Justice for Rizal!

Ka Ed Punzalan is a man on a mission. Since 1995 and up to the present, he has been deep in research, compiling facts and figures so that he could finally bring to the court of justice the killers of Dr. Jose Rizal—114 years after the hero was shot by a firing squad. The hero was executed here in Bagumbayan (now Luneta) at exactly 7:03 am, on December 30, 1896 by order of the Spanish Military Tribunal for the charges of sedition and rebellion against the government.Ka Ed believed--and rightly so--that Rizal's trial was a farce.

Fast forward December 30, 2010— Ka Ed was standing on the very ground where Rizal fell, distributing leaflets to people, giving impromptu speeches, and promising that he will re-open the Rizal murder case. This was where I met Ka Ed, as I was also on a pilgrimage to the exact execution ground of the Philippine National Hero.

A native of Pampanga, Philippines, Ka Ed grew up with stories of Rizal’s heroism and greatness embedded in his young mind. Although he didn’t get past Grade Six, Ka Ed was a voracious reader of history. As a young man, he read the various biographies of Rizal and became a staunch admirer of the dead hero. Fifteen years ago, he started his crusade to research on available resources so that he could prove once and for all there is still a case against those responsible for the patriot's death.

Earlier in the morning, Ka Ed attended the memorial ceremonies at the Rizal Monument led by President Benigno Aquino III. Ka Ed wanted to have an audience with President Aquino so that he could personally present his case to P-noy, but he could not get through the tight security around the president. I told him that presidents have daily schedules that should be followed and one cannot just go through him at whim.

Ka Ed was complacent. “I will go to Malacanang one day and ask for an appointment”, he said. Meanwhile he started giving out to pedestrians and tourists brochures documenting his various researches. “Here”, he said to me and some of the curious onlookers who stopped by to listen to his impromptu speech,“are the facts that we could use to sue the killers of Rizal.”

I could not for the moment believe what he was saying. Rizal has been dead for many years; whoever killed the hero couldn't still be around today. No mature person alive in 1896 could still be living in 2010. I was here in the Luneta to pay homage to the national hero; but meeting Ka Ed and knowing his strange case is totally unexpected. Indeed, I expected to meet some Rizalistas here as I have in the past—those who believe that Rizal is God and therefore still alive--they always flock to the Luneta on December 30 and June 19 to honor God Rizal. But Ka Ed is not the usual Rizalista you would meet in the Luneta, Calamba, and Mount Makiling. He doesn’t believe that Rizal is God. He believes that Rizal is only a human being like you and me—but a great one, and Rizal was wrongly executed on December 30, 1896 on false charges. Ka Ed is very determined to set the facts straight and correct the injustice. He will exert every effort to re-open the Rizal murder case.

Admittedly, I find Ka Ed’s thinking quite unique, if not downright bizarre. Here was a man trying to put Rizal’s killers to justice. This is the first time I have ever heard a man trying to pursue this long-forgotten, albeit obviously neglected murder case. Ka Ed may be a lone crusader but he was a very determined one. He produced several photocopied sheets of his researches. I was astounded they ran into hundred pages, obviously a task that required a lot of time and energy. I am not prone to judge a person, but Ka Ed doesn’t exactly fall into the category of lunatic—he was quite a sensible man—though his mission is quixotic and unusual.

One of Ka Ed’s audiences said: “Malabo na ho yang sinasabi nyo. Matagal na hong patay si Rizal. At isa pa, patay na rin yung mga pumatay sa kanya. Sino pa ang ikukulong natin?”

The audience smiled but Ka Ed quickly replied, “Tama ka, pero makakakuha tayo ng damages para sa pagpatay nilang ginawa kay Dr. Jose Rizal”.

“Eh sino po ba ang pumatay kay Rizal, di po ba mga Gwardiya Sibil?” said a young man, presumably a college student and one who already took a Rizal course.

“Napag-utusan lang ang mga Guwardiya Sibil. Hindi sila ang may kasalanan kungdi yung mga mastermind”, said Ka Ed quite emotionally.

“E sino po yung mga mastermind?”

“Aba e di yung Gobernador Heneral, yung Hari ng Espanya, at Papa sa Roma noong panahon na yun. Si Gobernador Heneral Camilo Polavieja, Haring Alfonso XIII, at Papa Leo XIII. Patay na sila pero mahahabol pa natin ang bansang Espanya at Roma na magbayad sa atin ng damages”

“Magkano naman po ang damages”, asked another listener.

“We will demand that they pay us 333 Billion U.S. Dollars for the 333 years that they occupied our country. That’s 1 billion every year”, Ka Ed said.

Suddenly a wild applause from the audience erupted and Ka Ed was visibly pleased. But for me, I was getting a little tired of this. After making some excuses, I prepared to leave. But Ka Ed wanted me to wait, because on this very day, he would go to the Department of Justice to file a case to against Rizal’s killers. Fortunately, December 30, 2010 is a working holiday and all the government offices were open. The only problem is that Ka Ed didn’t know where the Department of Justice office was located. I said it’s in Padre Faura street, in Malate.

“Can you accompany me?” Ka Ed said.

Right then and there I would have said no, and instead just give him directions, but I supposed if I helped him go to the Department of Justice (DOJ), and possibly meet with Secretary Leila De Lima, the country’s chief attorney could advise him to stop his fantasies. This way he could retire from his mission (he was already 70) and perhaps embark on another worthwhile and more realistic mission (say, find the true killer/s of the Vizcondes).

So we went to the DOJ. We walked the convoluted Ermita streets, stopping by a few moments to buy crackers and soft drinks from a sidewalk vendor. In half an hour, we were at the gates of the DOJ. The kindly guards at the gates inquired where we wished to go. Ka Ed could barely contain his excitement. He said “I am going to file a case to re-open Rizal’s murder case and bring to justice those who killed him”.

The guards looked at one another, but they realized that Ka Ed was serious and surmised I was a reporter with a camera. The guards requested us to log in our names and directed us to the second floor of the DOJ building so we can meet Secretary De Lima. Unfortunately, the secretary was in an important meeting that could not be disturbed, even for such a momentous case as the murder of Rizal. We were directed instead to the office of one of the government prosecutors.

A kindly middle-aged woman warmly greeted us. “How can I help you sir?” asked the lady who happened to be one of the DOJ’s prosecutors (she declined to give her name though after realizing I was a reporter)

“Madam”, said Ka Ed “I want to file a case”.

“Is it criminal or civil?” asked the lady prosecutor.

“It’s criminal madam!” said Ka Ed, barely containing his enthusiasm “I want to file a criminal case against the killers of Dr. Jose Rizal!”

Now, the lady prosecutor was very matter of fact, very professional, as one could expect from a lawyer--not a little bit shocked by Ka Ed’s statement. She said without a hint of exasperation: “Sir, Rizal was killed in 1896, a period of 114 years. The prescriptive period for a criminal case has already elapsed. For a murder case to be pursued, one must file a case twenty years from the commission of the crime.”

Undaunted, Ka Ed replied: “If it’s not possible to file a criminal case here in DOJ, then I will go to the International Court of Justice to file this case”.

“Well, you certainly can sir. But I doubt if your case will be entertained”, said the lady prosecutor.

“At least I will give it a try, and I'm the only Filipino who have tried to get justice for Rizal” said Ka Ed proudly. Ka Ed asked the lady prosecutor a file form so that he could still file a murder case. The lady gave him one and Ka Ed enthusiastically filled up the blanks. In the blank where it asked what case was being filed, Ka Ed wrote: "Murder Case Against the Killers of Rizal".

Still Ka Ed thought that the DOJ might just ignore his plea. He still wanted to go to the International Court of Justice. He asked me, “Do you know where the International Court of Justice is located?”

Unfortunately,or rather fortunately I do not know where the International Court of Justice is. I thought that I had helped him enough. While I was about to walk away, Ka Ed said to me “Thank you ha? Ite-text kita pag nanalo itong kaso. Kailangan nating bigyang katarungan ang kamatayan ni Rizal!”

I smiled and wished him the best.

Going to the DOJ

Explaining to the DOJ security guards his important case to bring to justice Rizal’s killers.

Filing the murder case for the “heinous crime of murdering Rizal”

Ka Ed with a new supporter, Princess Bae Catiguman

Lecturing the people about Rizal and why it’s important to put to justice those responsible for killing Rizal and other Philippine heroes like Diego Silang, Gabriela Silang, the Thirteen Martyrs of Cavite, and the Three Martyred Priests Gomburza.

***This article originally appeared at the Philippine Online Chronicles, the world's leading online news magazine about the Philippines. For more interesting articles and news please visit our website here.

Juvenile angiofibroma-CT

Juvenile angiofibroma (JNA) is a benign tumor that tends to occur in the nasopharynx of prepubertal and adolescent males. This is 14year old male with epistaxis.  The tumor starts adjacent to the sphenopalatine foramen.  This tumour is enhancing, bilobed or dumbbell-shaped, with one portion of the tumor filling the nasopharynx and the other portion extending to the pterygopalatine fossa. This mass is seen to erode into sphenoid sinus and displaces the posterior antral wall anteriorly (antral bow sign)

Benign perimesencephalic SAH

Findings

Figure 1, Figure 2, and Figure 3: Axial CT images of the brain demonstrate SAH in the premedullary, prepontine, suprasellar, and interpeduncular cisterns.
Other figures (not shown): Representative images from a 4-vessel cerebral angiogram demonstrate no evidence of aneurysm or vascular malformation.


Diagnosis: Benign perimesencephalic SAH


Trauma and aneurysm are the two most common causes of SAH. At least 80% of cases of atraumatic SAH are caused by rupture of an intracranial aneurysm. When SAH is present, many clinicians request CT or MR angiography in order to quickly and non-invasively diagnose aneurysm. If an aneurysm is not detected with one of these modalities, conventional cerebral angiography (the gold standard for exclusion of aneurysm) is necessary. If the initial angiogram is negative, a second cerebral angiogram, typically performed 1-3 weeks after the first, is mandatory. This is because occasionally an aneurysm will be missed on the initial angiogram due to spasm or partial/complete thrombosis. The diagnosis of non-aneurysmal SAH can be applied to patients who have two consecutive negative technically adequate 4-vessel cerebral angiograms. Additionally, many clinicians request MRI of the spine to exclude the possibility of spinal AVM as a source for SAH.

The classic variety of non-aneurysmal SAH is known as benign perimesencephalic SAH or pretruncal nonaneurysmal SAH. As the name implies, the hemorrhage is situated around the midbrain and anterior to the brainstem in the ambient, interpeduncular, and prepontine cisterns. The term “benign” refers to the fact that after recovery from the initial episode, there is no increased risk of repeat hemorrhage. Cerebral vasospasm is less likely in these patients, but does occur. Hydrocephalus also remains a possibility during the acute phase. Although not clearly understood, one proposed mechanism of benign perimesencephalic SAH is rupture of the venous plexus anterior to the pons (the anterior pontomesencephalic plexus). This is postulated to occur as a result of increased venous pressure from strenuous activities such as exercise. Intramural hematoma of the basilar artery and rupture of a basilar perforating artery have also been suggested as alternate hypotheses.

Although benign perimesencephalic SAH has been known as a distinct clinical entity for some time, patients may present with non-aneurysmal SAH in an atypical distribution (non-perimesencephalic). In some of these patients, the total volume of hemorrhage is increased such that blood is present throughout the basal cisterns and extends over the cerebral convexities. In other patients, the hemorrhage is confined to the convexities, quadrigeminal cistern, or other atypical locations. In today’s case, Patient #1 presented with the classic variety of benign perimesencephalic SAH. Patient #2 presented with atypical non-aneurysmal SAH. Both patients recovered, and have had no repeat episodes of hemorrhage to date.

Possible causes of SAH:
- Trauma
- Aneurysm
- AVM
- Vasculitis
- Dural AV fistula
- Extension from intraparenchymal hemorrhage
- Dural venous sinus thrombosis
- Infection
- Neoplasm
- Idiopathic

Arteriovenous Malformation-Urinary Bladder

Localized arteriovenous malformation of the bladder is extremely rare.  When arteriovenous malformation is suspected, an angiogram and pelvic computed tomography or magnetic resonance imaging is essential to delineate the extent of the disease and to plan appropriate therapy. Common symptoms include pain, gross hematuria and acute urinary retention. This is a 60 year old male with previous history of unknown pelvic surgery and flow voids in the bladder base involving the seminal vesicles and prostate as well.

PET Isotopes produced without cyclotron

Advantage of PET is the use of the positron emitting biologic radiotracers, e.g., 11C, 13N, 15O ,  and most important 18F (Half life = 110 min) that mimic natural substrate. However, due to relatively short half-lives, they are unable to be transported to sites at great distances from the production facility.

(Generator nuclides)

44Sc --- Bone disease

 68Ga  --- Blood–brain barrier; tumor localization

72As-- Toxicological study

82Rb Myocardial perfusion

118Sb First pass angiography

128Cs Myocardial perfusion

Post Cricoid Carcinoma-CT

This is a 45 year old female with post cricoid carcinoma. The postcricoid region, pyriform sinus, and posterior hypopharyngeal wall comprise the hypopharynx. Tumors rarely appear in the posterior pharyngeal wall or postcricoid region without also involving the pyriform sinus. Well known etiological association is with Plummer-Vinson syndrome (Paterson-Brown-Kelly syndrome). The syndrome includes hypopharyngeal webs, usually centered in the postcricoid area.

Possible Pancreatic Cystosis

1. Pancreatic involvement in cystic fibrosis can result in exocrine or endocrine insufficiency. 
2. The spectrum of pancreatic appearances has been described as follows: complete replacement of the pancreas by fibrofatty tissue, with enlargement of the pancreas corresponding to lipomatous pseudohypertrophy; partial replacement of the pancreas by fibrofatty tissue; complete atrophy of the pancreas without fatty replacement; diffuse pancreatic fibrosis; and cystic transformation of the pancreas. Calcifications may also be found.  
3. Macroscopic cysts measuring more than 1 cm are a rare condition. Macrocysts of different sizes distributed throughout the gland represent an extremely unusual form of pancreatic involvement in CF that has been described in only a few patients and is known as pancreatic cystosis.

Lumbar disc extrusion with a wrapped disc

Findings

There is a left central disc extrusion at L5-S1 that causes mild to moderate left lateral recess narrowing and nerve root displacement without nerve root compression. At this level there is also contrast enhancement traversing the left laminectomy defect and encasing the disc extrusion, consistent with a wrapped disc. There is enhancement in the left lateral recess, suggesting post-operative fibrosis.

Differential diagnosis:
- Wrapped disc
- Peridural fibrosis
- Epidural abscess
- Epidural metastasis
- Nerve sheath tumor
- Disc pseudobulge
- Intervertebral disc protrusion
- Intervertebral disc extrusion
- Recurrent intervertebral disc herniation


Diagnosis: Lumbar disc extrusion with a wrapped disc


Key points: "Wrapped" disc


Disc herniation (protrusion, extrusion, or fragment) may be caused by trauma, repetitive or acute, and are a common source of pain and subsequent back surgery in the general population. In the acute phase, the herniated disc stimulates a fibrovascular response. A "wrapped disc" is the focal herniation (protrusion, extrusion, or fragment) that is encased in vascular scar tissue stimulated by this response and is evident by enhancement on contrast-enhanced T1-weighted images.

Asymptomatic or low back pain and/or radiculopathy are most common in the lumbar spine at L4-L5 and L5-S1. A wrapped disc is a post-surgical sequela, particularly following surgery for spinal stenosis in which the surgical procedure is more extensive, involving a laminectomy and a medial facetectomy.

Best imaging modality: MR (sequences: sagittal and axial T2WI and T1WI, as well as contrast-enhanced axial and sagittal T1WI)
Other imaging modalities: CT, myelography


Imaging findings

MR: Anterior extradural mass contiguous with the disc space extending into the spinal canal
*Contrast-enhanced T1WI: Peripheral enhancement surrounding the disc herniation or fragment with/without central canal, lateral recess, or foraminal stenosis and cord or nerve root impingement. (*most helpful MR sequence)
Non-enhanced T1WI: Isointense to parent disc
T2WI: Iso- to hyper intense to parent disc
General disc hypointensity and height loss at the level of the herniation, as well as postoperative changes (laminectomy defects, etc), degenerative facet disease, and osteophytes, are common associated findings.
CT:
Non-contrast CT: An anterior extradural soft tissue mass that may displace the nerve root / indent the thecal sac
Contrast-enhanced CT: Mild peripheral enhancement of the disc herniation/fragment
Myelography: An extradural mass that indents the thecal sac and nerve root sleeves
Imaging findings of other common differential diagnoses
Peridural fibrosis: Scar within epidural space after lumbar surgery that infiltrates epidural fat, causing homogeneous enhancement that diffusely surrounds the thecal sac and nerve root; increased in T2 signal relative to adjacent disc herniation
Epidural abscess: A distinct fluid collection in the epidural space with peripheral enhancement on post-contrast images, often associated with findings of diskitis
Epidural metastasis: Elongated (cranial-caudal orientation) enhancing mass with osseous involvement and may demonstrate paravertebral extension
Nerve sheath tumor: Avid enhancement surrounding the nerve root, some of which are in a "dumbbell" shape
Disc pseudobulge: Smooth generalized extension of the disc margin without a focal defect due to "uncovering" of disc related to spondylolisthesis
Intervertebral disc protrusion: Anterior extradural mass contiguous with disc space and triangular in shape with broader base than apex; no enhancement
Intervertebral disc extrusion: Anterior extradural mass contiguous with disc space by a "neck," in which this herniated disc material then widens in the epidural space
Recurrent intervertebral disc herniation: Extradural mass contiguous with intervertebral disc margin, demonstrating enhancement peripherally but without central enhancement
Treatment
Conservative: Anti-inflammatory and pain medications, avoid trauma
Surgical: Repeat surgery to remove herniated disc (protrusion, extrusion, fragment)

Intramuscular Cyst-Rotator cuff

The cause of intramuscular cysts is not entirely clear but may be similar to that of paralabral cysts in the shoulder and hip and parameniscal cysts in the knee. As in those other types of cysts, a defect in the surface of a rotator cuff tendon may allow fluid from the glenohumeral joint (or associated bursae) to enter the substance of the rotator cuff tendon and then dissect along the tendon fibers and intramuscular planes to form a cyst either within the sheath or within the substance of a muscle.

Pseudotumor cerebri - Idiopathic Intracranial Hypertension (IIH)

Findings

T2W axial MRI (Figure 1) shows signs of increased ICP, but only increased fluid within the optic nerve sheaths, flattening of the posterior orbit, and a partially empty sella.
The 3D TOF MRV Towne and RPO projections (Figure 2 and Figure 3) show bilateral, right greater than left, focal transverse-sigmoid venous sinus junction narrowing’s. It is not a normal MRV given the pt’s history, with more explanation in the discussion. There is no aneurysm or collection of collateral blood vessels seen in these images.

The AP and lateral (Figure 4 and Figure 5) venous phase carotid arteriogram shows long segment stenosis at transverse-sigmoid venous sinus junction distal to the vein of Labbé. Pre procedure venography showed a venous pressure gradient across this lesion of 17 mmH2O with 37 mmH2O on transverse sinus side and 15 mmH2O on internal jugular vein side.

AP and lateral (Figure 6 and Figure 7) venous phase carotid arteriogram shows long segment stenosis at transverse-sigmoid venous sinus junction with a balloon crossing the gradient lesion.


Diagnosis: Pseudotumor cerebri - Idiopathic Intracranial Hypertension (IIH)


Pseudotumor cerebri is defined by typical clinical symptoms which occur in the setting of elevated “idiopathic” ICP and a normal composition of CSF. Classic clinical symptoms include diffuse recalcitrant headaches, vision changes (including vision loss), and hearing changes (e.g., tinnitus), and the disease is typically seen in obese women who are 20-50 years of age. Papilledema is the most common physical exam finding, but visual loss and sixth nerve palsy are also seen. Other symptoms include disabling headaches and blindness. LP opening pressure is greater than 25 cm H2O. Brain computed tomography (CT) and magnetic resonance imaging (MRI) are typically normal, however, the following suggestive non-pathognomonic findings are frequently present:

– Cerebral venous sinus stenoses
– Flattening of the bilateral posterior sclera
– Partially or fully empty sella; enlargement of the chiasmatic recess of the 3rd ventricle
– Distension of perioptic nerve subarachnoid space
– Intraocular protrusion of the optic nerve head
– Orbital optic nerve vertical tortuosity

Treatment for pseudotumor cerebri typically includes medical management with acetazolamide and pain control for headaches. Furosemide and corticosteroids have been used, as well. Surgical interventions to treat pseudotumor cerebri include lumboperitoneal shunt (LPS) and ventriculoperitoneal shunt (VPS), which often produce immediate results, however, eventual return of pseudotumor symptoms occur in approximately 50% within three years. Optic nerve sheath fenestration is also used to treat vision changes, with variable headache relief. Dominant transverse/sigmoid venous sinus angioplasty and stenting are relatively new methods for the treatment of pseudotumor cerebri for those who have significant dural sinus stenosis. Given that 80% of intracranial vascular compliance is provided from the venous vasculature, reduction of pressure in the sinuses reduces CSF pressure. Better results are achieved in patients with documented high pressure gradients, and greater efficacy is seen with regard to arrest of visual loss (>90%) than with headache relief (~50%). Long-term results are lacking. however.

In this case, cerebral angiography demonstrated bilateral high-grade transverse/sigmoid sinus stenoses distal to vein of Labbe insertions. Selective catheterization of the right transverse sinus revealed an estimated 80% narrowing to a luminal diameter of 1mm, and a pressure gradient across the stenosis of 13 mmHg (normal <5 mmHg). The contralateral sinus was smaller, but distally stenotic. A stent was placed across the right sided stenosis.
The patient was placed on antiplatelet medication to preserve stent patency immediately after the procedure. She had no headaches after the procedure and demonstrated objective visual improvement at her one- and six-week follow-up examinations.

Now Google for Learning Anatomy

Google body browser

"Google has released a new Body Browser experiment that shows a detailed 3D model of the human body in Google Chrome web browser beta. Users can view through the anatomical layers of human body, zoom in and navigate to explore the human body parts. The new Google Body Browser is pretty commendable for use in a medical education environment and especially for radiologists who need to look up anatomy every now and then."

Have a look here-

http://bodybrowser.googlelabs.com/index.html

Omental Fat Necrosis

This is case of chronic pancreatitis with calcification and atrophy in pancreas. Along with fat attenuation lesion in the omentum with surrounding capsule seen on STIR images and adhesion to parietal peritoneum and surrounding stranding.

Intracranial pseudotumor (Tolosa-Hunt syndrome)

Findings

Increased CSF signal demonstrated by T2 hyper intensity within the right optic sheath. Nodular enhancement at the superior aspect of the right optic nerve at the orbital apex, which extends with prominent nodular enhancement posteriorly along the dural reflection of the right cavernous sinus. Asymmetric dilatation of the right superior ophthalmic vein.

Differential diagnosis:
- Meningitis
- Sarcoidosis
- En plaque meningioma
- Meningeal metastases
- Meningeal Non-Hodgkin's lymphoma
- Tolosa-Hunt syndrome


Diagnosis: Intracranial pseudotumor (Tolosa-Hunt syndrome)


Discussion

Intracranial pseudotumor (Tolosa-Hunt syndrome) is a part of a spectrum of "quasineoplastic" lesions that demonstrate orbital, intracranial, or pulmonary involvement, and include such other disorders as plasma cell granuloma and hypertrophic cranial pachymeningitis. It is a chronic granulomatous disease of unknown origin, which has been hypothesized to represent a low grade fibrosarcoma of inflammatory cells versus an autoimmune phenomenon. While Tolosa-Hunt syndrome is rare, orbital pseudotumor is the third most common ophthalmic disorder, and encompasses 5-8% of all orbital masses. Histologically, the lesions of Tolosa-Hunt demonstrate mixed lymphocytic and plasma cell infiltrate, with a variable degree of fibrosis. Lesions favor the cavernous sinus and basal meninges, although falcine and tentorial lesions have been described.

Patients with intracranial lesions are more frequently young adults, who present initially with chronic headaches or cranial nerve palsies. Patients with orbital involvement are more frequently middle-aged, and may present with painful proptosis and vision loss . Symptoms may be intractable, leading to severe disability. Untreated or unresponsive disease may progress to death. First-line treatment is invariably high-dose steroids, with radiotherapy or surgical resection reserved for patients with incomplete response to steroids .


Radiologic Overview of the diagnosis

The imaging hallmarks of Tolosa-Hunt syndrome are characterized by an enhancing, infiltrating meningeal mass, which favors the cavernous sinus or basal meninges, although falcine and tentorial involvement has been described . Focal meningeal thickening may range from just a few millimeters to a greater than 2 cm rind. With intracranial pseudotumor, orbital involvement is spared more than 90% of the time. Tolosa-Hunt remains a diagnosis of exclusion, once meningitis, en plaque meningioma, and meningeal metastases are ruled out.

The imaging modality of choice for imaging patients with Tolosa-Hunt remains MRI, although useful information may be gleaned from other modalities. On non-contrast enhanced CT (NECT), there are no specific findings to suggest the diagnosis; however, this modality may be of some value in differentiating the lesion from en plaque meningioma. On contrast enhanced CT (CECT), salient imaging findings include enhancing, thickened meninges or a curvilinear appearance of a single meningeal region. As aforementioned, MRI remains the primary modality for diagnosis of Tolosa-Hunt syndrome, and each sequence may provide critical information required to make the diagnosis. On T1WI, one may find focal thickening of the meninges that is isointense to gray matter. On T2WI, lesions are characterized as iso- to hypo intense regions of focal meningeal thickening, which may be more hypo intense as they become more fibrotic. FLAIR is of little help in making the diagnosis, but it is unlikely to demonstrate focal brain edema underlying the lesion . Contrast enhanced T1WI is the single most valuable sequence for evaluation of Tolosa-Hunt syndrome, and is characterized by diffusely enhancing region of meningeal thickening, which may range from a few millimeters to greater than 2 cm in some cases. Diffuse boney infiltrates may be appreciated on fat saturated contrast enhanced T1 sequence. While angiography is not considered a primary modality, severe disease may result in carotid artery narrowing, thus MRA may be a useful adjunct in the appropriate clinical setting.

The appropriate differential diagnosis of Tolosa-Hunt syndrome includes meningitis, sarcoidosis, en plaque meningioma, meningeal metastases, and meningeal Non-Hodgkin's lymphoma.

Branchial cleft cyst-CT

First branchial cleft cysts are divided into type I and type II. Type I cysts are located near the external auditory canal. Type II cysts are associated with the submandibular gland or found in the anterior triangle of the neck.

The second branchial cleft are most frequently identified along the anterior border of the upper third of the sternocleidomastoid muscle and adjacent to the muscle. However, these cysts may present anywhere along the course of a second branchial fistula, which proceeds from the skin of the lateral neck, between the internal and external carotid arteries, and into the palatine tonsil .

Third branchial cleft cysts are rare. Third branchial cleft cyst are characteristically located deep to the sternocleidomastoid muscle as in our case which was diagnosed as third branchial cleft cyst.

Thrombosed Aortic Aneurysm

Old man with a history of coronary artery disease  & pain and numbness in the lower extremities. Computed tomography showed a thrombosed  infrarenal abdominal aortic aneurysm and diffuse aortic atherosclerosis.  

Os Navicularis Syndrome-MRI

Os naviculare is a large ossicle adjacent to the medial side of the navicular bone. The tibialis posterior tendon often inserts with a broad attachment onto the ossicle. Most cases are asymptomatic but in a small proportion it may cause a painful tendinosis due traction between the ossicle and the navicular. Such changes are best seen on MRI as in our case with marrow and soft tissue edema on STIR images in relation to the bony ossicle.

Sciatic Schwannoma-MRI

MRI scan through the pelvic area  in a 15 year old boy shows large soft tissue mass arising in the retroperitoneal portion of the left  hemipelvis, extruding out into the subgluteal area through the sciatic notch. This picture suggests the diagnosis of sciatic schwannoma spanning the sciatic notch.