Cubao Blogged!

I'm proud to announce here my new blog on Cubao. In a small way, this is my tribute to the place where I was born and grew up.
There is not much yet in this new blog as I've just started it a week ago. But I will try to post regularly so that you'll learn more about the Cubao that I know.
So if you plan to visit Cubao someday, please feel free to visit my Cubaorepublic blog to help guide you through its ins and outs and everything in between.
I welcome you to my Cubao blog. Please click here: Cubaorepublic.blogspot.com

Hemangioblastoma

Findings

There is a right parasagittal lesion along the medial aspect of the cerebellum. The cystic mass has pronounced mass-effect on the dorsal brainstem and tectum. Extending from the cyst wall along one of the septations is an enhancing nodule.

Differential diagnosis:
- Hemangioblastoma (given patient age, the most likely diagnosis)
- Medulloblastoma
- Pilocytic astrocytoma


Diagnosis: Hemangioblastoma


Key points

The hemangioblastoma (HB) is a vascular neoplasm of unknown etiologycular. Cerebellar hemangioblastoma is the most common primary brain neoplasm involving the infratentorial space in adults. This benign tumor is readily curable by surgery. More than 85% of hemangioblastomas occur in the cerebellum, with the remainder occurring in the spinal cord, medulla, and cerebrum in a 4:2:1 ratio. Approximately 10% of posterior fossae masses are hemangioblastomas. Men are more commonly affected than females, and patients are usually young adults. The common symptoms are headache, nausea, vomiting, ataxia, and vertigo. In 40% of patients, polycythemia is present secondary to increased erythropoietin produced by the tumor (more common in solid tumors). A spinal hemangioblastoma may present with subarachnoid hemorrhage.

The classic findings of an HB are that of a cystic mass with a solid mural nodule (60% of cases), which is highly vascular and has serpentine signal voids of feeding vessels. However, 40% of HBs are solid. Less commonly, these tumors may be purely cystic. Overall, HB is a rare tumor representing 1-2.5 % of primary CNS neoplasms; 10-20% of all cases are associated with with von-Hippel-Lindau syndrome; converesly, 45% of patients with VHL develop HBs.

Treatment: Treatment frequently requires removal of the mural nodule only, since the cyst is not truly neoplastic. Preoperative embolization aids in resection of the highly vascular tumors. Prognosis is very good with 5-year a survival rate of more than 85%.


Radiology

Angiography: Vascular nodule with intense, prolonged stain; +/- avascular cyst.
CT: Low-density cyst with strongly enhancing mural nodule that abuts a pial surface (75%)
MRI: Cyst slightly hyperintense to CSF on T1WI; hyperintense to brain on T2WI; mural nodule variable but typically enhances strongly

Acute subdural hematoma

Findings

There is acute subdural hematoma along the tentorium. This extends along the posterior interhemispheric fissure. The ventricles are prominent out of proportion to the sulci raising the possibility of obstructive hydrocephalus. The fourth ventricle is normal in size. No definite tectal mass is appreciated.

Differential diagnosis: "Bright tentorium"
- Subdural hematoma
- Epidural hematoma
- Aneurysmal bleed
- Metastatic disease to the cerebellum with local bleeding
- Isodense primary CNS tumor (meningioma) with focal bleeding

Other subdural fluid collection
- Hygroma (clear CSF, no encapsulating membranes)
- Effusion (xanthochromic fluid from extravasation of plasma from outer membrane; 20% evolve into chronic SDH)
- Empyema (peripheral enhancement, restricted diffusion centrally)

Epidural Hematoma
- Biconvex extra-axial collection
- Often associated with fracture
- May cross dural attachments, limited by sutures
- Pachymeningopathies (thickened dura)

Chronic meningitis (may be indistinguishable)
- Post-surgical (shunt, etc)
- Intracranial hypotension ("slumping" midbrain, tonsillar herniation)
- Sarcoid (nodular, "lumpy-bumpy")

Tumor
- Meningioma, lymphoma, leukemia, metastases
- Dural based, enhancing mass
- ± Skull involved


Diagnosis: Acute subdural hematoma


Key points

Acute (± 6 hrs-3 days) hemorrhagic collection in subdural space
Diagnostic clue: Crescent-shaped, homogenously hyperdense on CT, extra-axial collection that spreads diffusely over affected hemisphere
May cross sutures, not dural attachments
May extend along falx & tentorium
Compresses & displaces underlying brain
Recurrent, mixed-age hemorrhage in a child raises suspicion of non accidental trauma!
CT density & MR signal intensity vary with age & organization of hemorrhage
Protocol advice: Use wide window settings (150-200 HU) to identify small SDH

Etiology
- Trauma most common
Stretching & tearing of bridging cortical veins as they cross subdural space to drain into dural sinus
Both nonimpact as well as direct injury
Trauma may be minor, particularly in elderly

- Less common etiologies include
Dissection of intraparenchymal hematoma into subarachnoid, then subdural space
Aneurysm rupture
Vascular malformations: Dural AVF, AVM, cavernoma
Coagulopathy

Predisposing factors
- Atrophy
- Shunting (leads to increased traction on superior cortical veins)
- Arachnoid cyst (middle fossa most common site)

Epidemiology: SDH found in 10-20% imaged & 30% autopsy cases following craniocerebral trauma
Associated abnormalities: > 70% of aSDH have other significant associated traumatic lesions

Arachnoiditis-MRI Findings

MRI is the study of choice for the diagnostic evaluation of arachnoiditis. T1-weighted MRIs may reveal an indistinct or absent cord outline due to the increase in the signal intensity of the surrounding CSF. T2-weighted MRIs may demonstrate CSF loculation and obliteration of the subarachnoid space or irregularly thickened, clumped nerve roots, which occasionally may be misinterpreted as a tethered cord or a thickened filum terminale. With more severe arachnoiditis, progression of nerve root clumping and leptomeningeal adhesions may lead to angular defects in the dural sac. Peripheral adherence of the nerve roots to the walls of the thecal sac produces the so-called featureless, or empty, sac.
Case by-- Teleradiology Providers

Radiology Blog and Sumer Sethi feature in RT Image magazine's 25 most influential list

After eliciting reader nominations and debating for hours, RT Image is proud to present the 2007 roster of radiology’s most powerful people, institutions and organizations. Whether their influence comes in numbers or from the dedication of one, all those on our list demonstrate the drive, character and integrity that deserve the title of “Most Influential.” Check out the number 24th for a mention of yours truly Dr Sumer Sethi and his experience with Rad-Blogging. I am proud that the concept of rad-blogging is now recognized as one of the 25 most influential in the world of Radiology.

Here is the link--

25 Most Influential

Recognizing radiology’s movers and shakers

Right cerebellar infarct demonstrating luxury perfusion

Findings

CT shows right cerebellar hemispheric hypoattenuation with edema, mass effect, and effacement of the 4th ventricle. Angiogram shows contrast blush in the right inferior cerebellar hemisphere with an early draining vein ("luxury perfusion"). Anterior and inferior displacement of the right PICA branch. No evidence of vertebral dissection or vascular malformation.


Diagnosis: Right cerebellar infarct demonstrating luxury perfusion


Key points

Luxury perfusion is a term used to describe increased circulation through an area of infarcted brain.
Thought to be due do vasodilation secondary to lowered oxygen tension and decrease tissue pH. (Loss of normal CBF autoregulation).
Angiographically seen as capillary blush and early filling of local veins.
The blush may simulate a tumor
Luxury perfusion can be seen in minutes to hours after infarction, usually resolves in 3-5 days. Never seen after 2 weeks.

Persistent Trigeminal Artery (PTA)

Findings

In Figure 1, an artery can be seen branching from the cavernous portion of the left internal carotid artery and joining the basilar artery. Notice the absence of this vessel on the right.


Diagnosis: Persistent Trigeminal Artery (PTA)


In the 3-5 mm human embryo, approximately 29 days after ovulation, four important arterial anastamoses join the dorsal aorta (the future internal carotid artery) to the bilateral longitudinal neural arteries (the future basilar artery). They are the trigeminal, otic, hypoglossal and proatlantal intersegmental arteries. The largest of these is the trigeminal artery. These arteries persist about a week and regress as the posterior communicating and vertebral arteries develop. For reasons that are not fully understood, these arteries sometimes fail to regress.

The most common persistent carotid-vertebrobasilar anastamotic artery is the trigeminal artery. The incidence has been reported to be about 0.2%, but if undiagnosed and unreported cases are taken into account, this number may approach 1%. There are two main classifications of a persistent trigeminal artery based on its anatomic position; lateral and medial. The lateral type leaves the cavernous sinus to course with the trigeminal root on the lateral side of the sella turcica in a groove of the posterior petrosal process and joins the basilar artery between the origin of the anterior inferior cerebellar artery and superior cerebellar artery. The medial type penetrates the sella turcica to run in its own groove and perforates the dura near the clivus to join the basilar artery.

A persistent trigeminal artery is usually an incidental finding, but has been reported to present with several clinical manifestations. Patients with a persistent trigeminal artery are at an increased risk of developing aneurysms. These aneurysms can be located either at their origin from the internal carotid artery or at their connection with the basilar artery. Depending on the artery’s anatomic location relative to the trigeminal and abducens nerves, patients can present with trigeminal neuralgia or sixth nerve palsies. Patients can present with vertigo and ataxia from embolization of a carotid atherosclerotic plaque through a persistent trigeminal artery into the posterior circulation. Patients can present with the same symptoms with a carotid occlusion which can cause a vascular steal phenomenon from the basilar artery to the carotid system through a persistent trigeminal artery. Patients with complications from a persistent trigeminal artery can be treated with endovascular or surgical interventions.