Dr.

Suman Poudel
Department of pathology
Contents
CSF circulations
Definition of Hydrocephalous
Types and etiopathogenesis
Clinical pictures
Morphology
Treatment
Cerebral edema
Other intracranial expanding lesions
CSF
Review of
Source of CSF
productions
CSF Circulations
Hydrocephalous
Hydro- water
Kepholos- head
Excess of CSF in ventricular system
Types and etiopathogenesis
Primary
Actual increase in volume of CSF with increase in ICP

Secondary
Primary hydrocephalous
Etiopathogenesis
Obstruction to flow of CSF
Overproduction of CSF
Impairment in CSF reabsorption
Obstructive Hydrocephalos
Non-communicating
Obstruction in foramen of monro
Aqueduct of sylvius stenosis

Communicating
Overproduction of CSF
Defect in reabsorption of CSF
Secondary
Less common
Loss of neural tissue
Compensatory increase in CSF
ICP normal
Morphology
Gross
Dilatation of ventricles
Thinning and stretching of brain

Microscopic
Damage of ependymal lining of ventricles
Periventricular interstitial oedema
Hydrocephalus. Dilated lateral ventricles seen in a coronal section through the midthalamus
Early symptoms (infants)
* Enlargement of the
head
* Bulging fontanels
* Sutures are separated
* Vomiting
Late symptoms
* Decreased mental function
* Delayed movements
* Difficulty feeding
* Excessive sleepiness
* Brief, shrill, high-pitched
cry
* Slow growth (0-5 years)
Treatment
The main goal is to
minimize or prevent
brain damage by
improving CSF flow.

Surgical shunt
 Cerebral Edema
Edema of brain parenchyma
Two type:
Vasogenic edema
Cytotoxic edema

Vasogenic edema :
Occurs normal blood-brain barrier is disrupted.

Increased vascular permeability

Cytotoxic edema –
increase in intracellular fluid secondary to
neuronal, glial, or endothelial cell membrane
injury

Oedema can be
localized-because of abnormal permeability of
vessels adjacent to inflammation or tumors

generalized – it may be vasogenic or cytotoxic

Morphology :
The edematous brain is softer than normal and often
appears to "overfill" the cranial vault.

In generalized edema the gyri are flattened, the

intervening sulci are narrowed, and the ventricular
cavities are compressed
 Intracranial pressure (ICP)
• major components of ICP
– brain, CSF and blood

increased volume of any one will raise ICP, unless

compensatory reduction in one/both of other
components

presence of anything else “extra” inside skull will do

the same
 Common causes of raised ICP
intracranial expanding lesions (“space occupying
lesions”) – e.g. tumour, haematoma, abscess

hydrocephalus (excess CSF)

cerebral edema – increase in brain water content, due

to blood-brain barrier problem
– localised (e.g. around tumours)
– generalised (e.g. following severe head injury or hypoxic
brain damage)
 Herniation
 Cranial vault is subdivided by rigid dural folds (falx and
tentorium), a focal expansion of the brain causes it to be
displaced in relation to these partitions.

Sites of brain herniation

Subfalcine
(trans)tentorial
Tonsillar

(also through skull defect in trauma)

Subfalcine - ipsilateral cingulate gyrus herniates
under the free edge of falx
Transtentorial (uncinate)- medial aspect of the
temporal lobe is compressed against the free margin
of the tentorium.
Tonsillar- foramen magnum or foraminal herniation
= coning of cerebellar tonsils
Other intracranial expanding
lesions
Abscess
Tumor
Haematoma


 Thank you