Fast 10: Neuroradiology high speed case review part 6 – Cases 51-60
In this 6th video, we present 10 more neuroradiology high speed review cases so you can review them quickly before your exams. If you want to see more information about these cases, you can find longer versions on the channel under the Board review playlist
Fast 10: Neuroradiology high speed case review part 5 – Cases 41-50
In this 5th video, we present 10 more neuroradiology high speed review cases so you can review them quickly before your exams. If you want to see more information about these cases, you can find longer versions on the channel under the Board review playlist
Cases included in this set: Subependymoma CNS lymphoma Metastatic disease to calvarium Meningioma Metastatic melanoma Hypothalamic hamartoma Pituitary adenoma (with hemorrhage/apoplexy) Pilocytic astrocytoma Cerebellopontine angle meningioma Glioblastoma
Be sure to check back in for the remainder of the high speed cases.
Fast 10: Neuroradiology high speed case review part 4 – Cases 31-40
In this fourth video, we present 10 more neuroradiology high speed review cases so you can review them quickly before your exams. If you want to see more information about these cases, you can find longer versions on the channel under the Board review playlist
Cases included in this set: Renal cell carcinoma Tuberculosis discitis osteomyelitis Osteosarcoma of the spine Ischemia with penumbra (tissue at risk) Traumatic spine epidural hematoma Thoracic spine meningioma Benign perimesencephalic subarachnoid hemorrhage Chiari malformation Traumatic vertebral artery injury Temporal lobe anatomy – fusiform gyrus
Be sure to check back in for the remainder of the high speed cases.
Fast 10: Neuroradiology high speed case review part 3 – Cases 21-30
In this third video, we present some 10 more neuroradiology high speed review cases so you can review them quickly before your exams. If you want to see more information about these cases, you can find longer versions on the channel under the Board review playlist
Fast 10: Neuroradiology high speed case review part 2 – Cases 11-20
In this second video, we present some 10 more neuroradiology high speed review cases so you can review them quickly before your exams. If you want to see more information about these cases, you can find longer versions on the channel under the Board review playlist
These videos focus on going quickly through neuroradiology cases, spending about 1 minute per case to get you through 10 cases in 10 minutes. Ideal for a quick review before an exam or neuroradiology rotation. An ideal way to go through a lot of cases quickly.
Each case shows a couple of images with a multiple choice question, followed by a quick review of the answer and the diagnosis.
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
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.
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.
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