Hippocampal Commissure and Agenesis of the Corpus Callosum

The hippocampal commissure (commissura fornicis) is part of the fornix and crosses the midline to connect to the contralateral hippocampus inferior to the caudal body and rostral splenium of the corpus callosum. The normal hippocampal commissure small and difficult to visualize on MRI.

Because the crossing fibers of the hippocampal commissure are crucial in the formation of a normal hippocampus, a normal hippocampus can be taken as proof of the presence of a hippocampal commissure.

The hippocampal commissure may be enlarged in some patients with agenesis of the corpus callosum and can be mistaken for its splenium on sagittal views. The differentiating feature is that the enlarged hippocampal commissure connects the fornices on coronal views.

When there is question of callosal agenesis, look for a normal hippocampus. A normal hippocampus implies the presence of the hippocampal commissure, which may mimic the corpus callosum. Therefore, secondary signs of callosal agenesis should be sought, for example, absent cavum septum pellucidum, an elevated third ventricle extending into the interhemispheric fissure, and radial arrangement of the medial cerebral sulci perpendicular to the expected course of the corpus callosum.

On the other hand, the hippocampal commissure may be absent in patients with callosal agenesis; however, it is though that the two are separate forms of cerebral malformation and no definite association has been identified.

References

• Hannay HJ, Dennis M, Kramer L, Blaser S, Fletcher JM. Partial agenesis of the corpus callosum in spina bifida meningomyelocele and potential compensatory mechanisms. J Clin Exp Neuropsychol. 2009 Feb;31(2):180-94.
• Küker W, Mayrhofer H, Mader I, Nägele T, Krägeloh-Mann I. Malformations of the midline commissures: MRI findings in different forms of callosal dysgenesis. Eur Radiol. 2003 Mar;13(3):598-604. Epub 2002 Nov 1.

Milk Fistula

A milk fistula is a tract between the skin and a lactifenous duct. Milk fistulas usually form during lactation, often as a result of surgical intervention, but has also been seen after large-core needle biopsy. Peripheral lesions have a much lower risk of developing milk fistulas after open biopsy compared to deep, central lesions

While spontaneous closure has occurred during lactation, the only reliable way of closure is suppression of lactation. Lactation can be suppressed with breast binding and withholding sucking stimuli, or the use of bromocriptine. The former method usually takes about a week, but the patient may feel discomfort from breast engorgement during this time. Bromocriptine therapy takes about two weeks and may result in nausea in about 5% of patients and carries a slight risk of cardiovascular side effects.

References

Schackmuth EM, Harlow CL, Norton LW. Milk fistula: a complication after core breast biopsy. AJR Am J Roentgenol. 1993 Nov;161(5):961-2.

Differential Diagnosis of Masses on Mammograms Based on Density

Fatty mass on mammogram:

• Lipoma: Masses larger than 2 cm tend to be lipomas
• Fat necrosis: Seen at site of prior surgery or trauma
• Galactocele: Occur during or shortly after lactation.
• Focal breast fat simulating a mass

Mixed-density mass on mammogram:

• Fibroadenolipoma: Will contain fatty components. Looks for radiodense "capsule" when adjacent to fatty tissue.
• Intramammary lymph node: Look for fatty hilum.

Water-density mass on mammogram

• Cyst
• Fibroadenoma
• Cancer: Most tend to be more dense than surrounding fibroglandular tissue. The increased density is more apparent than real and is due to increased content of fibrous and sclerotic elements leading to decreased compressibility.

References

Sickles EA. Breast masses: mammographic evaluation. Radiology. 1989 Nov;173(2):297-303.

Spiculated Masses on Mammography

The differential diagnosis of a spiculated mass on mammography includes:

• Scar from biopsy: Most common etiology.
• Radial scar: Usually lacks central density. Thin radiolucent lines can be seen coursing through its center. May contain microcalcifications. Indistinguishable from tubular carcinoma on imaging.
• Fat necrosis: May contain microcalcifications.
• Abscess
• Hematoma
• Tuberculosis
• Sclerosing adenosis: May contain microcalcifications. May be difficult to differentiate from tubular carcinoma on histological evaluation.
• Cancer:

A hematoma or abscess may be suspected based on history and may resolve or decrease in size on short-term (1-month) follow-up. A scar at a recent biopsy site may also be followed to evaluate stability or partial resolution. Otherwise, the benign causes cannot be differentiated from neoplasm, and biopsy is often needed.

References

• Sickles EA. Breast masses: mammographic evaluation. Radiology. 1989 Nov;173(2):297-303.
• Cyrlak D, Carpenter PM, Rawal NB. Breast imaging case of the day. Florid sclerosing adenosis. Radiographics. 1999 Jan-Feb;19(1):245-7.

Os Peroneum

The os peroneum is an accessory ossicle found within the peroneus longus tendon near the calcaneocuboid joint. The ossicle may be single-part or multipartite (bipartite shown here). It is found in about 10% of radiographs, but is thought to be always present in a cartilaginous or fibrocartilaginous stage.

While most often an incidental finding, the os peroneum can be associated with pain. The os peroneum syndrome presents with lateral pain, tenderness and swelling along the course of the peroneus longus tendon. There is also lateral pain with plantar flexion of the foot against resistance.

Os peroneum syndrome can be initiated by:

• Os peroneum fracture
• Hypertrophic healing of an os peroneum fracture
• Diastasis of a multipartite os peroneum
• Attrition or tear of the peroneus longus tendon
• Enlarged peroneal tubercle of the calcaneus

References

• Mellado JM, Ramos A, Salvadó E, Camins A, Danús M, Saurí A. Accessory ossicles and sesamoid bones of the ankle and foot: imaging findings, clinical significance and differential diagnosis. Eur Radiol. 2003 Dec;13 Suppl 6:L164-77.
• Pierson JL, Inglis AE. Stenosing tenosynovitis of the peroneus longus tendon associated with hypertrophy of the peroneal tubercle and an os peroneum. A case report. J Bone Joint Surg Am. 1992 Mar;74(3):440-2.

Unnamed Ossicle Medial to Navicular

I couldn't find a name for this ossicle medial to the navicular. It's clearly not an os naviculare, as it is too distal and too medial. Keats simply calls it "an unnamed ossicle adjacent to the navicular."

References

Keats TE and Anderson MW. Atlas of Normal Roentgen Variants That May Simulate Disease. 8th edition, page 847; Mosby (2004).

Cerebrospinal Fluid Flow Void Sign

The cerebrospinal fluid (CSF) flow void sign (CFVS), also known as the aqueductal flow void sign, classically referred to hypointensity in the Sylvian aqueduct as a result of to-and-fro CSF flow. The to-and-fro flow is due to pulsatile motion of CSF related to the cardiac cycle. It can also be observed in the fourth ventricle (~95% of cases), the third ventricle (70% of cases), foramen of Magendie (~75% of cases), and the foramina of Monro (~30% of cases).

On T1-weighted images, CSF signal is replaced by signal that is lower than that of the contents of the lateral ventricles. On T2-weighted images, there is low signal instead of the expected hight fluid signal.

The CFVS can be seen in normal individuals, and in those with brain atrophy, but is more pronounced in patients with chronic, communicating normal pressure hydrocephalus (NPH). Unfortunately, the sign does not appear to be useful in differentiating patients with NPH from those with brain atrophy.

The presence of CFVS, along with more extensive periventricular hyperintensities, are felt to have positive prognostic value in patients who are treated for NPH.

References

• Bradley WG Jr, Kortman KE, Burgoyne B. Flowing cerebrospinal fluid in normal and hydrocephalic states: appearance on MR images. Radiology. 1986 Jun;159(3):611-6.
• Sherman JL, Citrin CM, Gangarosa RE, Bowen BJ. The MR appearance of CSF flow in patients with ventriculomegaly. AJR Am J Roentgenol. 1987 Jan;148(1):193-9.

Tumoral Calcinosis

Tumoral calcinosis is a term whose true meaning has been lost over the years. It is now a stand-in for any kind of periarticular calcification. However, it has a specific definition: a hereditary disease of phosphate metabolic dysfunction that leads to the formation of characteristic lobulated, well-demarcated soft tissue calcifications distributed most commonly around the extensor surface of large joints. The sedimentation sign may be seen on CT and upright radiographs when calcium layers dependently in cysts.

Many conditions that mimic tumoral calcinosis are mistakenly referred to by the same name. The most common mimicker is calcinosis of chronic renal failure, which is actually the case shown here. This is the most common cause of a periarticular calcified mass. Calcinosis of chronic renal failure is seen in about 1% of patients on hemodialysis. The cause is unknown, but is thought to be related to hyperparathyroidism. There is no radiologic or histologic difference between these lesions and the lesions of tumoral calcinosis.

Specific dental abnormalities can be seen in patients with tumoral calcinosis, including short bulbous roots of teeth, pulp stones, and partial obliteration of the pulp cavity.

References

• Burkes EJ Jr, Lyles KW, Dolan EA, Giammara B, Hanker J. Dental lesions in tumoral calcinosis. J Oral Pathol Med. 1991 May;20(5):222-7.
• Hug I, Gunçaga J. Tumoral calcinosis with sedimentation sign. Br J Radiol. 1974 Oct;47(562):734-6.
• Olsen KM, Chew FS. Tumoral calcinosis: pearls, polemics, and alternative possibilities. Radiographics. 2006 May-Jun;26(3):871-85.

Osmotic Demyelination Syndrome

Images are from a 40-year-old man transferred to our institution with history of "pancreatitis and hyponatremia." As is typical, no symptoms or other clinical history was provided in the 120-character-limit space for history (medicine by twitter).

Sagittal T1-weighted image shows a hypointense lesion in the pons, seen in the axial T1-weighted image as a trident-shaped lesion that spares the ventrolateral pons and the pontine portion of the corticospinal tracts. The axial T2-weighted image shows hyperintensity in this region, while the FLAIR image at the same level shows a trident-shaped area of hyperintensity surrounding an area of encephalomalacia in the central pons. The GRE image shows no evidence of hemorrhage. The diffusion-weighted image shows a trident-shaped rim of hyperintensity surrounding the central pons, while the apparent diffusion coefficient map at the same level shows no signal dropout in the region of hyperintensity, indicating T2 shine-through.

On the clinical side, symptoms typically occur 2-4 days after correction of hyponatremia. The earliest imaging finding of osmotic demyelination syndrome is restricted diffusion, which may be apparent as early as 24 hours after onset of clinical symptoms. The appearance of myelinolytic lesions on MRI lags clinical symptoms by 2 weeks:

• T1: Hypointense, but can also be isointense. Images obtained 1-4 months later may be normal or demonstrate hyperintensity, representing coagulative necrosis.
• T2: Hyperintensity that may also include the basal ganglia. Images obtained 1-4 months later may show complete resolution.
• FLAIR: Hyperintense
• GRE: Hyperintense. Hemorrhage is rare
• DWI: Hyperintense
• ADC: Normal to mildly hyperintense
• Post-contrast: Typically no enhancement, but may also see mild enhancement.

Differential considerations for T2-hyperintensity in the pons includes:

• Ischemia: Look for restricted diffusion.
• Infection: Look for enhancement.
• Brainstem glioma:
• Demyelination: Progressive multifocal leukoencephalopathy, osmotic demyelination syndrome.

References

• Hall J. Osmotic Demyelination Syndrome. StatDx. 2008-06-05.
• Howard SA, Barletta JA, Klufas RA, Saad A, De Girolami U. Best cases from the AFIP: osmotic demyelination syndrome. Radiographics. 2009 May-Jun;29(3):933-8.
• Ruzek KA, Campeau NG, Miller GM. Early diagnosis of central pontine myelinolysis with diffusion-weighted imaging. AJNR Am J Neuroradiol. 2004 Feb;25(2):210-3.

Cone-Shaped Epiphyses

Cone-shaped epiphyses (coned epiphyses) are epiphyses that invaginate into cupped metaphyses. They are more commonly found in the feet as a morphological variant, but can also be associated with symptoms or be seen with a variety of developmental disorders. Differential considerations for cone-shaped epiphyses include normal variant and ABCD MOST:

• Normal variant (shown above in three different patients)
• Achondroplasia, Acrodysostosis
• Beckwith Wiedemann syndrome
• Chondroplasia punctata, Cockayne syndrome, Conorenal syndrome (Mainzer-Saldino syndrome, association of chronic renal failure and phalangeal cone-shaped epiphyses of the hands), Cleidocranial dysplasia, Cartilage-hair hypoplasia
• Dactylitis, Dyggve-Melchior-Clausen syndrome
• Multiple epiphyseal dysplasia
• Osteomyelitis
• Sickle cell disease
• Thermal injury, Trichorhinophalangeal syndrome

References

• Freyschmidt J, Brossmann J, Wiens J, Sternberg A. The Hand - General Aspects. In Freyschmidt's Köhler and Zimmer: Borderlands of normal and early pathologic findings in skeletal radiography. Fifth revised edition. Thieme (2003). Pp 24-26.
• Differential Diagnosis in Pediatric Radiology. Edited by Ebel KD, Blickman H, Willich E, Richter E. Thieme. Stuttgart, New York, 1999.
• Medcyclopaedia.

Snapping Hip (Coxa Saltans)

Snapping hip, also known as coxa saltans (coxa=hip, saltans=dance/jump), refers to a snapping sensation about the hip on motion. It can be divided into intra-articular and extra-articular. The extra-articular category is further divided into external and internal.

Intra-articular snapping hip can be caused by a torn labrum, chondral defect, or loose bodies. The external type is due to snapping of the posterior iliotibial band or the anterior edge of the gluteus maximus muscle over the greater trochanter.

The internal type thought to occur when the musculotendinous iliopsoas snaps over the femoral head or the anterior capsule of the hip; however, a recent study with dynamic ultrasound suggests that the sudden flipping of the iliopsoas tendon over the iliac muscle is the most common cause of snapping hip. Snapping iliopsoas tendon can also be caused by acetabular dysplasia, as the tendon snaps over the uncovered femoral head. Therefore, hip dysplasia must be ruled out in patients with snapping iliopsoas tendon.

Coxa Saltans Externa

On MRI, patients with external snapping hip demonstrate thickening of the iliotibial tract or focal thickening of the anterior edge of gluteus maximus muscle. There may also be atrophy of the rest of the gluteus maximus muscle.

Coxa Saltans Interna

On MRI, patients with internal snapping hip will demonstrate edema around the iliopsoas tendon. The MRI image shown here shows edema (pink arrows) surrounding the iliopsoas tendon (blue arrow) on axial (A), coronal (B), and sagittal fluid-sensitive images from an MR arthrogram.

References

• Allen WC, Cope R. Coxa Saltans: The Snapping Hip Revisited. J Am Acad Orthop Surg. 1995 Oct;3(5):303-308.
• Deslandes M, Guillin R, Cardinal E, Hobden R, Bureau NJ. The snapping iliopsoas tendon: new mechanisms using dynamic sonography. AJR Am J Roentgenol. 2008 Mar;190(3):576-81.
• Garbuz DS, Masri BA, Haddad F, Duncan CP. Clinical and radiographic assessment of the young adult with symptomatic hip dysplasia. Clin Orthop Relat Res. 2004 Jan;(418):18-22.
• Krishnamurthy G, Connolly BL, Narayanan U, Babyn PS. Imaging findings in external snapping hip syndrome. Pediatr Radiol. 2007 Dec;37(12):1272-4.

Target and Fat Halo Signs of Bowel

Target Sign

The target sign refers to the enhanced CT appearance of edematous bowel, which demonstrates three layers:

• Inner: Contrast-enhanced inner mucosa
• Middle: Submocosal edema
• Outer: Muscularis propria and/or serosa

The target sign may also be see on nonenhanced CT when the edema is severe.

Differential considerations include:

• Inflammatory bowel disease (Crohn disease and ulcerative colitis)
• Ischemic bowel disease
• Intramural intestinal hemorrhage
• Vasculitis (Henoch-Schönlein purpura)
• Infection (infectious and pseudomembranous colitis)
• Radiation damage (radiation enteritis colitis)
• Portal hypertension

Fat Halo Sign

A similar sign is the fat halo sign, in which there are also three layers:

• Inner: Inner mucosa
• Middle: Fatty infiltration of the submucosa with Housnfield units lower than -10.
• Outer: Muscularis propria and/or serosa

The inner mucosal layer can be appreciated even without intravenous contrast due to the contrast between the soft tissue of the mucosa and the underlying low-attenuation fat.

Differential considerations include:

• Chronic inflammatory bowel disease (Crohn disease and ulcerative colitis)
• Cytoreductive therapy.
• Graft vs host disease.
• Normal appearance of underdistended bowel.

References

• Ahualli J. The target sign: bowel wall. Radiology. 2005 Feb;234(2):549-50.
• Ahualli J. The fat halo sign. Radiology. 2007 Mar;242(3):945-6.

Median Arcuate Ligament Syndrome

Median arcuate ligament syndrome (also known as celiac artery compression syndrome) refers to the compression of the celiac axis by an abnormally low median arcuate ligament. The median arcuate ligament is a fibrous band that connects the diaphragmatic crura at the aortic hiatus. In 10%–25% of people, it crosses in front of the celiac trunk and may cause symptoms. The arterial compression usually varies with respiration and worsens with expiration.

Median arcuate ligament syndrome does not respond to angioplasty, and stents are not used due to possible device fatigue. Surgery to enlarge the diaphragmatic hiatus or resect the celiac ganglion is the preferred.

On angiography, there is a characteristic focal narrowing in the proximal celiac axis with a hooked appearance. Injection of the superior mesenteric artery can lead to retrograde opacification of the celiac artery via the gastroduodenal and pancreaticoduodenal arteries if the compression is severe enough.

References

Horton KM, Talamini MA, Fishman EK. Median arcuate ligament syndrome: evaluation with CT angiography. Radiographics. 2005 Sep-Oct;25(5):1177-82.

Mammographic Appearance of the Breast after Breast Conservation Therapy

Expected mammographic changes in the breast 6 months after completion of radiation therapy as part of breast conservation therapy include:
Diffuse changes from radiation

• Generalized skin thickening: intra- and extra-cellular edema from radiation. Maximal at 6 months and either stable or decreasing on subsequent mammograms (may take years).
• Increased breast markings: Engorged breast lymphatics. Usually gone by 1 year.
• Overall increased breast density: Due to skin thickening and suboptimal compression of the treated breast.

Localized changes at the excisional biopsy site:

• Mass or vague density at operative site: From edema, hematoma, or seroma. Can assume to be post-surgical if there is histological proof of complete resection.
• Architectural distortion: From surgical damage. Can assume to be post-surgical if there is histological proof of complete resection. Should decrease in size as time goes on.
• Early fat necrosis: Most commonly lipid cyst, but can also see macroscopic (benign) calcifications. Benign-appearing microcalcifications that occur at the lumpectomy site within three years after treatment may be followed up.

References

• Dershaw DD, Shank B, Reisinger S. Mammographic findings after breast cancer treatment with local excision and definitive irradiation. Radiology. 1987 Aug;164(2):455-61.
• Vora SA, Wazer DE, Homer MJ. Management of microcalcifications that develop at the lumpectomy site after breast-conserving therapy. Radiology. 1997 Jun;203(3):667-71.

Fat Necrosis of the Breast

The mammographic and sonographic appearance of fat necrosis depends on the degree of fibrosis. The mammographic appearance is more specific than sonography. Mammographic presentations of fat necrosis include the following:

• Fat cyst: Minimal fibrosis. Radiolucent mass with thin wall. Linear and curvilinear calcifications develop early and central calcifications can be seen later. If there is more fibrosis the wall may be thick, irregular, spiculated, or ill-defined. Fat cysts may contain fat–fluid levels, serous–hemorrhagic contents, or spherical densities. Collapsed oil cysts may also be seen.
• Focal asymmetries: A fat cyst whose center has been replaced by reparative fibrotic reaction may appear as a focal asymmetric density.
• Spiculated mass: A fat cyst whose center has been replaced by reparative fibrotic reaction may appear as a spiculated mass.
• Coarse calcifications: May be smooth and round or curvilinear.
• Microcalcifications: More worrisome appearance of calcifications, including branching, rodlike, or angular, can also be seen.

The sonographic appearance is varied, ranging from a solid mass to an anechoic mass with posterior enhancement with margins ranging from well circumscribed to indistinct to spiculated. A specific sonographic appearance of fat necrosis is a mass with echogenic internal bands that shift in orientation with changes in patient position. The most common presentation of fat necrosis is a hyperechoic subcutaneous mass.

On MRI fat necrosis may be indistinguishable from malignancy and can mimic tumor recurrence after breast conservation therapy. The degree of enhancement on MRI depends on the degree of inflammatory reaction.

References

Taboada JL, Stephens TW, Krishnamurthy S, Brandt KR, Whitman GJ. The many faces of fat necrosis in the breast. AJR Am J Roentgenol. 2009 Mar;192(3):815-25.

Dilated Duct Pattern at Mammography

The appearance of symmetric bilateral subareolar ductal dilatation is usually of no clinical importance in postmenopausal women. Asymmetric dilatation is another story. Asymmetrically dilated ducts can be caused by:

• Primary: Intraductal growth of papilloma or intraductal carcinoma
• Secondary: Duct retraction by architectural distortion from adjacent mass, or ductal obstruction from mass.

The following should raise concern for malignancy in an asymmetrically dilated duct:

• Nonsubareolar location
• Interval change
• Suspicious microcalcifications

References

Huynh PT, Parellada JA, de Paredes ES, Harvey J, Smith D, Holley L, Maxin M. Dilated duct pattern at mammography. Radiology. 1997 Jul;204(1):137-41.

Intranodal Calcifications on Mammography

Calcifications may be seen within intramammary or axillary lymph nodes on mammography. Differential considerations include:

• Granulomatous disease: Histoplasmosis, tuberculosis, sarcoidosis. Usually coarse calcifications
• Fat necrosis:
• Metastatic disease: Rare
• Tattoo pigments
• Gold deposit: From gold therapy for rheumatoid arthritis
• Breast cancer:

References

Dunkin J, Hong R, and Fisher P. Axillary lymph node gold deposits. ACR Case in Point. Monday, June 18, 2007.

Axillary Lymph Nodes on Mammography

Differentiating benign from malignant lymph nodes on mammography is difficult due to the wide overlap in appearance. Three characteristics point toward malignancy and should prompt recommendation of biopsy:

• Nonfatty lymph nodes with microcalcifications. Intranodal gold in patients with RA who have received gold therapy may have a similar appearance
• Nonfatty lymph nodes with ill-defined or spiculated margins
• Nonfatty lymph nodes longer than 45 mm
• Documented increase in size or density

References

Walsh R, Kornguth PJ, Soo MS, Bentley R, DeLong DM. Axillary lymph nodes: mammographic, pathologic, and clinical correlation. AJR Am J Roentgenol. 1997 Jan;168(1):33-8.

Columnar Cell Lesions of the Breast

Columnar cell lesions (CCLs) of the breast, formerly known as columnar alteration with prominent apical snouts and secretions (CAPPS), are characterized by lining of enlarged terminal duct lobular units by columnar epithelium. They can cause microcalcifications and are frequently found at biopsy performed for tissue charcterization of microcalcifications.

CCLs can be broken down into:

• Columnar cell change (CCC): Corresponds to an increased relative risk of breast cancer. But the overall risk is low, therefore discovery at core needle biopsy requires no additional work-up.
• Columnar cell hyperplasia (CCH): Corresponds to an increased relative risk of breast cancer. But the overall risk is low, therefore discovery at core needle biopsy requires no additional work-up.
• Flat epithelial atypia (FEA): Commonly coexists with other more significant lesions, including ADH, DCIS, and tubular carcinoma. Therefore discovery at excisional biopsy should prompt in an excisional biopsy releveling of the block and a careful search for areas of ADH and DCIS.

Mmammographic findings of CCLs include clustered, amorphous, or fine pleomorphic microcalcifications within the lumen of terminal duct lobular units.

Differential considerations for amorphous calcifications in the lobule or the terminal ducts incldues:

• DCIS
• ADH
• CCLs
• Ordinary epithelial hyperplasia
• Papillomatosis
• sclerosing adenosis

Differential considerations for fine pleomorphic calcifications located in the terminal ducts of the terminal duct lobular units includes:

• DCIS
• ADH
• CCLs
• Typical ductal hyperplasia

References

Pandey S, Kornstein MJ, Shank W, de Paredes ES. Columnar cell lesions of the breast: mammographic findings with histopathologic correlation. Radiographics. 2007 Oct;27 Suppl 1:S79-89. Review.

Eustachian Valve

The eustachian valve, named after Bartolomeo Eustachi, is also known as valvula venae cavae inferioris. It is a remnant of the embryonic right valve of the sinus venosus.

In the fetal circulation the eustachian valve directs oxygenated blood from the inferior vena cava into the left atrium via the patent foramen ovale. The eustachian valve also directs deoxygenated blood from the superior vena cava toward the right ventricle through the tricuspid valve, preventing it from crossing into the left atrium.

References

Manson F. Eustachian valve. www.TheFetus.net. 2006-06-07-15

Idiopathic Pulmonary Hemosiderosis

Idiopathic pulmonary hemosiderosis (IPH) is a rare disease characterized by recurrent diffuse alveolar hemorrhage in the absence of vasculitis, leading to aggregates of hemosiderin-laden macrophages and eventual interstitial fibrosis. IPH is thought to be due to environmental triggers (household pathogenic molds have been suggested but not proven) in genetically predisposed individuals (e.g., decreased levels of von Willebrand factor). In addition, there is an association with celiac disease (known as Lane-Hamilton syndrome), suggesting a possible autoimmune process.

References

Gordon IO, Cipriani N, Arif Q, Mackinnon AC, Husain AN. Update in nonneoplastic lung diseases. Arch Pathol Lab Med. 2009 Jul;133(7):1096-105.

Lesions of the Psoas Compartment

Mass-like lesions in the psoas compartment include:

• Retroperitoneal hematoma: The case shown here. There is a heterogeneous mass in the expected region of the right psoas muscle.
• Muscle asymmetry
• Retroperitoneal fibrosis: Look for center of lesion surrounding the aorta and inferior vena cava.
• Paraspinal abscess
• Neoplasm

References

Federle MP. Mass in Iliopsoas Compartment. StatDx; 2008-10-17.

Annulus of Zinn

The annulus of Zinn is a fibrous ring that overlies the optic canal and the medial aspect of the superior orbital fissure and is continuous with the dura of the middle cranial fossa. It is divided into the superior Lockwood tendon and the inferior tendon of Zinn.

Six of the seven extraocular muscles arise from the annulus of Zinn: The four rectus muscles, the levator palpebrae superioris muscle, and the superior oblique muscle. The inferior oblique muscle arises from the medial orbital floor lateral to the lacrimal sac.

Cranial nerves II, III, nasocilliary branch of V1, and VI enter through the annulus of Zinn, while Cranial nerves IV and the frontal and lacrimal branches of the ophthalmic division of the trigeminal nerve (V1) enter the orbit through the superior orbital fissure lateral to the annulus of Zinn.

The ophthalmic artery also passes through the annulus of Zinn, while the superior ophthalmic vein enters the orbit through the superior orbital fissure lateral to the annulus of Zinn. The diagram, adapted from Petruzzelli and Hampson, shows the right orbit. 2=cranial nerve II; 3i=inferior division of cranial nerve III; 3s=superior division of cranial nerve III; 4=cranial nerve IV; 6=cranial nerve VI.

References

• Aviv RI, Casselman J. Orbital imaging: Part 1. Normal anatomy. Clin Radiol. 2005 Mar;60(3):279-87
• Petruzzelli GJ and Hampson CM. Orbit Anatomy. eMedicine. Mar 11, 2008.

Mounier-Kuhn Syndrome

Mounier-Kuhn syndrome, also known as tracheobronchomegaly, is a rare congenital abnormality of the trachea and main bronchi characterized by cystic dilatation of the tracheobronchial tree and recurrent respiratory infections. The characteristic demographic is middle-aged African-American men.

As the name suggests, there is enlargement of the trachea (coronal diameter > 25 mm measured 2 cm above the aortic arch) and central bronchi. There may be an undulating or corrugated appearance to the airways due to prolapse of redundant mucosa through tracheal rings. Tracheobronchial diverticula may also be seen. There may be collapse of the trachea and major airways on expiration. Recurrent infections leave behind areas of bronchiectasis.

Differential consideration include:

• Pulmonary fibrosis in the upper lobes: Retraction of the tracheobronchial walls, leading to tracheomegaly.
• Tracheobronchomalacia: Diffusely flaccid and dilated airway may simulate the appearance of the airway in Mounier-Kuhn syndrome. May lead to recurrent infections and bronchiectasis. May be primary or due to relapsing polychondritis, chronic airway inflammation or infection, chronic bronchitis, trauma (intubation) or cystic fibrosis.
• Allergic bronchopulmonary aspergillosis: May cause central bronchiectasis. Usually in patients with chronic asthma or cystic fibrosis. Look for central, round, or varicoid bronchiectasis; large mucoid impactions (finger-in-glove opacities); and fleeting peripheral air-space opacities.

See related post on tracheal stenosis.

Special thanks to Dr. Aiham Korbage for the case.

References

Marom EM, Goodman PC, McAdams HP. Diffuse abnormalities of the trachea and main bronchi. AJR Am J Roentgenol. 2001 Mar;176(3):713-7.

Reversible Cerebral Vasoconstriction Syndrome

Reversible cerebral vasoconstriction syndrome (RCVS) is characterized by the association of severe headaches and a segmental and multifocal string and beads appearance of the cerebral arteries. There may or may not be associated focal neurological symptoms and seizures. RCVS resolves spontaneously in 1–3 months.

RCVS may be primary or secondary (most common). Secondary causes include vasoactive substances (cannabis, SSRIs, nasal decongestants) and pregnancy.

RCVS is not as benign as it sounds. Complications can include intracranial hemorrhage (subarachnoid, parenchymal), seizures, reversible posterior leukoencephalopathy, transient ischemic attacks, and cerebral infarction.

Other vascular abnormalities have been noted in patients, including aneurysms and dissections.

References

Ducros A, Boukobza M, Porcher R, Sarov M, Valade D, Bousser MG. The clinical and radiological spectrum of reversible cerebral vasoconstriction syndrome. A prospective series of 67 patients. Brain. 2007 Dec;130(Pt 12):3091-101.

Digital Hypoperfusion Ischemic Syndrome

Digital hypoperfusion ischemic syndrome (DHIS) refers to hand ischemia due to peripheral hypoperfusion after arteriovenous access (e.g., for hemodialysis). Its older name, arterial steal syndrome, is felt to be less accurate, since a majority of patients with arteriovenous access demonstrate clinically silent arterial steal (i.e., retrograde flow).

The exact etiology is poorly understood, but is felt to be related to a combination of true steal from the distal arteries, arterial stenosis throught the arm (proximal and distal), and distal arteriopathy.

Patients commonly present with cold hand, numbness, and hand pain on and/or off dialysis. The radial pulse is usually diminished. In advanced cases, there may be ischemic ulcers and dry gangrene. DHIS is more common in patients with brachial artery than radial artery based accesses. Symptoms are also more frequent in patients with diabetes and in smokers.

The presentation may be acute or insidious. In the acute case, symptoms occur almost immediately after creation of the access. The treatment in these cases is ligation of the access.

The symptoms may also occur weeks or months after access. They may later resolve due to development of collateral circulation.

Differential Considerations

Differential considerations for hand pain in chronic dialysis patients can be narrowed somewhat:

• Carpal tunnel syndrome: Increased prevalence in long-term hemodialysis. There may be atrophy of the lateral thenar muscles.
• Tendopathy: Increased prevalence in long-term hemodialysis.
• Arthropathy: Increased prevalence in long-term hemodialysis. There may be deformity and instability of interphalangeal joints and localized tenderness.
• Reflex sympathetic dystrophy: Pain and swelling of an affected extremity.
• Ischemic monomelic neuropathy: Complication of vascular access seen almost exclusively in patients with diabetes, typically in those with peripheral neuropathy and atherosclerotic peripheral vascular disease. There is acute pain, weakness, and paralysis of forearm and hand muscles that occurs within minutes to hours after the creation of an arteriovenous access. The etiology is ischemic infarction of the vasa nervosa. As opposed to DHIS, the hand is typically warm. The radial pulse is variably present. Treatment is access ligation.
• Diabetic neuropathy.

References

Leon C, Asif A. Arteriovenous access and hand pain: the distal hypoperfusion ischemic syndrome. Clin J Am Soc Nephrol. 2007 Jan;2(1):175-83.

Aneurysm Aspect Ratio

The aspect ratio of an aneurysm is the ratio of its depth to the width of its neck. Aneurysms with high aspect ratios are thought to be more prone to rupture because they are low-flow and set the sac up for stasis, thrombosis, and the fibrinolytic cascade and resultant intimal breakdown. Initial studies suggested 1.6 as the cut-off for increased risk of rupture. Subsequent studies have come up with different numbers, and it's unclear to me what number should be used as a threshold in clinical practice.

References

Dhar S, Tremmel M, Mocco J, Kim M, Yamamoto J, Siddiqui AH, Hopkins LN, Meng H. Morphology parameters for intracranial aneurysm rupture risk assessment. Neurosurgery. 2008 Aug;63(2):185-96; discussion 196-7.

Thoracic Manifestations of Ankylosing Spondylitis

The most common thoracic manifestation of ankylosing spondylitis is ankylosis of the costovertebral joints limiting chest expansion. The lungs and pleura may also be involved in up to 30% of patients with ankylosing spondylitis.

Pleuropulmonary manifestations include:

• Upper lobe fibrosis: Cicatrization, cavitation, architectural distortion, and traction bronchiectasis.
• Nonapical interstitial lung disease: Follows the usual interstitial pneumonitis pattern: subpleural band opacities, thickened interlobular septae, parenchymal bands, ground-glass opacification, honeycombing.
• Bronchiectasis:
• Paraseptal emphysema:
• Tracheal abnormalities: Tracheobronchomegaly (Mounier-Kuhn syndrome, Rare)
• Mycetoma formation:
• Pleural thickening:
• Pleural effusion:
• Empyema:
• Pneumothorax:
• Cor pulmonale:
• Ankylosis of the costovertebral joints: Limits lung expansion

References

Fenlon HM, Casserly I, Sant SM, Breatnach E. Plain radiographs and thoracic high-resolution CT in patients with ankylosing spondylitis. AJR Am J Roentgenol. 1997 Apr;168(4):1067-72.

Quadrigeminal Plate Arachnoid Cyst

Compared to supratentorial arachnoid cysts, infratentorial arachnoid cysts are more frequently symptomatic. Typical locations are:

• Retrocerebellar: Common location.
• Cerebellopontine angle: Common location.
• Quadrigeminal plate cistern: Third most common infratentorial location. Located between the collicular plates and the incisural notch of the tentorium cerebelli.
• Along the lateral aspect of the cerebellum
• Along the clivus

Quadrigeminal plate cistern arachnoid cysts are also known as paracollicular arachnoid cysts, tentorial notch arachnoid cysts, arachnoid cysts of cisterna ambiens, paramesencephalic arachnoid cysts, and parapineal arachnoid cysts.

Symptoms may be related to normal pressure hydrocephalus, Parinaud syndrome, visual disturbances, nystagmus, hearing deficits, hemiparesis, paraparesis, generalized spasticity, clonus, diplopia caused by trochlear nerve compression, lateral rectus palsy caused by intracranial hypertension, and precocious puberty.

It's important to look for mass effect on adjacent structures, including the sylvian aqueduct. An important differential consideration is a cyst of the tectal plate, which is intraparenchymal. As such, a tectal plate cyst is covered by a rim of brain tissue whereas a quadrigeminal cistern cyst is not.

The standard differential is

• Epidermoid cyst: don't suppress on FLAIR and show restricted diffusion.
• Chronic subdural hematoma: Not identical to cerebrospinal fluid signal.
• Subdural hygroma: Often bilateral
• Other nonneoplastic cyst: porencephalic cyst, neurenteric cyst, neuroglial cyst

The image is that of a middle-aged man who presented with sudden onset dizziness. There is cystic lesion in the quadrigeminal plate cistern that follows cerebrospinal fluid signal without diffusion restriction or abnormal enhancement. The signal is completely suppressed on FLAIR. There is no hydrocephalus and the sylvian aqueduct is patent. There is, however, mass effect on the cerebellum.

References

• Kumar V, Peng EW, Fitzpatrick MO, Whittle IR. Tectal plate cyst in adults. Acta Neurochir (Wien). 2006 Jul;148(7):805-8.
• Little JR, Gomez MR, MacCarty CS. Infratentorial arachnoid cysts. J Neurosurg. 1973 Sep;39(3):380-6.
• Topsakal C, Kaplan M, Erol F, Cetin H, Ozercan I. Unusual arachnoid cyst of the quadrigeminal cistern in an adult presenting with apneic spells and normal pressure hydrocephalus--case report. Neurol Med Chir (Tokyo). 2002 Jan;42(1):44-50.

Pulmonary-Renal Syndromes

Pulmonary-renal syndromes are clinical syndromes defined by a combination of diffuse alveolar haemorrhage (blood on serial bronchoalveolar lavage) and glomerulonephritis.

• Primary systemic vasculitis (+ANCA): Wegener granulomatosis, microscopic polyangiitis, Churg–Strauss syndrome
• Primary systemic vasculitis (-ANCA): Henoch–Schönlein purpura, mixed cryoglobulinaemia, Behçet disease, IgA nephropathy
• Goodpasture syndrome: Autoantibodies to type IV collagen in alveolar and glomerular basement membrane.
• Autoimmune: Systemic lupus erythematosus, scleroderma, polymyositis, rheumatoid arthritis, mixed collagen vascular disease
• Drug-Related: Propylthiouracil, D-penicillamine, hydralazine, allopurinol, sulfasalazine
• Thrombotic microangiopathy: Antiphospholipid syndrome, thrombotic thrombocytopenic purpura, infection, neoplasm

References

Papiris SA, Manali ED, Kalomenidis I, Kapotsis GE, Karakatsani A, Roussos C. Bench-to-bedside review: pulmonary-renal syndromes--an update for the intensivist. Crit Care. 2007;11(3):213.

Cystitis Cystica and Cystitis Glandularis

Cystitis cystica and glandularis are common chronic reactive inflammatory disorders characterized by urothelial metaplasia in response to chronic irritants such as infection, calculi, outlet obstruction, or tumor.

Pathologically, there is proliferation of the urothelium into buds (nests of von Brunn), which extend into the lamina propria. Cystitis cystica results if the nests differentiate into cysts. If the nests differentiate into intestinal mucin-secreting glands (goblet cells), we get cystitis glandularis. Both are usually present at the same time.

If there is invasion of the muscular layer, adenocarcinoma must be considered.

References

Wong-You-Cheong JJ, Woodward PJ, Manning MA, Davis CJ. From the archives of the AFIP: Inflammatory and nonneoplastic bladder masses: radiologic-pathologic correlation. Radiographics. 2006 Nov-Dec;26(6):1847-68.