HYDROCEPHALUS

Presenter: Dr. Erasmo Fuime (Resident III)

Supervisor: Dr.Lilian (MD,Mmed )
:
 INTRODUCTION
• Total volume: 50 ml in newborn, 150 ml in
adult.
• *Composition: inorganic salts like those in
plasma, traces of protein + glucose.
• *Production: 0.3 - 0.4 ml/min resulting in 500
ml/day; secreted into ventricles by choroid
plexuses (80 - 90%), 10 - 20% formed by
parenchyma of the cerebrum + spinal cord.
*Circulation:
• From ventricles through foramina of Magendie +
Luschka of 4th ventricle into cisterna magna + basilar
cisterns;
• 80% of CSF flows initially into suprasellar cistern +
cistern of lamina terminalis, the ambient / superior
cerebellar cisterns, eventually ascending over supero-
lateral aspects of each hemisphere; 20% initially
enters spinal subarachnoid space + eventually
recirculates into cerebral subarachnoid space.
Absorption: into venous system by
(a) Arachnoid villi of superior sagittal sinus (villi behave as one-
way valves with an opening pressure between 20 - 50 mm of
CSF)
(b) Cranial + spinal nerves with eventual absorption by
lymphatics (50%)
(c) Prelymphatic channels of capillaries within brain
parenchyma
(d) Vertebral venous plexuses, intervertebral veins, posterior
intercostal + upper lumbar veins into azygos + hemiazygos
veins
DIAGRAM SHOWING THE VENTRICLES
 HYDROCEPHALUS
DEFINITION: excess of CSF (ventricular dilatation) due to
imbalance of CSF formation + absorption resulting in
increased intraventricular pressure.
PATHOPHYSIOLOGY:
A. Overproduction (rare).
B. Impaired absorption:
1. Blockage of CSF flow within ventricular system, cisterna
magna, basilar cisterns, cerebral convexities.
2. Blockage of arachnoid villi / lymphatic channels of cranial
nerves, spinal nerves, adventitia of cerebral vessels.
 COMMUNICATING HYDROCEPHALUS
• EXTRAVENTRICULAR HYDROCEPHALUS :

PATHOLOGY:
• Communicating i.e. free communication between ventricles &
basal cisterns with obstruction to CSF flow in subarachnoid
spaces or basal cisterns →dilatation of all ventricles and basal
cisterns.
• Elevated intraventricular pressure secondary to blockade beyond
the outlet of 4th ventricle within the subarachnoid pathways.
• Unimpeded CSF flow through ventricles impeded CSF flow over
convexities / impeded reabsorption by arachnoid villi.
 COMMUNICATING HYDROCEPHALUS
CAUSE:
1- Subarachnoid hemorrhage (most common cause).
2- Meningeal carcinomatosis (medulloblastoma,
germinoma, leukemia, lymphoma,
adenocarcinoma).
3- Purulent / tuberculous meningitis.
4-Subdural hematoma
 COMMUNICATING HYDROCEPHALUS

• Incidence: 38% of congenital hydrocephaly.

Radiology Features:
Plain film: as above
 IMAGING STUDIES
2-CT:
• Effects of obstruction
• Site of obstruction
• Cause of obstruction
• follow up the shunt operation
• (brain damage)
 IMAGING STUDIES
CT FINDINGS:
• Symmetric enlargement of lateral, 3rd, and often
4th ventricles
• Dilatation of subarachnoid cisterns
• Normal / effaced cerebral sulci.
• May be enlarged sylvian fissure
• Symmetric low attenuation of periventricular
white matter (transependymal migration of CSF).
• Ventriculitis. Contrast
enhanced CT image
showing
hydrocephalus with
rounding of the third
ventricle and evidence
of ventriculitis with
layering of debris in
the occipital horns
(arrowhead) and third
ventricle, ependymal
enhancement (arrow)
and subependymal
oedema.
• Hydrocephalus.
Contrast enhanced
CT shows
obstructive
hydrocephalus with
dilatation of the
lateral third and
fourth ventricles.
Note the small,
enhancing right
frontal subdural
empyema (arrow).
• Contrast-
enhanced CT
of brain
showing
hydrocephalus
and a thalamic
infarct
 IMAGING STUDIES
3-MRI: as CT.
4-NUCLEAR:
• Delayed ascent of radionuclide tracer over convexities
• Persistence of radionuclide tracer in lateral ventricles
for up to 48 hours
*CHANGES AFTER SUCCESSFUL SHUNTING:
• Diminished size of ventricles + increased prominence
of sulci.
• Cranial vault may thicken.
 IMAGING STUDIES
5-ANGIOGRAPHY:
• Ventricular dilatation can be diagnosed by
stretching anterior cerebral artery in lateral
view.
• Downward displacement of internal cerebral
vein.
COMPLICATION: subdural hematoma (result
from precipitous decompression)
NONCOMMUNICATING HYDROCEPHALUS

• INTRAVENTRICULAR HYDROCEPHALUS:

PATHOLOGY:
• Blockade of CNS flow within the ventricular system
with dilatation of ventricles proximal to obstruction.
• Increased CSF pressure causes ependymal flattening
with breakdown of CSF-brain barrier leading to myelin
destruction + compression of cerebral mantle.
NON COMMUNICATING HYDROCEPHALUS
LOCATION&CAUSE:
(a) LATERAL VENTRICULAR OBSTRUCTION:
• Cause: ependymoma, intraventricular glioma, meningioma.
(b) FORAMEN OF MONRO OBSTRUCTION:
• Cause: 3rd ventricular colloid cyst, tuber, papilloma,
meningioma, septum pellucidum cyst / glioma, fibrous
membrane (post infection), giant cell astrocytoma.
(c) THIRD VENTRICULAR OBSTRUCTION:
• Cause: large pituitary adenoma, teratoma,
craniopharyngioma, glioma of 3rd ventricle, hypothalamic
glioma.
(d) AQUEDUCTAL OBSTRUCTION:
• Cause: Congenital web / atresia (often associated with
Chiari malformation), fenestrated aqueduct, tumor of
mesencephalon / pineal gland, tentorial meningioma,
intraventricular hemorrhage or infection.
(e) FOURTH VENTRICULAR OBSTRUCTION:
• Cause: Congenital obstruction, Dandy-Walker
syndrome, inflammation (TB), tumor within 4th ventricle
(ependymoma), extrinsic compression of 4th ventricle
(astrocytoma, medulloblastoma, large CPA tumors,
posterior fossa mass), isolated / trapped 4th ventricle.
 IMAGING STUDIES

1-CT:
• Enlarged lateral ventricles (enlargement of occipital horns precedes
enlargement of frontal horns).
• Effaced cerebral sulci.
• Periventricular edema with indistinct margins (especially frontal horns).
• It can define site or level of obstruction e.g.
• -dilated single lateral ventricle  obstruction at foramen of Monro
• -both lateral ventricles  obstruction in 3rd ventricle
• -both lateral ventricles & 3rd ventricle: in aquiduct or 4th ventricle
 IMAGING STUDIES

• It can diagnose cause of obstruction as brain tumors:

• -obstructive hydrocephalus associated with smooth uniform
dilatation of ventricles .
• -with periventricular haze around frontal horns due to passage
of CSF through ependyma (subependymal leak).
3-MRI: as CT.

4-NUCLEAR:
• Radioisotope cisternography: no obstruction if tracer reaches
ventricle
• Noncommunicating
obstructive
hydrocephalus caused
by obstruction of the
foramina of Luschka
and Magendie. This
MRI sagittal image
demonstrates
dilatation of lateral
ventricles with
stretching of corpus
callosum and dilatation
of the fourth ventricle.
• Noncommunicating
obstructive
hydrocephalus
caused by
obstruction of
foramina of Luschka
and Magendie.
• This MRI axial
image
demonstrates
fourth ventricle
dilatation.
 NON OBSTRUCTIVE HYDROCEPHALUS

*PATHOLOGY:
• Secondary to rapid CSF production or
decreased CSF absorption.
• CAUSE: 1- Over production of CSF: Choroid
plexus papilloma.
• 2- Decreased absorption of CSF: due
to defective development of aracnoid villi.
 IMAGING STUDIES

1-CT:
• Ventricle near papilloma enlarges.
• No periventricular haze (only type with no haze).
• Enlarged subarachnoid system & sulci.
2-MRI: as CT.
3-NUCLEAR: intense radionuclide uptake in papilloma.
4-ANGIOGRAPHY: enlarged anterior / posterior
choroidal artery and blush.
 INFANTILE HYDROCEPHALUS

ETIOLOGY:
• 1. Communicating hydrocephalus
• 2. Aqueductal stenosis
• 3. Chiari II malformation
• 4. Dandy-Walker malformation
• =mnemonic: "A VP-Shunt Can Decompress The Hydrocephalic Child"
• Aqueductal stenosis
• Vein of Galen aneurysm
Postinfectious
• Superior vena cava obstruction
• Chiari malformation
• Dandy-Walker syndrome
• Tumor
• Hemorrhage
• Choroid plexus papilloma
 INFANTILE HYDROCEPHALUS
PRESENTATION:
• Ocular disturbances: paralysis of upward gaze,
abducens nerve paresis, nystagmus, ptosis,
diminished pupillary light response
• Spasticity of lower extremities (from
disproportionate stretching of paracentral
corticospinal fibers)
 IMAGING STUDIES

1-ULTRASOUND: before closure of anterior fontanel& in

utero
• It can detect congenital hydrocephalus in uterus in 17
weeks.
• It can diagnose midline shift in unilateral hydrocephalus.
• It can diagnose Dandy Walker syndrome.
• Follow up of shunting operation.
• Can diagnose intracranial haemorrahge.
3-CT: as above
 MEASUREMENTS
a. Ventricular atrium 1.2 cm.
b.      Medial separation of the choroid plexus from
the medial wall of the lateral ventricle.
i.      <3 mm = normal
ii.      3-5 mm = "gray zone".
iii.      >5 mm = abnormal separation.
c.       Hanging or dangling choroid plexus sign (the
dependent choroid plexus hangs down towards the
dependent part of the head by gravity.)
 NORMAL PRESSURE HYDROCEPHALUS

 PATHOLOGY:
• NPH = ADAM SYNDROME
• Pressure gradient between ventricle + brain parenchyma
in spite of normal CSF pressure
• CAUSE: communicating hydrocephalus with incomplete
arachnoidal obstruction from neonatal intraventricular
hemorrhage, spontaneous subarachnoid hemorrhage,
intracranial trauma, infection, surgery, and carcinomatosis.
• STATISTICS: Age: 50 - 70 years
• PRESENTATION: dementia, gait apraxia, incontinence
 IMAGING STUDIES
1-CT:
• Communicating hydrocephalus with prominent temporal horns
• Ventricles dilated out of proportion to any sulcal enlargement
2-MRI:
• Upward bowing of corpus callosum
• Flattening of cortical gyri against inner table of calvarium (DDx:
rounded gyri in generalized atrophy)
• Pronounced aqueductal flow void (due to diminished
compliance of normal pressure hydrocephalus)
• Periventricular hyperintensity (due to transependymal CSF
flow)
• T2-weighted MRI
showing dilatation
of ventricles out of
proportion to
sulcal atrophy in a
patient with
normal pressure
hydrocephalus.
The arrow points
to transependymal
flow
• CT head scan of
a patient with
normal pressure
hydrocephalus
showing dilated
ventricles. The
arrow points to a
rounded frontal
horn.
THANK YOU