Tuesday 25 August 2015

MCQ RADIOLOGY --INTRAVENTRICULAR LESIONS

Q.All are true regarding  intaventricular lesions except
a.. central neurocytoma typically show attachment to the septum pellucidum
b. Subependymomas in the lateral ventricles typically show intense  contrast enhancement
c. Heterotopic gray matter  neither enhance nor have calcifications and is not in contact with the septum
d. Intraventricular meningiomas and choroid plexus are usually situated  within the atrium of the lateral ventricle 
e. ependymoma, subependymoma, and oligodendroglioma are most often hyperintense to gray matter 

ANS --Pl post your answer 

Saturday 22 August 2015

WHAT IS CHORDOID GLIOMA?

273.All are true regarding chordoid glioma except

a. typical location in frontal lobe

b. thought to arise from the region of the lamina terminalis

c. signal abnormalities extending into the proximal optic tracts 
    bilaterally

d. appear to be benign

e. the strong staining for glial fibrillary acidic protein

273.---a


Chordoid glioma  is a recently recognized tumor that has a typical

 location in the anterior third ventricle and hypothalamic region, 

with histologic features distinct from those of other glial tumors 

. This lesion has shown cords and clusters of epithelioid cells with 

mucinous background, with low-grade lymphoplasmacytic 

infiltrate, similar to chordoma or chordoid meningioma.

Saturday 15 August 2015

MCQ FRCR ---RESTRICTED DIFFUSION

Q.All shows restricted diffusion except
a. lymphoma
b meningioma
c.glioblastoma multiforme
d. pyogenic abscesses

e.arachnoid cyst

ANS---?

15 AUG 2015


15 AUG 2015

HAPPY 
          INDEPENDANCE 
                                     DAY

Thursday 13 August 2015

signal on T2-Weighted and T1-Weighted Magnetic Resonance Images

Causes of Low Intensity in Tumors on T2-Weighted Magnetic Resonance Images
Paramagnetic effects
   Iron within dystrophic calcification or necrosis
   Ferritin/hemosiderin from prior hemorrhage
   Deoxyhemoglobin in acute hemorrhage
   Intracellular methemoglobin in early subacute hemorrhage
   Melanin (or other free radicals)
Low spin density
   Calcification
   Scant cytoplasm (high nucleus:cytoplasm ratio)
   Dense cellularity
Fibrocollagenous stroma
Macromolecule content
Very high (nonparamagnetic) protein concentration
Intratumoral vessels
   Signal void from rapid flow








Causes of High Intensity in Tumors on T1-Weighted Magnetic Resonance Images
Paramagnetic effects from hemorrhage
Subacute-chronic blood (methemoglobin)
Paramagnetic material without hemorrhage
Melanin
Naturally occurring ions associated with necrosis of calcification
   Manganese
   Iron
   Copper
Nonparamagnetic effects
Very high (nonparamagnetic) protein concentration
Fat
Flow-related enhancement in tumor vessels

Tuesday 11 August 2015

FRCR mcq ------Cortical malformation

230.All are true regarding malformation of cortical development except
a. dysembryoplastic neuroepithelial tumor is a glial abnormalities
b. tuberous sclerosis shows abnormal neuronal proliferation
c. hemimegalencephaly has contralateral ventricular enlargement,
d. cortical thickening and radial bands extending toward the ventricle noted in tuberous sclerosis
e. balloon cell focal cortical dysplasia of Taylor appears hyperintense on T2W






230.---c
 Features of hemimegalencephaly include hemispheric enlargement (or a portion of it), white matter hyperintensity, ipsilateral ventricular enlargement, heterotopia, and thickened cortex.

Glial abnormalities consist of developmental neoplasms such as dysembryoplastic neuroepithelial tumor , ganglioglioma, and gangliocytoma. These abnormalities are usually cortical in location and appear as focal lesions on MR, often with a cystic component.


 Abnormal neuronal proliferation is typified by disorders with “balloon cell” proliferation , such as tuberous sclerosis, balloon cell focal cortical dysplasia of Taylor, and hemimegalencephaly.
Balloon cells are large progenitor cells with both neural and glial characteristics.
The imaging findings in balloon cell focal cortical dysplasia(type II focal cortical dysplasia) and tuberous sclerosis are similar . Both have hyperintense cortical lesions on T2-weighted images, often with cortical thickening and radial bands extending toward the ventricle.
However, unlike tuberous sclerosis, the balloon cell focal cortical dysplasia is not associated with multiplicity of cortical lesions, subependymal nodules, or systemic manifestations (such as the cardiac, renal, and dermatologic abnormalities found in tuberous sclerosis).
Because of focal hyperintensity on T2-weighted images, balloon cell cortical dysplasia may mimic a tumor. Other features of balloon cell dysplasia (i.e., cortical thickening, homogeneous bright signal in subcortical white matter, and radial bands) facilitate the distinction . This differentiation may be crucial for surgical management



Sunday 9 August 2015

Radiology mcq frcr ---epilepsy imaging

223.All are true regarding imaging of hippocampus except
a. best performed in a slightly oblique coronal plane, perpendicular to the long axis of hippocampus
b. FLAIR is optimal for quantitative volumetry
c. high-resolution fast spin echo and inversion recovery sequences are important for depiction of hippocampal architecture
d. Conventional / fast spin echo T2-weighted acquisitions are sensitive for assessing hippocampal signal changes
e. Enhancement with intravenous gadolinium has been shown to be of no value in hippocampal sclerosis




223.----b

Coronal, T1-weighted, three-dimensional volume gradient echo is optimal for quantitative volumetry

Seize the seizure

 Cause of Epilepsy Categorized by the Age at Seizure Onset
cause Age at seizure onset (yr)
0–2 3–20 21–40 41–60 >60
Cerebral anoxia X    
Metabolic abnorma lities or inborn error of metabolism X
Congenital or developmental malformations X X
Infection X X
Phakomatoses (TS, SWS neurofibromatosis) X X
Primary generalized seizures   X
Hippocampal sclerosis X
Vascular malformation X X
Posttraumatic epilepsy X X X X
Tumor   X X X
Stroke   X X

Saturday 8 August 2015

Look Ahead: The Future of Medical Imaging

The essence of medical imaging lies in understanding the relationship between patterns of energy emanating from tissues and the underlying state—healthy or diseased—of those tissues. This fundamental paradigm will not change in the future. 
However, the way we study biological tissues with different forms of energy and how we draw inference from image data will change continuously at a relentless pace.

From Radiographs to Parametric Imaging

For the better part of 100 years, physics was the dominant scientific basis of radiology and X-ray attenuation was the paramount measureable parameter. Radiologists spoke of “images” and “radiographs” not “attenuation maps.” New energy sources—magnetic, radiofrequency, sonic, optical and nuclear—combined with fast, dynamic, digital methods of applying and recording them, have added dozens of parameters to the imaging toolkit.
The richness of measurable parameters has taken medical imaging beyond organ anatomy and pathology into the realms of physiology, pharmacology and cellular and molecular biology. The scale of measurement has been extended from centimeters and millimeters to encompass micrometers and nanometers. Taken together these developments are moving radiology into the age of molecular medicine and genomics.

Images as Data—Derivation of Additional Parameters

Digital images are more than pictures; they are sources of data that contain important information not qualitatively perceptible by human observers. 
Hundreds of secondarily derived parameters can be extracted from image data sets by advanced computational methods, such as analysis of tumor textures, that can be empirically linked to different tumor genotypes. Computationally derived images can depict information from multiple parameters allowing us to see how they relate to each other temporally and spatially. Going forward, we will still talk about images, but the conceptual key to diagnostic inference will be gaining an understanding either directly or empirically of what each parameter represents and how that parameter is manifest in a given disease process.

Radiation Dose Reduction and Phase Contrast Imaging

Improvements in X-ray based imaging in the next decade will result in reductions of radiation doses to the point where the issue will no longer be of discussion or concern. 
Current calculations projecting excess cancers and cancer deaths from CT seriously inflate the risks, because they are derived from 10-year-old data that don’t take into account new reconstruction methods and scanning systems developed in the last decade that have reduced radiation doses substantially.
Phase contrast X-ray imaging is likely to be the next new imaging method to be explored clinically.
 Compared to attenuation based X-ray imaging, phase contrast has the theoretical potential to reduce doses by 10- to 100-fold or more due to the inherently high contrast it affords. Predictably, it will take time to achieve these levels of benefit but the underlying physics is favorable—phase shift versus linear attenuation of X-rays in biological tissues will usher in the submillisievert era of CT imaging.

Information and Communication Systems

With the Internet, borders have blurred between the concepts of information and communication systems, making access to data and distribution of information faster and more efficient. Mobile and wearable media will accelerate these trends. Timing of information delivery will be tailored to medical need. Biometric and/or wearable patient identification media will facilitate the “electronic round trip”—automated patient identification and no reentry of patient data or selection from pick lists required from the time of computer order entry by a referring physician until report delivery.
Direct patient access to information will democratize the medical record; all physicians, including radiologists, will need to learn how to craft reports that convey necessary information without unduly alarming patients and be mindful that many patients are not medically literate. These are unsolved challenges today.

Big Data, Data Mining and Value Creation

Radiology led the way into the era of digital medicine. Now in the era of “big data,” radiology will continue to lead in mining and mobilizing data—turning dumb data into smart knowledge to be delivered in real time—just-in-time—at the point of care. 
Decision support (DS) systems for referring physicians will be built into the work process for computerized physician order entry (CPOE).
DS systems will guide radiologists in their recommendations and reduce wasteful variations in practice. 
Real-time data-mining during the reporting process will be used to help avoid errors—for example, checking consistent use of right versus left and comparing terms used in the body of the report versus the impression.
Standardized nomenclature based on imaging ontologies such as BIRADS™ and RADLEX™ and structured reporting will facilitate data-mining for many applications, including the aggregation of similar cases to look for new patterns in the image data or to test new imaging biomarkers for accuracy. Radiology subgroups and the specialty more generally must work together to agree on unambiguous standardized nomenclatures to avoid confusing referring physicians and each other—is it a heart attack or a myocardial infarction, a cyst or an inclusion cyst, a tumor or a mass?

Imaging in the Era of Precision (Personalized) Medicine

The fundamental principle of precision medicine or personalized medicine is a definition of ever smaller, more precise subgroups of patients with similar characteristics who have similar prognoses and are likely to benefit from the same therapies. 
The term “biomarker” is used for any finding that is linked to the presence or severity of a disease such as blood pressure, heart rate, hematocrit and other laboratory values. By analogy, what we have historically called “Roentgen Signs” may be thought of as imaging biomarkers.
Conceptually, the radiology report is an enumeration of the imaging biomarker and, as such, constitutes an “imaging phenotype” at that point in time. Imaging phenotypes are systems for scoring, categorizing and classifying disease processes and their severity. They define these “precise” subpopulations. 
Establishing linkages between genotypes and imaging phenotypes (radiogenomics) will serve as the foundation for surveillance of disease manifestation—occurrence, location, extent, severity—and discovery of genetic polymorphisms.
Radiologists should begin considering their interpretations in this conceptual framework if we are to take a leadership role in the era of precision medicine as productive, vital members who speak a common language.

Challenges and Opportunities

Future developments will certainly entail vastly increased complexity in imaging technology and radiology practice, and the increased educational activities those advancements will require. Competition, both clinically and in research for “ownership” of imaging methods, will continue to increase due to the high value inherent in medical information.
On a positive note, the future will bring new capabilities that have even greater medical value. We will see radiation dose continue to drop and utilization of imaging services become more efficient, with fewer healthcare resources wasted, including the increasingly scarce commodity of time—to the benefit of patients, physicians and workers in the healthcare system


Friday 7 August 2015

RADIOLGY ---CONTRAST

The above graph shows changing signal intensity over time in contrast agent bolus tracking.
Which curve is normal –one with down deflection (drop in signal) or one with no deflection?







ANS—
The curve with drop in signal is normal,other one reflect the ischemia.

Gadolinium passing through the capillary bed results in decreased T2 relaxation time, seen as a drop in signal intensity that then returns to normal as the contrast passes out of the capillary bed.  The normal tissue demonstrates an earlier decline in signal intensity and a greater overall decrease in signal intensity than the ischemic region.

Thursday 6 August 2015

RADIOLOGY MCQ --HIPPOCAMPAL SCLEROSIS

Q.All are true regarding hippocampal sclerosis except
a.associated with temporal lobe complex partial seizures
b.associated with pyramidal and granule cell neuronal loss
c the cornu ammonis and dentate sections of the hippocampus involved
d. abundance  of interneurons

e. anterior temporal lobectomy--- the most rewarding and most commonly performed  surgery

ANS -----d

Hippocampal reorganization and changes in energy metabolism are  associated with hippocampal sclerosis and may be the result of a brain insult occurring during brain maturation .Findings of reorganization include abnormal axonal sprouting and loss of interneurons, which is thought to change the balance of neuronal excitation and inhibition.

Wednesday 5 August 2015

RADIOLOGY MCQ---FRCR

Q. Hyperdense basal ganglia and thalami is seen In
a. Mucopolysaccharidoses
b. Zellweger syndrome
c. Alexander disease
d. MELAS
e.Krabbe disease


ANS.---e

Krabbe disease, or globoid cell leukodystrophy (GLD)----
An autosomal recessive inherited disorder that commonly presents within the first 6 months of life., Deficiency of the lysosomal enzyme galactocerebroside β-galactosidase (encoded by chromosome 14)  results in the accumulation of galactocerebroside in macrophages

The brain is small and weighs only 600 to 800 g The white matter is rubbery to firm, but the cortex is relatively unaffected .The pathologic hallmark of Krabbe disease is a massive accumulation of large multinucleated cells containing periodic acid-Schiff–positive material (globoid cells) 

. In contrast to other demyelinating diseases, lipid-laden macrophages are uncommon. Demyelination and dysmyelination are seen.

The most characteristic MR finding in both the infantile and late-onset forms of GLD is high signal intensity on the T2-weighted images found along the lengths of the corticospinal tracts.

The cerebellar white matter and deep gray nuclei are not involved in the late-onset form

The CT findings of hyperdense thalami, caudate nuclei, and corona radiata are characteristic but not specific for the disease and have been shown to correspond to fine calcifications at autopsy .

 Late-onset cases of GLD with primary involvement of the parietal periventricular white matter, splenium of the corpus callosum, and corticospinal tracts may appear similar on imaging to adrenoleukodystrophy. However, auditory pathway involvement is characteristic of adrenoleukodystrophy and is not seen in GLD.

Monday 3 August 2015

RADIOLOGY MCQ ---FRCR

189.Hypointense subependymal germinolytic cysts ,typically

 involving the caudothalamic grooves is seen on MR imaging of

a.Mucopolysaccharidoses

b.Zellweger Syndrome

c.Fabry Disease

d.Krabbe disease


e.MLD

ANS-----b --Zellweger Syndrome

Zellweger syndrome (ZS) is a peroxisomal disorder characterized by hepatomegaly, high levels of copper/iron, and visual symptoms

Hypointense subependymal germinolytic cysts (typically involving the caudothalamic grooves) is noted on on MR imaging of Zellweger Syndrome.Other associated MR finding are microgyria (predominantly in the frontal and perisylvian cortex), polymicrogyria, and pachygyria (particularly in the perirolandic and occipital regions).


MR imaging might be  useful for the in utero diagnosis of this condition (during the third trimester), showing abnormal cortical gyral patterns, abnormal myelin formation, and cerebral periventricular pseudocysts . MR spectra show similar peak heights of the two lipid peaks (CH2, CH3), elevated choline levels, and low NAA 

REMEMBER THIS TABLE-----AND WIN THE RACE

 Lysosomal Disorders
Disease Deficient enzyme or activator
Sphingolipidoses  
   Metachromatic leukodystrophy (MLD) Arylsulfatase A (sulfatidase)
   MLD variant Sulfatide activator
   Krabbe (globoid cell leukodystrophy) Galactosylceramidase
   GM1 gangliosidosis β-Galactosidase
   Tay-Sachs β-Hexosaminadase α-subunit
   Sandhoff β-Hexosaminadase β-subunit
   GM2 gangliosidosis AB variant GM2 activator
   Fabry α-Galactosidase A
   Niemann-Pick, types A and B Sphingomyelinase
   Gaucher Glucosylceramidase
   Gaucher variant β-Glucosidase activator (SAP-2)
   Farber (lipogranulomatosis) Ceramidase
   Galactosialidosis Protective protein/cathepsin A
Mucopolysaccharidoses (MPSs)  
   Hurler-Scheie syndrome (MPS I and V) α-Iduronidase
   Hunter syndrome (MPS II) α-Iduronidate sulfatase
   Sanfilippo disease (MPS III)  
      Type A Heparan N-sulfatase
      Type B N-Acetyl α-glucosaminidase
      Type C N-Acetyl CoA:α-glucosaminide
N-Acetyl transferase
      Type D N-Acetyl α-glucosaminide-6-sulfatase
   Morquio disease (MPS IV)  
      Type A N-Acetyl galactosamine-6-sulfatase
      Type B β-Galactosidase
   Maroteaux-Lamy (MPS VI) Arylsulfatase B
   Î²-Glucuronidase deficiency (MPS VII) β-Glucuronidase
Glycoprotein storage disease and mucolipidoses  
   Sialidosis (mucolipidosis I) α-Neuraminidase (sialidase)
   Î±-Mannosidosis α-Mannosidase
   Î²-Mannosidosis β-Mannosidase
   Î±-Fucosidosis α-Fucosidase
   Mucolipidosis IV Mucolipin-1
   I-cell disease and pseudo-Hurler UDP-glcNAc:lysosomal enzyme glcNAc
   Polydystrophy (mucolipidoses II and III) Phosphotransferase

Saturday 1 August 2015

General Guidelines for Temporal Evolution of Intracranial Hematomas

 General Guidelines for Temporal Evolution of Intracranial Hematomas AT 1.5 T


Clinical biochemical form
Approximate stage
Time of appearance
Intensity on T1-weighted imagea
Intensity on T2-weighted imagea
Oxyhemoglobin in RBCs
Hyperacute
Immediately to first several hours
Deoxyhemoglobin in RBCs
Acute
Hours to days
≈, ↓
↓↓
Methemoglobin in RBCs
Early subacute
First several days
↑↑
↓↓
Extracellular methemoglobin
Subacute to chronic
Days to months
↑↑
↑↑
Ferritin and hemosiderin
Remote
Days to indefinitely
≈, ↓
↓↓
RBC, red blood cell.
aSignal intensity is relative to normal brain parenchyma.