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Fabio Triulzi
Cristina Baldoli
Cecilia Parazzini
Andrea Righini

Perinatal
Neuroradiology
From the Fetus to
the Newborn

123

Perinatal Neuroradiology

Fabio Triulzi • Cristina Baldoli • Cecilia Parazzini
Andrea Righini

Perinatal Neuroradiology
From the Fetus to the Newborn

Fabio Triulzi
Department of Neuroradiology
Fondazione IRCCS Cà Granda
Ospedale Maggiore Policlinico
Milan
Italy
Cristina Baldoli
Department of Neuroradiology
IRCCS Ospedale San Raffaele
Milan
Italy

Cecilia Parazzini
Department of Radiology and Neuroradiology
Children’s Hospital V. Buzzi
Milan
Italy
Andrea Righini
Department of Radiology and Neuroradiology
Children’s Hospital V. Buzzi
Milan
Italy

ISBN 978-88-470-5324-3
ISBN 978-88-470-5325-0
DOI 10.1007/978-88-470-5325-0

(eBook)

Library of Congress Control Number: 2015956387
Springer Milan Heidelberg New York Dordrecht London
© Springer-Verlag Italia 2016
This work is subject to copyright. All rights are reserved by the Publisher, whether the whole or part of the material is
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The publisher, the authors and the editors are safe to assume that the advice and information in this book are believed
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Printed on acid-free paper
Springer-Verlag Italia Srl. is part of Springer Science+Business Media (www.springer.com)

Preface

This book originates from a very simple observation: for neuroradiologists which take care of
neonatal brain, knowledge of what happens to the fetal brain, regarding both physiology and
pathology, is essential to better understanding brain neonatal diseases. Nonetheless it is virtually impossible to assess the fetal brain by means of MRI without an appropriate knowledge of
neonatal brain diseases.
Therefore, “prenatal and neonatal worlds” cannot be separated from both conceptual and
practical point of view, but they should be studied together as a natural continuum regarding
normal and pathological brain development.
From these considerations arises the subtitle: “from the fetus to the newborn”. This is not a
classical and exhaustive textbook, but more properly a collection of cases organized in a systematic way, so as to follow, from midgestation until birth, the fate of brain anomalies, highlighting how they may change during the course of gestation and how it may be difficult to
predict how a lesion will eventually appear.
The cases are organized in a systematic index covering the most important prenatal and
postnatal brain diseases from the congenital genetic based to the acquired ones. Some conditions are not treated, because still predominantly better assessed by ultrasound, such as malformations of the spine or, extremely rare, such as prenatal metabolic or neoplastic brain diseases.
Together with fetal and neonatal MR cases, high-resolution images of fetal MR autopsy cases
are presented, either as a reference for normal anatomy or as a gross pathologic confirmation
of a previous fetal MR.
Milan, Italy

Fabio Triulzi
Cristina Baldoli
Cecilia Parazzini
Andrea Righini

v

Acknowledgements

This book could not have been concluded successfully without the support and collaboration
of many people.
Special thanks go to our colleagues, gynaecologists, neonatologists and pathologists of our
Institutions, Children’s Hospital V. Buzzi, Policlinico Maggiore Hospital and San Raffaele
Hospital in Milan.
We are grateful to our MRI technicians which strongly collaborated to guarantee the high
quality of MR studies and showed an enormous patience and empathy with small patients,
expectant mothers and parents.
Thanks to the parents and to the families for allowing the publication of the images, understanding the meaning and the importance of scientific divulgation.
Finally thanks to everyone who we could not mention but who are in our hearts as a source
of inspiration and motivation.
Milan, Italy

Fabio Triulzi
Cristina Baldoli
Cecilia Parazzini
Andrea Righini

vii

Contents

1

Normal Development . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1
Fabio Triulzi, Elisa Scola, and Sabrina Avignone
1.1 Fetal MR Autopsy Technique . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1
1.2 Fetal Anatomy on MR Autopsy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1
1.3 From the Fetus to the Newborn: In Vivo Anatomy . . . . . . . . . . . . . . . . . . . . . . . . 2
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 77

2

Normal and Abnormal Forebrain Commissures . . . . . . . . . . . . . . . . . . . . . . . . . . . 79
Fabio Triulzi, Cristina Baldoli, Cecilia Parazzini, and Andrea Righini
2.1 Commissure Development . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 79
2.1.1 Anterior Commissure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 80
2.1.2 Hippocampal Commissure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 80
2.1.3 Corpus Callosum . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 81
2.1.4 Corpus Callosum Development on Fetal MR
and Fetal MR Autopsy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 83
2.2 Commissure Malformations. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 83
2.2.1 Complete Commissural Agenesis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 83
2.2.2 Partial Commissural Agenesis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 84
2.2.3 Lipomas of the Corpus Callosum and Interhemispheric Cysts . . . . . . . . 84
2.3 Septum Pellucidum Anomalies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 86
2.4 Holoprosencephaly . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 88
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 107

3

Posterior Fossa Malformations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 109
Fabio Triulzi, Cristina Baldoli, Cecilia Parazzini,
Özgur Öztekin, and Andrea Righini
3.1 Fetal Cerebellar Anatomy and Development . . . . . . . . . . . . . . . . . . . . . . . . . . .
3.2 Classification of Posterior Fossa Malformations . . . . . . . . . . . . . . . . . . . . . . . .
3.2.1 Anomalies of CSF Spaces . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3.2.2 Predominantly Cerebellar Malformations . . . . . . . . . . . . . . . . . . . . . . .
3.2.3 Cerebellar and Brainstem Malformations . . . . . . . . . . . . . . . . . . . . . . .
3.2.4 Predominantly Brainstem/Midbrain Malformations? . . . . . . . . . . . . . .
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

4

109
110
111
118
125
127
138

Malformations of Cortical Development . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 141
Cecilia Parazzini and Fabio Triulzi
4.1 Classification . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 141
4.2 Malformations Secondary to Abnormal Neuronal and Glial
Proliferation or Apoptosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 141
4.2.1 Congenital Microcephaly . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 141

ix

x

Contents

4.2.2
4.2.3

Megalencephaly . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Cortical Dysgenesis with Abnormal Cell Proliferation
(Without Neoplasia) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
4.3 Malformations due to Abnormal Cortical Migration . . . . . . . . . . . . . . . . . . . . .
4.3.1 MCD with Neuroependymal Abnormalities:
Periventricular Heterotopia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
4.3.2 MCD due to Generalized Abnormal Transmantle
Migration Lissencephaly/Subcortical Band
Heterotopia (LIS/SBH) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
4.3.3 MCD Presumably due to Localized Abnormal Late Radial
or Tangential Transmantle Migration–Subcortical Heterotopia . . . . . .
4.3.4 MCD due to Abnormal Terminal Migration and Defects
in Pial Limiting Membrane: Cobblestone Malformations . . . . . . . . . . .
4.4 Malformations due to Abnormal Postmigrational Development . . . . . . . . . . . .
4.4.1 MCD with Polymicrogyria (PMG) or Cortical Malformations
Resembling PMG . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
4.4.2 Cortical Dysgenesis Secondary to Inborn Error of Metabolism . . . . . .
4.4.3 Focal Cortical Dysplasia due to Late
Developmental Disturbances . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
5

142
145
145

148
150
151
153
153
156
156
163

Malformations of the Eye and Orbit . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 165
Chiara Doneda and Fabio Triulzi
5.1 Embryology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
5.2 Biometric/Morphometric Assessment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
5.3 Hypotelorism and Hypertelorism. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
5.4 Anophthalmia. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
5.5 Microphthalmia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
5.6 Buphthalmos . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
5.7 Optic Nerve Head Coloboma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
5.8 Microphthalmos with Cyst. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
5.9 Congenital Cystic Eye . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
5.10 Persistent Hyperplastic Primary Vitreous . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
5.11 Optic Nerve Aplasia and Hypoplasia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
5.12 Dacryocystocele . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
5.13 Congenital Nonvascular Tumors of the Orbit . . . . . . . . . . . . . . . . . . . . . . . . . .
5.14 Capillary Hemangioma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

6

142

165
165
167
167
170
172
172
173
175
175
178
179
180
180
187

Vascular Malformations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 189
Cristina Baldoli, Silvia Pontesilli, Roberta Scotti, and Fabio Triulzi
6.1 Dural Sinus Malformations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 189
6.2 Vein of Galen Aneurysmal Malformation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 191
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 198

7

Ventriculomegaly. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 201
Elisa Scola and Fabio Triulzi
7.1 Diagnosis of Fetal Ventriculomegaly with Ultrasound
and Magnetic Resonance Imaging . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 201
7.2 Etiology-Based Classification . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 202
7.3 Ventriculomegaly and Associated Structural Abnormalities . . . . . . . . . . . . . . . 206

Contents

xi

7.4 Role of MRI in Ventriculomegaly Assessment . . . . . . . . . . . . . . . . . . . . . . . . .
7.5 When to Perform MR Examination . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
7.6 Outcome of Fetal Ventriculomegaly . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
8

Congenital Infections . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 221
Fabio Triulzi, Chiara Doneda, Cecilia Parazzini, and Andrea Righini
8.1 Cytomegalovirus Infection . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
8.2 Toxoplasmosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
8.3 Rubella Infection . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
8.4 HIV Infection and Parvovirus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
8.5 Herpes Virus Infection . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

9

221
228
229
230
230
235

Focal and Multifocal Ischemic/Hemorrhagic Lesions . . . . . . . . . . . . . . . . . . . . . . 237
Andrea Righini and Fabio Triulzi
9.1 Ischemic Lesions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
9.1.1 Focal Ischemic Lesions on Arterial Basis . . . . . . . . . . . . . . . . . . . . . . .
9.1.2 Focal Ischemic and Ischemic–Hemorrhagic Lesions
on Venous Side Basis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
9.2 Hemorrhagic Lesions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
9.2.1 Focal Cerebral Hemorrhagic Lesions . . . . . . . . . . . . . . . . . . . . . . . . . .
9.2.2 Focal Cerebellar Hemorrhagic Lesions . . . . . . . . . . . . . . . . . . . . . . . . .
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

10

208
209
210
219

237
237
239
239
239
242
252

Twin to Twin Transfusion Syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 255
Claudia Cinnante, Fabio Triulzi, and Andrea Righini
10.1 Clinical and Pathophysiological Background . . . . . . . . . . . . . . . . . . . . . . . . . 255
10.2 Fetal and Postnatal MRI. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 256
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 261

Contributors

Sabrina Avignone Department of Neuroradiology, Fondazione IRCCS Cà Granda,
Ospedale Maggiore Policlinico, Milan, Italy
Claudia Cinnante Department of Neuroradiology, Fondazione IRCCS Cà Granda,
Ospedale Maggiore Policlinico, Milan, Italy
Chiara Doneda Department of Radiology and Neuroradiology, Children’s Hospital V.
Buzzi, Milan, Italy
Özgur Öztekin Department of Radiology, Tepecik Education and Research Hospital,
Izmir, Turkey
Silvia Pontesilli Department of Neuroradiology, IRCCS Ospedale San Raffaele, Milan, Italy
Elisa Scola Department of Neuroradiology, Fondazione IRCCS Cà Granda, Ospedale
Maggiore Policlinico, Milan, Italy
Roberta Scotti Department of Neuroradiology, IRCCS Ospedale San Raffaele, Milan, Italy

xiii

Normal Development

1

Fabio Triulzi, Elisa Scola, and Sabrina Avignone

Fetal MR imaging covers a relatively long period of the fetal
brain development: from approximately 18–19 gestational
weeks (GW) until birth. Therefore, at present, it is possible
to study more than a half of the entire gestational period by
this technique.
Different authors and most of all, Catherine Garel, have
reviewed systematically the normal development of the fetal
brain as it appears on the MR images and reported normal
biometrics curves as measured by MRI; gyration and myelination process has been extensively reported as well [1–6].
Here we present the fetal brain normal anatomy by means
of MRI, with particular focus on the crucial period between
19 and 22 GW, taking into account the high-resolution
images of MR autopsy (Fig. 1.1) as reference guideline to
interpret the low-resolution fetal MR images.

1.1

however be noted that even though cooling may preserve fetal
brain from autolysis, it nevertheless decreases the T1 and T2
contrast between tissues [9], and of course postmortem imaging cannot be considered the same as clinical imaging in a
living being. The absence of blood pressure can change the
shape of vessels and of the brain, resulting for example in a
kinking of the brainstem. The vaginal delivery may cause
deformation of skull and brain as well. Blood elements sediment and intravascular clots may finally occur [10].
To obtain a reasonable compromise between acquisition
time in a clinical setting and spatial resolution, the total
acquisition time of a fetal MR autopsy is approximately
80 min by using a 3.0 T magnet. The T2-weighted images
shown in this chapter are obtained applying a turbo spinecho sequence (TR 6500 ms; TE 120 ms; FA 90°; NEX 4,
acquisition time 20 min.); the voxel size was 0.3 × 0.3 × 1.2
mm, equal to a true spatial resolution of 0.10 mm3 (100 nl).

Fetal MR Autopsy Technique

In order to prevent postmortem tissue autolysis, fetal MR
autopsy studies were carried out within 24 h from death, without any fixation, in an intact fetus conserved in a refrigerator at
4–5°C prior to MR examination. The fetuses with spontaneous death in utero were not considered due to their long permanence at body temperature that accelerates the autolysis.
To obtain comparable images with the in vivo study, it is
important to preserve the natural tissue contrast on T1 and
T2-weighted images. The standard fixation with formalin
causes a marked tissue dehydration and a modification of T1
and T2 contrast [7, 8]. On the contrary, an MR study performed within approximately 24–28 h from death without
any fixation and with the fetal brain in situ, allows to maintain
the normal contrast differences between tissues. It should

F. Triulzi (*) • E. Scola • S. Avignone
Department of Neuroradiology,
Fondazione IRCCS Cà Granda, Ospedale Maggiore Policlinico,
Milan, Italy
e-mail: fabio.triulzi@policlinico.mi.it

1.2

Fetal Anatomy on MR Autopsy

On the T2-weighted images of the fetal MR autopsy with spatial resolution of 100 nl, not only the three layers usually recognizable on in vivo fetal MR are visible, but also layer number
1, the marginal layer (Fig. 1.2), and, at least between 19 and 28
GW, a thin hypointense layer in the most external part of the
subplate (Fig. 1.3). According to Kostovic et al., this thin layer
could represent thalamocortical axons in the superficial layer
of subplate that are waiting to enter the cortical plate [11], but
at present, no correlation between these images and corresponding pathological specimens is available.
If we compare the single-shot T2-weighted images of the
in vivo fetal MR (Fig. 1.4) with the turbo spin-echo
T2-weighted images of the fetal MR autopsy (Fig. 1.5), we
can highlight some changes in tissue contrast in the period
between 19 and 22 GW that are barely visible on in vivo
studies. Between 19 and 20 GW, the internal capsule and in
particular the posterior limb of the internal capsule (PLIC) is
clearly more hypointense than surrounding lentiform nuclei

© Springer-Verlag Italia 2016
F. Triulzi et al., Perinatal Neuroradiology: From the Fetus to the Newborn, DOI 10.1007/978-88-470-5325-0_1

1

2

1 Normal Development

and thalami (Figs. 1.5, 1.6, 1.7, 1.8, 1.9, 1.10, 1.11, 1.12,
1.13, and 1.14); this is of course not due to the presence of
myelin, it develops later in the last phase of gestation, but
probably to the differences in contrast between the relatively
compacted unmyelinated fibers and the relatively poor synapse density of the basal ganglia and thalami. Starting from
21 to 22 GW, the anterolateral aspect of the thalami before
and the mesial part of the lentiform nuclei shortly after, begin
to decrease their signal intensity on T2-weighted images and
consequently PLIC becomes scarcely visible (Figs. 1.15,
1.16, 1.17, 1.18, 1.19, 1.20, 1.21, 1.22, 1.23, 1.24, 1.25, 1.26,
1.27, 1.28, and 1.29).
The posterior part of the thalami is particularly hyperintese on T2-weighted images at 19–21 GW; sometimes, this
aspect can be misinterpreted as a lesion on the in vivo fetal
images (Figs. 1.8h and 1.10f).
The maximum contrast between the intermediate zone and
the subplate is reached at 19–20 GW (Figs. 1.8, 1.10, 1.12,
and 1.14) and then rapidly decreases. At 28 GW the periventricular areas, and notably in the peritrigonal regions, are
clearly more hyperintense on T2-weighted images than the
surrounding parenchyma. At this stage, the classical threelayers aspect is no more detectable, and the subplate seems to
be formed by thin different layers (Figs. 1.30, 1.31, and 1.32).

1.3

From the Fetus to the Newborn:
In Vivo Anatomy

As previously reported, the fetal in vivo development was
extensively reviewed in different articles and books; it should
however be noted that the obstacle to an accurate and reliable
brain MR imaging in vivo during fetal life is not only related
to the poor spatial resolution but also to the poor contrast
resolution. The T2-weighted sequences typically used in

fetal MR imaging are single-shot fast spin-echo or steadystate free precession 2D or 3D acquisitions both with a significant decrease of contrast resolution if compared with a
turbo spin-echo sequence. This concept appears clear in the
direct comparison between in vivo and ex vivo fetal MR
images and also looking at the fetal MR in vivo imaging of
the late gestation period (Figs. 1.33, 1.34, 1.35, and 1.36). In
the case of Figs. 1.35 and 1.36, the spatial resolution is proportionally better than in the midgestation cases, but if we
compare the contrast resolution of the single-shot fast spinecho sequence of this fetal case with the T2-weighted image
obtained with the traditional turbo or fast spin echosequence
in the normal newborn (Fig. 1.37), the differences in contrast are quite obvious.
Modern MR imaging in newborns can at present take
more advantage by the progressive widespread use of 3.0
T. Without relevant reduction of contrast resolution, the
increase of signal-to-noise ratio of 3.0 T allows to significantly increase spatial resolution in a affordable acquisition
time. The increase in tissue border definition and the overall
better anatomical depiction in comparison with the 1.5 T
magnet are well appreciable in Figs. 1.37 and 1.38.
It is well known how T1 relaxation time is influenced by
the magnetic field and how tissues differences can be reduced
at high field strength [12]; however, at 3.0 T, it has been demonstrated how the 3D T1-weighted sequence can maintain an
optimal contrast resolution even in neonatal brain imaging
[13]. Moreover, the increase in signal-to-contrast ratio can
further reduce the size of the isotropic vowel even under the
cubic millimeter, allowing extremely detailed reformatted
images (Figs. 1.39. 1.40, 1.41, and 1.42). Normal anatomy
and myelination obtained by in vivo MR in the newborns
have been also extensively reviewed in different articles
[14–16] and book chapters [17, 18], please refer to the figure
legends for a detailed description.

1.3

From the Fetus to the Newborn: In Vivo Anatomy

a

3

b

Fig. 1.1 Fetal MR autopsy. Normal brain at 22 gestational weeks (GW) (a) and 21 GW (b) on T2-weighted images. Voxel size 100 nl.

a

b

c

d

Fig. 1.2 Marginal zone on fetal MR autopsy (22GW). Layer I or marginal zone is detectable on fetal MR autopsy with a voxel size of 100 nl
(arrows a, b). Correspondent histologic section stained with hematoxy-

lin–eosin (c) and closeup view on marginal zone shows a large Cajal–
Retzius cell (black arrow) (d) (courtesy C. Frassoni, Neurological
Institute C. Besta, Milan)

4

1 Normal Development

19 GW

20 GW

21 GW

Fig. 1.3 A diffuse T2 hypointense layer on the more external part of
subplate is recognizable on fetal MR autopsy between 19 and 28 GW
(arrows). According to Kostovic et al., it could represent thalamocorti-

22 GW

28 GW

cal axons in the superficial layer of subplate that are waiting to enter the
cortical plate

1.3

From the Fetus to the Newborn: In Vivo Anatomy

18.2

21.4

26.4

5

19.6

22.3

27.6

20.2

24

21

25.2

30

32.2

Fig. 1.4 Normal fetal brain development according to fetal MR. Twelve selected cases from 18.2 to 32.2 GW, axial T2-weighted images passing
approximately through the thalamus. For the acquisition technique, see the text

6

19 GW

22 GW

1 Normal Development

20 GW

21 GW

28 GW

Fig. 1.5 Fetal MR autopsy. Normal cases at 19, 20, 21, 22, and 28 GW, representative axial T2-weighted images passing through the thalamus.
Voxel size 100 nl. For the acquisition technique, see the text; all the cases are studied within 24 hours from termination of pregnancy (TOP)

1.3

From the Fetus to the Newborn: In Vivo Anatomy

Fig. 1.6 Fetal MR, normal brain at 18.2 GW. Fetal MR is usually not
performed before 19 GW. The fetal brain size is too small and the fetal
movement is more pronounced. In this case, the parenchymal thickness

7

is still relatively thin in comparison to the ventricular size (top row). T2
signal contrast differences between cortical plate, subplate, and intermediate zone are however already appreciable (bottom row)

8

1 Normal Development

Fig. 1.7 Fetal MR, normal brain at 19.6 GW, axial sections. At this age, the main brain mantle layers, including germinal matrix, are usually well
documented. Brain opercularization is going to become evident even though the surface of the brain is still substantially smooth

1.3

From the Fetus to the Newborn: In Vivo Anatomy

a
Fig. 1.8 Fetal MR autopsy, normal brain at 19 GW, axial sections with
correspondent fetal MR in vivo axial sections. Even without an appreciable myelination, corticospinal tracts are recognizable as relatively
T2 hypointense bilateral symmetric areas in the most antero-mesial part
of the medulla oblongata (dotted arrow a) and as a small oval areas in
the anterior pons (dotted arrow b). Similarly, the posterior limb of the
internal capsule is already present, and even without myelin, the fibers
appear as relatively hypointense structure with respect to the basal ganglia and thalamus (arrows g–h). The posterior part of the thalami,
mainly represented by the pulvinar, is relatively hyperintense on
T2-weighted images (asterisk g–h). Cerebellar hemispheres are still

9

b
small, but dentate nuclei are already visible (b arrow). Eye globes show
the typical immature aspect with an irregular oval morphology (c).
Germinal matrix is clearly visible as the thick most hypointense layer
along the median portion of the lateral ventricles, adiacent to the forming basal ganglia (g–k). Temporal lobes opercularization is going to be
visible (d–h). The three major layers, cortical plate, subplate, and intermediate zone, are easily visible; marginal zone or layer I is also visible
as well as the hypointense layer in the outer part of the subplate, likely
to be compatible with thalamocortical axons. The irregular indentations of cortical plate at the level of frontal lobes are postmortem artifacts (f–l)

10

c
Fig. 1.8 (continued)

1 Normal Development

d

1.3

From the Fetus to the Newborn: In Vivo Anatomy

e
Fig. 1.8 (continued)

11

f

12

1 Normal Development

*

g
Fig. 1.8 (continued)

h

*

1.3

From the Fetus to the Newborn: In Vivo Anatomy

i
Fig. 1.8 (continued)

13

j

14

k
Fig. 1.8 (continued)

1 Normal Development

l

1.3

From the Fetus to the Newborn: In Vivo Anatomy

15

Fig. 1.9 Fetal MR, normal brain at 19.6 GW, coronal sections. On coronal section, the ongoing process of opercularization is better seen. Pituitary
stalk is usually recognizable; the three major layers are clearly visible

16

a
Fig. 1.10 Fetal MR autopsy, normal brain at 19 GW, coronal sections
with correspondent fetal MR in vivo coronal sections. Corticospinal
tracts and the posterior limb of the internal capsule are visible in (c) and
(d) (arrows), again as a slight hypointense tracts. Dentate nuclei are
visible in (arrow g). Germinal matrix is clearly visible also in coronal
section, both around temporal horns and laterally to the body o the lateral ventricles (a–f). Temporal lobes opercularization together with the
developing hippocampus is visible in (b–f). The three major layers, cor-

1 Normal Development

b
tical plate, subplate, and intermediate zone, are easily visible (a–h);
marginal zone or layer I is also visible as well as the hypointense layer
in the external part of the subplate, probably compatible with thalamocortical axons. Pituitary stalk together with a marked hypointense pituitary is visible in (a). The irregular indentations of cortical plate at the
level of frontal lobes are postmortem artifacts (a–d)

1.3

From the Fetus to the Newborn: In Vivo Anatomy

c
Fig. 1.10 (continued)

17

d

18

e
Fig. 1.10 (continued)

1 Normal Development

f

1.3

From the Fetus to the Newborn: In Vivo Anatomy

g
Fig. 1.10 (continued)

19

h

20

1 Normal Development

Fig. 1.11 Fetal MR, normal brain at 20.2 GW, axial sections with FOV of 20 × 12 cm. Parenchymal thickness is progressively increasing. The
three major layers are clearly visible

1.3

From the Fetus to the Newborn: In Vivo Anatomy

a
Fig. 1.12 Fetal MR autopsy, normal brain at 20.2 GW, axial sections
with correspondent fetal MR in vivo axial sections. In comparison with
Fig. 1.8, a little increase of opercularization is visible; all the other features are quite similar. The dentate nuclei are visible in (a) and the three

21

b
major layers in (b) to (h). The internal capsule is still hypointense with
respect to the basal ganglia (arrows, e, f). Some minor irregular indentations of cortical plate at the level of frontal lobes due to postmortem
artifacts are visible also in this case (c–h)

22

c
Fig. 1.12 (continued)

1 Normal Development

d

1.3

From the Fetus to the Newborn: In Vivo Anatomy

e
Fig. 1.12 (continued)

23

f

24

g
Fig. 1.12 (continued)

1 Normal Development

h

1.3

From the Fetus to the Newborn: In Vivo Anatomy

25

Fig. 1.13 Fetal MR, normal brain at 20.2 GW, coronal sections with FOV of 20 × 12 cm. As for Fig. 1.9 on coronal section, the ongoing process
of opercularization is better visible. Pituitary stalk is recognizable, as well as a normal cochlea; the three mayor layers are clearly visible

26

a
Fig 1.14 Fetal MR autopsy, normal brain at 20.2 GW, coronal sections
with correspondent fetal MR in vivo coronal sections. In comparison
with Fig 1.9, a little increase of opercularization is visible; all the other
features are quite similar. On (a), olfactory bulbs are clearly visible.

1 Normal Development

b
Some minor irregular indentations of cortical plate at the level of frontal
lobes due to postmortem artifacts are visible also in this case (a, b). The
germinal matrix and the three major layers are still very well evident
(a–h)

1.3

From the Fetus to the Newborn: In Vivo Anatomy

c
Fig. 1.14 (continued)

27

d

28

e
Fig. 1.14 (continued)

1 Normal Development

f

1.3

From the Fetus to the Newborn: In Vivo Anatomy

g
Fig. 1.14 (continued)

29

h

30

1 Normal Development

Fig 1.15 Fetal MR, normal brain at 21 GW, axial sections with FOV of 20 × 12 cm. The three major layers are clearly visible. No significant
changes compared to Fig. 1.11

1.3

From the Fetus to the Newborn: In Vivo Anatomy

Fig 1.16 Fetal MR, normal brain at 21,4 GW, axial sections with FOV
of 20 × 12 cm. A subtle increase in parenchymal thickness compared to
Fig. 1.15 seems to be visible. Generally, it does not mean necessarily
this increase represents the expected increase of brain parenchymal

31

thickness in 4 days; of course GW datation is never so precise, but in
any case, it must be take into account how the brain parenchyma can
grow very rapidly around this gestational age

32

a
Fig. 1.17 Fetal MR autopsy, normal brain at 21 GW, axial sections
with corresponding fetal MR in vivo axial sections. The dentate nuclei
with a relative hyperintense hilum are visible in (a). A further little
increase of opercularization in comparison with Fig. 1.12 seems to be
visible (c–f). The anterior part of the internal capsule is still relatively
hypointense compared to the basal ganglia, whereas the posterior part

1 Normal Development

b
of the internal capsule is now partly confounded with the growing
hypointensity of the central part of the thalami (arrows, e); all the other
features are quite similar to the previous cases. Some minor irregular
indentations of cortical plate at the level of frontal lobes due to postmortem artifacts are visible also in this case (b–h)

1.3

From the Fetus to the Newborn: In Vivo Anatomy

C
Fig. 1.17 (continued)

33

d

34

e
Fig. 1.17 (continued)

1 Normal Development

f

1.3

From the Fetus to the Newborn: In Vivo Anatomy

g
Fig. 1.17 (continued)

35

h


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