Previously had multiple surgeries in the abdomen (cholecystectomy, splenectomy after trauma, aorto-femoral bypass because of left AIC stent occlusion)
The emergency team did not have the impression that the cause might be bowel obstruction
Abdominal X-ray at that time was reported as normal
An ultrasound of the abdomen was requested
Abdominal ultrasound showed multiple distended and fluid-filled small bowel loops with To-and-Fro peristalsis, colon was not distended – indicating small bowel obstruction
One of the most distended bowel loops had slower peristalsis. The lumen was also filled with more particulate matter, demonstrating the ultrasound analog of the small bowel feces sign. The sign is more commonly seen on CT scans
The small bowel feces sign is helpful in finding the point of obstruction. An abrupt change in caliber was noted in the vicinity, in the left lower quadrant
The diagnosis of small bowel obstruction (presumably because of post-operative adhesions) with at least one point of obstruction in the left lower quadrant was made
A CT scan was arranged for better anatomical delineation and to assess for complications
The CT scan confirmed the small bowel obstruction. Small bowel feces sign is demonstrated in the left lower quadrant
The CT confirmed the point of obstruction, seen on ultrasound. However, another part of the small bowel in the vicinity was also slightly narrowed
The mesenterium of the loop of bowel between these two points was edematous
What is the final diagnosis?
Come back next week to see the answer. In the meantime, check our social networks to leave your guesses!
Well-defined cystic lesion in subcutaneous plane of lateral margins of orbit on left
Underlying bone and adjacent lacrimal gland are unremarkable
Differential diagnosis includes:
Orbital dermoid cyst
Orbital teratoma
Orbital dermolipoma
Orbital hemangioma
Orbital rhabdomyosarcoma
Differential diagnosis includes:
Description:
Possible differential considerations include:
Orbital dermoid cyst – TRUE
Orbital teratoma – TRUE
Orbital dermolipoma – TRUE
Orbital hemangioma – TRUE
Orbital rhabdomyosarcoma – FALSE
Dermoid cysts
They are thought to occur as a developmental anomaly in which embryonic ectoderm and mesoderm are trapped in the closing neural tube between the 5th and 6th weeks of gestation
These lesions are usually extraconal, non-enhancing masses with smooth margins, cystic, and/or solid components
They are typically heterogeneous with soft tissue, fluid, and fatty (sebum) components; occasionally calcifications may be present
They are most commonly located superotemporally, arising from the zygomaticofrontal suture, followed by superonasally, arising from the frontoethmoidal or frontolacrimal sutures
Ruptured dermoids may show adjacent inflammatory changes
Superficial lesions barely require cosmetic excision, while a deeper lesions may require more invasive methods involving micro-dissection and orbitotomy
References:
Kudo K, Tsutsumi S, Suga Y et al. Orbital dermoid cyst with intratumoral inflammatory hemorrhage: case report. Neurol. Med. Chir. (Tokyo). 2008;48 (8): 359-62. Pubmed citation
Ahmed RA, Eltanamly RM. Orbital epidermoid cysts: a diagnosis to consider. J Ophthalmol. 08;2014: 508425. doi:10.1155/2014/508425 – Free text at pubmed – Pubmed citation
Chaudhry IA. Management of deep orbital dermoid cysts. Middle East Afr J Ophthalmol. 2008;15 (1): 43-5. doi:10.4103/0974-9233.53376 – Free text at pubmed – Pubmed citation
Acute onset left hemiplegia (Time of last known well two hours ago)
Code stroke activated
Imaging in our institution constituted of:
Non-contrast head CT
CTA of aortocervical and intracranial vessels
CT perfusion
Non-contrast head CT:
CT perfusion revealed a large ischemic core compared with the penumbra (approximately 2:1)
TTP rCBF
rCBV
Based on the CTA and non-contrast head CT, which arteries were occluded?
The CTP shows perfusion changes in the vascular territories of both the right MCA and ACA.
We know that the MCA is also most certainly occluded because of the dense MCA sign.
Based on this, there is either a simultaneous occlusion of both the MCA and the ACA or the occlusion is even more proximal – ICA.
CTA shows occlusion of the M1 segment of the right MCA, and the terminal segment of the ICA is patent
However, more proximal intracranial segments of the right ICA were not opacified with contrast
The cervical ICA segments were also not opacified with contrast.(ECA and vertebral artery on the right, no ICA)
Modified sagittal reformation of the bifurcation
Right (Almost) Normal left for comparison
Given the CTA appearance of the right ICA, which of the following are the reasonable differentials?
Occlusion of the right carotid bulb with near total distal ICA occlusion
ICA dissection
ICA pseudo-occlusion
Solution:
Occlusion of the right carotid bulb with near total distal ICA occlusion – FALSE
ICA dissection – TRUE
ICA pseudo-occlusion – TRUE
Explanation:
The carotid bulb is patent and contrast opacification stops 1 to 2 centimeters after the bulb. If the bulb would be really occluded, contrast opacification would stop (almost) at the level of the bulb and the atherosclerotic changes of the bulb would be more extensive.
The sagittal images nicely show the gradual tapering of contrast opacification in the proximal cervical ICA, which is known as the flame sign.
The flame sign can be seen in carotid artery dissections and pseudo-occlusions.
How would you differentiate a pseudo-occlusion from a real dissection or ICA occlusion, while the patient is still lying in the CT scanner?
Obtain a delayed CTA scan of the arteries.
In other words, repeat the CTA scan at a later time point. Preferably tell the technician at the moment you see the flame sign on the console to just fire the CTA scan again (additional contrast application is not needed).
(In our case, the clinical context might also have helped. Spontaneous carotid artery dissections are the leading cause of stroke in younger/middle-aged patients. Our patient was almost 100 years old, which made dissection not the most probable diagnosis.)
Normal vs delayed CTA: the unopacified parts of the ACI are now opacified:
A slightly confusing term, as the carotid artery is still occluded, just not in the extent you might think!
Carotid artery pseudo-occlusion is seen, when there is an occlusion of a distal segment (usually one of the intracranial ones) of the ICA. This occlusion makes it harder for the contrast bolus to flow through the normal ICA – as the cervical ICA segment has no branches. So, using normal timings for the CTA bolus, the cervical segment might still be unopacifed, compared with the normal side. If we wait a little bit and obtain a delayed scan, we give the ICA time to fill up and can assess the extent of the occlusion more accurately. This can be achieved with a delayed CTA scan and is also easily identified with DSA (today mostly performed as the first part of mechanical thrombectomy).
The cavernous segment was unopacified in both the normal and delayed CTA – representing the true level of the occlusion
Normal (early) CTAICA not seen
Delayed CTA
What are the final diagnoses?
Right MCA and right cavernous segment ICA occlusion with resultant ischemic stroke
Pseudo-occlusion of the proximal (mostly cervical) parts of the ICA
Chronic onset of symptoms that appeared approximately three years ago and got worse in the preceding weeks
T2-weighted axial image:
The MRI sequences demonstrated no signs of acute or chronic ischaemic lesions, also no mass lesions were detected.
The signal of the white and grey matter was also otherwise normal.
Supratentorially, no abnormalities were detected.
T2-weighted axial image:
Infratentorially, however, the brainstem appeared compressed anteriorly by the dens.
An additional sagittal T2-weighted image was obtained to clarify the anatomy and the cause of obstruction.
The sagittal slices demonstrated several congenital abnormalities.
Which of the congenital abnormalities contributes the most to the patient’s symptoms?
Which of the congenital abnormalities contributes the most to the patient’s symptoms?
Basilar invagination (in combination with mild retroflexion of the dens).
The high riding dens causes compression of the brainstem at the pontomedullary junction.
What other congenital anomaly is basilar invagination commonly associated with?
Platybasia
Definition of terminology:
Congenital basilar invagination and platybasia are often seen together.
Basilar invagination:
A congenital or acquired condition, where the dens protrudes more cranially than it should be, typically above the foramen magnum.
If the dens causes compression of the brainstem, symptoms might ensue.
Platybasia:
A congenital or acquired condition, denoting abnormal flattening of the skull base, formally described as an increased base of skull angle. A simple way to think about it is also a shape of the base of the skull, where the clivus lies more horizontally than it should be (the clivus normally has a downward sloping shape, as clivus is a latin word for slope/hill).
Translated directly from Greek, platybasia means “flat base” (of skull). And platypus means “flat foot”, just in the case you are wondering.
Platybasia does not cause symptoms on its own.
The sagittal slices demonstrated several congenital abnormalities:
In addition to basilar impression, platybasia and dens retroflexion, several other anomalies were seen or suspected on the sagittal slices.
The most obvious additional anomaly was a hypoplastic clivus/basioccipital hypoplasia.
What seemed to be the tip of the clivus also seemed oddly very sclerotic.
A CT of the cervical spine and base of skull was recommended to further evaluate the relationship of the bones:
Basilar impression, platybasia and clivus hypoplasia were redemonstrated.
CT also showed an additional ossicle/unfused bone immediately superior to the tip of the dens/posterior to the clivus – in the same place as the structure, that appeared to be the sclerotic tip of the dens.
Sagittal and axial reformats:
The reformats demonstrated a bony arch, which were isolated from the rest of the occipital bone, representing the very rare variant called prebasioccipital arch.
Sagittal and axial reformats, what would we expect in a normal examination from a different patient?
We are still not finished (Part 1):
Hypoplasia of the occipital condyles, which appear flattened. They are commonly observed together with the aforementioned anomalies.
Oblique sagittal reformats right and left occipital condyle.
Condylar hypoplasia, oblique coronal reformat.
Oblique right sagittal and coronal reformats, what we would expect (normal examination from a different patient)?
The normal occipital condyles are convex.
We are still not finished (Part 2):
Additionally, the angle of the foramen magnum and the plane of the atlas were tilted cranially and posteriorly, resulting in a so-called “lordotic angulation”. The atlas was also noted to be hypoplastic.
Sagittal reformat, what we would expect (normal examination from a different patient)?
Wait a minute! The dens doesn’t actually protrude through the foramen magnum, as the foramen itself is tilted. So…
Are we still dealing with a case of basilar invagination?
Yes, we are.
Although the usual definition of basilar invagination says that the dens should protrude through the foramen magnum, the condition might be defined by several craniometric lineas and measurements. They also take into account conditions, where the foramen magnum itself is abnormally positioned, as in our case.
On sagittal images, they include the McRae, McGregor and Chamberlain lines. On coronal images, the digastric and bimastoid line.
In our case, we used the Chamberlain line. It is a line connecting the posterior edge of the bony hard palate to the opisthion (the midline point of the posterior edge of the foramen magnum). If the tip of the dens lies more than 3 mm above this line, we are dealing with basilar invagination.
Chamberlain line; our case and a normal CT of the cervical spine. Basilar invagination is defined, if the tip of the dens lies more than 3 mm above this line (the measurement in our case was 22 mm).
Platybasia measurements
Platybasia is also defined by a craniometric measurement, namely by an abnormally high base of skull angle (>143°).
On CT and MRI, it is defined as angle between the line drawn from the bottom of the anterior cranial fossa (or the nasion) and the tuberculum sellae, and the line drawn from the tuberculum sellae down the posterior margin of the clivus.
Base of skull angle, our case and a normal CT of the cervical spine.
An angle measuring more than 143° defines platybasia. The measurements of the angle were 146° and 67°, respectively.
Conclusion:
When confronted with a congenital anomaly, always be on the lookout, as they are often not isolated.
In the region of the craniocervical junction, congenital basilar invagination and platybasia often occur together.
It is important though to try to put emphasis on the most clinically relevant anomalies. In our case, among the many findings, basilar invagination was the most important one, causing symptoms by exerting pressure on infratentorial structures. Severe cases of basilar invagination can be treated by neurosurgical operative decompression.
Congenital anomalies of the craniocervical junction represent a complex topic. When confronted with difficult or ambiguous cases, looking up and reviewing many craniometric lines and measurements might be helpful.
The case was initially interpreted as CSF seeding by a malignant choroid plexus tumor.
However, retrospective investigation of CTA showed another pathology.
This case demonstrates several small areas of cortical enhancement in the right hemisphere. These enhancing areas correspond to small regions of subacute cortical ischemia in the right MCA territory, caused by a ruptured carotid plaque with an intraluminal thrombus. The mass in the antrum of the left ventricle is an incidental intraventricular meningioma. Follow-up scans showed regression of the cortical enhancement and stable intraventricular meningioma on the left.
Teaching points:
Subacute ischemia may enhance and in some cases mimic tumors or CSF seeding.
Ruptured carotid plaque with intraluminal thrombus presents with finger-like filling defect of the internal carotid.
Choroid plexus carcinomas are rare in elderly patients with an intraventricular meningioma being way more common. Typical location, sharp tumor-brain interface, homogeneous enhancement and T2 hypointensity allow for a confident diagnosis of an intraventricular meningioma.
Post-primary pulmonary tuberculosis/ reactivation tuberculosis or secondary tuberculosis is the most likely diagnosis
Primary TB within the lungs develops in either posterior segments of the upper lobes or superior segments of the lower lobes
The development of an air-fluid level implies communication with the airway
A (tree-in-bud sign) denoting endobronchial spread along nearby airways
Cavitation is uncommon in post-primary TB
Indicate the abnormalities:
A cavitary lesion is seen at the superior segments of the right lower lobe surrounded by patchy consolidation and smaller cavitating nodules as well as tiny nodular opacities with tree-in-bud pattern.
Differential diagnosis includes:
Post-primary pulmonary tuberculosis/ reactivation tuberculosis or secondary tuberculosis is the most likely diagnosis
Primary TB within the lungs develops in either posterior segments of the upper lobes or superior segments of the lower lobes
The development of an air-fluid level implies communication with the airway
A (tree-in-bud sign) denoting endobronchial spread along nearby airways
Cavitation is uncommon in post-primary TB
Solution:
Post-primary pulmonary tuberculosis/ reactivation tuberculosis or secondary tuberculosis is the most likely diagnosis – TRUE
Primary TB within the lungs develops in either posterior segments of the upper lobes or superior segments of the lower lobes – FALSE
The development of an air-fluid level implies communication with the airway – TRUE
A (tree-in-bud sign) denoting endobronchial spread along nearby airways – TRUE
Cavitation is uncommon in post-primary TB – FALSE
Explanation:
Primary pulmonary tuberculosis
The initial focus of infection can be located anywhere within the lung. It has non-specific appearances of consolidation or even lobar consolidation
Cavitation is uncommon in primary TB
The more striking finding, especially in children, is that of ipsilateral hilar and contiguous mediastinal (paratracheal) lymphadenopathy, usually right-sided
Post-primary pulmonary tuberculosis
Post-primary pulmonary tuberculosis, known as reactivation tuberculosis or secondary tuberculosis, occurs within the lungs and develops in either posterior segments of the upper lobes or superior segments of the lower lobes
Post-primary infections are far more likely to cavitate. The development of an air-fluid level implies communication with the airway. Endobronchial spread along nearby airways is a relatively common finding, resulting in tree-in-bud sign
References:
Nestor Luiz Müller, Tomás Franquet, Kyung Soo Lee (MD.) et al. Imaging of Pulmonary Infections. (2007) ISBN: 9780781772327 – Google Books
Jannette Collins, Eric J. Stern. Chest Radiology. (2008) ISBN: 9780781763141 – Google Books
David P. Naidich, Nestor L. Müller, W. Richard Webb. Computed Tomography and Magnetic Resonance of the Thorax. (2007) ISBN: 9780781757652 – Google Books
Kazerooni EA, Gross BH. The Core Curriculum: Cardiopulmonary Imaging. (2003) ISBN: 9780781736558 – Google Books
Thomas W. Shields, Ronald B. Ponn. General Thoracic Surgery. (2005) ISBN: 9780781738897 – Google Books
Jeong Y & Lee K. Pulmonary Tuberculosis: Up-To-Date Imaging and Management. AJR Am J Roentgenol. 2008;191(3):834-44. doi:10.2214/AJR.07.3896 – Pubmed
What are the top 3 differential diagnoses for lesions involving the corpus callosum?
Glioblastoma (formerly known as glioblastoma multiforme/GBM).
Primary CNS lymphoma.
Demyelinating disorders (multiple sclerosis…).
Did the MRI help in narrowing your differential?
A T2/FLAIR hyperintense lesion with enhancement was seen in the mentioned location and it was reported as representing either lymphoma or GBM in the conclusion of the MRI by the neuroradiologist.
T2WI AxialT1WI Post-Contrast
Does the lesion have a complete or incomplete rim of enhancement?
The lesion has an incomplete rim of enhancement.
What type of enhancement would you expect in the top 3 differential diagnoses?
Primary CNS lymphoma: homogeneous enhancement. (In immunocompetent patients)
Demyelinating disease: incomplete ring enhancement.
A small digression:
A well-known mnemonic for remembering ring-enhancing CNS lesions is…
MAGICAL DR
M = Metastasis
A = Abscess
G = Glioblastoma (or other high-grade gliomas)
I = Infarct (subacute phase may show enhancement)/Infections (others – non-pyogenic pathogens: Mycobacteria, Toxoplasmosis, Cysticercosis, Cryptococcus)
C = Contusion and resolving hematomas
A = AIDS related: again, non-pyogenic infections (Cysticercosis, Cryptococcus)
L = Lymphoma
D = Demyelinating disease
R = Radiation necrosis
Can demyelinating disease simulate CNS tumors?
These lesions can closely resemble CNS tumors, and in such cases, they are referred to as tumefactive demyelinating lesions.
Back to our case:
Another odd thing was overlooked.
Do you notice it on the T2-weighted image?
Does it additionally help narrowing the differential?
We see concentric rings at the periphery of the lesion.
Alternating hyper- and hypo-intense bands. Resembling the layers of an onion bulb.
Meanwhile:
The patient was admitted to neurosurgery.
Thinking it was a tumor, the neurosurgeons resected most of the lesion.
The histological diagnosis was not consistent with GBM or lymphoma. It mentioned a focus of leukoencephalitis with fiber destruction.
While ad definitive diagnosis was not provided by the pathologists: it was presumed, however, that the lesion represented “some sort of demyelinating disease or MS”.
The bands were seen on multiple MRIs
2 weeks after the initial MRI, before surgery (performed as part of pre-op MR tractography).
T1 GRE sag and ax, without contrast.
After surgery (2 days after the previous MRI).
T2WI sag and ax.
1 year after the first presentation, after surgery.
T2WI ax and FLAIR cube sag.
The bands are quite obvious on all MRI examinations.
The alternating bands are characteristic of what disease?
The “onion bulb” or “bullseye” appearance is characteristic of Baló concentric sclerosis.
This is a case of Baló concentric sclerosis, a rare demyelinating disease, often considered a variant of multiple sclerosis (MS).
Unlike conventional MS, the clinical course of Baló’s sclerosis is typically monophasic, with more severe symptoms during a single episode of demyelination. Our patient has not developed additional focal neurological deficits or new lesions outside of the previously operated area.
The hallmark MRI findings are the “onion bulb” or “bullseye” appearance, most clearly seen on pre-contrast T1- and T2-weighted images. Similar to other demyelinating disease, contrast enhancement usually appears as an incomplete open ring. DWI might show diffusion restriction during the episode of active demyelination (representing in most part intramyelinic edema).
This case serves as a reminder thta, when faced with a complex diagnosis, it‘s important to pause,reflext and ask key questions.
Asking the right questions at the right time might help you to narrow the list of your differential diagnoses and rule out other possibilities.
In our case, if the possibility of tumefactive demyelination had been considered based on the pre-operative imaging, the extensive surgery could have been avoided.
The three most common tumor or tumor-like lesions of the corpus callosum are glioblastoma, primary CNS lymphoma and demyelinating disorders. Corpus callosum is composed of dense white matter tracts, that make it hard for hematogenous metastases to deposit in that area, so they are rarely seen in this region and not on the top of your differentials. The abundance of white matter tracts probably explains, however, why predominantly white matter diseases affect this region – namely glioblastoma and demyelinating diseases. CNS lymphoma has a predilection for periventricular regions, corpus callosum being one of those regions.
Enhancement can help in differentiating the three entities, with classically glioblastoma having irregular ring enhancement or heterogeneous enhancement, lymphoma having homogenous enhancement and demyelinating diseases having the open ring enhancement.
Knowing the epidemiology can also be helpful. Glioblastoma and CNS lymphoma are seen in slightly older/older patients (>40 years), with a slight male predominance. Tumefactive demyelinating lesions have, similar to other demyelinating disorders, a younger age of onset (<40 years) with a female predominance. Our patient was a female in her late teens.
What’s the radiological sign visible on the radiograph?
Capitellum fracture
The case represents a classic capitellum fracture, with a mildly displaced fragment on the lateral projection, which can easily be missed if one is not familiar with the double-arc sign.
Axial T2 image on the left shows partial obliteration of the right Meckel’s cave and an ill-defined T2 hypointense lesion on the right temporal fossa.
Axial T2 image on the right shows atrophy of the right-sided masticatory muscles.
Post-contrast 3D T1 FSE fat-saturated images showing an enhancing lesion overlying the right temporal fossa, with perineural spread along CN7, the auriculotemporal nerve and continuing intracranially via the right foramen ovale (note the asymmetry in enhancement).
3D bSSFP images (CISS) before (left) and after (right) contrast administration. bSSFP images contain both T1 and T2 information, therefore showing enhancement after contrast administration.
While pre-contrast image doesn’t depict any obvious pathology, the post-contrast image on the right clearly highlights tumor deposits (red arrows) along the lateral aspect of the right cavernous sinus. The tumor has encased the cranial nerves, leading to the patient’s symptoms. For comparison, the normal anatomy of the cranial nerves is shown on the left (green arrows).
This case shows a histologically verified squamous cell carcinoma of the temporal fossa spreading along the CN7, auriculotemporal nerve, mandibular nerve and into the right cavernous sinus.
Teaching points:
Multiple CN palsies of CN3-6 should raise a suspicion of cavernous sinus pathology.
Auriculotemporal nerve is an important connection between the facial and mandibular nerves.
bSSFP sequences like CISS contain both T1 and T2 information and therefore show post-contrast enhancement which can be diagnostically useful in conjunction to their excellent spatial resolution.
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