What Does Coning Look Like? Symptoms and Imaging

Coning, the clinical term for brain herniation, looks different depending on which part of the brain is being displaced and how far the process has advanced. In its earliest stages it may show up only as subtle behavioral changes or a worsening headache. As it progresses, the signs become unmistakable: a blown pupil on one side, abnormal body posturing, erratic breathing, and dangerous swings in heart rate and blood pressure. On imaging, the hallmarks include midline shift of brain structures, compression or disappearance of the fluid-filled spaces (cisterns) around the brainstem, and visible displacement of brain tissue past rigid internal boundaries like the tentorium or the base of the skull.

Types of Brain Herniation and Why They Matter

The brain sits inside a rigid skull divided into compartments by tough membrane folds. When swelling, bleeding, or a mass pushes brain tissue out of its normal compartment and into another, herniation occurs. Where the tissue goes determines what structures get compressed and, in turn, what symptoms appear. The main types are subfalcine herniation, where brain tissue slides under the midline membrane called the falx; transtentorial herniation, where tissue is pushed downward (or sometimes upward) past the tentorium, the membrane that separates the upper brain from the cerebellum; and tonsillar herniation, where the lowest part of the cerebellum drops through the opening at the skull base into the spinal canal.¹ Transtentorial herniation is further split into lateral (uncal) and central types, each with a somewhat different clinical picture.

Uncal herniation is perhaps the most widely taught form because it produces such a distinctive set of signs. The uncus, a hook-shaped piece of temporal lobe, gets squeezed over the edge of the tentorium and presses directly on the third cranial nerve and the brainstem. Central herniation involves a more symmetric downward push of both sides of the brain. Tonsillar herniation is the variety most people mean when they say “coning” in casual medical shorthand, because the cerebellar tonsils cone down through the foramen magnum like a plug and compress the lower brainstem, which controls breathing and heart rate. All three can be fatal, but they announce themselves differently at the bedside and on scans.

Early Warning Signs Before the Classic Picture

Coning rarely arrives without warning, though the early signs are easy to miss or misattribute. Before any dramatic pupil changes or posturing, rising intracranial pressure tends to produce restlessness, drowsiness that seems disproportionate to the situation, headache, visual changes, and nausea or vomiting.² In a patient recovering from head trauma or brain surgery, these complaints can look like ordinary post-injury fatigue or medication side effects. The key is context: if a patient has any reason to be at risk for rising pressure inside the skull, a new headache or a subtle drop in alertness should be treated as a possible red flag rather than brushed aside.

A declining score on the Glasgow Coma Scale, even by just a point or two, is one of the most reliable early indicators that something is shifting inside the skull. Repeated neurological checks exist specifically to catch these small changes before they cascade into full herniation. By the time the classic signs appear, the window for reversing the process is already narrowing.

The Blown Pupil and Other Cranial Nerve Signs

The single most recognizable bedside sign of uncal herniation is a dilated, unreactive pupil on the same side as the mass or swelling. This happens because the third cranial nerve, which controls the pupil’s constriction, runs right along the edge of the tentorium and is one of the first structures compressed when the temporal lobe herniates. At first the pupil may be only sluggish in its response to light, but as compression worsens, it dilates fully and stops reacting. The affected eye also tends to drift downward and outward because the third nerve controls most of the muscles that move the eye.³

A difference in pupil size between the two eyes, called anisocoria, is treated as a possible herald of uncal herniation in anyone with a head injury or known intracranial mass. Papilledema, which is swelling of the optic disc visible with an ophthalmoscope, can also appear, though it takes longer to develop and is more a sign of sustained high pressure than of acute herniation itself.³ In central herniation, pupil changes tend to be bilateral and appear later, sometimes preceded by very small, pinpoint pupils as the upper brainstem is compressed before the third nerve pathways are affected.

Cushing Response and Vital Sign Changes

The Cushing response, sometimes called the Cushing reflex or Cushing triad, is the body’s last-ditch attempt to maintain blood flow to a brain being squeezed by rising pressure. It classically involves high blood pressure, a slow heart rate, and irregular breathing. The physiology is straightforward in concept: as the brain gets compressed, the brainstem cardiovascular centers detect falling perfusion and drive blood pressure up. The heart then reflexively slows in response to that elevated pressure.

A study of children with severe traumatic brain injury found that the combination of high systolic blood pressure and low heart rate was significantly linked with severe brain injury, with an odds ratio of about 2.8 compared to children with normal vital signs. The association was clear in children aged 7 and older, though it was not statistically significant in younger children aged 2 to 6, possibly because their vital sign ranges are wider and harder to interpret.⁴ The practical takeaway is that the Cushing response is a late and ominous sign. Waiting for it to appear before acting means the herniation is already well underway.

Abnormal Posturing

As coning progresses and the brainstem comes under increasing pressure, patients develop abnormal motor patterns. Decorticate posturing, where the arms flex inward and the legs extend, indicates damage or compression above the level of the midbrain. Decerebrate posturing, where both arms and legs extend rigidly, suggests the damage has reached the midbrain or pons. A third pattern, opisthotonic posturing, involves arching of the entire spine and is associated with even deeper brainstem involvement.

Research in children with cerebral malaria found that posturing was independently linked to signs of raised intracranial pressure on eye examination. Decerebrate posturing carried roughly double the odds of recurrent seizures compared with patients who did not posture, and opisthotonic posturing nearly triple the odds.⁵ In the setting of herniation specifically, the transition from decorticate to decerebrate posturing is a clinical marker that compression is advancing downward through the brainstem. A study of 25 patients with acute midbrain syndrome showed that the pattern of decerebrate episodes was tied to the degree of obstruction at the tentorial notch and influenced blood pressure, intracranial pressure, and heart rate during each episode.⁶

What Coning Looks Like on CT

A non-contrast CT scan of the head is usually the first imaging study obtained when herniation is suspected, because it is fast and widely available. The CT signs that indicate or suggest herniation include midline shift of brain structures away from the side of a mass, effacement (compression or disappearance) of the basal cisterns, and visible displacement of brain tissue across anatomical boundaries.

The basal cisterns are fluid-filled spaces surrounding the brainstem. On a normal CT they appear as dark crescents of cerebrospinal fluid. When pressure rises and the brain starts herniating, these spaces get squeezed shut. Their effacement is one of the most important CT markers of impending or active herniation. Automated methods for measuring cistern compression have shown a strong inverse relationship between the degree of effacement and severity of traumatic brain injury, with statistically significant correlation to expert clinical assessment.⁷

Beyond cistern effacement, CT can show direct signs such as displacement of brain tissue under the falx (subfalcine herniation), compression of one or both cerebral peduncles against the tentorium, or low-lying cerebellar tonsils at the foramen magnum. The gray-to-white matter ratio on CT has also been studied as a prognostic marker. In cardiac arrest patients, reduced gray-to-white differentiation combined with cistern effacement on early CT scans showed promise as a predictor of poor outcome, though the imaging measures did not clearly outperform clinical assessment alone.⁸

MRI and the Measurement Problem

MRI provides far more anatomical detail than CT and is the preferred modality for evaluating certain types of herniation, particularly tonsillar herniation associated with Chiari I malformation. In this condition, the cerebellar tonsils sit lower than normal, poking through the foramen magnum. The standard diagnostic threshold is tonsillar descent of 5 millimeters or more below the foramen magnum on a midsagittal MRI slice.

That measurement turns out to be trickier than it sounds. The cerebellar tonsils are not midline structures; they sit slightly off-center on each side. A study of 50 Chiari I patients found that sagittal MRI routinely overestimated the degree of tonsillar descent compared with coronal imaging. Ten percent of patients who appeared to meet the diagnostic threshold on sagittal images actually had both tonsils less than 3 millimeters below the foramen magnum on coronal views, and 38 percent had at least one tonsil below that mark.⁹ The finding underscores that tonsillar herniation is almost always asymmetric. Relying on a single midline sagittal slice to judge the degree of descent can mislead clinicians into overdiagnosis.

Parasagittal and coronal MRI planes help resolve this by showing where each tonsil actually sits. Research into using parasagittal measurements of the extent of tonsillar herniation has explored this as a more accurate diagnostic approach.¹⁰ For clinicians and patients alike, the lesson is that a single number on a single image plane does not capture the full picture. If a Chiari diagnosis hinges on a borderline measurement, additional imaging planes are worth requesting.

Duret Hemorrhages on Imaging

One of the most ominous imaging findings in transtentorial herniation is the Duret hemorrhage: small bleeds that appear in the brainstem, typically in the upper pons and midbrain. These show up on CT as small, bright white dots or streaks in the center of the brainstem. On MRI they are even more conspicuous.

Duret hemorrhages occur because the downward displacement of the brain stretches or tears tiny blood vessels that perforate into the brainstem from the basilar artery. Whether the primary mechanism is arterial tearing or venous congestion and infarction remains debated; both probably contribute.¹¹ Regardless of cause, the appearance of Duret hemorrhages typically signals that irreversible brainstem damage has occurred or is imminent. Finding them on a scan drastically shifts the prognosis and can influence decisions about continuing aggressive treatment.

Ultrasound of the Optic Nerve Sheath

Not every patient with suspected rising intracranial pressure can be rushed to a CT scanner immediately. Bedside ultrasound of the optic nerve sheath diameter has gained traction as a rapid, noninvasive way to screen for dangerously high pressure. The optic nerve is surrounded by a sheath that is continuous with the membranes around the brain, so when intracranial pressure rises, the sheath balloons outward. Measuring its diameter behind the eye with a standard ultrasound probe takes only a few minutes.

A scoping review found that optic nerve sheath diameter measurements exhibit strong correlation with invasive intracranial pressure monitors and should be considered one of the most effective noninvasive methods for estimating intracranial pressure in traumatic brain injury patients.¹² A cross-sectional study at a trauma center in India reported that the technique had about 86 percent sensitivity and 64 percent specificity for detecting raised intracranial pressure when compared with CT findings, with an overall accuracy around 83 percent.¹³

The technique is not a replacement for definitive imaging but fills a practical gap. In emergency departments, austere settings, or situations where the patient is too unstable to move, a widened optic nerve sheath on ultrasound can prompt faster escalation.¹⁴ It is especially useful for serial monitoring, since repeated measurements can track whether pressure is rising or falling over hours.

When the Signs Point the Wrong Way

One of the more confounding aspects of brain herniation is that the clinical signs sometimes point to the wrong side of the brain. In the Kernohan-Woltman notch phenomenon, a mass on one side of the brain causes weakness on the same side rather than the expected opposite side. This happens because the herniating tissue pushes the brainstem sideways, pressing the opposite cerebral peduncle (the bundle of motor fibers on the side away from the mass) against the hard edge of the tentorium, producing a visible notch or indentation.¹⁵

The phenomenon was first described through post-mortem studies on 297 patients in 1929, and modern imaging has confirmed the underlying mechanism. A recent analysis of patients with ipsilateral hemiparesis found that about 75 percent of cases developed acutely after traumatic brain injury, and structural lesions of the contralateral cerebral peduncle could be demonstrated on contemporary imaging in the majority of patients.¹⁶ This false-localizing pattern can lead clinicians to look for a problem on the wrong side if they rely on motor signs alone without imaging. It is one reason why a CT scan, not the neurological exam alone, determines the side and type of intervention.¹⁷

Paradoxical Herniation After Surgery

Decompressive craniectomy, the surgical removal of a section of skull to relieve pressure, is sometimes the last resort for uncontrollable brain swelling. Paradoxically, this lifesaving procedure can itself lead to herniation. After the bone flap is removed, changes in pressure dynamics, particularly when cerebrospinal fluid is drained or the patient is positioned upright, can cause the brain to shift in unexpected directions. The brain may herniate downward through the tentorium or at the foramen magnum, even though the pressure was supposed to have been relieved.

A systematic review found that the most common imaging signs of paradoxical herniation included midline shift, transtentorial herniation, compression of the space in front of the brainstem, and crowding of the cerebellar tonsils at the foramen magnum. Clinically, the most frequent presentation was a drop in consciousness, unequal pupils, and sinking of the skin flap over the surgical defect. Some patients developed hemiparesis, positional headaches, or signs of autonomic instability including rapid heart rate and abnormal breathing patterns.¹⁸ Recognizing this complication matters because the treatment is the opposite of what you would do for ordinary herniation: instead of removing fluid or lowering pressure further, the solution involves replacing the bone flap, placing the patient flat, or infusing fluid to restore pressure equilibrium.

Outcomes After Herniation Is Reversed

The prognosis after brain herniation depends heavily on how far the process has advanced and how quickly it is reversed. A study of patients with transtentorial herniation from masses above the tentorium found that in-hospital mortality was 60 percent. Brain death accounted for most of the deaths, and care was withdrawn in eight patients. Having a second episode of herniation and involvement of the midbrain during the first episode were both independently associated with dying in the hospital. Among the survivors followed for an average of about 11 months, roughly two-thirds regained functional independence.¹⁹

Those numbers offer a counterpoint to the common assumption that herniation is always unsurvivable. Early recognition, aggressive medical management of intracranial pressure with agents like hypertonic saline or mannitol, and rapid surgical intervention when appropriate can pull some patients back from the brink. The survivors who do well tend to be those caught early, before posturing has progressed to decerebrate patterns and before Duret hemorrhages have appeared on imaging. Once those late signs are present, meaningful recovery becomes far less likely.

The Lumbar Puncture Question

One practical scenario where coning enters clinical decision-making is the question of whether to perform a lumbar puncture on someone who might have raised intracranial pressure. The fear is that removing cerebrospinal fluid from below the brain could create a pressure gradient that pulls brain tissue downward, triggering tonsillar herniation. This concern is most relevant when evaluating patients with suspected meningitis who might also have a brain abscess or mass.

Whether CT scanning should always precede lumbar puncture in these situations has been debated for decades. A review of the evidence found that the decision is complicated by the fact that much of the data comes from retrospective studies and theoretical reasoning rather than controlled trials.²⁰ In current practice, most guidelines recommend obtaining a CT before lumbar puncture in patients who have focal neurological deficits, altered consciousness, papilledema, seizures, or an immunocompromised state. In an otherwise alert patient with no focal signs, the risk of herniation from a lumbar puncture is extremely low, and delaying the procedure to get a scan can delay treatment for infections like bacterial meningitis where every hour counts.

Cerebral edema from traumatic brain injury is one of the most common clinical contexts in which herniation occurs. The swelling that follows a severe head injury can raise intracranial pressure enough to cause fatal herniation, compromise cerebral perfusion, and starve the brain of oxygen.²¹ Managing that edema before it tips into herniation is the central challenge of neurocritical care in trauma, and the imaging and clinical signs described throughout this article are the tools clinicians use to track that trajectory in real time.