How to read imaging of the orbits: a pathology based approach

In this video, Dr. Katie Bailey describes her approach to imaging of the orbit with a focus on common diseases that can affect the orbits. We’ll save neoplasms for another video and focus on other pathologies here.

Review of the anatomy of the orbits. The orbits are surrounded by orbital walls and contain the globes, extraocular muscles, nerves including the optic nerve, a variety of vessels and nerves, and the lacrimal gland.

The globes. Common pathologies involving the globes include ocular lens surgery/removal, retinal detachment and vitreous hemorrhage, and phthisis bulbi (a chronically shrunken and deformed injured globe). MRI is even better at seeing these pathologies and can see tumors within the globe, such as ocular melanoma.

The orbital walls. The most common pathology of the orbital walls are fractures, commonly of the medial or inferior orbital wall. Other common pathologies include invasion of sinusitis into the orbit or carcinoma invading the orbit.

Extraocular muscles. Thyroid orbitopathy often causes symmetric enlargement of the extraocular muscles. IgG related disease and lymphoma can also infiltrate the extraocular muscles. Of these, lymphoma and metastatic disease tend to be more masslike and well defined.

Optic nerve, disc, and sheath. The most common pathology is optic neuritis, which affects the nerve itself. This is common in demyelinating disease. Perineuritis is when the enhancement/inflammation is around the nerve and has a different differential diagnosis. Idiopathic intracranial hypertension (IIH) can cause distended and tortuous optic nerve sheaths as well as elevation of the optic disc (papilledema).

Vessels. The ophthalmic artery is the most visible vein and often can have aneurysms. The superior ophthalmic vein is the largest vessel, and can have varices or thrombosis (often in the setting of infection).

Retroorbital fat. The fat is important because it can be a sign that other structures are abnormal. This is most commonly abnormal in orbital cellulitis, but can also be abnormal if there is a hematoma or orbital inflammatory disease.

Thanks for checking out this quick video on orbital imaging and common non-neoplastic pathology. Be sure to check out the additional videos on other head and neck topics.

 

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5 ways to improve your brain aneurysm search pattern

In this video, I walk you through 5 quick tips that you might use to improve your brain aneurysm search pattern on CT angiograms of the brain. This is a longer version of a lecture I put together with Everlight Radiology, so be sure to check them out.

Have a standard search pattern. When I’m looking at a CTA of the head, I do the anterior circulation first and then move from right to left, then over to the posterior circulation.

Know the common aneurysm locations. The most common aneurysm location is the anterior communicating artery (35%) followed by the carotid terminus (30%) and middle cerebral artery (20%). Posterior circulation aneurysms are relatively uncommon (10%) but it’s important to look there as well. Try to use these tips on the sample case.

Use reformats and 3-D imaging. These supplemental tools can help you improve your sensitivity. Multiplanar reformats are thin slices that are displayed in the other planes, while maximum intensity projections (or MIPs) show you the brightest pixel in a thicker slice. Volume renderings are a nice way to make measurements and increase your sensitivity.

Using the MIPs can definitely make you more sensitive. The axial MIPS are great to see the MCAs, the sagittal MIPs are great to see the carotid terminus and ACAs, and the coronal MIPs are great to see the posterior circulation and MCAs again.

Follow the blood. This is my favorite tip. The location of the blood on the non-contrast CT is one of the best clues about where your aneurysm is going to be. You need to check that area very closely.

 

 

 

Recognize the mimics. There are some things which can mimic aneurysmal subarachnoid hemorrhage, but some features may help you know that it is less likely to be from an aneurysm. Atypical location, an unusual history, or unusual patient demographics can clue you in that it might be a different cause. Be sure to think about hypertensive hemorrhage, venous infarct, tumor (glioma, metastasis, or cavernous malformation), and benign perimesencephalic hemorrhage.

Summary. These 5 quick tips can help you be better at understanding aneurysms and being better and finding them.

If you haven’t already, be sure to check out the vascular imaging course and sample cases that you can scroll through.

See all of the search pattern videos on the Search Pattern Playlist.

Laryngeal Cancer Staging in 5 minutes

In this video, Dr. Katie Bailey walks us through cancers of the larynx and quickly describes how they are staged. This quick video will help you identify common laryngeal cancers and how to stage them.

Review of the anatomy of the larynx. The larynx consists of structures from the inferior aspect of the epiglottis down to the inferior part of the cricoid cartilage. There are three subsites, the supraglottis (between the epiglottis and the false cords), the glottis (the true vocal cords, anterior commissure, and posterior commissure), and subglottis (from the inferior vocal cords to the inferior cricoid cartilage). Key landmarks include the aryepiglottic folds, the pyriform sinus, the false cords, the true cords, the arytenoid cartilage, and the cricoid cartilage.

Laryngeal cancer staging is based on a T, N, M stage. Supraglottic cancers and glottic cancers are staged separately. For supraglottic cancers, it is important to know if the vocal cord is mobile or fixed, which can only be determined on exam. T4B tumors are unresectable because they involve adjacent structures such as the prevertebral space or carotid artery. Glottic cancers are staged based on their involvement of adjacent structures. Similarly unresectable tumors involve deep adjacent structures.

Example case 1. This case has thickening and nodularity of the right aryepiglottic fold. This is confined to the aryepiglottic fold with no involvement of adjacent structures. There are no nodes, making this a T1N0 tumor.

Example case 2. There is a subtle tumor along the anterior aspect of the right vocal cord with asymmetric hyperdensity. This is a glottic lesion involving only the right vocal cord with no nodes, consistent with a T1N0 glottic tumor.

Example case 3. This is a more dramatic mass involving the right vocal cord with erosion of the cricoid cartilage posteriorly and loss of paraglottic fat. There is supraglottic and glottic extension. This is a T3N0 lesion.

Example case 4. To see this lesion, you have to window the images pretty severely. There is hyperdensity involving the anterior commissure and both anterior vocal cords. The involvement of both vocal cords makes this a T1bN0 lesion.

Example case 5. This bulky mass extends across the anterior commissure and extends through both sides of the thyroid cartilage. Destruction of the cartilage makes this a T4a lesion. Left level 3 lymph node is abnormal, making this an N1 nodal stage.

Conclusion. Hopefully you learned from these examples of supraglottic and glottic tumors and can use some of your skills on your future cases.

Thanks for checking out this quick video on nasopharyngeal cancer staging. Be sure to tune back in for additional videos on staging of the other head and neck subsites.Also take a look at the head and neck topic page as well as all the head and neck videos on the site.

 

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Nasopharyngeal cancer staging – 5 minute review

In this video, Dr. Katie Bailey takes us quickly through the nasopharynx, a common location of malignancies in the head and neck, and walks us through some quick samples of how they are staged.

Review of the anatomy of the nasopharynx. The nasopharynx is behind the palate and includes the clivus.  The nasopharynx is largely lined by squamous mucosa with lymphoid tissues and muscles. An important landmark is the torus tubarius and fossa of Rosenmuller.   

Nasopharyngeal cancer staging, like other subsites, is based on a T, N, M stage. Nasopharyngeal cancers are predominantly staged based on whether adjacent structures, such as surrounding soft tissues or the skull base, are involved. Unlike the other tumor sites, size is not involved in the T staging.

Example case 1. There is a soft tissue mass filling the nasopharynx, asymmetrically larger on the right. Erosion of the adjacent bony structures, including the clivus, are important. The tumor is extending into the sphenoid sinus. Involvement of the bony structures and sinuses makes this is a T3 tumor, and there were no nodes or distant metastases (not shown).

There is a more subtle example of bone erosion of the posterior wall of the sphenoid sinus and left carotid canal along with the clivus.

Example case 2. There is a soft tissue mass eroding the petrous apex and left aspect of the clivus. MRI better shows the extent of the involvement, where you can see that there is intracranial involvement into Meckel’s cave (trigeminal foramen). The intracranial involvement makes this a T4 tumor. There were no nodes or distant metastases (not shown).

Example case 3. In this case, there are necrotic lymph nodes in the parapharyngeal and prevertebral space as well as extending down the neck at multiple internal jugular levels. The original CT did not show a mass in the nasopharynx, but because of the nodes, a nasopharyngeal cancer is suspected. The PET/CT is able to locate the abnormality along the left torus tubarius. The local nature of this tumor makes it T1, but the bilateral lymph nodes make it an N3 for nodes.

Extra case. An incidental polypoid mass is seen in the left nasopharynx on a brain MRI with minimal peripheral enhancement and central reduced diffusion. The homogeneously low T2 appearance and reduced diffusion make this suspicious for lymphoma, although you would not be able to tell until this lesion had been biopsied.

Thanks for checking out this quick video on nasopharyngeal cancer staging. Be sure to tune back in for additional videos on staging of the other head and neck subsites.Also take a look at the head and neck topic page as well as all the head and neck videos on the site.

 

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Oropharyngeal cancer staging – 5 minute review

In this video, Dr. Katie Bailey describes the anatomic subsites of the oropharynx and reviews how tumors are staged through four quick example cases.

Review of oropharynx anatomy. The oropharynx includes the tonsils (both lingual and palatine), the squamous mucosa of the pharynx, the uvula, and the vallecula.   oral cavity includes the lips, teeth, hard and soft palate, gingiva, retromolar trigone, the buccal mucosa, and anterior 2/3 of the tongue. Masticator space. Contains the muscles of mastication, the mandible, branches of the trigeminal nerve, lymph nodes, and minor salivary glands. 

Oropharyngeal cancer staging. Tumor (T) staging is based on the size of the tumor or invasion through adjacent structures. Nodal (N) staging is based on the number, location, and size of nodes, and metastasis (M) staging is based on the presence or absence of distant sites of disease.

Example case 1. There is a 2.4 cm mass of the right palatine tonsil. There is level 2 and 3 adenopathy. The lymphadenopathy compresses the jugular vein and displaces the adjacent sternocleidomastoid.  The size of the tumor makes this a T1 lesion, and the unilateral adenopathy less than 6 cm with multiple nodes makes it N2b. Because metastases can’t be evaluated with this information, it is given an ‘X’ for M staging right now.

Example case 2. There is a 3.2 cm mass in the tongue base and extending into the vallecula. There is no extension into the adjacent structures or fat. There is a single left sided level 2 lymph node that is somewhat prominent but isn’t definitely abnormal. That makes this a T2N0Mx tumor. If a PET or biopsy later shows that the node is positive, the staging can be changed.

Example case 3. There is a subtle mass of the right lateral wall of the oropharynx involving the tonsillar pillar and tongue base. This one is quite hard to see. There are cystic necrotic lymph nodes on the right, but none greater than 6 cm. A PET/CT showed no distant metastatic disease. That makes this a T1N2bM0 tumor.

Example case 4. This patient presented with cervical lymphadenopathy on the left but had no clear primary tumor in the oropharynx. There was no mass of the tongue base or elsewhere. The patient had a lung node suspicious for metastatic disease. A PET/CT showed that there was a primary in the soft palate. The mass was detected only by PET/CT. The final staging for this cancer is T1N2bM1.

Thanks for checking out this quick video on oropharyngeal cancer staging.

Thanks for checking out this quick video on oral cavity cancer staging. Be sure to tune back in for additional videos on staging of the other head and neck subsites. Also take a look at the head and neck topic page as well as all the head and neck videos on the site.

 

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Oral cavity cancer staging – 5 minute review

In this video, Dr. Katie Bailey takes on a common topic and describes how cancers of the oral cavity are staged through three quick example cases.

Review of oral cavity anatomy. The oral cavity includes the lips, teeth, hard and soft palate, gingiva, retromolar trigone, the buccal mucosa, and anterior 2/3 of the tongue. Masticator space. Contains the muscles of mastication, the mandible, branches of the trigeminal nerve, lymph nodes, and minor salivary glands. 

Retromolar trigone. The retromolar trigone is a common crossroads where a lot of pathology occurs and it can cause referred ear pain. Mandibular invasion can also occur with masses that occur in this location.

Oral cavity cancer staging. Tumor (T) staging is based on the size of the tumor and depth of invasion. Nodal (N) staging is based on the number, location, and size of nodes, and metastasis (M) staging is based on the presence or absence of distant sites of disease.

Example case 1. This example case involves the oral tongue and measures 2-4 cm. It has ipsilateral lymph nodes less than 3 cm. This makes this a T2N2 tumor. Because metastases can’t be evaluated with this information, it is given an ‘X’ for M staging right now.

Example case 2. This shows a subtle left tongue cancer measuring less than 2 cm. There are no lymph nodes. That makes this a T1N0Mx tumor.

Example case 3. This case is a hard palate tumor with bone erosion. The involvement through adjacent structures (the bone of the hard palate) makes this a T4 tumor. There is no nodal involvement, making this a T4N0Mx cancer.

Thanks for checking out this quick video on oral cavity cancer staging. Be sure to check out the head and neck topic page as well as all the head and neck videos on the site.

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Neuroradiology Board Review – Brain Tumors – Case 20 – Summary

Neuroradiology brain tumor board review. This lecture is geared towards the ABR core exam for residents, but it would be useful for review for the ABR certifying exam or certificate of added qualification (CAQ) exam for neuroradiology.

This video has both the final case of the series and a quick review summary!

Case 20

In this case, you are starting with an immunocompromised patient with HIV. Initial CT images show a hyperdense mass in the left basal ganglia with a lot of surrounding edema. This is helpful, because a few things are known for being hyperdense on CT.

MRI images confirm a mass in the basal ganglia. It is somewhat T2 hypointense with well-defined margins and surrounding edema. On postcontrast images, it has peripheral enhancement but central non-enhancement compatible with necrosis.

The differential diagnosis for a solitary enhancing parenchymal mass is different in an immunocompromised patient (or someone on immune suppressing agents. In an immune normal patient, the top diagnoses are

  • metastatic disease
  • high grade glioma
  • lymphoma

On the other hand in an immunocompromised patient the order of these diagnoses shifts to include:

  • lymphoma
  • infection
  • metastatic disease
  • high grade glioma

As you can see, lymphoma and infection jump to the top in an immunocompromised patient.

The diagnosis is: CNS lymphoma

CNS lymphoma can occur when associated with systemic lymphoma or primarily in the CNS, as in this case. This is most commonly a diffuse large B-cell lymphoma. It is more common in immune compromised patients. It often occurs in the basal ganglia and periventricular white matter and can often be multifocal. Lymphoma is one of the rare diseases which is T2 hypointense, so you should think about it if you see a T2 hypointense mass.

In immunocompetent patients, lymphoma most commonly has solid enhancement. However, in immunocompromised patients it is much more likely to show central necrosis, as in this case. Also, in an immunocompromised patient, it can be hard to differentiate lymphoma from infection, particularly toxoplasmosis. The two most common ways to try to differentiate this are to start a trial of toxoplasmosis therapy for a few weeks and see if the lesions improve and to perform a thallium-201 chloride nuclear medicine scan. Lymphoma has thallium uptake, while toxoplasmosis does not.

Summary

In this board review lecture, you’ve seen a lot of different tumors and how they manifest in different situations. In many cases, you can’t make a definitive diagnosis but you should always be able to come up with a reasonable differential diagnosis. It’s also helpful to know some of the basics about treatment and prognostic factors.

There are two key strategies that I hope can help you get a few additional points, the approach to CP angle masses and the approach to cortical tumors.

Cerebellopontine angle masses

As we’ve seen in some of the other cases, cerebellopontine angle masses can be solid or cystic. Solid masses that involve the IAC and expand it are likely schwannomas, while others outside the IAC are likely meningiomas. Arachnoid cysts and epidermoids are the most common cystic masses which are differentiated by DWI (which is bright in ependymomas.

Cortical tumors

Several of the cases in this series dealt with cortical temporal tumors. Ill-defined masses that are larger are more likely to be low grade gliomas (oligodendrogliomas and astrocytomas). Completely non-enhancing bubbly masses favor DNET. A little nodular enhancement favors ganglioglioma, while pleomorphic xanthoastrocytoma (PXA) can be more avidly enhancing and irregular.

Neuroradiology Board Review – Brain Tumors – Case 19

Neuroradiology brain tumor board review. This lecture is geared towards the ABR core exam for residents, but it would be useful for review for the ABR certifying exam or certificate of added qualification (CAQ) exam for neuroradiology.

More description and the answer (spoiler!) are seen below the video.

This case of a patient with diplopia (double vision) starts with a CT through the orbits. You can see there is a well-defined mass at the right orbital apex.

On MRI, you can see the lesion again is well-defined with well defined margins and is hyperintense on T2. On T1, the lesion is isointense to muscle on pre-contrast and then demonstrates heterogeneous enhancement on postcontrast. It looks like the lesion is enhancing more on the coronal image compared to the axial image.

The diagnosis is: orbital venous vascular malformation

Orbital venous vascular malformations are sometimes referred to as hemangiomas, although this term is falling out of favor because it is not neoplastic (unlike the neoplastic infantile and neonatal orbital hemangiomas). These are relatively benign lesions that can cause visual problems secondary to mass effect, but it’s relatively uncommon for them to enlarge.

One characteristic finding of orbital venous malformations is progressive enhancement on delayed images. On early images, it might be enhancing a little bit but if you have more delayed images, you might see more enhancement. If you don’t have more than one plane of contrast, you can bring them back and image them again 15-30 minutes later and it should fill in.

The primary differential considerations for orbital masses are sarcoidosis, idiopathic or IgG4 related orbital disease, metastatic disease, and lymphoma. When it is this well defined and has the characteristic delayed enhancement, the diagnosis is relatively certain.

Neuroradiology Board Review – Brain Tumors – Case 18

Neuroradiology brain tumor board review. This lecture is geared towards the ABR core exam for residents, but it would be useful for review for the ABR certifying exam or certificate of added qualification (CAQ) exam for neuroradiology.

More description and the answer (spoiler!) are seen below the video.

This case starts with 2 axial images from a CT through the posterior fossa followed by MRI images through the same region. There is a heterogeneous lesion to the left of the midline along the left foramen of Lushka. On postcontrast images, it is pretty avidly enhancing. The enhancing margins are pretty well defined and it looks like it is wholly in the ventricle.

The diagnosis is: ependymoma

Ependymomas are enhancing intraventricular tumors arising from the ependymal lining. They are commonly enhancing and conform to the ventricles and the ventricular outflow tract, which results in their description of “toothpaste” like lesions. In adults, they most commonly occur in the 4th ventricle although in pediatric patients they can occur elsewhere.

When in the posterior fossa, your main differential is choroid plexus papilloma/tumor. If you can’t tell that it’s an intraventricular lesion it can be harder because the differential diagnosis also include metastatic disease and possibly medulloblastoma. If you see a lesion that looks similar but doesn’t enhance very much, think about it’s sister lesion subependymoma.

Neuroradiology Board Review – Brain Tumors – Case 17

Neuroradiology brain tumor board review. This lecture is geared towards the ABR core exam for residents, but it would be useful for review for the ABR certifying exam or certificate of added qualification (CAQ) exam for neuroradiology.

More description and the answer (spoiler!) are seen below the video.

In this case, we have an MRI showing a FLAIR and T2 hyperintense mass in the left insula with relatively ill-defined margins. On SWI, there are some areas of susceptibility that probably represent calcification, although blood products could look similar. Postcontrast images demonstrate little or no contrast enhancement.

1:33 The diagnosis is: oligodendroglioma

Oligodendrogliomas are gliomas which are now defined by the characteristic genetic features of IDH mutation and 1p19q codeletion (loss of portions of both chromosomes 1 and 19). They can be WHO grade 2 (as in this case) or grade 3 (anaplastic oligodendroglioma). Theoretically, these lesions never degrade into WHO grade 4 lesions although the grade 3 lesions can be quite aggressive. In general, oligodendrogliomas have a better prognosis than their sister gliomas, astrocytomas. They respond better to radiation and have better overall survival.

Oligodendrogliomas are treated with a combination of resection and chemoradiotherapy.

The susceptibility seen within the tumor on this case represents areas of calcification. Oligodendrogliomas are one of the main considerations if you see an expansile tumor with calcification.