anomalies of the Septum Pellucidum

Absence of the cavum septum pellucidum has already been addressed in the section
on corpus callosum agenesis. Here in this section, we will address the question of
septal agenesis.
Septal Agenesis
It is generally in the coronal section passing through the interface between the ante-
rior third and the posterior two-thirds of the brain that this type of anomaly can best
be visualized. It is characterized by nonvisualization of the lateral walls of the
cavum septum pellucidum (Fig. 7.34a, b), giving a “butterfly wings” appearance
caused by fusion with the frontal lobes of the lateral ventricles. The anomaly is also
visible in the axial image. The corpus callosum is normal in appearance (Fig. 7.33).
The diagnosis, with semilobar or lobar holoprosencephaly, is based on
• Image shape: in holoprosencephaly the fusion of the septum with the anterior
horns of the frontal horns appears to be far more extensive in coronal images,
• The path taken by the anterior cerebral arteries, which, in septal agenesis, take
the usual path unlike the “cerebral artery crawling under the skull” appearance in
cases of holoprosencephaly (Fig. 7.15).
Fig. 7.33 Septal agenesis: triplane images illustrating the level of the coronal section (white
double arrow)
Fig. 7.34 (a) Septal agenesis

coronal image: lateral walls a
of the septum absent.
(b) Septal agenesis at 34 gw
(fetal pathology specimens)
Discovery of septal agenesis should prompt further examinations aiming to rule

out septo-optic dysplasia.
Although not constituting formal proof, if maternal estradiol levels are normal
(Lepinard et al. 2005), if the posterior branches of the optic chiasma are normal in
size by 3D ultrasound (Fig. 7.35a) (Bault 2006, 2007; Bault et al. 2011), and if the
olfactory bulbs can be visualized (Fig. 7.35b), this would tend to rule out septo-
optic dysplasia.
Special Features
The septum may on occasion be seen to have a particular appearance: the septum
pellucidum may appear to be enlarged (Fig. 7.36) or echogenic (Fig. 7.37). The
significance of these two signs is unknown, but they should prompt the sonographer
to conduct a very careful examination of cerebral structures (Jou et al. 1998).
Ventriculomegaly 181
a b
Fig. 7.35 (a) measurements of posterior branches of the optic chiasma (1 and 2), (b) olfactive
bulbs
Ventriculomegaly
Definitions
A ventricle is considered to be too wide if atrial diameter throughout pregnancy,

correctly measured (see the Chap. 3 on measurement of ventricles), exceeds 10 mm,
which corresponds to a value above the 97th percentile (this value appears to be
constant from 17 to 35 weeks of gestation) (Salomon et al. 2007).
Ventriculomegaly may be unilateral or bilateral for the lateral ventricles, triven-
tricular if also involving the V3, or quadriventricular if including the V3 and the V4.
Ventriculomegaly is considered to be mild if between 10 and 12 mm, moderate
if between 12 and 15 mm, and severe if greater than 15 mm (Fig. 7.38a, b, c).
Etiologies
The discovery of ventriculomegaly should prompt a full investigation for its

etiology.
In this chapter, we illustrate the main ultrasound signs that can point to the etiol-
ogy of ventriculomegaly.
Fig. 7.36 Large septum pellucidum at 32 gw (median at this time point: 6.42 mm)
Fig. 7.37 Echogenic septum

pellucidum
Chromosomal Anomalies and Ventriculomegaly

Trisomy 21 is the chromosomal aberration with the highest prevalence of ventricu-
lomegaly, even though this prevalence is fairly low (6 cases for 140 cases of trisomy
21) (Albig et al. 2006) (15/529 in a meta-analysis, i.e., an LHR of +9 as published
by Melchiorre et al. in 2009), 3.8 % for Pilu et al. in 1999. The frequency of such
ventriculomegaly, of course, depends on previous screening. Most cases of ven-
triculomegaly are mild (Fig. 7.38b).
a a
b c
Fig. 7.38 (a) Ventriculomegaly types: a mild, b moderate, c severe. (b) Ventriculomegaly in a
fetus with trisomy 21 (low risk in the first trimester, brachycephaly). (1) width of lateral ventricle
Ventriculomegaly Related to an Anomaly of the Cerebral Aqueduct
Ventriculomegaly Due to Aqueduct Stenosis

Generally, the image produced is that of triventricular ventriculomegaly. It may be
detected early, particularly in cases of dominant aqueduct stenosis (Robyr et al.
2005) (Fig. 7.39).
Fig. 7.39 Triventricular ventriculomegaly by stenosis of the cerebral aqueduct at 15 gw

This appearance is characteristic of X-linked hydrocephalus: Bickers-Adams

syndrome where triventricular hydrocephalus is associated with the presence of
clasped thumbs. This hydrocephalus is caused by a mutation of the L1CAM gene.
The discovery of triventricular ventriculomegaly in a male fetus should prompt
an investigation into family history, an ultrasound scan for clasped thumb, and,
depending on the outcome of the genetic consultation, a test for mutation of the
L1CAM gene (Figs. 7.39, 7.40, and 7.41).
• Ventriculomegaly due to atresia of the aqueduct: this form of ventriculomegaly

is related to a total absence of lumen in the aqueduct and in general stems from
lesions acquired through infection or hemorrhage. It may be found in malforma-
tions and may sometimes be biventricular.
16 gw
Fig. 7.40 Ventriculomegaly by mutation of the L1CAM gene in a male fetus: relapse at 16 gw
a b
c
Fig. 7.41 (a) Ventriculomegaly in Bickers-Adams syndrome (28 gw), image shows clasped
thumbs. (b) Bickers-Adams syndrome (fetal pathology specimens): a Triventricular hydrocepha-
lus at 18 gw, b clasped thumbs at 22 gw. (c) Atresia (forking) of the cerebral aqueduct extending to
the third ventricle at 32 gw, marked dilation of the lateral ventricles
Ventriculomegaly in a Setting of Neural Tube Closure Anomalies

The discovery of ventriculomegaly should prompt investigations for other cerebral
signs of neural tube closure anomalies: “lemon” sign by deformation of the frontal
bone, “banana” sign cerebellum, and Arnold-Chiari malformation (Fig. 7.42).
Obviously, special care must be taken when examining the spine for direct signs
(Fig. 7.43) while bearing in mind that approximately 10 % of spina bifida cases do
not show cerebral signs (Fig. 7.44) (Ghi et al. 2006).
a
a
b c
Fig. 7.42 (a) a Ventriculomegaly in spina bifida, b “lemon” signs, c Arnold-Chiari malformation.
(b) Open spina bifida (fetal pathology specimens): a macroscopic features, b ventricular dilation,
c Arnold-Chiari malformation
a b
c c c

Fig. 7.43 (a) Direct signs of spina bifida in the spinal cord. (b) Open spina bifida (fetal pathology
specimens), upper spinal anomalies by X-ray, lower myelomeningocele with ulceration at 26 gw

Fig. 7.44 “Closed” spina bifida devoid of cerebral signs at 26 gw

Ventriculomegaly Accompanied by Other CNS Malformations
Agenesis of the Corpus Callosum

In agenesis of the corpus callosum, ventriculomegaly takes the form of colpoceph-
aly (see section “Midline anomalies”). As indicated previously, investigations
should be made for other indirect and direct signs of agenesis of the corpus callo-
sum (Fig. 7.45).
Fig. 7.45 Ventriculomegaly in a case of complete agenesis of the corpus callosum (frontal horns
scalloped outward)
Ventriculomegaly may also be seen in cases of partial agenesis of the corpus cal-
losum (Fig. 7.46).
22 gw
Fig. 7.46 Severe ventriculomegaly and partial agenesis of the corpus callosum
Agenesis of the Septum Pellucidum

Ventriculomegaly may be associated with absence of the septum pellucidum. Here,
when making the diagnosis, it is essential to differentiate between agenesis of the
septum pellucidum with its risk of septo-optic dysplasia and the various types of
holoproscencephaly (see “Midline anomalies”) (Malinger et al. 2005).
Fig. 7.47 Ventriculomegaly with agenesis of the septum pellucidum
Arachnoid Cysts
Certain very large arachnoid cysts may cause compression of the cerebral aqueduct
and give the appearance of triventricular ventriculomegaly (Fig. 7.48).
Fig. 7.48 Triventricular ventriculomegaly caused by compression by a large arachnoid cyst

A good number of pathologies of the posterior fossa are accompanied by ventricu-

lomegaly (see chapter on pathologies of the posterior fossa).
In particular, we may cite Joubert’s syndrome (Fig. 7.49) and rhombencephalo-
synapsis (Fig. 7.50).
Fig. 7.49 Ventriculomegaly at 17 gw: Joubert’s syndrome (* dilated ventricles, arrows elongated
superior cerebellar peduncles around the abnormally large V4)
Fig. 7.50 (a) Ventriculomegaly with rhombencephalosynapsis. (b) Fetal pathology features of
rhombencephalosynapsis: cerebellum and ventriculomegaly
Anomalies of the Gyration
Gyration disorders such as type II lissencephaly are accompanied by ventriculo-

megaly (see the section “Gyration disorders”).
Fig. 7.51 (a) Ventriculomegaly at 24 gw. Type II lissencephaly: Walker-Warburg syndrome.

(b) Ventriculomegaly and rupture of the septum pellucidum at 24 gw: Walker-Warburg syndrome
(fetal pathology specimen)
Ventriculomegaly in Hemorrhagic or Ischemic-Hemorrhagic

Pathologies
Examination of the ventricular walls and contents may indicate a pathology that is
hemorrhagic or ischemic (often secondary to a hemorrhagic phase).
In cases of hemorrhage, the ventricular walls are echogenic, and the different
echogenic intraventricular structures by their shape and the location of the choroid
plexuses are suggestive of blood clots (Fig. 7.52).
Fig. 7.52 (a) Unilateral hemorrhagic ventriculomegaly at 23 gw (arrows blood clots). (b) Intra-
ventricular, parenchymatous hemorrhage, ventricular dilation at 26 gw (fetal pathology
specimen)
Fig. 7.53 Hemorrhagic ventriculomegaly at 32 gw (arrows blood clots)

Ischemic lesions may be detected in the form of irregular lesions of the ventricu-
lar walls which may appear to be “nibbled” (Fig. 7.54).
27 gw
Fig. 7.54 Ventriculomegaly at 27 gw: Ischemic lesions secondary to hemorrhagic lesions

Infectious Ventriculomegaly
The appearance of the ultrasound images obtained in such cases will be addressed
more in detail in the chapter devoted to infectious pathologies, but we may already
note here that the outcome of infectious ventriculomegaly is very different depend-
ing on the type of pathogen: very rapid increase in toxoplasmosis against a back-
ground of microencephaly for cytomegalovirus (Fig. 7.55).
Fig. 7.55 Infectious ventriculomegaly: left CMV intraventricular septa and echogenic periven-
tricular halo, right toxoplasmosis: calcification showing as occipital “candle wax drippings”
Ventriculomegaly in Cases of Brain Tumors

Such cases are generally asymmetrical and poorly codified. The cerebral paren-
chyma is pushed back or laminated by the tumoral tissue causing a “mass effect”
(see the section “Intracranial expansive processes”) (Fig. 7.56).
Fig. 7.56 (a) Tumoral ventriculomegaly. (b) Embryonic tumor at 36 gw and secondary hydro-
cephalus (fetal pathology specimens)
The discovery of ventriculomegaly should prompt a full investigation that includes

reference ultrasound scan, karyotyping, PCR for CMV and toxoplasmosis, fetal
blood sampling (FBS) for CBC, and study of fetal hemostasis if signs are evident of
hemorrhage, and genetic consultation in particular in cases of nonisolated ventricu-
lomegaly; MRI will be performed mainly for ventriculomegaly exceeding 12 mm.
Ultrasound scans should be repeated every 2–4 weeks to monitor course.
Finally, it is noteworthy that ventriculomegaly generally has a good prognosis
with 88 % of fetuses showing a favorable neurological outcome in the Melchiorre
meta-analysis that studied ten series reported and published in 2009 (Melchiorre
et al. 2009). The magnitude of the initial dilatation, the rate at which it increases,
and the presence of associated signs are all factors that determine postnatal progno-
sis (Beeghly et al. 2010; Gaglioti et al. 2005).

Ever since 2006 and publication of Laurent Guibaud’s algorithm (Guibaud and des
Portes 2006), the approach to anomalies of the posterior fossa has been far more
clearly codified:
1. The retrocerebellar cistern is increased:

• The torcula is raised: Dandy-Walker anomaly
• The torcula is in place: biometrics should be measured (transverse cerebellar
diameter) and cerebral anatomy investigated
– Cerebral anatomy is normal:
• Mega cisterna magna
• Arachnoid cyst
• Cysts in Blake’s pouch
– Cerebral biometrics are reduced (see § 2)
– Cerebral anatomy is abnormal (see § 3)
2. Cerebral biometrics are reduced:
(a) a-anatomy normal:
Focal reduction
Overall reduction concerning the vermis and in certain cases the brainstem
(b) b- cerebral anatomy abnormal: see § 3.
3. Cerebral anatomy abnormal:
Rhombencephalosynapsis
Chiari II anomaly
Agenesis of the vermis
4. Special forms:
Joubert’s syndrome and CHARGE syndrome are more difficult to classify since
the retrocerebellar cisterna is increased, but this in fact is related to an abnormal
small vermis.
The sonographer would be wise to analyze the posterior fossa using the algo-
rithm. The precise location of the torcula may be more easily determined by
measuring brainstem-tentorium (BT) angle as demonstrated in the work per-
formed by the Italian team headed by G. Pilu (Ghi et al. 2011) (Fig. 7.57).
Brainstem-vermis (BV) angle may also be measured.

Published normal values are 30° for BT angle and 10° for BV angle.
Fig. 7.57 Measuring angles

in the posterior fossa at 25
gw: yellow BT angle, green
BV angle
Thus, an open BT angle confirms that the cerebellar tentorium has been raised.
Also, a Doppler ultrasound scan could be used to locate the right sinus and there-
fore the cerebellar tentorium, particularly if large subtentorial arachnoid cysts are
present (Fig. 7.58).
Fig. 7.58 Cerebellar

tentorium (white arrows
right sinus, green arrow
torcula)
Ultrasound Images
Augmented Retrocerebellar Cisterna

• Raised torcula: Dandy-Walker malformation
Multiplane sections here are useful to visualize this anomaly most clearly
(Fig. 7.59) (Paladini and Volpe 2006; Pilu et al. 2006). Measurement of BT angle,
which is very abnormal, will confirm the raising of the torcula (Fig. 7.60).
Agenesis of the vermis may be complete in 25 % of cases and partial in 75 %.
Detection of a Dandy-Walker malformation should prompt karyotyping (Imataka
et al. 2007) and investigations for associated cerebral and extracerebral anomalies
that are common in such cases.
• Torcula in place:
• Cerebral anatomy normal:
• Mega cisterna magna:
The cerebellum shows normal morphology and biometrics. The morphology of the
vermis is normal in the sagittal image except for an increase in the size of the cisterna
magna (see the chapter on cerebral biometrics) (Robinson and Goldstein 2007).
a
Torcula Partial or complete agensis
of the vermis
Cystic dilation of V4
Fig. 7.59 (a) Dandy-Walker malformation at 27 gw, multiplanar view. (b) Dandy-Walker malfor-
mation at 30 gw: macroscopic and histological features
BT angle : 101
BV angle : 63°
Fig. 7.60 Dandy-Walker

malformations, angles
abnormal
32 gw
Fig. 7.61 Mega cisterna magna at 32 gw (measurements and anatomy normal for the cerebellum
and vermis)
Arachnoid Cyst
The cerebellum and vermis show normal biometrics but appear to be pushed back-
ward by an anechoic mass whose walls are generally visible. The cyst is commonly
lateralized and may be large, in which case it may compress the cerebral aqueduct
(see section “Ventriculomegaly”).
Fig. 7.62 (a) Simple arachnoid cyst. (b) Arachnoid cyst of the posterior fossa (fetal pathology
specimens)
Blake’s Pouch Cyst

A delay in the fenestration of Blake’s pouch and doubtless the Luschka foramens
leads to formation of a cyst that may slightly raise the cerebral vermis (Robinson
and Goldstein 2007; Paladini et al. 2012). The cerebellum is normal in size, though
it may appear to be slightly compressed by the mass of the cyst. The sonographer
will be able to visualize the lateral walls of the cyst on the axial image and its upper
wall on the sagittal image, giving the appearance of a “comet’s tail.” It should be
noted that a large cyst may slightly raise the cerebral vermis and the central part of
the cerebellar tentorium without causing any veritable elevation of the torcula.
Fig. 7.63 (a) Blake’s pouch cyst (arrow: upper wall of the cyst: “comet’s tail”). (b) Blake’s pouch
cyst: raised vermis
Fig. 7.64 (a) Blake’s pouch cyst axial image (arrows lateral walls of the cyst). (b) Remnants of
Blake’s pouch at 36 gw (pathology specimens)
Cerebral Biometrics Are Reduced

• Anatomy normal
• Focal reduction
The reduction concerns part of the cerebellum, which otherwise shows a normal
morphology as here where a cerebellar hemisphere is illustrated after an ischemic
lesion (Fig. 7.65).
Fig. 7.65 Focal reduction of the cerebellum: ischemic lesion of a cerebellar hemisphere (arrows)
• Overall reduction
Here, the reduction concerns both the cerebellum and the brainstem (causing
pons-cerebellar hypoplasia), which may be morphologically abnormal as in Walker-
Warburg syndrome (type II lissencephaly): the brainstem is reduced in size and has
an abnormal “Z” shape. The cerebral vermis is reduced in size.
Fig. 7.66 (a) Walker-Warburg syndrome: overall reduction concerning the brainstem (white
arrows) and the vermis (green arrow). (b) Cerebellar hypoplasia at 24 gw in Walker-Warburg
syndrome (type II lissencephaly): lower line, control at the same time point. (c) Overall hypoplasia
of the cerebellum at 30 gw (upper line) – Control at 29 gw (lower line). (d) Olivopontocerebellar
atrophy at 37 gw (fetal pathology specimens)

Cerebellar Anatomy Abnormal
Rhombencephalosynapsis
In this anomaly, the cerebellum appears to be made up of a single lobe without any
interposition of the vermis. The prognosis in this extremely rare anomaly is very
poor (McAuliffe et al. 2008). The disorder is often associated with ventriculomeg-
aly. Its ultrasonographic diagnosis is based on the shape of the cerebellum, which
appears overall to be scalloped rearward (Fig. 7.67), the observation that the gyra-
tion extends without interruption from one lateral side of the cerebellum to the other
(Fig. 7.68), the dysmorphic appearance of V4, and, of course, the absence of the
vermis (Fig. 7.67) (it should be noted that a strictly sagittal image may give the false
impression that the vermis is present (Fig. 7.69)).
Vermis absent
Scalloping of the posterior
edge of the cerebellum
a b c
d e
Fig. 7.67 (a) Rhombencephalosynapsis: typical images of the posterior edge of the cerebellum,
which appears to be scalloped rearward, cerebellum absent. (b) Rhombencephalosynapsis (fetal
pathology specimens): a, b, c: agenesis of the vermis, d fused hemispheres, e fused dentate nuclei
Fig. 7.68 Rhombencephalosynapsis: gyration extending from one lateral side of the cerebellum
to the other
Fig. 7.69 Rhombencephalosynapsis : false impression that the vermis is present
Type II Chiari Anomaly

This is an indirect sign of neural tube closure anomalies and is characterized by a
cerebellum of reduced size with rearward “banana sign” and pressed against the
occipital squama with disappearance of the cisterna magna (Fig. 7.70).
Fig. 7.70 (a) Chiari anomaly Type II: “banana sign”. (b) Arnold-Chiari malformation: Left coro-
nal image of the cerebral hemispheres showing biventricular dilatation and destruction of the sep-
tum pellucidum. Top right axial image of the mesencephalon showing deformation of the peduncles
and reduced-size cerebral aqueduct. Bottom right sagittal image of the brainstem and cerebellum
showing lengthening of the vermis and collapsed V4 by engagement of the cerebellum (Images
F. Razavi)
Cerebellar Agenesis
The cerebellum is entirely absent in cases of complete agenesis (Fig. 7.71).
Fig. 7.71 (a) Complete cerebellar agenesis. (b) Cerebellar agenesis at 19 gw (fetal pathology
specimens). Absent cerebellum (red circle)
Special Forms
Joubert’s Syndrome
The retrocerebellar cisterna appears to be enlarged due to dysgenesis of the vermis.
This causes an elongation of the superior cerebellar peduncles giving the “molar
tooth sign” on the axial image (Fig. 7.72) (Quarello et al. 2009; Pugash et al. 2011).
Also, the kidneys are hyperechoic in half of all cases (Quarello et al. 2009), (Quarello
et al. 2014).
b c
Fig. 7.72 (a) Joubert’s syndrome at 17 gw: left axial image showing “molar tooth sign”, right
sagittal image showing dysgenesis of the vermis. (b) Joubert’s syndrome at 33 gw. (c) Joubert’s
syndrome: fetal pathology specimen with “molar tooth” (Photo: F. Razavi)
CHARGE Syndrome
This malformative syndrome (Coloboma, Heart defects, Atresia of the nasal choa-
nae, Retardation of growth and/or development, Genital anomalies, Ear anomalies)
must be investigated should a cardiac anomaly be detected, and in particular if
tetralogy of Fallot, double outlet ventricle, or an atrioventricular septal defect is
detected. This syndrome may be accompanied by an anomaly of the vermis
(Fig. 7.73) (Guibaud and des Portes 2006).
Fig. 7.73 CHARGE syndrome: anomaly of the vermis (amputation of the inferior part of the
vermis)
In this syndrome, the ultrasound examination should be supplemented with tests

for coloboma of the iris, and a check should be made whether the olfactory bulbs are
present (Bault 2008a, b; Bault and Quarello 2009) (Fig. 7.74).
a b
Fig. 7.74 (a) CHARGE syndrome: a ocular asymmetry, b coloboma (white arrows) (virtual eye-
ground), c no olfactory sulci (green arrows). (b) CHARGE syndrome at 24 gw: arrhinencephaly
and coloboma of the optic papilla (fetal pathology specimens)
Intracranial Expansive Processes 223
Intracranial Expansive Processes
Brain Tumors
Brain tumors are rare (0.5–1.9 % of all pediatric tumors) and in most cases are dis-
covered fortuitously. All types of brain tumors can be detected antenatally, the most
common (62.5 %) being teratomas (Schlembach et al. 1999).
They create a variety of echoic images (solid, heterogeneous, mixed, cystic, etc.).
In the worst cases, no normal cerebral structures can be individualized. Such tumors
are often accompanied by macrocrania or hydrocephalus. Their growth is often very
rapid and may lead to a collapse of the cranial vault. Cases of polyhydramnios are
common and may be responsible for fetal anasarca through anemia and arteriove-
nous shunt. The figures below provide a few examples:
Fig. 7.75 (a) Cerebral teratoma (Images A. Sadji). (b) Teratoma at 23 gw: (fetal pathology speci-
mens): (a, b) prebrainstem tumor and solid and cystic, immature, multitissue temporal extension
(c, d), “yolk sac” component (e)
Intracranial expansive processes
a b
c d e

Fig. 7.76 (a) Cerebral hamartoma. (b) Hypothalamic hamartoma at 23 gw

Fig. 7.77 Cerebral hamartoma: Circle of Willis vessel pushed backward
Fig. 7.78 (a) Craniopharyngioma (Images B. Benoit). (b) Papillomas of the choroid plexuses
(white arrows) (Image Dr Louati Tunis)
Tuberous Sclerosis
The discovery of cardiac rhabdomyomas (Fig. 7.79) should prompt the sonographer
to look for cerebral cortex tubers, which often proves to be very difficult. The use of
high-frequency transvaginal transducers when the fetus is in cephalic presentation
can be of precious assistance (Fig. 7.80).
A family and genetic investigation for mutations of the TSC1 and TSC2 genes is
essential (Barozzino et al. 1998).
Fig. 7.79 Cardiac rhabdomyomas

Fig. 7.80 (a) Cortical tubers in a setting of tuberous sclerosis. (High-frequency transvaginal
transducer). (b) Tuberous sclerosis: cortical tubers at 35 gw, subependymal nodules at 33 gw (fetal
pathology specimens)
Corpus Callosum Lipomas
These lipomas are rare and may be tubulonodular or curvilinear. The tubulonodular
form is easy to diagnose (Fig. 7.81): the fatty lesion appears as hypoechoic on the
ultrasound scan. Diagnosing the curvilinear form is often more difficult (Fig. 7.82).
Associated signs should always be sought with great care, particularly corpus cal-
losum anomalies, which may include complete or partial agenesis. If no major asso-
ciated lesions are found, the neurological outcome may be favorable, but insufficient
cases have been assessed to evaluate this prognosis correctly.
32 gw
33 gw
Fig. 7.81 (a) Corpus callosum lipoma: tubulonodular form. (b) Pericallosal lipomas (tubulonodular
form) at 32 and 33 gw: macroscopic and histological appearance. Lipoma of corpus callosum (black
arrows)
27 gw
25 gw
23 gw
Fig. 7.82 (a) Corpus callosum lipomas, curvilinear form. (b) Pericallosal lipomas (curvilinear form)
at 34 gw: macroscopic and histological appearance. Lipoma of corpus callosum (black arrow)
Arachnoid Cysts
These cysts are rare (1 % of expansive processes in newborns). They may be pri-
mary or secondary to an infection, hemorrhage, or trauma. They may develop at any
location where meninges are present. They are independent of the ventricular sys-
tem. They contain CSF and therefore appear in ultrasonography as anechoic struc-
tures. Their diagnosis is generally suggested in the third trimester and should prompt
investigations for associated lesions. They may be very variable in size, and if large,
the route of delivery should be discussed. This pathology is illustrated by the exam-
ples below.
Fig. 7.83 Arachnoid cysts of the posterior fossa (third trimester)

Fig. 7.84 Temporal arachnoid cyst (24 gw)

Fig. 7.85 Midline arachnoid cysts (22 gw) associated with agenesis of the corpus callosum
Fig. 7.86 Parietal arachnoid cyst (32 gw)
Hematomas
Hematomas are rare and occur in a setting of coagulation disorders, anticoagulant

treatment, or injuries to the mother (Barozzino et al. 1998). Hematomas on the
ultrasound image appear as a finely echogenic collection beneath the cranium. They
do not give a signal on a Doppler ultrasound scan (Fig. 7.87).
Fig. 7.87 Subdural hematoma (mother treated with an anticoagulant)

Cysts of the Germinal Zone
These cysts can be found in 5 % of newborns. They arise from persisting germinal
matrix and are located on the edge of caudate nuclei or in the caudothalamic groove.
Their ultrasound appearance is that of an array of mostly bilateral, oblong,
anechoic structures (Fig. 7.88) that are generally discovered in the third trimester.
If isolated, the prognosis is excellent, and they regress spontaneously in a few
months after birth. By contrast, if associated with cerebral or extracerebral anoma-
lies in a setting of infectious, vascular, or chromosomal pathologies, the prognosis
is poor (Bats et al. 2002).
Fig. 7.88 Cysts of the germinal zone (32 gw)

Hemimegalencephaly
Hemimegalencephaly corresponds to a rare malformation of the cerebral cortex that

culminates in excessive enlargement of one of the cerebral hemispheres which thus
overlaps the midline (Fig. 7.89). Such anomalies may be isolated or associated with
neurological and skin conditions such as hypomelanosis of Ito, Proteus syndrome,
or Klippel-Weber-Trenaunay syndrome (Tinkle et al. 2005; Boer et al. 2007).
Fig. 7.89 Hemimegalencephaly: coronal and axial images: excessive development of one hemi-
sphere overlapping the midline (white arrows)
Infectious Pathologies 237
Infectious Pathologies
Cytomegalovirus (CMV)
General Aspects
Virology: Cytomegalovirus (CMV) is a member of the Herpesviridae group and there-
fore shares certain characteristics with other members of this group. For instance,
primary infection is followed by a latent infection harbored in various organs with
possible endogenous reactivations. Reinfections are also possible. All recurrences and
reinfections are called “secondary infections.” Pregnant women and patients who
have received a graft are more at risk of developing complications linked to this virus.
Epidemiology
• Target population: CMV infection outside pregnancy in immunocompetent
patients is benign. It is serious in immunocompromised patients or in kidney
transplant recipients.
• Seroprevalence in pregnant women: 50 % of women seropositive.
• Incidence of primary infection during pregnancy: 3 %.
Diagnosing Maternal Infection

• Clinical diagnosis: maternal infection is asymptomatic in 90 % of cases. Aspecific
infectious syndrome in other cases.
• Laboratory diagnosis: evidence of seroconversion (appearance of IgG).
• If difficulties are encountered in establishing the date of the primary infection in
the mother, a measurement of IgG avidity may be conducted (low avidity corre-
sponds to a recent infection). In addition, all previous sera must also be tested.
Maternal-fetal transmission: 30–50 %. Variations in vertical transmission rates

related to time point in the pregnancy are controversial.
Fetal involvement: This may be asymptomatic or symptomatic (signs present on
the ultrasound scan). These signs may be cerebral or extracerebral. Signs are noted
on the ultrasound in approximately 50 % of cases.
Antenatal diagnosis: This is possible by testing for the virus (by culturing) and/or the
viral genome (by PCR) in amniotic fluid removed by amniocentesis at least 6 weeks
after the presumed seroconversion date and after 20 gw (fetal diuresis established).
Prognostic factors: The prognosis depends mainly on the presence of anomalies
on the cerebral ultrasound scan, yet the individual weight of each sign taken indi-
vidually is unclear. In this matter, additional MRI of the fetal brain has an important
role to play (Picone et al. 2008). Fetal blood sampling is of prognostic value to
determine fetal platelets (the presence of fetal thrombocytopenia is an independent
prognostic factor), as is the assay of beta-2 microglobulin (an increase correlates
with an unfavorable prognosis) (Benoist et al. 2008; Fabbri et al. 2011).
Treatment of the fetal infection: no approved treatment available. Two therapeu-
tic “avenues”: high-dose valaciclovir (Jacquemard et al. 2007) and specific immu-
noglobulins (Nigro et al. 2005).
Cerebral Ultrasound Signs of Cytomegalovirus Infection
Microcephaly
Microcephaly in CMV infection is caused by microencephaly. Pericerebral spaces are
large, and development of the cerebral cortex is often retarded. This is a most impor-
tant prognostic sign for mental retardation and motor development (Malinger 2011).
Fig. 7.90 (a) Microcephaly at 26 gw: coronal image of the fetal brain showing enlarged pericere-
bral spaces and retarded development of the cerebral cortex. (b) CMV-related fetal pathology: fetal
pathology specimens: microcrania and microencephaly at 36 gw (brain biometrics corresponding
to 29 gw, cerebellar biometrics corresponding to 35 gw)
Ventriculomegaly
Ventriculomegaly is one of the most commonly observed of all cerebral signs seen
in CMV-infected fetuses. In cases where the fetal brain does not show massive
destruction, the ventriculomegaly is most often moderate. The ventricles in such
cases are 10 mm larger than normal at the atrium, but it is more the appearance of
the walls, the presence of synechiae, and the echogenicity of the periventricular
parenchyma that point to this infectious etiology.
Fig. 7.91 (a) Moderate ventriculomegaly at 27 gw: posterior coronal image showing hyperechoic
ventricle walls. (b) Ventriculomegaly at 36 gw, median and posterior coronal sections (pathology
specimens)
Periventricular Hyperechogenicity or “Periventricular Halo”

(Picone et al. 2010; Simonazzi et al. 2010)
Periventricular halo is in most cases an early sign in the natural history of
CMV-related brain damage and is generally seen around 20 gw. A transvaginal
examination is most often required to detect this sign. Histological examination
shows similar lesions to those observed with periventricular leukomalacia. The dis-
order may progress to cavitation (pseudocyst appearance).
Fig. 7.92 Periventricular halo hyperechogenicity of the occipital horns at 23 gw: Volume acquisi-
tion in the sagittal and parasagittal planes of the fetal brain with TUI. Buildup of an occipital
pseudocyst
Fig. 7.93 (a) Periventricular

halo hyperechogenicity of the a
occipital horns at 23 gw:
parasagittal image of the fetal
brain. (b) Periventricular
necrosis at 28 gw, occipital
horns, several developmental
stages: “periventricular halo”
(upper left), cavitary necrosis
(upper right and lower left),
extensive necrosis (lower
right)
Periventricular Pseudocysts
These generally develop in the occipital region and are in most cases surrounded by
a hyperechoic wall contiguous with the periventricular halo described above. They
arise from necrosis of the germinal matrix.
Fig. 7.94 Bilateral occipital

cysts (red arrows) of the
occipital horns, moderate
ventriculomegaly at 24 gw:
axial image
Fig. 7.95 (a) Cyst of the

occipital horn, moderate a
ventriculomegaly at 24 gw:
parasagittal image.
(b) Occipital cyst and
periventricular necrotic
lesions at 36 gw
b
Intraventricular Synechiae
Intraventricular synechiae give the appearance of septa between the ventricles. They
are often multiple and may be visible at any location within the lateral ventricles.
Fig. 7.96 Intraventricular

synechiae, moderate
ventriculomegaly: axial
image
Fig. 7.97 (a) Intraventricular

synechiae, moderate a
ventriculomegaly: parasagit-
tal image of the fetal brain.
(b) Intraventricular synechia
(black arrow) in a pathology
specimen at 36 gw
Calcifications
Calcifications are commonly encountered in infections and are not specific to CMV
infection (toxoplasmosis, HSV, etc.). They are generally punctiform, small, and dis-
seminated and do not cause any echogenicity. Calcifications may be found at any
location in the cerebral parenchyma, though they are most often seen in the periven-
tricular region.
Fig. 7.98 Calcifications:

pseudocoronal image
Fig. 7.99 (a) Calcifications (black arrows): coronal image. (b) Periventricular and parenchyma-
tous calcifications (black arrows) at 27 gw
“Candelabra” Images
These “classic” images are not specific to CMV infection. They correspond to
striated lenticular vasculopathy.
Fig. 7.100 (a) “Candelabra”

feature: coronal image. a
(b) Striated lenticular
vasculopathy at 37 gw
b
Fig. 7.101 “Candelabra”

feature: parasagittal image
Secondary Rupture of the Septum Pellucidum

One or two lateral walls of the cavum of the septum pellucidum may be ruptured
secondary to ventriculomegaly.
Fig. 7.102 Rupture of a wall

in the cavum and thalamic
calcification: coronal image
Fig. 7.103 Rupture of a wall

in the cavum. Bilateral
thalamic calcifications
Enlargement of the pericerebral spaces: coronal image.

Anomalies of Cortical Development

Retarded closure of the sylvian fissure may be seen, or the cortical sulci may fail to
appear. This may be associated with microencephaly and enlargement of the perice-
rebral spaces.
Fig. 7.104 (a) Enlargement of pericerebral spaces, retarded sylvian fissure (red arrow),
hyperechoic irregularity of the ventricular walls at 26 gw: axial image. (b) Microencephaly
(biometrics <5th centile) and micropolygyria at 27 gw
Anomalies of the Corpus Callosum

Fig. 7.105 (a) Destructive
lesion of the anterior portion a
of the corpus callosum:
sagittal image. (b)
Destructive lesions at 24 gw
b
Anomalies of the Cerebellum

The cerebellum may be the site of ischemic-hemorrhagic occurrences causing
destructive lesions of the vermis of asymmetry of the cerebellar hemispheres.
Fig. 7.106 (a) Enlargement of the posterior fossa (left red arrow), hyperechogenicity of part of
the posterior fossa. Fragmentary lesion of the vermis and asymmetry of the cerebellar hemispheres
(right red arrow): axial image (left red arrow: increased cisterna magna, right red arrow: atrophy
of the cerbellum vermian). (b) Asymmetric cerebellar hemispheres at 36 gw: hypotrophy of the
right hemisphere
Toxoplasmosis
General Aspects of Toxoplasma Gondii (TG) Infection During

Pregnancy
• Epidemiology: Seroprevalence in women of childbearing age: 54.3 %. This
increases with age and fluctuates according to geographic area (eating habits,
lifestyle, climate). Seroprevalence in pregnant women, incidence of seroconver-
sions: 0.5–1.5 %/100 seronegative women, 50–60 % of women of childbearing
age are seropositive.
• Maternal infection:
• Clinical infection: 80–90 % of forms are asymptomatic. Ten to twenty percent of
symptoms are unspecific (cervical or occipital polyadenopathy, asthenia, head-
aches, mild fever) and often resolve spontaneously. In these cases, a laboratory
diagnosis is essential (serology tests).
• Laboratory diagnosis: In France, serology tests have been mandatory since
1978. If IgGs are detected prior to pregnancy, no serological follow-up is nec-
essary as the patient is immune. If the patient is seronegative (IgG-), monthly
serology tests must be conducted up to delivery and for 3–4 weeks
thereafter.
• Diagnosis of maternal infection when seroconversion is detected: if specific IgG
anti-TG antibodies appear between two samples taken 3 weeks apart, the date of
the maternal infection can be determined by measuring IgM, IgA, IgG avidity
and performing the differential agglutination test.
• Mother-to-fetus transmission: This occurs consecutive to parasitemia. The infec-
tion is first placental, then fetal. Transmission is extremely rare during the peri-
conception period. Vertical transmission increases with time into pregnancy: 6 %
at 13 gw, 40 % at 40 gw, 72 % at 36 gw.
• Fetal damage: The risks for the fetus due to TG infection decrease with time into
pregnancy. Thus, clinical signs in children less than 3 years old in cases of con-
firmed vertical transmission manifest in 61 % of cases with maternal infection at
13 gw, 25 % at 26 gw, and 9 % at 36 gw.
• Antenatal diagnosis: Diagnosis is possible by analyzing amniotic fluid taken by
amniocentesis. The sample must be drawn after 18 gw and at least 4 weeks after
the presumed date of the maternal primary infection. PCR is used to detect the
parasite genome in the amniotic fluid. If fetal infection is confirmed, ultrasound
monitoring should be started to detect cerebral and extracerebral signs, which
may consist of increased thickness of the placenta associated or not with calcifi-
cations, liver calcification and/or hepatomegaly, ascites or pericardial or pleural
effusion, hyperechoic intestine, or intrauterine growth retardation
• Prognostic factors
• Time into pregnancy of the maternal primary infection (and on which depends
the risk of vertical transmission and the extent of fetal damage)
• Presence of signs on the ultrasound scan
• Parasite burden in the amniotic fluid by real-time PCR (for maternal infections
occurring before 20 gw)
• Treatment:
• In cases of maternal seroconversion: Spiramycin 3MIU three times daily. This
treatment should be continued up to delivery if tests for the parasite genome
continue to be negative in the amniotic fluid. Otherwise, the treatment should be
switched as described below.
• In cases of fetal infection: Pyrimethamine 50 mg/day, sulfadiazine 1.5 g twice
daily, folic acid 50 mg per week. This treatment should be continued up to deliv-
ery. It is contraindicated in cases of G6PG deficiency.
• Therapeutic aims are to prevent vertical transmission in cases of maternal sero-
conversion and reduce symptomatology in cases of documented fetal infection.
However, the exact methods by which these treatments are administered vary
between countries, and currently, a French clinical research hospital program
called TOXOGEST is undertaking to evaluate the efficacy of spiramycin com-
pared with the pyrimethamine-sulfonamide combination on the vertical trans-
mission of the parasite in cases of maternal infection. Finally, a meta-analysis of
SYROCOT study group raw data highlighted weaknesses in theoretical basis for
the administration of these treatments.
Cerebral Ultrasound Signs of Toxoplasma Gondii Infection

Ultrasound monitoring must take place monthly in cases of maternal seroconversion
and every 2 weeks in cases of fetal infection documented by positive parasite detec-
tion in the amniotic fluid.
Extracerebral lesions may be present: intra-abdominal hyperechoic areas, thick-
ening of the placenta, serous effusion, hyperechoic areas in the liver,
hepatomegaly.
Investigations for brain lesions should be a priority. These lesions, in cases of
documented fetal infection, are more common if the maternal infection occurred
during the first half of pregnancy. They are also the most serious.
Lesions Most Often Encountered
Ventricular Dilatation
Such dilatation is generally bilateral and symmetric. It begins in the occipital horns
and customarily progresses rapidly. Its onset may, however, be retarded (hence the
necessity to continue frequent ultrasound monitoring).
Such dilatation is generally visualized in the third trimester of pregnancy con-
secutive to maternal infection before 22 gw in most cases. The outcome may be
cerebral atrophy with microcephaly (far more rarely).
The onset of ventriculomegaly detected during monitoring of a fetal toxoplasma
gondii infection is associated with a poor prognosis.
Fig. 7.107 Ventriculomegaly

(toxoplasma infection): axial
image
Fig. 7.108 Ventriculomegaly

(toxoplasma infection):
coronal image
Fig. 7.109 (a) Ventriculomegaly (toxoplasma infection): parasagittal image. (b) Toxoplasma
infection: ventriculomegaly at 28 gw, periventricular necrosis and calcifications
Cerebral Hyperechoic Areas

These correspond to necrotic foci. They may show little calcification when the ultra-
sound examination is carried out and are therefore difficult to visualize. They are
more clearly evident in postnatal transfontanel ultrasonography using high-
frequency (7.5 MHz) transducers or by CT scan. These foci may be
Periventricular
Hyperechoic, punctiform, generally rounded structures with no shadow cones
are in most cases visible around the ventricles.
Fig. 7.110 Periventricular calcifications (toxoplasmosis): axial image (corresponding pathology

specimen and ultrasound image) (red arrows: small calcifications)
Fig. 7.111 Periventricular

calcifications (toxoplasmo-
sis): coronal image (red
arrows: small calcifications)
Intraparenchymatous
Hyperechoic, punctiform, generally rounded structures resembling “candle wax
drippings” with no shadow cones may also be visualized within the cerebral
parenchyma.
Fig. 7.112 (a) Intraparenchymatous calcifications (red arrows: small calcifications) (toxoplasmosis).
(b) Intraparenchymatous calcifications (black arrows) (toxoplasmosis), fetal pathology specimens
Hemorrhagic and Ischemic Pathologies
Hemorrhagic Pathologies
Hemorrhagic pathologies are graded using the classification system employed for
newborns:
Grade 1: hemorrhage restricted to the subependymal area.

Grade 2: hemorrhage extends to the ventricle but ventricle filled to no more than
50 % and does not exceed 15 mm atrial diameter.
Grade 3: intraventricular hemorrhage fills more than 50 % of the ventricle(s) with
ventriculomegaly.
Grade 4: Grades 1, 2, or 3 hemorrhage with intraparenchymatous hemorrhage.
The incidence of these hemorrhagic processes is difficult to estimate (1/10,000

for Ghi et al. (2003), but probably far higher) as the condition may be unrecognized
and identified as a case of isolated, moderate ventriculomegaly.
The neurological prognosis would appear to be dependent upon hemorrhagic
grade, but advising parents is still difficult in all cases (Ghi et al. 2003; Elchalal
et al. 2005).
Ultrasound Images
Grade 1: the hemorrhage appears as a fine echoic area in the subependymal area
(Fig. 7.113).
Grade 2: the walls of the ventricles are thickened by an echogenic margin; small
clots may be visible in the form of irregular echogenic formations separate from
the choroid plexuses; the ventricle shows little or no dilatation (Fig. 7.114).
Grade 3: the ventricles are highly dilated; their walls are echogenic; large clots may
be visualized within the enlarged ventricles (Fig. 7.115).
Grade 4: the intraparenchymatous hemorrhage manifests as a large, echoic, intrapa-
renchymatous formation with poorly defined edges (Fig. 7.116).
A few examples of antenatal cerebral hemorrhages are shown below.
Hemorrhagic and Ischemic Pathologies 259
Fig. 7.113 Subependymal cerebral hemorrhage (Grade 1)

Fig. 7.114 (a) Cerebral hemorrhage with restricted, unilateral intraventricular component: Grade
2 (arrow clot). (b) Subepidymal and intraventricular hemorrhage (Grade 2)
Fig. 7.115 Cerebral hemorrhage (Grade 3): severe ventriculomegaly with large blood clots (arrows)
Fig. 7.116 (a) Cerebral

hemorrhage: major intrapa- a
renchymatous hemorrhage
(Grade 4). (b) Grade 4
intracerebellar hemorrhage at
22 gw
b
Ischemic Pathologies
Ischemic lesions are often secondary to hemorrhage and/or cerebral anoxia. A clas-
sic example is that of monochorionic pregnancies where the surviving twin has a
high risk of secondary brain lesions (Simonazzi et al. 2006; Senat et al. 2002). An
attentive study of the fetal brain is imperative in these cases.
Ischemic lesions take the form of periventricular cysts within an area of leuko-
malacia (Fig. 7.117) or in regions where brain tissue has been destroyed. These
lesions appear as anechoic areas with very irregular contours corresponding to
porencephaly (Figs. 7.118 and 7.119). Finally, the lesion may create communica-
tion between pericerebral spaces and the ventricles, resulting in schizencephaly.
A recent study showed that schizencephaly occurs more readily in young moth-
ers and is often associated with septo-optic dysplasia, suggesting that they have a
common destructive origin (Howe et al. 2012).
Transvaginal ultrasonography is of precious assistance for the difficult diagnosis
of these lesions when the fetus is in cephalic presentation (De Vries 2003).
These destructive lesions generally have a poor neurological prognosis.
Fig. 7.117 Leukomalacia in

twin-to-twin transfusion
syndrome (Image M. Molho)
Fig. 7.118 (a) Destructive lesions of a ventricle wall (24 gw). (b) Ischemic and hemorrhagic
lesion of the temporal lobe at 34 gw: pathology specimen. (c) Parietal-occipital infarction and
ventricular dilatation at 18 gw (twin-to-twin transfusion syndrome)
Fig. 7.119 (a) Large lesions in poroencephaly. (b) Ischemic and hemorrhagic clastic lesions at 32
gw, asymmetric cerebral atrophy and porencephaly (pathology specimens). (c) Temporal atrophy
secondary to ischemia (white arrows), by TUI
Fig. 7.120 Schizencephaly (32 gw, surviving twin of a monochorionic diamniotic pregnancy)
It should be noted that schizencephaly may cause malformations as illustrated in

Fig. 7.121.
Fig. 7.121 Open-lip

schizencephaly at 33 gw
Vascular Pathologies
Vein of Galen Aneurysms
In fact, this term covers a range of arteriovenous malformations located in the cen-
tral region of the brain. Three types have been identified: arteriovenous fistulas,
arteriovenous malformations with ectasia of the vein of Galen, and vein of Galen
varices (Lasjaunias et al. 1986).
For the ultrasonographer, these malformations appear in the form of a very finely
echoic or even anechoic oblong lesion in the quadrigeminal cisterna. Doppler ultra-
sound can confirm the presence of a turbulent flow within this formation (Fig. 7.122)
(Pilu et al. 1997; Carletti et al. 2009). This formation may on occasion become
echogenic with no vascular flow being found. In this case, the efferent sinuses are
nevertheless dilated, corresponding to thrombosis of the aneurysm (Boopathy
Vijayaraghavan et al. 2006).
A 3D ultrasound scan is particularly useful in determining the afferent and effer-
ent vessels (Fig. 7.123) (Pilu et al. 2007). Investigations should be conducted to
detect dilatation of neck vessels, signs of heart failure: cardiomegaly, hepatospleno-
megaly, anasarca, or polyhydramnios.
Fig. 7.122 Vein of Galen aneurysm (Doppler ultrasound confirms the vascular nature of the lesion)
Vascular Pathologies 267
Fig. 7.123 (a) Vein of Galen aneurysm: 3D color ultrasound with glass body rendering showing
evidence of vascular connections and dilated cervical vessels. (b) Vein of Galen aneurysm: fetal
pathology specimen (Photo F. Razavi)
Thrombosis of the Dural Sinuses
The most common location for such anomalies is the torcula. This lesion appears by
ultrasonography to be very roughly triangular in shape with an anterior apex. It is
more or less echogenic but does not show any blood flow by Doppler ultrasound
(Fig. 7.124). Outcome is variable and may be favorable if there are no signs of car-
diac decompensation, if the lesion is isolated, and if it regresses spontaneously
(Laurichesse Delmas et al. 2006, 2008; Visentin et al. 2001).
a b
Fig. 7.124 (a) Thrombosis of the torcula (anechoic image of the posterior fossa), dilatation of the
superior sagittal sinus (right) (Images H. Laurichesse). (b) Thrombosis of the torcula: weakly
echogenic lesion in the posterior fossa with major stasis in the superior sagittal sinus (Images
H. Laurichesse). (c) Thromboses of the dural sinuses at 22 gw: a in the torcula (green arrow), b in
the anterior part of the sagittal sinus (pink arrow)
Vascular Pathologies 269
Other Vascular Lesions
Pial malformations are very rarely discovered by antenatal examinations, but aneu-
rismal lesions may be found at other locations such as this rare case of aneurysm of
the circle of Willis (Fig. 7.125).
Fig. 7.125 Aneurysm of the circle of Willis

Fig. 7.126 Aneurysm of the

circle of Willis, 3D ultra-
sound with glass body
rendering (arrows aneurysm)
Therefore, when faced with an anechoic or hypoechoic anomaly, the sonogra-

pher should check by Doppler ultrasound for the presence of blood flow in the
lesion detected.
Biometric Anomalies 271
Biometric Anomalies
Microcephaly
Detection of a “small cranium” anomaly has three prerequisites:
• Date of conception must be known exactly.

• The measurement technique used must be appropriate.
• The definition of the anomaly must be precise.
• Date of conception.
This is based on a precise measurement of crown-rump length in the first trimes-

ter of pregnancy, but it should be recognized that above a CRL of 60 mm, a mea-
surement of biparietal diameter is more precise (Fig. 7.127).
Fig. 7.127 Dating by CRL (double blue arrow) and BPD (double yellow arrow)
A rigorous measurement technique must be used (see the Chap. 4). The section
chosen must meet the quality criteria.
The charts on which the measurements are plotted must correspond to the method
employed, particularly as regards placement of the calipers. In the example below
(FMF charts, Snidjers), the ellipse must be placed at the external interface of the
skull.
Perimetre cranien
450
400
95%
350
5%
300
250
mm
200
150
100
50
0
14 16 18 20 22 24 26 28 30 32 34 36 38 40
Semaines
Fig. 7.128 Chart for the measurement of head circumference (Snijders and Nicolaides 1994)
The charts must be suitable for the population studied. In the example below,
FMF charts are the most suitable. All operators should study their data and thus
“customize” their charts after checking the measurement technique.
Chart suitable
HC
Fig. 7.129 Finding a suitable plot

• Precise Definition of the Anomaly
The definition of microencephaly is perfectly precise: head circumference is less

than a Z-score of –3, i.e. –3 SD.
Microcephaly: –3 SD, Z-score: –3
Microcephaly : –3 SD, Z-Score : –3
Fig. 7.130 Defining anomalies

The ultrasound image associates a head circumference of less than Z-score –3

and a characteristic receding forehead (Pilu et al. 1998; Le Ray et al. 2004).
a b
Fig. 7.131 (a) Microcephaly at 25 gw: HC: Z-score –3, receding forehead. (b) Microcephaly:
fetal pathology specimens, a: 20 gw, b: 36 gw
The discovery of microencephaly should prompt the conduct of a full investiga-

tion given that the risk of mental retardation is about 50 % for HC Z-scores between
–3 and –3.99 and practically 100 % for HC Z-scores of –4 (Stoler-Poria et al. 2010).
Ultrasonography should play a major role in this investigation:
• Evaluation of background intrauterine growth retardation: comparison of HC

measurements with other anomalies, detection of any vascular anomalies in par-
ticular by uterine Doppler ultrasound
• Careful verification of fetal profile
• Tests for infection, particularly for associated brain signs suggestive of
cytomegalovirus-related pathology (Benoist et al. 2008)
• Genetic tests: karyotype, 4p deletion, specialized consultation
• Family inquiry.
Major Hydrocephalus
Head circumference is very greatly increased (>Z-score: +2.5), the ventricles are
very clearly dilated, midline structures are often ruptured (Fig. 7.132), a differential
diagnosis must be made with respect to hydranencephaly where no cerebral struc-
tures are recognizable (Fig. 7.134).
Fig. 7.132 Major hydrocephalus (33 gw): rupture of the midline
Fig. 7.133 Major hydrocephalus: postnatal features

Fig. 7.134 Hydranencephaly
a b c
d d
Fig. 7.135 (a) Hydrocephalus at 22 gw with septal rupture and thin corpus callosum, (b, c) hydra-
nencephaly at 21 gw by a clastic mechanism, (d) hydranencephaly at 13 gw and multiple calcified
necrotic lesions in hydranencephaly-hydrocephalus syndrome (fetal pathology specimens)
Gyration Disorders 279
Gyration Disorders
Obviously, a study of gyration disorders is best conducted by nuclear magnetic

resonance imaging.
But ultrasonographers – thanks to their knowledge of simple anatomical land-
marks identified by ultrasonography (see Chap. 3 on the cerebral aqueduct and the
study of the gyration) – may in the course of their examinations be led to suspect
such anomalies (Malinger 2002), Malinger et al. 2007).
Major gyration disorders may be divided into three groups: lissencephaly, neuro-
nal migration disorders: heterotopia, and polymicrogyria.
Three Groups: Lissencephaly Type I (LIS I), II (LIS II), and III (LIS III)
It is often the discovery of other cerebral anomalies that prompts ultrasonographers

to conduct a careful study of the cerebral cortex: ventriculomegaly, thickened corpus
callosum, or small HC related to LIS I: Miller-Diecker syndrome (Fig. 7.136a, b)
(Fong et al. 2004), X-linked LIS I with corpus callosum anomalies.
a b c d
f g
e h
Fig. 7.136 (a) Miller-Diecker syndrome at 24 gw. Cerebral spaces are very large, the cerebral
aqueduct is not clearly defined. (b) Miller-Diecker syndrome (17p13.3 deletion syndrome): fetal
pathology specimens. a bitemporal narrowing, thin upper lip, micrognathia. b 5th percentile brain
biometrics, 5th percentile cerebellar biometrics, c agyria, abnormal cerebral aqueduct, d control at
25 gw, e abnormally thickened cortex, f, g four layers of the cortex, h vermis nodular heterotopia
LIS II with, for example, Walker-Warburg syndrome may be suspected when faced
with a picture of rapidly progressive hydrocephalus associated with meningocele and
brainstem and cerebellar anomalies or ocular anomalies (Fig. 7.137a, b).
Fig. 7.137 (a) Walker-Warburg syndrome at 24 gw: major ventriculomegaly, brainstem abnormal
(Z-shaped), ocular anomaly: microphthalmia and persistent primary vitreous. (b) Walker-Warburg
syndrome: fetal pathology specimens. a meningocele. b smooth brain, little sylvian fissure opercu-
lization, c control at 26 gw, d ventricular dilatation, fusion of the two hemispheres along the mid-
line, e thickened meninges, ventricular dilatation, hypoplasia of the corpus callosum,
f cytoarchitectonic anomalies of the cortex with massive neuronal migration into the meninges,
g retinal dysplasia, h mesencephalon: thickened meninges containing many neuroglial cells, i cer-
ebellar hypoplasia, smooth hemispheres, thickened meninges, j Z-shaped brainstem, partial agen-
esis of the vermis. (c): Nodular heterotopia at 22 gw by TUI
Regarding LIS III, a decrease in fetal motility, polyhydramnios, and microenceph-

aly lending the brain the appearance of a “hazelnut” may be seen by ultrasonography.

Heterotopia
Nodular heterotopia may be visualized by ultrasonography thanks to the use of

high-frequency transducers. It is recognizable in the form of small echogenic nod-
ules located in the ventricle walls (Fig. 7.137c).

Polymicrogyria
This anomaly is either hereditary or acquired. The cortex is seen to contain many
small irregular sulci but the condition may not be diagnosed if these lesions are very
localized. This anomaly is illustrated below by images drawn from a case of fetal
CMV infection at 22 gw (it should be noted that the sylvian fissure appears retro-
spectively to be very abnormal) (Dhombres 2008).
Fig. 7.138 (a) Polymicrogyria in a setting of CMV-related fetopathy (26 gw). (b) CMV-related
fetopathy: Polymicrogyria (fetal pathology specimens)
Fig. 7.139 CMV-related

fetopathy: abnormal sylvian
fissure (white arrow)
Part III
Biometric Tables
Biometric Tables
8
Table 8.1 Measurements of biparietal diameter

(SA ± 3J) BIP p3 BIP p10 BIP p50 BIP p90 BIP p97
11 12.08 13.12 15.36 17.60 18.63
12 15.81 16.96 19.40 21.81 22.92
13 19.47 20.71 23.30 25.92 27.12
14 23.05 24.36 27.14 29.92 31.23
15 26.56 27.93 30.89 33.82 35.23
16 29.97 31.41 34.53 37.62 39.08
17 33.32 34.85 38.12 41.35 42.87
18 36.55 38.15 41.58 44.97 46.56
19 39.76 41.46 45.00 48.52 50.18
20 42.85 44.56 48.22 51.90 53.64
21 45.86 47.66 51.43 55.23 57.00
22 48.79 50.61 54.53 58.44 60.30
23 51.63 53.48 57.51 61.54 63.45
24 54.38 56.31 60.42 64.57 66.50
25 57.04 59.00 63.25 67.48 69.42
26 59.62 61.64 65.94 70.24 72.27
27 62.12 64.15 68.35 72.92 75.00
28 64.50 66.61 71.03 75.52 77.60
29 66.84 68.98 73.50 77.97 80.09
30 69.07 71.21 75.80 80.37 82.52
31 71.22 73.39 78.00 82.63 84.80
32 73.30 75.49 80.16 84.80 87.00
33 75.24 77.46 82.14 86.84 89.04
34 77.14 79.36 84.07 88.80 91.00
35 78.94 81.14 85.90 90.61 92.83
36 80.64 82.88 87.61 92.35 94.56
37 82.27 84.50 89.24 93.97 96.19
38 83.78 86.00 90.70 95.42 97.66
39 85.22 87.43 92.10 96.86 99.05
40 86.57 88.78 93.45 98.13 100.31
41 87.00 89.00 94.00 99.00 101.00

290 8 Biometric Tables
Biparietal Diameter (Snidjers)

Table 8.2 Normal range for biparietal diameter (mm)
Biparietal diameter (mm)
Gestational age range (weeks + days) 5th centile Median 95th centile
14 + 0–14 + 6 28 31 34
15 + 0–15 + 6 31 34 37
16 + 0–16 + 6 34 37 40
17 + 0–17 + 6 36 40 43
18 + 0–18 + 6 39 43 47
19 + 0–19 + 6 42 46 50
20 + 0–20 + 6 45 49 54
21 + 0–21 + 6 48 52 57
22 + 0–22 + 6 51 56 61
23 + 0–23 + 6 54 59 64
24 + 0–24 + 6 57 62 68
25 + 0–25 + 6 60 66 71
26 + 0–26 + 6 63 69 75
27 + 0–27 + 6 66 72 78
28 + 0–28 + 6 69 75 81
29 + 0–29 + 6 72 78 85
30 + 0–30 + 6 74 81 88
31 + 0−31 + 6 77 83 90
32 + 0–32 + 6 79 86 93
33 + 0–33 + 6 81 88 96
34 + 0–34 + 6 83 90 98
35 + 0–35 + 6 85 92 100
36 + 0–36 + 6 86 94 102
37 + 0–37 + 6 87 95 103
38 + 0–38 + 6 88 96 104
39 + 0–39 + 6 89 97 105
Snijders RJM, Nicolaides KH (1994) Fetal biometry at 14–40 weeks gestation. Ultrasound Obstet
Gynecol 4:34–48 – With permission
Table 8.3 Measurements of cephalic perimeter

(SA±3J) PC p3 PC p10 PC p50 PC p90 PC p97
11
12
13
14
15
16 105.80 110.58 120.86 131.25 136.11
17 118.67 123.78 134.49 145.38 150.39
18 131.08 136.36 147.55 158.92 164.11
19 143.00 148.53 160.29 172.14 177.48
20 154.53 160.21 172.47 184.86 190.54
21 165.41 171.49 184.21 197.12 203.09
22 176.12 182.35 195.74 208.91 215.15
Biparietal Diameter (Snidjers) 291
Table 8.3 (continued)

(SA±3J) PC p3 PC p10 PC p50 PC p90 PC p97
23 186.32 192.31 206.64 220.26 226.76
24 196.19 203.00 217.18 231.39 238.00
25 205.50 212.40 227.32 241.91 248.81
26 214.44 221.57 236.72 252.00 259.23
27 222.87 230,33 246.00 261.75 269.13
28 231.00 238.56 254.77 271.00 278.57
29 238.40 246.35 263.00 279.71 287.56
30 245.86 253.74 270.84 288.13 296.00
31 252.54 260.81 278.33 296.00 304.27
32 258.86 267.22 285.29 303.54 312.00
33 264.62 273.38 292.00 310.40 319.10
34 270.14 279.00 298.10 317.00 325.91
35 275.33 284.23 303.62 323.00 332.16
36 279.79 289.00 308.81 328.75 338.00
37 283.90 293.32 313.52 334.00 343.34
38 287.63 297.29 317.88 338.64 348.29
39 290.88 300.76 321.86 343.00 352.67
40 293.00 303.00 324.00 346.00 356.00
41
Table 8.4 Normal range for head circumference (mm)

Head circumference (mm)
14 + 0–14 + 6 102 110 118
15 + 0–15 + 6 111 120 129
16 + 0−16 + 6 120 130 140
17 + 0–17 + 6 130 141 152
18 + 0–18 + 6 141 152 164
19 + 0–19 + 6 151 163 176
20 + 0–20 + 6 162 175 189
21 + 0–21 + 6 173 187 201
22 + 0–22 + 6 184 198 214
23 + 0–23 + 6 195 210 227
24 + 0–24 + 6 206 222 240
25 + 0–25 + 6 217 234 252
26 + 0–26 + 6 227 245 264
27 + 0–27 + 6 238 256 277
28 + 0–28 + 6 248 267 288
29 + 0–29 + 6 257 277 299
30 + 0–30 + 6 266 287 309
31 + 0–31 + 6 274 296 319
32 + 0–32 + 6 282 304 328
33 + 0–33 + 6 288 311 336
34 + 0–34 + 6 294 317 342
35 + 0–35 + 6 299 323 348
36 + 0–36 + 6 303 327 353
(continued)

Head circumference (mm)
37 + 0–37 + 6 306 330 356
38 + 0–38 + 6 308 332 358
39 + 0–39 + 6 309 333 359
Snijders RJM, Nicolaides KH (1994) Fetal biometry at 14–40 weeks’ gestation. Ultrasound Obstet
Table 8.5 Normal range for transverse cerebellar diameter (mm)

Transverse cerebellar diameter (mm)
14 + 0–14 + 6 12 14 15
15 + 0–15 + 6 13 15 17
16 + 0−16 + 6 14 16 18
17 + 0–17 + 6 15 17 19
18 + 0–18 + 6 16 18 21
19 + 0–19 + 6 17 20 22
20 + 0–20 + 6 19 21 24
21 + 0–21 + 6 20 22 25
22 + 0–22 + 6 21 24 27
23 + 0–23 + 6 22 25 28
24 + 0–24 + 6 24 26 30
25 + 0–25 + 6 25 28 31
26 + 0–26 + 6 26 29 33
27 + 0–27 + 6 27 31 34
28 + 0–28 + 6 29 32 36
29 + 0–29 + 6 30 33 37
30 + 0–30 + 6 31 35 39
31 + 0–31 + 6 32 36 40
32 + 0–32 + 6 34 37 42
33 + 0–33 + 6 35 39 43
34 + 0–34 + 6 36 40 44
35 + 0–35 + 6 37 41 46
36 + 0–36 + 6 38 42 47
37 + 0–37 + 6 39 43 48
38 + 0–38 + 6 40 44 49
39 + 0–39 + 6 41 45 51
Table 8.6 Normal range (mean, 5th, and 95th centile) for transverse cerebellar diameter (TCD)
in mm relative to gestational age (weeks)
Gestational age (weeks) 5th centile Mean 95th centile
17 15.87 17.50 19.29
18 16.87 18.50 20.40
19 17.75 19.57 21. 57
20 18.76 20.69 22.81
21 19.84 2l.88 24.l2
22 20.98 23.l3 25.51
23 22.l9 24.46 26.97
24 23.46 25.87 28.52
25 24.81 27.35 30.16
26 26.23 28.92 31.89
27 27.74 30.58 33.72
28 29.33 32.34 35.65
29 31.01 34.l9 37.70
(continued)

Gestational age (weeks) 5th centile Mean 95th centile
30 32.79 36.l6 39.87
31 34.68 38.23 42.l5
32 36.67 40.43 44.57
33 38.77 42.75 47.l3
34 41.00 45.20 49.84
Vinkesteijn ASM, Mulder PGH, Wladimiroff JW (2000) Fetal transverse cerebellar diameter mea-
surements in normal and reduced fetal growth. Ultrasound Obstet Gynecol 15:47–51 – With
permission
Table 8.7 Length of fetal corpus callosum by gestational age

Gestational age Lower 95% Mean length Upper 95%
(weeks) Observations (n) CI (mm) CI
16 4 2.95 3.75 4.55
17 8 4.77 6.24 7.70
18 7 10.04 12.51 14.99
19 18 14.51 15.78 17.05
20 21 18.13 18.95 19.77
21 21 19.54 20.38 21.23
22 18 21.53 22.39 23.24
23 22 23.19 24.45 25.72
24 18 26.32 27.61 28.90
25 23 28.66 29.65 30.64
26 18 29.91 31.44 32.98
27 12 32.75 34.33 35.92
28 9 32.30 34.44 36.59
29 10 34.21 36.40 38.59
30 12 37.14 38.33 39.52
31 10 36.18 37.30 38.42
32 7 38.37 40.43 42.49
33 4 31.44 38.50 45.56
34 6 41.40 42.50 43.60
35 5 40.82 45.60 50.38
36 2 40.00 44.00 45.00
37 3 42.5 44.67 46.84
Achiron R, Achiron A (2001) Development of the human fetal corpus callosum: a high-resolution,
cross-sectional sonographic study. Ultrasound Obstet Gynecol 18:343–347 – With permission
CI confidence interval
Table 8.8 Thickness of fetal corpus callosum by gestational age

Gestational age Lower 95% Mean thickness Upper 95%
(weeks) Observations (n) CI (mm) CI
16 4 0.42 0.75 1.08
17 8 0.58 1.12 1.32
18 7 1.12 1.30 1.48
19 18 1.03 1.13 1.24
20 21 1.31 1.47 1.63
21 21 1.60 1.73 1.86
22 18 1.82 2.00 2.18
23 22 1.87 2.04 2.20
24 18 1.90 2.07 2.24
25 23 1.89 2.11 2.34
26 18 1.87 2.09 2.31
27 12 1.94 2.14 2.35
28 9 1.66 2.14 2.63
29 10 1.73 1.99 2.25
30 12 2.04 2.35 2.66
31 10 1.93 2.37 2.81
32 7 1.96 2.66 3.36
33 4 2.13 2.75 3.37
34 6 2.20 2.62 3.03
35 5 2.21 2.76 3.31
36 2 2.20 2.50 3.00
37 3 1.98 2.27 2.55
Achiron R, Kivilevitch Z, Lipitz S, Gamzu R, Almog B, Zalel Y (2004) Development of the human
fetal pons: in utero ultrasonographic study. Ultrasound Obstet Gynecol 24:506–510 – With
permission
CI confidence interval
Table 8.9 Percentile measurements of the pons (anteroposterior diameter) according to gesta-
tional age
Anteroposterior diameter (mm)
GA (weeks) n 5th 25th 50th 75th 95th
19−20 18 4.2 6.3 6.8 7.0 7.5
21−22 114 6.8 7.2 7.5 8.0 8.3
23−24 82 7.2 7.7 8.2 8.5 9.1
25−26 20 8.4 9.3 9.6 10.2 11.0
27−28 15 9.3 10.0 10.3 10.9 11.5
29−30 11 9.9 10.7 11.4 11.7 12.0
31−32 13 10.9 11.7 12.3 12.8 14.0
33−34 14 12.0 12.4 12.8 13.5 15.7
cross-sectional sonographic study. Ultrasound Obstet Gynecol 18(4):343–347 – With permission
GA gestational age
Table 8.10 Raw data and smoothing data using the LMS procedure for the diameter of the pons:
mean, standard deviation, median, 5th, 10th, 25th, 75th, 90th, and 95th percentile values according
to gestational age for 883 normal fetuses
Raw data (mm) Smoothing data (percentiles) (mm)
GA Standard
(weeks) N Mean deviation 5th 10th 25 th Median 75th 90th 95th
21 82 7.9 0.7 6.7 7.0 7.4 7.9 8.4 8.9 9.1
22 267 8.4 0.9 6.9 7.3 7.8 8.4 9.0 9.5 9.8
23 92 8.8 1.1 7.2 7.6 8.2 8.8 9.5 10.1 10.4
24 25 9.2 0.7 7.6 8.0 8.6 9.3 10.0 10.6 11.0
25 11 10.4 1.1 8.1 8.5 9.2 9.9 10.6 11.2 11.6
26 21 10.4 1.0 8.5 9.0 9.6 10.4 11.1 11.7 12.1
27 20 10.7 1.0 8.9 9.4 10.1 10.8 11.6 12.2 12.6
28 13 11.3 1.3 9.4 9.8 10.5 11.3 12.0 12.7 13.1
29 13 11.4 1.4 9.8 10.2 10.9 11.7 12.4 13.2 13.5
30 9 12.2 0.7 10.2 10.6 11.3 12.1 12.9 13.6 14.0
31 45 12.6 1.2 10.5 11.0 11.7 12.5 13.3 14.0 14.4
32 169 12.8 1.2 10.8 11.3 12.0 12.9 13.7 14.5 14.9
33 71 13.2 1.6 11.0 11.5 12.3 13.3 14.2 15.1 15.6
34 24 14.0 1.5 11.2 11.8 12.7 13.7 14.7 15.7 16.3
35 10 13.5 1.1 11.4 12.0 13.0 14.1 15.3 16.3 16.9
36 11 14.7 2.0 11.6 12.3 13.3 14.5 15.8 16.9 17.6
Mirlesse V, Courtiol C, Althuser M, CFEF, M. Duyme M (2010) Ultrasonography of the fetal
brainstem: a biometric and anatomical, multioperator, cross-sectional study of 913 fetuses of
21–36 weeks of gestation. Prenat Diagn 30:739–745
GA gestational age
Table 8.11 Percentile measurement of cerebellar vermis (superoinferior diameter) according to

gestational age
Superoinferior diameter (mm)
GA (weeks) n 5th 25th 50th 75th 95th
19−20 18 6.5 9.1 9.5 10.0 11.1
21−22 114 10.1 10.9 11.7 12.1 13.2
23−24 82 11.4 12.3 13.0 13.6 15.2
25−26 20 13.1 14.3 14.8 15.4 16.4
27−28 15 15.3 16.0 16.8 17.9 18.6
29−30 11 15.6 17.5 18.5 20.3 20.9
31−32 13 17.2 19.6 20.1 20.7 21.0
33−34 14 18.3 20.6 21.5 22.8 24.0
fetal pons: in utero ultrasonographic study. Ultrasound Obstet Gynecol 24:506–510 – With permission
GA gestational age
Table 8.12 Vermis size (width and height) according to gestational age (mean ± SD)
Number of Vermis width (mean, mm Vermis height (mean, mm
Gestational week patients (SD)) (SD))
18−20 8 5 (0.76) 5.88 (0.85)
21 17 5.76 (0.83) 6.47 (0.94)
22 17 6.24 (0.66) 6.88 (0.60)
23 31 6.90 (0.54) 7.71 (0.90)
24 25 8.12 (0.67) 8.44 (0.71)
25 26 8.58 (0.81) 8.62 (0.75)
26 18 9.11 (0.96) 9.17 (0.71)
27 18 9.78 (0.81) 10.00 (0.91)
28−29 17 10.4 (1.17) 10.5 (0.87)
30−31 12 11.3 (1.22) 11.6 (0.79)
32 14 12.3 (1.54) 12.1 (1.27)
33 16 11.8 (1.29) 12.2 (1.11)
34 10 13.0 (1.05) 13.0 (0.94)
35−36 18 14.2 (1.25) 14.2 (1.20)
37−38 9 15.4 (1.01) 15.3 (0.87)
Total 256
Zalel Y, Seidman DS, Brandt N, Lipitz S, Achiron R (2002) The development of the fetal vermis:
an inutero sonographic evaluation. Ultrasound Obstet Gynecol 19:136–139 – With permission
SD standard deviation
Table 8.13 Raw data and smoothing data using the LMS procedure for the diameter of the ver-
mis: mean, standard deviation, median, 3rd, 5th, 10th, 25th, 75th, 90th, 95th, and 97th percentile
values according to gestational age for 643 normal fetuses
Raw data (mm) Smoothing data (percentiles) (mm)
GA Standard
(weeks) N Mean deviation 5th 10th 25th Median 75th 90th 95th
21 79 11.8 0.8 10.6 10.8 11.2 11.7 12.2 12.8 13.1
22 203 12.4 0.9 11.1 11.4 11.8 12.4 13.1 13.7 14.2
23 55 13.4 1.3 11.6 12.0 12.5 13.2 13.9 14.7 15.2
24 20 13.9 0.8 12.3 12.7 13.2 14.0 14.8 15.7 16.2
25 11 15.6 1.5 12.9 13.3 14.0 14.8 15.7 16.6 17.2
26 19 15.4 1.3 13.6 14.1 14.8 15.7 16.6 17.5 18.1
27 17 16.8 1.5 14.5 14.9 15.6 16.5 17.4 18.3 18.9
28 11 17.11 0.6 15.3 15.7 16.4 17.3 18.3 19.2 19.8
29 13 17.87 1.5 16.1 16.5 17.3 18.1 19.0 19.9 20.5
30 6 19.82 1.2 16.9 17.3 18.0 18.9 19.8 20.7 21.2
31 39 19.92 1.3 17.6 18.0 18.7 19.6 20.5 21.3 21.9
32 112 20.29 1.3 18.1 18.6 19.4 20.3 21.2 22.0 22.6
33 3 20.74 1.5 18.6 19.1 19.9 20.9 21.8 22.7 23.3
34 13 21.12 1.4 18.9 19.5 20.4 21.5 22.5 23.5 24.0
35 8 21.86 2.0 19.2 19.8 20.9 22.1 23.2 24.2 24.8
36 7 22.49 1.9 19.4 20.2 21.4 22.6 23.9 25.0 25.6
Mirlesse V, Courtiol C, Althuser M, CFEF, Duyme M (2010) Ultrasonography of the fetal brain-
stem: a biometric and anatomical, multioperator, cross-sectional study of 913 fetuses of 21–36
weeks of gestation. Prenat Diagn 30:739–745
GA gestational age
Table 8.14 Normal range for cisterna magna diameter (mm)

Cisterna magna diameter (mm)
Gestational age range (weeks + day) 5th centile Median 95th centile
14 + 0–14 + 6 1.9 3.5 5.3
15 + 0 – 15 + 6 2.1 3.8 5.7
16 + 0–16 + 6 2.4 4.1 6.0
17 + 0 – 17 + 6 2.6 4.3 6.3
18 + 0– 18 + 6 2.8 4.6 6.6
19 + 0–19 + 6 3.1 4.9 6.9
20 + 0–20 + 6 3.3 5.1 7.2
21 + 0–21 + 6 3.5 5.4 7.5
22 + 0–22 + 6 3.7 5.6 7.7
23 + 0–23 + 6 3.9 5.8 8.0
24 + 0–24 + 6 4.1 6.0 8.2
25 + 0–25 + 6 4.3 6.2 8.5
26 + 0–26 + 6 4.4 6.4 8.7
27 + 0–27 + 6 4.6 6.6 8.9
28 + 0–28 + 6 4.7 6.8 9.1
29 + 0–29 + 6 4.9 6.9 9.3
30 + 0–30 + 6 5.0 7.0 9.4
3 1 + 0–31 + 6 5.1 7.2 9.6
32 + 0–32 + 6 5.2 7.3 9.7
33 + 0–33 + 6 5.3 7.4 9.8
34 + 0–34 + 6 5.3 7.5 9.9
35 + 0–35 + 6 5.4 7.5 1 0.0
36 + 0–36 + 6 5.4 7.6 10.0
37 + 0–37 + 6 5.4 7.6 10.1
38 + 0–38 + 6 5.5 7.6 10.1
39 + 0–39 + 6 5.5 7.6 1 0.1
Table 8.15 Mean and dispersion of the measurement (cm) of the fetal cisterna magna in the nor-
mal control population
Weeks n One SD Average less 2.5 SD Average Average plus 2.5 SD
15 48 0.09 0.11 0.33 0.56
16 66 0.09 0.15 0.37 0.59
17 44 0.09 0.16 0.38 0.60
18 65 0.11 0.18 0.46 0.74
19 53 0.12 0.21 0.51 0.82
20 51 0.10 0.31 0.55 0.79
21 30 0.13 0.24 0.55 0.86
22 30 0.15 0.25 0.62 0.99
23 21 0.15 0.26 0.64 1.02
24 21 0.15 0.24 0.62 0.99
25–26 40 0.19 0.22 0.70 1.17
27−28 31 0.19 0.31 0.78 1.25

Weeks n One SD Average less 2.5 SD Average Average plus 2.5 SD
29−30 25 0.24 0.15 0.77 1.37
31−32 23 0.22 0.30 0.84 1.38
33−35 24 0.25 0.24 0.85 1.47
Steiger RM, Porto M, Lagrew DC, Randall R (1995) Biometry of the fetal cisterna magna esti-
mates of the ability to detect trisomy 18. Ultrasound Obstet Gynecol 5:384–390 – With
permission
The recommended normal range of ±2.5 standard deviations (SD) is indicated. The groups were
chosen so that there were at least 20 studies in each cell. Studies less than 15 weeks and greater
than 35 weeks are excluded, as the sample sizes were too small
Conclusion
We hope that this Atlas will be of assistance to all ultrasonographers whether they
work in screening or in diagnosis, and that it will help them better understand the
anatomy of the fetal brain and its pathologies.
This book demonstrates that many tools are available to ultrasonographers, both
for conventional and 3D/4D ultrasonography.
3D/4D ultrasonography can in particular be used to situate accurately the ana-
tomic relationship of the lesions detected with other brain structures.
Comparisons with reference fetal pathology specimens provide a clearer picture
of the exact nature of the lesions and their translation into ultrasound images.
Obviously, comparisons with other fetal imaging techniques, particularly nuclear
magnetic resonance imaging, is often indispensable. These comparisons would best
be made during meetings at multidisciplinary diagnostic centers.
The authors wish to thank their fellow physicians for their invaluable input during
these multidisciplinary meetings.

Ultrasonographic Features, DOI 10.1007/978-3-319-19971-9
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Part II: The Pathological Brain

First Trimester Pathologies
Bernard JP, Suarez B, Rambaud C, Muller F, Ville Y (1997) Prenatal diagnosis of neural tube
defect before 12 weeks’ gestation: direct and indirect ultrasonographic semeiology. Ultrasound
Bernard J-P, Cuckle HS, Bernard MA, Brochet C, Salomon LJ, Ville Y (2013) Combined screen-
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Chaoui R, Nicolaides KH (2010) From nuchal translucency to intracranial translucency: towards
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Roszkowski T, Kucinska-Chahwan A, Garwolinski J, Szyszka M, Jakiel G (2009) P16.10: first
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Second and Third Trimester Pathologies
Skull Anomalies
Buckmiller LM, Richter GT, Suen JY (2010) Diagnosis and management of hemangiomas and
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Delahaye S, Bernard JP, Rénier D, Ville Y (2003) Prenatal ultrasound diagnosis of fetal craniosyn-
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half of pregnancy. Ultrasound Obstet Gynecol 24(4):412–416
Ghi T, Pilu G, Falco P, Segata M, Carletti A, Cocchi G, Santini D, Bonasoni P, Tani G, Rizzo N
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Midline Anomalies
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Ventriculomegalies
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Salomon LJ, Bernard JP, Ville Y (2007) Reference ranges for fetal ventricular width: a non-normal
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Posterior Fossa Anomalies
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Guibaud L, des Portes V (2006) Plea for an anatomical approach to abnormalities of the posterior
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Paladini D, Volpe P (2006) Posterior fossa and vermian morphometry in the characterization of
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Medical, Montpellier, France
Garel C (2002) Imagerie du cerveau fœtal pathologique. Sauramps Medical, Montpellier, France
Govaert P, De Vries L (2010) An atlas of neonatal brain sonography. Mac Keith Press, London, UK
Guibaud L (2009) Contribution of fetal cerebral MRI for diagnosis of structural anomalies. Prenat
Diagn 29(4):420–433
International Society of Ultrasound in Obstetrics & Gynecology Education Committee (2007)
Sonographic examination of the fetal central nervous system: guidelines for performing the
‘basic examination’ and the ‘fetal neurosonogram’. Ultrasound Obstet Gynecol 29(1):109–116
Pathologie fœtale et placentaire pratique. Sauramps Medical 2008. Ouvrage collectif de la Société
Française de Fœtopathologie. Coordonné par FE Razavi et D Carles
Index
A C
Acrania, 137, 153 Calcarine fissure, 88
Agenesis Calcifications, 244–245
of the corpus callosum, 167–174, 192 Calipers, 124
of the septum pellucidum, 194 “Candelabra”images, 246–247
of the vermis, 203 Caudate nucleus, 35
Alobar holoproscencephaly, 141 Cavity of the septum pellucidum, 30
Alobar holoprosencephaly, 163 Cavum of the septum pellucidum, 33–34, 62
Anencephaly, 153 Central gray nuclei, 35
Aneurysm of the circle Cerebellar agenesis, 151, 219
of Willis, 269 Cerebellar and Brainstem, 128–129
Anomalies of the cerebellum, 251 Cerebellar tentorium, 91, 205
Anomalies of the posterior fossa, Cerebellar vermis, 16, 128–129
151–152, 195–196 Cerebral aqueduct, 8
Anterior complex, 31, 32 “Cerebral artery crawling under the skull”, 179
Anterior fontanel, 118 Cerebral circulation, 104
Aqueduct stenosis, 182–184 Cerebral hamartoma, 225
Arachnoid cyst, 151, 203, 209, 231–234 Cerebral hemorrhage, 260
Arnold-Chiari malformation, 187 Cerebral hyperechoic areas, 256–257
Arteries of Central Gray Cerebral vesicles, 3
Nuclei, 110 CHARGE syndrome, 203, 221–222
Ascent of the V3, 171 Chiari II anomaly, 203
Atrial diameter, 125 Choroid plexuses, 35
Chromosomal anomalies, 182–184
Cingulate sulcus, 53, 56, 91
B Cisterna magna, 91, 97, 125
“Banana”sign cerebellum, 187 Clasped thumbs, 186
‘Bichat’s fissures, 12, 148 “Cloverleaf”skull, 161
Bickers-Adams, 186 Coronal sutures, 118, 120
Biparietal diameter (BPD), 123–124 Corpus callosum, 24, 30, 62–73, 126
Blake’s pouch, 92 anomalies, 167–181
cyst, 210–211 lipomas, 228–230
Blood clots, 198 Cortex, 3
Body, 63 Craniopharyngioma, 226
Brainstem, 91 Craniosynostoses, 158–160
Brainstem-tentorium (BT) angle, 204 Craniosynostosis, 162
Brainstem-vermis (BV) angle, 204 Crura of fornix, 26
Brain tumors, 223–226 Curvilinear form, 230
“Bulls horn”, 167 Cyclopia, 163

Ultrasonographic Features, DOI 10.1007/978-3-319-19971-9
312 Index
Cyst of the ccipital horn, 242 Ischemic, 198

‘Cysts in Blake’s pouch, 203 lesions, 200
Cysts of the Germinal Zone, 235 pathologies, 262–265
Cytomegalovirus (CMV), 237 ‘ISUOG’s guidelines, 73
D J
Dandy-Walker ‘Joubert’s syndrome, 195, 203, 220
anomaly, 203
malformation, 206
Destructive lesions, 263 K
Diencephalon, 12 Kidney anomalies, 146
Dysmorphic corpus callosum, 176
L
E L1CAM gene, 185
Echogenic septum ellucidum, 182 Lamboid sutures, 118
Exencephaly, 139 Large septum pellucidum, 182
Lateral Ventricles, 29, 73–77
Laurent Guibaud’s score, 73
F “Lemon” sign, 148, 187
Falx cerebri, 8, 31 Lentiform nucleus, 35
Focal reduction, 212 Lissencephaly Type I (LIS I), 278–282
Fourth ventricles, 12, 16, 18, 62 Lissencephaly Type II (LIS II), 278–282
Frontal bones, 156 Lissencephaly Type III (LIS III), 278–282
Frontal sulcus, 53 Lobar holoprosencephaly, 165
Fusion of the frontal bones, 163
M
G Main sinuses, 115
Genu, 63 Main Venous Sinuses, 115–116
of the corpus callosum, 65 Major Hydrocephalus, 276–278
Gyration, 53, 197 Mastoid fontanels, 118
Meckel-Gruber syndrome, 146
Mega cisterna magna, 203, 208
H Meningocele, 145, 154–156
Head Circumference (HC), 123–124 Meningoencephalocele, 145, 154–156
Hemangioma of the scalp, 156 Mesencephalon, 3
Hematomas, 234 Metopic suture, 118, 120
Hemimegalencephaly, 236 Microcephaly, 238, 271–276
Hemorrhagic, 198 Middle cerebral artery peak systolic
Hemorrhagic Pathologies, 258 velocity, 114
Heterotopia, 283 Miller-Diecker syndrome, 280
Holoprosencephaly, 141, 163–166 Moving the Fetus, 133
Hydranencephaly, 278
Hypotelorism, 163
Hypothalamic hamartoma, 225 N
Neural Tube Closure Anomalies, 148, 156–157
I
Infectious Ventriculomegaly, 201 O
Interorbital distance, 130 Olfactory sulci, 54, 56
Intracranial translucency, 149 Open-lip chizencephaly, 265
Intraparenchymatous trabecula, 48 Optic stems, 3
Intraventricular synechiae, 243–244 Overall reduction, 203, 213
Index 313
P Sutures and fontanels, 116–122

Partial agenesis, 175–176 Sylvian fissures, 24, 78
of the corpus callosum, 193 operculization, 48
Pericallosal artery, 172
Pericallosal circulation, 105–109
Periventricular halo, 240–241 T
Periventricular Pseudocysts, 241–242 Tear drop, 168
Petrous pyramids, 98 Telencephalic vesicles, 8
Polymicrogyria, 284 Temporal lobes, 48
Poroencephaly, 264 Temporal Sulcus, 91
Posterior fontanel, 118 Thalami, 35
Posterior fossa, 30, 91–92, 97–103 Thick corpus callosum, 176–178
Posterior Fossa and Cerebellum, 35–47 Third ventricle, 12, 16, 18, 35, 48, 62
Posterior horn, 35 Thrombosis of the dural
Precallosal fissure, 31 sinuses, 268
Proboscis, 163 Torcular, 91
Prosencephalon, 3 Tower skull, 162
Toxoplasma Gondii (TG), 252
Transvaginal approach, 132
Q Transverse diameter, 127
Quadriventricular, 181 Transverse sinuses, 116
Trigonocephaly, 162
Triple leaf, 168
R Trisomy 18, 157
Radial folds, 169 Trisomy 21, 157, 182
Rhombencephalic vesicle, 8 Tuberous Sclerosis, 227–228
Rhombencephalon, 3 TSC1, 227
Rhombencephalosynapsis, 195, 203, TSC2, 227
215–217 Tubulonodular form, 229
Rhomboencephalic vesicles, 12 Type II Chiari anomaly, 217–218
Right sinus, 115 Type II lissence, 197
Rostrum, 63
U
S Use of 3D Ultrasound, 134
Scaphocephaly, 160
Schizencephaly, 265
Secondary Rupture of the Septum V
Pellucidum, 247–249 V3, 181
Semilobar holoproscencephaly, 143 Vein of Galen, 115
Semilobar holoprosencephaly, 164 Aneurysms, 266–267
Septal Agenesis, 179 Venous circulation, 115
Septo-optic dysplasia, 180, 194 Ventricular dilatation, 253–255
Shortening of biparietal diameter, 149 Ventriculomegaly, 35, 181–183, 239
Signs of Toxoplasma Gondii Volume reconstruction, 72
Infection, 253
Single nostril, 163
Single ventricle, 163 W
Skull contours, 29 Walker-Warburg syndrome, 281
Splenium, 63 Willis’ circle, 111–114
Strawberry sign, 157 Wormian bones, 122
Subependymal cerebral hemorrhage, 259
Subtentorial arachnoid cysts, 205
Superior frontal sulcus, 56, 91 X
Superior sagittal sinus, 115 X-linked hydrocephalus, 185

The Normal and Pathological Fetal Brain - Ultrasonographic Features

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The Normal

The Normal and

ISBN 978-3-319-19970-2 ISBN 978-3-319-19971-9 (eBook)

Library of Congress Control Number: 2015947148

Springer Cham Heidelberg New York Dordrecht London

Printed on acid-free paper

Springer International Publishing AG Switzerland is part of Springer Science+Business Media

Part I The Normal Brain

1 Brief Review of Embryology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3

Part II The Pathological Brain

6 First-Trimester Pathologies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 137

Midline Anomalies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 163

Part III Biometric Tables

8 Biometric Tables . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 289

© Springer International Publishing Switzerland 2015 3

Fig. 1.1 Segmentation of the neural tube

Fig. 1.2 Bending of the neural tube

Fig. 1.5 Cerebral vesicles “inversion mode”

Fig. 1.6 Cerebral vesicles:

From 8 to 10 GW: Early Morphological Examination

© Springer International Publishing Switzerland 2015 7

From 11 to 13 GW: Early Morphological Examination

Fig. 2.5 Fourth ventricle: histology at 13 gw (coronal sections) V4 intracerebral transluscency,

From 14 to 16 GW: Morphological Examination

Fig. 2.6 (continued)

Fig. 2.7 Corresponding specimens and histology at 15 gw

At 14 weeks, the fourth ventricle is clearly visible (yellow arrow).

From 18 to 20 GW: Morphological Examination

Fig. 2.9 (continued)

Fig. 2.11 (continued)

Fig. 2.12 Corresponding ultrasound images and fetal pathology specimens at 18 gw

Fig. 2.13 Fetal pathology specimen at 18 gw

Fig. 2.14 Fetal pathology specimen at 20 gw: coronal section

From 21 to 23 GW: Morphological Examination

Fig. 2.16 (continued)

Fig. 2.17 Fetal pathology specimen: axial section at 21 gw

Fig. 2.18 Fetal pathology specimen: coronal section

Fig. 2.19 Fetal pathology specimen: sagittal section at 22 gw

In its recommendations, the Comité National Technique de l’Echographie (French

Figs. 2.20 and 2.21 Skull contours (yellow arrows): sutures

Fig. 2.23 Transfrontal

Fig. 2.26 Fetal pathology specimen: anterior complex

Fig. 2.27 False septal cavity

Fig. 2.28 Cavum of the septum pellucidum in three planes (*)

Cavum of the Septum Pellucidum

Posterior Fossa and Cerebellum

• Visualization of the choroid plexuses and the third ventricle

• Choroid plexuses, third ventricle:

Fig. 2.30 (continued)

Fig. 2.31 Fetal pathology

Fig. 2.33 Fetal pathology

Fig. 2.34 Central gray

Fig. 2.35 Histology at

Fig. 2.36 Cerebral aqueduct (white arrows)

Fig. 2.37 Measurement of

From 24 to 26 GW: Morphological Examination

Fig. 2.38 (continued)

Fig. 2.39 Macroscopic appearance at 24 gw

Fig. 2.40 (continued)

Fig. 2.41 Fetal pathology specimens: coronal sections at 26 gw

Fig. 2.42 Sylvian fissure operculization (dotted green arrows)

Fig. 2.45 Fetal pathology specimens at 26 gw

Sylvian fissure operculization (Figs. 2.42 and 2.43).