Brain Herniation Syndromes on CT: Board Imaging Clues

Board exams test four main brain herniation syndromes, and each one has a signature finding. Uncal herniation blows the pupil on the same side as the mass and weakens the opposite side of the body. Central herniation gives small pupils, then midposition fixed pupils, with breathing that worsens in a predictable order as the brainstem is pushed down. Subfalcine herniation causes contralateral leg weakness from anterior cerebral artery compression, and tonsillar herniation stops breathing by crushing the medulla.

The CT shows you the mass effect. The stem gives you the pupil, the motor exam, the breathing pattern and the vital signs. Your job is to match the two, name the herniation, and pick the step that lowers intracranial pressure before the patient dies. That is the whole game, and it shows up on COMLEX Level 1, USMLE Step 1, and in more management-heavy form on Level 2-CE and Step 2 CK.

Why does the brain herniate in the first place?

The skull is a closed box. The Monro-Kellie doctrine says the volume inside it (brain, blood and CSF) is fixed, so when a hematoma, tumor, abscess or swelling adds volume, something else has to leave. CSF drains into the spinal canal first and venous blood gets squeezed out next. Once those buffers are used up, intracranial pressure climbs fast and brain tissue starts sliding past the rigid walls that divide the skull.

There are three walls that matter for boards. The falx cerebri separates the two hemispheres. The tentorium cerebelli separates the cerebrum above from the cerebellum and brainstem below, with a gap in the middle (the tentorial notch) where the midbrain passes. The foramen magnum is the hole at the bottom of the skull where the medulla becomes the spinal cord.

Every herniation syndrome is named by which wall the brain slips past. If you know what sits next to that wall, you can predict the deficit without memorizing a list. The cingulate gyrus slides under the falx and pinches the anterior cerebral artery. The uncus slides over the tentorial edge and pinches CN III and the cerebral peduncle. The tonsils slide through the foramen magnum and crush the medulla.

How do you read a head CT for herniation on boards?

Non-contrast head CT is the first study in any acute neurologic emergency because it is fast and shows blood well. On a board question, check five things in this order.

1. The lesion. A biconvex (lens-shaped) collection that does not cross suture lines is an epidural hematoma, classically from a temporal bone fracture tearing the middle meningeal artery. A crescent that crosses sutures is a subdural hematoma from torn bridging veins. A bright mass in the deep brain of a hypertensive patient is an intraparenchymal hemorrhage.
2. Midline shift. Look at the septum pellucidum, the thin membrane between the lateral ventricles. If it is pushed away from the side of the lesion, there is subfalcine herniation.
3. The ventricles. The lateral ventricle next to the mass gets compressed. The opposite ventricle can enlarge because its outflow at the foramen of Monro is kinked shut.
4. The basal cisterns. The CSF spaces around the midbrain (suprasellar, ambient and quadrigeminal cisterns) should be dark and open. When they fill in with tissue and disappear, the brain is herniating downward through the tentorial notch.
5. The posterior fossa. Check the fourth ventricle and the cisterna magna behind the medulla. If they are squeezed shut by a cerebellar mass, tonsillar herniation and obstructive hydrocephalus are next.

Effaced sulci and loss of the gray-white boundary across both hemispheres point to diffuse cerebral edema, which is the usual setup for central herniation.

Uncal herniation: the blown pupil on the same side

What moves and what gets compressed

In uncal herniation (also called lateral transtentorial herniation), the uncus of the medial temporal lobe slides over the free edge of the tentorium. It is the classic complication of an expanding temporal or lateral mass, and an epidural hematoma is the board favorite. The stem often describes a patient hit in the side of the head who talks normally for a while (the lucid interval) and then deteriorates.

Three structures get hit, and each gives a finding.

Why the pupil goes first

The parasympathetic fibers that constrict the pupil run on the outside of CN III. Pressure from the uncus hits those surface fibers before the deeper motor fibers that move the eye. That is why a unilateral fixed, dilated pupil in a head trauma stem is CN III compression until proven otherwise, and why a blown pupil with a normal-looking eye position still counts.

Compare that with diabetic CN III palsy, which is a common board distractor. Diabetic microvascular infarction damages the center of the nerve and spares the outer pupillary fibers. So a "down and out" eye with a normal pupil points to diabetes, and a "down and out" eye with a blown pupil points to compression (aneurysm of the posterior communicating artery or uncal herniation).

The Kernohan notch trap

Sometimes the mass pushes the whole midbrain sideways, and the opposite cerebral peduncle gets jammed against the opposite edge of the tentorium. The notch it leaves in the peduncle is the Kernohan notch. The patient now has weakness on the same side as the lesion, which is a false localizing sign. If a stem gives you a left epidural hematoma, a blown left pupil and left-sided weakness, the pupil is still the reliable sign. Trust it for side, not the hemiparesis.

CT clues for uncal herniation

The medial temporal lobe pushes into the suprasellar cistern on one side, and the ambient cistern on that side is effaced. The midbrain may look rotated or flattened. You will usually see the cause too: an epidural or subdural hematoma, or a temporal lobe mass with surrounding edema.

Central herniation: rostrocaudal deterioration

What moves

In central (downward transtentorial) herniation, both hemispheres and the diencephalon are pushed straight down through the tentorial notch. The setup is something that raises pressure evenly from above. Diffuse cerebral edema after trauma or anoxia, bilateral subdural hematomas, and a large midline mass are the usual causes.

Pupils, breathing and posture by level

Central herniation compresses the brainstem from the top down, so the exam gets worse in a fixed order. Boards love this because each level has a matching pupil, breathing pattern and posture.

The posturing rule is simple. Decorticate posturing means the lesion is above the red nucleus, so the arms flex. Decerebrate posturing means the lesion is at or below the red nucleus in the midbrain, so the arms extend. Moving from decorticate to decerebrate is the patient getting worse.

Two other clues worth knowing

Downward pressure stretches the long, thin abducens nerve (CN VI) over the petrous ridge. That can cause a lateral rectus palsy that does not localize the lesion, another false localizing sign. Stretching of the pituitary stalk can also cause central diabetes insipidus.

The late and often fatal finding is a Duret hemorrhage. These are small midline bleeds in the midbrain and pons from tearing of the basilar artery's paramedian perforating branches as the brainstem drops. On CT they look like a bright streak in the center of the brainstem.

CT clues for central herniation

The basal cisterns are effaced on both sides. Sulci are lost across both hemispheres, the ventricles look slit-like, and gray-white differentiation fades. There may be no single dramatic mass, which is exactly why students miss it.

Subfalcine herniation: the most common type and the leg finding

What moves and what gets compressed

In subfalcine (cingulate) herniation, the cingulate gyrus slides under the free edge of the falx cerebri toward the other side. It is the most common herniation and the easiest one to see on CT, because it is the midline shift.

The anterior cerebral artery runs along the medial surface of the hemisphere next to the falx. When the cingulate gyrus pushes under the falx, it can pinch the ACA (or its pericallosal and callosomarginal branches) against the edge. The ACA supplies the medial motor and sensory cortex, which is where the leg is mapped on the homunculus. So the result is contralateral leg weakness and numbness, with the face and arm relatively spared.

CT clues for subfalcine herniation

The septum pellucidum shifts away from the mass. The lateral ventricle next to the mass is compressed, and the opposite ventricle may enlarge as its foramen of Monro gets trapped. Midline shift is the number neurosurgery uses. The Brain Trauma Foundation guidelines recommend evacuating an acute subdural hematoma with a midline shift over 5 mm or a thickness over 10 mm, regardless of the Glasgow Coma Scale score.

Subfalcine herniation on its own is often not the immediate killer. It is the warning that the same mass is about to push the uncus or the whole diencephalon downward.

Tonsillar herniation: the one that stops breathing

What moves and what gets compressed

In tonsillar herniation, the cerebellar tonsils are pushed down through the foramen magnum and compress the medulla. The medulla holds the respiratory and cardiovascular centers, so this is the herniation that kills by apnea and cardiovascular collapse.

The usual causes are a posterior fossa mass (cerebellar hemorrhage, a swollen cerebellar infarct, a tumor) or the final stage of any supratentorial process. Boards also love the iatrogenic version. A lumbar puncture in a patient with raised intracranial pressure from a mass drops the pressure below the foramen magnum, and the tonsils get pulled down.

Clinical clues

Early signs are occipital headache, neck stiffness and a head tilt as the tonsils irritate the upper cervical roots. Then comes the Cushing triad: hypertension with a widening pulse pressure, bradycardia, and irregular breathing. The Cushing triad is a late sign of raised intracranial pressure from any cause, but in a posterior fossa stem it points straight at the medulla. Respiratory arrest can come before the patient loses consciousness.

CT and MRI clues

The fourth ventricle and cisterna magna are effaced. Obstructive hydrocephalus may enlarge the lateral and third ventricles upstream. On MRI, the tonsils sit below the foramen magnum and look crowded and pointed.

The Chiari I trap

Do not confuse tonsillar herniation with a Chiari I malformation. Chiari I is a congenital, chronic downward position of the cerebellar tonsils (generally more than 5 mm below the foramen magnum), often found in a teenager or adult with occipital headaches worsened by coughing or straining. It is associated with syringomyelia, which causes a cape-like loss of pain and temperature sensation over the shoulders. Same anatomy, completely different stem. Chiari I is a slow outpatient problem, and tonsillar herniation is a code.

Upward herniation, briefly

A posterior fossa mass can also push the cerebellum up through the tentorial notch. This upward transtentorial herniation compresses the midbrain and can kink the superior cerebellar arteries. It is less commonly tested, but a classic setup is a patient with a cerebellar mass who deteriorates after a ventricular drain is placed above the tentorium, since draining CSF from above lets the posterior fossa push upward.

One-glance summary for the stem

What is the board answer for management?

Level 1 and Step 1 mostly ask you to name the herniation and the compressed structure. Level 2-CE and Step 2 CK ask what to do next, and the answers are consistent.

Get a non-contrast head CT first, and do not do a lumbar puncture when there are signs of a mass or raised pressure (papilledema, focal deficits, altered mental status). Lower intracranial pressure quickly by raising the head of the bed to 30 degrees and giving hyperosmolar therapy with mannitol or hypertonic saline. Intubating and briefly hyperventilating the patient lowers CO2, which constricts cerebral vessels and drops pressure within minutes. That is only a short bridge to definitive treatment, because sustained vasoconstriction can cause ischemia.

The definitive answer for a hematoma is surgical evacuation, and for refractory swelling it can be a decompressive craniectomy. Dexamethasone helps the vasogenic edema around a brain tumor or abscess. It is the wrong answer in traumatic brain injury, because the CRASH trial showed that corticosteroids increased mortality after head injury.

How to spot the herniation fast on test day

Read the last sentence of the stem first so you know whether the question wants a diagnosis, a structure or a next step. Then jump to the pupils. One blown pupil means uncal herniation on that side. Small pupils with Cheyne-Stokes breathing means early central herniation. Leg weakness with a midline shift means subfalcine herniation. Hypertension, bradycardia and irregular breathing in a patient with a posterior fossa lesion, or after a lumbar puncture, means tonsillar herniation.

After that, confirm with the CT description and use the lesion to tell you the cause. A lucid interval with a biconvex bleed is an epidural hematoma, and an elderly patient on anticoagulation with a crescent is a subdural. That pairing of cause and syndrome is what turns a scary imaging question into an easy point.

Frequently asked questions about brain herniation syndromes

What is the difference between uncal and tonsillar herniation on boards?

Uncal herniation happens at the tentorium, and tonsillar herniation happens at the foramen magnum. Uncal herniation compresses CN III and the cerebral peduncle, so the clue is an ipsilateral blown pupil with contralateral weakness, usually from a temporal mass or epidural hematoma. Tonsillar herniation compresses the medulla, so the clue is the Cushing triad and respiratory arrest, usually from a posterior fossa mass or a lumbar puncture done with raised pressure.

Why does uncal herniation cause a fixed, dilated pupil before eye movement problems?

The parasympathetic fibers that constrict the pupil run on the outer surface of CN III. External compression from the uncus damages those surface fibers first, so the pupil dilates and stops reacting before the motor fibers fail. The eye drifts "down and out" and the lid droops later as compression deepens.

What is the Kernohan notch phenomenon?

It is weakness on the same side as the brain lesion caused by uncal herniation. The mass pushes the midbrain sideways until the opposite cerebral peduncle is pressed against the tentorial edge. That opposite peduncle controls the body on the side of the mass, so the weakness appears on the same side as the lesion, which makes it a false localizing sign. The blown pupil still points to the correct side.

Which herniation causes leg weakness?

Subfalcine herniation. The cingulate gyrus slides under the falx and can compress the anterior cerebral artery, which supplies the medial cortex where the leg is represented. The result is contralateral leg weakness and sensory loss, and the CT shows midline shift of the septum pellucidum.

Why is a lumbar puncture contraindicated when a CT shows a mass?

A mass with raised intracranial pressure sets up a pressure difference between the skull and the spinal canal. Removing CSF from below widens that difference and can pull the cerebellar tonsils through the foramen magnum. That compresses the medulla and can cause respiratory arrest, so the board answer is to image first and hold the tap.

What is a Duret hemorrhage?

A Duret hemorrhage is a small bleed in the midline of the midbrain or pons that happens late in downward transtentorial herniation. As the brainstem is pushed down, the basilar artery's paramedian perforating branches stretch and tear. On CT it appears as a bright spot in the center of the brainstem, and it carries a very poor prognosis.

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