EDEMA, HYDROCEPHALUS AND
HERNIATION
EDEMA, HYDROCEPHALUS AND HERNIATION
• a) Define and differentiate
• b) Discuss the causes
• c) Compare and contrast different types
• d) Explain the pathophysiology
• e) Discuss the morphologic features of cerebral
edema
• f) Discuss clinical manifestations
Brain edema, hydrocephalus, Herniation
- CSF Circulation (production, flow, resorption)
- Increase in intracranial pressure ICP
- Anatomical limitation structure (Rigid container)
- Treatable
- Intra cranial compartment volume =(CSF volume+blood+
brain).
CSF ↔ Blood ↔ Brain tissue
- Causes;
1. Generalized brain edema.
2. Focally expanding mass lesions- tumor,
aneurysm
bleeding , etc……………………………
Cerebral Edema
1- Definition: is the accumulation of excess fluid
within the brain intercellular& intracellular spaces, in
the paucity of lymphatic vessels and may lead to
increased intracranial pressure.
2- Causes
1- Traumatic causes- Physical injury.
2- Non-traumatic causes
a. Inflammation(meningitis, encephalitis ) .
b. Ischemic Stroke.
c. Tumor
d. Toxins exposure.
Cerebral Edema
3-Explain the pathophysiology:
Two underlying mechanisms (often occur together):
1- Vasogenic Mechanism: (Extracellular Edema)
2- Cytotoxic Mechanism (Intracellular Edema)
1- Extracellular Edema- Vasogenic mechanism
due to disruption of the integrity of the Endothelial
cell (blood-brain barrier BBB), on effect of
(vasoactive, free radicals, destructive material).
- With increased vascular permeability, fluid shifts
from the vessels into the extracellular spaces of the
brain, can be either: a)localized b)Generalized.
- Causes
–Acute inflammation (e.g., meningitis, encephalitis)
–Metastasis, trauma, lead poisoning.
–Fast travel to high altitude without proper acclimatization
2- Intracellular Edema -Cytotoxic mechanism :
- Water moves into cells (Cytotoxic): e.g. hypoxic cell injury
increase permeability of cell membrane (neuronal, glial and
endothelial cells membrane injury ).
- The BBB remains intact
- Caused by:
1- Generalized hypoxic/ischemic insult Dysfunctional
Na+/K+-ATPase pump retention of Na&H2oosmotic
shift
2- Exposure to some toxins.
3- metabolic damage.
In practice, conditions a\w generalized edema often have
elements of both vasogenic ,cytotoxic edema.
Cerebral edema
4- Morphology:
- The edematous brain is softer than normal
appears to "overfill" the cranial vault.
- In generalized edema the gyri are flattened, the
intervening sulci are narrowed.
- The ventricular cavities are compressed.
Cerebral edema: The surfaces of the gyri are widened&
flattened, the sulci are narrowed
-Cerebral edema- CF
5- Clinical manifestations: Symptoms – signs of ↑↑ ICP
- Nausea, vomiting, blurred vision, faintness., headache
- Severe cases- disorientation, seizures and coma.
Clinical consequences:
a.- Intracranial compartmental shifts  ↑↑Intracranial
pressure Compression of vital brain structures.+
ventricular cavity compression.
c. Herniation  Respiratory arrest
b- Cerebral ischemia compromised blood flow.
Treatment: - Osmotherapy using mannitol, diuretics
- corticosteroids, surgical decompression .
Hydrocephalus
Definition: is abnormal excessive accumulation of CSFwithin ventricular system & subarachnoid spaces 
Abnormal dilatation  This dilation causes potentially
harmful pressure on the tissues of the brain
Brain CT scan - Hydrocephalous
Dilated ventricles
2-What is the pathogenesis of Hydrocephalous?
- Hydrocephalus results from an imbalance between the
(CSF) inflow and outflow.
1. Decreased resorption of the CSF- e.g (scarring of
arachnoid granulation).
2. Overproduction of CSF- e.g. (choroid plexus tumor ,
hypertrophy).
3. Impaired flow- e.g. (Stenosis of the cerebral aqueduct,
Obstruction of the interventricular foramina - secondary
tumor, Hemorrhage)
Hydrocephalus (infancy) < fusion of the cranial sutures
hydrocephalus occurs acutely or occurs > fusion of the cranial sutures
Periventricular brain edema and ischemia  leading to atrophy of the
white matter. )Progressive ventricular dilatation disrupt ependmya)
Hydrocephalus - Etiology
- Related condition to the Hydrocephlus:
a- Congenital Hydrocephalus ( at birth ):
1 - Neural tube defect: spina bifida, encephalocele .
2 - CNS malformations: Dandy-Walker, Chiari syndrome
3- Choroid plexus papilloma or carcinoma
4 - Intrauterine infection: Rubella, Toxoplasmosis, CMV
5- X-linked type hydrocephalus (genetic defect)
b- Acquired Hydrocephalus
1- CNS infections: meningitis, Viral infection.
2- Brain tumors: medulloblastomas, astrocytomas.
3- Post-hemorrhagic: trauma, AV malformation, Aneurysm
Hydrocephalus - types
- two types:
1- Obstructive (noncommunicating)
2- Non-obstructive (communicating).
Both forms can be either congenital or acquired.
Hydrocephalus – types
1-Communicating, non-obstructive:LESS COMMON
• Non-obstructive = Open communication between ventricles
and subarachnoid space, a\w enlargement of all of the
ventricular system , caused by:
1.Increased CSF production e.g Choroid plexus papilloma
2.Impaired CSF resorption by arachnoid granulations e.g
arachnoid granulations (scarring- meningitis)
• Main predisposing factors:
1- Subarachnoidal hemorrhage,
2- Infection, Tuberculous, Pneumococcal infections
3- Congenital absence of arachnoids villi.
1. Meningitis.
2.
Subarachnoid hemorrhage
• Overproduction of CSF
(choroid plexus tumor)
Communicating Hydrocephalous.
Hydrocephalus - types
2-Noncommunicating (obstructive): COMMON
Caused by a CSF-flow obstruction from flowing into the
subarachnoid space (either due to external compression or
intraventricular mass lesions)+ a\w enlargement of a
portion of the ventricles
Causes:
1- Aqueductal stenosis\ stricture.
2- Tumor of 4th ventricle e.g. Ependymoma, Medulloblastoma.
3- Malformations of posterior fossa.
4- Fourth ventricle obstruction “chiari syndrome”
5- The foramina of Luschka and foramen of Magendie
may be obstructed “Dandy-Walker syndrome”
Non communicating Hydrocephalous (Obstructive)
Medulloblastoma,
Ependymoma
Chiari
Dandy-Walker malformation
Hydrocephalus – clinical features
- Vary with Age, duration= disease progression, Site of obstruction and
.- CF depend on dilatation of the ventricles and ICP
- 1- Rapid increase in head circumference (Newborn)
-2-Headache followed by vomiting, nausea.
-3- Eye: papilledema. deviation of the eyes-Sun-setting (midbrain
pressure) , CN Compression of the 3rd , 6th - Diplopia
-4- Balance, poor coordination, Gait disturbance& -Urinary, fecal
incontinence (Stretching of sacral motor fibers near dilated ventricle).
-6- Slowing or loss of development ,
7- Mental retard , memory.
8- Behavioral change(unsceratin)
9- Dementia (limbic fibers pressure)
Hydrocephalus : dilated ventricles , Dysjunction of sutures,
Tense fontanelle, etc…
Head enlargement, Setting-sun sign
Brain Herniation
1- Definition: Is displacement of brain tissue from one
compartment (separated by dural boundaries) to another,
squeezed across structures within the skull, secondary to
increased intracranial volume = (brain, blood, CSF)
- It is a medical emergency, needed urgent intervention.
- Increases compartmental volume
2- Causes of volume increase:
1- tumors & trauma Local edema
2- hemorrhage (subdural)  blood clot formation.
3- infections  abscess formation
Herniation- can occur in absence of Increase ICP
Causes- mass
S 1. blood clot
2. Tumor
3. Edema
4. Abscess
T
5. Trauma
3- The usual clinical consequence of displacement
a- Compression of blood supply resulting in infarction
b- Compression of other structures& (parenchyma, cranial
nerves, ventricle).
4- Herniation are named either by 1- Part of the brain that is displaced .
2- The structure across which it moves.
Supratentorial herniation
1- Uncal (transtentorial)
2- Central
3- Cingulate (subfalcine)
4- Transcalvarial
Infratentorial herniation
5- Upward (upward cerebellar
or upward transtentorial)
6- Tonsillar (downward cerebellar)
Causes
1- Subfalcine Hern.
2-Transtentorial Hern.
3- Tonsillar Herniation
T
Types of Herniation:
1- Subfalcine Herniation (cingulate)
2-Transtentorial Herniation (uncal)
3- Tonsillar Herniation
I- Subfalcine (cingulate) Herniation:Mass in cerebral hemisphere forces brain tissue under falx to opposite side ( cingulat gyri is a part of frontal brain lobe)  This may be
associated with:
A. Compression of branches of the anterior cerebral Artery.-lead to:- a. Gait problem b. headach, contralateral weak-
B. Effacement of ant. horn of the lateral ventricle-
Patterns of brain herniation: subfalcine (cingulate), transtentorial
(uncinate), and tonsillar.
II- Transtentorial (Uncal) herniation:
- Supratentorial mass effect forces cerebral structures (uncal)
downward through opening of tentorium, may lead to:- 1. Temporal lobe is displaced Cerebellum The third cranial
nerve + post ganglionic Parasympathetic is compromised  
Resulting in pupillary dilation and impairment of ocular
movements on the Side of the lesion.
2. The Posterior cerebral artery may also be compressed, resulting
 ischemic injury to the area supplied by this vessel Infraction
of occipital lobe visual field defect
- 3. Duret hemorrhages- hemorrhagic infarcted lesions in the
midbrain and pons. (branches of the basilar artery are kinked).
Duret hemorrhage: midline hemorrhages involving the
brainstem at the junction of the pons and midbrain
III- Tonsillar herniation:
-Posterior fossa mass effect forces cerebellar tonsils
downward through the foramen magnum.
- This pattern of herniation is life-threatening, because it causes brain
stem compression and compromises vital respiratory and cardiac
centers in the medulla.
Clinical features:
•Headache, * Coma
• Cardiac arrest.
* Loss of reflexes
* Respiratory arrest.
• Complications:
•
Death
Permanent neurologic deficit
Thank you