Brain herniation

brain herniation

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.

3. 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

4. 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

5. 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 .

6. 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.

7. 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

8. 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

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

10. 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

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

12. Puts pressure on midbrain squeezing the 3 rd 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

13. 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 3 rd nerve palsy. So side of the dilated pupil is a much more reliable sign

14. 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.

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

16. Central Herniation - Stages Early diencephalic stage Late diencephalic stage Midbrain – upper pons stage Lower pons – Medullary stage Medullary stage.

17. 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

18. 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.

19. 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

20. 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

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

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

23. 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

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

25. Surgical : Decompressive craniectomy

26. Thank you