various fetal cns anamolies described with ante nantal and postnatal imaging features of ultrasound, barium study CT and MRI in each entity with representative iamges

1. FETAL CENTRAL NERVOUS SYSTEM
ANOMALIES
MODERATOR- DR C N PRADEEP KUMAR SIR
PRESENTER- DR SUSHMITA

2. INTRODUCTION
• Central nervous system (CNS) anomalies are common and most devastating.
They occur in frequency of about 1.4 to 1.6 per 1000 live births but are seen in
about 3-6% of stillbirths.
• CNS develops from 3 to 20 weeks of intrauterine life. Almost all CNS anomalies
are result of the insult in embryogenesis at some point of development.
• Ultrasound can diagnose many CNS anomalies in first and early second trimester.
Some develop or become apparent in late pregnancy.
• Earlier is the detection more is the time available for the clinician and parents to
plan about the outcome of pregnancy.

3. INDUCTION
NEURAL TUBE FORMATION
HISTOGENESIS
PROLIFERATION AND MIGRATION
LOBULATION AND OPERCULIZATION
SULCATION AND GYRATION
MYELINATION

4. EMBRYOLOGY

7. NORMAL VARIANTS
• Cavum Veli Interpositi
• small cystic collection in the midline
• dilatation of the normal cistern of the velum
interpositum
• usually seen below the splenium of the corpus
callosum, behind the upper brainstem and above the
region of the pineal gland.

8. Choroid Plexus Cysts
• Only CPCs over 3 mm should be considered substantial enough to be termed
“choroid plexus cyst.”
• They are common and seen in 1% to 6% of foetuses between 14 and 24 weeks’
gestation.

9. Blake’s Pouch Cyst
• Cystic appearing structure that represents posterior ballooning of the inferior
medullary velum into the cisterna magna, below and posterior to the
vermis, that communicates with an open fourth ventricle.
• It is caused by a failure of the regression of Blake's pouch secondary to the
non-perforation of the foramen of Megendie.
• Transient structure that regresses[12Wks]

10. ERRORS OF DORSAL INDUCTION

11. Anencephaly
• Anencephaly occurs when the cephalic
portion of the neural tube fails to close
• Resulting in absence of the cranial vault,
cerebral hemispheres, & diencephalic
structures.
• Replaced by a flattened, amorphous
vascular-neural mass (area
cerebrovasculosa).
• Visible ossification of frontal bones may
not be apparent until 10 weeks -should
not be diagnosed before this gestational
age

13. Acrania - Anencephaly Sequence
Failure of normal migration of mesenchymal tissue
calvarium, muscles of scalp and dura fail to form (Acrania)
exposes brain to amniotic fluid with risk of friction with uterine wall,
placenta and fetal parts (exencephaly)
unprotected brain tissue undergoes progressive destruction and
degeneration due to mechanical and chemical trauma
complete or almost complete disappearance of the brain from 14 weeks'
gestation onward (Anencephaly)

14. USG
• No parenchymal tissue is seen above
the orbits and calvarium is absent: parts
of the occipital bone and mid brain
may be present
• If a small amount of neural tissue is
present, it is then termed
EXENCEPHALY
• A "frog eye" or "mickey mouse"
appearance .
• Polyhydramnios: due to impaired
swallowing.

15. Cephaloceles
Skull defects with herniations of
intracranial contents due to failure of
closure of normal diverticulation
• Types
• Meningoceles
• Meningoencephaloceles
• Atretic cephaloceles - parietal,
occipital
• Glioceles
• Since many are skin covered, MS-AFP
is elevated in only 33% compared with
spina bifida (62%) and anencephaly
(92%). This makes ultrasound the
primary diagnostic

16. Encephalocele
 Herniation of brain tissue through a defect in the cranium.
 Most occur in the midline - occipital (75%) or frontal.
 Can extend into the mouth, nasal, and sphenoid areas
 Isolated lesions / associated with other anomalies/ Chromosomal
abnormalities.
Meckel Gruber Syndrome, Walker Warburg Syndrome, Joubert Syndrome,
Trisomy 13/18, Dandy Walker Continuum, CVS Abnormalities, etc

17. A) Occipital encephalocele on axial view at 22 menstrual weeks shows brain tissue
(arrow) herniating through the occipital bony skull defect
B) (B) In another fetus, a small skull defect is seen with only meninges and no brain
tissue in this fetus with ventriculomegaly and meningocele.
C) Atretic Encephalocele

19. CHIARI MALFORMATIONS
Chiari I
– Downward displacement of the cerebellar tonsils, without displacement of the fourth ventricle
or medulla- Tonsillar Ectopia
-Tonsillar ectopia measuring ≥ 5 mm as sufficient to establish the diagnosis of CM1.
-Syringomyelia is present in 40-80% of individuals with symptomatic CM1.

20. Chiari II- Most common, almost universal association with
lumbar myelomeningocele.
• Myelomeningocele (almost always)
• Lacunar skull
• Small posterior fossa
• Abnormal dura (gaping FM, heart-shaped incisura,
fenestrated falx)
• Inferiorly displaced medulla, vermis lead to “cascade”
of tissue
• Cervicomedullary “kink,” medullary “spur”
• “Towering” and “creeping” cerebellum
• “Soda straw” 4th ventricle
• Prominent massa intermedia
• Hydrocephalus, shunted ventricles appear scalloped
• Callosal dysgenesis

21. CHIARI – II MALFORMATION

22. • Chiari III- Occipital/High cervical encephalomeningocele in which
the medulla, fourth ventricle, and virtually the entire cerebellum are
involved.
• Chiari IV- Cerebellar Hypoplasia without descent
• Chiari V- Absent cerebellum with herniation of occipital lobe through
foramen magnum

23. Errors of Ventral Induction

24. Holoprosencephaly
• Holoprosencephaly results from
incomplete cleavage of the
primitive forebrain into two
cerebral hemispheres.
• Axial views of the normal fetal
head in the first trimester have
the symmetric shape of a
butterfly including clear
demarcation of the midline.
• Absence of this butterfly sign is
seen in holoprosencephaly.

25. Alobar
Holoprosencephaly
• Failure of cleavage of the
prosencephalon which gives rise to
the cerebral hemispheres and
thalamus during early first
trimester (5-6 weeks)
• Single forebrain ventricle
• Absent midline structure
(interhemispheric fissure, olfactory
tracts, cavum septum and corpus
callosum)
• Non seperation of deep grey nuclei
• Dorsal cyst
Coronal view- shows fused thalamus capped by a single
hemisphere and underlying monoventricle.
There is no falx or interhemispheric fissure.

27. Facial anomalies
Extreme hypotelorism or even
cyclopia
Cebocephaly (a flat nose or a
nasal-like tubular appendix
[proboscis] with hypotelorism)
Ethmocephaly (extreme
hypotelorism with arhinia with
proboscis and median cleft palate).

28. Semilobar
Holoprosencephaly
• There is a single monoventricle but also
rudimentary development of falx and inter-
hemispheric fissure.
• Incomplete anterior hemisphere division
• Absent olfactory tracts and corpus
callosum
• Variable non seperation of deep gray
nuclei.

29. Lobar Holoproscencephaly
• Least severe form
• Fusion of the frontal horns of the lateral
ventricles with a wide communication
with the third ventricle.
• Fusion of the fornices
• Absence of septum pellucidum
• Unlike semilobar holoprosencephaly,
the falx is present, the interhemispheric
fissure is fully formed and
the thalami are not fused.

30. Septo-Optic Dysplasia
(SOD)
• Two cardinal pathologic features
define SOD:
• (1) Absence of the septum
pellucidum
• (2) Optic nerve hypoplasia.
• The major differential diagnosis
of SOD is well-differentiated
lobar holoprosencephaly. The
cerebral hemispheres and basal
ganglia are completely separated
in SOD

31. Hydranencephaly
• In hydranencephaly, the cerebral
hemispheres are completely or almost
completely missing. Instead, a
membranous sac filled with CSF, glial
tissue, and ependyma is present.
• The most important differential
diagnosis of hydranencephaly is severe,
“maximal” obstructive hydrocephalus
(OH). In severe OH (e.g., secondary to
aqueductal stenosis), a thin cortex can
be seen compressed against the dura
and inner table of the calvarium

32. DIFFERENTIAL DIAGNOSIS OF “WATER-BAG” BRAIN
Maximal” Obstructive Hydrocephalus
• Large head
• Thinned but normal cortex
• Massively enlarged ventricles Normal
horns
• Falx present
• Basal ganglia separated
Alobar Holoprosencephaly
• Small head
• Smooth or minimally sulcated brain •
“Horseshoe” monoventricle
• Absent falx, interhemispheric fissure
• Basal ganglia fused
“Open Lip” Schizencephaly
• Remnant “nubbins” of brain
• No cortex external to huge “open”
clefts
• Dysplastic cortex lines sides of open
cleft
• Falx, interhemispheric fissure present
• Basal ganglia separated

33. POSTERIOR FOSSA
MALFORMATIONS

35. • Fastigial point.
• Tegmento-vermian angle to about 10
degrees.
• the fastigium-declive line
• Nomograms are available for vermian
dimensions. Vermian fissures become visible
after about 18 weeks and can be used to help
determine normal vermis development.

36. DANDY-WALKER
MALFORMATION
Classic- Triad:
1. Cystic dilation of the fourth ventricle
communicating with a posterior fossa fluid
space
2. Elevated tentorium and high position of
the torcula- "lambdoid-torcular inversion
(confluence of the superior sagittal and
lateral venous sinuses)
3. Small, rotated, raised, or absent vermis

38. Vermis hypoplasia or dysplasia (Dandy-Walker Variant )
• Conspicuous cleft separating the
inferior parts of the cerebellar
hemispheres due to absence of
the lower part of vermis.
• Communication between the
fourth ventricle & cisterna
magna
• 4th ventricle -slightly to
moderately enlarged.
• Posterior fossa –normal size
• Small vermis but normal
cerebellar hemispheres.
• No associated hydrocephalus.

39. Megacisterna Magna
Enlargement of the cisterna magna
beyond 10 mm with normal vermis
 No mass effect on vermis or
cerebellum
Fluid crossed by veins, falx cerebelli.
Isolated finding, 97%-100% are normal.
The majority of non isolated cases have
ventriculomegaly, congenital infection,
or karyotype abnormalities, especially
trisomy 18.
When a large cisterna magna is found,
there should be a careful search for
other abnormalities

40. Arachnoid cyst
• Benign, non-communicating fluid
collections within arachnoid
membranes.
• Stable and require no surgical
treatment.
• They can occur intracranially and in
the spinal canal.
• No communication of the cyst with the
fourth ventricle.
• Normal fourth ventricle, vermis, and
cerebellum are displaced by the
arachnoid cyst.

41. Commissural and Cortical
Maldevelopment

42. ABNORMAL NEURONAL
PROLIFERATION OR
APOPTOSIS
Microcephaly
Megalencephaly
Hemimegalencephaly
ABNORMAL NEURONAL
MIGRATION
Classical Lissencephaly and subcortical band heterotopia
Cobblestone Lissencephaly and complex or congenital
muscular dystrophy
Heterotopia (periventricular nodular)
ABNORMAL CORTICAL
ORGANIZATION
Polymicrogyria
Schizencephaly
NOT OTHERWISE
CLASSIFIED
Secondary to inborn errors of metabolism
Peroxisomal disorders

43. HOLOPROSENCEPHALI
ES, RELATED
DISORDERS, AND
MIMICS
HOLOPROSENCEPHALY(LOBAR, SEMILOBAR,ALOBAR)
RELATED MIDLINE DISORDERS - SEPTO-OPTIC DYSPLASIA
HOLOPROSENCEPHALY MIMICS - HYDRANENCEPHALY

44. Malformations
Secondary to Abnormal
Neuronal Migration

45. Heterotopia
• Arrest of normal neuronal migration along the radial glial cells can result in grossly visible masses of
"heterotopic" gray matter.
• These collections come in many shapes and sizes and can be found virtually anywhere between the
ventricles and the pia.
• They can be solitary or multifocal and exist either as an isolated phenomenon or in association with other
malformations

46. • On MRI three types are described:
Periventricular Nodular Heterotopia,
Focal Subcortical Heterotopia, and Band
Heterotopia.
• Only the Periventricular nodules are readily
detectable on prenatal ultrasound and visible
as irregular lining of the ventricular surface
• DD- Subependymal nodules of tuberous
sclerosis which calcify.

47. LISSENCEPHALY
• The term lissencephaly (LIS) literally means "smooth brain."
• The spectrum ranges from severe (agyria) to milder forms, including abnormally
broad folds (pachygyria) or a heterotopic layer of gray matter embedded in the white
matter below the cortex (subcortical band heterotopia)
• Between 5 and 22 gestational weeks, primitive neurons are generated from mitotic
neural stem cells in the ventricular zone. Guided by radial glial fibers, postmitotic
neuroblasts migrate outward from the VZ to populate the cortical plate.

48. Type 1 /Classic Lissencephaly
Neurons fail to migrate to the cortex.
Smooth cortex & hourglass-shaped
brain with mild VM. Vermis spared.
The normal six-layer cortex is
replaced by a thick four-layer
cortex
Variants : Miller-Dieker syndrome
- congenital heart disease,
omphalocele, genitourinary
abnormalities, IUGR, and dystrophic
facies.

49. TYPE 2 LISSENCEPHALY
• Cobblestone cortex results from
abnormalities caused by defects in the
limiting pial basement membrane.
• Over migration of neuroblasts through
these breaches results in an extracortical
layer of aberrant gray matter nodules—the
"cobblestones"—on the brain surfaces.

51. Malformations Secondary to
Abnormal Post migrational
Development

52. Polymicrogyria
• The signature feature of PMG is an
irregular cortex with numerous
small convolutions and shallow or
obliterated sulci. The appearance is
that of tiny miniature gyri piled on
top of other disorganized gyri
• It can involve a single gyrus or most
of an entire cerebral hemisphere. It
can be uni or bilateral, symmetric or
asymmetric, and focal or diffuse.

53. • Bilateral perisylvian PMG is the most common location
• Associated periventricular GM heterotopias are found in 11% of cases, and
other anomalies, such as schizencephaly, are common.
• Thickened or overfolded cortex with nodular surfaces and irregular
“stippled” GM-WM interfaces are the most characteristic findings on
imaging
• The major differential diagnosis of PMG is type 2 lissencephaly
(cobblestone malformation).The absence of congenital muscular dystrophy
and “Z-shaped” brainstem is a helpful clinical distinction.
• The cortex in PMG is thin, nodular, and excessively folded. In focal cortical
dysplasia, the GM is thickened, and the GM-WM interface is blurred.
• In schizencephaly, the dysplastic cortex lining the cleft may appear
“pebbled,” but the cleft distinguishes it from PMG.

54. Schizencephaly ("Split Brain")
• Gray-matter lined cleft that extends from the
ventricular ependyma to the pial surface of the cortex.
• Etiology - destructive (encephaloclastic- vascular
injury, teratogens, infections-CMV and trauma) or
developmental.
• The diagnosis rests on detection of cleft surrounded
and lined by disorganized, dysmorphic- appearing
cortex traversing from ventricle to cortex (The cleft
spans the full thickness of the affected hemisphere)
• The "lips“ of the cleft can be fused or closely apposed
("closed lip“ schizencephaly) or appear widely
separated ("open lip“ schizencephaly).
• The key imaging features of schizencephaly are (1) a
CSF-filled defect extending from the ventricle wall to
the pial surface and (2) dysplastic GM lining the cleft.
• DD- porencephaly, the cleft is lined by gliotic white
matter, not dysplastic gray matter.

55. Agenesis of Corpus Callosum
• 3 major commissural tracts: the CC, which is the largest and
most prominent, the anterior commissure (AC), and the
hippocampal (posterior) commissure (HC).
• Anteroposterior manner.
• Development of the corpus callosum starts at about 12 weeks
from the lamina terminalis near the anterior end of the third
ventricle; it becomes detectable by about 15 weeks and is
complete by about 20 weeks
• The corpus callosum measures 4 mm at 16 weeks and grows
to 45 mm by term.
• By 10 months of age, the overall appearance resembles that
of a normal adult.

56. Probust bundles
consist of
misdirected
commissural fibers,
which should have
crossed the midline
but instead course
from front to back,
indenting the medial
walls of the lateral
ventricles.

57. Callosal development is associated
with the development of the septal
leaflets and the CSP. When septal
leaflets are present, at least the
anterior portion of the corpus
callosum has formed.
• On routine scans reliance for
screening for callosal and other
midline abnormalities is placed on
indirect findings on the standard
views, especially the CSP, which
should be sought on all axial scans
after about 16 to 17 weeks
• Color Doppler scans can be used to
demonstrate an abnormal course of
pericallosal and cingulate arteries,
which normally follow the contour
of the callosomarginal sulcus, but
with ACC they assume a more
radial course.

58. VEIN OF GALEN MALFORMATION
• Cerebral arteriovenous fistula of the median prosencephalic vein (MPV) (a precursor of the vein of Galen)
• Anechoic cystic lesion in midline posterior to the foramen of Monro, superior to the third ventricle.
• On color Doppler- shows extensive vascularity .
• Fed by large arteries off the anterior or posterior cerebral artery.

59. SPINE

60. 1. The lateral edges of neural fold
begins to close dorsally in to a
closed neural tube. in the
occipitocervical region leaving a
opening at the cranial end
called cranial neuropore and
the caudal end called caudal
neuropore
2. The hollow center of the neural
tube is the neural canal which
becomes the central canal of
spinal cord and ventricular
system of the brain
3. The neural tube zippers both
cranially and caudally

61. TERM DEFINITION COMMENT
Spinal dysraphism
(neural tubedefect, NTD)
Failure of part of neural tube to close This disrupts both differentiation of central
nervous system and induction of vertebral
arches
Spina bifida Defect in posterior midline neural arch. Arches fail to fuse along dorsal midline and fail
to enclose vertebral canal
Spina bifida occulta Vertebral arches of a single vertebra fail to fuse Underlying neural tube differentiates normally;
does not protrude from vertebral canal.
Meningocele Dura and arachnoid protrude from vertebral canal
through spina bifida defect in posterior midline neural arches
Myelomeningocele Dura, arachnoid, and neural tissue protrude from
vertebral canal through spina bifida defect in posterior midline neural
arches.
Rachischisis (e.g.,
myeloschisis)
Neural folds corresponding to future spinal cord fail to fuse and fail to
differentiate (myeloschisis), invaginate, and separate from surface
ectoderm.
The deformed underdeveloped spinal cord is
exposed dorsally.This is the most severe form of
spinal neural tube defect
Cranioschisis (e.g.,
exencephaly,
anencephaly)
Neural folds corresponding to future brain fail to fuse and fail to
differentiate, invaginate (exencephaly, anencephaly), and separate from
surface ectoderm.
The brain is represented by an exposed dorsal
mass of undifferentiated neural tissue.

62. SPINA BIFIDA:
• Result of nondisjunction of the cutaneous ectoderm from the neural ectoderm and
failure of neural tube closure.
• The non-neurulated cord or placode is exposed through a dural, bony and cutaneous
defect
• The dorsal and ventral nerve roots exit from the ventral surface of the placode.
• May be associated with diastematomyelia or dermal sinus.

63. PATHOGENESIS AND PATHOLOGY
• Due to failure of closure of the embryologic neural tube.
• Some may be caused by rupture of the neural tube after primary closure.
ASSOCIATIONS
• Chromosomal abnormalities (mostly trisomy 18 and trisomy 13)
• Autosomal dominant conditions: Lehman syndrome.
• Autosomal recessive conditions: Meckel-Gruber syndrome and VACTERL syndrome
(vertebral defect, imperforate anus, tracheoesophageal fistula, radial and renal
dysplasia).
• X-linked conditions : Mathias laterality sequence and X-linked neural tube defects

64. • Spina Bifida Occulta
• Restricted to involvement of the mesoderm of the posterior vertebral arch and rarely
exhibits intrinsic maldevelopment of the spinal cord.
• This may result from an insult occurring at the end of the fourth embryologic week
(sixth menstrual week), causing failure of complete formation of the posterior midline
structures.
• About 66% of spina bifida occulta cases have skin manifestations: nevi, lumbosacral
lipomas, dermal sinus, hypertrichosis (tuft of hair, “horse’s tail or fawn’s tail”), or
scarred area.
• May be associated with urologic dysfunction and tethered cord syndrome, foot
deformity, increased incidence of spondylolisthesis, and intervertebral disc herniation.
• Spina bifida occulta is difficult to detect with prenatal ultrasound unless it is associated
with a lipoma, a simple meningocele, or tethered cord.

65. Myeloschisis
• Most severe form- Embryologic neural tube (the precursor to the spinal cord) remains
open in addition to the overlying mesodermal structures [neural arch, muscles, and skin]
• The open, flattened spinal cord is exposed posteriorly through a wide defect in the
posterior neural arch and associated musculature and skin.
• Less severe cases-
• Major anatomic defect is in the structures derived from the mesodermal tissues
overlying the embryologic neural tube.
• Meningocele
• Myelomenigocele

66. SONOGRAPHIC FINDINGS:
• Common site- Lumbo sacral area
• Spina bifida-
• Posterior transaxial plane- lamina fails to converge on midline
• Lateral transaxial and Lateral Longitudinal- pedicles are displaced more laterally
• They usually demonstrate meningocele or myelomeningocele
• In most cases of spina bifida, there is abnormal divergence or splaying of the pedicles over
several vertebral levels. This is best appreciated in 3-D images and in lateral longitudinal
views, where multiple interpedicular distances can be evaluated simultaneously.

67. Normal spine demonstrated in
a lateral longitudinal scan
spine of a fetus
with spina
bifida.
there is a
separation of
the pedicles

68. AXIAL SECTIONS
Separation of the posterior ossification centers is observed, along with a skin defect and
exposure of neural contents to the amniotic fluid. In most cases, a myelomeningocele sac
can be seen

69. Posterior Longitudinal sections :
lumbosacral vertebrae of a normal fetus
lumbosacral spine of a fetus with spina bifida.

70. LUMBAR MENINGOCELE:
Post longitudinal and Posterior trans axial scan demonstrates fluid filled sac
in the back with a small defect in neural arch.

71. MYELOMENINGOCELE
Posterior transaxial scan
of the mid lumbar spine shows the
splaying of the laminae and the
myelomeningocele sac

72. MYELOSCHISIS
Posterior Trans axial scan showing splaying
of lamina and only a thin membrane
overlies the spinal defect
Lateral trans axial scan shows
increased interpedicular distance

73. • Lateral longitudinal scan progressive
increase in transpedicular distance
Posterior longitudinal scan abrupt truncation
of soft tissues of fetal back and the site of
open neural tube defect

74. ASSOCIATED CRANIAL ABNORMALITIES
• Effacement of cisterna magna
• Deformation of cerebellum [Banana sign]
• Bifrontal indentation [Lemon sign]
• Ventriculomegaly
• BPD lower than the expected.

75. • Spinal dysraphism allows a leak of CSF from the spinal canal into the
amniotic fluid, which causes low intracranial pressure (ICP) early in
pregnancy.
• Low ICP induces a smaller-than-normal posterior fossa
compartment.
• The cerebellum then grows into this abnormally small space, which
leads to obliteration of the cisterna magna, compression of the
cerebellar hemispheres, herniation of the cerebellar tonsils into the
cervical spinal canal, and related abnormalities such as
ventriculomegaly.

76. ASSOCIATED NON CRANIAL ABNORMALITIES
• Club foot
• Congenital dislocation of hip
• Renal abnormalities
• Choroid plexus cyst
• IUGR
• Omphalocele
• Associated chromosomal abnormalities

77. PROGNOSIS
• The outcome is better for low lesions (lower lumbar or sacral),
closed defects, and those with minimal or no hydrocephalus and
no compression of the hindbrain from Chiari II malformation.
• Multiple impairments may affect the individual, including motor
function, bladder and bowel dysfunction, and intellectual
impairment.
• Degree of muscle dysfunction is defined by the highest level of
the open NTD, not by the number of involved vertebrae or the
size of the overlying sac.

78. MYELOCYSTOCELE
• Uncommon form of spinal dysraphism.
• Dilatation of central cord of spinal cord
which herniates posteriorly through
the spinal cord and posterior neural
arch to form an exterior sac.
• No spina bifida
• Occur at any level and is associated
with Chiari 2 malformation

79. Prenatal ultrasound demonstrate cyst with in a cyst appearance.
Splaying of the laminae and pedicles may or may not be present

80. DIASTEMATOMYELIA
• Complete or partial cleft of spinal cord,
distal conus of the cord or filum
terminale.
• characterized by a sagittal osseous or
fibrous septum in the spinal cord.
• May be asssociated with spina bifida
and hydromyelia.
• Visceral malformations such as
horseshoe or ectopic kidney, utero-
ovarian malformation, and anorectal
malformation.

81. Transaxial and Longitudinal sonogram demonstrating two
echogenic foci within the spinal canal with intact skin along
the fetal back

82. References
• Diagnostic Ultrasound- Carol M Rumack
• Callen’s Ultrasonography in Obstetrics & Gynecology

83. THANK YOU!!!