Monday, July 30, 2007

Radiology Grand Rounds XIV



Here is a case of leaking aneurysm for the Radiology Grand Rounds submitted by Dr MGK Murthy of Teleradiology Providers

Concept of the Radiology Grand Rounds is available at- Radiology Grand Rounds.


Idiopathic dural dysplasia









Findings

Figure 1 and Figure 2: Axial and sagittal CT images demonstrate dural ectasia with a capacious thecal sac to the level of the sacrum.
Figure 3 and Figure 4: Sagittal T1 postcontrast and T2-weighted MR images reveal a dilated terminal thecal sac without a tethered cord. Benign subtle scalloping of the posterior margin of the lumbar and sacral vertebral bodies (Figure 4) is best visualized on the T2-weighted images.
Figure 5 and Figure 6: Axial T1 postgadolinium and axial T2-weighted MR images reveal a dilated thecal sac with root sleeve prominence.

Differential diagnosis:
- Idiopathic dural dysplasia
- Neurofibromatosis I
- Marfan syndrome
- Ehlers-Danlos syndrome
- Homocystinuria
- Achondroplasia
- Hurler syndrome (MPS IH)
- Syringomyelia
- Ankylosing spondylitis


Diagnosis: Idiopathic dural dysplasia


This case is an example of an expanded dural sac with posterior vertebral scalloping of the lumbar spine and sacrum. Findings include a capacious thecal sac with smooth scalloping of the posterior aspect of the involved vertebral bodies. Dural dysplasia most often occurs in the lumbar spine but can involve the cervical and thoracic spinal canal as well. The case described herein is mild as there is no resulting kyphoscoliosis or erosion of the pedicles which occurs in more severe cases. Making the diagnosis of dural dysplasia requires that one excludes other causes of the expansion of the canal such as syrinx, tumor or meningeal cyst. The differential diagnosis and etiology of dural dysplasia is extensive and should be distinguished from meningeal cysts. The patient in this case had no known cause for the dural dysplasia and only complained of back pain.


Meningeal cysts
- Type I meningeal cysts: are extradural cysts that do not contain nerve root fibers. Type IA cysts are extradural arachnoid cysts. Occult sacral meningoceles (OIM) are considered type IB meningeal cysts which are also extradural and do not contain nerve root fibers. OIMs present with smooth remodeling and enlargement of the sacral canal with an extradural arachnoid sacral cyst adjacent to the thecal sac.
- Type II meningeal cysts are extradural cysts that contain nerve root fibers. These include Tarlov cysts and spinal nerve root diverticula. Tarlov cysts are cystic dilatation of the sacral root pouches with associated bone erosion which may or may not be symptomatic.
- Type III meningeal cysts are true intradural arachnoid cysts.

Sunday, July 29, 2007

Avenida Then and Now!

Which of the two pictures below do you think looks better? The first photo I shot October 2006, while the second just last week(July 2007). I took both photos from the mezzanine floor of the Carriedo LRT station.


The Avenida of 2006 during Mayor Atienza's term?



Or the Avenida of today (2007) under Mayor Lim?

Vote now! (Not for Mayor..it's already finished with Lim as winner...) You can vote for the picture though.

Saturday, July 28, 2007

Image case-Osteosarcoma




Here is another case a 20 year old boy with a lower femoral swelling pain. CT scan done in a remote area was referred to us via Teleradiology.


Note the characteristic Spiculated (Sunray appearance) periosteal reaction & characteristic osseous destruction.


Friday, July 27, 2007

Arachnoid cyst with hemorrhage












Findings

Figure 1: CT of the brain without contrast demonstrates a left extra-axial mass occupying the left frontotemporal region, which is relatively isointense to the white matter, measuring approximately 20 Hounsfield units.
Figure 2 : CT of the brain with bone windows demonstrates slight deformity of the calvarium with thinning related to a long-standing process.
Figure 3, 4, 5, 6, 7 and 8: Axial T1, T2, FLAIR and SPGR sequences demonstrate increased signal intensity compatible with subacute hemorrhage into left middle cranial fossa arachnoid cyst with left-to-right midline shift. Note that this is an atypical arachnoid cyst as it does not follow CSF on all sequences.
Figure 9: DWI image from original study obtained several months prior shows characteristic low signal consistent with uncomplicated arachnoid cyst.


Diagnosis: Arachnoid cyst with hemorrhage


Arachnoid cysts are cerebrospinal fluid (CSF) collections contained within a wall of normal arachnoid cells. These structures represent the most common intracranial congenital cystic lesions. They arise during development when the embryonic meninges fail to merge with resultant splitting of the arachnoid membrane. Importantly, they do not openly communicate with the ventricular system or subarachnoid space and typically show delayed opacification upon intrathecal contrast administration.

These lesions account for approximately 1% of all intracranial masses. There is a predilection for males (3:1) and they may be seen in any age group with 75% occurring in the pediatric population. Most cases are incidental findings in adult patients with brain imaging performed for unrelated symptoms. They usually do not enlarge over time however, can expand when CSF pulsations become entrapped in the arachnoid cyst.

When symptoms are present, they are related to the location and size of the lesion. Small cysts are typically asymptomatic whereas large masses present with various clinical features. The most common symptoms and signs include headache, seizures, developmental delay, hydrocephalus, and increased intracranial pressure. Focal neurological signs secondary to direct compression occurring less frequently.

These lesions demonstrate characteristic features on imaging studies as cystic cisternal masses with thin walls containing CSF density (CT) or intensity (MR) fluid. CT findings include a CSF attenuation mass (0 to 20 Hounsfield units) with sulcal effacement, displacement of surrounding structures, and remodeling or erosion of adjacent bone. There is no enhancement of the cystic contents or wall and calcification is rare. Occasionally, hemorrhagic products or proteinaceous fluid may result in higher attenuation and in these cases, MR is often the diagnostic modality of choice. On MR imaging, the extra-axial mass demonstrates signal intensity identical to CSF on all pulse sequences. Thus, it has low signal intensity on T1WI and high signal intensity on T2WI. Additionally, the FLAIR sequence shows a low signal (fluid-attenuated) lesion and diffusion-weighted imaging (DWI) also reveals a low intensity mass demonstrating absence of restricted diffusion.

Most cases do not require treatment and surgery is reserved for cases where symptoms correlate with anatomic location. Treatment options include conventional shunt placement for drainage into the peritoneal cavity or alternatively, cyst fenestration into normal CSF pathways (decompression) through an endoscopic approach or open craniotomy. Patients should be followed with serial scans for progressive cyst enlargement. As this case demonstrates, intracystic hemorrhage is a potential complication. Additional sequelae include secondary infection of the cyst or development of a subdural hematoma/hygroma.

Thursday, July 26, 2007

Neurosarcoidosis









Findings

There is demonstrate diffuse, nodular meningeal thickening and enhancement along the convexities, interhemispheric fissures, and skull base. There is associated underlying parenchymal edema within the frontal lobes.

Differential diagnosis
- Granulomatous disease (namely, sarcoid)
- Meningitis
- Metastases
- Meningioma
- Histiocytosis


Diagnosis: Neurosarcoidosis (dural and parenchymal involvement)


Key points

Multisystem inflammatory disease characterized by noncaseating epithelioid-cell granulomas; etiology unknown
CNS involved in 5% clinically (27% autopsy); 10-20 per 100k in North America

Involves
- Dura, leptomeninges, subarachnoid space
- Brain parenchyma to include hypothalamus>brain stem>cerebral hemispheres>cerebellar hemispheres

Solitary or multifocal CNS mass(es)
Approximately 50% have periventricular T2 hyperintense lesions
Perivascular infiltrative involvement Virchow Robin spaces
May induce a small vessel vasculitis

Clinical Presentation:
- Most common symptom - CN deficit(s); most often CN VII; up to 50% asymptomatic
- Age of onset – 3rd-4th decade; 3-5% children; M:F 2:1; African American: Caucasian 10:1
- Pulmonary involvement in >90% of patients (abnormal CXR in association with CNS involvement strong evidence)

Course/Treatment:
- 2/3 have self limited monophasic illness; remainder have chronic remitting-relapsing course
- No known cure


Radiology

CT:
- May show basilar leptomeningeal enhancement
- Osteolytic skull lesions

MR:
- T1 + Contrast
Wide spectrum of enhancement
1/3 have multiple parenchymal lesions
>1/3 have leptomeningeal involvement, nodular and/or diffuse
10% solitary intra-axial mass
5-10% hypothalamus, infundibular thickening
- FLAIR:
Approximately 50% with periventricular T2 hyperintense lesions
Hyperintense vasogenic edema secondary to perivascular infiltrates or small vessel vasculitis
- T2:
Lacune (brainstem, BG)
Hypointense material within subarachnoid space
Hypointense dural lesion(s)
Hydrocephalus

Saturday, July 21, 2007

I went to downtown Manila this afternoon to buy some camera accessories. It was raining when I arrived in the train station of Recto and proceeded to Avenida.

I was surprised to see that Avenida Park is now once again open to traffic, with the familiar jeepneys now plying it's stretch from Recto to Sta. Cruz. I found that mayor Lim ordered its opening to traffic immediately after taking his office.

It can be remembered that during Mayor Atienza's term, he turned this stretch of Avenida into a public park, complete with tiled flooring, sculptured plants and cozy benches. I was so happy with this project of Mayor Atienza and even wrote something about the daily life of downtown Manila here.

Now Mayor Lim ordered to open it once again to traffic. I'm quite angry at this development. When I see something that has already been developed and beautified, and then recklessly ignored and turned back to what was ugly before, I feel angry.

Mayor Lim justified his action by saying that Avenida Park has become a haven for pickpockets, drug dealers, and prostitutes.
To my knowledge, these problems already existed in Avenida even during his first term as Manila Mayor, so the park should not be blamed for these happenings. Maybe Mayor Lim should have just increased police presence in the area..

Well, inasmuch as I want to rant about this, I can't do anything about it. But it definitely calms down my nerves a bit when I voice out my anger.



Jeepneys once again ply in this portion of Avenida that was previously made into a park during Mayor Atienza's term.


....and what it was before, a public park with cozy benches and tiled colored flooring...

Friday, July 20, 2007

Teleradiology business models

I found an interesting article in J Telemed Telecare. 2005;11(6):271-5 on various business models followed by various teleradiology providers worldwide. According to Mun Sk et al A number of new diagnostic radiology services have emerged which use teleradiology. The main themes include: (1) stand-alone teleradiology practice; (2) the "Nighthawk"/on-call coverage; (3) solo radiologist practice; (4) expert/second-opinion teleradiology; (5) a global virtual radiology service based on workload sharing and reallocation.

In our own company Teleradiology Providers we follow the model of expert opinion as we have done in various centres around Delhi and Second opinions as sent over to us & sharing of work in the inetrnational market.

Thursday, July 19, 2007

Juvenile angiofibroma







Findings

CT shows a soft tissue mass extending from pterygopalatine fissure into sphenoid sinus with some erosion and expansion of adjacent bony structures. Angiography shows a major hyper vascular tumor supplied by sphenopalatine branch of right internal maxillary artery, without ascending pharyngeal artery supply. Minimal tumor blood supply from sphenopalatine branch of left internal maxillary artery. Super selective embolization of left and right sphenopalatine arteries was performed using Echelon-14 micro catheter and RVA particles (150-250 microns).


Diagnosis: Juvenile angiofibroma


Key points

Epidemiology:
- 1 of every 5,000-6,000 otolaryngological admissions.
- Approximately 0.5% of all head and neck neoplasms.
- Occurs exclusively in adolescent males.

Pathophysiology:
- Highly vascular tumors, locally invasive, non-encapsulated tumors.
- Usually arise at posterior attachment of middle turbinate, near the sphenopalatine foramen.
- Superior growth occurs towards sphenoid sinus, with erosion possible. Invasion into cavernous sinus may also occur.

Clinical:
- Symptoms: epistaxis (45-60%), nasal obstruction (80-90%), headache (25%), facial swelling (10-18%).

Treatment:
- Definitive therapy is usually surgical, with pre-operative embolization to control intraoperative bleeding.
- Hormonal therapy (with testosterone blockers) and radiotherapy have been tried with mixed results.


Radiologic overview

Usually suspected via findings on CT, but angiography used for definitive diagnosis and possible embolization prior to definitive surgery.
Most suggestive finding is a homogenous, nasopharyngeal soft tissue mass causing expansion of the nasal cavity, sometimes with septal deviation, and extending into the pterygopalatine fossa and sphenoid sinus.
Often see anterior bowing of the posterior wall of the ipsilateral maxillary sinus, but rarely with breakthrough into the antrum. Conversely, the tumor often extends superiorly with erosion into the sphenoid sinus, and possibly with extension into the cavernous sinus.
Angiography: 94% of the time, primary feeder system comes from branches of the external carotid system (usually from maxillary artery, but may also include ascending pharyngeal or vidian arteries).

Wednesday, July 18, 2007

Sjogren syndrome involving the parotid glands





Findings

Figure 1 and Figure 2: There are diffusely enlarged, heterogeneous parotid glands with invasion of the carotid space and punctate calcifications in the left parotid gland. Discrete areas of low attenuation likely represent areas of parenchymal destruction or contained saliva.


Diagnosis: Sjogren syndrome involving the parotid glands


Sjogren’s syndrome is a chronic, systemic exocrinopathy secondary to lymphocytic infiltration of the salivary and lacrimal glands. Sjogren’s is the second most common autoimmune disorder after rheumatoid arthritis. Sjogren’s affects patients between 50-70 years of age with a 90% to 95% female predominance. Sjogren’s is primarily characterized by dry eyes (keratoconjunctivitis sicca) and dry mouth (xerostomia) although patients may develop symptoms referable to multiple organ systems similar to systemic lupus erythematosus. Certain systemic manifestations are unique to Sjogren’s syndrome such as interstitial nephritis, hyperglobulinemic purpura, and an increased risk of lymphoma. On the opposite end are patients complaining of dry eyes and mouth with vague symptoms of fatigue, myalgia, and cognitive dysfunction which may be difficult to distinguish from fibromylagia or depression.

The diagnosis of Sjogren’s syndrome involves both subjective and objective criteria. Patient’s complain of inadequate tear production and decreased saliva production. Ocular signs of corneal damage are present on physical exam (Schirmer’s or Rose Bengal) with a slit lamp exam. Laboratory diagnosis of Sjogren’s syndrome involves detection of antibodies to the Sjogren A or B antigen, SS-A (Ro) and SS-B (La). Labial biopsy and additional test indicating impaired salivary gland function may also be performed.

There are primary and secondary forms of the Sjogren’s syndrome. Primary Sjogren’s syndrome generally consists of dry eyes and mouth due to salivary and lacrimal gland destruction via autoimmune activation of lymphocytes. Secondary Sjogren’s syndrome, usually due to rheumatoid arthritis, causes symptoms related to exocrinopathy and collagen vascular disease. These patients have high titers of the SS-A antibody. Other secondary causes of Sjogren’s syndrome include systemic lupus erythematosus or scleroderma.

The imaging appearance of the parotid glands in Sjogren’s syndrome is varied and depends on the stage of the disease. The parotid glands may appear normal in the early stages. Multiple small cysts in both parotids can be seen in the intermediate form of the disease. Late stage Sjogren’s syndrome of the parotids involves large cystic and solid masses. The cystic components represent areas of destroyed gland or collections of saliva while the solid masses represent lymphoid aggregates which actively destroy the gland. Contrast enhanced CT typically demonstrates bilateral parotid enlargement, heterogeneous enhancement of solid and mixed cystic lesions and punctate calcifications. MR sialography is the best imaging test if Sjogren’s syndrome is suspected because of its ability to accurately stage the severity of the disease.

No radiology professionals in the google advisory board!!

Google’s decision to set up an advisory group has sparked controversy as well as congratulation. While the lack of nursing professionals or health librarians has caused a storm of protest on health blogs, it also appears it’s also a ‘no show’ from the radiology community too. The stated composition includes healthcare experts from “provider organizations, consumer and disease-based groups, physician organizations, research institutions, policy foundations, and other fields”.While the list of participants is impressive there’s no obvious representation from medical imaging professionals. In response the head of the American College for Radiology (ACR) Arl Van Moore wrote to Google to say it was pleased to hear that the advisory group was being established: "However, it is unfortunate, and frankly quite puzzling, that Google has apparently chosen not include a representative from radiology, a vital, and increasingly far reaching area of medicine."
Reference-
Author: Stuart Hall

Tuesday, July 17, 2007

Maganese in brain on MRI

"Manganese (Mn) accumulation in the brain is detected as symmetrical high signal intensity in the globus pallidi on T1-weighted MR images without an abnormal signal on T2-weighted images. Mn accuulation in the brain is due to acquired or congenital diseases of the abdomen including hepatic cirrhosis with a portosystemic shunt, congenital biliary atresia, primary biliary cirrhosis, congenital intrahepatic portosystemic shunt without liver dysfunction, Rendu-Osler-Weber syndrome with a diffuse intrahepatic portosystemic shunt, and patent ductus venosus. Other causes of Mn accumulation in the brain are Mn overload from total parenteral nutrition and welding-related Mn intoxication."

Neuroradiology 2007 Jul 12; [Epub ahead of print]

Monday, July 16, 2007

PACS reporting room-How Dark Should It be?



According to RSNA news Not pitch black, but about 40-25 lux, comparable to a dim hotel room at night, according to one study.


RSNA News May 2007 (p 13-14).


Hat tip--MidEssexRay

Saturday, July 14, 2007

Nikon D40x Sample Shots

I have a new camera in my hand, the cheapest and smallest dslr today, a Nikon D40x. I am amazed at how small this camera is, and how easy it is to use. It's amazing how Nikon could have managed to create a dslr of this tiny size.

The grip is fatter than my Canon 400D, and much easier to hold than my Nikon D80. The LCD screen is bright, and the viewfinder is large. It is tiny in size, it can fit into my small backpack and carry it anywhere without feeling a burden of carrying a dslr.
What about pictures? I took some test shots and I'm amazed at how well saturated the colors are, even just using the standard kit lens. Nikon D40x + kit lens is much better than my more expensive Nikon D80+ kit lens.

Now I'm thinking of selling my Nikon D80 in Ebay, and just keep my D40x forever. It is cheap, it is light and it delivers amazing images.
Here then are some sample shots of this camera. All images taken with the supplied cheapy 18-55mm II lens



Eurotel Hotel. My favorite hotel in Cubao.


New Frontier Theater. Closed for renovation. A place of my vivid romantic memories of yesteryears. I liked the KKK part of this theater. Kataas-taasan, kasuluk-sulukan, at kadilimdiliman.


Araneta Center Bus Terminal Station

A fruit market



Divisoria Night Market

A Macro shot of Dancing Buddha



A Lion's Head

Submissions are requested for the Upcoming Radiology Grand Rounds

Next Radiology Grand Rounds will be hosted on last sunday 29-7-2007 of this month at John Hopkins MRI by Christopher , so hurry send all your Radiology Related submissions to me at sumerdoc@yahoo.com or to christopher at christopheraj@poczta.wprost.pl

If you are not familiar with the concept of the Radiology Grand Rounds check out the archive and concept here-Radiology Grand Rounds

Friday, July 13, 2007

Radiology Wiki

"Recent developments in online collaborative technologies such as Wikipedia (http://www.wikipedia.org/) have demonstrated the potential usefulness of an online reference resource produced as the collective effort of many users. Although this type of resource has enjoyed success in the public arena, however, its value remains unproved in the academic community. RadiologyWiki (http://www.radiologywiki.org/) applies the technology and methods of collaborative authorship to create a dynamic online radiology educational resource. The World Wide Web site capitalizes on the core technology of Wikipedia, allowing individuals with little technical experience to easily create, categorize, and search for articles by using a standard Web browser."
Ref-
RadiologyWiki.org: The Free Radiology Resource That Anyone Can Edit. Jonathan L. Streeter, Michael T. Lu, and Frank J. Rybicki. RadioGraphics 2007;27:1193-1200

Thursday, July 12, 2007

Bilateral optic nerve glioma




Additional clinical history: Patient also has café au lait spots, and his mother has a history of Neurofibromatosis Type 1.


Findings

CT Head: There is enlargement of the bilateral optic nerves and optic chiasm.
MRI Brain: There is fusiform enlargement of the optic nerves bilaterally, with extension to the optic chiasm. The optic nerves demonstrate isointense signal to grey matter on T1 (and, not shown, also on T2 and FLAIR images), with contrast enhancement.

Differential diagnosis:
- Optic nerve sheath meningioma
- Optic neuritis
- Pseudotumor (Idiopathic orbital inflammatory disease)
- Adult malignant optic glioma
- Bilateral optic nerve glioma associated with NF-1


Diagnosis: Presumed bilateral optic nerve glioma in NF-1 patient


Key points

General:
- Most common cause of optic nerve enlargement
- Much more common than optic nerve sheath meningioma (up to 4 times more common)
- 3% of all orbital tumors
- Treatment may include radiation, chemotherapy, or surgery if needed
- Strong association with NF-1
Up to 50% of cases of optic nerve glioma involve patients with NF-1
Conversely, 15% of patients with optic nerve glioma have NF-1
May be bilateral in NF-1

Clinical Presentation
- Patients present with progressive vision loss
- May have proptosis
- Age at presentation is median of 5 years old
- Approximately 80% occur by 10 years of age
- Rarely progress after 6 years old, with cases of spontaneous regression

Pathology
- Grade I astrocytoma of the optic nerve
- Same histologic appearance as juvenile pilocytic astrocytoma


Radiology

Fusiform or sausage like enlargement of the optic nerve
Resulting in kinking of the optic nerve
May extend into proximal optic pathway, including optic chiasm, optic tracts, lateral geniculate body, and optic radiations
Demonstrates variable enhancement
Causes enlargement of optic canal

CT
- Isodense optic nerve enlargement
- Rare to have calcification (different from meningioma)

MR
- T1 iso/hypointense
- T2 variable signal
- Variable enhancement

Corpus callosum lipoma, Agenesis of the corpus callosum, and Chiari I malformation









Findings

Nonenhanced axial CT demonstrates a well-defined, very low attenuation (fat) mass in the region of the roof of the third ventricle/genu of the corpus callosum. More inferiorly (Figure 2 and Figure 3), extension of the mass through the foramina of Monroe is noted (Figure 2). There are bilateral linear calcifications, which are classic for callosal lipoma (Figure 1, Figure 2, and Figure 3). In addition, there is parallel alignment of the lateral ventricles, suggestive of dysgenesis of the corpus callosum. There is also prominence of the occipital horns of the lateral ventricles (Figure 2), termed colpocephaly.
Axial T1 (Figure 4) weighted MR image through the center of the mass demonstrates a homogeneous very high signal mass in the region of the genu of the corpus callosum. Parallel orientation of the lateral ventricles is again seen. Incidentally noted is a large scalp lipoma.
Axial FLAIR (Figure 5) MR image in the same location demonstrates the callosal mass and the the scalp lipoma.
Sagittal T1 (Figure 6) weighted MR image in the midline demonstrates a fat intensity mass with absence of the corpus callosum. In addition, the cerebellar tonsils protrude approximately 5 mm below the level of the foramen magnum (blue arrow), consistent with a Chiari I malformation. Another scalp lipoma is also noted.


Diagnosis: Corpus callosum lipoma, Agenesis of the corpus callosum, and Chiari I malformation


CNS lipoma is an uncommon congenital lesion and constitutes less than 1% of brain tumors. Its most frequent location is the genu of the corpus callosum, tuber cinereum, and quadrigeminal plate cistern. The optic chiasm, interpeduncular cistern, sylvian fissure, cerebellopontine angle, and cerebellomedullary cisterns are less common locations.

CNS lipoma has the classic appearance of a discrete fatty mass. It often (especially when located within the corpus callosum) has a calcified rim, which can form a “bracket sign” on frontal radiographs, and this appearance is pathognomonic. It is very low attenuation on CT, homogeneously high in signal on T1- and T2-weighted MR images, and demonstrates no enhancement.

Approximately half of patients are asymptomatic at the time of discovery. Agenesis of the corpus callosum can be associated with colpocephaly, the disproportionate dilation of the occipital horns of the lateral ventricles compared to the frontal horns. This is felt by most to be due to decreased brain volume within the posterior fossa. However, colpocephaly and hydrocephalus can coexist, and the frontal and temporal horns should be carefully evaluated in the context of the clinical presentation.

There is a known association between callosal agenesis and other midline defects, including Chiari malformations, Dandy-Walker cyst, encephalocele, and others. A careful search should be undertaken for these congenital anomalies in any patient with callosal agenesis. In this patient, multiple scalp lipomas were also noted, raising the possibility of a lipomatosis syndrome.