Juvenile angiofibroma

Findings

Axial T1 and T2 (Figure 1 and Figure 2) demonstrate a mass with intermediate T1-weighted signal and intermediate-to-high T2-weighted signal.
Axial T1 postcontrast (Figure 3) demonstrates avidly enhancing mass in right maxillary sinus that widens the sphenopalatine foramen.
Figure 4 (coronal) contrast enhanced T1-weighted images demonstrate flow voids within the enhancing mass. Flow voids are characteristic of a juvenile angiofibroma.
Flow voids are seen as dark areas on T2-weighted image (Figure 2) as well.


Diagnosis: Juvenile angiofibroma


Juvenile angiofibroma (JAF) presents in adolescent males (median age 15) with unilateral nasal obstruction and epistaxis. JAF is rare, representing 0.5 % all head and neck neoplasms; however, it is the most common benign neoplasm of the nasopharynx. Although the commonly used synonym is juvenile nasopharyngeal angiofibroma, true JAF entity arises in the nasal cavity, not the nasopharynx. However, it may spread into the nasopharyx.

JAF is considered benign but locally aggressive. Approximately 20 % have skull base invasion at diagnosis.

On imaging, JAF is a highly enhancing mass that is lobulated and nonencapsulated. Microscopically, it is composed of delicate thin-walled vessels on a background of connective tissue stroma. These delicate vessels lend the mass its tendency to bleed easily.

JAF originates at the posterior nasal cavity along the superior margin of the sphenopalatine foramen and posterior aspect of middle turbinate As it enlarges, this mass may fill the unilateral nasal cavity, and extend into the nasopharynx and pterygopalatine fossa (90%). If there is superior extension, it will involve the sphenoid sinus (60%). When it pushes anteriorly against the posterior wall of the maxillary sinus, it results in the classic “antral bowing sign” on CT examination. A small number may actually invade into the middle cranial fossa via the foramen rotundum or vidian canal. In these cases, bony destruction is evident.

On MRI, there is T1 intermediate signal and T2 intermediate-to-high signal. Flow voids are often seen in these very vascular tumors. Biopsy of this lesion is considered unnecessary and dangerous, given its propensity to bleed. An angiogram of both ECA and ICA with embolization using polyvinyl alcohol particles or Gelfoam is often performed 1-2 days before surgery to reduce surgical blood loss and decrease rate of recurrence. Local recurrence after surgery is 6-24%. Low dose radiation may be used in conjunction with surgery for cure. Rarely, chemotherapy has been utilized in cases of intracranial extension with favorable results.

Several staging systems have been described to help predict outcome. Chandler et al (1984) described the following:
- I) Tumor confined to nasopharyngeal vault.
- II) Tumor extends into nasal cavity or sphenoid sinus
- III) Tumor extends into antrum, ethmoid sinus, pterygomaxillary fissure, orbit, and/or cheek
- IV) Intracranial tumor

Electromagnetic Breast Imaging

Electromagnetic breast imaging: results of a pilot study in women with abnormal mammograms. Radiology 2007 May;243(2):350-9. Epub 2007 Mar 30

Study by Poplack SP et al published in Radiology May 2007 used three EM imaging methods: electrical impedance spectroscopy (EIS), microwave imaging spectroscopy (MIS), and near-infrared spectral tomography (NIR).Results from EM breast examinations provide statistical evidence of a mean increase in image contrast of 150%-200% between abnormal (benign and malignant) and normal breast tissue.

Sumer's Radiology Site-Features in Journal Of Thoracic Imaging

The concept of Rad-blogging as used in Sumer's Radiology Site which is one of the earliest Radiology Blogs now has now been accepted in "Journal of thoracic imaging" as a review article.

Blog/Web Log-A New Easy and Interactive Website Building Tool for a Non-net Savvy Radiologist.
Review Article

Journal of Thoracic Imaging. 22(2):115-119, May 2007.

Sethi, Sumer K. MD

I Feel Great To be A Filipino...Sometimes

I was tagged by my friend Gerry about what makes me feel great being a Filipino. I was dumbfounded because there are times when I feel great to be a Filipino and there are times when I feel depressed that I'm a Filipino.

Well, I feel great to be a Filipino when:

1. I see the natural beauty of our Philippines. The beautiful countrysides, the spreading beaches, the beautiful sunsets, the valleys, the natural wonders of of our beautiful country. We may not have the Grand Canyon, the Yosemite, the Disneyland, but I will never exchange our natural wonders with them.
2. I read in the history books the noble deeds of our great heroes like Mabini, Bonifacio, or Rizal.
3. I realize that brown skin is the best skin to have. Brown is beautiful. I don't need skin whiteners. I feel great to be brown! Hahahah!

But then, I feel depressed being a Filipino when:

1. I see bad politicians being elected into office( I heard that one of the Mayors in Cebu who has been charged with overpricing the city lamposts- so he could get a big kickback-has been reelected) Grrrrr!
2. I see Filipinos leaving the Philippines for good, immigrating to other countries....while wealthy foreigners flock to our country to enjoy our resources.
3. I travel to the Visayas, and from my airplane I see the massive deforestation caused by obnoxious loggers who should be punished with garrote
4. I watch the television and see Filipino movie stars talk Taglish...like "Well, you know naman na need ko mag-reduce nang fat noh?" I feel devastated how they murder the beautiful Tagalog language.
5. I pick up the newspapers, and read about the poverty of the Filipinos... then a few pages later I look at the Lifestyle section and see the lavish weddings of movie stars, pulitikos, that costs millions of pesos, and sometimes attended by the President of the Philippines.

There are more...and more....but I don't want to go further..I'm sick to the stomach

Well, I have been tagged...I have to answer honestly...I feel proud to Be a Filipino! Well, sometimes!

Radiology Grand Rounds XII

Here is the the twelth Radiology Grand Rounds, hosted on the last sunday of each month with archives maintained by me here-
Radiology Grand Rounds

We start this radiology Grand rounds with a Radiology Quiz
It goes like-
Radiology Quiz!
"A young lady in her 30s was referred to me for having serous mixed with blood(haemoserous) discharge from her previous abdominal incision. This discharge increased during her menses and with the same consistency. She had an emergency surgery a year ago for a ruptured uterus from pyometra (pus within the uterus) She was found to have a congenital (from birth) anomaly. This is her hysterogram"

Blast from the Past

Here is an interesting write up about the X-ray discovery
""Is it light?""No.""Is it electricity?""Not in any known form.""What is it?""I don't know."And the discoverer of the X rays thus stated as calmly his ignorance of their essence as has everybody else who has written on the phenomena thus far."

Radiology Journal Section

Choosing and using bibliographic software
"I’m sure most of you out there have a collection of articles gathered from many journals, and neatly (or not) filed away in your office. Reading and indexing information from the literature used to mean trips to the library with the photocopy card and sitting down with the highlighter to read them.Starting in the late 90’s, many journals started posting abstracts and full text articles online. Pubmed also became a huge resource for searching the most recent literature for citations. All of these electronic references need to be stored somewhere, and paperless filing is becoming a much more viable option. Hard drives have almost limitless memory, and interfaces for saving references electronically have become much more user friendly. Now you need to decide how to choose bibliographic software, and how you will use it."

Alvaro Fernandez presents Lifelong Learning and New Neurons in Adults posted at Brain Fitness. We will need new imaging methods to see this in action-not even fMRI allows us to see neurogenesis take place.

Somethings to think about

MR/PET hybrid on the way too....

Anatomy Trivia

The Azygos lobe

Radiological Sign

"Heart of Stone" image

That wraps up this month's highlights of the Radiology blogosphere. Hope the readers enjoyed the XII edition of the Radiology Grand Rounds. If you liked any of these blogs, keep visiting them. Please email me at sumerdoc@yahoo.com if you are interested in hosting future Radiology Grand Rounds. Also visit our sister concern Teleradiology Providers. Archive for the Radiology Grand Rounds here-Radiology Grand Rounds. Be sure to tune in Next Month Last Sunday 24th June, when Grand Rounds will be hosted at- NeuroRaziology Blog mail to- eytan.raz@gmail.com or sumerdoc@yahoo.com

MR/PET hybrid on the way too....

Siemens proves feasibility of MR/PET hybrid

"The first brain images produced simultaneously with a prototype MR/PET scanner were shown at the Siemens Medical Solutions booth and in a scientific session in Berlin. The device, currently in development at a Siemens lab, integrates a PET detector into the bore of a 3T scanner. "

Read the full article here-

Diagnostic Imaging Webcast

Pseudohypoparathyroidism

Additional clinical data: The patient has a history of hypocalcemia.


Findings

Diffuse, symmetric calcification of the deep gray matter and bilateral immediate subcortical white matter (U-fibers). No acute intracranial hemorrhage or abnormal extra-axial fluid collections. No focal mass, mass effect, or shift of midline structures. Stable, normal ventricle sizes and configuration.

Differential Diagnosis:
- Pseudohypoparathyroidism
- Hypoparathyroidism
- Hyperparathyroidism
- Fahr's disease
- Post-infectious (e.g. toxoplasmosis)
- Post-radiation therapy


Diagnosis: Pseudohypoparathyroidism


Discussion

Pseudohypoparathyroidism (PHP) is a congenital hereditary abnormality that appears to be transmitted as an X-linked dominant trait characterized by hypocalcemia, hyperphosphatemia, and basal ganglia / soft tissue calcification. In PHP, biochemical hypoparathyroidism results from end-organ resistance to parathyroid hormone, due to a defect in the receptor-adenylate cyclase system. As a result, the kidney and, less commonly, the bones are unable to respond to parathyroid hormone.


Radiologic overview

Afflicted patients may be short-statured with rounded faces. Brain calcinosis may be seen in conditions with PHP, the severity and distribution of which varies in individual reports. Bilateral calcifications may present in the basal ganglia, thalamus, cerebral white matter, and cerebellum on head CT. The intracranial calcifications of the basal ganglia may later coalesce into homogeneous masses. Osteosclerosis, which may be generalized or localized, is the most common skeletal abnormality, including calvarial thickening. Subcutaneous calcifications can be seen, especially in the area of the hips and shoulders.

Dermoid cyst

Findings

Axial images show a heterogeneous mass in the anterior left temporal lobe. T1-weighted images show hyperintense regions suggesting fat involving the left parietal and temporal lobe leptomeninges suggesting fat and/or blood products. These same areas show patchy foci of hypointense signal on fat-suppressed T2. Postcontrast axial images do not show enhancement of the left temporal mass.

Differential diagnosis:
- Dermoid cyst
- Epidermoid
- Lipoma
- Metastatic lesion
- Meningioma


Diagnosis: Dermoid cyst


Key points

Dermoid cysts are comprised of connective tissue, squamous epithelium, lipid, and glandular tissue. They sometimes also include calcifications.
Congenital lesions, which are usually midline. Most commonly in the posterior fossa or suprasellar region. Can be seen in the spine, often involving the conus medullaris and cauda equina.
Benign and slow-growing due to glandular secretions and accumulation of epithelial debris. Symptoms are secondary to mass effect.
Dermoid cysts can rupture and release lipid contents into the subarachnoid spaces, which can cause chemical meningitis. Most common symptom postrupture is headache. Meningeal inflammation can (but rarely does) lead to arterial vasospasm and stroke or death.
No role for chemotherapy or radiation therapy in treating dermoid cysts. Resection must include the contents and entire connective tissue lining. Special care must be taken not to spill contents or meningitis will ensue.
On CT, hypodensity suggesting significant fat composition suggests the diagnosis.
On MR, a heterogeneous often midline mass showing hyperintense regions on T1-weighted images may represent a dermoid cyst. Diffuse subarachnoid or intraventricular foci of hyperintensity on T1-weighted imaging that lose signal on fat-suppressed images are concerning for rupture and subsequent chemical meningitis.

Dysembryoplastic Neuroepithelial Tumor (DNET)

Findings

Axial T1-WI (Figure 1) demonstrates a well-defined, cortical based intraxial mass in the right temporal lobe which is hypointense to brain parenchyma. The mass is hyperintense on T2-WI (Figure 2). No surrounding edema is seen. The right temporal horn is seen normally. No enhancement is detected on post-gadolinium T1-WI (Figure 3). Scalloping of the adjacent skull is noted with the lesion “pointing” towards the ventricle (Figure 3).


Diagnosis: Dysembryoplastic Neuroepithelial Tumor (DNET)


DNET is an uncommon benign intracortical lesion that is classified by WHO as a “neuronal and mixed neuronoglial tumor”. These are commonly associated with cortical dysplasia. DNETs show no or very slow growth over time and are WHO Grade I.

These tumors virtually always manifest in patients with medically refractory partial seizures. The vast majority of patients are younger than 20 years, and males are more commonly affected. The temporal lobe is the most common site (62%), followed by the frontal lobe (31%).

The imaging appearance of dysembryoplastic neuroepithelial tumor is similar to those of other low-grade glial tumors. On CT, a wedge shaped low-density area is seen in a cortical/ subcortical location “pointing” towards the ventricle. Calcification may be seen in 25% of cases. Scalloping of the adjacent inner table of the skull suggests long standing nature of the lesion.

At MR imaging, DNET tumors most commonly manifest as cortical masses that are hypointense on T1-weighted images and hyperintense on T2-weighted images without surrounding vasogenic edema. Pseudocystic, multinodular “bubbly” mass may be seen. DNETs usually do not enhance- faint focal punctuate or nodular enhancement may be seen in 20% cases.

The prognosis is excellent with long survival even with incomplete tumor resection. Most patients have a significant reduction in seizure frequency. Tumor recurrence is very rare.

A Visit to Jose Rizal's House

I have been an admirer of Rizal for as long as I can remember. As a child, I heard countless stories about his greatness and heroism. Well, I wasn't sure if all the stories were true, but one thing I was certain of, Jose Rizal was a great man. Like most Filipino school children, I learned from school about his life and works, that he wrote two novels (back then I could pronounce the Noli Me Tangere perfectly but I always mispronounce the mouthful El Filibusterismo). I also learned from school that Rizal was shot by the Spaniards. Back then, I was very angry at the Spaniards.

As a young Manila student in the 1990s I collected books about Rizal. I usually purchased my books in the bangketas of Recto. I read the unexpurgated Noli Me Tangere and the El Filbusterismo that were both superbly translated into Tagalog by Maria Odulio De Guzman. Some of my early books on Rizal were the biographies by Gregorio F. Zaide, Rafael Palma, Leon Ma. Guerrero, and Austin Coates. All these books gave me a fascinating insight on the national hero. I still keep these books and I re-read them from time to time (especially when I'm not so enamored by my latest Hustler issue).


Thinking about Rizal one hot summer afternoon, I decided to drive to Laguna and visit the birthplace of my hero. From Cubao, it took me almost two hours to reach Calamba. I arrived at at three in the afternoon and quickly found the old house of Dr. Rizal, which is the most important landmark in Calamba.

Even to this day, Rizal's house makes a striking impression. It is the biggest house in the area. It was here that Rizal was born. I closed my eyes for a moment to visualize in my mind what it was like standing in front of this beautiful house. Instead of cars, there were horse-drawn carriages. Instead of people in modern clothes, I visualize men and women wearing 19th century Barong Tagalogs and Maria Clara attires. Visiting Rizal's house was like a time travel to the world of the young Jose Rizal.

Rizal's parents were Don Francisco Mercado and Donya Teodora Alonso, a well-to-do couple who originally came from Binan, Laguna. After they married, Rizal's parents migrated to Calamba where they built one of the first stone and hardwood houses there. The house was patterned after the "Bahay na Bato" architectural style that was popular among the ilustrados of the 19th century.

On June 19, 1861, Rizal was born inside that house and was the seventh among the eleven children of Don Francisco and Dona Teodora. He was baptized “José Rizal y Mercado” at the Calamba Church right next door. Young Jose was the first in the family to use the name Rizal in accordance with the 1849 decree of then Governor Narciso Claveria to change the surnames of Filipinos.

In 1891, due to Rizal's activism, the family came under attack of the friars who own the land where the Rizal house stood. Rizal's family was evicted from the house due to pressure from the friars. Eventually the house was sold to a Spaniard named Don Isidro for 24,000 pesos. Rizal's mother and sisters transferred to Hongkong where they reunited with Rizal in a place called Rednaxela Terrace, where Rizal maintained an eye-clinic. Meanwhile other family members sought refuge with relatives in Binan.

The Rizal house was destroyed during the Second World War, and after the war, the Philippine government bought what remained of the property for 27,000 pesos. Then in 1948, by virtue of Executive Order No. 145 signed by President Elpidio Quirino, the house was rebuilt by architect Juan F. Nakpil. Funded in part through schoolchildren contributions, Nakpil rebuilt the Rizal house exactly as it looked like during Rizal's time, using as reference old photos, the written memoirs of Rizal, and the recollections of Rizal's surviving siblings and relatives.The re-built house was inaugurated in 1950 and opened to public.

Viewing the house today, one would imagine that the Rizal's were one of the richest families in Calamba during those times. Imagine a huge house like this complete with daughters' bedrooms, sons' bedrooms, two dining rooms, a master's bedroom, a huge library, a living room, cocina, and toilet and bath! Not to mention the garage for the horse-drawn carriage owned by the family, and the huge backyard. Indeed, only the richest principalias of town like the Rizals were the only ones able to build a house like this. In today's standards, the house could qualify as a mansion.

At present, though, the Rizal house has become a shrine that serves as a museum containing some original furniture, books, and memorabilia that once belonged to the Rizal family (donated in part by Rizal family). On the grounds are statues of the boy Rizal and his pet dog. The lot is also where Rizal’s parents remains were transferred.

I have photographed the entire house of Jose Rizal from room to room (including the bathroom!), and I would like to invite you to go with me today for this virtual tour of the National Hero's house. Of course, nothing beats going there yourself and immerse yourself with culture and history. But if you're too busy to make the drive down to Calamba, then consider this tour as your virtual introduction to Rizal's historic house and lovely hometown.

The famous landmark of Calamba, the gigantic jar which has all the Calamba towns written on its surface.

The street where he lived..the town plaza is at the left side and the town's church at the right.

A frontal view

A historical marker

The grand staircase that leads to the main hall of the house

The original karwahe (carriage) of the Rizal family, still intact after all these years. Unfortunately, the horse died many many years ago.

The living room.

A window in the living room

A view from the front window of the Rizal house.

The comida or the dining room

The main dining room

The platera

The cocina

Rizal's bedroom. The bed was a replica of the original one used by Rizal.

The family well located at the back of the house

A most important seat in the house. No instant flush, though.

The back of the Rizal house

A replica of the little nipa playhouse that Rizal's father built for his son, Pepe

The Church of Calamba beside the Rizal house.

Ahhh it's the monsoon season once again in the Philippines. It is the time of the year when the mornings and afternoons are hot and humid..and then in late afternoons, out of nowhere, clouds will begin to form and lash out heavy rains-complete with peals of thunder and bursts of lighning.

After an hour or so, the rain would suddenly stop, the sun would shine again, and the heat and humidity continues.

On these rainy afternoons, I often sleep in my room with the airconditioning on, and then I wrap myself tightly in a thick blanket. I find it very relaxing, the sweet sound of the rain like sweet music lulling me to sleep.

Indeed, nothing compares to this blissful feeling...of sleeping comfortably in your own bed, hugging a soft pillow...dreaming of beautiful things.....Half-awake and half-asleep..I visualize that I'm in paradise... ahhh how relaxing!

And then I sensed something in my forehead....what is it?

It feels cold ...and it feels wet...

My ceiling is dripping rain...right on my forehead.

At first it was one drip...and then two...and then in a maddening rush it continues until it's a steady trickle.......Lazily, I get up to remedy the situation.

I have to stop this trickle of rain. If I don't act sooner, my whole bed will get soaked. And then my room..and then my books...My quick but stupid thinking led me to look at my arinola....oh no..it shouldn't be..I didn't want my arinola to be filled with rainwater..overflowing in my bed..

Piling clothes and sheets to where the rain was dripping, I frantically searched my toolbox and found Mighty Bond..but my common sense tells me it wouldn't work....How about a masking tape?

Why not?

I started taping masking tape in the very spot where the rain was dripping. Here..there ..and even farther....my ceiling now looks like it had gotten a serious injury.....but at least the dripping had stopped.... I'm always succesful at fixing things....

Well, the actual reason was that the rain had suddenly stopped too.

It is indeed monsoon season in the Philippines. I have to sleep again and try to imagine that it's raining.

After all sleeping during rainy afternoons is one of the best free things in life.

That is, unless you don't have a hole in your ceiling....

Submissions Requested for Radiology Grand Rounds-XII

Dear Readers
As you all know we have hosting Radiology Grand Rounds sucessfully for one year where we summarize the best in the radiology blogosphere at one location, this is hosted on last sunday of each month.Your radiology related blog posts can be submitted over to us.
This month's Radiology Grand Rounds will be hosted at my site-
Sumer's Radiology Site on Last sunday May 27 2007

So hurry up send your submissions to me at -
sumerdoc-AT-yahoo-DOT-com
Archives and links to previous issue of Radiology Grand Rounds Here-
Radiology Grand Rounds

Carbon monoxide poisoning

Findings

NECT images show low density in the bilateral globus pallidi. The remainder of the basal ganglia and hemispheric white matter is unremarkable.

Differential diagnosis:
- Carbon monoxide poisoning
- Acute hypoxia of other causes
- Small vessel ischemic disease
- Creutzfeldt-Jakob disease (and other encephalidites)
- Wilson’s disease (and other metabolic processes)


Diagnosis: Carbon monoxide poisoning


Bilateral GP low density on NECT is virtually pathognomonic of CO poisoning.
MRI is more accurate and should be used for follow-up.
Normal CT on arrival correlates with better prognosis.

Carbon monoxide poisoning remains an important cause of morbidity/mortality in the US despite improvements in automobile and home safety. While nearly 50% are due to suicide and many are associated with fires, a large number of unintentional CO poisonings still occur. Race and source of CO are also important, as CO poisoning in Caucasians is more likely to be suicidal and fatal than in African- or Asian-Americans. Also, toxicity from automobile exhaust is more likely to be fatal, and malfunctioning heating equipment is a more common source.

Patient clinical history may include unresponsiveness, seizure, or adjunctive information such as multiple patients from the same household. Nausea, vomiting and headache are more general symptoms which are often associated with a lower degree of toxicity.

For most patients the initial imaging study is a NECT following ER evaluation. Hypodensity in the bilateral GP is a strong indicator for this process and is virtually pathognomonic. CT findings are also indicative of outcome. A patient with a normal head CT is very unlikely to have long-term neurological abnormalities.

MRI is much more accurate than CT in defining the extent of disease (e.g. white matter ischemic changes, internal capsule or caudate nucleus involvement). As such, this is the preferred modality for follow-up. Findings include T1 hypointensity (necrosis) or hyperintensity (hemorrhage), T2 and FLAIR hyperintensity, hypointense rim on T2 (hemosiderin deposition), and DWI hyperintensity in the acute setting.

The Azygos lobe

NEJM features a case of azygos lobe with fissure along with metastatic nodule from osteogenic sarcoma, check out images and case details here-
NEJM-Azygos lobe


What is azygos lobe?

"Abnormal fissures and lobes of the lungs are common and usually insignificant. A lobe of the azygos vein appears in the right lung in about 1 percent of people. It develops when the apical bronchus grows superiorly medial to the arch of the azygos vein instead of lateral to it. As a result, the azygos vein comes to lie at the bottom of a deep fissure in the superior lobe of the right lung."

Tornwaldt cyst

Findings

Figure 1: Sagittal T1 demonstrates midline cystic structure in the posterior pharynx which demonstrates increased signal intensity on T1WI.
Figure 2 and Figure 3: Axial T1 and T2 demonstrate the lesion with variable signal intensity based on protein content. When increased protein content is present, T2WI is decreased as in Figure 3. The lesion is anterior and adjacent to the superior pharyngeal constrictors.


Diagnosis: Tornwaldt cyst


Described by Gustav Ludwig Tornwaldt (1843-1910), a Tornwaldt cyst, or bursa pharingea, is a benign developmental cyst which is found in posterior nasopharyngeal soft tissues, anterior to the superior pharyngeal constrictors. The lesion is nearly always midline, although off-midline is possible. Identified in about 3% of patients, this cyst has no sex predilection with a peak incidence in patients from 15-30 years of age.

The cyst is formed during development, from a diverticulum which results from an adhesion between the notocord and endoderm of the posterior pharynx. As the notocord retracts normally into the clivus and cervical spinal column, a midline nasopharyngeal epithelial lined outpouching may close, forming a cyst. This is a part of the pharyngeal roof and a remanant of the Rathke’s pouch. Some authors believe that the lesion arises from a remnant of the notochord itself.

On CT, Tornwaldt cyst appears as a hypodense lesion in the midline in nasopharyngeal soft tissues. On MRI they demonstrate variable intensity depending on the degree of proteinaceous content, however are typically hyperintense on T1, T2 as well as FLAIR sequence images. The size of the lesion can vary from 5mm to a few centimeters.

These cysts are nearly always asymptomatic. They infrequently become infected resulting in neck pain or muscle spasm. If the cyst ruptures due to infection or trauma, the release of anaerobic contents may result in halitosis, eustachian tube obstruction or possibly an upper respiratory tract infection.

When symptomatic, treatment option includes surgical excision or marsupialization.

Upcoming Radiology Conferences

Upcoming Events:

ESSR 2007 - 14th Annual Meeting - European Society of Musculoskeletal Radiology - Izmir, Turkey (June 1-2)

SIIM 2007 Annual Meeting - Providence, RI USA (June 9-15)

UKRC 2007 - UK Radiological Congress - Manchester, UK (June 11-13)

25th EuroPACS Congress 2007 - Berlin, Germany (June 27-309)

Sagittal synostosis

Findings

3-D CT images demonstrate sagittal synostosis. Markedly increased anteroposterior diameter of the head (dolichocephaly) with flattening of the superior contour is noted. The sagittal suture is fused (Figure 1 and Figure 2), with widening of both the coronal (Figure 2) and lambdoid sutures (Figure 1 and Figure 2).


Diagnosis: Sagittal synostosis


Premature fusion of the cranial sutures is termed craniosynostosis. Approximately 80-90% cases involve isolated defects, while the remaining cases are part of a recognized syndrome. In the isolated cases, the sagittal suture is affected most often (55%), followed by the coronal (20%), lambdoid (5%), and metopic (5%) sutures. Syndromes associated with synostosis include Crouzon disease and Chotzen and Apert syndromes.

The anterior fontanel represents the intersection of the metopic, coronal, and sagittal sutures. It normally closes in children by the age of 20 months. The posterior fontanel, located at the junction of the lambdoid and sagittal sutures, closes by the age of 3 months. Skull growth is restricted in the plane perpendicular to the prematurely fused suture and enhanced in the plane parallel to it.

Sagittal synostosis produces a long and narrow skull, called scaphocephaly or dolichocephaly. The AP diameter of the skull is increased, whereas the transverse diameter is decreased. Actual head volume is normal and there is no increase in ICP, no hydrocephalus, and no neurologic deficit.

Coronal synostosis can occur bilaterally or unilaterally and is called brachycephaly and plagiocephaly (twisted and asymmetric skull), respectively. Brachycephaly results in a short, wide skull, with a shortened AP diameter with a flattened occiput and forehead. It has a higher incidence of neurologic complications, including increased ICP, optic atrophy, and mental retardation.

Lamboid synostosis produces a marked flattening and underdevelopment of the posterior fossa and overgrowth of the bregma may occur, resulting in a tall tower like shape called oxycephalic or turricephalic skull.

Metopic synostosis occurs in utero. It is rare, and results in a pointed forehead and hypotelorism called trigonocephaly, and has an increased risk for associated anomalies of the forebrain.

The most severe form is called the kleeblattschädel deformity or cloverleaf skull, in which the coronal, sagittal, and lambdoid sutures are all affected. The skull resembles a cloverleaf shape, and patients typically have a bulging forehead, proptotic eyes, and severe neurologic impairment.

The signs of craniosynostosis on plain radiography include bony bridging across the suture that produces beaking or heaping up of bone as well as sclerosis, straightening and narrowing of the suture.

The diagnostic value of the CT scan outweighs that of plain radiography because the sutures can be identified more accurately. In addition, CT helps in evaluating the brain for structural abnormalities (eg, hydrocephalus, agenesis of the corpus callosum) and in excluding other causes of asymmetric vault growth (eg, brain hemiatrophy, chronic subdural hematoma). Three-dimensional surface CT reconstructions can help the surgeon to accurately delineate the craniofacial deformity and plan surgical management.

"Heart of Stone" image in Mayo Clinic Proceedings

Here is a link to a interesting case known as Heart of Stone that i discovered surfing the medical image (free) section on Mayo Clinic Proceedings.

Heart Of Stone-pdf

Mayo Clinic Proceedings-Medical Images

ABC's

Noah is a singer. For all of you that have not heard Noah sing his ABC's, I posted a video of him doing it. There's no picture, but the sound is pretty good. Every time he sees the lens of my camera phone he wants to play with it.

Who is the only entertainer to be honored with one of each of the five stars on the Hollywood Walk of Fame?

Stars can be honored for five types of entertainment styles with a star on the Hollywood Walk of Fame. The categories include: contribution to the film industry; contribution to the broadcast television industry; contribution to the recording industry; contribution to the broadcast radio industry; and contribution to live theater.

The singing cowboy Gene Autry is the only person to be honored with each of the five stars on the Hollywood Walk of Fame!

Creutzfeldt-Jakob Disease - Sporadic form

Findings

Figure 1, Figure 2, and Figure 3: T2, DWI, and ADC map show increased signal and restricted diffusion in the basal ganglia. More specifically there is symmetrically increased signal in the caudate and putamen with sparing of the globus pallidus. Additional areas of increased signal are seen in the right and left parietal cortex (Figure 4). No contrast enhancement was seen.


Diagnosis: Creutzfeldt-Jakob Disease - Sporadic form


CJD is a progressive fatal neurodegenerative disorder caused by prion proteins accumulating within the neurons.

There are three forms of CJD. A familial form, a sporadic form, and a variant or iatrogenic. form. The sporadic form (sCJD) is identified in 85% of cases. No genetic or infectious cause can be identified in these patients.

The familial or genetic form (fCJD) is seen in 15% of cases. These cases are identified by DNA analysis of the PRPC gene mutations.

Though it receives the most media attention, the infectious variant or iatrogenic form (vCJD) is the rarest, accounting for 1% of cases.

Diagnosis is based on clinical presentation, EEG findings, and a positive CSF analysis showing 14-3-3 proteins. MRI is reported to have high sensitivity and specificity for the disease with characteristic symmetric signal abnormalities in the basal ganglia and cortical abnormalities. The caudate and putamen are the most frequently involved nuclei. Thalamic involvement is only seen in 14% of patients with the sporadic form. However, thalamic involvement is seen in 78-100% of the variant/iatrogenic forms of CJD. The globus pallidus is usually spared. Diffusion weighted sequences are the most sensitive. Abnormalities are also well seen on T2 and FLAIR weighted sequences. The basal ganglia and cortical lesions show increased signal on T2 and FLAIR with persistent restricted diffusion. The cause of the restricted diffusion is not completely understood.

No treatment is available for the disorder at this time. The clinical course is usually progressive and rapid with most patients expiring within six months to one year from the time of diagnosis.

Radiology Quiz-What is the Diagnosis?

On popular demand here is the Radiology quiz. What is the diagnosis? this is a T2 weighted axial MRI image. Kindly submit your answers in the comments section. Correct answer will be put up here within this week.

DIAGNOSIS-

Diastematomyelia

Discussion: The congenital entity of diastematomyelia results from a splitting of the notochord during early development; the etiology of this phenomenon is, at present, uncertain. The result is a complete, longitudinal division of the spinal cord over a variable distance. The abnormality is most frequently encountered in the upper lumbar region, but may occur anywhere else along the length of the spinal cord. Division of the cord is often asymmetrical (i.e.), parasagittal); however, each hemicord possesses it's corresponding anterior and posterior horn cells and ipselateral nerve roots. Two subdivisions are recognized, and are described as follows:
Type I (50%): split cord, surrounded by a normal undivided arachnoid-dural sleeve; no septum (diastem)
Type II (50%): split cord; however, each hemicord is invested by a separate dural sleeve, divided by a fibrous, cartilaginous or bony septum (diastem).
Associated clinical/radiographic findings:
Vertebral anomalies associated with defective neural tubeclosure, resulting in the gamut of spinal dysraphisms.
Tethered cord, thickend filum terminale )75%)
Meningomyelocele
Intra/extradural lipoma
Dermal sinus

Case submitted by Dr MGK Murthy Senior Consultant Teleradiology Providers

Craniometaphyseal dysplasia

Findings

Marked thickening of the skull base with narrowing of all the neural foramina. Hydrocephalus.

Differential diagnosis:
- Craniometaphyseal dysplasia
- Frontometaphyseal dysplasia
- Craniodiaphyseal dysplasia
- Osteopetrosis


Diagnosis: Craniometaphyseal dysplasia


Discussion

Craniometaphyseal dysplasia is a rare genetic disorder whereby stromal cells are not able to differentiate osteoclast precursors, resulting in craniofacial and long bone abnormalities and cranial nerve palsies.
Autosomal dominant form has variable expression. Autosomal recessive is more severe.
Radiologic findings include hyperostosis of the skull base, narrowing of the neural foramina which exit the skull base, and fraying or "celery stalking" of the metaphyses, usually in the lower extremities.
These children have normal growth, normal intelligence, no bone fragility and no growth retardation.

In this particular case:
- This patient has had bilateral cranial nerve VII decompression secondary to bony overgrowth of the neural pathway. This patient also has optic canals which are 50% smaller than normal
- This patient developed new hydrocephalus due to stenosis of the jugular foramina. The resultant venous hypertension created hydrocephalus by disturbing the pressure gradient which is necessary for CSF drainage into the venous system

Other dysplasias similarly affecting parts of the skull:
- Craniodiaphyseal dysplasia: children have mental retardation, massive sclerosis of the skull, retarded growth
- Frontometaphyseal dysplasia: X linked, hyperostosis of the skull base and vertex, mandibular hypoplasia, sinus obliteration