Head and Neck #19

Clinical Data

80-year-old female:

  • With left-sided dyspraxia

  • Duration uncertain

What do you see?

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.

Chest and Thorax #3

Clinical Data

53-year-old male:

  • With chronic cough

1. Indicate the abnormalities:

2. Which of the following statements are correct?

  • 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:

      1. Nestor Luiz Müller, Tomás Franquet, Kyung Soo Lee (MD.) et al. Imaging of Pulmonary Infections. (2007) ISBN: 9780781772327 – Google Books

      2. Jannette Collins, Eric J. Stern. Chest Radiology. (2008) ISBN: 9780781763141 – Google Books

      3. David P. Naidich, Nestor L. Müller, W. Richard Webb. Computed Tomography and Magnetic Resonance of the Thorax. (2007) ISBN: 9780781757652 – Google Books

      4. Kazerooni EA, Gross BH. The Core Curriculum: Cardiopulmonary Imaging. (2003) ISBN: 9780781736558 – Google Books

      5. Thomas W. Shields, Ronald B. Ponn. General Thoracic Surgery. (2005) ISBN: 9780781738897 – Google Books

      6. 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

Neuroradiology #40

Clinical Data

19-year-old female presents to the neuro-emergency department with:

  • Right-sided hypesthesias and sensorimotor aphasia

  • Subacute onset: the symptoms did not develop extremely quickly as we would expect in a stroke

  • Unremarkable past medical history (mild gastroesophageal reflux)

  • Non-contrast CT was ordered


Describe the findings:
  • An ill-defined hypodense lesion primarily located in the deep white matter of the left parietal lobe.

MRI was performed:



FLAIR / T1 FFE / DWI / ADC / T2 / T1 FFE post-contrast AX / SAG / COR
(T1 FFE: a volumetric gradient echo T1-weighted sequence).

MRI was performed (superior slices):



FLAIR / T1 FFE / DWI / ADC / T2 / T1 FFE post-contrast AX / SAG / COR
(T1 FFE: a volumetric gradient echo T1-weighted sequence).
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.

Imagen axial T2-weighted: [Describir hallazgos, ej. 'lesión hiperintensa en región X']
T2WI Axial
Imagen axial T1-weighted post-contraste: [Describir realce o anatomía relevante]
T1WI 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?
  • Glioblastoma: complete ring, irregular enhancement.

  • 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.

Reference:

Musculoskeletal #42

Clinical Data

55-year-old female:

  • With trauma

  • Painful elbow after a fall from height

  • Supination and pronation painful



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.

Head and Neck #18

Clinical Data

73-year-old male:

  • With worsening paresis of cranial nerves CN3-7







What do you see?


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.

Chest and Thorax #2

69-year-old male patient with:

  • Dysphagia
  • Chronic food regurgitation
  • Barium swallow (oesophagogram) was performed
Lateral projection, early
Lateral projection, early
AP projection
AP projection
Lateral projection, late
Lateral projection, late
What do you see?

Findings:

Retroesophageal outpouching located along the midline at the C5-C7 level, with barium retention.

What is the most likely diagnosis?

Zenker diverticulum

Neuroradiology #39

Clinical Data

40-year-old female presents with:
  • Fever

  • Progressive headache

  • Confusion in the last two days

  • Previous medical history was unremarkable

  • CT brain without contrast was performed in the emergency department

CT images:

Unenhanced CT
Unenhanced CT
What are the most important findings on CT?
  • Subtle hypodensity in the medial temporal lobe on the right side.

  • Sparing of the basal nuclei on the right side.

What are your next steps?
  • Immediately call the ordering physician to communicate that the imaging (and clinical) findings are suggestive of Herpes Simplex Encephalitis.

    • This will prompt the clinician to directly start with an antiretroviral agent (acyclovir) if not started already and to perform a lumbar puncture to confirm HSV in CSF.

MRI was performed:

T2
Coronal T2 FLAIR
T1 + C
What are the findings on MRI?
  • T2 hyperintense regions with swelling/oedema and involvement of both white matter and cortex centered around the right sylvian fissure with involvement of the right temporal, frontal and insular region. Subtle patchy and leptomeningeal enhancement in the right temporal lobe can be seen.

What is the most likely diagnosis?

Herpes Simplex Encephalitis

  • The clinical picture is already highly suggestive of this diagnosis with supporting imaging findings. The diagnosis was confirmed with positive PCR for HSV-1 in CSF.

  • Typical imaging findings of herpes encephalitis are T2(/FLAIR) hyperintense swollen areas of cortex and white matter with bilateral but asymmetrical involvement of the fronto-temporo-insular regions. Characteristic is sparing of the lentiform nuclei, which distinguishes it from ischemia due to vessel occlusion. Diffusion restriction and hemorrhage can be present.

  • This is a radiological emergency and the phone must be picked up directly to alert the clinician and to prevent significant mortality and morbidity.

Reference:

Neuroradiology #38

Clinical Data

35-year-old male presents with:
  • Progressive headache and ataxia
  • Previous medical history was unremarkable
  • MRI brain was performed
T1 + C
T1 + C
T1 C+
T1 C+
T2
T2
T2
T2
T2 FLAIR
T2 FLAIR
What do you see?
  • Cystic lesion with an enhancing lesion in the posterior fossa on the left side. No enhancement of the cystic wall. Discrete flow voids in the solid nodule.
  • Relevant mass effect with compression on the 4th ventricle and obstructing supratentorial hydrocephalus.
What is your differential diagnosis?
  • The differential diagnosis of a cyst with an enhancing mural nodule in the posterior fossa includes hemangioblastoma, pilocytic astrocytoma, ganglioglioma and cystic metastasis.
What are the most likely diagnoses?
  • When a cystic lesion with a mural nodule is encountered in the posterior fossa, the most likely diagnosis is hemangioblastoma in an adult in the absence of a primary tumor elsewhere. The imaging findings support hemangioblastoma, since the mural nodule shows flow voids on T2 and no enhancing cystic wall. Typically, the cystic wall of hemangioblastoma does not enhance, while a subtle enhancing wall can be discerned in pilocytic astrocytomas.
  • The majority of hemangioblastomas occur spontaneously. In case of multiple hemangioblastomas, think about Von Hippel-Lindau syndrome.
  • Reference:

  • Raz et al. Cyst with a mural nodule tumor of the brain. Cancer Imaging. 2012 Aug 10;12(1):237–244. doi: 10.1102/1470-7330.2012.0028

Chest and Thorax #1

56-year-old male patient:
After kidney transplantion presented with cough

Findings:

Multiple intrapulmonary consolidations with peripheral ground-glass opacities . No bronchial obstruction. No pathologically enlarged lymph nodes

What is the most likely diagnosis?

Fungal infection (Rhizopus infection)

Fungal infections in immunocompromised patients may manifest as intrapulmonary nodules or consolidations with peripheral ground glass opacities. May lead to cavitation, pseudoaneurysm formation and bleeding.

Treatment in this case: Anti-fungal systemic therapy

Patient died 5 months thereafter from pulmonary artery aneurysmal bleeding.

Urogenital #3

87-year-old woman:
* Presented with lower abdominal discomfort and weight loss.
* Pelvic MRI is performed.


What can be seen in the uterine cavity?

Blood, hematometra

In this case what is the cause?

Cervical cancer

What are some congenital causes of hematometra?

Imperforate hymen, vaginal septum, vaginal hypoplasia

Explanation:

In non-adolescent women, hematometra can often be caused by malignancy, so a search for cervical/endometrial cancer must be done.