- 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
Blakes Pouch Cyst
It is a posterior fossa developmental variant that often causes confusion because it sits on the border between normal maturation and malformation.
• Blake’s pouch is a transient embryologic structure
• It is the inferior posterior ballooning of the 4th ventricle
• Normally regresses when the foramen of Magendie opens (around 18–20 weeks)
Blake’s pouch cyst = failure or delay of this perforation
Pathophysiology
• Non-perforation or delayed perforation of the foramen of Magendie
• CSF accumulates posteriorly
• Vermis is normally formed, but pushed upward and appears rotated
• Vermis is present and intact. It is displaced, not absent or hypoplastic.
Etiology
Primary / developmental
• Delayed maturation of posterior fossa CSF pathways
• Often isolated
• Considered part of the Dandy–Walker spectrum, but at the mild end Secondary associations
• Mild CSF circulation imbalance
• Rare association with aqueductal flow issues
Ultrasound diagnostic features (essential)
Mandatory criteria
1. Normal vermian size and morphology
2. Upward rotation of vermis (not hypoplastic)
3. Cystic dilatation of the 4th ventricle
4. Normal posterior fossa size
5. Normal tentorium position
Helpful measurements
• Vermian height appropriate for GA
• Tegmento-vermian angle mildly increased (usually < 30°)
What you should NOT see
• Enlarged posterior fossa
• Elevated tentorium
• Absent vermis
• Cerebellar hemispheric hypoplasia
Differentiation
| Condition | Vermis | Posterior fossa | Tentorium | Prognosis |
|---|---|---|---|---|
| Blake’s pouch cyst | Normal, rotated | Normal size | Normal | Usually good |
| Dandy–Walker malformation | Absent / hypoplastic | Enlarged | Elevated | Poor–variable |
| Vermian hypoplasia | Small | Normal | Normal | Variable |
| Arachnoid cyst | Normal | Mass effect | Normal | Depends |
Genetics
Isolated BPC
• Usually sporadic
• No single gene consistently implicated
• Most cases have normal karyotype and CMA
When genetics matter
Consider genetic testing if BPC is associated with:
• Other CNS anomalies
• Cardiac defects
• Facial anomalies
• Growth restriction
Natural history and progression
During pregnancy
• Many cases remain stable
• Some show gradual decrease in cyst size
• Vermian rotation often improves with gestation
Resolution
• Spontaneous prenatal resolution in ~50–70%
• Postnatal resolution even more common
Mechanism:
• Late opening of the foramen of Magendie
• Maturation of CSF circulation
Postnatal outcome
If isolated
• Normal neurodevelopment in the vast majority
• Normal motor and cognitive outcomes
• Rare need for neurosurgical intervention
Prognosis
| Scenario | Prognosis |
|---|---|
| Isolated BPC | Excellent |
| BPC + mild ventriculomegaly | Usually good |
| BPC + additional anomalies | Depends on associations |
| Misdiagnosed DWM actually BPC | Prognosis much better |
Common interpretation mistakes
• Calling BPC “vermian hypoplasia” too early
• Over-interpreting mild vermian rotation before 22 weeks
• Confusing arachnoid cyst with BPC
• Assuming Dandy–Walker prognosis
Practical counseling language
• “This is a common developmental variant of the posterior fossa.”
• “The cerebellum is formed normally and just temporarily displaced.”
• “In most cases, it improves or resolves before or after birth.”
• “When isolated, long-term development is usually normal.”