Welco

Everyon
 Brain Herniation

Department of Neurosurgery,The First

Affiliated Hospital of Zhengzhou University
Xu Bin
Cerebral falx and tentorium of
cerebellum divided the whole
cranial cavity into three tunes,
which communicated each other.
When there is an occupying
lesion in one tune, the
pressure of the tune must be
higher than contiguous tune,
which result in migration of
cerebral tissues from one
part in body to another. This
is called herniation.
Brain herniation is a condition in
which a portion of the brain is
displaced because of increased
pressure inside the skull. Increase
in pressure results in progressive
damage to brain tissue that may
include life-threatening damage to
the brainstem.
These are generally complications of
mass effect whether from tumor,
trauma or infection. We will discuss
the imaging findings, clinical
characteristics and possible
complications involved in brain
herniations. The key to recognizing
all herniations of the brain is
evaluation of the cisterns.
 According to position of lesions, it
is mainly composed of tentorial
herniation and foramen magnum
herniation.Tentorial hernation also
called tentoral incisure of cerebellar
herniation or temporal herniation of
hippocampal herniation.Foramen
magnum herniation also called tonsil
of cerebellar herniation.
Large right-
sided subdural
hematoma
producing
right to left
midline shift
and right uncal
(red arrow)
herniation.
Tentorial and Tonsillar Herniation
Two common types:
– Tentorial: medial portion of the temporal lobe herniates into
the tentorial notch and compresses the midbrain, cerebral
peduncle and third nerve
– Tonsillar: herniation of the cerebellar tonsils through the
foramen magnum
Etiology can include cerebral edema, space occupying lesions
(abscesses, tumors, hematomas), hydrocephalus,et al
 Tentorial Herniation

Definition:
Cerebral tissues of temporal lobe
are squeezed to posterior cranial
fossa through tentorial incisure.
Transtentorial herniations occur
when the brain traverses across the
tentorium at the level of the incisura.
These can be divided into ascending
and descending transtentorial
herniations.The latter is common.So
we emphasis on discussing it.
Descending transtentorial
herniations are a larger
category caused by mass effect
in the cerebrum which pushes
the supratentorial brain tissue
through the incisura to the
posterior fossa.
Ascending transtentorial
herniation is caused by
mass effect in the posterior
fossa which leads to brain
extending through the
incisura in an upward.
 Clinical Manifestation
1. Severe headache: caused by IIP.
2. Disturbance of consciousness,
drowsiness, especially coma,et al.
The reticular formation of midbrain
is involved.
3. Pupillary Alteration,from one
pupil dilated to bilateral pupils
dilated:Due to involvement of the
third cranial nerve.
4.Motor disturbance, hemiplegia,
decerebrate rigidity:pyramidal
tract of brain stem is involved.
5.Vital signs disorder: Cushing’s
response
All of them are very important and
must be kept in mind, because the
diagnosis is based on these clinical
findings.
These clinical situation may be isolated
or occur together. Ipsilateral pupil
dilatation occurs as the parasympathetic
fibers, which are located around the
outer aspect of the third nerve, are
compressed by the uncus. This leads to
dysfunction of the parasympathetic
fibers with subsequent unopposed
sympathetic responds. This will dilate
the ipsilateral pupil.
Contralateral hemiparesis
occurs with compression of the
ipsilateral cerebral peduncle.
Since the cortical spinal tracts
decussate (cross over) below
the mid brain in the level of
pons, the hemiparesis is
contralateral.
In some cases, an ipsilateral hemiparesis
can occur with a contralateral dilated
pupil or oculomotor paresis. This occurs
when the lateral translation of the
brainstem is so great as to push the
midbrain and cerebral peduncles all the
way across the perimesencephalic
cistern, so that the opposite
(contralateral) third nerve and cerebral
peduncle are pressed against the opposite
This phenomenon is called a
Kernohan’s notch - a hemorrhage
that occurs in the contralateral
cerebral peduncle (image shows
damage of the right peduncle with
hemorrhage centrally from
Durette hemorrhage).
Thus causing ipsilateral
hemiparesis. This neurologic sign
can be termed a "false localizer",
since it can be confusing or
misleading for lateralization of the
inciting lesion's location.
Imaging findings of descending
transtentorial herniations include
ipsilateral ambient cistern widening and
ipsilateral prepontine cistern widening.
A contralateral temporal horn is also
widened. These findings occur as the
ipsilateral, lateral ventricle is
compressed with subsequent dilatation
of the contralateral ventricle to
maintain the same volume.
ipsilateral ambient cistern widening
ipsilateral prepontine cistern widening
contralateral temporal horn is also widened
The ipsilateral
cistern is widened
because of the fact
that the brain
stem is inferiorly
contiguous with
the spinal cord
leading to a long
rigid structure as
shown in the
coronal CT image.
Note the mass on the right with
widening of the ipsilateral, right
ambient cistern. As the
supratentorial brain shifts to
the right, the superior aspect of
this long column of mid brain
and cord also shifts to the right.
This will
narrow the
contralateral
cistern and
widen the
ipsilateral
cistern at the
anterolateral
aspects of the
brain stem.
Uncal herniation is a subset of
descending transtentorial herniations.
The uncus is displaced into the
suprasellar cistern. The usual six
pointed star appearance of the
suprasellar cistern then becomes
truncated on the ipsilateral side of the
herniation. Coronal imaging can also
demonstrate uncal herniation either
by CT or MRI.
usual six pointed star appearance of the
suprasellar cistern
truncated on the ipsilateral side of the
herniation
This CT scan demonstrates a Durette
hemorrhage, descending transtentorial
shift to the left, widening of the
contralateral, right temporal horn and
a residual ipsilateral ambient cistern
(left) still remaining. The uncus is also
filling the left aspect of the suprasellar
cistern.
Complications of descending
transtentorial herniations include
occipital infarction. The posterior
cerebral artery becomes
compressed as the ipsilateral uncus
and parahippocampal gyrus
compresses the artery against the
ipsilateral cerebral peduncle.
The gross specimen associated with
the CT of occipital infarcts
demonstrates the excellent
correlation. This can occur
unilaterally or bilaterally depending
on the extent of injury and amount of
mass effect. Generally, an ipsilateral
occipital infarct will appear first
followed by contralateral infarction.
Another
complication of
descending
transtentorial
herniation includes
Durette
hemorrhage. This
is due to pontine
perforators which
are displaced
downward by mass
effect.
The basilar artery
sends these
perforators
posteriorly into the
pons. As the pons
shifts inferiorly,
these perforators
are stretch and can
cause hemorrhage
within the brain
stem or pons.
Sagittal and axial MRI demonstrates the
hemorrhage in the dorsal lateral pons.
Kernohan’s notch is another type of
hemorrhagic damage caused by
transtentorial herniation. This is due
to compression of the contralateral
cerebral peduncle against the
incisura. If this occurs, it leads to
ipsilateral hemiparesis since the
cortical spinal tracts become
damaged.
The gross specimen demonstrates
hemorrhage in the left central midbrain from
Durette hemorrhage and cortical damage
with some hemorrhage at the right cerebral
peduncle consistent with Kernohan’s notch.
There is also a left uncal herniation.
Foramen Magnum Herniation
Defination:
Cerebellar tonsil is squeezed to
cervical vertebral canal through
foramen magnum and compresses
the medulla oblongata and
cervical spinal cord.
 Clinical Manifestation
A neurologic examination would show an
impaired level of consciousness.
Depending on the severity of the
herniation, one or several brainstem
reflexes and cranial nerve functions will
be impaired. The patient would show an
inability to breathe consistently, and
heart rhythms would be irregular.
❂1. Severe headache:

the manifestation of IIP

❂2. Sudden arrest of
respiration: respiratory center
in medulla is involved.
❂3. Disturbance of consciousness:
This always happened later than.
❂4. Neckstiffness and head tilt
from impaction of the foramen
magnum.
❂5.Bradycardia and wide pulse
pressure.
Clinical symptomatology maybe
subtle in foramen magnum
herniation until the patient becomes
obtunded. Patients with a Chiari
malformation may have little or no
clinical symptomatology or may
demonstrate Lhermitte’s
phenomenon.
This is changed or dysesthesia in
the arms or legs with forward
bending of the head. This is
postulated to occur as the
anterior spinal tracts within the
ventral spinal cord, become
compressed against the bone of
the posterior vertebral bodies.
Acute foramen magnum herniation
clinically can be catastrophic as the
brains extrudes through the
foramen magnum. Again, this is
generally associated with other
herniations such as ascending
transtentorial herniation depending
on the level of the mass.
Imaging
findings include
on the axial
images,
cerebellar
tonsils at the
level of the dens.
In general if the
tonsils are located
at the level of the
dens on the axial
images, this
generally is an
indicator of
foramen magnum
herniation.
Excessive cerebellar
tissue can be seen at
the foramen
magnum but it may
be best to visualize
the dens and
cerebellum together
since the CT gantry
angle can yield
different
appearances at the
foramen magnum.
A sagittal MRI is a much easier method
of determining if foramen magnum
herniation is present as in this patient
with a tentorial subdural and shift
through the foramen magnum. This is
because the association between the
inferior aspect of the clivus and inferior
aspect of the occipital bone is much
easier to demonstrate on the sagittal
images.
tentorial subdural and shift through the
foramen magnum
This gross specimen also shows a crease on the
cerebellar tonsils as they extend through the
foramen magnum. Clinical complications would
include obturation and death as this progresses.
Treatment of cerebral herniation
Brain herniation is a medical
emergency! The goal of treatment is
to save the patient's life.
To help reverse or prevent a brain
herniation, the medical team will
treat increased swelling and pressure
in the brain. This can be
accomplished by:
Ⅰ.Nonoperative treatment:
1.Dehydration drug: 20%Mannitol
250ml iv drop q6h–
q6h 1g/kg over 15
minutes,Effects last 4-6 hours or
other diuretics
2.Cortisone:dexamethasone 10~20mg
iv qd, especially in cases where a
tumor is involved.
3. A drain placed into the brain
to drain off fluid, in the case of a
mechanical obstruction causing
herniation.
4. Removing the blood if a
massive hemorrhage is present
and causing herniation, although
the outlook in these cases is poor.
5.Keeping the respiratory tract
unobstructed: Placing a tube in the
airway and mechanically ventilating
(forced breathing) at a rapid rate to
reduce the levels of carbon dioxide
(CO2) in the blood for patients with
breathlessness.
Ⅱ.Operative treatment:

1.Removing the etiology: such as

resection of tumor, remove of
hematoma,et al.
2.Brain ventricle drainage:
such as hydrocephalus .
3.Operation of decompression:
such as temporal decompression
for cerebral edema.
4.Cerebral spinal fluid shunt:
such as ventricle-abdominal
cavity shunt.
•Expectations (prognosis)
Once herniation in the brain's temporal lobe
or the cerebellum occurs, death is often
inevitable. Herniation of other areas of the
brain areas has a more variable outlook.
•Complications
Permanent and significant neurologic
problems
Brain death
The end result of herniation is compression and
Duret hemorrhages, as seen here in the pons.
Here is another example of uncal herniation. Also
seen with such herniation can be Duret hemorrhages
in the brainstem.
 Brain Death
When ICP increased suddenly and reach
to or beyond the mean artery pressure
(MAP), brain circulation completely
stopped. The patient was deep coma, no
autonomous breathing. Applying
artificial respiration and some medicine,
the heartbeat can be sustained for 1~2
week or so.
Diagnosis standard of brain death
(1) No autonomous breathing;
(2) deep coma;
(3) Bilateral pupil dilation and light
reflex disappear;
(4) brain stem reflex disappear: such as
swallowing reflex, corneal reflex, et al.
(5) the blood pressure must be
maintained by medicine, such as
dopamine, adrenaline.
(6) Electroencephalogram (EEG) display
resting potential.
(7) to inject atropine 1~3mg
intravenously, no heartbeat acceleration
was found.
(8) Brain stem auditory evoked potential
(BAEP) display resting potential;
(9) ICP monitoring found that ICP reach
to or beyond the mean artery pressure.
When manifestation above-mentioned
sustained at least 6 hours and examined
by 2 doctors, the diagnosis can be made.
 The summary
Brain tumor Intracranial Hematoma
Chronic IIP acute IIP
headache, vomiting, headache, vomiting,
papilloedema Cushing’s response
Herniation
(Tentorial H or Foramen magnum H)
brain death
Questions?