Imaging description

The spectrum of chronic sinusitis is wide and includes diverse etiologies such as pyogenic, allergic, and fungal. In patients with a known history of allergies and with sinonasal polyposis, the body’s immune system responds to the presence of fungal elements within the paranasal sinus infection, leading to overproduction of eosinophilic mucin [1]. This is generally seen in immunocompetent, non-diabetic, and otherwise healthy populations. It is most commonly seen in young male adults in warm and humid climates.

On CT, there is opacification and expansion of multiple paranasal sinuses containing a centrally high-attenuating dense material (Fig. 68.1). On MRI, a central variable T1 and low T2 signal representing eosinophilic mucous is surrounded by low T1 and high T2 signal of the thickened mucosa (Fig. 68.2) [2,3]. The signal may be so low on T2-weighted images that it can mimic air (Fig. 68.2B).

Importance

The clinical spectrum of chronic rhinosinusitis represents diverse etiologies. Making the correct diagnosis of allergic fungal sinusitis allows for more accurate treatment options for this condition, including surgical resection and debridement.

Typical clinical scenario

The presence of chronic rhinosinusitis with nasal discharge and congestion, headaches, fever, and facial pain and pressure is common. The maxillary sinus is the most commonly involved sinus. The pain may be infraorbital or periauricular. Involvement of frontal sinus results in headache of forehead and supraorbital region. A history of allergies and underlying nasal polyp is common in these patients. In severe cases with bony remodeling and orbital complications, facial deformity, proptosis, and diplopia can be seen.

Imaging description

Cavernous malformations (CMs) are angiographically cryptic vascular malformations of the brain and spinal cord that consist of discrete, honeycomb-like masses of endothelial-lined sinusoidal spaces. These are circumscribed lesions and consist of thrombosed blood. While the majority of these lesions are solitary, multiplicity may occur in nearly 20% of patients. Multiple lesions are more common in genetic/familial forms of CMs.

Cross-sectional studies identify and characterize the majority of these lesions, and these are nearly always occult on angiography [1]. CT demonstrates well-defined, focal hyperdense masses that may have internal, speckled calcifications. There is a lack of mass effect or edema, differentiating these from brain neoplasms. MRI is far more sensitive, as well as more specific, in the diagnosis of CMs. The MR appearances parallel the pathoanatomic changes on histologic exam. There is internal heterogeneity, and “popcorn”-type areas of high T1 signal from subacute blood products (methemoglobin) are often noted [1]. There is a peripheral rim of hemosiderin around the lesion, generally indicative of seepage of blood breakdown products in the periphery of the mass. This rim is best noted on T2-weighted sequences, although even more marked blooming is observed on gradient echo (GRE) and susceptibility-weighted imaging (SWI) sequences (Fig. 17.1). There is no edema and generally no adjacent arterial vessels. CMs have a known association with developmental venous anomalies.

Imaging description

Repeated otorrhea and recurrent parotid swelling in infancy and childhood should prompt further cross-sectional imaging. One of the most important causes for this condition is infected first branchial cleft cyst. The branchial anomalies occur as a result of persistence of vestigial remnants of first branchial apparatus [1,2]. They are rare lesions. The first branchial cleft cyst accounts for only 8–10% of branchial cleft anomalies. They are divided into two major types [3]. Type I first branchial cleft cyst occurs in the preauricular area and lies parallel to the external artery canal (EAC) and lateral to the facial nerve (Fig. 76.1). Type II first branchial cysts are located posterior or inferior to the angle of the mandible and are intimately associated with the parotid gland and facial nerve (Fig. 76.2). There is generally presence of a sinus track reaching up to the junction of the membranous and bony portion of the external auditory canal and in close proximity to the facial nerve [2,3].

Importance

The first branchial cleft anomalies are relatively rare. A high index of suspicion in patients with a cyst or sinus around EAC and within the parotid gland is important. Incision and drainage of suppurative fluid collection can result in repeated recurrence. Definitive total surgical excision, achieved with a superficial parotidectomy approach with facial nerve identification and facial nerve exposure, results in excellent outcomes [4].

Imaging description

Cervical myelopathy (CM) can result from extrinsic compression of the cord or cord inflammation, demyelination, ischemia, or infection. The most common reason for CM is spondylosis of the cervical spine. MRI is the modality of choice in the work-up of CM, and it can differentiate intrinsic cord lesions from extrinsic ones such as cervical spondylosis. In patients with CM secondary to cervical spondylotic changes, MRI shows narrowing of the spinal canal, complete effacement of the CSF spaces at the stenotic level(s), and deformity of the cord, although presence of these findings does not always predict clinically detectable CM. Although the primary mechanism of cervical spondylotic myelopathy is the compression of nervous tissue, there is some evidence that ischemia at the cellular level may be a contributing factor [1].

Increased T2 signal within the cord at the level of compression can be seen in some patients and heralds a worse outcome after surgical decompression compared to patients who do not have increased T2 signal in their cords [2]. Other factors that are associated with lack or diminished levels of improvement following surgery include old age, longer duration of symptoms, diminished T1 signal in the cord, and worse preoperative neurologic status [2–4].

Imaging description

Invasive fungal sinusitis occurs predominantly in immunocompromised patients or patients who are on chronic steroid therapy or have diabetes. The most dreaded acute invasive form is seen in severely immunocompromised patients, while the chronic form is more common in diabetics.

In acute invasive fungal sinusitis, there is rapid invasion of mucosa, submucosa, and blood vessels with neutrophilic infiltrates. On CT, there is complete or partial soft tissue opacification of the paranasal sinus with mucosal thickening. Areas of bone erosion are common, with infiltration of adjacent fat and soft tissues (Fig. 69.1), but can be subtle. Intraorbital and intracranial extension takes place along the perivascular or perineural spread [1] or through direct bony invasion (Fig. 69.2). On MRI, the sinus secretions exhibit low T1 and high T2 signal [2]; however, high T1 signal may suggest proteinaceous content or fungal aggregation [3]. Fungal elements may also cause low T2 signal, which can look analogous to air within the sinuses (Fig. 69.3). When the sphenoid sinus is involved, there is a high incidence of cavernous sinus thrombosis and obliteration of the internal carotid artery (Fig. 69.2). Intracranial extension through cribriform plate and orbital invasion is common when ethmoidal sinuses are involved. Involvement of the maxillary sinus results in encroachment of retroantral fat or premaxillary soft tissue. Mucormycosis is more commonly associated with acute invasive fungal sinusitis, while in more than 50% of cases with chronic invasive fungal sinusitis Aspergillus fumigatus is the culprit.

Imaging description

Malignant otitis externa (MOE) is an uncommon infection of the external auditory canal (EAC) that has a propensity to spread outside the temporal bone. MOE is seen in elderly diabetic patients, and Pseudomonas aeruginosa is the most common organism responsible. Infection from the EAC spreads through the small perforations along the floor of the cartilaginous portion of the EAC and extends medially to the skull base including the jugular canal and stylomastoid foramen, nasopharynx, parapharyngeal space, parotid space, and infratemporal fossa. More medial and superior extension results in involvement of the petrous apex, dural sinuses, meningies, and brain [1]. Involvement of the stylomastoid foramen leads to facial nerve paralysis, and this is the most commonly involved cranial nerve in MOE. Involvement of the jugular foramen causes deficits of cranial nerves IX, X, and XI, and petrous apex involvement may result in trigeminal and abducens nerve palsies.

The diagnosis of MOE is difficult and requires the presence of clinical, radiologic, and microbiologic findings. Demonstration of bone involvement in the mastoid and soft tissue involvement outside the EAC is diagnostic of MOE in the appropriate clinical setting (Figs. 66.1, 66.2). CT is usually the first imaging study obtained, and it is very accurate in demonstrating bone erosion, which is present in about 70% of cases [2]. Often, cortical bone erosion is very subtle and requires careful scrutiny of all cortical margins of the mastoid bone. Tc-99m MDP bone scan is much more sensitive than CT and is positive in essentially all cases of MOE, although its specificity is quite poor. Soft tissue involvement outside the EAC can be seen on CT, although findings are often subtle. MRI is much more accurate in the assessment of the extent of disease because of its superior contrast resolution and multiplanar capability (Fig. 66.1).

Imaging description

Cystic mass lesions of the nasopharynx are common and often encountered incidentally on CTs and MRIs done for other reasons. The most common cystic masses seen in the nasopharynx are mucous retention cysts (MRC), which are often asymptomatic. MRC can occur anywhere in the upper aerodigestive system, but the nasopharynx is the most frequent site, followed by the valleculae. MRC wall has a pseudostratified ciliated epithelium and the cyst contains fluid that appears hypoattenuating on CT, hypointense on T1-weighted MRI, and markedly hyperintense on T2-weighted MRI, although cysts with a high protein content can demonstrate increased T1 and decreased T2 signal (Fig. 77.1) [1].

MRCs can be found anywhere in the nasopharynx but most commonly involve the lateral recesses and occasionally obstruct the Eustachian canals. They range from a few millimeters up to 20mm in size. MRCs are covered with intact mucosa on endoscopic exam and may only be appreciated if they create a bulge on the nasopharyngeal wall.