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CSF CIRCULATION
AND
MECHANICS OF
HYDROCEPHALUS
 CSF formation - 0.4 mL/min per gram
of choroid plexus or 0.35 mL/min
 Choroidal blood flow- 4 mL/min per
gram
 80% - Lateral, 3rd and 4th ventricles
 20% - Interstitial space and
ependymal lining
INTRODUCTION
Total CSF volume
◦ Infant - 50 mL
◦ Adults - 150 mL
Production rate
◦ Infant - 25 mL/day
◦ Adults - 500 mL/day
Intracranial pressure
◦ Infants - 9 to 12 cm H2O
◦ Adults - less than 18 to 20 cm H2O
The Monro-Kellie Doctrine
The sum of intracranial contents to
include blood, CSF, and brain should
remain constant in a fixed container,
such as the skull.
 < 2 to 3 years of age – this does not
apply
CHOROID PLEXUS
BLOOD SUPPLY OF CHOROID
PLEXUS
A
T
P
3Na
2K
A
T
P
Na
Na Na
Na
K 2Cl- Cl-
Cl-
HCO3
-
HCO3
-
HCO3
-
HCO3
-
H+
CA
H2O + CO 2  HCO3
- +H+
H2O
AQ 1
CSF
INTERSTITIUM
Choroidal cell
Apica
l
Basolater
al
REGULATION OF
CEREBROSPINAL
FLUID FORMATION
 Neurohumoral Ligands and Receptors
 Sympathetic
 Parasympathetic
 Serotonin (5HTc)
 AVP
 ANP
 Diuretic Agents and Ion Transporters
 Ouabain
 Digoxin
 Bumetanide
 Furosemide
CEREBROSPINAL FLUID
FLOW
CSF flow rate depends on
◦ Upstream choroidal
◦ Mainstream ventriculocisternal
◦ Downstream arachnoidal fluid throughput
 Slowing of CSF flow disturbs both
trophic and excretory functions in the
CNS
 Pulsatile movement during each
cardiac cycle – CSF movement
Anterograde caudal flow
Retrograde cranial flow
ABSORPTION OF
CEREBROSPINAL FLUID
The only proven force responsible for
bulk CSF absorption is that of a
hydrostatic gradient
 Absorption via the Arachnoid Villus
 Absorption into the Lymphatic System
 Absorption via the Brain
 Absorption via Blood Vessels
 Absorption at the Nerve Root Sleeves
 Absorption from the Subarachnoid
Space
CLASSIFICATION OF
HYDROCEPHALUS
A. Over production of CSF (a rare entity)
B. Obstructive: wherein there is
obstruction to the flow of CSF in the
◦ Lateral ventricles
◦ Foramen of Monroe
◦ Third ventricle
◦ Aqueduct of Sylvius
◦ Fourth ventricle
◦ Subarachnoid spaces
C. Absorption defect
Based on the site of blockage :
 Monoventricular
 Biventricular
 Triventricular
 Panventricular
Based on exact aetiology
1. Congenital
2. Traumatic
3. Inflammatory
4. Neoplastic
5. Degenerative
CSF FORMATION RATE IN
HYDROCEPHALUS
 Reduced fluid turnover in hydrocephalus:
◦ Reduced choroid plexus blood flow
◦ Epithelial cell shrinkage or damage
◦ Diminution of blood-CSF surface area
 Ventricular pressure = Net fluid
filtration
 ICP  Release of neurohumoral agents
 Choroid plexus epithelial receptor–
mediated inhibition of CSF production.
PATHOPHYSIOLOGIC MECHANISMS
Gliosis and Inflammation
 Glial fibrillary acidic protein (GFAP)
 Aquaporin 4 (AQP4)
 Minocycline as a specific inhibitor of
microglial cells
Intracranial Pulsatility
 Ventricular dilation can be caused by
abnormal intracranial pulsatility
 Dissipation of cerebral arterial
pulsatility, resulting in minimal
(homeostatic) capillary and venous
pulse pressure, is believed to be
critical for normal cerebrovascular
function
CSF Absorption
 Lymphatic, Arachnoid, Microvascular
 Latest in vivo studies - cranial
lymphatics, most notably the nasal
pathways surrounding the olfactory
nerves, are capable of transporting
large volumes of CSF.
A
T
P
3Na
2K
A
T
P
Na
Na Na
Na
K 2Cl- Cl-
Cl-
HCO3
-
HCO3
-
HCO3
-
HCO3
-
H+
CA
H2O + CO 2  HCO3
- +H+
H2O
AQ 1
CSF
INTERSTITIUM
Choroidal cell
Apica
l
Basolater
al
Ouabain Bumetanide
Digoxin
Furosemide
Furosemide
Acetazolamide
Amiloride
Post-Haemorrhagic
 Premature infants born before 34
weeks have a high incidence of
intracranial haemorrhage
 majority occurs within the first few
days of birth
Meningomyelocoele
 It may manifest after closure of the
meningomyelocoele, as the sac acts
as a CSF sump
Aqueduct Stenosis
 Communicating hydrocephalus with
external pressure on the
mesencephalon
 Scaring and gliosis following infection
or haemorrhage
 Tumours from the surrounding
structures
Dandy Walker Syndrome
 Agenesis of the cerebellar vermis
 Cystic dilation of the fourth ventricle
 Enlargement of the posterior fossa
 Hydrocephalus
Post-Meningitic
 Bacterial, parasitic and granulomatous
 infections like tuberculosis and fungal
infections.
 Hydatidosis
 Toxocara
 Viral infections
Subarachnoid Haemorrhage
 Can occur in 10–15% of patients with
subarachnoid haemorrhage
 Impaired absorption due to blockage
at multiple sites.
Normal Pressure
Hydrocephalus
 In some cases, it may be secondary to
infection or haemorrhage in the past
Hydrocephalus and Venous
Hypertension
 Otitic-hydrocephalus
 Seen in anchondroplasia and
syndromic craniostenosis
Arrested Hydrocephalus
 Persistent ventricular enlargement
with normal CSF pressures
 Disproportionate headgrowth,
progression of ventricular size and
intellectual decline are indications for
intervention
Multiloculated Hydrocephalus
 Usually occurs after an initial episode
of neonatal meningitis or a germinal
matrix haemorrhage
 Different from cysts associated with
hydrocephalus - Dorsal cyst
malformations.
Hydrocephalus Ex-vacuo
 Enlargement of the ventricles
secondary to cerebral parenchymal
damage.
 Ageing, head trauma, severe infection,
hypoxia or ischaemic insults,
radiotherapy ,chemotherapy
 Associated with white matter loss and
concomitant enlargement of the
cortical sub-arachnoid spaces and
basal cisterns.

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Nano-gold for Cancer Therapy chemistry investigatory projectNano-gold for Cancer Therapy chemistry investigatory project
Nano-gold for Cancer Therapy chemistry investigatory project
 

CSF physiology and Mechanics of Hydrocephalus

  • 2.  CSF formation - 0.4 mL/min per gram of choroid plexus or 0.35 mL/min  Choroidal blood flow- 4 mL/min per gram  80% - Lateral, 3rd and 4th ventricles  20% - Interstitial space and ependymal lining INTRODUCTION
  • 3. Total CSF volume ◦ Infant - 50 mL ◦ Adults - 150 mL Production rate ◦ Infant - 25 mL/day ◦ Adults - 500 mL/day Intracranial pressure ◦ Infants - 9 to 12 cm H2O ◦ Adults - less than 18 to 20 cm H2O
  • 4. The Monro-Kellie Doctrine The sum of intracranial contents to include blood, CSF, and brain should remain constant in a fixed container, such as the skull.  < 2 to 3 years of age – this does not apply
  • 6. BLOOD SUPPLY OF CHOROID PLEXUS
  • 7.
  • 8. A T P 3Na 2K A T P Na Na Na Na K 2Cl- Cl- Cl- HCO3 - HCO3 - HCO3 - HCO3 - H+ CA H2O + CO 2  HCO3 - +H+ H2O AQ 1 CSF INTERSTITIUM Choroidal cell Apica l Basolater al
  • 9. REGULATION OF CEREBROSPINAL FLUID FORMATION  Neurohumoral Ligands and Receptors  Sympathetic  Parasympathetic  Serotonin (5HTc)  AVP  ANP  Diuretic Agents and Ion Transporters  Ouabain  Digoxin  Bumetanide  Furosemide
  • 10. CEREBROSPINAL FLUID FLOW CSF flow rate depends on ◦ Upstream choroidal ◦ Mainstream ventriculocisternal ◦ Downstream arachnoidal fluid throughput
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  • 12.  Slowing of CSF flow disturbs both trophic and excretory functions in the CNS  Pulsatile movement during each cardiac cycle – CSF movement Anterograde caudal flow Retrograde cranial flow
  • 13. ABSORPTION OF CEREBROSPINAL FLUID The only proven force responsible for bulk CSF absorption is that of a hydrostatic gradient
  • 14.  Absorption via the Arachnoid Villus  Absorption into the Lymphatic System  Absorption via the Brain  Absorption via Blood Vessels  Absorption at the Nerve Root Sleeves  Absorption from the Subarachnoid Space
  • 16. A. Over production of CSF (a rare entity) B. Obstructive: wherein there is obstruction to the flow of CSF in the ◦ Lateral ventricles ◦ Foramen of Monroe ◦ Third ventricle ◦ Aqueduct of Sylvius ◦ Fourth ventricle ◦ Subarachnoid spaces C. Absorption defect
  • 17. Based on the site of blockage :  Monoventricular  Biventricular  Triventricular  Panventricular
  • 18. Based on exact aetiology 1. Congenital 2. Traumatic 3. Inflammatory 4. Neoplastic 5. Degenerative
  • 19. CSF FORMATION RATE IN HYDROCEPHALUS
  • 20.  Reduced fluid turnover in hydrocephalus: ◦ Reduced choroid plexus blood flow ◦ Epithelial cell shrinkage or damage ◦ Diminution of blood-CSF surface area  Ventricular pressure = Net fluid filtration  ICP  Release of neurohumoral agents  Choroid plexus epithelial receptor– mediated inhibition of CSF production.
  • 21. PATHOPHYSIOLOGIC MECHANISMS Gliosis and Inflammation  Glial fibrillary acidic protein (GFAP)  Aquaporin 4 (AQP4)  Minocycline as a specific inhibitor of microglial cells
  • 22. Intracranial Pulsatility  Ventricular dilation can be caused by abnormal intracranial pulsatility  Dissipation of cerebral arterial pulsatility, resulting in minimal (homeostatic) capillary and venous pulse pressure, is believed to be critical for normal cerebrovascular function
  • 23. CSF Absorption  Lymphatic, Arachnoid, Microvascular  Latest in vivo studies - cranial lymphatics, most notably the nasal pathways surrounding the olfactory nerves, are capable of transporting large volumes of CSF.
  • 24. A T P 3Na 2K A T P Na Na Na Na K 2Cl- Cl- Cl- HCO3 - HCO3 - HCO3 - HCO3 - H+ CA H2O + CO 2  HCO3 - +H+ H2O AQ 1 CSF INTERSTITIUM Choroidal cell Apica l Basolater al Ouabain Bumetanide Digoxin Furosemide Furosemide Acetazolamide Amiloride
  • 25. Post-Haemorrhagic  Premature infants born before 34 weeks have a high incidence of intracranial haemorrhage  majority occurs within the first few days of birth
  • 26. Meningomyelocoele  It may manifest after closure of the meningomyelocoele, as the sac acts as a CSF sump
  • 27. Aqueduct Stenosis  Communicating hydrocephalus with external pressure on the mesencephalon  Scaring and gliosis following infection or haemorrhage  Tumours from the surrounding structures
  • 28. Dandy Walker Syndrome  Agenesis of the cerebellar vermis  Cystic dilation of the fourth ventricle  Enlargement of the posterior fossa  Hydrocephalus
  • 29. Post-Meningitic  Bacterial, parasitic and granulomatous  infections like tuberculosis and fungal infections.  Hydatidosis  Toxocara  Viral infections
  • 30. Subarachnoid Haemorrhage  Can occur in 10–15% of patients with subarachnoid haemorrhage  Impaired absorption due to blockage at multiple sites.
  • 31. Normal Pressure Hydrocephalus  In some cases, it may be secondary to infection or haemorrhage in the past
  • 32. Hydrocephalus and Venous Hypertension  Otitic-hydrocephalus  Seen in anchondroplasia and syndromic craniostenosis
  • 33. Arrested Hydrocephalus  Persistent ventricular enlargement with normal CSF pressures  Disproportionate headgrowth, progression of ventricular size and intellectual decline are indications for intervention
  • 34. Multiloculated Hydrocephalus  Usually occurs after an initial episode of neonatal meningitis or a germinal matrix haemorrhage  Different from cysts associated with hydrocephalus - Dorsal cyst malformations.
  • 35. Hydrocephalus Ex-vacuo  Enlargement of the ventricles secondary to cerebral parenchymal damage.  Ageing, head trauma, severe infection, hypoxia or ischaemic insults, radiotherapy ,chemotherapy  Associated with white matter loss and concomitant enlargement of the cortical sub-arachnoid spaces and basal cisterns.