Low grade vs High grade Brain Neoplasms

- Some benign intracranial tumors like Pilocytic Astrocytoma, Pleomorphic Xanthoastrocytoma(PXA), GanglioGlioma(GG) can have cystic areas and PXA and GG can have enhancement.

Approximate Normal ADC Values

Gray matter  - 0.85 +/- 0.13 x 10 e-3 mm2 / s

White Matter - 0.80 +/- 0.13 x 10 e -3 mm2/s

CSF   - 3.63 +/- 0.30

DIffusion Restriction Areas ~ 0.60 - 0.65

Proton MR Spectroscopy - ppm of Minor Metabolites

Metabolite                PPM

Valine
Leucine                         --->      0.9 ppm
Isoleucine

Alanine                          --->     1.48 ppm

Acetate                          --->     1.9 ppm

Succinate                      ---->     2.4 ppm

Lipid / Lactate              ---->     0.8 to 1.3 ppm


PS: To differentiate Lipids vs Lactate which occur at the 1.3ppm in the short TE acquisition, and additional TE = 135ms imaging is done in which the lipids do not invert.

       Pic F - Short TE                                           Pic G - Intermediate TE

Distinguishing the Amino acid peaks of Valine, Leucine and Isoleucine at the 0.9ppm and the lactate/lipid at 0.8-1.3ppm is important in distinguishing between Cystic Tumors (Both primary and mets) from Brain Abscesses - by doing the Intermediate TE (135ms) Spectroscopy, which causes the inversion of Aminoacids and lactate peak, but not of lipid.

Image showing the inversion of lipid in intermediate TE..

Fibrodysplasia Ossificans Progressiva

1. Bilateral Hallux Valgus - with malformed first metatarsal and phalanges.

2. Medial cortical thickening with formation of Pseudo-exostosis ( Calcification of Gracilis / Semitendinosus tendons).

3. Shortened first metacarpals

4. Usually the hetrotopic ossification begins in the soft tissues of neck, even after trivial trauma.

5. FNAC is contraindicated as it can result in permanent deforming ossification.

6. F.O.P is an AD disease with complete penetrance,, but with variable expressivity.

7. Can be diagnosed by the HALLUX VALGUS. Genetic testing is available.

8. Small vertebral bodies, enlarged pedicles, small spinal canal may be seen.

9. Starts by 2-5yrs, Death by 3rd decade by recurrent pulmonary infections due to prevention of expansion of thoracic cage (Impairing Respiration).

Causes of CT Bowel Fat Halo Sign

CT Bowel Fat Halo Sign

Seen in 

1. Chronic Inflammatory Bowel Disease

2. Cytoreductive therapy

3. GVHD.

4. Normal patients ~20% of normal, with increased BMI can have this sign positive.

"When seen in both the small and large bowel, the halo sign has been considered specific evidence of Crohn’s disease. When only the colon is affected, the degree and geographic distribution

of bowel wall thickness are signs used to distinguish ulcerative colitis from Crohn’s disease. '

(Gore RM, Balthazar EJ, Ghahremani GG, MillerFH. CT features of ulcerative colitis and Crohn's, AJR, 1996)

Fluid-blood levels in Intracranial Hemorrhage

Excerpt from the Stroke Article
ref: http://stroke.ahajournals.org/content/24/4/554.full.pdf

"The cause of lobar hemorrhage after fibrinolytic treatment remains puzzling. We speculate, but have
proof in only one patient, that the presence of amyloid angiopathy may be an important risk factor. We cannot exclude the possibility, however, of hemorrhage into a prior silent infarction as the mechanism in some of these patients. Long-standing hypertension has been specifically implicated as a risk factor for cerebral
hemorrhage.
However, the site of hemorrhage associated with hypertension is usually in the distribution of perforating vessels, not lobar.
Patients with hypertension alone usually have bleeding into sites such as basal ganglionic, posterior lateral thalamus, pons, and cerebellar hemispheres.
Patients with hypertension and lobar hemorrhages may have amyloid angiopathy as well.

One recent study of surgically treated patients with lobar hematomas indeed suggested that amyloid angiopathy is a major contributing factor. 

In two series of patients with lobar hemorrhage but without anticoagulant or fibrinolytic treatment, hypertension was found in only one third of the patients. Although hemorrhage into the cerebellum has traditionally been linked to hypertension, blood pressure was normal in our one patient with a massive vermis hemorrhage. Furthermore, one study claimed that vermis hemorrhages were relatively frequent in anticoagulated patients."

" We suspect, therefore, that cerebral amyloid angiopathy may be a contributing, if not crucial, factor in

fibrinolysis-associated hemorrhages. Intracerebral lobar hemorrhage is frequently associated with cerebral amyloid angiopathy in patients in the sixth or seventh decade of life. It encompasses multiple, usually superficially located, areas of hemorrhage on CT scans. Frontal or parietal lobe hemorrhages are common, but cerebellar and putaminal locations have been described in association with amyloid angiopathy. Recently, it was also noted that cerebral amyloid angiopathy associated with lobar intracerebral hemorrhage resulted in good outcome in the vast majority of patients."

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.

Elevated Hemidiaphragm on Chest X-Ray

Causes of an elevated hemidiaphragm are:

 1) Above the diaphragm – decreased lung volume (atelectasis, collapse, lobectomy, pneumonectomy, pulmonary hypoplasia).

2) Diaphragm – phrenic nerve palsy, diaphragmatic eventration

3) Below the diaphragm – abdominal tumour, subphrenic abscess, distended stomach or colon.

Differential diagnoses which may mimic an elevated hemidiaphragm are subpulmonic effusion, diaphragmatic hernia, diaphragmatic rupture and a tumour of the pleura or diaphragm

White Out Lung on Chest X-Ray

Complete White Out’ on the CXR has a limited number of causes.


The differential diagnosis can be shortened further with one simple observation - the position of the trachea.


Is it central, pulled or pushed from the side of opacification?


Pulled 


-Pneumonectomy(usually associated with a segmental rib defect)
-Total Lung Collapse
-Pulmonary Agenesis


Central:


-Consolidation
-Mesothelioma


Pushed:


-Pleural effusion
-Diaphragmatic hernia

Osteoscerotic Lesions : Mnemonic

'Regular sex makes occasional perversions much more pleasurable and fantastic.'




Mnemonic for osteosclerosis


Renal osteodystrophy
Sickle cell disease
Myelofibrosis
Osteopetrosis
Pyknodysostosis
Metastases
Mastocytosis
Paget disease
Athletes
Fluorosis

BASILAR INVAGINATION

PF ROACH

Paget disease
Fibrous dysplasia
Rickets
Osteogenesis imperfecta, Osteomalacia
Achondroplasia
Cleidocranial dysplasia
Hyperparathyroidism, Hurler syndrome

Shapes of Ventricles

1. Viking horn / Steer Horn / Long-Horn appearance of Lateral Ventricles – 
Agenesis  of Corpus Callosum.


2. Bullet shaped third ventricle – Joubert’s Syndrome.


3. Bat(wing) shaped fourth ventricle – Joubert’s Syndrome.


4. Horshoe shaped monoventricle – Alobar Holoprosencephaly.

Bullet shape in Radiology

1. Bullet shaped Posterior Urethra – in PUV MCU.

2. Bullet shaped Thoraco-lumbar vertebrae in Lateral XR spine in Achondroplasia.

3. Bullet shaped metacarpals - MPS

4. Tumbling bullet sign : is seen in bullet within a post-traumatic bone cyst.

5. Bullet shaped third ventricle  : Joubert Syndrome.

SIEMENS New 1.5T MRI with TIM and DOT

TrueForm Magnet and Gradient Design - now available for 1.5T!


The cylindrical magnet and gradient homogeneity volume is shaped closer to the 'true form' of the human body. This enables better image quality even at the edges.


Better fat saturation


Less overlap needed for multi-station exams.



Tim+Dot. Together, they enable improved scans.


The real power of Tim+Dot in MAGNETOM Aera is all about diagnostic consistency. With the accuracy of Tim 4G integrated with the unique on-board guidance of Dot, you will achieve excellent image quality with fewer errors and recalls.


Tim's new ultra high-density array, with up to 204 coil elements, combines with a new RF design, with up to 64 RF channels, for an SNR increase of up to 20%*. This enables high-resolution imaging that holds up even when zooming in on multi-station images.


For further details see SIEMENS WEBSITE : CLICK HERE

Silver Bromide Emulsion Types

Silver Bromide Emulsion Types in X-Ray


1. Monochromatic Emulsion - No colour sensitizers added, so emulsion will be sensitive to the blue-violet spectrum of the light.


It usually requires prolonged exposure to red light to produce any Photographic Effect on the film. This is the reason why RED LIGHT is used in dark rooms.


2. Orthochromatic Emulsion - Spectral Resolution extended upto green(570nm), with colour sensitizers added.


3. Panchromatic Emulsion - extended upto Red light.(700nm).

Spotter 6 ?

Notch in the Film

You must have noticed a 'notch' in most of the CT films we use. What is the purpose of this notch in a CT / XR film?


Ans: This so called notch is seen only in a 'single sided' = ' single coated' film, where the emulsion is coated only on one side of the film, and to help identify the emulsion side of the film a notch is given in the top right hand corner. Once the film is kept with notch is on our top-right, the emulsion side is nearer to us. This side should be made in contact with the intensifying screen while mounting into a cassette for XR. 


Of course while mounting films on to the lobby, the notch is usually should be on the top-right hand corner.