– Chronic sensory polyneuropathy (autoimmune). Long-term corticosteroid therapy.
– Forefoot pain for three weeks (acute onset without trauma).
– Physical examination: no haematoma , mild swelling.
– X-ray performed on day 2 after initial pain.
– MRI performed on day 25 after initial pain.
What are the findings?
X-Ray: No obvious fracture.
– Bone marrow heterogeneous oedema within the third metatarsal diaphysis (hypointense on T1W image, hyperintense on Proton Density (PD) FatSat image).
– Linear low signal intensity fracture identified in all sequences.
– Periosteal reaction due to callus formation. Periosteal thickening and enhancement (contrast administration is not necessary for diagnosis).
– Surrounding soft-tissue oedema (adjacent fat and interosseous muscles).
Metatarsal stress fracture (“march fracture”)
– Stress fractures are caused by overuse and repetitive activity.
– Everyday activities may result in a stress fracture if there is any disease or therapy that weakens the bone such as osteoporosis or long-term use of steroids (bone insufficiency: long-term treatment with steroids in this case).
– Classically affects the 2nd or 3rd metatarsal of the foot “march fracture”: named after its prevalence in soldiers who often undertake repeated and prolonged periods of walking as part of their training or work.
– Bone changes are usually not evident on X-rays before 10 to 21 days following the injury. May not be visible for several weeks later, until callus bone formation (the sensitivity range, for detecting stress fractures on initial examinations, is 15-35%; it increases to 30-70% at follow-up studies due to bone reaction).
– The fluid-sensitive sequences (T2-weighted images with chemically selective fat suppression or STIR sequences) are very useful for the detection of the earliest changes of stress reaction, such as periosteal reaction, muscle, or bone marrow oedema.
– T1-weighted sequences depict the anatomy and more advanced stress-related findings.
Grading based on MRI (Arendt and Griffiths)🙂
1: Mild – moderate periosteal oedema on STIR, no marrow changes.
2: Moderate – severe periosteal oedema on STIR + marrow changes on T2-weighted.
3: Grade 2+ marrow changes on T1-weighted.
4: Fracture line visible.
– Feels a lump in the upper lateral corner of right eye.
– MRI was made.
What do you see?
Preseptal lesion right supero-lateral corner, lateral to lacrimal gland.
T2 and T1 hyperintense, low signal after fat suppression.
No enhancement (right upper picture).
Slight remodeling of bone.
No invasive growth no post-septal component.
What is the most likely diagnosis?
Diagnosis: dermoid cyst, also fits with age and location of lesion.
Left carotid sheath posterior to the carotid bulb, internal, and external carotid arteries.
How does it look like?
Large oval avidly enhancing lesion displacing the carotid bifurcation anteriorly.
What is the differential diagnosis?
– 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.
– 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).
What are your findings?
Widened infraorbital canal left eye with thickening of the infraorbital nerve.
What is your differential diagnosis and do you want more imaging?
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.
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!
– Fracture?What do you see?
Showing the supine AP and lateral view, due to the inability to stand on the right leg.
Click here to see the answer
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 tibia plateau classification
– Schatzker I: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:pure depression of the lateral tibial plateau; divided into two subtypes:
– Schatzker IIIa: with lateral depression
– Schatzker IIIb: with central depression
– Schatzker IV:medial tibial plateau fracture with a split or depressed component
– Schatzker V: wedge fracture of both lateral and medial tibial plateau
– Schatzker VI:transverse tibial metadiaphyseal fracture, along with any type of tibial plateau fracture (metaphyseal-diaphyseal discontinuity)
– Known breast cancer
– Arm paresis and soft-tissue lump
What are the salient findings?
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.
What is the differential diagnosis?
DIFFERENTIAL DIAGNOSIS FOR TRANS-DIPLOIC SKULL VAULT LESION WITH AGGRESSIVE-LIKE BONE AFFECTATION
– Always consider in older patients
– Multiplicity and known primary
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
MULTIPLE MYELOMA (MM)/SOLITARY PLASMOCYTOMA
MULTIPLE MYELOMA (MM)/SOLITARY PLASMOCYTOMA
– Affects older patients (median 68-70 years). Very rare under 40 years (<10%)
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
– 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
– 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
*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:
Could meningiomas condition aggress periosteal reaction? Does it go against its diagnosis
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.
Bonus clues and some advance imaging pearls
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:
ARE THE ADVANCED IMAGING TECHNIQUES HELPFUL?
FINAL DIAGNOSIS: MENINGIOMA (WHO GRADE 2)
TAKE HOME MESSAGE REGARDING MENINGIOMA
– 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
– 66-year-old female:
– Feels a lump in the neck when swallowing
In what space houses this lesion?
Mass in the right parapharyngeal space or deep part of parotid space. No parapharyngeal fat is visible, so either the lesion displaces the fat or it arises from it. It is certainly not from the carotid space, since the carotid arteries are displaced posteriorly. It is also not from the mucosal space since it compresses the lateral oropharyngeal wall, instead of arising from it.
Do you want further imaging to make a diagnosis and what?
MRI will provide you more details in head and neck lesions where the lesion arises from exactly, and what the origin is. MRI is made with T1, T2, and T1 with Gad and fat suppression.
What is your differential diagnosis?
Origin from deep parotid lobe, so DD benign or malignant salivary gland tumor, such as pleiomorphic adenoma, adenoid cystic of mucoepidermoid cell carcinoma. Radiologists are not good in differentiating benign from malignant lesions on MRI. Histopathology has to be done. DWI will help you a little, in that, malignant lesions have often lower ADC values, but also Wharthin tumors do so. DD rare schwannoma arises from V3 (mandibular nerve) in the true parapharyngeal space.
We performed ultrasound and cytologic punction. This turned out to be a fairly rare acinic cell carcinoma.
Teaching point: Malignant tumors of the salivary glands are well delineated and do not have to present as ill-defined lesions, nor have to have lymph node metastasis or perineural spread.