Herniation Syndromes

Cerebral herniations

1. HERNIATION SYNDROMES Dr CSN Vittal

2.  Cerebral Herniation Occurs when brain tissue, blood, and cerebrospinal fluid (CSF) shifts from their normal position inside the skull. A brain herniation is a medical emergency and requires immediate medical attention. The condition is usually caused by swelling from a head injury, stroke, bleeding, or brain tumor – primary or metastatic.

3. Cerebral herniation is caused by a number of factors that cause a mass effect within the skull and increase the intracranial pressure including:  Cerebral edema  Hematoma  Stroke  Tumor  Infection  Cerebral Herniation

4. Intracranial hypertension Intracranial hypertension is defined as a sustained (>5 min) elevation of ICP above 20 mmHg  the mass effect of a hematoma causes a decrease in the volume of CSF and venous blood within the brain to maintain a normal ICP Normal ICP is < 10 mm Hg Degrees: Mild : 20-29 mm Hg Moderate: 30-40 mm Hg Severe : > 40 mm Hg

5. Metabolic Regulation Pressure Regulation Regulation of Cerebral Blood Flow

6. Pressure Regulation CPP = MAP - ICP  CPP= effective pressure that results in blood flow to the brain.  MAP=Mean Arterial Blood Pressure. • CBF remains constant with variations in MAP in the range (50-150 mmHg). Beyond these limits or with acute brain insult this autoregulation is disturbed.

7. Metabolic Regulation Hypoventilation g h PaCO 2 g h CBF g h ICP Hyperventilation g i PaCO 2 g i CBF g i ICP Arterial hypoxemia > h CBF and h ICP Increase in PaCO 2 > cerebral vasoconstriction Cerebral blood flow is sensitive to changes in PaCO 2 and PaO 2

8. Monro Kellie Doctrine The intracranial compartment is incompressible and the volume inside the cranium is a fixed volume The intracranial volume constituents are brain tissue, blood and cerebrospinal fluid (CSF) Changes in ICP may result from an increase in volume of brain tissue, blood or CSF Compensatory mechanisms maintain a normal ICP for any increase in volume of 100-120 ml

9. Cerebral herniation is caused by a number of factors that cause a mass effect within the skull and increase the intracranial pressure including :  Subfalcine  Central or downward transtentorial  Temporal transtentorial or uncal  Cerebellar tonsillar  Cerebral Herniation - Types

10. Shift of the septum pellucidum from midline can be measured in millimeters and compared over time to determine any change Present clinically as headache and as the herniation progresses, contralateral leg weakness Compression of anterior cerebral artery leads to paraparesis. Subfalcine (Cingulate) Herniation The most common form of herniation Presence does not necessarily lead to severe clinical symptomatology or harm

11. Puts pressure on the midbrain squeezing the 3rd cranial nerve affecting the parasympathetic input to the eye causing and pupillary dilation and a lack of pupillary constriction to light. (ipsilateral) a second key feature of uncal herniation is a decreasing level of consciousness (LOC) due to distortion of the ascending arousal systems as they pass through the midbrain Contralateral hemiparesis occurs with compression of the ipsilateral cerebral peduncle of the midbrain Uncal Herniation Subset of transtentorial herniations The uncus, the medial part of the temporal lobe, is displaced into the suprasellar cistern

12. In some cases of uncal herniation the lateral translation of the brainstem is so severe that the midbrain is is pushed against the opposite edge of the tentorium A false localizing sign occurs as the shift of the midbrain causes compression of the contra-lateral cortico-spinal tract causing ipsilateral hemiperesis and less frequently, the contra-lateral 3rd nerve The side of the dilated pupil is a much more reliable sign (90%) of the side of the lesion than the side of the hemiparesis Uncal Herniation - Kernohan’s Notch Kernohan-Woltman notch

13. In the first phase of central herniation, the diencephalon (the thalamus and hypothalamus) and the medial parts of both temporal lobes are forced through a notch in the tentorioum cerebelli Central Herniation

14.  Diffuse cerebral edema as seen in patients with severe traumatic brain injury CT Scan shows effacement of the peri-mesencephalic cisterns and loss of gray -white matter differentiation Central Herniation

15. Early diencephalic stage (reversible) Decreasing level of consciousness with difficulty concentrating, agitation and drowsiness Pupils are small (1-3 mm) but reactive Pupils dilate briskly in response to a pinch of the skin on the neck ( ciliospinal reflex) Oculocephalic & oculovertebral reflexes are intact (Doll’s eyes) Plantar responses are flexor Respirations contain deep sighs, yawns and occasional pauses then progress to Cheyne- Stokes Central Herniation - Stages Early diencephalic stage Late diencephalic stage Midbrain-upper pons stage Lower pons-medullary stage Medullary stage

16. Late diencephalic stage Patient becomes more difficult to arouse Localizing motor responses to pain disappear 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 Central Herniation - Stages Early diencephalic stage Late diencephalic stage Midbrain-upper pons stage Lower pons-medullary stage Medullary stage

17. Midbrain-upper pons stage Motor tone is increased Decerebrate posturing Signs of oculomotor failure appear The pupils irregular and fixed at mid position Oculocephalic movements become more difficult to elicit Plantar responses are extensor Hyperventilation Central Herniation - Stages Early diencephalic stage Late diencephalic stage Midbrain-upper pons stage Lower pons-medullary stage Medullary stage

18. Lower pons – medullary stage no spontaneous motor activity. lower extremities may withdraw to plantar stimulation mid-position fixed pupils. absent oculocephalic and oculovestibular reflexes. ataxic respirations.  Central Herniation - Stages Early diencephalic stage Late diencephalic stage Midbrain-upper pons stage Lower pons-medullary stage Medullary stage

19. Meullary stage generalized flaccidity. absent pupillary reflexes and ocular movements. slow irregular respirations. death. Central Herniation - Stages Early diencephalic stage Late diencephalic stage Midbrain-upper pons stage Lower pons-medullary stage Medullary stage

20. The cerebellar tonsils move downward through the foramen magnum causing compression of the medulla oblongata and upper cervical spinal cord Increased pressure in the posterior fossa May cause cardiac and respiratory dysfunction Loss of consciousness (RAS). Focal lower cranial nerve dysfunction. Relative preservation of upper brainstem function, such as pupillary light reflexes and vertical eye movements.   Tonsillar Herniation

21. Chiari malformations are hindbrain herniation syndromes Chiari Malformations Classification of Chiari Malformations Type I Displacement of cerebellar tonsils below foramen magnum Type II Displacement of the cerebellar vermis, fourth ventricle, and lower brainstem below foramen magnum Type III Displacement of cerebellum and brainstem into a high cervical meningocele Type IV Cerebellar hypoplasia

22. Management of Cerebral Herniation The first treatment of raised ICP is to remove the lesion causing mass effect within the brain such as a tumor , hematoma or abcess Hydrocephalus caused by a mass lesion or intraventricular blood should be aggressively treated by removing the mass lesion and/or placing a ventriculostomy

23. Management of Cerebral Herniation Tier System 3 Decompressive craniectomy 2 Forced Hyperventilation Barbiturate coma Hypothermia Tris Buffer Other medications 1 Positioning Hyperventilation Hyperosmolar therapy Induced arterial hypertension

24. Management of Cerebral Herniation Tier 1 Positioning Hyperventilation Hyperosmolar therapy Induced arterial hypertension Positioning : Moderate head elevation at an angle of 15-30 to h cerebral venous return and i ICP Maintain neutral position (t urning head to one side will reduce cerebral venous return ) Hyperventiation Rescue manoeuvre in impending or frank herniation Keep PaCO 2 between 30-35 mmHg. (Lowering paCO 2 by 1 mmHg reduces CBF by 4%) Induced arterial hypertension Drug of choice: Norepinephrine o.1 mic/kg/min OR Dopamine 4-10 mic/kg/min Goal : MAP = > 70 mm Hg

25. h ICP Text Text h CBV i CVR i CPP CPP Concept CPP = MAP - ICP h MAP

26. Management of Cerebral Herniation Tier 1 Positioning Hyperventilation Hyperosmolar therapy Induced arterial hypertension Hyperosmolar Therapy : Mannitol Osmotic diuresis Decreases blood viscosity Free radical scavenger Hypertonic Saline Can be used till S osmolality 360 mOsm Maintains MAP

27. Management of Cerebral Herniation Tier 2 Forced Hyperventilation Barbiturate coma Tris Buffer Hypothermia Other medications Forced Hyperventilation Down to PaCO 2 of 25-30 mm Hg Risk of cerebral ischemia Barbiturate coma Suppresses the cerebral metabolic rate of Oxygen (CMRO) Terminates convulsions Scavenge free oxygen radicals Decrease a cerebral hyperthermic response to ischemia

28. Management of Cerebral Herniation Tier 2 Forced Hyperventilation Barbiturate coma Hypothermia Tris Buffer Other medications Hypothermia Moderate (32–35°C) hypothermia, if implemented early and maintained for at least 48 hours, may benefit TBI patients Tris Buffer Acidosis removes the Mg lock from the NMDA receptor— facilitating excitotoxicity. High pH protects energy-dependent glutamate porter sytsems and thus delays onset of excitotoxicity. Corrects intracellular acidosis and increases the buffering capacity of CSF. Tham ( trishydroxy methylaminomethane ) 1 mg/kg IV

29. Management of Cerebral Herniation Tier 2 Forced Hyperventilation Barbiturate coma Hypothermia Tris Buffer Other medications Steroids: In vasogenic brain edema around brain tumors, hematoma or postoperative Dexamethasone .25 mg/kg every 6 h IV. Methyl predinsolone 1-2 mg/kg every 6 h Indomethacine : Non selective cyclo-oxygenase inhibitor - in TBI or intracranial surgery Dihydroergotamine(DHE): Hyperoncotic therapy - precapilary arterioles are constricted Also constricts cerebral veins Dose : 4 mic/kg IV

30. Summary Cerebral herniation is the result of increased intracranial pressure which exceeds the body’s compensatory mechanisms. Understanding the types of cerebral herniation is essential to making the diagnosis and determining the best course of treatment

31. Dr CSN Vittal Thank You