1. The document provides information on tips for using a PowerPoint presentation (ppt) for teaching. It recommends freely editing the ppt, not worrying about number of slides as some are blank, showing blank slides and asking students questions before providing information. 2. The document then discusses hydrocephalus including causes such as congenital defects, infections, tumors, classifications as communicating or non-communicating, symptoms in infants like head enlargement and older children like headaches, and investigations including imaging and tissue diagnosis. 3. Imaging findings of conditions like aqueduct stenosis, tumors, and investigations for hydrocephalus are also covered.

1. Tips on using my ppt.
1. You can freely download, edit, modify and put your
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2. Don’t be concerned about number of slides. Half the
slides are blanks except for the title.
3. First show the blank slides (eg. Aetiology ) > Ask
students what they already know about ethology of
today's topic. > Then show next slide which enumerates
aetiologies.
4. At the end rerun the show – show blank> ask questions >
show next slide.
5. This will be an ACTIVE LEARNING SESSION x
three revisions.
6. Good for self study also.
7. See notes for bibliography.

2. Pathology
The aqueduct may become stenotic as a
consequence of compression from mass lesions
or because of intrinsic pathology (“non-tumoral
aqueductal stenosis”) .
 congenital
aqueductal webs or diaphragms
Gliosis
acquired
intrinsic
infection: meningitis / ventriculitis
subarachnoid hemorrhage
idiopathic (called late-onset idiopathic aqueductal
stenosis

3. Pathology cont…
extrinsic compression
tectal plate glioma
pineal tumor
posterior fossa tumor
cerebral vascular malformation
decreased aqueductal stroke volume and
peak systolic velocity

4. Tectal plate glioma
Tectal gliomas fall under the grouping of
childhood brainstem gliomas and unlike the
other tumors in that group they are typically
low grade astrocytomas with good prognosis.
Tectal plate gliomas are encountered in
children and adolescents
Their expansion within the brainstem causes
narrowing the aqueduct of Sylvius and
causing obstructive hydrocephalus

5. Radiographic features
CT
Typical CT finding is homogeneous expansion
of tectal plate, isodense to grey matter with
minimal enhancement on postcontrast
images 1,3. On CT it is not uncommon to find a
central tectal calcification 2-3.

6. MRI
Typically the tumors demonstrate expansion of
the tectal plate by a solid nodule of tissue.
T1: iso to slightly hypointense to grey matter 1-
3
T2: hyperintense to grey matter
T1 C+ (Gd): usually no enhancement
With time the mass can develop small cystic
spaces (sometimes associated with neurological
deficits) or calcification 3.

7. .
T1+C tectal glioma
t2w

8. .

9. .
Tectal plate glioma with radiological progression but without clinical deterioration. A:
Brain MRI revealed a tectal plate lesion with hyperintensity on T2-weighted images. B:
After gadolinium administration, the lesion showed a focal enhancement. C:
Postoperative follow-up brain MRI revealed a tectal plate glioma without hydrocephalus.
D, E: In a follow-up 5.1 years after endoscopic third ventriculostomy, the brain MRI
showed that the size of the tectal plate glioma was increased without contrast media
enhancement. F: On C-methionine brain PET/CT images, a hypermetabolic lesion was
detected.

10. .
Typical MRI features of tectal glioma. a Sagittal post-contrast T1-weighted
image shows a typical non-enhancing, T1 hypointense lesion obstructing the
cerebral aqueduct (*). b Axial T2-weighted image shows typical T2
hyperintensity of the lesion (*), and periventricular CSF accumulation
indicative of hydrocephalus. c on ADC map, tectal gliomas (*) are typically
high in signal (“facilitated” diffusion)

11. Non- contrast CT (tectal glioma)

12. T1: iso to slightly hypointense to grey matter
(tectal plate glioma)

13. .
Axial (above left) and coronal (above right) T1 MRI without contrast of
the brain show dilation of the lateral and third ventricles. Sagittal T2
MRI without contrast of the brain (below) shows narrowing at the
aqueduct of Silvius with a decreased amount of CSF within it. The
fourth ventricle is normal in size.
A B
C

14. .
Typical features of aqueductal stenosis on sagittal T1 and
Axial T2 weghted imaging, with dilatation of the lateral and
now third ventricles. There is thinning of the corpus
callosum, especially posteriorly, due to long term pressure
effects. Note fornices have “fallen down” due to lack of
support from the perforated septum pellucidum. Sulcal
development is appropriate.

15. .
Sagittal balanced steady-state free precession sequence from fetal MR
imaging (A) of a 33-week fetus and a postnatal sagittal T1-weighted
sequence (B) of the same patient demonstrating stenosis of the inferior
cerebral aqueduct with associated aqueductal funneling (arrow). As a
result, there is marked enlarged of the lateral and third ventricles with
dilation of the inferior third ventricular recesses (white arrowheads)
depicted by bowing of the lamina terminalis and inferior third
ventricular floor. The corpus callosum is thin and superiorly bowed
(black arrowheads). Note also the normal size of the fourth ventricle.

16. .
Fetal MR imaging of a 30-week fetus (A) and postnatal MR
imaging correlation (B) of prenatally diagnosed aqueductal
stenosis with tectal thickening and loss of intercollicular
sulcus (arrows). There is subtle early prominence of the
supraoptic recess of the third ventricle on fetal MR imaging
(white arrowhead), which progressed to more obvious dilation
of both supraoptic and infundibular recesses on postnatal
imaging (white arrowheads). Note also the presence of a
superiorly bowed and thinned corpus callosum (black
arrowheads).

17. ?
MRI sagittal view showing Aqueduct Stenosis causing
Hydrocephalus
17

18. . Enlarged third ventricle with expansion of the supraoptic recess (SOR),
infundibular recess (IR) and pineal recess (PR). Basilar tip (red arrow) is
closely related to the inferiorly displaced floor of the third ventricle.
On flow studies, flow induced signal can be seen passing in front of the
basilar tip and into the third ventricle.

19. .
.

20. .
.

21. .
Aqueductal stenosis. (A) Sagittal T1-weighted (T1W) magnetic resonance
imaging (MRI) and axial T2W (B) MRI demonstrating stenosis of the cereb
aqueduct with concomitant hydrocephalus.
View chapterPurchase book

22. .
Coronal (left) and sagittal (right) US of the brain show
dilation of the lateral and third ventricles. The fourth
ventricle is normal in size.
A B

23. .
AP and lateral radiographs of the skull (above) show throughout skull
vault prominence of convolutional markings from gyral impressions on
the inner table of the skull, which is also well demonstrated on the axial
CT without contrast of the brain (below).
A B

24. Imaging findings cont
In the case of tectal plate gliomas MRI will
demonstrate expansion of the tectal plate by a
solid nodule of tissues , that is iso to slightly
hypointense to gray matter on T1 ,
hyperintense to gray matter on T2 and usually
non-enhance on T1+C

25. Diagnostic
Studies
Imaging modalities
• X-Ray-erosion of sella turcica, or
"beaten copper cranium" (or "beaten
silver cranium")
• MRI
• USG
• CT
• Angiography
• Endoscopy
• Nuclear scan

26. T2: hyperintense to grey matter

27. ,
Pineal tumor

28. .

29. .
T1Wpineal tumor

30. DWI/ADC

31. .
.
Pineal tumor

32. Pineoblastomas are tumors that are best
thought of as small round blue cell
tumors located in the pineal region and thus,
they closely resemble (both on imaging and on
histology) medulloblastomas and retinoblastom
as. They are the most aggressive and highest
grade tumor among pineal parenchymal
tumors and are considered WHO grade 4
tumors

33. Pineoblastomas are the most aggressive pineal
parenchymal tumor and account for a
substantial proportion of such tumors (24-
50%) 7. They are typically found in young
children.
Pineoblastomas are typically large and almost
always associated with obstructive
hydrocephalus, due to compression of the
cerebral aqueduct. Compression of the tectal
plate may also result in the Parinaud syndrome.

34. Pineoblastomas originate from pinealocytes
and/or their precursors

35. .
Radiographic features
Pineoblastomas tend to be large poorly defined
masses, with frequent CSF seeding at
presentation. They have a tendency to involve
directly adjacent brain structures, which helps
distinguish them from other pineal tumors that
tend to be better circumscribed.
CT : The solid component tends to be slightly
hyperdense compared to the adjacent brain due
to high cellularity. This is a characteristic
shared by other small round blue cell tumors
such as PNET and medulloblastoma.

36. .
MRI
Pineoblastomas tend to appear as sizable (>4
cm) irregular masses often with evidence of
invasion into the adjacent brain 6,9. Typical
signal characteristics include 9:
T1: isointense to hypointense to adjacent brain
T2
isointense to adjacent brain
areas of cyst formation or necrosis may be present
T1 C+ (Gd): vivid heterogeneous enhancement
DWI/ADC
restricted diffusion due to dense cellular packing
ADC values are typically ~400-800 mm2/s 7

37. Introduction & History.

38. Introduction & History.
Term derived from two Greek words-
 “hydro” means water and
 “cephalus” means head.
Hydrocephalus can be defined broadly as a
disturbance of formation, flow, or
absorption of cerebrospinal fluid (CSF) that
leads to an increase in its volume.

39. Etiology

40. Etiology
• Idiopathic
• Congenital
• Traumatic
• Infections /Infestation
• Autoimmune
• Neoplastic (Benign/Malignant)
• Degenerative

41. Etiology
1.CONGENITAL HYDROCEPHALUS
I. Intrauterine infections: Rubella,
Cytomegalovirus, Toxoplasmosis.
II. Trauma: Subarachnoid, Intracranial,
Intraventricular haemorrhages.
III. Congenital malformations:
Dandy-walker syndrome: posterior fossa
cyst continuous with 4th ventricle.

42. Etiology
• Aqueduct stenosis: it accounts for
33% of hydrocephalus cases. Stenosis
of aqueduct of sylvius causes dilation
of lateral and 3rd ventricles. In 2% of
cases this could be familial with X
linked recessive inheritance.
• Arnold-Chiari syndrome- Portions of
cerebellum & brainstem herniating
into cervical spinal canal, blocking
the flow of CSF to the posterior fossa.

43. Etiology
2) ACQUIRED HYDROCEPHALUS: -
• Tuberculosis,chronic & pyogenic
meningitis.
• Post-intraventricular hemorrhage.
• Posterior fossatumors:
medulloblastoma, astrocytoma,
ependymoma.
• Arteriovenous malformation,
intracranial hemorrhage, ruptured
aneurysm.

44. Physiology of csf production &
flow
⦿CSF is secreted at the choroid plexus within the ventricles
by ultra filtration & active secretion.
Lateral ventricles
FORAMEN OF MONRO
3rd ventricle
AQUEDUCT OF SYLVIUS
4th ventricle
CONTD…

45. Contd……
Via lateral foramen of Luschka & foramen
of Magendie
Cistern magna
Cerebral & cerebellar subarachnoid
spaces

46. ……Contd
• A large portion is absorbed through the
arachnoid villi, but the sinuses, veins, brain
substance & dura also participate in
absorption.
• About 20ml of CSF is secreted in an hour.
The total of CSF approximates 50ml in an
infant and 150ml in adults.

47. Pathophysiology & Classification

48. Pathophysiology & Classification
There are two types of hydrocephalus: -
1) Noncommunicating (intraventricular or
obstructive)
2) Communicating hydrocephalus.

49. Noncommunicating
hydrocephalus

50. Noncommunicating
hydrocephalus
• There is blockage between the ventricular &
subarachnoid systems, resulting in an
interference with circulation of CSF & lack
of access to the subarachnoid spaces.
• CSFdistends the ventricles.
• There is a gradual thinning of the brain
substance, which is compressed between the
distended ventricles & the expanding skull.

51. Noncommunicating
hydrocephalus
• Stenosis of the aqueduct of sylivus, either a
congenital defect or acquired.
• postnatally from brain tumors that put
pressure on or extend into the ventricles or
circulation pathways.

52. Communicating
hydrocephalus.

53. Communicating
hydrocephalus.
• There is normal communication between
the ventricles & the subarachnoid space.
• There is an interference with the absorption
of CSF caused by an occlusion of the
subarachnoid cisterns around the brain
stem.
• The fluid that is not absorbed in the
subarachnoid space accumulates,
compressing the brain & distending the
cranial cavity.

54. Communicating
hydrocephalus
• Subarachnoid hemorrhage
• Meningitis
• Toxoplasmosis or cytomegalovirus
infection,
there is obliteration of the subarachnoid
spaces by fibrous tissue reaction, or to
diseases of connective tissue.

55. Clinical Features

56. Clinical Features
• Demography
• Symptoms
• Signs
• Prognosis
• Complications

57. Demography

58. Demography
• Incidence of primary hydrocephalus 1 in
2500 live births,
• one of the most common developmental
disabilities
• Equal male :female.

59. Symptoms & Signs

60. Symptoms & Signs
IN INFANTS-
• Head grows at abnormal rate.
• Anterior fontanel is tense, often bulging, & non pulsatile.
• Scalp veins are dilated & markedly so when infant cries.
• Macewen’s sign- with increase in intracranial volume, the
bones of the skull become thin & the sutures become
palpably separated to produce the cracked pot sound on the
percussion of the skull.
• Frontal bossing with depressed eyes.
• Setting-sun sign- eyes rotated downward, in which sclera
may be visible above iris.

61. Setting sun sign

62. Symptoms & Signs
• Feeds poorly
• Pupils are sluggish, with unequal response to light
• Changes in level of consciousness.
• Opisthotonus position & lower extremity spasticity.
• Cries when picked up & quiets when allowed to lie
still.
• If hydrocephalus is allowed to progress- there will
be disruption in the lower brainstem function as
manifested by difficulty in feeding & a shrill, brief,
high-pitched cry. Eventually the skull becomes
enlarged, & the cortex is destroyed.

63. Symptoms & Signs
• If the condition progress rapidly, the infant
may display emesis, somnolence, seizures &
cardiopulmonary distress.

64. Symptoms & Signs
IN CHILDHOOD-
• Headache on awakening with improvement
following emesis or upright posture.
• Papilledema, strabismus (Squint).
• Irritable & lethargic, Drowsiness
• Apathetic, confused & often incoherent.
• Bulging occiput, nystagmus, ataxia & cranial nerve
palsies.
• Stunted growth and sexual maturation

65. Symptoms & Signs
• IN Adults:
• Cognitive deterioration:
• Headaches: Headache is rarely if ever present in
normal pressure hydrocephalus (NPH).
• Neck pain:
• Nausea Vomiting:
• Blurred vision
• Double vision (horizontal diplopia) from sixth
nerve palsy
• Difficulty in walking
• Drowsiness
• Incontinence (urinary first, fecal later if condition
remains untreated):

66. Investigations

67. Investigations
• Laboratory Studies
– Routine
– Special
• Imaging Studies
• Tissue diagnosis
– Cytology
• FNAC
– Histlogy

68. Diagnostic Studies

69. Diagnostic Studies
Imaging Studies
• X-Ray-erosion of sella turcica, or "beaten
copper cranium" (or "beaten silver
cranium")
• USG
• CT
• Angiography
• MRI
• Endoscopy
• Nuclear scan

70. CT

71. Non Operative Therapy

72. Non Operative Therapy
This can be tried in mild cases of
hydrocephalus.
• Acetozolamide: dose of 50mg/kg/day
dimnishes CSF production.
• Oral glycerol has also been used for the
similar purpose.

73. Operative Therapy

74. Operative Therapy
It may consist of
• The removal of the obstruction (tumor, hemorrhage
or cyst) to the flow of CSF.
• Reduction in the amount of CSF produced through
destruction of a portion of the choroid plexus or a
third or fourth ventriculostomy.
• Shunting of CSF from the ventricle to another site in
the normal circulatory passageway of this fluid.
• Shunting of CSF from the ventricle to an area
outside the CNS, an extracranial body compartment.

75. Operative Therapy
Shunting is the most common procedure to
be done in the surgical management of
hydrocephalus.
Most shunt systems consist of a ventricular
catheter, a flush pump, a unidirectional flow
valve & a distal catheter

76. Types of shunts-
..

77. Types of shunts-
..
1. Ventriculoperitonial(VP) shunt.
2. Ventriculoatrial(VA) shunt.
3. Ventriculopleural shunt.

78. Minimally invasive Therapy

79. Minimally invasive Therapy
• Endoscopic third ventriculostomy- It is a
procedure that has potential for greater
independence from VP or VA shunting in
children with noncommunicating
hydrocephalus. In this procedure a small
opening is made in the floor of the 3rd
ventricle, allowing CSF to flow freely
through previously blocked ventricle, thus
bypassing the aqueduct of sylvius.

80. External drainage

81. External drainage
Rapid-onset hydrocephalus with increased
intracranial pressure (ICP) is an emergency.
• Ventricular tap in infants
• Open ventricular drainage in children and
adults
• LP in posthemorrhagic and postmeningitic
hydrocephalus

82. NPH
• Normal Pressure Hydrocephalus.
• Variant of communicating Hydrocephalus
• Triad of
– Abnormal gait
– Urinary incontinence
– Dementia

83. NPH
• Elderly
• Normal muscle strength; no sensory loss
• Increased reflexes and Babinski response in
one or both feet:
• Variable difficulty in walking:
• Frontal release signs (in late stages):
Appearance of suckling and grasping
reflexes

84. NPH
• Imaging -Ventriculomegaly,
• Diagnostic CSF removal
• Surgical CSF shunting.

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