Slit ventricles refer to complete collapse of the ventricles. Slit ventricle syndrome involves intermittent headaches in shunted patients with small ventricles and slow reservoir refilling. It is usually caused by chronic, nonphysiologic CSF drainage from the shunt. Management involves adjusting shunt valve pressure or adding an antisiphon device to drain less CSF while maintaining stable ventricle size. Evaluation assesses CSF pressure and attempts to identify patients who may no longer require the shunt.

1. SLIT VENTRICLES
AND
SLIT VENTRICLES SYNDROME
Dr SAMEEP KOSHTI

2. • "Slit ventricles" refers to
• complete collapse of the ventricles.
• In a survey, a frontaloccipital horn ratio< 0.2 was most often interpreted as representing
SVS.
•Slit ventricle triad :
• Intermittent headaches,
• small ventricles, and
• a slowly filling reservoir.

3. • PRESENTATION OF SLIT VENTRICLES:
• AYMPTOMATIC
• The pediatric literature has estimated that
• small ventricles exist in as many as 80% of shunted children,
• only 10% of whom have symptoms
• SLIT VENTRICLE SYNDROME
• INTRAVENOUS HYPOTENSION (POSTURAL DUE TO TRUE OVERSHUNTING)
• usually self limited,
• Bed rest and analgesic
• Trial with tight abdominal binder
• if symptoms persist after 3 days
• the valve should be checked for proper closing pressure.
• If it is low  replace with a higher pressure valve.
• If it is not low  an antisiphon device (ASD) WITH or WITHOUT HIGHER PRESSURE VALVE
• ASD  also increases the resistance of the system•

4. SLIT VENTRICLE SYNDROME
• Definition of SVS:
• development of intermittent headaches, usually lasting 10 to 30 minutes, in a
shunted patient with smaller than usual ventricles.
• In addition, the reservoir refill may be slow.

5. Etiology
• The general etiology of SVS is
1. chronic, nonphysiologic CSF drainage.
• Because the intraventricular pulse amplitude hypothesized to maintain ventricular size may also be
reduced by the pressure regulation of the shunt.
2. pressure differential and a higher than normal brain compliance could be the cause of
the slit ventricles.
• Because the observation of the sudden conversion of slit ventricles into large ventricles with
• progressive increase in opening pressure or
• after reduction of subarachnoid volume and pressure via lumbar puncture (LP)
• The etiology of the pain that is described
1. May be low.
2. may be associated with high pressures even as the ventricles remain small.
• considered due to evidence of reduced compliance.
• May be due to ependymal or glial scarring (no evidence rather).
• May be due to Vascular engorgement

7. Subtypes of SVS
• A. intermittent shunt occlusion:
• overshunting leads to ventricular collapse (slit ventricles) -> which causes the ependymal lining to occlude the inlet ports of the
ventricular catheter (by coaptation) producing shunt obstruction.  With time, many of these patients develop low ventricular
compliance, where even minimal dilatation results in high pressure which produces symptoms.-Expansion then eventually
reopens the inlet ports allowing resumption of drainage (hence the intermittent symptoms).
• Symptoms (of shunt malfunction)
• intermittent headaches unrelated to posture,
• often with NN, drowsiness, irritability and impaired mentation.
• Signs may
• include 6th cranial nerve palsy.
• Incidence in shunted patients: 2-5%
• CT or MRI scans may also show evidence of transependymal absorption of CSF
• B. total shunt malfunction (AKA normal volume hydrocephalus):
• may occur and yet ventricles remain slit-like if the ventricles cannot expand
• because of subependymal gliosis, or
• due to the law of Laplace (which states that the pressure required to expand a large container is lower than the pressure required to expand a small
container).
• C. venous hypertension with normal shunt function:
• may result from partial venous occlusion that occurs in some conditions (e.g. at the level of the jugular foramen in Crouzon's
syndrome).
• Usually subsides by adulthood

8. TRUE SHUNT FAILURE
• Present more acutely with
• unremitting headache, papilledema, cranial nerve deficits, and
• more ominous signs of impending herniation : including Cushing's phenomenon.
• Because the radiographic findings are usually
• unremarkable or lag behind the clinical symptoms,
• true shunt obstruction may be recognized late.

9. D/D of HEADACHE IN SHUNTED PATIENT AND SMALL
VENTRICLES (BASED ON ICP )
1. CSF leak (LOW PRESSURE)
• pressures may be consistently low, or low with standing.
• Headache is positional, But effect is variable.
• Etiology :
• Shunt overdrainage
• Spontaneous CSF leak
• Leak caused by LP
• Lumbar shunt (for treatment of SVS)
• Treatment:
• decreasing the drainage with a different valve, a shunt assist device, or an adjustable valve adjustment
is the treatment of choice.

10. • 2.EPISODIC INTERMITTENT BLOCKAGE OF SHUNT BY VENTRICULAR
EPENDYMAL LINING (NORMAL PRESSURE)
• Described as intermittent shunt occlusion.

11. • 3.TOTAL SHUNT OCCLUSION AND VENOUS HYPERTENSION (HIGH PRESSURE)
• blocked shunt,
• usually at the site where the catheter and tissue are adherent.
• Treatment:
• Shunt exploration and revision are appropriate.
• other possible causes:
• IIH,
• elevated venous pressure may also be considered.
• Magnetic resonance venograms or formal angiograms to rule out venous outflow obstruction or jugular
foramen compression

12. • 4. IATROGENIC CEPHALOCRANIAL DISPROPORTION (Due to Chronic
shunting from infancy)
• Skull fails to expand because of LOW CSF HYDROSTATIC PRESSURE.
• Treatment:
• the use of cisternal catheters: effective method to drain CSF.
• The addition of a lumboperitoneal shunt: for refractory cases
• form of cranial expansion : for the root cause.
• Hemispheric or occipital expansion,
• including enlarging the foramen magnum,
• Other less radical surgeries, including
• subtemporal decompression (occasionally)

13. EVALUATION OF SLIT VENTRICLES
• The shunt valve fills slowly if pumped when the ventricles are
collapsed.
• Monitoring CSF pressure:
• either via lumbar drain, or
• with a butterfly inserted into the shunt reservoir
• (with this method, pressure can be followed during postural changes to look for negative
pressure when upright; possibly higher risk of infection with this).
• These patients are also monitored for pressure spikes, especially during sleep.
• "shunt-o-gram"

14. • MANAGEMENT OF SVS
MANAGING SHUNTS IN CHILDREN TO PREVENT SVS
• Children with small or collapsed ventricles may undergo:
• exchange of their low-resistance valve to a high-resistance valve ,
• incorporation of antisiphon devices, or
• conversion to programmable systems with the intent to slowly adjust the valve pressure
upward as the child grows.
• Children with progressive collapse of ventricles,
• the long-term benefits should be considered.
• With the use of adjustable systems from the beginning of shunting
• opening pressures may be increased gradually without surgical intervention as the patient develops
from infant to full-grown adult.
• Even if the child is clinically doing well, if the ventricles are small or decreasing in size,
• adjustments may proceed in a stepwise fashion over years
• An antisiphon device may be added during this process only if needed.

15. REMOVAL OF SHUNT TIMINGS?
• The overriding concept is
• to drain as little CSF as possible and still achieve stable ventricles and a stable clinical status.
• Patients reaching adolescence or adulthood who have avoided shunt revision until then :
• are best evaluated for shunt independence with clamping and monitoring of symptoms and pressure.
• Baskin and colleagues described a shunt removal protocol designed
• to identify those SVS patients in whom a shunt is no longer needed,
• and another group who still demonstrated a need for drainage, who were treated with ETV.
• Shunt independence may be difficult to determine
• even with extended inpatient monitoring.
• Although the number of children growing into adulthood and becoming shunt independent
• estimated it as low as 3.2%