Allergic fungal sinusitis is the most common form of fungal sinusitis. It is particularly common in warm, humid climates. The overall prevalence of allergic fungal sinusitis is estimated at 5%–10% of all patients with chronic hypertrophic sinus disease going to surgery.

The underlying cause is thought to be a hypersensitivity reaction to certain inhaled fungal organisms resulting in a chronic noninfectious, inflammatory process, similar to that seen in allergic bronchopulmonary aspergillosis of the lung. Although the exact pathophysiology is not yet clear, immunologically, immunoglobulin E–mediated type I immediate hypersensitivity and type III delayed hypersensitivity are thought to be involved.

Common implicated fungi are the dematiaceous (pigmented) fungi—Bipolaris, Curvularia, Alternaria—and the hyaline molds such as Aspergillus and Fusarium. Allergic fungal sinusitis is characterized by the presence within the affected sinuses of “allergic mucin”—inspissated mucus that is yellow-green, white-tan, gray, brown, or black with the consistency of peanut butter.

Allergic fungal sinusitis tends to be a disease of younger individuals, usually in their third decade. Typically, afflicted individuals are immunocompetent. There is a frequent associated history of atopy including allergic rhinitis and asthma. Patients usually experience chronic headaches, nasal congestion, and chronic sinusitis for several years. There is often a history of sinus surgery.

There is usually involvement of multiple sinuses if not pansinusitis and rhinitis. Disease tends to be bilateral, and there is a frequent nasal component. The majority of the sinuses show near-complete opacification and are expanded. Expansion, remodeling, or thinning of involved sinus walls is common in allergic fungal sinusitis (AFS) and is thought to be caused by the expansile nature of the accumulating mucin. Areas of high attenuation are found within the expanded paranasal sinuses in all patients. Similar radiographic findings can be caused by rare osteoid/chondroid matrix-producing sinonasal sarcomas or meningiomas.

Noncontrast CT demonstrates hyperattenuating allergic mucin within the lumen of the paranasal sinus.

Bony erosion of the sinus walls and extension into adjacent cavities have been mentioned in many reports, usually focusing on intracranial extension, as depicted in the 1st image above. In most series, a rate of approximately 20% bony erosion with extension into surrounding vital cavities is reported.

The ethmoid sinus was the most commonly involved sinus, while the adjacent lamina papyracea was the most common bone to exhibit demineralization, as depicted in the image below. Extension of allergic fungal sinusitis (AFS) beyond the confines of the paranasal sinuses most commonly occurred into the orbit, followed by the anterior, middle, and posterior cranial fossae, respectively

Although low signal intensity of the sinus contents has been described on T1-weighted images, we have frequently observed high signal intensity or mixed low, intermediate, and high signal intensity on T1-weighted images in these patients. There is characteristic low signal intensity or signal void on T2-weighted images. The T2 signal void is attributed to a high concentration of various metals such as iron, magnesium, and manganese concentrated by the fungal organisms. The T2 signal void is also attributed to a high protein and low free-water content of the allergic mucin.

The inflamed mucosal lining is relatively hypointense on T1-weighted images and hyperintense on T2-weighted images and demonstrates enhancement after intravenous administration of gadolinium contrast material.

There is no enhancement in the center or in majority of the sinus contents, which distinguishes this condition from neoplastic entities.

Although the condition is not considered invasive, if left untreated, the involved sinuses expand and there is smooth bone erosion with subsequent intracranial or intraorbital extension and resulting cranial or orbital symptoms. Intracranial extension is usually limited by the dura to the extradural space.

Reference:

https://doi.org/10.1148/rg.275065189

Vertebral haemangiomas are common vascular lesions affecting 11% of the population according to autopsy series. These lesions are usually asymptomatic and are discovered as incidental findings on multiple imaging modalities. Nevertheless, in some instances, these lesions can behave aggressively and cause pain or neurological deficit secondary to expansion of the vertebral body or paravertebral or epidural soft-tissue extension with spinal cord/nerve root compression.

Histologically, haemangiomas are predominantly composed of vascular lined spaces and non-vascular components that may include adipose tissue, smooth muscle, fibrous tissue, bone, haemosiderin and thrombus.

 There are two histological subtypes of haemangioma: the cavernous type which is the most common subtype and is characterized by large sinusoidal spaces, and the capillary type which demonstrates smaller vascular channels.

Vertebral haemangiomas classically have a coarse, vertical, trabecular pattern on radiographs which are seen on axial CT scan as punctate areas of sclerosis on axial imaging called “polka-dot” appearance or “jail-bar”, or “corduroy-cloth appearance” on sagittal or coronal reconstructions.

On MRI imaging, the signal intensity (SI) of typical asymptomatic haemangiomas is usually hyperintense on both T1 and T2 weighted sequences; however, aggressive haemangiomas have been shown to have low T2 SI related to paucity of adipose tissue.

The presence of adipose tissue in haemangiomas therefore has been suggested as a predictor of benign nature in some studies.

Laredo et al investigated the appearance of the stroma between the osseous trabeculae on vertebral haemangiomas and demonstrated absence of fat attenuation on CT in aggressive haemangiomas, in comparison to asymptomatic haemangiomas. In their study, aggressive haemangiomas showed numerous packed, thin-walled vascular cavities with absence of fatty replacement on histopathological evaluation. Ross et al  and Pastushyn et al also demonstrated that the paravertebral extraosseous component of aggressive haemangiomas is hypointense on T1. In the study by Ross et al, histopathological evaluation of the extraosseous portion of the tumour showed a preponderance of angiomatous tumour vessels and fibrous tissue, with little adipose tissue. Although a few of the previous studies showed hyperintensity on STIR sequence in their published figures of aggressive haemangioma.

Reference:

10.1259/bjr.20150557

The septum pellucidum is a structure that is marginated by the corpus callosum and body of the fornix. It is composed of white matter leaves along the medial walls of the lateral ventricles and is lined by ependyma along its ventricular surfaces . The entire space between the leaves of the septi pellucidi is the cavum septi pellucidi et vergae, with the space anterior to either the foramina of Monro or an arbitrary vertical plane formed by the forniceal columns being the CSP and the space posterior being the cavum vergae.

When the two leaves fail to fuse and form the septum pellucidum, a number of postnatal anatomic variants can result including the CSP, cavum vergae, and cavum veli interpositi. The CSP and the cavum vergae usually freely communicate with one another. Usually a cavum vergae is seen in association with a CSP, although it can also occasionally be seen in isolation . In general, persistence of the CSP in postnatal life is considered a normal variant.

The leaves of the septi pellucidi begin to close at approximately 6 months’ gestational age from back to front. Nearly all term infants have closure of the cavum vergae and the majority of infants 3–6 months old have closure of the cavum septi as well . The cavum sometimes persists into adulthood as a normal variant, typically small, measuring less than 4 mm in transverse diameter, in healthy individuals . The terminology can be confusing. In general, when the two leaves are separated, this may be referred to as the “cavum septi pellucidi” or “CSP”; when the leaves are fused to form a single structure, it is referred to as the “septum pellucidum”

Reference: https://www.ajronline.org/doi/10.2214/AJR.17.19219

The usual clinical presentation of PTT is that of a long-standing, subcutaneous, cystic nodule that slowly progresses to a large, nodular mass, often following a history of trauma or inflammation. The tumor preferentially arises in areas of dense hair follicle concentrations, and about 90% of cases occur on the scalp, with the residual 10% occurring mainly on the back. Other, less common locations include the vulva, nose, mons pubis, buttock, wrist, chest, and elbow.

Women are affected in more than 80% of cases, and the average age of patients is 65 years . The presentation is nearly always that of a single lesion, but, rarely, multiple lesions are seen.

Areas of necrosis, calcification, and hyalinization may be seen. The stroma is usually fibrous and shows a variable inflammatory reaction, including foreign body giant cells.

Although PTT is generally considered biologically benign, even though histologically indistinguishable from squamous cell carcinoma in some cases, malignant PTT has been reported. Saida et al suggested three stages in the oncologic development of a malignant PTT: the adenomatous stage of the trichilemmal cyst, the epitheliomatous stage of the PTT, and the carcinomatous stage of the malignant PTT. A rare occurrence of PTT with spindle cell carcinoma has also been reported .

Reference:

American Journal of Neuroradiology January 2001, 22 (1) 180-183;