Emergency Imaging of Brain Tumors: Oligodendrogliomas & Others

This video is the fourth video in an overview about the emergent approach to brain tumor imaging. This video talks about different presentations of oligodendrogliomas, ranging from grade 2 to grade 3, showing representative emergency presentations and CT examples with emphasis on how to report the CT and next steps. The video also shows some of the more common lower grade circumscribed gliomas like DNET, ganglioglioma, PXA, and pilocytic astrocytoma.

Types of oligodendrogliomas.

Oligodendrogliomas range from grade 2 to grade 3 and are characterized by IDH mutation and 1p19q codeletion. Theoretically, they do not transform into grade 4 tumors.

Case 1. Grade 2 Oligodendroglioma.

We start with a scout image from a CT. If you look closely, you can see calcification which is confirmed on the axial CT images. There is a a pretty ill-defined hypodense mass in the right posterior frontal and inferior parietal lobe. There is extremely dense calcification centrally. Your initial differential should include calcified tumors (such as oligodendroglioma, calcifying metastasis, or vascular malformation). The MRI confirms what was seen on CT, an expansile mass with central calcification. There is very little if any enhancement.

Grade 2 oligodendrogliomas tend to be middle age patients and are characterized by IDH mutation a. Common locations are the frontal and temporal lobe. Calcification and cystic changes are pretty common, but grade 2 tumors rarely enhance.

Case 2. Grade 3 Oligodendroglioma.

In this case, we go straight to MRI. There is a really heterogeneous mass in the left frontal lobe with cyst, hematocrit/fluid levels, and probably some calcification and blood products. Compared to the grade 2 tumor, there is definitely more mass effect. There is lots of heterogeneous enhancement. In your differential, you would think about an high grade tumor, including a glioblastoma.

Grade 3 oligodendrogliomas, or anaplastic oligodendrogliomas, look a lot like high grade tumors, and you will almost never make the diagnosis on imaging as you should suggest high grade tumors like glioblastoma as well. Like GBMs, they have, cysts, enhancement, and hemorrhage.

Other low grade tumors

There are a number of other low grade gliomas that are well circumscribed and are usually low grade (grade 1 or 2). This includes pilocytic astrocytomas, dysembroplastic neuroepithelial tumors (DNET), gangliogliomas, and pleomorphic xanthoastroctyomas (PXA).

Tumors with an enhancing nodule have a short differential, including pilocytic astrocytoma, PXA, and ganglioglioma.

If you see a small lesion with a cystic appearance, if there is no enhancement, favor DNET and if there is some enhancement favor ganglioglioma.


In this video, we’ve seen a couple of oligodendrogliomas and how they can appear on imaging, and covered some of the more common lower grade tumors.

Be sure to tune in for upcoming videos which will cover other common tumors, and some red flags to be alert to in the ER setting.

Thanks for tuning in. Be sure to check out the other videos on the brain tumor topic page if you want to learn more about brain tumors. Also check out the Emergency Imaging of Brain Tumors Playlist to see all the videos from this lecture.


Emergency Imaging of Brain Tumors: Astrocytomas

This video is the third video in an overview about the emergent approach to brain tumor imaging. This video talks about different presentations of the most common primary brain tumor type, astrocytomas, ranging from grade 2 to grade 4, showing representative emergency presentations and CT examples with emphasis on how to report the CT and next steps.

Types of astrocytomas.

Astrocytomas range from grade 2 to grade 4, with the highest grade IDH wild type tumors being glioblastomas. Some lower grade gliomas behave like higher grade tumors if they have specific molecular features.

Case 1. Grade 2 Astrocytoma.

There is a low density mass in the insula and temporal lobe with moderately well-defined margins. The differential primarily includes tumor and infection with stroke and metastatic disease less likely. The MRI shows primarily a non-enhancing mass in the medial temporal lobe and insula with a lot of expansion.

Grade 2 astrocytomas tend to be younger patients and have IDH mutation. Common locations are the frontal and temporal lobe. Enhancement, hemorrhage, and cyst formation are relatively rare.

Case 2. Grade 3 Astroctyoma.

In this case, there is a more heterogenous mass in the right basal ganglia and corona radiata. Internal areas of high density may represent some areas of calcification or hemorrhage. There is definitely more mass effect. In your differential, you would think about an intermediate grade tumor or metastatic disease. The MRI confirms that there is a more heterogeneous mass with some faint/subtle areas of enhancement centrally. This makes you think of an intermediate to higher grade tumor.

Grade 3 astrocytomas, or anaplastic astrocytomas, make but about 25% of astrocytomas. They tend to be a little less defined and are more likely to have cysts, enhancement, and hemorrhage

Case 3. Grade 4 Astrocytoma

The CT in this case shows a much more heterogeneous mass spanning both frontal lobes and involving the corpus callosum. The high density material internally likely represents hemorrhage. There is a lot of mass effect on the frontal horns bilaterally. In this case, you are definitely thinking about a high grade mass or metastatic disease. Lymphoma would be less likely. The MRI confirms what you saw on the CT, with lots of internal hemorrhage, mass effect, and extension across the corpus callosum. There is a lot of heterogeneous and ill-defined enhancement.

Grade 4 astrocytomas are either glioblastomas (if they are IDH wild type) or IDH-mutated grade 4 astrocytomas. This was a case of glioblastoma. These tumors frequently have a hemorrhage, mass effect, and heterogeneous enhancement.


In this video, we’ve seen a range of astrocytomas and how they can appear on imaging, particularly on CT. Hopefully you learned a little bit about how to form a differential on CT and give an appropriate differential.

Be sure to tune in for upcoming videos which will cover oligodendrogliomas, other common tumors, and some red flags to be alert to in the ER setting.

Thanks for tuning in. Be sure to check out the other videos on the brain tumor topic page if you want to learn more about brain tumors. Also check out the Emergency Imaging of Brain Tumors Playlist to see all the videos from this lecture.


Emergency Imaging of Brain Tumors: Tumor Classification

This video is the second video in an overview about the emergent approach to brain tumor imaging.  The first video talked about the role of imaging in an emergent setting and how to approach cases. This tells you a little bit more about the common types of tumors you might encounter and how they are classified.

Common types of brain tumors. The most common brain tumors you may encounter are primary gliomas, meningioma, metastatic disease, and lymphoma. Calvarial tumors, or those centered in the skull, have a somewhat special differential.

Primary gliomas. The primary gliomas encompass all the grade 2, 3, and 4 oligodendrogliomas and astrocytomas. In 2016, the WHO started using genetic testing more to classify these tumors, and further refined these classifications in 2021. In general, tumors are first classified by whether they have isocitrate dehydrogenase (IDH) mutation. Mutated tumors tend to be lower grade astrocytomas and oligodendrogliomas. If they have 1p19q co-deletion, they are oligodendrogliomas, and otherwise astrocytomas. IDH wild type tumors are the most aggressive and include glioblastomas. Now, there are some tumors that have genetic features that make them a lot like glioblastomas.

Pearls about primary gliomas.

  • Higher grade tumors will be characterized by mor mass effect, hemorrhage, and enhancement, although you aren’t always going to be able to tell.
  • The term “multiforme” has fallen out of use, so you can just call them glioblastomas or GBM.
  • Gliosarcomas are a special subset of tumors that have features of both gliomas and sarcomas. They are often characterized by broad dural involvement or bone involvement, but sometimes you can’t tell.
  • Oligoastrocytoma is a deprecated term no longer used. If it has 1p19q codeletion and IDH mutation, it’s an oligodendroglioma.
  • Gliomatosis cerebri is no longer it’s own diagnosis but simply a pattern of brain involvement

Pearls about other common tumors

  • Meningiomas are the most common primary intracranial tumors. If you see an extra-axial tumor, it is likely a meningioma.
  • Metastatic disease is the overall most common intracranial tumor and should be suspected in older patients and those with other malignancies
  • Lymphoma can cause solid enhancing multifocal disease
  • Calvarial tumors have a special differential including meningioma, lymphoma, myeloma, and metastatic disease

Thanks for tuning in. Be sure to check out the other videos on the brain tumor topic page if you want to learn more about brain tumors. Also check out the Emergency Imaging of Brain Tumors Playlist to see all the videos from this lecture.

Emergency Imaging of Brain Tumors: Introduction/Role of Imaging

Hi everyone! In this video, we’re going to talk about the emergent imaging of brain tumors, particularly as it applies to a general approach when you might see patients like this coming through the emergency department. We’ll have a special emphasis on computed tomography throughout this lecture. This is the ideal lecture for someone who practices neuroradiology and sees some patients with brain tumors, but isn’t exactly a brain tumor expert.

Role of imaging brain tumors in emergencies. There are 2 main tools for imaging brain tumors, CT and MRI. CT is the screening tool for initial identification of a potential mass and then evaluating complications such as hemorrhage, edema, mass effect, hydrocephalus, and herniation. However, MRI is the mainstay of tumor evaluation used for evaluation of tumor type, tumor worsening, and tumor details.

MRI. MRI is used to make a more specific initial diagnosis, for pre-treatment planning, and for follow-up after surgery and treatment. It will almost always have FLAIR, diffusion weighted imaging (DWI), and pre- and post-contrast T1 imaging. A few other tools are used for troubleshooting, such as perfusion and functional MRI (fMRI).

FLAIR. This is a key sequence for evaluating a mix of edema and infiltrative tumor. It is the best comparison for CT

Pre- and post-contrast T1. Areas of post-contrast enhancement show areas of breakdown of the blood brain barrier. This can happen when the tumor itself has disrupted it or when there has been tissue damage from radiation therapy. More aggressive tumors have more enhancement

Role of emergent imaging. When a patient comes to the ER, if a patient doesn’t have a known tumor, you might use it to identify a potential tumor, give a practical differential, and recommend next steps. In patients with tumors, you might use it to identify urgent complications. The role of emergent imaging is not to give an exact diagnosis or assess tumor progression.

Summary. In this video, we have covered some of the basics of imaging patients with brain tumors in emergent situations, including when CT and MRI are most appropriate.

This is the first lecture in this series about imaging brain tumors in the emergent setting. Hopefully you learned a little bit about the role of different imaging types. The next lectures are going to discuss some additional topics in detail, including how to classify these tumors, how to interpret common imaging studies, and how to avoid red flags.

Thanks for tuning in. Be sure to check out the other videos on the brain tumor topic page if you want to learn more about brain tumors.

Imaging of the sella

In this video from Dr. Katie Bailey, we go through imaging of the sella, including a brief review of the contents of the sella, common pathologies on MRI, and an algorithm for refining your differential diagnosis based on location.

Normal sellar anatomy. The pituitary gland sits in the sella and in general should measure less than 1 cm. The posterior pituitary is intrinsically T1 bright. The gland and infundibulum enhance on postcontrast images. Sometimes the pituitary can appear more convex if the carotid arteries and cavernous sinuses are more medial than expected, which is a normal variant

Empty sella. When the sella is expanded and filled with CSF, this is called an empty sella. Sometimes you can see a thinned pituitary at the bottom or it may be completely compressed. This is most commonly seen in the setting of intracranial hypertension.

Pituitary cysts. These are relatively common lesions, often hypointense on T1 and hyperintense on T2 and do not enhance. Rathke cleft cysts can be T1 hyperintense if they have proteinaceous content. Pars intermedia cysts and Ratke cleft cysts are terms that refer to the same pathologic diagnosis but some people use them differently based on the size/location of the lesions. Adenomas can also have cystic degeneration, particularly if they have been treated.

Pituitary adenomas. These are hypoenhancing lesions which enhance less and more slowly than the adjacent gland. They may fill in with time. Microadenomas are by definition less than 1 cm. The infundibulum will often be deflected away from the pathology because of mass effect.

Macroadenomas. These are pituitary tumors that are greater than 1 cm and may have a snowman appearance with mass effect on the adjacent optic chiasm. These will often involve the cavernous sinuses. Involvement greater than 270 degrees around the carotid is highly suggestive of cavernous sinus invasion, and classification systems such as the Knosp classification can help you be more exact about cavernous sinus involvement.

Other lesions. Other common lesions in the pituitary are metastases, apoplexy (hemorrhage most commonly into a pre-existing adenoma), and meningiomas.

Autoimmune hypophysitis. This is a special type of inflammation of the sella most commonly occurring in patients getting immunotherapy for metastatic melanoma (ipilimumab). The pituitary and infundibulum are commonly diffusely enlarged and enhancing.

Lymphocytic hypophysitis is an inflammatory disease of the infundibulum which may involve the gland itself, but often spares it.

Metastatic disease. Metastases can occur in the pituitary gland or infundibulum. If you see an irregular mass filling the sella in a patient with known malignancy, consider metastases.

Other lesions. Aneurysms of the internal carotid artery, epidermoids, chondrosarcomas, and other vascular variants can all involve the sellar region and infundibulum, so it is important to keep those in mind.

Hopefully you learned a bit from this video about approaching sellar lesions. Be sure to check out the other videos on search patterns as well as all the other

head and neck topics.

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Emergency Imaging of Brain Tumors

This playlist covers the imaging of brain tumors in an emergency setting, with particular emphasis on how a general radiologist might approach these cases and how to formulate a smart differential on CT.

You can learn more about brain tumors on the brain tumor topic page. Also, please check out our full channel on Youtube.

Facial fractures

This video is an overview from Dr. Katie Bailey about fractures of the face, including their CT findings and complications. Facial fractures are among the most commonly encountered emergencies, particularly in busy trauma hospitals.

Simple fractures. These involve isolated fractures of one of the sinus walls, the zygomatic arch, or the nasal bones.

Frontal sinus fractures. Consider whether they involve the outer table, inner table, or both. Complications of frontal sinus fractures include CSF leak, mucocele, or meningitis. Brain parenchymal contusions can also accompany frontal sinus fractures.

Other common isolated fractures. Common fractures include the zygomatic arch and mandible. When you have a fracture of the mandible, it is very common to have a fracture elsewhere in the mandibular ring. Nasal fractures are commonly seen and are worse if there is displacement because they can result in poor cosmetic outcomes. Nasal septal fractures are sometimes challenging to see and soft tissue swelling is probably your best clue. A nasal septal hematoma, if present, can result in necrosis of the nasal septum.

Lamina papyracea fractures. These are fractures of the medial wall of the orbit. Most commonly, these result from a blow to the eye. Soft tissue swelling within the orbit or blood in the sinus can tell you if you are likely dealing with a more acute fracture. A retroorbital hematoma can accompany these fractures, and are characterized by stranding or soft tissue density in the retroorbital fat. These require more rapid intervention to avoid risks to vision

Orbital floor fractures. These can have displacement of fragments into the adjacent maxillary sinus, and it is important to report if the muscles are displaced into the sinus. Entrapment of the muscle can result in loss of eye movement and may need to be managed surgically.

Single sinus fractures. Sometimes you will have a fracture of only a single sinus, often from a direct blow. These can involve one or more walls of the sinus. Sphenoid sinus fractures can be complicated by extension into the carotid canal which increases the risk of vascular injury.

Lefort fractures. Lefort fractures involve the pterygoid plates and are subdivided into 3 types. They can be unilateral or bilateral. Lefort I fractures extend through the inferior maxilla and not the roof of the sinus. This is a transverse pattern which is low across the maxillary sinus. Lefort 2 fracture extend through the inferior lateral maxilla but extend superiorly as they go medially through the midface and inferior orbital wall. A Lefort III fracture is a transvere fracture which is higher and goes through the lateral orbital wall and potentially the zygoma.

ZMC fractures. These are fractures of the zygomaticomaxillary complex. They involve the struts of the zygoma, including the anterior maxillary wall, posterior maxillary wall, zygoma, and frontal sinus.

NOE fractures. Nasal-orbital ethmoidal fractures are a pattern of injury etending from the nasal bones through the septum, ethmoid sinuses, and medial orbital walls across the bridge of the nose. These can cause injury to the nasolacrimal duct or medial canthus, reducing eye movement.

Hopefully you learned a bit from this video about how to categorize facial fractures on CT. Be sure to check out the other videos on search patterns as well as all the other head and neck topics.

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How to read a Sinus CT

In this video, Dr. Katie Bailey gives us an overview of how to approach a CT of the sinuses, including an overview of anatomy, some common pathology, and red flags to look out for as you interpret the images.

Overview of sinus anatomy. There are 4 main sinuses, the maxillary, ethmoid, sphenoid, and frontal, which are both paired. The nasal cavity and orbits are also important structures to discuss.

Maxillary sinus. When evaluating the maxillary sinus, you should describe whether there is opacification, the appearance of the bony walls, and the outflow tract (the ostiomeatal complex).

Frontal sinus. The paired frontal sinuses should also be described in terms of aeration and bony walls. They drain through the frontoethmoid recess into the anterior ethmoid air cells.

Ethmoid air cells. There are anterior and posterior ethmoid air cells which can have mucosal thickening or opacification. The Haller cell is an important variant in which an ethmoid cell is found below the medial orbit that can contribute to obstruction. Ethmoid sinusitis can extend into the orbits and cause orbital cellulitis, an important complication.

Sphenoid sinus. The sphenoid sinus is posterior to the ethmoids and may have a fluid level, as it is a dependent sinus. The drainage is into the posterior ethmoids via the sphenoethmoid recess. Adjacent structures including the sella, internal carotid artery, and clivus can all be affected by sphenoid sinus disease.

Nasal cavity. Important features of the nasal cavity are the nasal septum, turbinates, and any potential polyps. An important variant is the concha bullosa, which is an aerated middle turbinate, which can contribute to sinus outflow obstruction.

Anatomic variants. Important anatomic variants can affect the optic canal, such as absence of the bone. The olfactory fossa can also have variants where the depth is greater or less. Keros is a classification used to describe how deep the olfactory fossa is. The vidian canal contains the vidian nerve and is best seen on the coronal images just above the pterygoid plates. It can be medially directed and run in the wall of the sphenoid sinus, which exposes it to injury. The carotid canal can be medially positioned and very close to the sphenoid sinus, also putting it at risk of injury. There are variants in the sphenoid septa, in which it attaches along one lateral wall rather than in the midline.

Red flags of sinus imaging. Abnormal soft tissue or stranding in the retromaxillary fat or pterygopalatine fossa is an important red flag which can signal invasive (possibly fungal) sinusitis. Similarly, stranding in the orbit can raise the possibility of invasive sinusitis. Another red flag is bony disruption, particularly along the sinus walls or in the nasal cavity.

Conclusion. Don’t forget to look at other things in the images, including the brain, sella, nasopharynx, mandible, teeth, orbits, and more.

Thanks for checking out this quick video on the internal auditory canal. Be sure to check out the additional videos on other
head and neck topics.


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Imaging findings in Pulsatile Tinnitus

In this video, Dr. Katie Bailey talks about the imaging findings of pulsatile tinnitus. Pulsatile tinnitus is a ringing or abnormal sound sensation in the ear, but unlike the most common high frequency tinnitus, it has a pulsatile or wavelike quality that can often oscillate with arterial or venous flow. Causes of pulsatile tinnitus are unique and a different approach is warranted.

General approach and common causes. Some findings are best seen on CT and others are best seen on MRI. For this reason, you can often perform either a CT or MRI when you begin. There are a wide range of possible causes that can be categorized into neoplasm, arterial, and venous.

Paragangliomas. Glomus tympanicum, or tympanicum paraganglioma, is the most common middle ear tumor. These are more common in women than men. The most common location is along the floor of the middle ear adjacent to the cochlea. A glomus tympanicojugulare has features of both a jugular paraganglioma and tympanic paraganglioma, often connecting them. On MRI, these appear as permeative masses with bone destruction and enhancement.

Vestibular schwannoma is the most common tumor of the internal auditory canal and usually arise from the inferior vestibular nerve. These are solidly enhancing masses that extend from the IAC into the cerebellopontine angle.

Other tumors that can occur in or around the region include meningiomas and chondrosarcomas. Meningiomas are usually homogeneously enhancing and may have dural tails. Chondrosarcomas are often centered around the petroclival junction.

Arterial anomalies can also cause pulsatile tinnitus. If the internal carotid artery extends into the middle ear with no bony covering, this is an aberrant ICA. A persistent stapedial artery can also cause pulsatile tinnitus. The absence of foramen spinosum suggests a variant with no middle meningeal artery and a persistent stapedial artery.

Other vascular causes include vascular loops and microvascular compression of the nerves in the IAC. These can also cause pulsatile tinnitus, although the role of an AICA loop has been controversial. Other carotid abnormalities such as carotid stenosis, dissection, or fibromuscular dysplasia are also associated with tinnitus.Hemangiomas, or encapsulated venous vascular malformations, are benign vascular malformations which have high flow

Venous abnormalities can also cause tinnitus. These may be a more constant tinnitus or hum with less arterial type pulsation. Absence of the bony wall around the jugular bulb is known as a dehiscent jugular bulb. Venous diverticula from the sigmoid sinus or jugular vein are small outpouchings of the vein, almost like aneurysms. Other vascular malformations such as dural AV fistulas and arteriovenous malformations can cause tinnitus, and can be confirmed on vascular imaging studies. Idiopathic intracranial hypertension causes stenosis of the lateral transverse sinuses which can also cause tinnitus.

A few other things can cause pulsatile tinnitus, such as cotospongiosis/otosclerosis and Paget disease.

Overall, a number of things can cause pulsatile tinnitus, but a few of these things are more common so you should keep your eye out for them.

Thanks for checking out this quick video on the internal auditory canal. Be sure to check out the additional videos on other

head and neck topics.


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Imaging the internal auditory canals

In this video, Dr. Katie Bailey describes the internal auditory canal including the anatomy and some of the common pathology that you may encounter.

Review of internal auditory canal (IAC) anatomy. The IAC includes arteries and nerves. The most easily seen structures are the facial (cranial nerve VII) and vestibulocochlear (cranial nerve VIII) nerves. On a sagittal view, the anterior portion of the canal contains the facial nerve (superior) and cochlear nerve (inferior). This can be remembered by the mnemonic “7up, Coke down”. 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. 

Vascular loop. Sometimes an arterial branch can compress the nerves as they enter the IAC. If you see mass effect, this is particularly possible. Smaller loops of the anterior inferior cerebellar artery are more controversial but has been previously described as associated with hemifacial spasm. If you see it, you can be descriptive about which portion of the nerve is involved.

Vascular malformations are a rare cause of symptoms, but if you see an unusual tangle or cluster of vessels in the region you should

Vestibular schwannomas are the most common tumor affecting the IAC. They usually arise from the inferior vestibular nerve, and have previously been referred to as “acoustic neuromas”. With these tumors, you will see an enhancing mass with pretty homogeneous enhancement centered in the IAC with extension into the porus acousticus. They can sometimes be quite small but still symptomatic.

Meningiomas are the second most common solid mass. They are also solid enhancing masses near the IAC. Key clues that they are not schwannomas are a center outside of the IAC. Dural tails, or linear areas of tumor tracking along the dura, can be helpful, but schwannomas can also have them.

Epidermoids are relatively uncommon non-enhancing masses of the CP angle and IAC. They look cystic on T2 and can be close to CSF, but their key distinguishing feature is hyperintensity on DWI.

Bell’s Palsy is an idiopathic facial paralysis on one side. Imaging can often be normal, but if you see linear enhancement in the distal auditory canal this can be a sign of Bell’s palsy. The geniculate and mastoid portions of the facial nerve can enhance in normal cases, so in those cases you must consider the symmetry.

Red flags in the IAC include nodular enhancement and multiple cranial nerves enhancing. This should make you think of unusual pathology such as lymphoma, sarcoidosis, metastatic disease, perineural spread of tumor, and Lyme disease.

Thanks for checking out this quick video on the internal auditory canal. Be sure to check out the additional videos on other head and neck topics.


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