CSF and CSF Circulation

Dr. Asis S. Encarnacion Aug. 23, 2011

Legend: lecture /powerpoint, notes, 2012trans, emphasized – Most numerous at the superior surfaces of the cerebral
hemispheres
Physiology of the Cerebrospinal Fluid – Rate of absorption is pressure dependent
Adult average Intracranial volume 1700cc
- Brain 1400cc
- Blood 150cc
- CSF 50-160cc
• Varies with age
• 50% cranial; 50% spinal in adult
• 10% of intracranial/intraspinal space

Formation of the CSF

*formation rate is independent of ICP
• 18-22cc per hour
• Approx 450-528 cc per day
• CSF is renewed 3-5 times per day
• The rate of formation is independent of the intracranial pressure
(except in cases when ICP becomes so high that cerebral blood
flow is reduced)
• Formed by:
• Choroid Plexus Function
• Main source (80%) • Mechanical
• Lateral ventricles; 3rd and 4th ventricle – 1500 g brain (80% water) weighs only approx 50 g when suspended
• Thin walled vessels in CSF
• Passive diffusion from blood plasma to – Serves as shock absorber
extracellular space surrounding the choroid • “lymphatic”
plexus – “Alternative circulation”
• Presence of organelles indicating Active Clearing function
transport – Removes waste products
• Blood vessels in the subependymal regions and pia • C02
• meninges • lactate
• Electrolytes and glucose equilibrate with the CSF at all points in the • Mediates Intracranial compliance- Monro-Kellie hypothesis - any
ventricular and subarachnoid increase in volume of one of the cranial constituents must be
• Sodium transport, is accomplished by the action of an ATP compensated by a decrease in volume of another
dependent sodium-potassium-ion exchange pump in the choroid
plexus cells
• drugs that inhibit the ATP system reduce CSF formation

Normal CSF production, volumes and pressure

Property Newborn 1-10 Adult

Total volume 5ml 150 (50%

cranial, 50%
spinal)

Formation 25ml/day 18-22 cc/hr

rate approx
500cc/day

Pressure 9-12 Mean:10 7-15 (>18

abnormal)
Normal <15
Circulation of CSF
from Handbook of Neurosurgery, Mark Greenberg 6th edition choroid plexus → lateral ventricles → foramen of Monro (Interventricular
foramen)→ third ventricle → aqueduct of Sylvius (Cerebral aqueduct)→
• Sodium fourth ventricle→ foramen of Magendie (Median aperture) and foramina of
– Main cation Luschka (Lateral apertures)→ subarachnoid space→ arachnoid granulations
– Na-K ion exchange pump
• Other substances like drugs and metabolites depends on lipid Lumbar Puncture
solubility –enter when they are lipophilic Although CSF pressure may be measured during LP, this method is of limited
• Protein entry is dependent on diffusion gradient value in Intracranial pressure measurement.
• Water and sodium diffuse as readily from blood to CSF and - an isolated pressure reading does not indicate the trend in ICP and pressure
intercellular spaces as in the reverse direction. waves cannot be monitored.
• Rapid effects of intravenously injected hypotonic and hypertonic - lumbar puncture is contraindicated in the presence of an intracranial mass
fluids. .- pressure gradients exist between different intracranial and spinal
– Hypertonic saline to reduce increases in ICP compartments, especially in the presence of brain shift.
• Water enter sub-arachnoid space(SAS)>ventricles
• Electrolytes enter ventricles>SAS
•
Absorption
• Arachnoid Villi
– Outgrowth of arachnoid membrane which penetrate the dura
and protrude into the dural venous sinuses mainly the superior
sagittal sinus

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TAMARAY, Ethel Grace; TAN LIM, Pamela; TAN, Bernadine Joy
Function 3. Check if CSF is Clear - compare with water.
1. Diagnostic – CSF protein - >100mg/10ml >>>faintly yellow (could also be
 CSF sample caused by ↑papaya or carrot diet)
 Cell count, chemistries, GS-CS – 200 - 300 WBCs - cause CSF cloudiness
 Infectious – Dark CSF - metastatic melanoma, jaundice with
 Gamma globulin for MS hyperbilirubinemia
 SAH – Xanthochromia – SDH
 Pressure dynamics
 Quekenstedt test - for spinal block (i↑venous 4. Check CSF for cells within 1 hr or sooner
pressure = ↑ ICP done by compressing (No polymorphonuclear neutrophils-PMNs)
jugular or pressing duodenum, also (No more than 5 mononuclear cells)
therapeutic) – Distinguish bet RBCs & WBCs
 Administration of contrast material – Do Gram Stain or acid fast stain on centrifuged sediment(bact. vs
 myelography TB)
2. Therapeutic – India ink preparation(fungal disease eg Cryptococcus org)
 Spinal anesthesia – Millipore, Cytocentrifuge, or cytologic exam (tumor cells)
 Intrathecal antineoplastic drugs
 Removal of CSF in benign intracranial hypertension CSF Constituents
 Intraoperative maneuver to decrease the intracranial • Cellular components
pressure – 0-5 lymphocytes
Method: – No polys and RBC
 Midline bet L3-L4 or L4-L5 interspaces level of ASIS • Solutes
 Insert the bevel of the needle parallel to long axis of the spine – Sodium
 Use 20 - 22-gauge needle small gauge to avoid spinal trauma – Glucose >45 mg/dl
 Note opening and closing pressure & amount of fluid removed – Protein 15-50mg/dl
 Proper positioning is crucial – K+
 +Cisternal or Cervical (C1-C2) tap under fluoroscopy – Magnesium
– Ca++
Contraindications to Lumbar Puncture – Cl-
1. Infection at site of puncture – Bicarbonate
2. Bleeding disorder or with severe thrombocytopenia – Non protein nitrogen
3. Suspected mass lesion – Amonia
4. Presence of papilledema (relative) – Uric acid
 Idiopathic intracranial hypertension (pseudotumor cerebri) – Urea
 CSF examination is crucial – creatinine
 Elevated opening pressure
 Normal sugar and cell count: normal or low protein Examination of the CSF
 Mass lesion must be ruled out by CT or MRI
 ↑ ICP is not an absolute contraindication
 Mass lesion suspected esp pt with lateralized neuro finding or signs
or a possible mass in posterior fossa
Suspect: brain abscess in congenital heart disw with right to left
shunts, otitismedia or lung disease
 brain tumors - lead to herniation after LP esp post fossa
 subdural hematoma - not usually dx by LP, may be harmful
 ICH best dx by CT scan

Examination of the CSF

1. Collect four tubes:
– #1 tube - cell count – WBC, RBC
– #2 tube – chemistries – protein and glucose most impt in
clinical setting
– #3 tube - bacteriologic studies - culture
– #4 tube - saved for future use
2. If RBCs are present, count in 1st and 3rd tubes
– Analyze individually if RBC is present, this will determine SAH vs
Trauma
– If bottle 1-3 has consistent bleeding with increase WBC  SAH
o Bacterial = predominantly PMN
o TB = predominantly lymphocyte

SAH vs. Traumatic Tap

RBC count >100,000; changes Declines as CSF
little as CSF drains drains

WBC:RBC Ratio Elevated WBC Same ratio as in

peripheral

Supernatant Xanthochromic Clear

Clotting of fluid Does not clot Clots if RBC

>200,000

Protein 1mg/1000 RBC >1mg/1000 RBC

Repeat LP Remains bloody Usually clear

Opening pressure Usually elevated Usually normal

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 CT/MRI Criteria
Size of Temporal Horn (TH) is =>2mm W
- the sylvian and interhemispheric fissures
and cerebral sulci are not visible
Both TH are => 2mm, & the ratio FH/ID > 0.5
(FH - largest width of frontal horns, and ID -
internal diameter from inner table to inner table at
this level)
Evan’s ratio: ratio of FH to maximal biparietal
diameter > 30%
Disorders of CSF circulation
1. HYDROCEPHALUS
Pathogenesis and Classification of Hydrocephalus: Most experienced clinicians can recognize HCP by its appearance on CT or
CSF overproduction: MRI : “Eye-balling”
 choroid plexus tumor Eye balling is different from the encounter you have after an exchange of text
CSF flow obstruction: most common messages with a stranger.
 Functional Classification Numerous methods have attempted to quantitatively define HCP (most date
 Obstructive/Non communicating Hydrocephalus back to the early CT experience).
o -intraventricular
o -no communication b/n ventricle and subarachnoid Some presented here for completeness:
space (adams) Hydrostatic HCP is suggested:
o Block proximal to arachnoid granulation with a. Size of temporal horn is = > 2mm in width
enlargement of ventricles proximal to the block e.g., -in the absence of HCP, the TH should be barely visible
aqueductal stenosis >>> triventricular -The sylvian and interhemispheric fissures and cerebral sulci are
hydrocephalus) not visible
o Levels of CSF obstruction: Foramen of Monro, b. FH/ID >0.5
anterior third ventricle, posterior third ventricle
(aqueduct-pineal-quadrigeminal region), 4th Ventricles and CSF spaces:
ventricle, 4th ventricular outlet. Remember!
 Communicating Hydrocephalus World war II (WATER is WHITE on T2)
o -basal cisterns to subarachnoid space Bright on T2, dark on T1
o -there is connection b/n ventricles and spinal
arachnoid space T1 (dark) T2 (bright)
o Block at level of arachnoid granulation
CSF absorption disturbance at arachnoid granulations –venous sinus –
External Hydrocephalus
Estimated prevalence: 1-1.5%
Incidence of congenital hydrocephalus is =
0.9 - 1.8 /1000 births (reported range from 0.2 to 3.5 / 1000 births)
• Hydrocephalus Ex Vacuo
-enlargement of the ventricles due to loss of cerebral tissue (cerebral
T2 (Sagittal) T2 (Coronal)
atrophy), usually as a function of normal aging, but accelerated or accentuated
by certain disease processes.
– from severe head injury, infarction or cerebral hypoxia.
– Not true hydrocephalus.

Signs and Symptoms of Active HCP:

 In young children
 Cranium enlarges at a rate > facial growth
 Irritability, poor head control, N/V
 Fontanelle full and bulging
 Enlargement and engorgement of scalp veins
 Macewen’s sign (cracked pot sound on percussing over dilated V) CT/MRI Criteria:Other Features:
 6th nerve(abducens) palsy – Ballooning of frontal horns of lateral ventricles (“Mickey Mouse”
 “setting sun sign” (upward gaze palsy, Parinauds syndrome) ventricles) and 3rd ventricle
 Hyperactive reflexes – Transependymal absorption (periventricular low density)
 Irregular respirations with apneic spells
 Splaying of cranial sutures(seen on plain skull x-ray)

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 The current recommendation is that women at high risk* for the development
on NTD ingest 4 mg / day of folic acid from 1 month before pregnancy through
the first trimester.

Incidence in US and Europe

Before 1980 1,5 x 1000 live births
By 1990 0,6
Nowadays 0,4
– Evan’s ratio: ratio of FH to maximal biparietal diameter > 30% Termination of pregnancy after prenatal diagnosis was responsible for 20% to
– Sagittal MRI may show upward bowing of the corpus callosum 31 % of the decline.
(Cuckle H.et al 1987, Cragan J.et al 1995, Van Dorsten et al. 1998)

Associated pathology:
Hydrocephalus
A shunt is indicated at the 1st sign of increased ICP.

Shunt revision vs Endoscopic 3rd ventriculostomy

Approximately 15% of patients with a MY are born with severe hydrocephalus
evident at birth and require immediate shunt placement.

If the shunt is not performed, the increase of CSF pressure after MY repair
Causes: increases the chance of wound dehiscence and CSF leak from the back repair.
Congenital
– Chiari Type 2 malformation and/or myelomeningocele Repair:
– Chiari Type 1 malformation: HCP with 4th outlet obst. Timing:
– 1* aqueductal stenosis- presents in infancy Can be performed up to 72 hours after birth
– 2* aqueductal gliosis - intrauterine infxn Delayed repair: 75% shunt infection, 13% mortality (negative culture is
– Dandy-Walker malformation mandatory; if with infection, Treatment: EVD + Antibiotic)
– X-linked inherited disorder
Acquired More recently no clear association has been found between the timing of
– Infectious surgery and: survival, development of infection, worsening of the neurological
– Post-hemorrhagic deficits and developmental delay.The use of antibiotics significantly reduced
– Secondary to masses the risk of infection.
– Post-op Charney EB, 1985
– Asstd Spinal tumor
2. ARACHNOID CYSTS Objectives:
See below 1. Protect the functional tissue in the neural placode
3. SPINAL DYSRAPHYSM 2. Prevent loss of CSF
Chiari II with MM 3. Minimize the risk of meningitis
OJ
-CSF leak at birth until 2 wks old GOAL of SURGERY IN MM CLOSURE:
-enlarging cystic mass at LS area 1. Eliminate CSF leak
2. Prevention of infection
3. Preserve neural functions

Early Complications of Myelomeningocoele Repair:

1. Significant wound dehiscence
2. Wound infection

1985 to present
Chiari II Malformation -Child Abuse Prevention Act mandates treatment for every infant unless: the
infant is chronically and irreversibly comatose and treatment would merely
• Associated with 34-38% mortality prolong dying or be virtually futile and inhumane.
• Intermittent obstructive or central apnea, cyanosis, bradycardia, dysphagia,
nystagmus, stridor, vocal cord paralysis, torticollis, opisthotonus, -Closure of MM within first 72 h. practiced widely.
hypotonia, upper ext. weakness and spaticity. -MRI allows timely surgical treatment of the late neurologic deteriorations.
• 23% symptomatic, 17% required decompression
Hydrocephalus
*Myelomeningocele: Illustration given:
Neural placode – flat plate of neural tissue; unfused spinal cord during primary Delicia Roldan 55 yr F Jan 2006 UE
neurulation -HA
-Cervical pain
Closure of the posterior neuropore: (stage 12, 26 days) -Unsteadiness
-Extremity weakness
Location:
85% thoracolumbar Hydrocephalus: Causes
10% thoracic
Aqueductal Stenosis
5% cervical
-may result from a congenital malformation of the aqueduct
80-90% have HCP
-result from gliosis around aqueduct of Sylvius in response to an
40-80% have Hydrosyringomyelia
inflammatory process.
Prognosis:
Illustration given:
95% 2 year survival
R.F. 1 yr old boy
10-15% Die before age 6
-Increasing head circumference
75-80% Normal intelligence with aggressive management
-Irritability
60% Ambulatory (Motor level determines the ambulatory status)
-Poor suck
6-17% Normal urinary continence
-Distended scalp veins
86% Social fecal continence

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 2. Infections
-congenital or neonatal herpes
-toxoplasmosis
-equine virus

Hydranencephaly vs. HCP

Means to differentiate:
EEG - best way
Hydranencephaly - no cortical activity
Diagnostic studies demonstrate enlargement of lateral and third ventricles but HCP - abnormal with background activity
not fourth ventricle.
• CT, MRI, US
Hydrocephalus – Majority of IC spaces occupied by CSF
- due to subnormal CSF reabsorption, rarely to CSF over production (choroid – Brainstem nodule - rounded thalamic masses, hypothalamus and medial
plexus papilloma). occipital lobes sitting on the tentorium occupies midline position
surrounded by CSF
Even her reabsorption is probably defective in some as normal individual could – Posterior fossa grossly intact
probably tolerate slight increase in CSF production.
• Transillumination of the skull
Congenital: HCP - ordinarily does not transilluminate unless
1. Chiari Type ll and /or myelomeningocele (MM) usually occur together. <9 month old, cortical mantle <1cm thick
If fluid displaces cortex inward - subdural effusion
2. Chiari type l - Too nonspecific
- hcp may occur with 4th ventricular outlet obstruction
• Angiography
3. Primary aqueduct stenosis – Bilateral ICA occlusion - no flow through supraclinoid carotids
- usually presents in infancy, rarely in adulthood – Normal posterior circulation

4. Secondary aqueductal stenosis Hydrocephalus: Causes

- due to intrauterine infection or germinal matrix hemorrhage – Intracranial Tumors or Cyst
– Vein of Galen Aneurysm
5, Dandy-Walker amlformation – Periventricular hemorrhage in premature infants
- atresia of of foramina of Luschka and Magendie – Leptomeningeal Inflammation from Infection- TBM, SAH
-the incidence of this in patient with HCP is 2.4% – Post-op
– Associated Spinal tumor
6. Rare X- linked inherited disorder
Choroid Plexus Papilloma
Severe Hydrocephalus -Secretes too much CSF; problem also in absorption
Illustration given:
J.C. 3 month old girl Illustration given:
-Increasing head circumference Baby boy with history of vomiting and irritability and increasing head
-Irritability circumference.

Hydranencephaly
-Post-neurulation defect
-Total or near-total absence of the cerebrum

Small bands of cerebrum may be consistent with the diagnosis with intact
cranial vault and meninges, the intracranial cavity being filled with CSF.

IVH with HCP after trauma

Hydranencephaly Illustration given:
- there is usually progressive macrocrania, but head size may be normal (esp. AT, 15 yr old boy
at birth), and occasionally microcephaly may occur. -Mauling victim
- facial dysmorphism is rare -Presented with no verbal and eye opening response
-Withdraws to pain
-Was hit on the leg and fell hitting occipital area first
-2hr post trauma CT: ns status GCS 6
-11 hrs after initial ct: ns status
-Ventriculostomy done
-Presently:3rd week post trauma - sustained eye opening

Third Ventricular Cyst

Illustration given:
Trauma:
Kelly Cuesta 4yr old girl with history of trauma
Hydranencephaly: Causes Later deteriorated to decreased sensorium
1. Bilateral ICA infarcts
-results in absence of brain tissue supplied by the anterior and middle cerebral TB Meningitis
arteries with preservation in the distribution of the PCA -causes problem in CSF

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VP Shunt Procedure External Hydrocephalus
-tip of catheter should end at frontal horn - enlarged subarachnoid space (cortical sulci & basal cisterns) seen in
childhood.
- inc head circumference with normal or mildly
dilated ventricles.
- no other signs and symptoms
- benign subddural collections (or extra-axial fluid) of infancy
- maybe variant of communicating HCP.
- vs. symptomatic chronic extra-axial fluid colllections.

*Symptomatic chronic extra-axial fluid collections are accompanied by seizure,

vomiting, and headache.

“Arrested Hydrocephalus”
- refer to a situation where there is no progression or deleterious sequelae due
to hydrocephalus that would require the presence of a CSF shunt.
- “compensated hydrocephalus”
- Satisfies the ff criteria in the absence of a CSF shunt:
Shunt Complications:
-Near normal ventricular size
1. Infection: shunt perforates skin
-Normal head growth curve
2. Distal Shunt Obstruction -if enveloped in omentum, fluid can’t escape
-Continued psychomotor development
3. External Hydrocephalus -enlarged subarachnoid space
Arrested or compensated HCP
4. Arrested Hydrocephalus -no signs and symptoms that would require
- exact definition not generally agreed upon, used interchangeably.
shunt
- most clinicians use to refer to a situation.
Third Ventriculostomy Concept of becoming independent of a shunt is not universally accepted.
Indications: Some feel that shunt independence occurs more commonly when HCP is due
• Obstructive HCP to a block in the subarachnoid granulations (comm. HCP), but others have
• Shunt infxn - option shown that it can occur regardless of etiology. The patients must closely
• Slit ventricle followed up because there are reports of death as late as five years after
• SDH after shunting apparent shunt independence, sometimes without warning.
Overall success rate 56%; 20% if with preexisting pathology.
Highest maintained patency rate is with previously untreated acquired Ventriculostomy
aqueductal stenosis.
Poor in infants - not have normally developed SA space.

Endoscopic cauterization of the choroid plexus

Shunt problems:
1. Undershunting - obstruction
2. Infection
3. Overshunting: slit ventricle syndrome, subdural hemaTOMA
4. SEIZURES
5. Problem related to distal catheter
6. Skin breakdown
7. One & two acct for most common shunt prob
Skin breakdown over hardware: infections or silicone allergy.

Distal shunt obstruction

Illustration given:
Mark Yanez 30 yr old Arachnoid Cyst
-Diagnosed with Pilocytic Astrocytoma, operated when he was 12 yr old and
shunted
-HA and Vomiting few hrs PTA
-Distal shunt obstruction secondary to shunt breakage

• Congenital lesion which arise during development wherein there is

splitting of the arachnoid membrane
• Technically an intra-arachnoid cyst
• Usually supratentorial, heterogenous lesion

True arachnoid cysts

- Fluid collections within the arachnoid membrane
- Produce symptoms by pressure
- Focal bulging of skull may result

Hydrocephalus
• Hydrocephalus Ex Vacuo
- certain disease processes eg SDAT, Creutzfeldt-Jacob accelerates ex
vacuo.
- ventric enlargement due to loss of brain parenchyma rather than from
overproduction or underabsorption of CSF or an obstruction of CSF flow.

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False arachnoid cysts
- Fluid accumulations resulting from pos-tinflammatory location of the
subarachnoid space (head injury, intracranial infection, hemorrhage)

Management:
Conservative: -in asymptomatic patients with normal CSF pressure
Surgical:in symptomatic patients

Aim of the surgical treatment:

 To eliminate the pressure exerted by the lesion
 To restore CSF circulation

FAILURES: 25% are caused by too limited cyst wall excision, impaired
CSF circulation/absorption,late obliteration of the cyst opening)
Surgical options:
1. Drainage- High rate of recurence
2. Craniotomy- Cyst wall excision/marsupialization and Fenestration
into the Subarachnoid space.
3. Shunt –cons: patient becomes dependent on shunt
a. Ventriculo-peritoneal or Cysto-peritoneal
b. Probably the best surgical option
c. Shunt dependent
4. Endoscopy
a. Fenestration into the subarachnoid space

No % No %
• SUPRATENTORIAL: 161 77 336 77
• Sylvian fissure 103 50 162 34
• Sellar region 18 9 73 15
• Cerebral convexity 9 4 70 15
• Interhemispheric 10 5 36 8
• Quadrigeminal 21 10 25 5
No % No %
• INFRATENTORIAL: 47 23 112 23
• Cerebellar midline 19 9 86 17.5
• Cerebellar hemisph 22 11 24 5
• Retroclival 6 3 2 0.5

Arachnoid cyst:
Natural history:
-Quiescient throughout life Sellar region cysts: Risk for visula impairment
-Dormant for years before showing clinical manifestations
-Occasionally disappearing spontaneously
-Progressively enlarging, compressing and dislocating surrounding structures,
and interferring with CSF circulation.

RUPTURE
-Gradual resolution after spontaneous rupture into the subdural space.

Pathogenesis of enlargement:
• Osmotic gradient
• Ball-valve mechanism (microsurgical and endoscopic observations)
• Fluid production by the cyst wall cells (similar to the subdural
neuroepithelium)

Arachnoid cyst – picture next column

Conclusions:
1. Arachnoid cyst are heterogeneous lesions
2. Clinical manifestations as well as surgical indication depend on cyst location
3. Surgical indication is doubtful in several cases
4.The choice of surgical modalities is difficult because of the unpredictability of
results however, some procedures should be preferred for specific locations
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(e.g.endoscopic fenestration for sellar cysts, cyst excision for interhemispheric Hehe, may siningit ako from doc bka makatulong.
cysts). Dr. Encarnacion said: “I typically start with a bugbee wire electrode and
SURGICAL INDICATION( in adult) : use it as a blunt probe. If the membrane is not penetrable with the probe
YES- for symptomatic cysts (intracranial hypertension, neurological deficits, I will then shrink it by applying cauterizing energy to the probe. If I am
epilepsy); working the superior wall of a suprasellar arachnoid cyst or the lateral
NO- for asymptomatic cysts incidentally found after completion of the cerebral wall of a quadrigeminal cyst I will use the probe to cut an opening using
development. cautery. If necessary I will cut a series of openings close to one another
SURGICAL INDICATION( caution in children!!!!) and then use a pair of scissors to connect these openings to make a
NO - asymptomatic cysts located in particular areas (e.g. Sylvian fissure: note large one. Cautery can also be used to shrink the membrane tissue
for bleeding) adjacent to the opening and in doing so further enlarge the opening. I will
YES for asymptomatic cysts found in neonates and infants (e.g. then navigate the scope through the opening. When dealing with the
interhemispheric cysts:impairment in cerebral growth) inferior cyst wall of a suprasellar cyst or medial wall of a middle fossa cyst
Dandy Walker Syndrome: I will use the bugbee as a blunt probe to make the opening without
applying cautery. These membranes are typically diaphanous and easily
penetrated. I then will use a fogarty balloon to enlarge the opening or
simply navigate the scope through the opening made by the probe to
ensure communication with the adjacent CSF space.”

Checker’s comments: I don’t want to comment. Just be calm. Inhale.

Exhale. Inhale. Exhale. Do a better job next time.

- consists of a small malformed cerebellum, a large posterior fossa

cyst in communicqation with the fourth ventricle, and obstruction to
the flow of CSF from the fourth to the subarachnoid cisterns.
- enlargement of the posterior fossa results in a prominent occiput.
ARACHNOIDAL CYST TECHNIQUES:
1. PENETRATION: BLUNT, CAUTERY, LASER, SHARP
2. ENLARGEMENT

*There are several techniques available to the endoscopists that will

make an opening through tissue.
a. Blunt probes- it can be pushed through tissue. This is a technique
used by many when performing a third ventriculostomy.
* With arachnoidal cysts, however, the membrane is typically very tough
and the cyst will tend to move with the probe as it is advanced thus
resisting penetration. The membrane can be tightened and thinned using
cautery.
b. Cautery- it can also be used to cut through the membrane but this can
be dangerous when vital structures line the membrane as is the case with
the medial wall of a middle fossa cyst or the inferior wall of a suprasellar
arachnoidal cyst.
*Care must also be used when a laser is chosen to cut through a
membrane. Fibers that lend themselves to endoscopy deliver a beam
and that beam can continue to travel. It can hit a vessel or other critical
tissue once it has cut through the membrane.
d. Sharp instruments such as scissors or blades can be used to cut
openings through the membrane.
* Once the opening has been made it usually needs to be enlarged both
to insure patency over time and to allow for the scopes advancement
through the opening to ensure a clear path. This can be done by
spreading an instrument such as scissors or forceps as they straddle the
opening. Further enlargement occurs when the scope is advanced
through the opening.

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