brain herniation syndrome

Herniation Syndrome

Dr Sarah ‘Atiqah Mohd Zamri

Medical Officer

Neurosurgery Department

Hospital Sultanah Nur Zahirah1

Outline• Anatomy of cisterns• 5 most common herniation• Supratentorial, infratentorial• Mechanism • Imaging• Clinical manifestation

• Summary stages of herniation• Breathing pattern• References

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Interpeduncular cistern

Ambient cistern

Quadrigeminal cistern

Incisular cistern

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Pentagon of basal cistern(suprasellar cistern)

Pontine cistern

Pontocerebellar cistern

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5 most common herniation syndrome1. Cingulate herniation – a.k.a. subfalcine herniation2. Central (transtentorial) herniation3. Uncal herniation4. Tonsillar herniation5. Upward cerebellar

Supratentorial herniation

Infratentorial herniation

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Central herniation (a.k.a transtentorial a.k.a tentorial herniation)• Usually more chronic than uncal herniation• E.g. tumor – frontal, parietal or occipital lobes• Diencephalon forced through tentorial incisura• Pituitary stalk may be sheared diabetes insipidus• PCAs may be trapped along the open edge of the incisura – may

occlude cortical blindness• Brainstem ischemia from compression and shearing perforating

arteries from basilar artery haemorrhage within brainstem Duret Hemorrhage

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• Mechanism : downward displacement of cerebral hemisphere and the basal nuclei compressing and displacing the diencephalon and the midbrain rostrocaudally through the tentorial notch

• Imaging findings :• Effacement of sulci• Obliteration of suprasellar cistern• Compression and posterior displacement of quadrigeminal cistern

• Clinical manifestations:• Medium sized, fixed pupils• Somnolence, Early coma• Decorticate posturing• Cheyne stokes respiration

• a cyclical crescendo-decrescendo pattern of breathing, followed by periods of central apnea • Diabetes insipidus

Central herniation

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• Duret hemmorhage

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Uncal herniation

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Uncal herniation • Mechanism : Rapidly expanding hematoma at middle-fossa or temporal

lobe pushing medial uncus and hippocampal gyrus over edge of tentorium, entrapping 3rd nerve and directly compressing midbrain• Imaging:

• Contralateral temporal horn widening• Ipsilateral ambient cistern widening• Ipsilateral prepontine cistern widening• Uncus extending into suprasellar cistern

• Clinical Manifestation• Earliest sign : ipsilateral pupil dilatation/anisocoria• Opthalmoplegia• Contralateral hemiparesis

• Contralateral cerebral peduncle may be compressed against the tentorial edge causing ipsilateral hemiplegia (Kernohan’s phenomenon, false localizing sign)

• Somnolence • Decerebrate posturing• Variable impairment in consciousness

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• Kernohan notch - made by tentorial edge on cerebral peduncle contralateral to side of hemispheric mass lesion.

• Kernohan's notch phenomenon is the ipsilateral hemiplegia caused by compression of the contralateral cerebral peduncle against the tentorial edge by a supratentorial mass

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Right hemispheric chronic SDH with gross midline shift and effacement of perimesencephalic cistern, subfalcine and transtentorial herniation. Postoperative axial CT head showing left PCA territory infarct.

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Uncal herniation

• Bilateral uncal herniation – suprasellar cistern obliterated

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Subfalcine herniation aka cingulate herniation

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Subfalcine herniation

• Mechanism : brain tissue extending under the falx in supratentorial cerebrum• Imaging :

• Attenuation of ipsilateral aspect of frontal horn• Asymmetric anterior falx• Obliteration of ipsilateral atrium of lateral ventricle• Septum pellucidum shift

• Clinical manifestation• Small reactive pupils• Headache• Somnolence • Contralateral leg paralysis

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Tonsillar herniation• Mechanism : a mass effect in the posterior fossa causing the

cerebellar tonsils herniating/protruding below the foramen magnum compressing the medulla and upper cervical cord• Imaging :• Cerebellar tonsils at level of dens on axial images• Cerebellar tonsils on sagittal images 5mm below foramen magnum (7mm in

children)

• Clinical manifestation • Hypertension-bradycardia-bradypnea• Coma• Respiratory arrest• Cardiac arrhytmia• Bilateral arm dyesthesia

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Tonsillar herniation

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Upward cerebellar herniation

• Mechanism : infratentorial mass effect protruding upward compressing the midbrain• Imaging :

• Spinning top appearance of midbrain• due to compression bilaterally on the posterolateral aspects of the midbrain as the posterior fossa

squeezes through the incisura from below• Narrowing of bilateral ambient cisterns• Filling of quadrigeminal cisterns/’crooked smile’• Hydrocephalus if aqueduct of sylvius compressed

• Clinical manifestation :• Nausea/vomiting• Progressive stupor

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Consciousness Respirations Pupils Oculomotor Motor

CE

Diencephalic stage

Altered alertnessLethargyAgitationLater: stupor -> coma

SighsYawnsLater : Cheyne - Stokes

Small (1-3mm), small range of contraction

Conjugate or slightly divergent roving eyes; if conjugate the brainstem intact.Usually positive Doll’s eyes and conjugate ipsilateral response to Cold Water Calorics (CWC). Impaired upgaze due to compression of superior colliculi and diencephalic pretectum (Parinaud’s syndrome)

Early: appropriate response to noxious stimuli, bilateral Babinski, gegenhelten (para tonic resistance). If previously hemiparetic, may worsen. Later : motionlessness & grasp reflexes, then Decorticate (initially contralateral to lesion)

NT

Midbrain – upper pons stage

Cheyne – Stokes sustained tachypnea

3-5mm, fixed Doll’s eyes & CWC impaired, may be dysconjugate. MLF lesion internuclear opthalmoplegia (when doll’s or CWC elicited and dysconjugate, medially moving eye moves less than laterally moving eye.

Decorticate bilaterally Decerebrate (occasionally spontaneously)

R Lower pons – upper medullary stage

Regular, shallow and rapid (20-40/min)

3-5mm fixed Doll’s eyes and CWC unelicitable Flaccid. Blateral Babinski. Occasionally LE flexion to pain

AL

Medullary stage (terminal stage)

Slow, irregular rate and depth, sighs/gasps. Hyperpnea alternate with apnea.

Dilated widely with hypoxia

U Early 3rd nerve stage

Normal Unilaterally dilated/sluggish pupil;85% ipsilateral to lesion

Doll’s = normal or dysconjugate. CWC = slow ipsilateral deviation, impaired nystagmus, may be dysconjugate if external oculomotor ophthalmoplegia (EOO)

Appropriate response to nociceptive stimulus. Contralateral babinski

NCAL

Late 3rd nerve stage

Once EOO, stuporous -> comatose

Sustained hyperventilation, rarely cheyne stokes.

Fully dilates Once pupil blown, then EOO Contralateral weakness. Sometimes with ipsilateral weakness, kernohans phenomenon. Then, bilateral decerebration (decortication unusual)

Mid brain upper pons stage

Sustained hyperpnea Contralateral pupil fixes in mid position or full dilation. Eventually, both midposition (5-6mm) and fixed

Impaired or absent Bilateral decerebrate rigidity24

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• Thank you

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References 1. Handbook of Neurosurgery. Seventh Edition. Mark S. Greenberg. Thieme.2. Intracranial Hypertension and Brain Herniation Syndromes. Radiology Cases in

Pediatric Emergency Medicine Volume 5, Case 6. Loren G. Yamamoto, MD, MPH

https://www.hawaii.edu/medicine/pediatrics/pemxray/v5c06.html

3. Neurology and Neurosurgery Illustrated. Third Edition. Kenneth W Lindsay. Churchill Livingstone.

1. Vv2. vv

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