In 1993, neurosurgeon Gregory Grabb and his colleague Edward Oakes published a measurement technique for quantifying ventral brainstem compression at the craniocervical junction. It was not flashy. It was a line on a sagittal MRI — from the opisthion (the posterior lip of the foramen magnum) to the posterior axial line (the posterior cortex of the C2 body and odontoid process). The perpendicular distance from this line to the most ventral point of the brainstem (or the cord at that level) was, they argued, a direct, reproducible, clinically meaningful measure of how much the brainstem was being encroached upon from the front. They were right. Three decades later, the Grabb-Oakes measurement remains one of the most important numbers in the evaluation of craniocervical pathology — and one of the most systematically unmade.

Measurement 1 of 2

The Grabb-Oakes Measurement (pB-C2)

How it is made: step by step

The measurement is performed on a midsagittal MRI or CT image — the image slice passing through the midline of the spine.

The four steps are: identify the posterior axial line (the posterior cortex of the C2 body, extended superiorly along the posterior cortex of the odontoid process — this is a single, continuous line following the back of the C2 structure); locate the opisthion (the posterior midline rim of the foramen magnum); identify the most ventral point of the brainstem or cord at the level of the opisthion-pAL line; and draw a perpendicular from the ventral brainstem to the posterior axial line. That perpendicular distance, in millimetres, is the Grabb-Oakes value.

What the measurement captures is the degree to which the brainstem or cord has been displaced posteriorly — pushed backward, away from where it should sit — by the encroaching odontoid or retro-odontoid tissue. A high value means more posterior displacement, which means more compression, which means more clinical consequence.

What compresses: odontoid vs. pannus

The compressing structure is not always bone alone. In chronic atlantoaxial instability — including CCI in hypermobile connective tissue disorders — the body responds to chronic abnormal motion at the C1-C2 joint by laying down retro-odontoid pannus: a mass of fibrocartilaginous and fibrovascular tissue that accumulates behind the odontoid process and in the retro-odontoid space. This pannus can add several millimetres to the effective anterior compression — and it is only visible on MRI, not on CT. A patient assessed only with CT may have their compression underestimated because the pannus is invisible to that modality.

The clinical implication is important: on MRI, the measurement should be made to the most anterior compressing tissue — whether that is bone (odontoid) or soft tissue (pannus). Using bone alone on MRI will underestimate compression in pannus-positive patients. This is one reason why the measurement must always be made on MRI when pannus is clinically suspected, and why CT-based Grabb-Oakes values should be interpreted with awareness that soft-tissue compression is not captured.

A Grabb-Oakes of 8 mm on CT in a patient with known atlantoaxial instability may represent 12 mm of actual compression — with 4 mm of retro-odontoid pannus sitting invisibly in the retro-odontoid space, absent from the CT image.

The surgical threshold — and the context-dependence problem

The original Grabb-Oakes paper used > 9 mm as the threshold of significance. Neurosurgeon Fraser Henderson subsequently proposed > 13 mm as the threshold for surgical intervention — a number widely referenced in CCI surgery discussions. These thresholds matter, but they should not be applied in isolation from clinical context.

The threshold problem — critical for CCI patients to understand

A Grabb-Oakes value of 11 mm is "between the thresholds" — above Grabb's original 9 mm but below Henderson's 13 mm surgical threshold. In a patient with severe positional neurological symptoms, progressive myelopathy signs, and confirmed hEDS causing ligamentous laxity at the craniocervical junction, 11 mm may well represent a surgical indication. In an asymptomatic healthy adult found incidentally to have a value of 10 mm, it may not. The measurement is one data point in a clinical picture — not a binary on/off switch for surgical decision-making. Specialist neurosurgical evaluation is required whenever the value is elevated in a symptomatic patient.

Measurement 2 of 2

The Clivoaxial Angle (CXA)

Bony CXA vs. soft-tissue CXA — a distinction that changes the diagnosis

Bony CXA

Measured from the posterior cortex of the clivus to the posterior cortex of the C2 body (the same posterior axial line used in Grabb-Oakes). Uses bony landmarks only. Can be measured on either CT or MRI. Reflects the bony geometry of the junction. Does not account for the actual trajectory of the brainstem within that geometry. In EDS/CCI, the brainstem may be more displaced than the bony angle suggests, because ligamentous laxity allows the soft tissues to translate beyond what bony alignment predicts.

Soft-Tissue CXA

Measured from the line of the posterior clivus to the line of the posterior brainstem/cord at the pontomedullary junction. Requires MRI. Reflects the actual angulation of the neural tissue — not just the bony geometry around it. In CCI, the soft-tissue CXA is often more abnormal than the bony CXA — meaning the brainstem is kinked more severely than the bones alone suggest. Missing the soft-tissue variant means underestimating compression in a substantial proportion of CCI patients.

The practical implication: both should be measured on MRI. Reporting only the bony CXA — or confusing the two — can result in a patient being told their angle is "borderline normal" when their soft-tissue CXA is clearly pathological. This distinction is not universally acknowledged in radiological reporting, and patients reviewing their own imaging reports should be aware that the report may not specify which variant was measured.

What a reduced CXA does to a human body

The brainstem is not merely a cable running through this junction. It is an active regulatory centre — containing the nuclei of cranial nerves V through XII, the reticular formation (which governs arousal and consciousness), the cardiovascular and respiratory centres, and the principal relay structures for sensory and motor pathways to and from the entire body below the head. When it is kinked at an acute angle, multiple mechanisms of injury occur simultaneously.

CXA Range Mechanical effect Typical clinical consequences Urgency
≥ 135° Normal brainstem trajectory; no kinking None attributable to CXA alone Normal
125° – 134° Mild kinking; early cord/brainstem angulation Positional headache, cognitive symptoms, early dysautonomia, neck pain; myelopathy signs may be subtle Monitor
115° – 124° Moderate kinking; impaired CSF flow; vascular compromise possible Progressive myelopathy, worsening POTS, swallowing difficulty, proprioceptive deficits, significant cognitive impairment Specialist referral
< 115° Severe kinking; high-grade compression; CSF obstruction likely Severe myelopathy, spasticity, respiratory symptoms, cranial nerve deficits, possible drop attacks; surgical emergency territory Urgent
These ranges represent clinical heuristics drawn from published surgical series, not absolute categorical thresholds. A patient with a CXA of 130° and severe, progressive symptoms deserves the same urgency of evaluation as one with a CXA of 120°. The angle is one measurement in a clinical picture.

A CXA below 125° is not a "borderline" result to be watched. In a symptomatic patient, it is evidence that the brainstem is being kinked at the most critical junction in the human nervous system.

Pitfalls

Where These Measurements Go Wrong

Both the Grabb-Oakes measurement and the CXA have characteristic error modes — pitfalls that can produce falsely reassuring values in patients with genuine pathology. Understanding these pitfalls is essential both for the clinicians making the measurements and for patients reviewing reports.

1
Supine imaging hides positional pathology
Both measurements can be near-normal on supine MRI and significantly abnormal on upright or flexion imaging. The craniocervical junction is most stable when lying flat; the ligaments are unstressed; the odontoid sits in its least invaginated position. A Grabb-Oakes of 8 mm supine may become 12–14 mm in an upright loaded position. This is perhaps the single most important pitfall in CCI imaging — and the most common reason patients with genuine structural pathology receive normal radiology reports.
2
Incorrect identification of the posterior axial line
The posterior axial line must follow the posterior cortex of both the C2 body and the odontoid process as a single continuous line. A common error is using only the posterior cortex of the C2 body without extending it along the posterior odontoid — this moves the reference line anteriorly and artificially inflates the measured pB-C2 distance. Conversely, extending the line along only the posterior odontoid tip without reference to the C2 body can place the line too posteriorly, deflating the measurement. Landmark precision here directly determines clinical accuracy.
3
Confusing bony and soft-tissue CXA
The bony CXA uses the posterior clivus cortex and the posterior C2 cortex. The soft-tissue CXA uses the posterior clivus cortex and the dorsal brainstem surface at the pontomedullary junction. These measure different things and will differ in value — sometimes substantially. A report stating "CXA 138°" without specifying which variant was measured cannot be reliably interpreted. In patients with CCI/EDS, the soft-tissue CXA is the more clinically relevant value, and it is the one more likely to be abnormal.
4
Missing retro-odontoid pannus on CT
CT does not visualise soft tissue adequately to detect retro-odontoid pannus. A Grabb-Oakes measurement on CT in a patient with chronic atlantoaxial instability will underestimate the true compression if pannus is present. MRI is mandatory in this population. When both CT and MRI are available, both should be reviewed — and any discrepancy should prompt specific investigation of the retro-odontoid space on MRI T1 and T2 sequences.
5
Isolating these measurements from the clinical picture
Neither measurement has an absolute threshold that independently mandates or excludes surgery. A Grabb-Oakes of 11 mm in a patient with rapidly progressive myelopathy and failed conservative management is different from the same value in a mildly symptomatic patient who has not yet trialled non-surgical management. The measurements provide the quantitative evidence. The clinical decision requires a specialist who understands both the measurements and the patient.
6
Failure to measure at all
The most common pitfall: neither measurement is made. Standard cervical MRI protocols do not include craniocervical morphometric measurements. Standard radiology training does not routinely cover them. Unless the referring clinician specifically requests these measurements — or the radiologist is one of the small number who know to make them proactively — the imaging will be reviewed without them. The evidence sits in the scan; the scan is reported as unremarkable; the patient is told they are fine.
Clinical Integration

Grabb-Oakes and CXA Together — Reading the Complete Picture

The Grabb-Oakes and CXA are complementary measurements, not alternatives. Grabb-Oakes quantifies the anteroposterior compression — how far the ventral brainstem has been displaced toward the posterior elements. CXA quantifies the angular deformity — the degree to which the brainstem is being bent. A patient can have an elevated Grabb-Oakes without a severely reduced CXA, and vice versa — but in most significant CCI presentations, both will be abnormal, and the combination provides a more complete picture of the compressive pathology than either alone.

The combination that changes the clinical picture

Elevated Grabb-Oakes (say, 11–14 mm) with a reduced CXA (say, 120–128°) in a symptomatic patient with hEDS, POTS, and positional neurological symptoms is not a coincidence of mild findings. It is evidence of a structural neurological emergency that has been developing — often for years — while a series of normal supine MRI reports accumulated in the patient's notes. When both measurements are abnormal on upright or dynamic imaging, the case for specialist craniocervical evaluation is not merely supported. It is compelling.

Associated conditions to look for when these values are abnormal

An elevated Grabb-Oakes or reduced CXA is rarely an isolated finding. In most CCI presentations, the abnormal morphometric values are accompanied by — or causally related to — a cluster of other findings that paint the full structural picture:

For Patients

What to Do With This Information

If you have CCI or are pursuing a diagnosis, and you have existing imaging, here is what you can ask your current clinician or a specialist to do:

For existing MRI: Ask specifically whether the Grabb-Oakes (pB-C2) measurement has been made, and whether both the bony and soft-tissue clivoaxial angles have been reported. If not, ask for the imaging to be reviewed by a radiologist or neurosurgeon familiar with CCI morphometrics. In some cases, this means seeking out a specialist centre.

For new imaging: The referral should specifically request craniocervical morphometric measurements including Grabb-Oakes and CXA (both variants). If upright or open-bore MRI is available, this is strongly preferable for CCI evaluation. Flexion-extension sequences should be included where possible.

When reviewing a report: Look for the words "Grabb-Oakes," "pB-C2," "clivoaxial angle," or "CXA." Their absence from a report does not mean the values were checked and normal — it almost always means they were not checked at all. An MRI report that does not mention these measurements is not a reassurance that compression is absent. It is a statement that compression was not looked for.


Grabb-Oakes and the clivoaxial angle are not abstract academic constructs. They are the numbers that describe, precisely and reproducibly, the degree to which the most critical regulatory centre in the human nervous system is being mechanically deformed. When those numbers are elevated and abnormal, the body that contains them is in structural trouble — trouble that has a location, a mechanism, and in the right hands, a treatment. The first step is making the measurement. The second is finding the clinician who understands what the number means.