- Cerebral herniation occurs when brain tissue shifts from its normal position inside the skull due to increased intracranial pressure. This is a medical emergency. - Common causes are cerebral edema, hematoma, stroke, tumor, and infections. - There are several types of cerebral herniations including subfalcine, central, uncal, and tonsillar. Uncal herniation can cause pupillary dilation and decreased consciousness as it compresses the midbrain. - Increased intracranial pressure can be managed medically with positioning, hyperventilation, hyperosmolar therapy, and induced hypertension or surgically with decompressive craniectomy.

1. Brain Herniation
Dr SANJOG CHANDANA

2. Monro Kellie Doctrine
• The intracranial compartment in incompressible and the volume
inside the cranium is a fixed volume.

4. Cerebral Herniation
• Occurs when brain tissue, blood and CSF shifts from their normal
position inside the skull
• Is a medical emergency and requires immediate medical attention

5. Cerebral herniation
• Cerebral herniation is caused by number of factors that cause mass
effect within the skull and increase the intracranial pressure
• Includes
• Cerebral edema
• Hematoma
• Stroke
• Tumor
• Infections

6. Intracranial Hypertension
• Defined as sustained elevation of ICP above 20 mm hg for > 5 mins.
• The mass effect of a hematoma causes decrease in the volume of CSF
and venous blood within the brain to maintain Normal ICP.
• Degrees
• Mild : 20-29 mmhg
• Moderate : 30-40 mmhg
• Severe : >40 mmhg.

8. Pressure regulation
• CPP = MAP – ICP.
• CBF remains constant with variations in the MAP ( 50-150 mmhg)
• Beyond this limits or with acute brain insult this autoregulation is
disturbed.

9. Metabolic Regulation
• Cerebral blood flow is sensitive to changes in PaCO2 and PaO2
• Hypoventilation  increase PaCO2  increase CBF  Increase ICP
• Hyperventialtion  Decrasede PaCO2  Decrease CBF  Decrease
ICP.
• Arterial hypoxemia  Increase CBF and ICP
• Increase in PaCO2  Cerebral vasoconstriction

10. Cerebral Herniations
• Cerebral herniation Is caused by
number of factors that create
mass effect within the skull and
increased ICP.
• Subflacine / cinugulate
• Central
• Uncal / Temporal
• Tonsillar

11. Subfalcine / Cingulate Herniation
• MC type of cerebral herniation
• Presence does not neccesarily
lead to severe clinical
symptomatology.
• May lead to contralateral
hemiparesis
• Drowsiness

12. • Shift of Septum Pellucidam from
midline can be measured in mm
and compared over time to
determine change
• Present Clinically as
• Headache – increased
herniation
• Contralateral limb weakness
• Compression of ACA -
Paraperesis

14. Uncal herniation
• Subset of transtentorial
herniation
• The uncus, medial part
of temporal lobe is
displaced into
suprasellar cistern.

15. • Puts pressure on midbrain squeezing
the 3rd cranial N affecting para-
sympathatic input to eye causing
pupillary dilatation and lack of
pupillary constriction ( ipsilateral )
• A second key feature of uncal
herniation is a decreasing level of LOC
due to distortion of the ascending
arousal system as they pass through
the midbrain.
• Contralateral hemiparesis occurs with
compression of the ipsilateral cerebral
peduncles

17. Uncal herniation – Kernohan’s Notch
• In some cases of uncal herniation the
lateral translation of the brainstem is so
severe that the brainstem is pushed
against the opposite edge of tentorium.
• A false localizing sign occurs as the shift
of the midbrain causes compression of
contralateral corticospinal tract causing
ipsilateral hemiparesis and less
frequently contralateral 3rd nerve palsy.
• So side of the dilated pupil is a much
more reliable sign

18. Central herniation
• In the first phase of central herniation, the diencephelon ( the
thalamus and hypothalamus ) and the medial part of both temporal
lobes are forced through a notch in tentorium cerebelli.

19. Central herniation
• Diffuse cerebral
edema
• CT – effacement of
peri-messencephalic
cistern and loss of
grey white
differientiation

20. Central Herniation - Stages
1. Early diencephalic stage
2. Late diencephalic stage
3. Midbrain – upper pons stage
4. Lower pons – Medullary stage
5. Medullary stage.

21. Early diencephalic stage ( reversible)
• Decreasing level of consciousness with difficulty in concentrating,
agitation and drowsiness
• Pupils are small but reactive
• Pupils may dilate briskly in response to a pinch if the skin on the neck
( ciliospinal reflex)
• Oculocephalic and oculovertebral reflexes are intact.
• Planters are flexors
• Respiration contains deep sighs, yawns and occasional pauses 
progress to Cheyne- Stokes

22. Late Diencephalic
• Patient becomes more difficult to arouse
• Localizing motor response to pain disappears
• Decorticate posturing
• Sighing and yawning
• Progressive diencephalic impairment is thought to be the result of
stretching of the small penetrating vessels of the posterior cerebral
and communicating arteries which supply the hypothalamus and
thalamus.

23. Midbrain – upper pons stage
• Motor tone is increased
• Decrebrate posturing
• Signs of oculomotor failure appear
• The pupils are irregular and fixed at mid position
• Occulo-cephalic movements are difficult to elicit
• Platers – extensor
• Hyperventilation

24. Lower pons – Medullary stage
• No spontaneous motor activity
• Lower extremities – may withdraw to planter stimulation
• Mid position – fixed pupils
• Absent oculocephalic and oculovestibular reflexes
• Ataxic respirations

25. Medullary stage
• Generalized Flaccidity
• Absent pupillary reflexes and ocular movements
• Slow irregular respirations
• Death.

26. Duret hemorrhage
• due to stretching of small veins in the
midbrain and pons.

27. Tonsillar herniation
• The cerebral tonsils move downward thorough the
foramen magnum causing compression of the
medulla oblongata and upper cervical spinal cord
• Increased pressure in posterior fossa
• May cause cardiac and respiratory dysfunction
• Loss of Consciousness( RAS)
• Focal lower cranial N dysfunction
• Relative preservation of Upper brain stem function –
Such as pupillary light reflexes and verticle eye
movements

29. Management of cerebral herniation
• Medical management
• 1st tier
• Positioning – elevated 30 degree
• Hyperventilation
• Hyperosmolar therapy
• Induced arterial hypertension
• 2nd tier
• Forced hyperventilation
• Barbiturate coma
• Hypothermia
• Tris buffer

30. • Surgical : Decompressive craniectomy