Mineralization of Substantia Nigra and red nucleus in SWI

Dolichoectasia of the Vertebrobasilar System

The Rt VA is measuring 6.2mm and left VA is hypoplastic, with non-visualized V4. Basilar artery measued maximum diameter of 6.9mm and is seen compressing the antero-lateral pons on the right side.


Other names for this disorder include dolichoectasia, megadolichoectasia, fusiform aneurysm of the vertebral and basilar arteries, and tortuous vertebrobasilar system.


The mean diameter of the normal basilar artery is 3.17 mm at the level of the pons, and the bifurcation is located in the interpeduncular cistern adjacent to the dorsum sellae or in the suprasellar cistern below the level of the floor of the third ventricle.The major criteria for diagnosis of VBDE are an arterial diameter of over 4.5 mm at any location along its course and deviation of any portion by over 10 mm from the shortest expected course.

The vertebrobasilar system can be considered elongated if the basilar artery lies lateral to the margin of the clivus or dorsum sellae, or if it bifurcates above the plane of the suprasellar cistern. Ectasia can be considered to be present if the basilar artery has a diameter greater than 4.5 mm.
(Ref - Smoker WR, Corbett JJ, Gentry LR, Keyes WD, Price MJ, Mc- Kusker S. High-resolution computed tomography of the basilar artery, 2: vertebrobasilar dolichoectasia: clinical-pathological correlation
and review. AJNR Am J Neuroradiol 1986;7:61–72)


While many patients are asymptomatic, these cases illustrate some of the diversity of symptoms associated with vertebrobasilar dolichoectasia. Patients may present with cranial nerve dysfunction, transient ischemic attacks, hydrocephalus, and subarachnoid hemorrhage, rarely midbrain infarct associated with vertebral artery dissection, an unusual complication of dolichoectasia.
Ref : Vertebrobasilar Dolichoectasia: Evaluation with CT Angiography
Pedro T. Vieco, Edward E. Maurin III, and Cordell E. Gross, AJNR 1997


NOTE: Dolichoectasia has been also described in Anterior Circulation.
Ref : http://www.ajnr.org/content/16/7/1548.full.pdf

Another case of Fenestrated Left SCA - MRA

Strange..another case of fenestrated left Superior cerebellar artery..another patient.

Fenestration of Left Superior Cerebellar Artery

Looks like a fenestrated left Superior Cerebellar Artery, incidental finding  in a patient evaluated for right hemiparesis.

Similar cases:

1. Acta Neurochir (Wien). 1991;109(1-2):66-71.

Anomalies of the P1 segment of the posterior cerebral artery: early bifurcation or duplication, fenestration, common trunk with the superior cerebellar artery.

Caruso G, Vincentelli F, Rabehanta P, Giudicelli G, Grisoli F.

http://www.ncbi.nlm.nih.gov/pubmed/2068971?dopt=Abstract

Mesenteric Venous Thrombosis Part 1

Mesenteric Venous Thrombosis

Mesenteric ischemia encompasses a broad spectrum of diseases

   1.     acute arterial occlusive disease,

   2.     nonobstructive mesenteric arterial insufficiency,

   3.     mesenteric venous occlusion, and

   4.     chronic mesenteric ischemia

Venous occlusions account for a relatively small percentage of such cases, about 15%–20%.

Mesenteric venous thrombosis can be classified on the basis of its cause as primary or secondary.

Spontaneous, idiopathic thrombosis of the splanchnic veins not associated with any predisposing conditions has been termed primary mesenteric venous thrombosis.

Patients with known medical conditions or factors associated with portal or mesenteric venous thrombosis, such as pancreatitis, hypercoagulability states, cirrhosis, or surgery, are said to have secondary mesenteric venous thrombosis.

Cases may also be classified into acute and chronic presentations for management purposes. Acute mesenteric venous thrombosis is defined as the process that exists in those patients with presenting symptoms of less than 4 weeks duration.

 Typical signs and symptoms of acute bowel ischemia were found to include pain out of proportion to the physical findings.

The differential diagnosis for acute mesenteric ischemia is extensive, comprising both 

intravascular and extravascular causes.

-         Arterial causes include embolic or atheromatous disease, dissecting aortic aneurysm, arteritis, fibromuscular dysplasia, endotoxin shock, hypoperfusion (shock, hypovolemia), direct trauma, and disseminated intravascular coagulation. Arterial causes can be further subdivided into occlusive mesenteric infarction (embolus lodging distal to the middle colic artery or thrombosis of the superior mesenteric artery) and nonocclusive mesenteric ischemia (pre-existing atherosclerosis with a systemic low-flow state).

-         Venous causes make up a much smaller percentage of cases and are generally seen in younger patients, typically in the setting of abdominal surgery.

-         Extravascular causes include incarcerated hernia, volvulus, intussusception, and constricting adhesive bands.

Chronic mesenteric ischemia

-    

      Most patients with chronic disease are asymptomatic until late complications occur, such as variceal bleeding due to portal hypertension. Weight loss, food avoidance, vague postprandial abdominal pain, or distention may also be demonstrated. The pain usually occurs within the first hour after eating, diminishing over the next 1–2 hours.

Radiologic Findings of MVT

-         Radiographic findings of bowel ischemia or infarction demonstrated on plain radiograph or barium studies are usually nonspecific;

o   most often, these studies demonstrate a nonspecific ileus pattern with dilated, fluid-filled loops of bowel.

o    Thumbprinting (focal mural thickening secondary to submucosal hemorrhage), separation of bowel loops due to mesenteric thickening, intramural pneumatosis, and mesenteric or portal venous gas may occasionally be seen but usually indicate late-stage disease.

     Doppler Ultrasonography

Venous flow anomalies or thrombus, a thickened bowel wall, free intraperitoneal fluid, and biliary disease can also be demonstrated.

Cortical Laminar Necrosis

“Cortical laminar necrosis” was defined as hyperintense cortical lesions on T1-weighted imaging found during the subacute or chronic phase of brain damage.

(** Ref : Susceptibility-Weighted Imaging Findings of Cortical Laminar Necrosis in Pediatric Patients
T. Niwaa, N. Aidaa, A. Shishikuraa, K. Fujitaa and T. Inoueb (AJNR oct 2008))

Although, the mechanism of T1 shortening in cortical laminar necrosis remains unclear, high cortical intensity on a T1-weighted image is believed to occur by neuronal damage and reactive tissue change of glia and deposition of fat-laden macrophages

The gray matter has six layers. The third layer is the most vulnerable to depletion of oxygen and glucose. Cortical laminar necrosis is a specific type of cortical infarction, which usually develops as a result of generalized hypoxia rather than a local vascular abnormality. Depletion of oxygen or glucose as in anoxia, hypoglycemia, status epilepticus, and ischemic stroke has been attributed as an underlying cause of cortical laminar necrosis.

Immunosuppressive therapy (cyclosporin A and FK506), and polychemotherapy (vincristine and methotrexate) have been observed to cause laminar necrosis due to hypoxic-ischemic-insult. Hypoxic insult leads to death of neurons, glia and blood vessels along with degradation of proteins

Chronic brain infarcts are typically seen as low-intensity lesions on T1-weighted and high-intensity lesions on T2-weighted MR images due to prolonged T1 and T2 values

Ref : http://komiyama.me/Kodomo/lun_wen_files/PDF42.pdf

Rasmussen Encephalitis

- Rasmussen encephalitis, also known as chronic focal encephalitis, is an extremely rare chronic inflammatory neurodegenerative disease resulting in untreatable seizures and progressive neurologic deficit.

- It usually begins in childhood, between 6 and 8 years of age, in previously normal children.

- Clinically, an abrupt onset of severe and intractable epilepsy occurs, most frequently epilepsia partialis continua and, less often, generalized status epilepticus.

- Rasmussen encephalitis is a diagnosis of exclusion in patients with intractable seizures and advancing motor and cognitive deterioration.

- The disease tends to affect one hemisphere, although bilateral involvement at initial presentation has also been reported.

- The earliest abnormal MRI feature has been described as cortical swelling with hyperintensity on T2-weighted images.

- Serial scans show focal or hemispheric atrophy, and T2-weighted images may reveal areas of increased signal in the white matter and/or putamen. After seizures, a transient hyperintensity T2-weighted imaging in the temporal lobe and hippocampus may be seen related to postictal changes .

- Classification and staging criteria have been proposed based on MR imaging findings on T2-weighted and FLAIR images:

 normal volume and signal (stage 0),
 swelling and hyperintense signal (stage 1),
 normal volume and hyperintense signal (stage 2),
 atrophy and hyperintense signal (stage 3), and
 progressive atrophy and normal signal (stage 4)

- MR spectroscopy demonstrates a reduction in NAA levels that at some point may be reversible after seizure control and may be related to recovery of neuronal function. Increased choline peaks have been described, although a reduction in this metabolite was observed in one study related to a transient increase in turnover and loss of membrane components. Slightly increased myo-inositol and glutamine/glutamate peaks and markedly increased lactate levels were noted.

- Diffusion and ADC ---> shows high ADC value.

Ref : Scott.

DDs of Unilateral Brain Atrophy

1. Dyke-Davidoff-Mason Syndrome.
2. Sturge-Weber Syndrome
3. MELAS

Other Common Catheters and Guidewires

1.Pig Tail Catheter 

2. Spinnaker Microcatheter
- is a flow directed catheter

3. Terumo Guidewire with the curved J-tip

4. Transcend Microwire

5. Mani's Head Hunter Catheter

Simmons Catheter

Simmons Catheter

Sim-1, 4F, 100cm.

Right Coronary Catheter

Right Coronary Catheter

6F, 100cm.

Diagram showing R and L Coronary Catheters

Left Coronary Catheter

Left Coronary Catheter

6F, 100cm.

Diagramatic depiction of RCC and LCC

TNM Staging of HepatoCellular Carcinoma (HCC)

Development Of Spleen

Ref : AJR http://www.ajronline.org/content/155/4/805.abstract

Cystic Lesions of the Spleen

Ref : http://bjr.birjournals.org/cgi/content/abstract/83/990/e126

Extrahepatic metastasis of hepatocellular carcinoma Part 1

Extrahepatic metastasis of hepatocellular carcinoma: incidence and risk factors.

REFERENCE from PUBMED

RESULTS:
During the average observation period of 3.9 years, extrahepatic metastasis was diagnosed in 123 in the treatment-naïve and 53 in the patients treated previously. The incidence rate of extrahepatic metastasis, as detected during the lifetime after medical treatment of HCC, was approximately 13% at 5 years.

Multivariate analysis with Cox proportional hazard model revealed that positivity for viral markers, larger tumour diameter, multiple tumour nodules, presence of vascular tumour invasion and elevated tumour markers were associated with the development of extrahepatic metastasis.

CONCLUSION:
The incidence of extrahepatic metastasis of HCC diagnosed during clinical course was not frequent. Advanced intrahepatic lesions, presence of vascular tumour invasion, elevated tumour markers and presence of viral hepatitis were risk factors for extrahepatic metastasis.