Introduction
Normal brain myelination is a process that begins during the fifth fetal month and continues in the postnatal brain. It has important implications in nor- mal brain development. The organized order of myelination emphasizes the role of imaging exami- nations of developmentally delayed children who of- ten show no structural brain alterations despite sus- picion of brain maturation delay. During the first months of life, the myelination process follows well- defined steps. Even the appearance of the normal fe- tal brain follows predictable steps. The timing of the appearance of the different sulci in the fetal brain is available using MR imaging. It is considered to be a good marker of fetal brain maturation. In general, in the postnatal brain the myelination progresses from caudal to cephalad and from dorsal to ventral. There- fore the occipital lobes myelinate before the frontal lobes and the dorsal brainstem does so before the ventral brainstem. The myelination progresses more rapidly in the functional areas used early in life. The myelination progresses rapidly during the two first years of life and slows markedly after that. MR imag- ing studies suggest that white matter myelination can be considered as an indicator of functional brain maturation. Myelination also progresses differently in compact (corpus callosum, internal capsule, cere- bral peduncle) than in non-compact (peripheral white matter and corona radiata) white matter. Al- though myelination is initially greater in compact white matter, the change in myelination may be greater in non-compact white matter during the first few years of infancy.
From the imaging point of view, brain maturation can be followed in both T1- and T2-weighted images, although it occurs at different rates in T1 and T2 im- ages. The newborn T1-weighted image is grossly sim- ilar to the adult T2-weighted image in that white mat- ter has lower signal intensity than gray matter. The overall appearance of the newborn brain on the T2-
weighted image is grossly similar to that of the adult on the T1-weighted image in that the white matter has higher signal intensity than the gray matter. The brain myelination reaches the adult appearance at the age of 2years. The only area that can still exhibit a persistent T2 hyperintensity on MR images at about 2years of age (and well beyond that) is considered to be the peritrigonal region, the so-called terminal zone. However, a persistent T2 hyperintensity has been noted in the frontotemporal subcortical regions beyond that age in normal children suggesting, that the so-called terminal zones are subcortical areas rather than the peritrigonal area. The terminal zones do not stain for myelin until the fourth decade of life.
Persistent T2 hyperintensity may be seen until the second decade in these areas. Complete myelination takes place by about age 3years in the subcortical re- gions. It is important to differentiate the terminal ar- eas from white matter injury, such as periventricular leukomalacia.
Diffusion images and ADC maps give the same in- formation: in both the signal intensity is proportion- al to water diffusion only. On DW images of the neonatal brain there is marked contrast between the hyperintense gray matter and the hypointense white matter. This contrast is more marked in premature neonates than in term neonates. The ventrolateral thalami of the newborn stand out on DW image and should not be misinterpreted as pathological restrict- ed diffusion in the neonatal brain. It becomes pro- gressively less hyperintense until the age of 4 months when it is isointense to the rest of the gray matter. As the brain matures, the contrast between the gray and white matter diminishes.
Normal Brain Myelination
and Normal Variants
Suggested Reading
1. Carmody DP, Dunn SM, Boddie-Willis AS, DeMarco JK, Lewis M (2004) A quantitative measure of myelination de- velopment in infants, using MR images. Neuroradiology 8 Jul (Epub ahead of print) DOI: 10.1007/s00234-004-1241-z 2. McGraw P, Liang L, Provenzale JM (2002) Evaluation of normal age-related changes in anisotropy during infancy and childhood as shown by diffusion tensor imaging. AJR Am J Roentgenol 6:1515–1522
3. Parazzini C, Baldoli C, Scotti G, Triulzi F (2002) Terminal zones of myelination: MR evaluation of children aged 20–40 months. AJNR Am J Neuroradiol 10:1669–1673
Chronological Imaging Atlas of Normal Myelination
Figures1.1 to 1.8 illustrate the process of normal
myelination starting with a fetus aged 28weeks and
ending with a normal pattern in a 7-year-old. We
have included MR spectroscopy for all cases avail-
able.
Figure 1.1
28 gestational week fetus (courtesy Susan Blazer, M.D.)
T2-weighted image.
Medulla
T2-weighted image.
Pons
T2-weighted image.
Midbrain
T2-weighted image.
Basal ganglia
A B C D
T2-weighted image.
Sylvian fissure level
T2-weighted image.
Centrum semiovale
E F G H
I
M N
J K L
Figure 1.2 17-day-old male
T1-weighted image.
Posterior fossa
T1-weighted image.
Suprasellar cistern
T1-weighted image.
Basal ganglia
T1-weighted image.
Centrum semiovale
MR spectroscopy. TE=144 ms MR spectroscopy. TE=35 ms
A B C D
T2-weighted image.
Posterior fossa
T2-weighted image.
Suprasellar cistern
T2-weighted image.
Basal ganglia
T2-weighted image.
Centrum semiovale
E F G H
DW image.
Posterior fossa
DW image.
Suprasellar cistern
DW image.
Basal ganglia
DW image.
Centrum semiovale I
M N
J K L
Figure 1.3
4-month-old female
T1-weighted image.
Posterior fossa
T1-weighted image.
Suprasellar cistern
T1-weighted image.
Basal ganglia
T1-weighted image.
Centrum semiovale
MR spectroscopy. TE=144 ms MR spectroscopy. TE=35 ms
A B C D
T2-weighted image.
Posterior fossa
T2-weighted image.
Suprasellar cistern
T2-weighted image.
Basal ganglia
T2-weighted image.
Centrum semiovale
E F G H
DW image.
Posterior fossa
DW image.
Suprasellar cistern
DW image.
Basal ganglia
DW image.
Centrum semiovale I
M N
J K L
Figure 1.4 6-month-old male
T1-weighted image.
Posterior fossa
T1-weighted image.
Suprasellar cistern
T1-weighted image.
Basal ganglia
T1-weighted image.
Centrum semiovale
MR spectroscopy. TE=144 ms MR spectroscopy. TE=35 ms
A B C D
T2-weighted image.
Posterior fossa
T2-weighted image.
Suprasellar cistern
T2-weighted image.
Basal ganglia
T2-weighted image.
Centrum semiovale
E F G H
DW image.
Posterior fossa
DW image.
Suprasellar cistern
DW image.
Basal ganglia
DW image.
Centrum semiovale I
M N
J K L
Coronal T2-weighted image O
Figure 1.5 10-month-old male
Contrast-enhanced T1-weighted image.
Posterior fossa
Contrast-enhanced T1-weighted image.
Suprasellar cistern
Contrast-enhanced T1-weighted image.
Basal ganglia
Contrast-enhanced T1-weighted image.
Centrum semiovale
MR spectroscopy. TE=144 ms MR spectroscopy. TE=35 ms
A B C D
T2-weighted image.
Posterior fossa
T2-weighted image.
Suprasellar cistern
T2-weighted image.
Basal ganglia
T2-weighted image.
Centrum semiovale
E F G H
DW image.
Posterior fossa
DW image.
Suprasellar cistern
DW image.
Basal ganglia
DW image.
Centrum semiovale I
M N
J K L
Figure 1.6 13-month-old male
T1-weighted image.
Posterior fossa
T1-weighted image.
Suprasellar cistern
T1-weighted image.
Basal ganglia
T1-weighted image.
Centrum semiovale
MR spectroscopy. TE=144 ms
A B C D
T2-weighted image.
Posterior fossa
T2-weighted image.
Suprasellar cistern
T2-weighted image.
Basal ganglia
T2-weighted image.
Centrum semiovale
E F G H
DW image.
Posterior fossa
DW image.
Suprasellar cistern
DW image.
Basal ganglia
DW image.
Centrum semiovale I
M
N
J K L
Figure 1.7
25-month-old female
Contrast-enhanced T1-weighted image.
Posterior fossa
Contrast-enhanced T1-weighted image.
Suprasellar cistern
Contrast-enhanced T1-weighted image.
Basal ganglia
Contrast-enhanced T1-weighted image.
Centrum semiovale
MR spectroscopy. TE=144 ms MR spectroscopy. TE=35 ms
A B C D
T2-weighted image.
Posterior fossa
T2-weighted image.
Suprasellar cistern
T2-weighted image.
Basal ganglia
T2-weighted image.
Centrum semiovale
E F G H
DW image.
Posterior fossa
DW image.
Suprasellar cistern
DW image.
Basal ganglia
DW image.
Centrum semiovale I
M N
J K L
Figure 1.8 7-year-old male
T1-weighted image.
Posterior fossa
T1-weighted image.
Suprasellar cistern
T1-weighted image.
Basal ganglia
T1-weighted image.
Centrum semiovale
MR spectroscopy. TE=144 ms
A B C D
T2-weighted image.
Posterior fossa
T2-weighted image.
Suprasellar cistern
T2-weighted image.
Basal ganglia
T2-weighted image.
Centrum semiovale
E F G H
DW image.
Posterior fossa
DW image.
Suprasellar cistern
DW image.
Basal ganglia
DW image.
Centrum semiovale I
M
N
J K L
Cavum Septi Pellucidi, Cavum Vergae and Cavum Velum Interpositum Cavum Septi Pellucidi and Vergae Clinical Presentation
A 21-month-old male with developmental delay.
Images (Fig. 1.9)
A. T2-weighted image shows cavum septi pellucidi between the frontal horns (arrow).
B. T2-weighted image shows cavum vergae between the bodies of the lateral ventricles (arrow) C. T1 FLAIR image. The CSF in the cavum follows
CSF signal in all sequences
Figure 1.9
Cavum septi pellucidi and vergae
A B C
Cavum Velum Interpositum Clinical Presentation
A 6-year-old female with headaches. Cavum is con- sidered as an incidental finding.
Images (Fig. 1.10)
A. T2-weighted image shows a triangular CSF space (arrow) between and below the fornices (arrow- heads) with its apex pointed anteriorly
B. FLAIR image reveals the signal intensity of the CSF inside the cavum to be near isointense to the ventricle CSF. This is due to different velocities of the CSF
C. Coronal SPGR image confirms the location of the cavum
A B
C
Figure 1.10
Cavum velum interpositum
Discussion
Cavum septi pellucidi is a CSF collection between the two leaves of the septum pellucidum posterior to the genu of the corpus callosum and anterior to the foramina of Monro. It is present in most fetuses and in 80% of term infants up to the age of 3months. Al- though until recently it was considered an incidental finding, cavum septi pellucidi is more commonly seen in pugilists and after a head trauma. Recently it has also been associated with schizophrenia. The in- creased prevalence of cavum septi pellucidi, cavum vergae and corpus callosum dysgenesis in schizo- phrenics supports the concept that abnormal devel- opment of the brain may play an important role in this disorder. These structures are closely related de- velopmentally to the limbic system, which has been implicated in the etiology of schizophrenia. The por- tion of the cavum septi pellucidi extending posterior to the fornices is known as the cavum vergae. It is rarely seen without cavum septi pellucidi. The cavum vergae is bordered posteriorly by the splenium of the corpus callosum, and superiorly by the body of the corpus callosum. Although it usually is an incidental finding, it may become very large and cause com- pression upon the foramina of Monro leading to hy- drocephalus.
Cavum veli interpositum is produced by an infold- ing of pia matter between the roof of the third ventri- cle and forniceal fibers. This CSF space between the pial layers is known as the cistern of the velum inter- positum and it contains the posterior medial choroidal arteries and the internal cerebral veins. On MR images and CT scan it appears as a triangular CSF space with its apex pointed anteriorly. When the cistern is very large it is called the cavum. The cavum lies below the fornices and above the internal cere- bral veins. It should not be confused with an arach- noid cyst or an epidermoid tumor that can be present is this region.
Suggested Reading
Chen CY, Chen FH, Lee CC, Lee KW, Hsiao HS (1998) Sono- graphic characteristics of the cavum velum interpositum.
AJNR Am J Neuroradiol 19:1631–1635
Degreef G, Lantos G, Bogerts B, Ashtari M, Lieberman J (1992) Abnormalities of the septum pellucidum on MR scans in first-episode schizophrenic patients AJNR Am J Neurora- diol 13:835–840
Ventriculus Terminalis Clinical Presentation
A 2-year-old girl was examined because of walking difficulties and suspicion of tethered cord.
Images (Fig. 1.11)
A. Sagittal T2-weighted image of the lumbosacral spine reveals normal location of the conus. It shows a large cystic dilatation in the conus B. Sagittal T2-weighted magnified image of the
conus shows again a smooth cystic dilatation that is hyperintense on T2-weighted image
C. On T1-weighted image the cyst follows the CSF signal
D. Axial T2-weighted image shows the central loca- tion of the ventriculus terminalis
Figure 1.11
Ventriculus terminalis
A D
B C
Discussion
The final stage of development of the distal spinal cord begins at about 38days of gestation. In this process the central lumen of the caudal neural tube decreases in size and the segment formed includes the conus, filum terminale and ventriculus termi- nalis. Thus the ventriculus terminalis is a cavity situ- ated at the conus medullaris enclosed by ependymal tissue and normally present as a virtual cavity or as a mere ependymal residue. In rare cases, and almost exclusively in children, the ventriculus terminalis may be wide enough to be visualized by imaging studies, such as MR imaging. It represents a transient finding in young children. On rare occasions, a cystic dilatation of the central conus medullaris may be seen and this is probably the result of a persistent ventriculus terminalis. Cystic dilatation is usually de- scribed in children in association with a tethered cord. However, an asymptomatic, localized dilatation of the ventriculus terminalis is considered a normal developmental phenomenon that can be seen on im- aging.
Suggested Reading
Celli P, D’Andrea G, Trillo G, Roperto R, Acqui M, Ferrante L (2002) Cyst of the medullary conus: malformative persist- ence of terminal ventricle or compressive dilatation? Neu- rosurg Rev 1/2:103–106
Coleman LT, Zimmerman RA, Rorke LB (1995) Ventriculus ter- minalis of the conus medullaris: MR findings in children.
AJNR Am J Neuroradiol 7:1421–1426
