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CSF Production Dynamics and Physiology
Dr Fakir MohanSahu
Dept. ofNeurosurgery
AIIMS Bhubaneswar
13/04/2021
Dr Fakir Mohan Sahu
Dept. of Neurosurgery
AIIMS Bhubaneswar
Learning Objectives
• Historical Backgrounds
• CSF anatomy and Physiology
• CSF Production, Circulation and Absorption
• CSF Dynamics, ICP, CPP
• Consequences of altered CSF Hydrodynamics
• Applied Anatomy
Historical Background
• Hippocrates described fluid in brain
• Galen described ventricles
• Vesalius showed the anatomy
• Megendi performed first cisternal puncture in animals
• Quinke performed first LP(1891)
• Quekensted did first cisternal puncture in humans(1916)
• Dandy was credited first ventricular puncture(1918)
• Mixter in 1923 performed the first ETV in a child with
congenital hydrocephalus using a urethroscope and probe
Introduction
• CSF clear, Colourless, Odourless fluid present within and around the CNS
• Tela choroidea
• Choroid plexus
• Arachnoid villi(Endothelial cell Vesicular Channels)
• Arachnoid granules
• CSF Flow(Unidirectional, from arachnoid villi to Dural Venous sinuses,
Pressure of 1.5 mmHg higher)
• Foramens
CSF Anatomy and Physiology
CSF Flow
Choroid Plexus
AQP1
Mechanism of choroidal
production
Tight junction
 Epithelial cells
 Active process:
Uses ATP
 movement ofions
 osmotic
gradient 
secretion ofH2O
 high expressionof
AQP1 on apical
membrane
Factors Decreasing CSF
production
Endogenous Exogenous
CSF Pressure Acetazolamide
Choroid plexus ischemia Frusemide
Hypoxia Amiloride
Acidosis/ Alkalosis Omeprazole
Hypoglycemia Glycosides
Neural Cholera toxins
Johnston, I et al. Child's Nerv Syst. 2000
CSF Production, Dynamics and Physiology
CSF Production, Dynamics and Physiology
Sylvian cistern
Chiasmatic/
suprasellar cistern
Interpeduncular cistern
Ambient cistern
Quadrigeminal cistern
Crural cistern
Mechanism of CSF
flow
The pressure gradient is highest in the lateral ventricles and diminishes
successively along the subarachnoid space
b, the negative venous pressure
(dark blue) produced during
inspiration causes
pressure decrease in
temporary
intracranial
compartment, resulting in CSF
outflow (Dreha-Kulaczewski et al.
2017)
Delaidelli, Aet al. Journal of Neuroscience 2017
a. Arterial pulse wave (red) causes
temporary pressure increase in
intracranial compartment, resulting
in CSF outflow (O'Connell,1943)
Absorptio
n
Arachnoid villi
 microscopic one-way valves
(modified pia andarachnoid)
 penetrate meningeal dural
layer lining venous sinuses
arachnoid villi =
granulations =
Clumps of
arachnoid
macroscopic
Mechanism of
absorption
Hydrostatic pressure in
subarachnoid space (11mmHg)
> dural sinuses (5mmHg)
Arachnoid villi open : pressure
in SAS ~1.5 mm Hg > pressure
in dural sinuses
Passive process
Papaiconomou,C.et al News Physiol Sci 2002
Possible alternative sites of CSF
absorption
 Arachnoid endothelium &
membrane
 Adventitia of bloodvessels
and lymphatics
 Cranial/ spinal nerveroots
sleeves/ lymphatics
 Capillary endothelium
 Spinal arachnoid
projections Johnston, I et al. Child's Nerv Syst. 2000
Papaiconomou,C.et al News Physiol Sci 2002
Functions of CSF
• Cushion around the CNS
• Protection(Coup Counter coup injury concept)
• Buoyancy /Floating in CSF(Sp. gravity almost equal 140050gm)
Post LP-- excess fluid-- traction in foramens - Headache incre.
• Haemostasis/Reservoir/ Control
• Nourishes- Lipid, Glucose, Electrolytes
• Vehicle to remove metabolic waste (ECF and CSF easily exchange)
• Carries hormonal Products of CNS
• Immune Function- Immunoglobulin and immune Protection
The Monroe-Kellie
doctrine
Sum of volumes of the 3 components
is constant  an increase in volume
of any one component 
accompanied by a reduction in
volume of at least one of the
remaining two components
ICP : Function of the volume and
compliance of each component of the
intracranial compartment
The magnitude and the rate of
change in the volume of each
component determines its effect on
ICP
Intra Cranial Pressure
(ICP)
≤ 15mmHg inadults
Intracranial hypertension (ICH) : pressure≥ 20 mmHg
Normally lower in children than adults
Homeostatic mechanisms stabilize ICP
Intracranial contents include :
Brain parenchyma — 80 %
Cerebrospinal fluid — 10 %
Blood — 10%
Cerebral Perfusion Pressure
(CPP)
The pressure needed to overcome ICP in order to deliver O2
& nutrients.
Clinical surrogate for the adequacy of cerebral perfusion.
MAP is the DRIVING FORCE ---------- ICP is the RESISTENCE
CPP = MAP – ICP = 100 mmHg – 15mmHg = 85 mmHg (Normal)
CPP < 50 mmHg → cerebral ischemia
CPP < 30 mmHg→ brain death
Features of CSF
• Volume -150ml
• 550ml/day @ 5.5 ml /min
• Pressure – 50-150 cm H2O
• No RBCs, No Neutrophils, Few Lymphocytes- < 5 / cumm
• Glucose- 2/3rd level of plasma(In LP Study always take the venous sample)
• Protein-Immune mediated diseases of CNS
CSF Production, Dynamics and Physiology
CSF Production, Dynamics and Physiology
OP(CM APPEAR CELLS PROTEI GLUCO MISC.
H20) ANCE N(MG%) SE
FUNGAL
MENINGITIS
INCREASED OPALASCENT 30-300
(LYMPHO)
100-700 <30 +INDIA
INK IN
CRYPTO.
TB
MENINGITIS
INCREASED OPALASCENT 50-500LY
MPHO
60-700 20-40 ZN STAIN
+/AFB CS
WITH
CLOT
+
BRAIN INCREAS CLEAR/ INCREAS INCREAS NORMAL LESS
ABSCESS TURBID / SENSITIV
DECREAS
Other Biomarkers in CSF
 CSF HCG- Central choriocarcinoma
 CEA- breast,lungbladdermetsin CNS
 Alfafetoprotein – germcelltumors, metastatictesticularandhepatic ca.
 Spermidine– meningiomas
 Polyaminein leukemia
 Desmosterol in gliomas
 betaglucuronidaseinleptomeningeal involvement
VENTRICULAR CATHETERIZATION
POINTS AND TRAJECTORIES OF ACCESS TO VENTRICLES
—Kocherʼs point – 3 cm latto midline and 1cm ant to coronal suture
—Keenʼs point 2.5 -3 cm above and 2.5-3cm behind pinna
—Dandyʼ s point – 3 cm above inion and 2 cm lateral to midline
—Frazierʼs point - 6 cm above inion and 4 cm latto midline
—Orbital point – 1-2 cm behind superior orbital rim
—Supra orbital – 4 cm above orbital rim in midpupillary line
CSF Production, Dynamics and Physiology
Intraoperative CSF Puncture points
Consequences of altered CSF
hydrodynamics
Abnormal fluid movement (transependymal/transparenchymal)
Effects of raised ICP
Circulatory changes (micro and macro)  Ischemia
Changes in brain morphology/parenchymal damage
Changes in CSF circulatory path : obstruction/ shunt/ surgery 
Effects of loss or misdistribution of CSF
Post-shunt or other post-surgical changes
Johnston, I et al. Child's Nerv Syst. 2000
Classification of CSF circulation
disorders
Johnston, I et al. Child's Nerv Syst. 2000
Types of HCP
Causes of HCP
Congenital Acquired
Aqueductal stenosis (MC) SAH/ IVH
Dandy-Walker malformation Infections : TBM
Arnold-Chiari malformation Mass lesions /Tumors
Agenesis of the foramen of Monro Posterior fossa cyst/ Arachnoid cyst
Congenital toxoplasmosis Increased venous sinus pressure
Bickers-Adams syndrome Traumatic brain injury
Neural tube defects Idiopathic
Diagnostic
techniques
USG
 in infants (due to open fontanel)
and in utero
CT/MRI scanning : the mainstay of diagnosis
CSF Flow study
CSF pressure measurement
CT/MRI
features
 Increased frontal horn radius
(Mickey mouse ventricle)
 Dilatation of the temporal horns
(>2mm)
 Acute ventricular angles
CT/MRI
features
 Periventricular interstitial edema
from the transependymal flow :
high T2 signal on MRI or low-
density change on CT
 Intra-ventricular flow void from
CSF movement
CT/MRI
Features
 Inferior displacement of the
floor of the 3rd ventricle
 Outward bowing / ballooning
of the lateral walls & recesses
of the third ventricle
(infundibular, optic and pineal
recesses)
 Ballooning of the suprapineal
recess
CT/MRI
Features
On mid-sagittal plane :
 Upward displacement of corpus
callosum
 Thinned out corpus callosum
 Depression of the posterior
fornix
 Decreased mamillopontine
distance ( normal >5.5mm)
CSF flow study
To qualitatively assess and quantify pulsatile CSF flow
MC technique : Time-resolved 2D phase contrast MRI
with velocity encoding (VENC)
CSF flow in the context of imaging : pulsatile to-and-fro
flow due to vascular pulsations NOT bulk transport of CSF
Typical CSF flow is 5-8 cm/s
Hyperdynamic circulation : higher velocities : up to 25 cm/s
Clinical applications
 Aqueduct stenosis
 Normal pressure hydrocephalus(NPH)
 Patency of third ventriculostomy
 Flow at the Cervico-medullary junction
(foramen magnum)
 Chiari I malformation
CSF flow
study
Images are typically presented in sets of 3 for each
plane and velocity obtained.
The set comprises of
 Re-phased image (magnitude of flow compensated
signal)
• flow is of highsignal
• background isvisible
CSF flow
study
 Magnitude image (magnitude of difference
signal)
• flow is of high signal (regardless of direction)
• background is suppressed
 Phase image (phase of difference
signal)
• signal is dependent on direction:
forward flow is of high
signal; reverse flow is
of low signal
• background is mid-grey
CSF pressure
measurement
Direct assessmentof elevated ICP
Surgical placement of ventricular /
intraparenchymal pressure transducer
Intraparenchymal transducer : more
invasive /real time data/ accurate
determination of ICP
Helps in management decisions
CSF Pressure Management
The main goal is to minimize or prevent brain damage by decreasing ICP
and improving CSFflow.
Medical management- Acetazolamide, Diuretics therapy
Temporary procedures
 External ventriculardrainage
 Spinal tap
Surgical management
 Shunt
 Endoscopic Third Ventriculostomy (ETV)/other endoscopic procedure
 Eliminating the cause of obstruction
Endoscopic Third
Ventriculostomy Indications:
 Aqueductal stenosis
 Posterior fossa tumors and cysts with
hydrocephalus
 Postinfectious hydrocephalus
 Tuberculous meningitis with
hydrocephalus
 Hydrocephalus associated with
myelomeningocoele and
Chiari malformation
 Hydrocephalus secondary to intracerebral
/ intraventricular hemorrhage
 Shunt dysfunction
Involves creating an opening in the floor of third
ventricle to allow CSF to flow into pre-pontine
cistern and subarachnoid space
Absolute contraindication : obstruction at the
level of the arachnoid villi or the venous flow in
the superior sagittal sinus
CSF Production, Dynamics and Physiology
Additional Radiological
findings
 The Evans' index
Ratio of maximum width of the frontal horns of the lateral ventricles (A)
and maximal internal diameter of skull (B) at the same level
Employed in axial CT / MRI images
Varies with the age and sex
Marker of ventricular volume
A/B > 0.3 - Hydrocephalus
 Narrow callosal angle:
Angle measured on a coronal image perpendicular to the anterior
commissure - posterior commissure (AC-PC) plane at the level of the
posterior commissure
Normal = 100-120°
NPH = 50-80°
 Cingulate sulcus sign :
Denotes the posterior part of the cingulate sulcus being narrower than
the anteriorpart.
Divider b/w anterior and posterior parts of the sulcus : line drawn parallel
to the floor of 4th ventricle
 Cerebral aqueductflow void
Loss of signal in the aqueduct ofSylvius
Represents higher-than-normal flow velocity of CSF in the aqueduct
(Disproportionately
 DESH
enlarged subarachnoid space
hydrocephalus)
Characterized by:
• Ventriculomegaly
• Tight high-convexity and medial
subarachnoid spaces
• Disproportionate enlargement of
the Sylvianfissures
• Focally dilated or entrapped sulci
without adjacent cortical atrophy
• Acute callosal angle
Hydrocephalus ex
vacuo
Compensatory enlargement of the CSF spaces
Seen in :
 asymptomatic elderly people : aging brain with related volume loss
 pathological conditions that promote brain shrinkage:
degeneration (e.g. Alzheimer disease and
due to focal damage (e.g. stroke and traumatic
• generalised brain
leukodystrophies)
• encephalomalacia
injuries)
Benign external
hydrocephalus
Enlargement of the subarachnoid space
 frontal or
 frontoparietal regions
Ventriculomegaly : absent or mild.
Clinically, infants have macrocephaly but otherwise well-appearing and
have normal development.
Presentation : progressive increase in the head circumference with normal
anterior fontanel.
Family history of macrocephaly :Frequent
Self-limited
Do not require any intervention
Arrested
hydrocephalus
Asymptomatic/ occult/ compensated/ long standing
overt ventriculomegaly of adulthood/ late onset
idiopathic aqueductal stenosis
Moderate to severe tri-ventricular enlargement
No evidenceof periventricular fluid
accumulation on imaging
Stable for years
Incidental diagnosis
Conservative approach with serial imaging
May be associated with cognitive decline or
sudden decompensation
Intracranial Hypotension
Defined as CSF pressure < 60 mm H2O in
patients with clinical presentation
compatible with intracranial hypotension
Most commonly results from a CSF leak
somewhere along the neuraxis
Intracranial hypotension can broadly be divided
into:
 primary: referred to as spontaneous intracranial
hypotension (SIH)
 secondary:
• iatrogenic (lumbar puncture or surgery)
• over-shunting due to diversion devices,
• traumatic
Presentation : positional headache
 relieved by lying in recumbent position
within 15-30minutes
 Nausea/vomiting/vertigo/neck pain
Traumatic or iatrogenic intracranial
hypotension : history of abundant,
clear rhinorrhea or otorrhea present.
Occasionally, presentation is more
sinister, with reported cases of decreased
level of consciousness and coma
Radiographic
features
Imaging is crucial both for confirming the diagnosis of intracranial
hypotension and identifying the location of the leak
CT
 Subdural collection
 Acquired tonsillar ectopia
 Dural venous sinus distention
MR
I
 Pachymeningeal enhancement
 Venous distensionsign
 Subdural effusions / hematomas
 Sagging brainstem /
acquired tonsillar ectopia
 Pituitary enlargement
 Diffuse cerebral edema
 Reduced CSFvolume
 Decreased fluid within the
optic nerve sheath
Intracranial HypotensionManagement
strict bed rest and the possible
Conservative
 Avoidance of the upright position :
addition of analgesics.
 Restoring CSF volume : oral or i.v. hydration, high oral caffeine intake,
and high saltintake
Epidural blood patches : firstline
 Infusion of 10 to 20 cc of autologous blood into the epidural space
 May be repeated
 Adverse effects : back pain, radiculopathy, leg paresthesias, and fever
Epidural fibrin glue
Surgical repair
CSF Production, Dynamics and Physiology

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CSF Production, Dynamics and Physiology

  • 1. CSF Production Dynamics and Physiology Dr Fakir MohanSahu Dept. ofNeurosurgery AIIMS Bhubaneswar 13/04/2021 Dr Fakir Mohan Sahu Dept. of Neurosurgery AIIMS Bhubaneswar
  • 2. Learning Objectives • Historical Backgrounds • CSF anatomy and Physiology • CSF Production, Circulation and Absorption • CSF Dynamics, ICP, CPP • Consequences of altered CSF Hydrodynamics • Applied Anatomy
  • 3. Historical Background • Hippocrates described fluid in brain • Galen described ventricles • Vesalius showed the anatomy • Megendi performed first cisternal puncture in animals • Quinke performed first LP(1891) • Quekensted did first cisternal puncture in humans(1916) • Dandy was credited first ventricular puncture(1918) • Mixter in 1923 performed the first ETV in a child with congenital hydrocephalus using a urethroscope and probe
  • 4. Introduction • CSF clear, Colourless, Odourless fluid present within and around the CNS • Tela choroidea • Choroid plexus • Arachnoid villi(Endothelial cell Vesicular Channels) • Arachnoid granules • CSF Flow(Unidirectional, from arachnoid villi to Dural Venous sinuses, Pressure of 1.5 mmHg higher) • Foramens
  • 5. CSF Anatomy and Physiology
  • 7. AQP1 Mechanism of choroidal production Tight junction  Epithelial cells  Active process: Uses ATP  movement ofions  osmotic gradient  secretion ofH2O  high expressionof AQP1 on apical membrane
  • 8. Factors Decreasing CSF production Endogenous Exogenous CSF Pressure Acetazolamide Choroid plexus ischemia Frusemide Hypoxia Amiloride Acidosis/ Alkalosis Omeprazole Hypoglycemia Glycosides Neural Cholera toxins Johnston, I et al. Child's Nerv Syst. 2000
  • 11. Sylvian cistern Chiasmatic/ suprasellar cistern Interpeduncular cistern Ambient cistern Quadrigeminal cistern Crural cistern
  • 12. Mechanism of CSF flow The pressure gradient is highest in the lateral ventricles and diminishes successively along the subarachnoid space b, the negative venous pressure (dark blue) produced during inspiration causes pressure decrease in temporary intracranial compartment, resulting in CSF outflow (Dreha-Kulaczewski et al. 2017) Delaidelli, Aet al. Journal of Neuroscience 2017 a. Arterial pulse wave (red) causes temporary pressure increase in intracranial compartment, resulting in CSF outflow (O'Connell,1943)
  • 13. Absorptio n Arachnoid villi  microscopic one-way valves (modified pia andarachnoid)  penetrate meningeal dural layer lining venous sinuses arachnoid villi = granulations = Clumps of arachnoid macroscopic
  • 14. Mechanism of absorption Hydrostatic pressure in subarachnoid space (11mmHg) > dural sinuses (5mmHg) Arachnoid villi open : pressure in SAS ~1.5 mm Hg > pressure in dural sinuses Passive process Papaiconomou,C.et al News Physiol Sci 2002
  • 15. Possible alternative sites of CSF absorption  Arachnoid endothelium & membrane  Adventitia of bloodvessels and lymphatics  Cranial/ spinal nerveroots sleeves/ lymphatics  Capillary endothelium  Spinal arachnoid projections Johnston, I et al. Child's Nerv Syst. 2000 Papaiconomou,C.et al News Physiol Sci 2002
  • 16. Functions of CSF • Cushion around the CNS • Protection(Coup Counter coup injury concept) • Buoyancy /Floating in CSF(Sp. gravity almost equal 140050gm) Post LP-- excess fluid-- traction in foramens - Headache incre. • Haemostasis/Reservoir/ Control • Nourishes- Lipid, Glucose, Electrolytes • Vehicle to remove metabolic waste (ECF and CSF easily exchange) • Carries hormonal Products of CNS • Immune Function- Immunoglobulin and immune Protection
  • 17. The Monroe-Kellie doctrine Sum of volumes of the 3 components is constant  an increase in volume of any one component  accompanied by a reduction in volume of at least one of the remaining two components ICP : Function of the volume and compliance of each component of the intracranial compartment The magnitude and the rate of change in the volume of each component determines its effect on ICP
  • 18. Intra Cranial Pressure (ICP) ≤ 15mmHg inadults Intracranial hypertension (ICH) : pressure≥ 20 mmHg Normally lower in children than adults Homeostatic mechanisms stabilize ICP Intracranial contents include : Brain parenchyma — 80 % Cerebrospinal fluid — 10 % Blood — 10%
  • 19. Cerebral Perfusion Pressure (CPP) The pressure needed to overcome ICP in order to deliver O2 & nutrients. Clinical surrogate for the adequacy of cerebral perfusion. MAP is the DRIVING FORCE ---------- ICP is the RESISTENCE CPP = MAP – ICP = 100 mmHg – 15mmHg = 85 mmHg (Normal) CPP < 50 mmHg → cerebral ischemia CPP < 30 mmHg→ brain death
  • 20. Features of CSF • Volume -150ml • 550ml/day @ 5.5 ml /min • Pressure – 50-150 cm H2O • No RBCs, No Neutrophils, Few Lymphocytes- < 5 / cumm • Glucose- 2/3rd level of plasma(In LP Study always take the venous sample) • Protein-Immune mediated diseases of CNS
  • 23. OP(CM APPEAR CELLS PROTEI GLUCO MISC. H20) ANCE N(MG%) SE FUNGAL MENINGITIS INCREASED OPALASCENT 30-300 (LYMPHO) 100-700 <30 +INDIA INK IN CRYPTO. TB MENINGITIS INCREASED OPALASCENT 50-500LY MPHO 60-700 20-40 ZN STAIN +/AFB CS WITH CLOT + BRAIN INCREAS CLEAR/ INCREAS INCREAS NORMAL LESS ABSCESS TURBID / SENSITIV DECREAS
  • 24. Other Biomarkers in CSF  CSF HCG- Central choriocarcinoma  CEA- breast,lungbladdermetsin CNS  Alfafetoprotein – germcelltumors, metastatictesticularandhepatic ca.  Spermidine– meningiomas  Polyaminein leukemia  Desmosterol in gliomas  betaglucuronidaseinleptomeningeal involvement
  • 25. VENTRICULAR CATHETERIZATION POINTS AND TRAJECTORIES OF ACCESS TO VENTRICLES —Kocherʼs point – 3 cm latto midline and 1cm ant to coronal suture —Keenʼs point 2.5 -3 cm above and 2.5-3cm behind pinna —Dandyʼ s point – 3 cm above inion and 2 cm lateral to midline —Frazierʼs point - 6 cm above inion and 4 cm latto midline —Orbital point – 1-2 cm behind superior orbital rim —Supra orbital – 4 cm above orbital rim in midpupillary line
  • 28. Consequences of altered CSF hydrodynamics Abnormal fluid movement (transependymal/transparenchymal) Effects of raised ICP Circulatory changes (micro and macro)  Ischemia Changes in brain morphology/parenchymal damage Changes in CSF circulatory path : obstruction/ shunt/ surgery  Effects of loss or misdistribution of CSF Post-shunt or other post-surgical changes Johnston, I et al. Child's Nerv Syst. 2000
  • 29. Classification of CSF circulation disorders Johnston, I et al. Child's Nerv Syst. 2000
  • 31. Causes of HCP Congenital Acquired Aqueductal stenosis (MC) SAH/ IVH Dandy-Walker malformation Infections : TBM Arnold-Chiari malformation Mass lesions /Tumors Agenesis of the foramen of Monro Posterior fossa cyst/ Arachnoid cyst Congenital toxoplasmosis Increased venous sinus pressure Bickers-Adams syndrome Traumatic brain injury Neural tube defects Idiopathic
  • 32. Diagnostic techniques USG  in infants (due to open fontanel) and in utero CT/MRI scanning : the mainstay of diagnosis CSF Flow study CSF pressure measurement
  • 33. CT/MRI features  Increased frontal horn radius (Mickey mouse ventricle)  Dilatation of the temporal horns (>2mm)  Acute ventricular angles
  • 34. CT/MRI features  Periventricular interstitial edema from the transependymal flow : high T2 signal on MRI or low- density change on CT  Intra-ventricular flow void from CSF movement
  • 35. CT/MRI Features  Inferior displacement of the floor of the 3rd ventricle  Outward bowing / ballooning of the lateral walls & recesses of the third ventricle (infundibular, optic and pineal recesses)  Ballooning of the suprapineal recess
  • 36. CT/MRI Features On mid-sagittal plane :  Upward displacement of corpus callosum  Thinned out corpus callosum  Depression of the posterior fornix  Decreased mamillopontine distance ( normal >5.5mm)
  • 37. CSF flow study To qualitatively assess and quantify pulsatile CSF flow MC technique : Time-resolved 2D phase contrast MRI with velocity encoding (VENC) CSF flow in the context of imaging : pulsatile to-and-fro flow due to vascular pulsations NOT bulk transport of CSF Typical CSF flow is 5-8 cm/s Hyperdynamic circulation : higher velocities : up to 25 cm/s Clinical applications  Aqueduct stenosis  Normal pressure hydrocephalus(NPH)  Patency of third ventriculostomy  Flow at the Cervico-medullary junction (foramen magnum)  Chiari I malformation
  • 38. CSF flow study Images are typically presented in sets of 3 for each plane and velocity obtained. The set comprises of  Re-phased image (magnitude of flow compensated signal) • flow is of highsignal • background isvisible
  • 39. CSF flow study  Magnitude image (magnitude of difference signal) • flow is of high signal (regardless of direction) • background is suppressed  Phase image (phase of difference signal) • signal is dependent on direction: forward flow is of high signal; reverse flow is of low signal • background is mid-grey
  • 40. CSF pressure measurement Direct assessmentof elevated ICP Surgical placement of ventricular / intraparenchymal pressure transducer Intraparenchymal transducer : more invasive /real time data/ accurate determination of ICP Helps in management decisions
  • 41. CSF Pressure Management The main goal is to minimize or prevent brain damage by decreasing ICP and improving CSFflow. Medical management- Acetazolamide, Diuretics therapy Temporary procedures  External ventriculardrainage  Spinal tap Surgical management  Shunt  Endoscopic Third Ventriculostomy (ETV)/other endoscopic procedure  Eliminating the cause of obstruction
  • 42. Endoscopic Third Ventriculostomy Indications:  Aqueductal stenosis  Posterior fossa tumors and cysts with hydrocephalus  Postinfectious hydrocephalus  Tuberculous meningitis with hydrocephalus  Hydrocephalus associated with myelomeningocoele and Chiari malformation  Hydrocephalus secondary to intracerebral / intraventricular hemorrhage  Shunt dysfunction Involves creating an opening in the floor of third ventricle to allow CSF to flow into pre-pontine cistern and subarachnoid space Absolute contraindication : obstruction at the level of the arachnoid villi or the venous flow in the superior sagittal sinus
  • 44. Additional Radiological findings  The Evans' index Ratio of maximum width of the frontal horns of the lateral ventricles (A) and maximal internal diameter of skull (B) at the same level Employed in axial CT / MRI images Varies with the age and sex Marker of ventricular volume A/B > 0.3 - Hydrocephalus
  • 45.  Narrow callosal angle: Angle measured on a coronal image perpendicular to the anterior commissure - posterior commissure (AC-PC) plane at the level of the posterior commissure Normal = 100-120° NPH = 50-80°
  • 46.  Cingulate sulcus sign : Denotes the posterior part of the cingulate sulcus being narrower than the anteriorpart. Divider b/w anterior and posterior parts of the sulcus : line drawn parallel to the floor of 4th ventricle
  • 47.  Cerebral aqueductflow void Loss of signal in the aqueduct ofSylvius Represents higher-than-normal flow velocity of CSF in the aqueduct
  • 48. (Disproportionately  DESH enlarged subarachnoid space hydrocephalus) Characterized by: • Ventriculomegaly • Tight high-convexity and medial subarachnoid spaces • Disproportionate enlargement of the Sylvianfissures • Focally dilated or entrapped sulci without adjacent cortical atrophy • Acute callosal angle
  • 49. Hydrocephalus ex vacuo Compensatory enlargement of the CSF spaces Seen in :  asymptomatic elderly people : aging brain with related volume loss  pathological conditions that promote brain shrinkage: degeneration (e.g. Alzheimer disease and due to focal damage (e.g. stroke and traumatic • generalised brain leukodystrophies) • encephalomalacia injuries)
  • 50. Benign external hydrocephalus Enlargement of the subarachnoid space  frontal or  frontoparietal regions Ventriculomegaly : absent or mild. Clinically, infants have macrocephaly but otherwise well-appearing and have normal development. Presentation : progressive increase in the head circumference with normal anterior fontanel. Family history of macrocephaly :Frequent Self-limited Do not require any intervention
  • 51. Arrested hydrocephalus Asymptomatic/ occult/ compensated/ long standing overt ventriculomegaly of adulthood/ late onset idiopathic aqueductal stenosis Moderate to severe tri-ventricular enlargement No evidenceof periventricular fluid accumulation on imaging Stable for years Incidental diagnosis Conservative approach with serial imaging May be associated with cognitive decline or sudden decompensation
  • 52. Intracranial Hypotension Defined as CSF pressure < 60 mm H2O in patients with clinical presentation compatible with intracranial hypotension Most commonly results from a CSF leak somewhere along the neuraxis Intracranial hypotension can broadly be divided into:  primary: referred to as spontaneous intracranial hypotension (SIH)  secondary: • iatrogenic (lumbar puncture or surgery) • over-shunting due to diversion devices, • traumatic Presentation : positional headache  relieved by lying in recumbent position within 15-30minutes  Nausea/vomiting/vertigo/neck pain Traumatic or iatrogenic intracranial hypotension : history of abundant, clear rhinorrhea or otorrhea present. Occasionally, presentation is more sinister, with reported cases of decreased level of consciousness and coma
  • 53. Radiographic features Imaging is crucial both for confirming the diagnosis of intracranial hypotension and identifying the location of the leak CT  Subdural collection  Acquired tonsillar ectopia  Dural venous sinus distention
  • 54. MR I  Pachymeningeal enhancement  Venous distensionsign  Subdural effusions / hematomas  Sagging brainstem / acquired tonsillar ectopia  Pituitary enlargement  Diffuse cerebral edema  Reduced CSFvolume  Decreased fluid within the optic nerve sheath
  • 55. Intracranial HypotensionManagement strict bed rest and the possible Conservative  Avoidance of the upright position : addition of analgesics.  Restoring CSF volume : oral or i.v. hydration, high oral caffeine intake, and high saltintake Epidural blood patches : firstline  Infusion of 10 to 20 cc of autologous blood into the epidural space  May be repeated  Adverse effects : back pain, radiculopathy, leg paresthesias, and fever Epidural fibrin glue Surgical repair