Diagnostic ultrasound ( PDFDrive )

1218 PART IV Obstetric and Fetal Sonography
TABLE 35.1 Spine Embryology During Third and Fourth Weeks After Conception
Menstrual Age
(Days)
Conceptual Age
(Days)
Embryo Length
(mm)
Sac Diameter
(mm)
Landmarks
31 17 0.5 2 Trilaminar disc
Notochordal process
Paraxial mesoderm (Fig. 35.1A)
35 21 2 4 Notochord
Neural plate
Somites (Fig. 35.1B)
42 28 5 10 Neural tube
Notochord
Sclerotome (Fig. 35.1C)
remnant corresponds to the nucleus pulposus of the intervertebral
discs. 11
Abnormalities of neural tube closure not only afect the spinal
cord and brain but also interfere with normal development of
surrounding vertebral arches, which are derived from adjacent
mesodermal somites. Disturbances of neural tube closure underlie
spina biida and anencephaly defects.
Caudal regression defects may be related to defective development
of the mesoderm layer in week 3 conceptual age, during
transformation of the germ disc from two layers (bilaminar) to
three layers (trilaminar). Various degrees of abnormal mesoderm
development account for the wide spectrum of abnormalities
found in caudal regression.
A failure of part of the neural tube to close, called spinal
dysraphism, disrupts development of the nervous system and
disrupts the induction of the overlying vertebral arches. he
resulting open vertebral canal is called spina biida. If dura and
arachnoid protrude from the spinal canal, the result is a meningocele.
If neural tissue and meninges protrude, the result is a
myelomeningocele. In the most severe NTDs, the neural tube
fails to form and fails to separate from the overlying ectoderm.
In the spine, this condition is called rachischisis or myeloschisis;
the open spinal cord is exposed along the dorsal surface of the
fetus. If the defect involves the cranial neural tube, the brain is
represented by an exposed dorsal mass of undiferentiated neural
tissue, called exencephaly, anencephaly, or craniorachischisis.
Diferentiated brain and meninges may bulge from a nonossiied
gap in the skull (meningoencephalocele), but this is not related
to failure of neural tube closure.
In animals, certain teratogens can induce NTDs: retinoic
acid, insulin, and high plasma glucose levels. In humans,
implicated factors include valproic acid (antiepileptic), maternal
diabetes, and hyperthermia. Valproic acid may interfere with
folate metabolism.
Ossiication of the Fetal Spine
Prenatal sonography readily portrays the ossiied portions of the
fetal spine, whereas the nonossiied cartilage is more diicult to
delineate. It is therefore important for sonographers and sonologists
to understand the temporal and spatial ossiication patterns
during fetal development in order to optimize spinal
evaluation.
Each vertebra will develop three ossiication centers: the
centrum, right neural process, and let neural process. 12 he
centrum will form the central part of the vertebral body, and
the neural process will form the posterolateral parts of the
vertebral body and pedicles, the transverse processes, the laminae,
and the articular processes.
Ossiication begins in the lower thoracic fetal spine at approximately
10 weeks’ gestation (menstrual age). 13 Ossiication of the
centra progresses in cranial and caudal directions simultaneously.
Neural arch ossiication proceeds caudally from the lower thoracic
(T) spine to the lumbar (L) spine. It proceeds sequentially from
L1 through L5 and then into the sacral (S) spine. By 13 weeks’
menstrual age, there are three ossiication centers in vertebrae
C1 through L3 14 (Fig. 35.2). Neural arch ossiication begins as
a small focus at the base of the transverse process and extends
simultaneously into the pedicle anteriorly and into the lamina
posteriorly (Fig. 35.3).
Ultrasound evaluation for spina biida usually occurs between
16 and 22 weeks’ gestation. By 16 weeks, there is enough ossiication
in the neural arches to assess for spina biida to level L5, 15
by 19 weeks to level S1, and by 22 weeks to level S2 (Figs. 35.4
and 35.5). In some fetuses, there may be enough neural arch
ossiication to assess for spina biida before these gestational
ages. Braithwaite et al. 16 assessed the fetal anatomy at 12 to 13
weeks’ gestation by a combination of transabdominal and
transvaginal sonography and reported successful examination
of the vertebrae and overlying skin in both the transverse and
the coronal plane in all cases. Others have reported successful
prenatal diagnosis of spina biida at 12 to 14 weeks’ gestation
on the basis of abnormal cranial indings. 17-19 hey caution that
although the characteristic cranial indings may be present at
11 to 14 weeks, the prevalence of these indings in the irst
trimester remains to be determined (Table 35.2). Furthermore,
closed NTDs are less likely to be associated with abnormal cranial
indings and therefore are more diicult to detect in the irst
trimester.
Normal Position of the Spinal Cord
For fetuses at 19 to 33 weeks’ gestation, the conus medullaris
is normally situated at level L2-L3 or higher (Fig. 35.6). Level
L3 is taken to be indeterminate and L3-L4 or lower as abnormal. 20
For those fetuses with tethered cord, the position of the conus