- Umbilical vein varix
- Timing of Cranial Markers in Open NTD
- Real world experience Open Neural tube defect and Brain Signs
- Real world experience First Trimester Megacystis – Management
- Real world experience Fetal Megacystis
- Abnormal facial profile
- Azygous Vein & ARSA
- Blakes Pouch Cyst
- Absent nasal bone (ANB)
- Choroid plexus cysts
- Chronic placental abruption
- Fetal Alcohol Syndrome
- Placenta-First Risk Stratification
Real World Experience Open Neural Tube Defect And Brain Signs
Open Neural Tube Defect
• Open lumbosacral spina bifida (myelomeningocele)
Because the neural placode is exposed, CSF continuously leaks into the amniotic cavity.
Chronic CSF Leak → Intracranial Hypotension
Persistent CSF loss causes:
• Reduced intracranial CSF volume
• Lower intracranial pressure
• Underexpansion of the embryonic ventricular system
• Small posterior fossa volume development
This is not an acute drop. It’s chronic pressure depletion during a critical period of brain morphogenesis.
Posterior Fossa Crowding → Banana Sign
Because of low intracranial pressure and reduced CSF distension:
• The posterior fossa remains small.
• The cerebellum gets pulled caudally.
• The cerebellar hemispheres wrap around the brainstem.
Banana sign
• Curved cerebellum
• Obliterated cisterna magna
• Effaced posterior fossa CSF space
This is one of the earliest and most specific cranial markers of open NTD.
It’s not just “compression.” It’s a developmental under-expansion plus downward traction phenomenon.
Brainstem and Peduncular Descent
As posterior fossa volume remains restricted:
• Brainstem shifts caudally.
• Cerebellar vermis is displaced.
• Cerebral peduncles and midbrain structures are pulled downward.
• Cisterna magna becomes obliterated.
This is essentially the fetal equivalent of Chiari II malformation.
Intracranial Hypotension → Frontal Bone Scalloping (Lemon Sign)
Low intracranial pressure also affects calvarial molding.
Mechanism:
• Reduced internal pressure
• External uterine pressure dominates
• Frontal bones collapse inward
This causes: Lemon sign
• Bilateral frontal scalloping
• Flattened or concave frontal contour
Key points:
• More common before 24 weeks
• May disappear later in gestation
• Not specific, but highly suggestive in the right setting
Progressive Ventricular Obstruction
As hindbrain herniation worsens:
• Fourth ventricle becomes compressed
• Aqueduct becomes kinked or obstructed
• CSF outflow from lateral ventricles is impaired
Now the pathophysiology shifts:
From intracranial hypotension → To obstructive hydrocephalus
This transition is crucial.
Development of Hydrocephalus
Because of:
• Aqueductal obstruction
• Fourth ventricle compression
• Impaired CSF circulation
You get:
• Progressive ventriculomegaly
• Dilated lateral ventricles
• Increasing head size later in gestation
This is why ventriculomegaly often appears after the posterior fossa signs.
Dangling Choroid Sign
As ventricles enlarge:
• Choroid plexus no longer fills the ventricular cavity
• It hangs dependently in dilated CSF
On ultrasound: “Dangling choroid sign”
• Choroid seen floating centrally
• Surrounded by anechoic CSF
This indicates: True ventriculomegaly
• Significant ventricular dilation
Putting It All Together — The Sequence
Open NTD
↓
Chronic CSF leakage
↓
Intracranial hypotension
↓
Small posterior fossa development
↓
Cerebellar wrapping (Banana sign)
↓
Brainstem and peduncular descent
↓
Frontal bone scalloping (Lemon sign)
↓
Aqueduct compression
↓
Obstructive hydrocephalus
↓
Ventriculomegaly
↓
Dangling choroid sign
Banana sign precedes hydrocephalus
Posterior fossa signs usually appear before ventriculomegaly.
Lemon sign may resolve
As skull ossifies and ventricles enlarge, frontal scalloping may disappear.
Hydrocephalus is secondary
In open NTD, hydrocephalus is not primary — it is secondary to hindbrain herniation.
Cisterna magna effacement is key
Absent cisterna magna is more specific than lemon sign.