This is a 5-year old female who is brought to the 
emergency department at 8:00 a.m. because she was 
poorly responsive when her mother awoke her in the 
morning.   This prompted her mother to drive her to the 
E.D.  There is a history of headache and vomiting 
during the evening and night.  There is no history of 
trauma.
     Exam:  VS T36.7 (rectal), P92, R32, BP 137/97.  
She is minimally responsive.  Pupils equal and reactive.  
There are no signs of external trauma.
     Within minutes of arrival, she exhibits extensor 
posturing.  She is orally intubated using the rapid 
sequence induction method with atropine, thiopental, 
and vecuronium.  She is hyperventilated.  End-tidal 
CO2 monitoring is used to keep her pCO2 in the 25 
mmHg range.  A loading dose of phenytoin is 
administered.
     An emergency CT scan is ordered.

View CT scan.

     There is obvious bilateral intraventricular 
hemorrhage and ventricular dilatation.  Clinically, 
extensor posturing suggests the possibility of impending 
herniation.  She sustains episodes of bradycardia which 
respond to doses of IV mannitol.  A neurosurgeon 
decompresses her ventricles immediately.  She 
recovers well without neurological deficits.  Subsequent 
studies demonstrate the presence of a choroid plexus 
arteriovenous malformation.  This is neurosurgically 
ablated.

Discussion
     Increases in intracranial pressure (ICP) compress 
the brain within the rigid skull.  This reduces cerebral 
blood flow prompting reflex hypertension to maintain 
cerebral perfusion.  As intracranial pressure increases 
further, the contents of the skull can no longer remain in 
place.  Focal increases in pressure, such as with 
tumors and acute hemorrhages, result in focal 
deviations in anatomy.  While the term "herniation" is 
used loosely when intracranial pressure increases, 
there are specific herniation syndromes with different 
mechanisms and outcomes.  Identifying increases in 
intracranial pressure by clinical and radiographic means 
is important to intervene early to prevent herniation.
     Clinical signs and symptoms of acute increased 
intracranial pressure include, headache, vomiting, vision 
distortion, diminished sensorium, pupillary dysfunction, 
hypertension, bradycardia, flexor/extensor posturing, 
etc.  Papilledema may not be present if ICP increases 
acutely.
     When intracranial hypertension is suspected, an 
immediate CT scan should be obtained to assess the 
degree of ICP increase and to identify the cause of the 
this.
     The following areas should be assessed on CT 
when attempting to determine the presence and 
severity of intracranial hypertension.  These are 
discussed in more detail below.
     1.  Prominence of sulci/gyri.
     2.  Lateral ventricle size.
     3.  Grey/White matter distinction.
     4.  Suprasellar cistern.
     5.  Quadrigeminal cistern.

     There are several brain herniation syndromes.  
These are discussed in more detail below.
     1.  Uncal  herniation.
     2.  Transtentorial herniation.
     3.  Tonsillar herniation.
     4.  Subfalcine herniation.
     5.  Superior vermian herniation.


CT signs of intracranial hypertension:

1.  Prominence of sulci/gyri:
     When intracranial pressure increases, this 
compresses the cerebral cortex against the calvarium.  
This attenuates the visibility of the sulci and gyri.  
Additionally, the space between the cortex and the 
calvarium is minimal when ICP increases.

View loss of sulci/gyri.

    The image on the left is a high CT cut which should 
show the sulci and gyri well.  Due to increased ICP, the 
cortex is compressed up against the calvarium losing 
the distinctness of the sulci and gyri.  The space 
between the cortex and the calvarium is obliterated.

     The sulci/gyri sign cannot be totally relied upon in 
some instances.  In cases of external hydrocephalus or 
chronic (or subacute) subdural effusions, fluid collects 
over the cortex.  The fluid space between the cortex 
and the calvarium appears to be increased and the 
sulci/gyri may appear prominent.  

View prominent sulci/gyri.

     Shown here is a focal extra-axial hematoma.  Note 
the prominent sulci and gyri despite intracranial 
hemorrhage.


2.  Lateral ventricle size:
     In acute hydrocephalus, due to obstruction in the 
outflow of CSF, the lateral ventricles will be enlarged.  
Similarly, in acute intraventricular hemorrhage, the 
lateral ventricles will be enlarged.

View dilated ventricles.

     Shown here are bilateral dilated lateral ventricles 
due to acute intraventricular hemorrhage.

     In other causes of intracranial hypertension, the 
lateral ventricles will be compressed (slit-like) or 
obliterated due to increases in pressure in 
compartments other than the lateral ventricles.  This is 
the case in generalized cerebral edema, subdural 
hematoma, epidural hematoma, etc.

View compressed ventricles.

    Shown here are two cuts showing subarachnoid 
hemorrhage.  The ventricles are slit-like due to cerebral 
edema and acute hemorrhage resulting in intracranial 
hypertension.


3.  Grey/White matter distinction:
     This is mostly a sign of cerebral edema in 
association with elevated ICP.

View good grey/white matter distinction.



View poor grey/white matter distinction.



4.  Suprasellar cistern:
     The suprasellar cistern is a fluid-filled space above 
the sella turcica.  It contains the circle of Willis and the 
optic chiasm.  On CT scan, it has a star-shaped 
appearance.  Anteriorly, the top point of the star is 
formed by the interhemispheric fissure between the two 
frontal lobes.  The lateral border of the suprasellar 
cistern is formed by the uncal portion of the temporal 
lobes.  The posterior border is formed by the pons in 
lower cuts and the cerebral peduncles of the midbrain in 
higher cuts.  In lower cuts where the pons forms the 
posterior border of the suprasellar cistern, the 
suprasellar cistern takes on the shape of a 5-pointed 
star.  In cuts where the cerebral peduncles (which have 
a central cleft) form the posterior border of the 
suprasellar cistern, the suprasellar cistern takes on the 
shape of a 6-pointed star.

View the midline anatomic diagram of the brain.


This is a midline sagittal cut of an MRI scan.  Identify 
the following structures:
     S - suprasellar cistern
     Po - pons
     P - cerebral peduncles (midbrain)
     M - medulla
     C - quadrigeminal plate (superior and inferior colliculi)
     V - fourth ventricle
     Q - quadrigeminal cistern

     Note that the fourth ventricle is connected to the 
third ventricle by the cerebral aqueduct which is very 
thin and may not be visible on CT.

View the anatomic diagram of the suprasellar cistern.


     The midline sagittal MRI scan shows the levels of 
the axial diagrams.  Note that the fourth ventricle is at 
roughly the same level of the suprasellar cistern, but 
depending on the angle of the axial cut, the fourth 
ventricle may be seen in cuts above, below, or at the 
same level as the suprasellar cistern.  The suprasellar 
cistern is seen in cuts 7 and 8.
     In the lower cut (7), the suprasellar cistern (s) takes 
on the shape of a five pointed star.  The frontal lobes 
(F) form the anterior border with the anterior 
interhemispheric fissure between the frontal lobes 
forming the apex of the star.  The uncus (U) of the 
temporal lobes forms the lateral borders.  The pons 
(Po) forms the posterior border.  The fourth ventricle (V) 
is also seen in this cut.
     In the higher cut (8), the suprasellar cistern (s) takes 
on the shape of a six pointed star.  The only difference 
higher up is that the posterior border is formed by the 
cerebral peduncles (p) of the midbrain.  The cleft 
between the cerebral peduncles forms the sixth point of 
the star.  The inferior colliculi (c) can also be seen at 
this level of the suprasellar cistern.

View CT scan of suprasellar cistern.

     The left and center images show the suprasellar 
cistern.  Its anterior borders are formed by the frontal 
lobes (F).  Its lateral borders are formed by the uncus 
(U) of the temporal lobes.  The left image shows the 
5-pointed star appearance of the suprasellar cistern 
where the posterior border is formed by the pons (Po).  
The black arrow points to the fourth ventricle.  The 
center image shows a higher cut where the suprasellar 
cistern has a 6-pointed star appearance since the 
posterior border is formed by the cerebral peduncles 
(P) which have a central cleft.
     When ICP increases, the suprasellar cistern space 
is compressed.  The space may still be visible; 
however, with severe intracranial hypertension, the 
cistern is obliterated due to encroachment of brain 
tissue that normally forms the borders of the suprasellar 
cistern.  Depending on the cause of the intracranial 
hypertension, the suprasellar cistern may be totally 
obliterated in global or severe ICP increase.  In focal 
lesions, brain tissue may encroach into only one part of 
the suprasellar cistern.  In early unilateral uncal 
herniation, the uncus of the temporal lobe (lateral 
border of the suprasellar cistern) will protrude into the 
suprasellar cistern.


5.  Quadrigeminal cistern:
     Also known as the quadrigeminal plate cistern, this 
fluid filled space is located cephalad to the fourth 
ventricle.

View the anatomic diagram of the quadrigeminal 
     cistern.

     The midline sagittal MRI scan shows the levels of 
the axial diagrams.  The quadrigeminal cistern is 
located above (anterior to) the "Q" in the highest cut 
shown (number 9).  The anterior border of the 
quadrigeminal cistern is formed by the superior colliculi 
(c).  Image 8 (lower cut) also shows the quadrigeminal 
cistern.  In this case, its anterior border is formed by the 
inferior colliculi (c).  This gives the anterior border of the 
quadrigeminal cistern the appearance of a "baby's 
bottom".  The quadrigeminal plate is comprised of the 
superior and inferior colliculi.  The quadrigeminal cistern 
is posterior to this quadrigeminal plate, thus its anterior 
border may be formed by the inferior or superior 
colliculi.

View CT scan of quadrigeminal cistern.

     The right image shows the quadrigeminal cistern 
(black arrow).  Note the "baby's bottom" appearance of 
its anterior border.  When ICP is increased, the 
quadrigeminal cistern space is compressed or 
obliterated.  


Identify the suprasellar and quadrigeminal cisterns in 
the following examples.

View moderately increased ICP.

     The suprasellar cistern is slightly smaller than its 
normal size (the right uncus is pushing into the 
suprasellar cistern) and the quadrigeminal cistern is 
compressed.  An epidural hematoma is noted.

View severe ICP increase.

     The suprasellar cistern (left image)  is tissue-filled, 
indicating the presence of brain tissue herniating into 
this space.  The quadrigeminal cistern is very 
compressed and pushed posteriorly (center image).  
The suprasellar cistern is located just above the base of 
the skull (above the sella).  It should be visible in the 
cuts near the base of the brain.  If it is not visible, it 
suggests that the suprasellar cistern is obliterated.  
Similarly, the quadrigeminal cistern should be located in 
the cut above the suprasellar cistern.  A subdural 
hematoma is noted with a midline shift.


Brain Herniation Syndromes:

1.  Uncal herniation:
     When mass effects within or adjacent to the 
temporal lobe occur, the medial portion of the temporal 
lobe (uncus) is forced medially and downward over the 
tentorium.  There is ipsilateral pupillary dilation.  The 
uncus is pushed medially into the suprasellar cistern.  

View uncal herniation.

     There is bilateral uncal herniation.  The suprasellar 
cistern is obliterated. 

View early uncal herniation.

     The right uncus is pushing into the suprasellar 
cistern; early right uncal herniation.


2.  Transtentorial herniation:
     It should be noted that this term is somewhat vague.  
It is used rather loosely and it may sometimes be used 
similarly to the terms temporal lobe herniation and uncal 
herniation.  The uncus may herniate over the tentorium 
as described above.  Supratentorial lesions on one side 
may initially result in uncal herniation.  As ICP increases 
further, bilateral temporal lobe herniation occurs 
transtentorially.  Early unilateral uncal herniation is 
more accurately called uncal herniation.  The terms 
cranial-caudal transtentorial herniation, rostro-caudal 
transtentorial herniation, or central transtentorial 
herniation more accurately describe what is generally 
meant by "transtentorial herniation".  Thus, uncal 
herniation is described separately above.
     In transtentorial herniation the medial portions of the 
temporal lobes (uncus) and the brainstem herniate 
downward from supratentorial to the infratentorial 
compartment.  The clinical signs include headache, 
decreasing level of consciousness and ipsilateral fixed 
dilated pupil (from compression of the third cranial 
nerve on the ipsilateral side).  As herniation worsens, 
decerebrate (extensor) posturing, contralateral (ie., 
bilateral) pupillary dilation and Cushing's triad occur.  
Cushing's triad includes alteration in respiration, 
bradycardia, and systemic hypertension.  It is rare to 
have all three present in children. Often there is just 
bradycardia alone.  Children tolerate brainstem 
compression produced by herniation better than adults.  
Immediate early intervention can result in recovery.  
Intervention at the stage of unilateral pupillary 
dysfunction is likely to have a better prognosis 
than intervention at the stage of bilateral pupillary 
dysfunction, decerebrate posturing and bradycardia.  
CT scan shows obliteration of the suprasellar and 
quadrigeminal cisterns.  Later findings include infarcts 
and brainstem hemorrhage.
     
View transtentorial herniation.

     The suprasellar cistern (left image) is obliterated.  
The quadrigeminal cistern is very compressed and 
pushed posteriorly (center image).  A subdural 
hematoma with a midline shift is noted.  There is central 
transtentorial and subfalcine herniation.


 3.  Tonsillar herniation:
     In tonsillar herniation (rare), a mass effect in the 
posterior fossa causes the cerebellar tonsils to 
herniate inferiorly through the foramen magnum 
compressing the medulla and upper cervical spinal 
cord.  Conscious patients complain of neck pain and 
vomiting.  They may have nystagmus, pupillary 
dilatation, bradycardia, hypertension and respiratory 
depression.  Early tonsillar herniation is difficult to 
recognize in an unconscious patient.  It may not be 
evident on CT scan since axial views cannot see the 
pathology well.  It is best seen on sagittal MRI.  
Clinically changes in vital signs may be the only clinical 
clue in an unconscious patient.

4.  Subfalcine herniation (cingulate herniation):
     A unilateral supratentorial mass or hemorrhage 
results in a midline shift.  If the pressure pushing the 
brain to one side is great enough, one of the 
hemispheres is pushed under the falx (subfalcine).  This 
may compress the anterior cerebral artery.  There is 
ipsilateral lateral ventricle compression and 
contralateral lateral ventricle dilation (due to obstruction 
of the foramen of Monroe).

View subfalcine herniation.

     The suprasellar cistern (left image) is obliterated.  
The quadrigeminal cistern is very compressed and 
pushed posteriorly (center image).  A subdural 
hematoma with a midline shift is noted.  There is central 
transtentorial and subfalcine herniation.


5.  Superior vermian herniation:
     Also called ascending transtentorial herniation, this 
involves upward herniation of the vermis and cerebellar 
hemispheres through the tentorial incisura due to a 
mass effect in the posterior fossa.  There is effacement 
of the quadrigeminal cistern.  There is hydrocephalus 
due to compression of the aqueduct of Sylvius.
  

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