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Brain herniation
- 1. Brain Herniation Dr SANJOGCHANDANA
- 2. Monro Kellie Doctrine •The intracranial compartment in incompressible and the volume inside the cranium is a fixed volume.
- 4. Cerebral Herniation • Occurswhen 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 • Cerebralherniation 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 • Definedas 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 • Cerebralblood 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 • Cerebralherniation Is caused by number of factors that create mass effect within the skull and increased ICP. • Subflacine / cinugulate • Central • Uncal / Temporal • Tonsillar
- 11. Subfalcine / CingulateHerniation • MC type of cerebral herniation • Presence does not neccesarily lead to severe clinical symptomatology. • May lead to contralateral hemiparesis • Drowsiness
- 12. • Shift ofSeptum 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 • Subsetof transtentorial herniation • The uncus, medial part of temporal lobe is displaced into suprasellar cistern.
- 15. • Puts pressureon 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 • Inthe 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 • Diffusecerebral 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 • Patientbecomes 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 – upperpons 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 • GeneralizedFlaccidity • Absent pupillary reflexes and ocular movements • Slow irregular respirations • Death.
- 26. Duret hemorrhage • dueto stretching of small veins in the midbrain and pons.
- 27. Tonsillar herniation • Thecerebral 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 cerebralherniation • 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