Salivary Glands

In this video, Dr. Bailey gives us an overview of salivary gland lesions, including briefly reviewing the normal anatomy and appearance of the salivary glands, common benign and malignant neoplasms, and other infectious, inflammatory, and systemic processes that may affect the salivary glands.

Salivary gland overview

There are three major sets of salivary glands, the parotid, submandibular, and sublingual glands. There are also minor salivary rests elsewhere. The parotid gland is the largest salivary gland, and drains through Stinson’s duct which empties near the 2nd molar. The submandibular and sublingual glands are in the floor of the mouth in the sublingual space.

Benign salivary gland neoplasms

There are a lot of salivary gland neoplasms, most of which are benign. A good tip is that the larger glands are more likely to have benign lesions. Most parotid lesions are benign, while minor glands have a higher percentage of malignant gland. The parotid is the most common location for both benign and malignant lesions.

The most common benign lesions are pleomorphic adenoma (benign mixed tumor) and Warthin tumors. Pleomorphic adenomas are the most common and tend to be homogeneously dense on CT. On MRI, they are relatively homogeneous, hypointense on T1, and VERY hyperintense on T2. They may have a fibrous rim. Warthin tumors are also benign, and are more common in older men. They are often bilateral, and tend to be more heterogeneous and less T2 hyperintense than pleomorphic adenomas. Bilateral tumors are more likely to be Warthin tumors.

Malignant salivary gland neoplasms

Mucoepidermoid carcinomas are the most common parotid malignancy. There is a lot of overlap with the appearance of benign lesions, but the margins tend to be more irregular. They may also have lower signal on T2. When you have malignant salivary gland lesions, you should check specifically for perineural spread, which can occur along the facial nerve up to the geniculate ganglion or along the trigeminal nerve to the foramen ovale.

Adenoid cystic carcinomas are more common in minor salivary glands and are the most common sinonasal salivary tumor. As the grade increases, they tend to be more T2 hypointense. There are also well known for perineural spread.

Parotid metastases are quite common because of intraparotid lymph nodes. Skin cancers and melanoma as well as lymphoma are common causes of metastatic disease. Like the other malignancies, they tend to have very irregular margins.

Inflammatory and other

Sjogren disease is an autoimmune disease of exocrine glands which results in a multinodular appearance of the parotid glands. Patients may have atrophy of the lacrimal glands. These patients have an increased risk of lymphoma.

Lymphoepithelial cysts are multifocal cystic lesions which are most often seen in patients with HIV due to lymphatic obstruction. They appear as bilateral parotid gland cysts.

Sialolithiasis is formation of stones (calculi) in the duct or parenchyma of glands. They are most common in middle age me and in the submandibular gland. This appears as very dense, calcified and well defined lesions either in gland or along the duct.

Sialadenitis is inflammation of the gland which can be caused by infection or inflammatory conditions. Ascending bacteria from the pharynx is the most common, but viruses and immune mediated causes are also possible.

Practice case

This is a relatively well-defined lesion in the superficial aspect of the left parotid gland. It is hyperdense and somewhat homogeneous, but superficial to the gland. If you review further, there is an additional superficial nodule, and this is spread of an adjacent malignancy. So, this case is malignant. An important lesson in evaluating salivary gland lesions is that you often cannot tell the difference between benign and malignant lesions, so biopsy is required.


Hopefully these cases taught you something about the normal appearance and anatomy of the salivary glands, some common tumors (both benign and malignant), and other conditions affecting the salivary glands. Be sure to check out the other videos on other head and neck topics.

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Stroke vascular distributions – Imaging Case Review

Dr. Bailey is back for a case-based review of stroke and the vascular distributions commonly seen in stroke.


In this video, we’ll review vascular territories in the brain as well as typical appearance of acute infarcts. This covers the distribution of the anterior cerebral artery (ACA), middle cerebral artery (MCA), posterior cerebral artery (PCA), cerebellar arteries, and basilar artery.

Case 1 – ACA infarct

This case shows an infarct in the right anterior cerebral artery distribution. There is loss of gray white differentiation on the CT. On MRI, it is even more apparent, with DWI abnormality which is dark on ADC. There is a corresponding abrupt occlusion of the ACA.

Case 2 – MCA infarct

In this case, there is hypoattenuation in the left posterior temporal lobe and inferior parietal lobe and posterior insular cortex. The MRI confirms that there is a stroke in this region. This is the posterior MCA distribution, with a posterior M2 branch occlusion

Case 3 – PCA infarct

There is subtle hypodensity in the left occipital lobe seen both on axial and sagittal CT. This is again confirmed on MRI, where there is T2 hyperintensity and diffusion abnormality. The MRA shows an abrupt cutoff of the left PCA.

Case 4 – Cerebellar infarct

This case shows a small, wedge shaped hypodensity in the left inferior cerebellum. MRI confirms abnormal diffusion in the left inferior cerebellum. In this case, the neck MRA shows

Case 5 – Multiple infarcts

This case shows multiple infarcts, including a right occipital and a left frontal infarct. When you have infarcts in multiple vascular territories, you should consider the possibility of a central source of thrombi, such as atrial fibrillation or cardiac disease, or vasculitis.

Case 6 – PCA plus

This case has an infarct in the left occipital lobe, but there is also hypoattenuation in the left midbrain and cerebral peduncle. MRI reveals even more areas of ischemia, including a small area in the right occipital lobe and multiple areas in the left thalamus. This indicates that the occlusion is more proximal and likely includes the basilar artery.

Case 7 – Medulla

This is a specific location which is frequently involved in infarcts, the lateral medulla. There is associated severe stenosis of the right vertebral artery.

Case 8 – Border zone

These are often seen as linear low attenuation along the border between vascular territories. In this case, it is the border between the ACA and MCA territories.

Special bonus case – artery of Percheron

This bonus case shows bilateral thalamic infarcts from an artery of percheron, a variant where the arterial supply for both thalami comes from a perforating branch on one PCA. This can also come from central venous thrombosis, so that is the other consideration

Special bonus case – venous infarct

If you have an infarction in an unusual location, particularly if associated with hemorrhage, then think about the possibility of sinus thrombosis. In this case, the straight sinus is dense and occluded on an MRV.


Hopefully these cases taught you something about the common locations of infarcts and their typical appearance on CT. Please check out the rest of the vascular and stroke content on the site.

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MRI of the Orbits

In this video, Dr. Bailey reviews the orbit on MRI, with a focus on anatomy and a few of the most common pathologies.


In this video, we’ll review the normal anatomy of the orbit and its appearance on MRI.

Orbital contents and normal anatomy

The postseptal orbit includes the intraconal (within the extraocular muscles) contents and extraconal contents. The muscles themselves are a muscular compartment, but it is useful to think of them in the extraconal compartment. There are many things you’ll find in the orbit, including the muscles, the optic nerve, arteries and veins, and fat.

On pre- and post-contrast imaging, you can identify which structures enhance. The optic nerves, for example, should not normally enhance. Lacrimal glands, the extraocular muscles, and sinus mucosa enhance normally.

Optic nerve

The optic nerve can be affected by masses, infection and inflammation, demyelination, and other pathologies. Optic neuritis is inflammation of the nerve, which is usually seen by enhancement in the optic nerve itself. Radiation can cause optic neuropathy, which may even be bilateral. Optic gliomas are tumors that affect the optic nerve and are associated with neurofibromatosis. Optic nerve ischemia can also cause optic neuropathy, often in the acute setting. Optic nerve atrophy is chronic volume loss that can occur from prior insult. It can be hard to determine which of the nerves is abnormal when they are asymmetric.

Optic nerve sheath and retroorbital fat

The optic nerve sheath and periorbital fat are subject to different pathologies, including perineuritis, idiopathic orbital inflammation, sarcoid, certain tumors such as meningioma, lymphoma, and metastatic disease, and idiopathic intracranial hypertension.


The globes can be affected by inflammation, tumors, and degenerative changes. Inflammation can affect the entire globe or only portions, such as the posterior sclera. Phthisis bulbi is a chronic atrophy of a non-functional globe. Melanoma is a relatively common malignancy of the uvea, but can be hard to see. It is sometimes manifested as an intrinsic T1 hyperintense mass. Retinal detachment can often be seen on MRI as well.

Orbital apex

Cranial nerves and vessels are the main things passing through the orbital apex, and pathologies that you see probably arise from one of them. Slow flow venous malformations (previously called hemangiomas) are well circumscribed vascular lesions often occurring in the orbital apex and orbit. Masses such as meningioma also occur at the orbital apex.

Extraconal compartment

The extraconal structures include the muscles, lacrimal ducts, fat, and the periosteum. A common cause of extraocular muscle abnormality is thyroid ophthalmopathy, which causes bilateral symmetric enlargement that spares the myotendinous junction. Lymphoma can cause masses of the extraocular muscles or lacrimal ducts and often restricts diffusion. Infection can extend from the sinuses into the extraconal compartment and even extend intracranially. The lacrimal glands are subject to their own specific pathology. They can get inflammatory changes related to idiopathic orbital inflammation or sarcoidosis. Dermoids are well-defined masses in the orbit, likely near suture lines. Osseous lesions can also extend from the orbits into the orbital walls.


Hopefully you learned a little bit about the anatomy and common pathology of the orbit. 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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Brain Vascular Malformations

In this video, Dr. Bailey discusses the most common vascular malformations and reviews the most common grading system for arteriovenous malformations (AVMs), the Spetzler-Martin grading scale.

Introduction to arteriovenous malformations

Arteriovenous malformations are vascular anomalies consisting of feeding arteries, a nidus where the shunt is located, and one or more draining veins. AVMs can be compact or have a diffuse nidus. There can be surrounding gliosis and potentially calcification on CT or calcium sensitive imaging. Imaging will demonstrate flow voids,

Spetzler-Martin grading scale

The Spetzler-Martin scale gives a score between 1-5, with points assigned based on size (< 3 cm, 1 point; 3-6 cm, 2 points, and > 6 cm, 3 points), involvement of eloquent cortex (1 point), and involvement of deep veins (1 point). This score can help predict the potential surgical morbidity and mortality.

Arteriovenous fistulas

Arteriovenous fistulas (AVFs) are abnormal shunts most commonly from dural vessels. These are abnormal connections between these arteries and the dural venous drainage. Often external carotid artery branches will be dilated as they are the abnormal supply. There is arterialization of the dural venous sinuses. These are most common at the transverse-sigmoid sinus junction.

Cavernous malformations

Cavernous malformations are slow flow venous malformations that have well contained abnormal veins and vessels. They have areas of hemosiderin with T1 hyperintensity, T2 hyperintensity centrally and a peripheral hemosiderin rim. They may have an abnormal adjacent vessel or developmental venous anomaly (DVA). On CT, they may be hyperdense and can be confused with hemorrhage, but central calcification is a good clue. Multiple cavernous malformations can occur in familial syndromes.

Developmental venous anomaly (DVA)

DVAs are congenital venous malformations draining normal veins. These are the most common vascular malformation and are benign. They appear as a branching tree of abnormal venous drainage going to normal veins.

Capillary telangiectasia

These are slow flow capillary malformations that are incidentally found. They have stippled enhancement and you may see something on the blood sensitive imaging (GRE or SWI). There is usually no abnormal edema or FLAIR.

Thanks for tuning in to this video about intracranial vascular malformations. Please check out the additional vascular videos on the site.

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Circle of Willis

In this video, Dr. Bailey reviews the anatomy of the Circle of Willis, or the confluence of the internal cerebral and basilar arteries within the brain. She reviews the normal anatomy, talks about some common variants you may encounter, and introduces a few less common variants.

Introduction to the Circle of Willis

The Circle of Willis is the circular anatomical construct of vessels made up by the internal carotid arteries, the basilar artery, and their intracranial proximal branches. This includes the anterior and posterior communicating arteries and the anterior, middle, and posterior cerebral arteries.

Posterior circulation

The posterior circulation includes the posterior cerebral arteries, the basilar artery, the superior cerebellar artery, the anterior inferior cerebellar artery (AICA), and the posterior inferior cerebellar artery (PICA). The AICA is particularly variable and may be hard to see, particularly on 3D imaging. The PICA arises from the vertebral artery and may also vary in size from one side to the other.

Common variants

One particularly common variant is a vertebral artery that terminates in PICA. That is, there is either no or a very vertebral artery is seen distal to the PICA origin. Dolichoectasia is a tortuous and prominent basilar artery larger than 4.5 mm in transverse diameter. It is also a common variant to have no posterior communicating arteries (P-comms). A fetal PCA, is vessel that arises from the posterior communicating artery with an absent or very small P1 segment of the PCA. A hypoplastic A1 is a small A1 on one side, with both A2 segments arising from one side. The A1 segments may arise at various levels and be tortuous. An azygous ACA is a single, or unpaired, ACA in the A2 segment where both sides fuse and there is a common ACA. Sometimes you can have the opposite and have 3 A2 segments. Any of the arteries can also be duplicated, or you can have a fenestration, a small wall within the center of the vessel. Fenestrations can mimic thrombus but they are often very linear along the course of the vessel.

Less common variants

The persistent trigeminal artery is a persistent fetal connection between the anterior and posterior circulation at the level of trigeminal artery. It is the most common persistent fetal connection and passes through Meckel’s cave (the trigeminal cistern).  

It’s also possible to see a missing vessel, such as an absent ICA. In these cases, they may be congenitally absent or chronically occluded.

Thanks for tuning in to this video about the normal and variant anatomy of the circle of willis. Please check out the vascular imaging page on the site.

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Intracranial aneurysms

In this video, Dr. Bailey reviews intracranial aneurysms, including an overview of what an aneurysm is, how to find them, and tips for searching for aneurysms. The first part of this video covers general principles of aneurysm evaluation and the second part shows 3 sample cases that you can go through to test your individual skills.

Introduction and definition of aneurysm

An aneurysm is an abnormal outpouching of the intracranial vessel. Intracranial aneurysms are true aneurysms, which typically involve all of the layers of the vessel. To find aneurysms, a type of vascular imaging known as an angiogram (which can also be done with CT or MRI) is done to evaluate the arteries.

How to find aneurysms

To find aneurysms, you should be looking for an abnormal dilation of the vessel. Then you should look at the most common locations, which are the anterior communicating artery, the carotid terminus/posterior communicating artery, the middle cerebral artery, and the posterior circulation/basilar tip.

Saccular versus fusiform aneurysm

Saccular aneurysms are the most common type of aneurysm. They are rounded outpouchings of the vessel. Fusiform aneurysms are circumferential areas of enlargement of the vessel, meaning the whole diameter is increased.

Thrombosed aneurysm

Sometimes aneurysms can be thrombosed, meaning they no longer have blood flow. In these cases, their imaging appearance can change, and they may not show up on angiographic imaging.

Tips for reporting aneurysms

When creating a report about an aneurysm, you should describe where the aneurysm is, which direction it points, and its size. It’s common to measure three sizes, the maximal width, the height, and the width at the neck.

Aneurysm treatment

The two most common treatments for aneurysm are surgical clipping, in which a clamp is placed over the base of the aneurysm, and endovascular coiling, in which small coils are placed within the vessel from inside. It is also possible to use stents to treat aneurysms, either in combination with coils or alone.

Practice cases

Take a crack at 3 practice cases at the end of the video.

Hopefully you learned a little bit about finding and reporting intracranial aneurysms. Please check out the additional vascular videos on the site, including the video on 5 quick ways to improve your aneurysm search pattern.

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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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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.

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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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