Spaces of the Head and Neck

This video describes the soft tissue spaces of the head and neck, including common normal anatomy and structures found in each region as well as potential pathology that can commonly arise there. By knowing the spaces, you can be more prepared to determine what diseases might occur there and formulate a better differential diagnosis.

 

Masticator space. Contains the muscles of mastication, the mandible, branches of the trigeminal nerve, lymph nodes, and minor salivary glands. 

Parotid space. Contains deep and superficial portions of the parotid gland, branches of the facial nerve, lymph nodes, the retromandibular vein, and the external carotid artery and its branches.

Carotid space. Contains the carotid sheath, internal jugular vein, cranial nerves IX-VI, sympathetic nervous system branches, and lymph nodes.

Parapharyngeal space. Predominantly composed of fat, with minor salivary glands and lymph nodes. Most useful for how it is displaced (medially if it is in the masticator space, carotid space, or parotid space, or laterally if it is a mucosal lesion)

Retropharyngeal space. Contains, fat, lymph nodes, and minor salivary glands. 

Perivertebral/vertebral space. Contains muscles, the vertebral bodies, fat, blood vessels, and nerve roots.   

Infrahyoid visceral space. Contains the thyroid and parathyroid gland, the esophagus, and the trachea. Vessels and nerves are also found here.

Check out more of our content on head and neck imaging by seeing all H&N related posts or on the H&N Imaging Topic page.

 

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Head and neck anatomy landmarks

Today, Dr. Bailey is back with a video about her approach to head and neck anatomy using landmarks. With this quick video, in about 5 minutes you can learn to quickly differentiate the important anatomical subsites of the head and neck on computed tomography.

 

Nasal cavity versus the nasopharynx. The nasal cavity and nasopharynx are both above the hard palate up to the cribriform plate. The nasopharynx begins just behind the posterior margin of the hard palate

Oral cavity vs oropharynx. Similarly, the oral cavity includes the tissue below the hard palate and anterior to its posterior margin, while the oropharynx includes what is posterior to the margin of the hard palate.

Floor of the mouth. The floor of the mouth is predominantly made of muscular structures, including the genioglossus, hyoglossus, and mylohyoid.

Hypopharynx. The hypopharynx consists of the pyriform sinuses, the lateral and posterior pharyngeal walls, and the posterior surfaces of the larynx extending to the cervical esophagus.

Supraglottic larynx. The supraglottic larynx includes everything from the tip of the epiglottis down to the laryngeal ventricle.

Larynx-glottis. The glottis includes the larynx and true vocal cords, including the anterior and posterior commissures.

Larynx-subglottis. The subglottis extends from the inferior aspect of the true vocal cords to the cricoid cartilage. Below the cricoid cartilage is the trachea.

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Cervical Lymph Node Stations – a landmark approach

In this quick video, Dr. Bailey walks us through a quick overview of 6 of the common cervical nodal stations in the neck. Each lymph node in the neck is assigned one of these 6 levels based on their relationship with normal anatomic structures in the neck. These stations are important in communicating with other physicians which abnormal nodes we are talking about.

By using only these 8 landmarks, you can feel confident that you are properly identifying the right nodal locations:

1. Anterior belly digastric
2. Submandibular gland
3. Hyoid bone
4. Cricoid cartilage
5. Sternocleidomastoid muscle
6. Clavicles
7. Carotids
8. Sternum

Hopefully this helps you be more clear in your reports and better understand the different lymph node levels in the neck.

Thanks for tuning in and 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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Temporal bone CT – Pathology based approach

In this second video about the temporal bone, Dr. Katie Bailey from the University of South Florida goes over some common pathology of the temporal bone. If you haven’t seen the first video and want to learn more about a general approach to reviewing temporal bone CT, go back and check out the first video.

The overview puts this video in the context of the outside-in approach reviewed in the first video. You can think about which diseases are most prevalent in each compartment based on location. A general differential of infection, inflammation, and tumor is a good place to start.

Otitis externa – a common pathology characterized by thickening of the mucosa of the external auditory canal. It may be accompanied by fluid in the mastoids and middle ear.

Malignant otitis externa – a variant of otitis externa in which you have destruction of the adjacent bone. You can also have soft tissue or intracranial abscesses as a complication.

External auditory canal neoplasm – soft tissue in the external auditory canal with adjacent bone destruction. The imaging appearance overlaps with malignant otitis.

Otitis media – characterized by fluid within the middle ear and around the ossicles. Most commonly in the mesotympanum and hypotympanum. There is often associated fluid in the mastoid air cells (otomastoiditis).

Cholesteatoma – a soft tissue mass often originating in Prussak’s space which results in blunting of the scutum and bone erosion.

Ossicular disruption – the ossicular chain can be disrupted, most often in trauma. The most common disruption is the malleoincudal joint, or loss of the “ice cream cone”.

Aberrant ICA – as a variant, the internal carotid artery can be located too medially, where it will lack a complete bony covering in the foramen lacerum. This can lead to complications of mastoid surgery and is important not to miss.

Dehiscent jugular bulb – the jugular vein should also have a bony covering between it and the middle ear.

Tympanicum paraganglioma (glomus tympanicum) – a vascular tumor of the middle ear starting at the cochlear promontory.

Labyrinthitis ossificans – sclerosis of the cochlea or semicircular canals. The cochlea or semicircular canals may be narrowed or sclerotic, usually from prior infection.

Semicircular canal dehiscence – loss of bone adjacent to the semicircular canal. This most commonly occurs along the superior aspect of the superior semicircular canal.

Otosclerosis – abnormal bone most commonly in the fissula ante fenestrum, manifested by lucent bone where it should be dense cortical bone.

Facial nerve – the facial nerve should have a smooth bony covering around it. If you see loss of bone, you should think about a hemangioma or a facial nerve schwannoma, two tumors that frequently occur in this area.

Thanks for tuning in and be sure to come back to check out part 1, temporal bone CT search pattern. Or you can see all of the temporal bone videos or all the search pattern videos.

 

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Temporal bone CT search pattern

Today we have a special guest, Dr. Katie Bailey from the University of South Florida who is presenting her approach to the temporal bone. Special thanks to her for this great video, and hopefully we will be having a lot of great new content from her in the future. This video will be part 1 of 2 in overviewing a starting approach to reviewing the temporal bone.

In this video, she goes through her structure approach to CT of the temporal bone. This approach is based upon an outside-in strategy, where you first look at the external ear, the middle ear, and then the inner ear. The coronal view is a nice place to start.

The key feature of the external ear is the external auditory canal, which should be patent but have a thin lining of mucosa. The external auditory canal ends at the scutum a thin sliver of bone along the top of the EAC.

The middle ear begins at the tympanic membrane, which should be so thin you can barely see it. The tympanic membrane articulates with the long arm of the malleus. A key space above the scutum is called Prussak’s space, which is a common location for cholesteatomas. The middle ear should only contain soft tissue and air. The middle ear is divided into upper (epitympanum), middle (mesotympanum), and lower (hypotempanum) segments. You should also be able to see the footplate of the stapes articulating with the oval window.

The mastoids connect with the middle ear and should be filled with air (no fluid or soft tissue). The roof of the mastoids is the tegmen mastoideum.

The inner ear contains the cochlea and semicircular canals. The cochlea should have 2 ½ turns and be surrounded by bright cortical bone. You have 3 semicircular canals (superior, lateral, and inferior) and should be about the same width. The internal auditory canal is hard to evaluate by CT but should be roughly a similar diameter with no expansion or loss of bone.

The facial nerve canal can be confusing. It is easiest to find at the stylomastoid foramen. You can follow it superiorly before turning and going under the lateral semicircular canal. The bone should be intact until it reaches the geniculate ganglion.

You can then turn to the axial views and review the ossicles. The malleus and incus should look like an ice cream cone. Another key feature is the fissula ante fenestrum, or the cortical bone next to the cochlea. This is a common place where otosclerosis can begin.

Finally, you want to review the axial images for everything out of the temporal bone. This includes the brain, sinuses, orbits, nasal cavity, salivary glands, and visible portions of the pharynx.

Summary. A coronal, outside-in approach to the temporal bone is a nice way to systematically review the temporal bone.

Thanks for tuning in and be sure to come back to check out part 2, temporal bone pathology. Or you can see all of the temporal bone videos or all the search pattern videos.

 

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Vascular imaging of the head and neck course

This is a short course in learning about vascular imaging of the head and neck. The first videos have an overview of how to approach these studies, while the additional videos show you specific cases.

The cases are accessible on the vascular capstone page to view them yourself.

Multiple sclerosis – white spots and red flags – part 2

Mimics and Variants

Demyelinating disease is a common situation we encounter in neuroradiology, and properly diagnosing and tracking it using MRI is a key skill for neuroradiologists. In this second part of the lecture, Dr. Michael Hoch gives us some tips about other causes of white matter lesion, and information we can use to make our imaging diagnosis of multiple sclerosis more specific.

Clinical history has an important role in determining how specific imaging findings are for multiple sclerosis. Some features may suggest that a patient does not have multiple sclerosis, such as if they are the wrong age (< 20 or > 50 years old), if they have abrupt swift progression, if they have systemic symptoms such as fever or weight loss, and if they have uncommon CNS symptoms such as a movement disorder or meningitis signs. MS lesions also usually occur in some specific locations, such as in the corpus callosum, temporal lobe, periventricular white matter, and juxtacortical white matter.

Mimics of Multiple sclerosis

So, what are some of the common mimics of MS?

Migraine – migraine is the most common cause of non-specific white matter abnormalities in young patients, occurring in more than 50% of patients with migraine

Chronic small vessel ischemia – more common with increasing age, and worsening with risk factors such as diabetes, hypertension, and smoking

CNS vasculitis – an inflammatory syndrome of the intracranial vessels. Be on the lookout if someone has a history of TIAs or thunderclap headache, or systemic symptoms.

Behcet’s disease – a vasculitis most common in young males, characterized by brainstem involvement and oral ulcers

Susac syndrome – an autoimmune microangiopathy overlapping MS in age distribution. However, patients more often have a triad of encephalopathy, hearing loss, and visual changes. Corpus callosum involvement is more likely to be central. 

CADASIL – an autosomal dominant syndrome characterized by frequent infarcts. Look out for the characteristic locations in the temporal poles, external capsules, and paramedian superior frontla lobes. It is also usually quite symmetric.

Other rarer mimics are Neuro-Sweets disease and Lyme disease, which can cause white matter abnormalities.

Key take home points of this lecture include:

  • Multiple sclerosis is a clinical diagnosis, not an MRI diagnosis
  • White spot lesion location matters
  • Juxtacortical lesions must touch the cortex
  • Aggressively window the spine to look for cord lesions
  • Leptomeningeal enhancement is possible in multiple sclerosis

Variants of demyelinating disease

There are several common variants that you should know about across the demyelinating spectrum:

ADEM – acute disseminated encephalomyelitis – an autoimmune mediated and often self limited fulminant demyelinating process. May be related to a viral illness or vaccination.

Marburg disease – a clinically fulminant demyelinating disease usually affecting younger patients with a febrile prodrome.

Balo concentric sclerosis – a rare and monophasic demyelinating disease characterized by large lesions with alternating zones of demyelination/myelination

Tumefactive demyelinating lesions (TDL) – large and often fulminant demyelinating lesions that have mass effect and can mimic tumors. Perfusion imaging with low blood volumes can help differentiate from masses.

Neuromyelitis optica (NMO) – a demyelinating syndrome characterized by post-chiasmatic optic neuritis and long segment spine lesions. This is mediated by an aquaporin-4 antibody.

Progressive multifocal leukoencepalopathy (PML) – a JC virus mediated demyelinating lesion that occurs in immune suppressed patients. Usually has little or no enhancement and favors a subcortical location.

Summary

In summary, there are a couple of key things to keep in mind when evaluating potential demyelinating lesions:

  • Read the chart for clinical red flags
  • Look at the MRI for imaging red flags, like strokes, hemorrhages, cysts, findings that are too symmetric, subcortical, or normal
  • Remember that white matter lesions from migraine and microvascular disease are far more common that multiple sclerosis
  • NMO has differentiating features
  • PML is a rare complication of immune suppressing medications in MS patients

 

The level of this lecture is appropriate for radiology residents, radiology fellows, and trainees in other specialties who have an interest in imaging or treating patients with potential demyelinating diseases.

This video is part of a two part series on multiple sclerosis presented by Dr. Hoch.

If you haven’t seen it already, go back and check out part 1, in which Dr. Hoch discusses the key findings of demyelinating lesions.

Multiple sclerosis – white spots and red flags

Demyelinating disease is a common situation we encounter in neuroradiology, and properly diagnosing and tracking it using MRI is a key skill for neuroradiologists. In this two part lecture, Dr. Michael Hoch instructs us on how to approach white matter abnormalities in the brain and use them towards making a diagnosis of multiple sclerosis. The first part is focused on key tips on making a diagnosis of demyelinating disease while the second is focused on potential pitfalls.

Be sure to watch them both to get the complete overview of imaging findings of common autoimmune and inflammatory conditions.

Multiple sclerosis – white spots and red flags – part 1

Making the diagnosis

Demyelinating disease is a common situation we encounter in neuroradiology, and properly diagnosing and tracking it using MRI is a key skill for neuroradiologists. Today, Dr. Michael Hoch gives the first part of a two part lecture on how to approach white matter abnormalties in the brain and use them towards making a diagnosis of multiple sclerosis.

Multiple sclerosis is a clinical diagnosis that depends on several possible presenting signs (such as depression, fatigue, vertigo, numbness or other neurological symptoms, bladder dysfunction, visual changes, or other phenomena including L’Hermitte’s sign or Uhthoff’s phenomenon) and other clinical sign (including tremor, decreased perception, hyperreflexia, and ataxia).

The imaging diagnosis of multiple sclerosis is based on the McDonald criteria, most recently revised in 2017. This requires dissemination in space, dissemination in time, and lack of an alternate explanation. You should evaluate different spaces for white matter abnormality, including the cortex, juxtacortical, subcortical and deep white matter, corpus callosum, and deep white matter, periventricular white matter. 

The locations of the lesions can provide a clue as to whether white matter lesions are more likely to be caused by demyelinating disease or other nonspecific insults, such as chronic microvascular ischemia. For instance, central lesions in the pons or lesions in the deep white matter are more nonspecific, while cortical/juxtacortical, periventricular, and anterior temporal lesions are more specific for multiple sclerosis.

The enhancement pattern is also a clue to whether a lesion might be demyelinating. Demyelinating lesions typically have an incomplete rim of enhancement, where the post-contrast enhancement has a broken circle type of appearance. Leptomeningeal enhancement can often be seen in patients with MS, although it is an alarm bell if patients don’t have a known diagnosis, as it can represent other diseases such as leptomeningeal carcinomatosis.

Key take home points of this lecture include:

  • Multiple sclerosis is a clinical diagnosis, not an MRI diagnosis
  • White spot lesion location matters
  • Juxtacortical lesions must touch the cortex
  • Aggressively window the spine to look for cord lesions
  • Leptomeningeal enhancement is possible in multiple sclerosis

 

The level of this lecture is appropriate for radiology residents, radiology fellows, and trainees in other specialties who have an interest in imaging or treating patients with potential demyelinating diseases.

This video is part of a two part series on multiple sclerosis presented by Dr. Hoch.

For the next part of the lecture, check out part 2, in which Dr. Hoch discusses potential mimics and pitfalls when assessing for demyelinating disease.

Imaging CNS autoimmune and inflammatory disease

Vascular Processes

This is the sixth and final lecture in a case based review of imaging of the brain and spine for autoimmune and inflammatory conditions. We will cover the MRI findings of some of the common conditions and some potential pitfalls and mimics.

This lecture covers intracranial vasculopathies, including central nervous system (CNS) vasculitis, Moya Moya disease, CADASIL, and MELAS. These vasculopathies can have a similar imaging appearance.

CNS vasculitis

CNS vasculitis is a process affecting the vessels which supply the brain with blood/oxygen. This can be a primary CNS process or can be associated with other systemic vasculopathies, such as lupus. The imaging manifestations are unexpected infarcts that are out of proportion for age and other causes of infarct. On vascular imaging, you will see areas of narrowing followed by areas of dilation or normal caliber, almost like beads on a string. While this can be caused by atherosclerotic disease, usually it will be out of proportion for age.

Vessel wall imaging

Vessel wall imaging is a specialized technique to look for inflammation in the walls of intracranial vessels. This consists of specialized sequences that suppress both fat and flow so you can see enhancement in the walls. On vessel wall imaging, vasculitis tends to enhance circumferentially while atherosclerotic disease enhancement is more eccentric. This is a useful advanced technique.

Moya Moya disease

Moya moya disease is a primary obliterative angiopathy which primarily occurs in young Asian women. In this disease, the large vessels of the circle of Willis, namely the middle cerebral artery, are obliterated and replaced with a number of abnormal collateral vessesl. This leads to a characteristic “puff of smoke” appearance on angiography. Patients may present with multiple strokes or hemorrhage and can be treated with ECA/ICA bypass. There are other causes of a moya moya like appearance, as it can happen with anything that causes chronic obliterative angiopathy, like sickle cell disease. However, although the terms are used interchangeably, this is really a moya moya syndrome, not the primary disease..

CADASIL

CADASIL, or cerebral autosomal dominant arteriopathy with subcortical infarcts and leukencephalopathy, is a genetic condition associated with the NOTCH3 gene abnormality. These patients have small and middle vessel abnormalities which manifest as a number of subcortical strokes and white matter abnormality in the bilateral temporal lobes. If you see abnormal subcortical temporal white matter, think about CADASIL.

MELAS

MELAS, or mitochondrial encephalopathy with lactic acidosis and stroke-like symptoms, is a similar syndrome where you get stroke-like episodes often preferentially involving the temporal and parietal lobes. They can often improve with time, but it can mimic other vasculopathies and strokes.

Summary and Conclusion

There are a number of vasculopathies which can affect the brain, with the most common being CNS vasculitis and moya moya disease or syndrome. CADASIL and MELAS can also have a similar appearance. This is the last lecture in this series. Please be sure to check out the other lectures in this series.

The level of this lecture is appropriate for radiology residents, radiology fellows, and trainees in other specialties, such as neurology, who have an interest in neuroradiology or may see patients with CNS demyelinating or inflammatory conditions.

Other videos on the autoimmune and demyelinating playlist are found here