The anatomy of the ventricular system, the physiology in production of CSF, the pathogenesis, and the different paediatric and adult forms of hydrocephalus.

1. HYDROCEPHALUS
MED/1004/16- DAUDI CHIRANZI
FACILITATOR: DR. KIRONGO

2. Definition
• Hydrocephalus is a diverse group of conditions that result to impaired
circulation of and/or absorption of CSF and also from increased production of
CSF.
CSF functions
• Physical protection for the brain and spinal cord through buoyancy.
• Reservoir to get rid of metabolites and toxins from the brain.
• Circulation of nutrients and chemical buffering.

3. CSF PRODUCTION
• CSF is an ultrafiltrate of the plasma in the ventricular system, by the choroid plexus in each
ventricle (60-80%).
• Remainder of the CSF is produced by cerebral tissue, directly into the extracellular space.
• The choroid plexus tissue consist of villous folds lined by epithelium and a central core of
highly vascularized connective tissue.
• The fluid is formed by active transport (and diffusion) dependent on the action carbonic
anhydrase.
• Active neurogenic control.

4. CSF PRODUCTION cont-
• CSF production daily:
1. 20-30 ml/hour
• About 500 ml of CSF produced daily.
• Constantly absorbed such that:
1. 50 ml (Infants)
2. 150 ml (Adults)

5. Histology of Choroid plexus

6. GROSS ANATOMY

7. RELATIONS
1. Lateral ventricles
• In the cerebral cortex
• Four parts-
Anterior horn and body–
Roof- Trunk of corpus callosum
Floor- Rostrum of the corpus callosum
Medial wall- Septum pellucidum
Lateral wall- Head of caudate nucleus

8. Posterior horn
In the occipital lobe
Inferior horn
Roof- Tapetum and tail of caudate nucleus
Floor- Collateral eminence, hippocampus, choroid plexus

9. 2. Third ventricle
• In the diencephalon between the two thalami.
• Its relations include:
Roof- body of fornix, choroid plexus.
Floor- Optic chiasm, infundibulum of the hypothalamus, tuber cinerium, mammillary bodies,
posterior perforated substance, the anterior part of the tegmentum of the midbrain.
Anterior wall- Foramina of Monro, Columns of fornix, anterior commissure, lamina terminalis,
optic recess, optic chiasm

10. Posterior wall- Suprapineal recess, Habenular commissure, pineal body, posterior commissure,
Aqeuduct of Sylvius.
Lateral walls- medial aspects of thalami and hypothalamus.
• The cavity extends into four recesses:
1. Supra-optic recess
2. Infundibular recess
3. Pineal recess
4. Suprapineal recess

11. 3. Fourth ventricle
• Lies behind the pons and forms the rhomboid fossa.
• The fourth ventricle has the following brain relations:
Floor- The trigeminal, abducens, facial, vestibular and cochlear nuclei, vagal and hypoglossal
triangles.
Roof- the superior and inferior medullary vela.

12. CSF CIRCULATION

13. CSF CIRCULATION cont-
Lateral ventricles
3rd Ventricle
4th Ventricle
Subarachnoid space and the cistern system
Foramina of Monro
Aqueduct of Sylvius (1.4-1.5cm)
lateral foramina of Luschka and
midline foramen of Magendie

14. CSF ABSORPTION
• CSF is absorbed into the systemic venous circulation primarily across the
arachnoid villi into the venous channels of the major sinuses.
• The arachnoid villi act as a one-way valve, allowing passive absorption of CSF
down a pressure gradient.

15. CSF ABSORPTION

16. ETIOLOGY OF HYDROCEPHALUS

17. PATHOGENESIS OF HYDROCEPHALUS
• Hydrocephalus results from an imbalance between the intracranial CSF inflow and outflow. It
is caused by obstruction of CSF circulation, by inadequate absorption of CSF, or rarely by
overproduction of the CSF.
• Regardless of the cause, the excessive volume of CSF causes increased ventricular pressure
and leads to ventricular dilatation.
• Many cases have both obstructive and absorptive components.

18. 1. Obstruction (obstructive hydrocephalus)
The most common mechanism. Involves anatomic or functional obstruction to CSF flow. The
obstruction occurs at the foramen of Monro, at the aqueduct of Sylvius or at the fourth ventricle
and its outlets.
Dilatation of the ventricular system occurs proximal to the obstruction.
• Obstruction of the aqueduct of Sylvius causes dilatation of the lateral and third ventricles,
while the size of the fourth ventricle remains relatively normal.
• Obstruction at the body of the lateral ventricle causes dilation of the distal temporal horn and
atrium.
• Obstruction of one foramenof monro causes dilatation of the lateral ventricle on that side
• Obstuction of flow from the fourth ventricle causes dilation of all four ventricles

19. 2. Impaired absorption (communicating hydrocephalus)
Typically due to inflammation of the subarachnoid villi but also may be caused by impaired
CSF absorption or increased pressure in the venous sinuses.
3. Excessive production
Rare cause. May occur with a functional choroid plexus papilloma

20. PATHOPHYSIOLOGY OF HYDROCEPHALUS
• Depends on the underlying cause, how quickly the condition develops and the presence or
absence of compensatory mechanisms.
• Hydrocephalus that begins in infancy before the fusion of the cranial sutures, if untreated,
typically results in marked enlargement of the head and in less compromise of brain tissue,
compared with hydrocephalus that develops acutely.
• This is because the skull expands, partially relieving the ICP. In addition, the force of the ICP
is distributed over the greater surface area of an enlarged ventricular system, so there is less
pressure on the brain parenchyma compared with hydrocephalus that develops in a ventricular
system that is not previously enlarged.
• If it occurs acutely or occurs after the fusion of the cranial sutures, the head does not
enlarge. This results in significantly increased ICP and in more rapid destruction of brain
tissue.

21. • The progression of ventricular dilatation is usually uneven. The frontal and occipital horns
typically enlarge first and to the greatest extent.
• Their progressive enlargement disrupts the ependymal lining to the ventricles, allowing the
CSF to move directly in to the brain tissue. This reduces CSF pressure but also leads to
edema of the subependymal areas and to progressive involvement of the white matter.
• As the hydrocephalus progresses, edema and ischemia develop in the periventricular brain
tissue, leading to atrophy of the white matter
• The gyri become flattened, and the sulci become compressed against the cranium, obliterating
the subarachnoid space over the hemispheres.
• The width of the cerebral mantle may be substantially reduced, gray matter is better preserved
than white matter, even in advanced stages.
• The vascular system is compressed and the venous pressure in the dural sinuses increases.

22. • There may absorption along nerve root sleeves (which may result in enlarged optic nerve
sheaths).
• May also result in elevation of the corpus callosum, stretching or perforation of the septum
pellucidum, thinning of the cerebral mantle, or enlargement of the third ventricle
downward into the pituitary fossa (which may cause pituitary dysfunction) as well as dorsal
midbrain compression resulting in Parinaud’s syndrome (paralysis of upward gaze, Pseudo-
Argyll Roberson pupils, convergence-retraction nystagmus, eyelid retraction and setting sun
sign).
The mechanism of NPH has not been elucidated compeletely.
• Current theories include increased resistance to flow of CSF within the ventricular system or
subarachnoid villi; intermittently elevated CSF pressure, usually at night and ventricular
enlargement caused by an initial rise in CSF pressure. The enlargement is maintained despite
normal pressure because of the Laplace law. Although pressure is normal, the enlarged
ventricular area reflects increased force on the ventricular wall.

23. CLASSIFICATION OF HYDROCEPHALUS
A.OBSTRUCTIVE VS. COMMUNICATING
HYDROCEPHALUS

24. OBSTUCTIVE/ NON-COMMUNICATING
HYDROCEPHALUS
• Caused by any lesion blocking the CSF pathways from the lateral ventricles to the fourth
ventricle.
• Ventricular fluid does not communicate with CSF in the spinal subarachnoid spaces or in the
basal cisterns.
• Proximal dilatation from site of obstruction.
• Susceptible sites include the foramen of Munro (colloid cyst of the third ventricle) and
cerebral aqueduct (congenital aqueduct stenosis, tectal plate glioma).
• Lesions may be within the ventricle, in the ventricular wall or distant from the ventricle but
exerting mass effect on it
• Posterior fossa mass lesions are more likely than supratentorial lesions to present with
obstructive hydrocephalus because the fourth ventricle is easily compressed within the
relatively small posterior fossa.

25. CAUSES OF OBSTRUCTIVE HYDROCEPHALUS
1. An abnormality of the Aqueduct:
• Stenosis; Congenital - inherited as a sex-linked recessive trait ,Acquired in Neurofibromatosis
• Gliosis; Intrauterine viral infections, SAH in a premature infant, Neonatal meningitis,Mumps
meningoencephalitis
2.Lesions in the fourth ventricle:
Chiari malformation
• Type II is characterized by progressive hydrocephalus and a myelomeningocele which results in
elongation of the fourth ventricle and kinking of the brain stem, with displacement of the inferior
vermis, pons, and medulla into the cervical canal.
• Produce symptoms during infancy consisting of stridor, weak cry, and apnea, which may be relieved
by shunting or by posterior fossa decompression.
• Type I produces symptoms during adolescence or adult life and is usually not associated with
hydrocephalus.
• These patients complain of recurrent headache, neck pain, urinary frequency, and progressive lower
extremity spasticity. The deformity consists of tonsilar herniation.

26. Dandy-Walker syndrome
• Consists of a cystic expansion of the fourth ventricle in the posterior fossa, which results from
a developmental failure of the roof of the 4th ventricle during embryogenesis.
Posterior fossa brain tumors - Meduloblastomas, hemangiomas, epindymomas.
3.Space occupying lesions may obstruct the flow along anywhere along the ventricular system-
Tumors, bleeds etc.

27. COMMUNICATING HYDROCEPHALUS
•Communicating hydrocephalus refers to circumstances in which the intracerebral CSF pathways
are patent but there is accumulation of CSF, usually due to impaired CSF absorption
•Mostly resulting from obliteration of the subarachnoid cisterns or malfunction of the
arachnoid granulations.
•The block is outside the ventricular system, and fluid within the ventricles communicates with
the spinal subarachnoid space and basal cisterns.
•This may be because the CSF constituents have altered such as in cases of meningitis or
subarachnoid haemorrhage (SAH).

28. CAUSES OF COMMUNICATING
HYDROCEPHALUS
1.Infections;
Intrauterine infections may destroy the CSF pathways. Pneumococcal and TB meningitis have a
propensity to produce a thick, tenacious exudate that obstructs the basal cisterns.
2.SAH
Blood in the subarachnoid spaces may cause obliteration of the cisterns or arachnoid villi, and
obstruction of CSF flow.
3.Leukemic infiltrates
May seed the subarachnoid space and produce communicating hydrocephalus
4. Superior sagittal sinus thrombosis
This impairs venous drainage and impairs re-absorption through the arachnoid villi.
5. Overproduction of CSF-choroid plexus papilloma

29. Cont…
Normal pressure hydrocephalus
•Is a specific form of communicating hydrocephalus that tends to affect the elderly.
•Cerebral ventricular dilation with normal lumbar CSF pressure (5-18cmH2O)
•The clinical triad is ataxia, cognitive decline and urinary incontinence, and there is
ventriculomegaly on imaging.
•Although one-off measurements of CSF pressure may be normal the syndrome is thought to
arise from impaired CSF absorption, resulting in intermittent high pressure, and some patients
respond clinically to CSF diversion with ventriculoperitoneal shunting.

30. B. CONGENITAL VS. ACQUIRED


31. 1. Congenital hydrocephalus
• Present at birth or during infancy
• Caused by events or influences that occur during fetal development, or genetic abnormalities
• Hydrocephalus presenting after 6 months is less likely to be congenital.

32. Causes of congenital hydrocephalus
ØIntrauterine infections: rubella, cytomegalovirus, toxoplasmosis
ØTrauma : intracranial subarachnoid, intraventricular hemorrhages.
ØCongenital malformations
Arachnoid cysts: may occur anywhere in the brain.
-In children, they are often located in the back of the brain and in the region of the third ventricle.
-They are CSF-filled cysts that are lined with the arachnoid membrane.
- Some arachnoid cysts are self-contained, while others may be connected by a passageway with
the ventricles or subarachnoid space.
- The entrapped fluid may block the CSF pathways, producing hydrocephalus.

33.  Dandy-Walker malformation: characterized by agenesis or hypoplasia of the cerebellar
vermis, cystic dilatation of the fourth ventricle and enlargement of the posterior fossa.
 Aqueduct stenosis: accounts for 33% of hydrocephalus.
stenosis of the aqueduct of sylvius causes dilation of the lateral and 3rd ventricles.
 Arnold Chiari syndrome: portion of the cerebellum and brainstem herniate into foramen
magnum blocking flow of csf

34. 2. Acquired hydrocephalus
ØINFECTIONS:
• Tuberculosis
• Meningitis by bacterial infections or, less frequently, viral infections, which can scar-
restricts or obstructs the flow of CSF ventricles or as it passes over the surfaces of the
brain in the subarachnoid space.
ØTRAUMA:
• A head injury can damage the brain's tissues, nerves or blood vessels.
• Blood from these ruptured vessels may enter the CSF pathways.
• Blood causes inflammation, there may be scarring of the meninges, or blood cells may block
the CSF absorptive sites.
• When this occurs, the CSF flow becomes restricted and hydrocephalus develops.

35. ØTUMORS:
 In children, brain tumors most commonly occur in the back of the brain (posterior fossa).
 As a tumor grows it may fill or compress the fourth ventricle, blocking the flow of spinal fluid.
In other areas of the brain a tumor may similarly block or compress the ventricular system
causing hydrocephalus.
E.g. Medulloblastoma, astrocytoma and ependymoma.

36. Clinical Presentation in Children
• Accelerated rate of enlargement of the head is the most prominent sign
• Irritability, lethargy, poor appetite, and vomiting
• Headaches
• Delayed milestones
• Failure to thrive
• Family history
• Premature delivery
• Previous history of treatment for meningitis
• Maternal infections and drug intake in prenatal period.
History

37. Physical Examination
• The head grows at an abnormal rate- At birth the head circumference is 35cm +/- 2 then
increases by
2cm per month for the first 3 months
1cm per month in the next 3 months
½ cm per month for the next 6 months
¼ cm per month from 1-3 years old
At 5 years : 50 cm
At 10 years : 56-57 cm

38. • Setting-sun sign– impairment of upward gaze. Eyes rotated downward in which the sclera may
be visible above the iris. This is caused by dilatation of the 3rd ventricle and the supra-pineal
recess which then impinges on the tectum causing the eyes to deviate downwards.
• Collier’s Sign – Displacement of the upper eyelid superiorly or lower eyelid inferiorly.
• Long tract signs- due to stretching and compression of cortico-spinal tract e.g. brisk tendon
reflexes, spasticity, clonus in lower extremities, babinski reflex up going
Spasticity in the extremities, especially the legs, may develop as the fibers from the cortical
motor areas are stretched around the bodies of the dilated ventricles in their course to the cerebral
peduncles.
• Macewen sign “cracked pot”. With increase in intracranial volume, the bones of the skull
become thin and the sutures become palpably separated to produce the “cracked pot” sound on
the percussion of the skull.

39. • Frontal bossing- Unusually prominent forehead
• Anterior fontanel is wide open and bulging
• Scalp veins may be dilated and prominent
• Fundoscopy- Papilloedema is observed in older children but is rarely present in infants
because the cranial sutures separate as a result of the increased pressure
• In the older child, the cranial sutures are partially closed so that the signs of hydrocephalus
may be more subtle. The signs of increased ICP become more prominent.
• Disturbances in growth, accelerated pubertal development, and fluid and electrolyte
homeostasis may develop from pressure exerted on the hypothalamus by the dilated third
ventricle.

40. Complications of hydrocephalus
• Visual changes
• Cognitive dysfunction
• Gait changes
• Incontinence

41. Treatment options

42. • Ventricular shunting
• Third ventriculostomy
• Removal of mass
• Non surgical

43. Ventriculoperitoneal shunt
• A ventriculoperitoneal shunt involves the insertion of a catheter into the lateral ventricle
(usually right frontal or occipital)
• The catheter is then connected to a shunt valve under the scalp and finally to a distal catheter,
which is tunneled subcutaneously down to the abdomen and inserted into the peritoneal cavity.
• If the CSF pressure exceeds the shunt valve pressure, then CSF will flow out of the distal
catheter and be absorbed by the peritoneal lining.

45. Other shunts
• Ventriculo-atrial shunt
• Ventriculopleural shunt
• Lumboperitoneal shunt- only used for communicating hydrocephalus, CSF fistula
• Torkildsen shunt- ventriculocisternostomy

46. Endoscopic third Ventriculostomy(ETV)
• Involves the insertion of a neuroendoscope into the frontal horn of the lateral ventricle and
then into the third ventricle through the foramen of Monro.
• Stoma can be created in the floor of the third ventricle
• This allows CSF to bypass any obstruction in the CSF pathway and be absorbed by the
arachnoid villi

48. External drains
• External drains can be placed within the ventricle (EVD) or the lumbar thecal sac (lumbar
drain).
• These are useful for temporary CSF drainage and can be used to administer intrathecal
antibiotics to treat CSF infection.
Alternatives to shunting
• Choroid plexectomy
• Opening of a stenosed aqueduct
• Endescopic fenestration of floor of third ventricle

49. Removal of causative mass lesion
• Tumor removal
• Decompression of CSF pathways

50. Non- surgical interventions
• Diuretics- furosemide and acetazolamide decrease CSF production.
• Serial lumbar punctures- Repeated lumbar punctures have been used as a temporizing measure
in preterm infants with posthemorrhagic hydrocephalus.
• Fibrinolytic therapy- Intraventricular administration of fibrinolytic agents has been used in
newborns with posthemorrhagic hydrocephalus in an attempt to prevent permanent obstruction
to CSF flow.

51. Complications of VP shunting
• Approximately 15–20% of shunts are revised within the first 3 years due to complications.
1. Mechanical obstruction
2. Infections
3. Seizures [5%]
4. CSF leak
5. Stroke
6. Intracerebral hemorrhage [< 1%] & Hematoma formation.
7. Perforation of viscus

52. Complications
8. Intestinal obstruction
9. Ascites
10.Pseudo-peritoneal cyst
11.Hydrocele
12.Inguinal hernia
13.Route for metastasis
14.Shunt nephritis

53. Complications related to medical treatment
• Electrolyte imbalance
• Metabolic acidosis

54. Mechanical malfunction
Suspected in patients with shunts who develop new or worsening signs or symptoms of elevated
intracranial pressure such as
• headache,
• vomiting,
• lethargy,
• papilledema,
• irritability.

55. Evaluation
• Neurologic examination,
• Neuroimaging (usually with computed tomography [CT] or rapid brain magnetic resonance
imaging [MRI]), and plain radiographs of the shunt tubing pathway (shunt series).

56. Diagnosis
Shunt malfunction can be diagnosed on the basis of any of the following:
• Interval increase in ventricular size on neuroimaging study.
• Highly concerning neurologic findings (eg, new focal deficits, papilledema, severe lethargy),
even in the absence of increased ventricular size.
• Fractured, displaced, or kinked shunt tubing seen on imaging (in the setting of suggestive
signs or symptoms).
• Elevated CSF pressure and/or poor CSF flow as assessed by tapping of the shunt.

57. Management
• Shunt malfunction is managed surgically. Treatments include;
• Multiple shunt placement,
• Ventricular catheters with multiple perforations or openings.
• Craniotomy and fenestration (opening) of the intraventricular loculations.

58. Infections
• Is a common complication, occurring in approx. 5 to 15 percent of procedures.
• Usually caused by skin commensals, such as Staphylococcus epidermidis.
• Neonates are susceptible to Escherichia coli and haemolytic streptococcal infections.

59. • Shunt infections may also develop via direct contamination of the distal end of the shunt or via
hematogenous seeding.
• Distal-end contamination of ventriculo- Peritoneal shunts occurs in the setting of bowel
perforation or peritonitis.
• Most infections become apparent clinically by 6 weeks and over 90% are apparent within 6
months.

60. • Risk factors for infection include:
o very young children
o open myelomeningocele
o longer operative time
o excessive staff movement into and out of theatre during shunt placement
o Previous shunt infection
o Certain causes of hydrocephalus (more likely after purulent meningitis, hemorrhage, or myelomeningocele)
o Intraoperative use of a neuroendoscope
o Improper patient skin preparation
o Shaving of skin
o Exposure of large areas of the patient's skin during the procedure
o Shunt revision, particularly if the patient has undergone ≥3 revisions

61. 1. Ventriculitis
2. Multiloculated hydrocephalus
3. impaired cognitive function
4. Death

62. Clinical presentation
• Often asymptomatic.
• In Neonates manifests as alteration of feeding, irritability, vomiting, fever and bulging
fontanelle.
• Headache,
• Nausea/vomiting,
• Lethargy,
• Altered mental status.

63. • VP shunt infections should be suspected in patients with symptoms of peritonitis; [fever,
abdominal pain, and anorexia]
• Abdominal ultrasound may demonstrate pseudocyst. [Large loculated pockets in the
peritoneum because of diminished CSF absorption in the setting of inflammation]

64. Diagnosis
• Taping of the CSF fluid may be necessary.
• CDC has described healthcare-associated ventriculitis or meningitis as being present
in patients who meet at least one of the following criteria;
1. An organism cultured from the CSF
2. At least two of the following signs or symptoms with no other recognized cause in
patients aged >1 year of age: fever >38°C or headache, meningeal signs, or cranial
nerve signs,

65. 3. At least two of the following signs or symptoms with no other recognized cause in patients
aged ≤1 year of age: fever >38°C or hypothermia <36°C, apnea, bradycardia, or irritability
4. At least one of the following:
o Increased CSF white blood cell count, elevated CSF protein, and decreased CSF
glucose
o Organisms seen on a CSF Gram stain
o Organisms cultured from the blood

66. Management
• Complete removal of the device,
• External drainage,
• Treatment of the infection with antibiotic therapy and
• Subsequent shunt replacement at a different site once CSF is sterile

67. Treatment
Pediatric antibiotic therapy
• vancomycin [15 mg/kg IV per dose every 6 hours]
• cefotaxime [200 mg/kg IV per day in four divided doses] or ceftriaxone [100 mg/kg IV per
day in two divided doses;
Adult antibiotic therapy
• Vancomycin (15 to 20 mg/kg intravenously [IV] per dose every 8 to 12 hours,
• (ceftazidime [2 g IV every 8 hours], cefepime [2 g IV every 8 hours], or meropenem [2 g IV
every 8 hours])

68. Antiobiotic prophylaxis
• Perioperative antibiotic prophylaxis reduces the risk of shunt infection by
approximately 50 percent.
• The use of antibiotic-impregnated catheters also appears to lower the risk of
infection.

69. Seizures
• Past studies have shown that children with hydrocephalus who have been treated with
a shunt and who also have significant cognitive delay or motor disability are more
likely to experience seizures than those without cognitive or motor delays.
• Studies have also indicated that seizures are not likely to occur at the time of shunt
malfunction, and that the most likely explanation of seizure disorder is the presence of
associated malformations of the cerebral cortex.

70. Adult Onset Hydrocephalus

71. Introduction;
• The average adult produces about 500 ml of csf daily. When an injury or illness alters the csf
one or more of the ventricles becomes enlarged as csf accumulates.
• In adults; it occur mostly in age 60 and above
• Affecting both males and females equally, as well as people of different races.

72. Aetiology;
• Congenital with a late onset
• Idiopathic
• Subarachnoid haemorrhage
• Tumours
• Aqueductal stenosis.

73. High pressure hydrocephalus
• As the volume of the brain increases, CSF is displaced and the vasculature is compressed,
leading to increasing pressure within the cranial cavity.
• When the increase is beyond the limit permitted by compression of veins and displacement of
CSF, tissue herniates between compartments across the pressure gradient.

74. • Herniation is mostly associated with mass effect, either diffuse (generalized brain edema) or
focal (tumors, abscesses, or hemorrhages).
• Elevated intracranial pressure may also reduce perfusion of the brain, further exacerbating
cerebral edema. If the expansion is sufficiently severe, herniation may occur in multiple
anatomic locations such as;
1. Subfalcine (cingulate) herniation
2. Transtentorial (uncinate, mesial temporal)
3. Tonsillar herniation

75. Low pressure hydrocephalus
• A rare type of hydrocephalus with low ICP and ventriculomegally
• LPH has been described in intraventricular haemorrhage, cranial trauma, spinal tap,
meningitis, parasitosis, posterior fossa tumors, congenital aqueductal stenosis, spinal
arachnoid cyst and hemispherectomy
• The individual experiences dementia inability to walk, and incontinence despite very low
pressure
• LPH appears to be a more acute form of normal pressure hydrocephalus.
• If not diagnosed early the patient runs a rusk of remaining in LPH state.
• Shunt revision even when they are set to drain at a low ICP are not always effective. The
pressure in the brain does not get high enough to allow CSF to drain in a shunt system,
therefore the shunt is open but malfunctioning in LPH.

76. • One treatment is an external ventricular drain EVD set at negative pressures. Caution
against dropping or raising the pressures of the EVD to quickly as it may increase risk and
also destabilizes the ventricles. Getting the ventricles smaller is the initial step stabilizing
them is the next step before placing a shunt.

77. Normal pressure hydrocephalus;
• Results from gradual blockage of the CSF draining pathways in the brain.
• Ventricles enlarge to handle the increased volume of CSF, and the compression of the brain
from within by the fluid filled ventricles destroy or damage brain tissue.
• Ventricles enlarge with little or no increase in pressure.
• Occurs as a result of head injury, brain surgery, haemorrhage, meningitis or tumour. Majority
are of unknown cause.

78. Symptoms and signs;
1. Headaches
2. Nausea
3. Difficulty focusing the eyes
4. Unsteady walking
5. Weakness of the legs
6. Sudden falls
7. Inability to walk forwards as if the feet are stuck to the floor.

79. • As the condition progresses ;
1. Decreased mental activity
2. Withdrawal behaviour
3. Lethargy
4. Apathy
5. Impaired memory
6. Speech problems
7. Dementia involving loss of movement, sensory functions and
cognitive abilities

80. Diagnosis;
CT – will show if the ventricles are enlarged or if there is obvious blockage
I. MRI – will show if ventricles are enlarged and evaluate csf flow
II. Isotopic cisternography – injection of radioactive isotope into the lower back through a
spinal tap. This allows absorption of csf to be monitored over a period of time; up to 4 days.
III. Lumbar puncture – measure csf pressure and analyse the fluid
IV. Intercranial pressure monitoring – detects abnormal pressure patterns.

81. Treatment
• Shunt; tube inserted into the ventricles to drain the fluid away usually peritoneal cavity, CSF is
eventually absorbed into the blood stream.
• Endoscopic third ventriculotomy; a tiny burr hole is made in the skull and a neuroendoscope
enters the brain. The neurosurgeon will the male a small hole in the floor of the third ventricle
creating a new pathway for the CSF to flow.

82. Thank You!