HERNIATION

SYNDROMES

Dr CSN Vittal
 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.
 Cerebral Herniation
• 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
 Intracranial hypertension

• Intracranial hypertension is
defined as a sustained (>5 min)
• Normal ICP is
elevation of ICP above 20 mmHg
< 10 mm Hg • 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
Degrees:
• Mild : 20-29 mm Hg
• Moderate: 30-40 mm Hg
• Severe : > 40 mm Hg
 Regulation of Cerebral
Blood Flow

Pressure Metabolic
Regulation Regulation
 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.
 Metabolic Regulation
• Cerebral blood flow is sensitive to changes in
PaCO2 and PaO2

• Hypoventilation g hPaCO2 g hCBF g hICP

• Hyperventilation g iPaCO2 g iCBF g iICP

• Arterial hypoxemia > hCBF and hICP

• Increase in PaCO2 > cerebral vasoconstriction
 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
Cerebral Herniation - Types

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
 Subfalcine (Cingulate) Herniation
• The most common form of herniation
• Presence does not necessarily lead
to severe clinical symptomatology or
harm

• 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.
 Uncal Herniation
• Subset of transtentorial herniations
• The uncus, the medial part of the temporal
lobe, is displaced into the suprasellar cistern
• 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 - Kernohan’s Notch
• 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

Kernohan-Woltman notch
 Central Herniation
• 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
• 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 - Stages
1. Early diencephalic
stage
2. Late diencephalic Early diencephalic stage (reversible)
stage
3. Midbrain-upper
pons stage
• Decreasing level of consciousness with difficulty
4. Lower pons- concentrating, agitation and drowsiness
medullary stage • Pupils are small (1-3 mm) but reactive
5. Medullary stage
• 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
1. Early diencephalic
stage
2. Late diencephalic Late diencephalic stage
stage
3. Midbrain-upper
pons stage • Patient becomes more difficult to arouse
4. Lower pons-
medullary stage • Localizing motor responses to pain
5. Medullary stage 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
1. Early diencephalic
stage
2. Late diencephalic Midbrain-upper pons stage
stage
3. Midbrain-upper
pons stage
• Motor tone is increased
4. Lower pons-
medullary stage
• Decerebrate posturing
5. Medullary stage • 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
1. Early diencephalic
stage
2. Late diencephalic Lower pons – medullary stage
stage
3. Midbrain-upper
pons stage
• no spontaneous motor activity.
4. Lower pons-
medullary stage
• lower extremities may withdraw to
5. Medullary stage plantar stimulation
• mid-position fixed pupils.
• absent oculocephalic and
oculovestibular reflexes.
• ataxic respirations.
 Central Herniation - Stages
1. Early diencephalic
stage
2. Late diencephalic Meullary stage
stage
3. Midbrain-upper
pons stage
• generalized flaccidity.
4. Lower pons-
medullary stage
• absent pupillary reflexes and ocular
5. Medullary stage movements.
• slow irregular respirations.
• death.
Tonsillar Herniation
• 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.
 Chiari Malformations
• Chiari malformations are hindbrain herniation syndromes

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

 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
 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
 Management of Cerebral Herniation

Tier 1 • Positioning:
•
•
Positioning
Hyperventilation
– Moderate head elevation at an angle of 15-300
• Hyperosmolar to h cerebral venous return and i ICP
therapy
• Induced arterial – Maintain neutral position (turning head to one side
hypertension will reduce cerebral venous return )
• Hyperventiation
– Rescue manoeuvre in impending or frank herniation
– Keep PaCO2 between 30-35 mmHg.
(Lowering paCO2 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
 CPP
h MAP
Concept

h ICP

iCPP
Text
Text
hCBV
iCVR
 Management of Cerebral Herniation

Tier 1
• Positioning Hyperosmolar Therapy:
• Hyperventilation
• Hyperosmolar • Mannitol
therapy
• Induced arterial
– Osmotic diuresis
hypertension – Decreases blood viscosity
– Free radical scavenger
• Hypertonic Saline
– Can be used till S osmolality 360 mOsm
– Maintains MAP
 Management of Cerebral Herniation
Tier 2
• Forced
Hyperventilation • Forced Hyperventilation
• Barbiturate
coma – Down to PaCO2 of 25-30 mm Hg
• Tris Buffer
• Hypothermia
– Risk of cerebral ischemia
• Other
medications
• Barbiturate coma
– Suppresses the cerebral metabolic rate of
Oxygen (CMRO)
– Terminates convulsions
– Scavenge free oxygen radicals
– Decrease a cerebral hyperthermic response to
ischemia
 Management of Cerebral Herniation

•
Tier 2
Forced
• Hypothermia
Hyperventilation – Moderate (32–35°C) hypothermia, if
• Barbiturate
coma
implemented early and maintained for at least 48
• Hypothermia hours, may benefit TBI patients
• Tris Buffer
• Other • Tris Buffer
medications
– 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
 Management of Cerebral Herniation
Tier 2 • Steroids: In vasogenic brain edema
• Forced around brain tumors, hematoma or
Hyperventilation postoperative
• Barbiturate
coma
– Dexamethasone .25 mg/kg every 6 h IV.
• Hypothermia – Methyl predinsolone 1-2 mg/kg every 6 h
• Tris Buffer
• Other
• Indomethacine: Non selective cyclo-
medications oxygenase inhibitor - in TBI or
intracranial surgery
• Dihydroergotamine(DHE):
Hyperoncotic therapy- precapilary
arterioles are constricted
– Also constricts cerebral veins
– Dose : 4 mic/kg IV
 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
• Dr CSN Vittal