

What do you see?
Dehiscent left jugular bulb
Absence of the sigmoid plate that normally separates the jugular bulb from the middle ear cavity with a resultant bulging of the jugular bulb into the middle ear cavity


Dehiscent left jugular bulb
Absence of the sigmoid plate that normally separates the jugular bulb from the middle ear cavity with a resultant bulging of the jugular bulb into the middle ear cavity

51-year-old female:
– Known with hypertension.
– Presents with hemiballism right.

What do you see?
Infarct? Other pathology?
– Unilateral hyperdense caudate nucleus, globus pallidus, and putamen
– Dx: Non-ketotic hyperglycemic hemichorea
– Key message: Basal Ganglia are a known site for metabolic- and toxic-related pathology, as is the diffuse cortical grey matter
– Key message: Usually bilateral changes in BG indicate toxic or metabolic pathology, but do not forget this in your differential diagnosis if you only see unilateral pathology!
– This woman was not known with diabetes, but the radiologist suggested it

94-year-old female:
– Lower consciousness. E1M3V2
– CT brain: Ischemia? Bleeding? Malignancy?

Complete hypodense right hemisphere with no grey-white matter differentiation possible indicative of ischemia. Large mass effect with subfalcine herniation (midline shift), uncal, and transtentorial herniation. Obliteration basal cisternsOld infarct left frontal and global cortical atrophy
Dx: Malignant medial artery infarction
Coincidental finding: Bilateral course calcifications in basal ganglia and dentate nuclei
Dx: M. Fahr: striato pallido dentate calcinosis


47-year-old male:
– Headache since 2 months, nausea, and vomiting.
– Papilledema but no loss of vision.
– MRI is made.

Expansive mass in the midline centered in the clivus (basiocciput and basisphenoid) with high signal on FLAIR (upper left), intermediate to low T1 signal, high T2 signal, and moderate heterogeneous enhancement after contrast administration.
No diffusion restriction.
ADC value is around 1350. No dural tail.
No encasement of basilar artery.
Compression on pons but no invasive growth.
Upward displacement of chaism, anterior displacement of pituitary gland and stalk.
Diagnosis: chordoma.
Does not fit with meningioma, pituitary macroadenoma, chondrosarcoma, lymphoma, or plasmacytoma.This
was histologically proven.


Left carotid sheath posterior to the carotid bulb, internal, and external carotid arteries.
Large oval avidly enhancing lesion displacing the carotid bifurcation anteriorly.
– Carotid bulb paraganglioma: avidly enhancing lesion with characteristic splaying of the internal and external carotid arteries (lyre sign).
– Glomus vagale: paragangliomas but of the vagus nerve, located posterior to the carotid arteries displacing them anteriorly.
– Vagal schwannoma: those that arises within the carotid sheath posteriorly but usually shows moderate enhancement compared with the avid enhancement of the paragangliomas.
Glomus vagale

47-year-old female:
– Found EMV 3 after assault
What do you see?



– Diagnosis: Diffuse subdural hematomas of multiple ages (convexities, parafalcine, tentorium)But more important:
– Diffuse swelling of gyri and edema with effacement of the CSF-containing spaces
– Diffuse loss of normal grey-white differentiation
– Decreased bilateral basal ganglia attenuation
– = Sequelae of traumatic brain injury (TBI) indicating hypoxic-ischemic injury, with poor prognostic outcome. Patient died several hours later
– Note: We do not see here the reversal sign (reversal of the normal CT attenuation of grey and white matter) or white cerebellum sign (diffuse oedema and hypoattenuation of the cerebral hemispheres with sparing of the cerebellum and brainstem, resulting in apparent high attenuation of the cerebellum and brainstem relative to the cerebral hemispheres)



Bilateral sacroiliac joint space narrowing, subchondral erosions, subchondral sclerosis, and subchondral fatty marrow infiltration.
Bilateral symmetrical:
Ankylosing spondylitis
Inflammatory bowel disease.Â
Bilateral asymmetrical:
Psoriasis
Reactive arthritis (Reiter syndrome)Â
Ankylosing spondylitis
Erosions with high signal intensity on STIR or T2- weighted images, subchondral edema, and enhancement within or adjacent to the sacroiliac joint.
Low signal intensity on T1- and T2- weighted images, subchondral sclerosis, narrowing of the joint spaces, bone bridging, and ankylosis.

60-year-old female:
– Since a few weeks eye movement disorder and diplopia of the left eye, tinnitus, and sinusitis.
– Non-enhanced CT of the orbits is performed (due to contrast allergy).

Widened infraorbital canal left eye with thickening of the infraorbital nerve.
Yes, we want MRI to sort things out more.
Findings: Smoothly thickened T2 hyperintense, enhancing infraorbital nerve in its canal. No continuation posteriorly to the vidian canal or anteriorly to the pre-antral region. No pathologic paranasal sinus mass or pharyngeal mucosal mass indicating perineural tumor spread.
Differential diagnosis:
Schwannoma.
Less likely malignant cause like perineural tumour spread.

Biopsy is performed of right lacrimal gland, since clinically this was found to be prominent (radiologically slight asymmetry, slightly higher T2 signal).
Histopathology: IgG4 disease or dacryoadenitis.
After this, whole body scanning showed evidence of IgG4 disease in the pancreas also. Patient was treated with steroids.
Follow-up MRI: Decrease in size of the infraorbital nerve from 11 to 5 mm. Still high T2 signal, however, the decrease in size on steroids suggests other diagnosis than schwannoma, in this case probably involved in orbital IgG4 disease. Rare!


61-year-old female:
– Trauma
– Fracture?What do you see?
Showing the supine AP and lateral view, due to the inability to stand on the right leg.

Diagnosis: Lipohemarthrosis (fat-blood level) indicating intra-articular #
Comminutive though non-displaced tibia plateau fractureAvulsion fracture proximal fibula (Segond fracture – 100% association with ACL injury)
CT: Schatzker type VI

– Schatzker I:Â wedge-shaped pure cleavage fracture of the lateral tibial plateau, having less than 4 mm of depression or displacement
– Schatzker II: splitting and depression of the lateral tibial plateau; namely, type I fracture with a depressed component
– Schatzker III:Â pure depression of the lateral tibial plateau;Â divided into two subtypes:
– Schatzker IIIa: with lateral depression
– Schatzker IIIb: with central depression
– Schatzker IV:Â Â medial tibial plateau fracture with a split or depressed component
– Schatzker V:Â wedge fracture of both lateral and medial tibial plateau
– Schatzker VI:Â transverse tibial metadiaphyseal fracture, along with any type of tibial plateau fracture (metaphyseal-diaphyseal discontinuity)

54-year-old woman:
– Known breast cancer
– Arm paresis and soft-tissue lump

Left: NECT, bone algorithm. Aggressive-like bone lesion with permeative pattern and hair on end periosteal reaction
Right: MRI T1 post-Gd. Associated trans-diploic soft-tissue mass with extracranial and intracranial-extraaxial components. Solid, homogeneous and avidly enhancing. Contiguous dural thickening and enhancement.
1- Metastasis
2 – Myeloma/Plasmocytoma
3 – Lymphoma
4 – Primary Bone Tumour (Osteosarcoma)
5 – Dural Lesion (Meningioma+++, Hemangiopericytoma)
– Always consider in older patients
– Multiplicity and known primary
Imaging
Varies depending on tumor type and aggressiveness
– Lytic: Most tumor types
– Permeative: Highly cellular and small-round cell tumors (PNET, small cell lung, lymphoma)
– Sclerotic/mixed: Prostate, breast. Less frequently: Transitional cell, neuroendocrine, PNET
– Hypervascular: Renal cell, melanoma, thyroid, hepatocarcinoma, lung, neuroendocrine
Possible soft-tissue components
LYTIC AGGRESSIVE BONE LESION/S IN PATIENT >40 years old. METASTASES vs MYELOMA




– Affects older patients (median 68-70 years). Very rare under 40 years (<10%)
Imaging
MM 4 patterns of bone involvement
– Diffuse lytic bone infiltration simulating osteopenia
– Multiple focal lytic well-defined lesions
– Solitary plasmacytoma
– Sclerotic bone lesions (exclusively associated with POEMS sd)
Solitary plasmacytoma in the skull: lytic, aggressive trans-diploic, soft tissues, and hypervascular aspect


– 7% of all bone malignancy; 5% of extranodal lymphoma
– All ages; predominates in adults (peak 50-60 years); men/women 1.5:1
– Secondary dissemination >>> primary bone lymphoma
– Imaging characteristics of a hypercellular small round cell tumour
Imaging
– Trans-diploic permeative bone pattern and abundant of tissue components (small round blue cells spread through Haversian canals conditioning a striking relatively little bone destruction in comparison to important soft-tissue lesions)
– Hyperdensity on NECT, T2 hypodensity and striking diffusion restriction on DWI (all signs related to hypercellularity)
– Homogenous enhancement
– No or little necrosis

– Most common primary high-grade bone sarcoma
– Bimodal distribution: 10-14 and >40 years old
– Extremely rare in the skull in adults, and much more frequently arising from coexisting Paget’s disease> >previously irradiated bone> or bone infarction
– Clinically, quickly growing painful mass
Imaging
– Destructive, aggressive lesion, with periosteal reaction, soft tissue-mixed lytic-blastic component. May show “fluffy”, “cloud-like” osteoid matrix.

– Most common brain tumor (36% of all brain tumors)
– Predilection for middle-aged females
– Can produce neurologic symptoms due to compression
– Most do not infiltrate bone, but when they do it, the hyperostosis is very specific, virtually pathognomonic
– Intra-diploic or trans-diploic meningiomas are less frequent
Imaging
Key signs:
– Calcifications
– “Dural tail” and extra-axial semiology
– Hyperostosis (very specific)
– Hypervascular with intense homogenous enhancement
*Even the great specificity of the hyperostosis, bone involvement can be VERY VARIABLE including aggressive-like lysis and periosteal reactions that do not exclude or go against the diagnostic
Ddx: Hemangiopericytoma (Solitary Fibrous Tumor New WHO 2016 classification). Younger, frequently male patients. Osteolysis possible, but NO hyperostosis. NO calcifications. The rest of imaging features identical to meningioma, differentiation is very difficult and challenging

EXAMPLES OF THE MULTIPLE FACES OF MENINGIOMAS AND THEIR BONE INVOLVEMENT. REMEMBER, POLYMORPHISM IS AN IMPORTANT FEATURE OF THIS ENTITY
With all the information mentioned above:
Meningiomas are very frequent, specially in middle-aged woman, if all or the vast majority of features favour this diagnosis, a relatively atypical bone affectation (lysis, periosteal reaction instead of the virtually pathognomonic hyperostosis) may not change the diagnostic orientation.
Diffusion: Striking restriction in lymphomas
Perfusion: Striking high rCBV in meningiomas
Spectroscopy: Alanine (and GLX) in meningiomas. Striking high Cho in lymphoma and plasmacytoma. Striking high lipids in metastases

Back to the case:

FINAL DIAGNOSIS: MENINGIOMA (WHO GRADE 2)
– Very frequent, specially middle-aged women
– Important to know the classic characteristic features, some of them are very specific; but recognize the great polymorphism/many faces of this entity
– Advanced imaging can be helpful
– Not all the lesions in a neoplastic patient are metastases