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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Spine tumors 6 – Cysts and Summary

A few lesions within the spinal canal are predominantly cystic or nonenhancing. They are almost always intradural extramedullary. The three most common entities are arachnoid cysts, dermoid cysts, and neuroenteric cysts. A contrast enhanced myelogram can often give you a little bit more information about what the entity is by determining if it fills with contrast.

Case 1. Arachnoid cyst. Arachnoid cysts in the spine are somewhat uncommon but will have the same characteristics as CSF on all images. They may often be identified only by their deflection of the spinal cord and mass effect. Their main differential is arachnoid webs or adhesions which cause similar mass effect on the spinal cord. On myelography, they often fill with contrast but more slowly than the surrounding CSF.

Case 2. Dermoid. Dermal inclusion cysts, or dermoids, are complex lesions made out of tissue from more than one embryonal layer. Their characteristic feature is internal fat contents. Like intracranial dermoids, they can rupture and cause a chemical meningitis. Their appearance overlap with lipomas but they are more likely to have complex features

Case 3. Neuroenteric cysts. Neuroenteric cysts are relatively simple cystic lesions which often occur ventral to the brainstem or spinal cord. They often are similar to but not exactly like CSF, and can be T1 hyperintense. They are indolent lesions but can cause mass effect. They do not fill on myelography.

Cyst summary. These are three of the most common cystic lesions. They are best differentiated by whether they communicate with the thecal sac (arachoid cysts), have complex or fatty features (dermoids), or are ventral to the cord and slightly differ from CSF (neuroenteric cysts).

Summary of spine tumors by location. Overall, when thinking about spine tumor, you should take a location-based approach. If you haven’t seen the introduction video yet, then definitely check it out. When divided by intramedullary, intradural extramedullary, and extradural, this can help you decide what type of lesion you are dealing with. Overall, always remember that the spine is an extension of the central nervous system, and consider imaging the brain because that may help you hone your differential diagnosis.

The level of this lecture is appropriate for radiology residents, radiology fellows, and trainees in other specialties who have an interest in neuroradiology or may see patients with spine tumors.

Other videos on the spine tumor playlist are found here.

Spine tumors 5 – Extradural lesions

Lesions outside the thecal sac are categorized as extradural lesions. Remember that everything that isn’t in the thecal sac is extradural, including discs, bones, meninges, nerves, and blood vessels. Anything that can occur in the surrounding areas can have extradural components. Look for lesions that have mass effect on the dura and deflect both the dura and the thecal sac to the side. Many of these lesions will require a biopsy as they have a differential diagnosis on imaging. CT and diffusion weighted imaging are useful adjunct tools that can help you refine your diagnosis.

The rest of this lecture consists of a mix of case presentations of different extradural lesions with tips on how to refine your differential diagnosis.

Case 1 – Disc extrusion. These are one of the most common extradural pathologies, particularly in patients with a history of degenerative disc disease. They tend to be contiguous with the disc and follow the disc in signal. Don’t be alarmed if they have enhancement, particularly if the enhancement pattern is peripheral. These can be confused with schwannomas and meningiomas.

Case 2 – Lymphoma. Lymphoma can involve the bones at any spinal level and can result in pathologic fracture. Anytime you see involvement of the pedicles and posterior elements you should worry about pathologic fracture, particularly if there is soft tissue or epidural involvement and enhancement. When the bone is involved, think about performing a CT to see the pattern and extent of bone destruction. This lesion has a mixed lytic and sclerotic appearance with bone destruction and was ultimately proven to be lymphoma.

CT pattern of different bone lesions. When you have a bone lesion, the trabecular pattern and pattern of bone destruction can be helpful. Lesions such as benign vascular malformations (hemangiomas) have a classic trabecular or corduroy pattern, while Paget’s disease is characterized by cortical thickening.

Case 3 – Osteosarcoma. Bone sarcomas are aggressive lesions that have bone destruction and can have soft tissue components. Their characteristic finding is matrix deposition which is best seen on CT. Osteosarcomas tend to have fluffy cloudlike matrix (osteoid) while chondrosarcomas have arcs and rings with interrupted calcification (chondroid). This was a case of osteosarcoma.

 Benign versus pathologic fractures. It can be challenging to differentiate fractures from bone insufficiency or trauma from those with an underlying lesion (pathologic fracture). Pathologic fractures are more likely to have bowing of the posterior cortex, a surrounding soft tissue mass, and abnormality on DWI. Looking for lesions elsewhere in the body can be a clue that it is metastatic disease, lymphoma, or myeloma. Sometimes these diseases can also have diffuse involvement of all of the marrow which can manifest as low T1 intensity throughout all the vertebral bodies.

Epidural tumor. Ventral epidural tumor can form a curtain or drape appearance because the dorsal dura is tacked down to the vertebral body at the midline. When it becomes more circumferential, it can extent completely around the thecal sac and extent both cranially and caudally.

Case 4 – Chordoma. Chordoma’s are aggressive tumors arising from notochordal remnant cells that can occur anywhere along the spinal axis. They are most common in the sacrum > clivus > remaining spine. Their characteristic appearance is a lytic lesion with bone destruction and marked T2 hyperintensity.

Enhancement pattern of extradural lesions. The enhancement pattern can help differentiate extradural lesions which may look similar. Tumors tend to have solid enhancement, abscess has peripheral enhancement, and a hematoma may have little or no enhancement.

Case 5 – Spinal dural arteriovenous fistula (dural AVF). These lesions have a classic presentation in older gentlemen with progressive myelopathy and are often missed. On MRI, they usually have edema and possibly enhancement in the cord, but the key finding is squiggly vascular enhancement along the margins of the cord. The pathology is from an abnormal connection between a vein and artery in the nerve root sleeve and can be treated endovascularly or with surgery.

Case 6 – Angiolipoma. These are fat containing lesions most common in the thoracic spine along the dorsal epidural space. They will have fat density on CT and can slowly increase in size, causing myelopathy.

Summary. There are a lot of things that can cause extradural masses, but they most commonly arise from the surrounding structures like discs and bones. Hopefully this video will help you refine your differential in the future.

The level of this lecture is appropriate for radiology residents, radiology fellows, and trainees in other specialties who have an interest in neuroradiology or may see patients with spine tumors.

Basics of Spine Interpretation in 5 minutes

In this lecture, Dr. Katie Bailey walks us through a rapid lecture about how to approach the basics of the spine. In about 5 minutes, you can learn most of what you need to know about spine interpretation when you first sit down to look at spine imaging.

This approach is based on the ABCDEs of spine. Each letter tells you something about what you should be looking for on the imaging.

Alignment. The way the vertebral bodies are oriented with respect to one another is alignment. This means lateral curvature (scoliosis), AP curvature (lordosis or kyphosis), and translation. Listhesis is conventionally described based on the level above with respect to the level below.

Bones. When thinking about the bones, you should look at the characteristics of the bones themselves. On CT, that could mean loss of normal bone density (lytic) or increased bone density (sclerotic). On MRI, you describe the appearance of a lesion with respect to the adjacent marrow. It is either hyperintense (more intense) or hypointense (less intense) compared to the normal marrow.

Cord/cauda equina. The cord itself is a key part of the image and you should look for any lesions within the cord or cauda equina. The cauda equina should be around the L1 level.

Disc. The discs have a wide range of degenerative pathology, which is discussed elsewhere. You should describe degenerative disease as well as any other abnormal conditions of the disc, such as infection.

Everything else. Finally, you should look at soft tissues and surrounding structures outside the spine. This is slightly different at each level of the spine where the structures vary slightly.

Summary. With this quick approach, you can rapidly move from a spine novice to a spine apprentice and you’re ready to learn more about different pathology within the spine. Check out some of the other spine videos to learn more about topics such as spine tumors, demyelinating disease, and degenerative disease.

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Spine tumors 4 – Intradural Extramedullary Lesions

Lesions that occur within the thecal sac are categorized as intradural extramedullary lesions. The vast majority of these lesions are tumors. The most common are schwannomas (and other nerve sheath tumors) and meningiomas, but there are others that include ependymoma, metastatic disease, and lymphoma. Also remember that the intradural extramedullary space contains cerebrospinal fluid (CSF), so any process that diffusely affects CSF can affect this space.

Peripheral nerve sheath tumors are a group of benign and malignant nerve tumors including schwannomas and neurofibromas. These can expand the neural foramen and usually have well defined margins. Schwannomas tend to enhance a lot while neurofibromas enhance less.   Sarcoidosis is another common granulomatous disease that can affect the cord. The most common appearance is T2 abnormality within the cord with some enhancement. Enhancement is often along the surface of the cord.

Neurofibromatosis is a genetic syndrome with two types, type 1 and type 2. NF type 1 is characterized by multiple plexiform (involving more than one adjacent nerve root) neurofibromas. If neurofibromas increase in size rapidly, have necrosis, or cause pain, that can be a sign of malignant degeneration. NF type 2 is characterized by multiple masses including schwannomas, meningiomas, or ependymomas. NF type 2 is sometimes called MISME syndrome.

Schwannomas are probably the most common intradural extramedullary lesions. They are well defined lesions with avid enhancement. They often have central non-enhancement or cystic degeneration, but calcification or hemorrhage are less common.

Case 1 – Meningioma. Meningiomas are well demarcated intradural lesions which occur along the dura and deflect the spinal cord. They enhance avidly and usually don’t have necrosis. They frequently calcify, which you may appreciate more on CT. If they are more elongated and plaquelike they may be referred to as “en plaque” menigiomas. They can cross the dura and have components outside the dura as well.

Case 2 – Myxopapillary ependymoma. Myxopapillary ependymomas are relatively common tumors that occur around the conus and cauda equina. They usually enhance avidly. Necrosis or hemorrhage are more common than in schwannomas. They were previously grade 1 tumors but have been upgraded to grade 2 because they frequently recur.

Leptomeningeal metastases are a consideration anytime you see multiple intradural nodules. In adults, these are most commonly from the most common tumors such as melanoma, lung, and breat cancer. Lymphoma can also occur along the cauda equina. In pediatric patients you should also think about intracranial tumors that spread in the CSF, like medulloblastoma, pineal

Case 3 – Paraganglioma. Spinal paragangliomas are rare spine tumors that have a lot of abnormal surrounding vessels and are prone to hemorrhage. Think about them anytime you see an enhancing tumor in the spine with a lot of flow voids. The other thing you might think about is a hemangioblastoma, but they are more likely to be cystic.

Case 4 – Lipoma. Fat containing lesions along the conus are common and can be lipomas or dermoids. Clues are fat-suppression of FS images, chemical shift artifact, and fat density on CT. If it is thin and linear along the filum terminale, it is likely a benign fatty filum terminale.

Summary. Intradural extramedullary lesions are among the most common spinal lesions and it is important to have a clear differential when you see them.

The level of this lecture is appropriate for radiology residents, radiology fellows, and trainees in other specialties who have an interest in neuroradiology or may see patients with spine tumors.

Other videos on the spine tumor playlist are found here