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HYDROCEPHALUS
Overview of CSF production
Choroid plexus
Circulates in ventricular system
Through foramina of Luschka & Magendie
Enter cisterna magna
Absorbed by arachnoid granulations
Definition
• Hydrocephalus refers to accumulation of
excessive CSF within the ventricular system.
• increased volume of CSF within the skull,
accompanied by dilatation of ventricles
INCIDENCE
• Dilatation occurs due to intermittent rise in CSF
mostly occurring at night
• Occurring in old age commonly in combination
with gait apraxia, dementia & urinary
incontinence
TYPES
PRIMARY
Communicating
hydrocephalus
Non- Communicating
hydrocephalus
SECONDARY
Primary hydrocephalus
• Actual increase in CSF within the skull along
with elevated ICP
• MECHANISMS:
– Obstruction to flow of CSF
– Overproduction of CSF
– Deficient reabsorption of CSF
• Commonest cause : obstruction to flow
Non- Communicating hydrocephalus
• Enlargement of only a portion of ventricular
system
• Major sites of obstruction
– 3rd ventricle
– Exit foramina in 4th ventricle
CSF can’t pass to subarachnoid space
Enlargement
Causes of Non- Communicating
hydrocephalus
1) Congenital non-communicating hydrocephalus
– Stenosis of aqueduct
– Arnold chiari malformation
– Progressive gliosis of Aqueduct
– Intra- uterine meningitis
Causes of Non- Communicating hydrocephalus
2) Acquired non—communicating hydrocephalus
• Occur due to expanding lesions of skull
– Tumor adjacent to ventricular system :
ependymoma, choroid plexus papilloma,
medulloblastoma etc.
– Inflammatory lesions : cerebral abscess, meningitis
– Hemorrhage : parenchymal hemorrhage, intra-
ventricular hemorrhage, epidural & subdural
hematoma
Communicating hydrocephalus
• Entire ventricular system is enlarged
• Causes are mostly non-obstructive like
–Overproduction of CSF : choroid plexus
papilloma
–Deficient reabsorption of CSF : following
meningitis, sub-arachnois hemorrhage &
dural sinus thrombosis
Communicating hydrocephalus
• When causes are obstructive:
Obstruction at subarachnoid space at base of
brain
Enlargement of ventricular system
CSF flows freely between dilated ventricles and
spinal canal
Hydrocephalus ex vacuo
• Dilatation of ventricular system with
compensatory increase in CSF volume
secondary to a loss of brain parenchyma
Secondary hydrocephalus
• Less common
• Compensatory increase in CSF due to loss of
neural tissue without associated rise in ICP
• Seen in cerebral atrophy & infarction
GROSS features
• Dilation of ventricles depending upon site of
obstruction
• Thining & stretching of brain
• Engorgement of Scalp veins overlying enlarged
head
• Fontanelle remain open
MICROSCOPIC features
In severe hydrocephalus,
• Damage to ependymal lining of ventricles
• Periventricular interstitial edema
CLINICAL FEATURES
• Develops in infancy before closure of cranial
sutures which leads to increase head
circumference
• In Hydrocephalus developing after closure of
sutures, there is increase in ICP & dilatation of
ventricles without change in head
circumference
THANK YOU

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Hydrocephalus

  • 2. Overview of CSF production Choroid plexus Circulates in ventricular system Through foramina of Luschka & Magendie Enter cisterna magna Absorbed by arachnoid granulations
  • 3. Definition • Hydrocephalus refers to accumulation of excessive CSF within the ventricular system. • increased volume of CSF within the skull, accompanied by dilatation of ventricles
  • 4. INCIDENCE • Dilatation occurs due to intermittent rise in CSF mostly occurring at night • Occurring in old age commonly in combination with gait apraxia, dementia & urinary incontinence
  • 6. Primary hydrocephalus • Actual increase in CSF within the skull along with elevated ICP • MECHANISMS: – Obstruction to flow of CSF – Overproduction of CSF – Deficient reabsorption of CSF • Commonest cause : obstruction to flow
  • 7. Non- Communicating hydrocephalus • Enlargement of only a portion of ventricular system • Major sites of obstruction – 3rd ventricle – Exit foramina in 4th ventricle CSF can’t pass to subarachnoid space Enlargement
  • 8. Causes of Non- Communicating hydrocephalus 1) Congenital non-communicating hydrocephalus – Stenosis of aqueduct – Arnold chiari malformation – Progressive gliosis of Aqueduct – Intra- uterine meningitis
  • 9. Causes of Non- Communicating hydrocephalus 2) Acquired non—communicating hydrocephalus • Occur due to expanding lesions of skull – Tumor adjacent to ventricular system : ependymoma, choroid plexus papilloma, medulloblastoma etc. – Inflammatory lesions : cerebral abscess, meningitis – Hemorrhage : parenchymal hemorrhage, intra- ventricular hemorrhage, epidural & subdural hematoma
  • 10. Communicating hydrocephalus • Entire ventricular system is enlarged • Causes are mostly non-obstructive like –Overproduction of CSF : choroid plexus papilloma –Deficient reabsorption of CSF : following meningitis, sub-arachnois hemorrhage & dural sinus thrombosis
  • 11. Communicating hydrocephalus • When causes are obstructive: Obstruction at subarachnoid space at base of brain Enlargement of ventricular system CSF flows freely between dilated ventricles and spinal canal
  • 12. Hydrocephalus ex vacuo • Dilatation of ventricular system with compensatory increase in CSF volume secondary to a loss of brain parenchyma
  • 13. Secondary hydrocephalus • Less common • Compensatory increase in CSF due to loss of neural tissue without associated rise in ICP • Seen in cerebral atrophy & infarction
  • 14. GROSS features • Dilation of ventricles depending upon site of obstruction • Thining & stretching of brain • Engorgement of Scalp veins overlying enlarged head • Fontanelle remain open
  • 15. MICROSCOPIC features In severe hydrocephalus, • Damage to ependymal lining of ventricles • Periventricular interstitial edema
  • 16. CLINICAL FEATURES • Develops in infancy before closure of cranial sutures which leads to increase head circumference • In Hydrocephalus developing after closure of sutures, there is increase in ICP & dilatation of ventricles without change in head circumference