Inferior Accessory Ossicle of the Anterior Arch of C1

A large ossicle occasionally seen along the inferior surface of the anterior arch of C1 should not to be mistaken for a fracture. Keats has named this the inferior accessory ossicle of the anterior arch of the atlas. On the lateral view of radiographs and on sagittal CT or MR images, it appears as a triangle with its base along the undersurface of the anterior arch of C1. On coronal reformations, however, we see that it has more of a diamond shape.

References

Keats TE. The inferior accessory ossicle of the anterior arch of the atlas. Am J Roentgenol Radium Ther Nucl Med. 1967 Dec;101(4):834-6.

Transient Hepatic Attenuation Difference

Transient hepatic attenuation difference (THAD) is an area of enhancement seen during the hepatic arterial phase of dynamic CT that is caused by an increase in arterial flow. This increase may be primary or in response to decreased portal flow.

Primary causes include hypervascular lesions (the sump effect), inflammation of adjacent organs (e.g., gallbladder, pancreas), or an aberrant hepatic arterial supply.

Decreased portal flow, in turn, can be caused by portal or hepatic vein thrombosis, compression by focal lesions, long-standing biliary obstruction, parenchymal trauma, and arterioportal shunts.

Transient hepatic attenuation difference is classified into four types based on morphology:

• Lobar multisegmental: All or almost all segments of one hepatic lobe is involved. Usually caused by a hypervascular lesion that sucks in extra blood to the whole segment. The shape is not triangular shape and a straight border sign (see below) is not seen.
• Sectorial: Triangular wedge- or fan-shaped areas with at least one straight border that separates the area of increased attenuation from adjacent normally attenuating liver. Caused by increased arterial flow in response to a portal venous obstruction. A malignant lesion may cause sectorial THAD by compression or infiltration of a portal vein branch. Benign lesions causing sectorial THAD are usually subcapsular. Alternatively, a focal liver abscess can cause portal hypoperfusion by the spread of inflammatory mediators.
• Polymorphous: Have various shapes and sizes without a straight border. Present as areas of irregular enhancement around or lateral to an injury. The polymorphous pattern may be caused by an aberrant blood supply, inflammation, physical parenchymal injury (contusion, percutaneous biopsy), chemical parenchymal injury (e.g., ethanol injection for tumor), extrinsic compression by ribs or stretched diaphragmatic pillars, and radiofrequency ablation.
• Diffuse: Involves the entire hepatic parenchyma. This pattern is caused by a generalized blood flow obstruction before, at, or after the level of sinusoids, with resultant portal hypoperfusion. The appearance depends on the level of obstruction.
  • Before: For example, portal vein thrombosis, cirrhosis. Portal flow is inadequate for the periphery of the liver, resulting in a central-peripheral appearance (peripheral subcapsular hepatic enhancement with relative low attenuation of the central perihilar area.
  • At: For example with dilatation of the biliary tree from choledocholithiasis or pancreatic cancer. The appearance is a peribiliary pattern of transient hepatic attenuation difference.
  • After: For example, Budd Chiari syndrome, right heart failure. Results in generalized central lobular enhancement with a marbled appearance.

References

• Colagrande S, Centi N, La Villa G, Villari N. Transient hepatic attenuation differences. AJR Am J Roentgenol. 2004 Aug;183(2):459-64.
• Itai Y, Moss AA, Goldberg HI. Transient hepatic attenuation difference of lobar or segmental distribution detected by dynamic computed tomography. Radiology. 1982 Sep;144(4):835-9.
• Itai Y, Murata S, Kurosaki Y. Straight border sign of the liver: spectrum of CT appearances and causes. Radiographics. 1995 Sep;15(5):1089-102.

Platybasia: MR Measurement

Platybasia refers to abnormal flattening of the skull base and can be seen with congenital (craniofacial anomalies, osteogenesis imperfecta, cleidocranial dysplasia, Chiari malformation, etc.), or acquired conditions (Paget disease, osteomalacia, rickets, trauma, etc.)

On radiographs, the Welcher basal angle can be used to diagnose platybasia. Lines are drawn from the nasion to the tuberculum sellae and from the tuberculum sellae to the basion. The angle should be less than 140°.

On MR imaging, the basal angle is measure based on landmarks consistently reproducible on midline sagittal T1 images. The angle is measured between a line extending across the anterior cranial fossa to the tip to the dorsum sellae and another line drawn along the posterior margin of the clivus. Using this technique, the 95% confidence limits of the means were 116°–118° for adults and 113°–115° for children.

The image above shows midsagittal MR images from two different 14-year-old children. The first child has a normal MRI basal angle of 110°, while the second child has an abnormally elevated basal angle of 124° associated with a Chiari I malformation (not shown).

References

• Koenigsberg RA, Vakil N, Hong TA, Htaik T, Faerber E, Maiorano T, Dua M, Faro S, Gonzales C. Evaluation of platybasia with MR imaging. AJNR Am J Neuroradiol. 2005 Jan;26(1):89-92.
• Smoker WR. Craniovertebral junction: normal anatomy, craniometry, and congenital anomalies. Radiographics. 1994 Mar;14(2):255-77.

Adrenal Hemangioma

Hemangiomas can uncommonly affect the adrenal glands and are not hormonally active. They occur in people between the ages of 50 and 70 years, more commonly in women. Adrenal hemangiomas are well delimited and encapsulated and usually involve the cortex.

Radiographs reveal calcifications in more than half of cases, and CT reveals these calcifications to be phleboliths. For this reason, CT is preferred over MRI, as calcifications can suggest the diagnosis but are poorly seen with MRI. CT also shows multiple low-attenuation areas corresponding to necrotic cavities. Peripheral contrast enhancement is also seen; however, unlike liver hemangiomas, centripetal enhancement is not commonly seen due to the higher frequency of central necrosis and fibrosis.

On MR, adrenal hemangiomas present as heterogeneous, T1-hypointense, T2-hyperintense lesions with central fibrotic areas. There is peripheral contrast enhancement with centripetal enhancement being uncommon, as explained above.

Differential consideration at imaging include malignant hemangioblastoma, adrenal carcinoma, pheochromocytoma, and neuroblastoma. Metastases and tuberculosis can also show calcifications and should be considered.

References

• Marotti M, Sucić Z, Krolo I, Dimanovski J, Klarić R, Ferencić Z, Karapanda N, Babić N, Pavleković K. Adrenal cavernous hemangioma: MRI, CT, and US appearance. Eur Radiol. 1997;7(5):691-4.
• Otal P, Escourrou G, Mazerolles C, Janne d'Othee B, Mezghani S, Musso S, Colombier D, Rousseau H, Joffre F. Imaging features of uncommon adrenal masses with histopathologic correlation. Radiographics. 1999 May-Jun;19(3):569-81.

Central Neurocytoma

Central neurocytomas are intraventricular neuroepithelial tumors that characteristically present as bubbly, lobulated masses in the frontal horn or body of the lateral ventricles attached to the septum pellucidum. They account for about half of all intraventricular masses in patients between the ages of 20-40 years.

On CT, central neurocytomas have mixed solid and cystic components and calcifications in up to 70% of cases. The lesions are highly vascular and may be complicated by hemorrhage, but this is rare. There is moderate, heterogeneous enhancement. Hydrocephalus may be seen with obstruction of the foramina of Monro.

MRI similarly shows a heterogeneous mass with cystic and solid components. Flow voids and calcifications present as low-signal areas. The lesion is predominantly hyperintense on FLAIR sequences. Post contrast images show heterogeneous, moderate enhancement.

The lesions are typically low metabolism on FDG-PET.

Differential considerations include:

• Subependymoma: May have a similar appearance. More commonly in the 4th ventricle. Enhancement is usually weaker.
• Choroid plexus papilloma: Intense enhancement. Found in the lateral ventricles in younger patients. More common in the 4th ventricle in older patients.
• Metastasis: Look for primary, other lesions.
• Meningioma: Well defined mass with intense enhancement. Typical location is the trigone of the lateral ventricles and is seen in older patients.
• Subependymal giant cell astrocytoma: Seen with tuberous sclerosis.
• Ependymoma: Rare for a supratentorial ependymoma to be intraventricular. Has much more aggressive appearance.

Colitis Cystica

Colitis cystica is the cystic dilatation of the mucous glands of the colon and can be classified as superficialis and profunda.

The cysts in colitis cystica superficialis are small, located in the mucosa, and distributed throughout the entire colon. Colitis cystica superficialis is often associated with vitamin deficiencies and tropical sprue, but can also be seen with terminal leukemia, thyrotoxicosis, uremia, and mercury poisoning.

Contrast enema shows multiple, small filling defects resembling pseudopolyposis extending from the rectum to the cecum.

The cysts in colitis cystica profunda may be large and are submucosal and primarily seen in the pelvic colon and rectum. A diffuse variety of colitis cystica profunda has also been described. It is thought that colitis cystica profunda is the result of herniation or extension of regenerating surface epithelium into the submucosa through mucosal ulcerations. This is supported by the fact that these submucosal cysts may be preceded by superficial mucosal ulcerations or chronic inflammation.

Contrast enema shows multiple, irregular, large filling defects in the rectum. The retrorectal space may be widened. Differential considerations include polyps, ulcerative colitis, pneumatosis intestinalis, endometriosis, and carcinoma.

References

• Ledesma-Medina J, Reid BS, Girdany BR. Colitis cystica profunda. AJR Am J Roentgenol. 1978 Sep;131(3):529-30.
• Morris MW, Wyatt AP. Colitis cystica superficialis. Proc R Soc Med. 1973 Sep;66(9):908-10.

Currarino Triad

Currarino triad is a rare constellation of anorectal malformation, sacrococcygeal defect, and a presacral mass. It is also known as ASP syndrome (Anorectal, Sacrococcygeal, Presacral), is inherited in an autosomal dominant manner in more than 50% of cases, and is diagnosed by age 16 in more than 80% of cases. Incomplete forms also exist.

• Anorectal malformations: Anal stenosis (with or without fistulas to the spinal canal) or anal atresia.
• Sacrococcygeal bony defect: Range from a small lateral deviation of the coccyx to asymmetric hypoplasia of multiple sacral segments ("scimitar sacrum").
• Presacral mass: Mature teratomas, dermoid or neurenteric cysts, lipomas, among others, often in combination with an anterior meningocele.

In addition to the above, other malformations may be seen in patients with Currarino triad, including tethered cord (and its neurological sequelae), intraspinal lipomas, rectovaginal fistulas, and partial duplication of the vagina, uterus or urinary tract.

While patients with caudal regression syndrome can also have anorectal, spinal and urogenital findings, a presacral mass is only found in patients with the Currarino triad.

References

Riebel T, Mäurer J, Teichgräber UK, Bassir C. The spectrum of imaging in Currarino triad. Eur Radiol. 1999;9(7):1348-53.