http://media.medeserv.com.au/RANZCR2007/MMR-5125/viewer_lrgvid.html
Tuesday, 9 December 2008
Tuesday, 25 November 2008
- Nick Miller
- November 26, 2008
ELECTIVE surgery and outpatient appointments at some Victorian hospitals could be hit by cancellations for the rest of the week, because of industrial action by imaging staff.
Employees of Symbion Imaging, which does X-rays, ultrasounds and other medical imaging for the Northern and Broadmeadows public hospitals, the Epworth in Richmond and 30 other private hospitals and clinics, voted to take industrial action yesterday.
From today until the end of Friday, striking staff will work on imaging only for emergency patients, said Health Services Union national secretary Kathy Jackson. "If it is elective, rather than urgent, it won't be done," she said.
Symbion's staff, including radiographers, administrative workers and technicians, were frustrated by a long-running enterprise bargaining process.
"This is one of the worst employers I have ever dealt with," Ms Jackson said. "For months, they were not prepared to negotiate, then last week they offered a 2 per cent first-and-final offer. They are ripping their staff off." The Age attempted to contact Symbion and its parent, Primary Health Care, but calls were not returned.
However, hospitals contacted by The Age differed on the expected effect of the action.
A spokesman for Northern Health, which includes the Northern Hospital and Broadmeadows, said imaging staff involved in the action had agreed to perform X-rays that were deemed "medically urgent".
"We don't know what will be deemed medically urgent — it will be discussed between medical staff and radiologists," he said. "There will be no impact on emergency or ICU (intensive care) or (operating) theatre. It will be more other inpatient and outpatient services deemed not medically urgent." He believed elective surgery would go ahead.
A spokeswoman for the Epworth said: "We believe there will be no major disruption."
Wednesday, 19 November 2008
Civil Liability Act 2002 (NSW)
An Act to make provision in relation to the recovery of damages for
death or personal injury caused by the fault of a person; to amend the
Legal Profession Act 1987 in relation to costs in civil claims; and for
other purposes.
Compensation to Relatives Act 1897 (NSW)
An Act to consolidate enactments relating to compensation to relatives of person's killed by accidents.
Limitation Act 1969 (NSW)
An Act to amend and consolidate the law relating to the limitation of
actions; to repeal section 5 of the Imperial Act known as the Common
Informers Act 1588 and certain other Imperial enactments; to repeal the
unrepealed portion of the Act passed in the fourth year of the ...
Minors (Property and Contracts) Act 1970 (NSW)
Health Administration Act 1982 (NSW)
Health Care Complaints Act 1993 (NSW)
Medical Practice Act 1992 (NSW)
Privacy and Personal Information Protection Act 1998 (NSW)
Virtual Colonoscopy: A Storm is Brewing
David J. Vining, MD
Appl Radiol. 2008;37(11):12-16.
Appl Radiol. 2008;37(11):12-16.
Abstract and Introduction
Abstract
The
author performed the first virtual colonoscopy (VC) in 1993. In this
article, he addresses the issues related to the turf battles between
radiologists and gastroenterologists in the use of this technology.
Reviewing common myths associated with VC, he warns that radiologists
must retain expertise in this area.
Introduction
A storm
is brewing around virtual colonoscopy (VC) and whether radiologists or
gastroenterologists will ultimately control this technology. Imagine
the following: in the near future, a patient who requires colorectal
cancer (CRC) screening walks into a local gastroenterologist's office,
obtains a VC examination, which is read by a nurse practitioner, and,
following consultation with a gastroenterologist, undergoes immediate
optical colonoscopy (OC) for evaluation of tiny polyps that either
cannot be found or turn out to be residual feces. Meanwhile, a
radiologist working with this practice interprets the CT data for
extracolonic findings in exchange for a small percentage of the total
professional fee. The patient's insurance (ie, Medicare) is billed for
both the VC and OC, which taxpayers ultimately pay. If this sounds
far-fetched, read on....
Virtual Colonoscopy Development
Colorectal
cancer is the second leading cause of cancer death in the United
States, but it is also one of the most preventable when screening is
used to detect and treat early disease. The 5-year survival rate for
early stage I CRC is 93%, but when it metastasizes to distant organs
and becomes stage IV disease, the survival rate decreases to 8%.[1]
Unfortunately, many adults over the age of 50 do not undergo screening,
and, as a result, CRC is more often diagnosed in advanced stages.[2] Virtual colonoscopy offers the public a more appealing and less invasive alternative for screening.
I
performed the first VC, also known as CT colonography (CTC), at the
Wake Forest University Health Sciences Center in 1993. It has taken
nearly 15 years for VC to mature and gain acceptance by policy makers.
The basic technique consists of: 1) bowel cleansing and stool tagging,
2) gas insufflation of the colon, 3) CT scanning of the abdomen/pelvis,
and 4) 2- and 3-dimensional image analysis of the data to identify
polyps and masses (Figure 1). The first VC examination took 60 seconds
to scan a patient using a single-slice helical CT scanner and nearly 8
hours to process the data for a fly-through, but today multidetector CT
scanners acquire the data in a few seconds, and processing occurs in
real time using inexpensive computers.
Despite the technological advances that have occurred during the past decade (eg, CO2
insufflation, multidetector CT scanners, stool tagging,
computer-assisted diagnosis), a strong lobbying effort on the part of
gastroenterologists has delayed the availability of VC in the United
States. Since Congress approved reimbursement for CRC screening in the
1997 Balanced Budget Act, the number of colonoscopies conducted
annually in the United States has increased from 4 million in 2000 to
>14 million in 2002.[3]
Handwriting on the Wall
Clinical
trials that compared VC with OC have shown a dramatic improvement in VC
accuracy in the last few years, culminating in 2 major trials that were
announced in September 2007. The ACRIN National Colonography Trial
enrolled over 2500 patients at 15 sites, and it reported that VC had a
90% sensitivity for the detection of polyps >10 mm.[4] Within a week, Kim[5]
published a study comparing VC screening in 3120 patients with OC
screening in 3163 patients. Remarkably, VC and OC found an equivalent
number of advanced adenomas in each group; more surprisingly, a larger
number of cancers were found in the VC group.[5] These 2
studies plus multiple prior published trials from the United States and
abroad led the American Cancer Society, the American College of
Radiology (ACR), and the United States Multi-Society Task Force to
incorporate VC in its screening recommendations that were published in
March 2008.[6]
As VC has gained acceptance,
gastroenterologists now realize that VC will impact their practice.
After years of bashing VC as not being good enough and requiring more
clinical data, the Future Trends Committee of the American
Gastroenterological Association (AGA) published a report in October
2006 stating that they see the handwriting on the wall.[7]
This Committee proposed that gastroenterologists should position
themselves to play a role in performing and interpreting VC, including
advocating for CPT codes in the 91000 series that will allow
gastroenterologists to be reimbursed for interpreting and providing VC
services, as well as developing specialized training and training
requirements for those interested in performing VC interpretation. In
an effort to make good on its promise, the AGA published a set of
guidelines in 2007 listing the minimum requirements that a
gastroenterologist must satisfy in order to become certified to read VC
examinations.[8]
Battle Lines are Drawn
Currently
the Centers for Medicare and Medicaid Services (CMS) approve
reimbursement for VC only when it follows a failed "diagnostic"
colonoscopy, not a failed "screening" colonoscopy (Figure 2).[9]
Following the inclusion of VC in the American Cancer Society's
screening guidelines, CMS launched a National Coverage Analysis for
Screening Computed Tomography Colonography for Colorectal Cancer
(CAG-00396N) in May 2008. This seeks to expand reimbursement for
screening indications. The final report of this analysis is due in
February 2009.[10] Expanded reimbursement could have a huge
impact on increasing screening and reducing CRC deaths, but it could
also have substantial economic consequences for CMS and taxpayers. A
public comment period held May-June 2008 drew responses from many
individuals and organizations, including the ACR and the AGA. Of
course, the ACR is in favor of expanded reimbursement, but the AGA
stated that it would support VC only if certain conditions were met,[11] including:
1. Reporting of
ALL polyps (which is contradictory to the ACR Practice Guideline for
the Performance of CTC in Adults that states reporting of polyps <5
mm is not recommended because of the low incidence of those lesions
having malignant potential);[12]
2. Allowing patients in consultation with their physician to determine whether or not to remove those polyps; and
3.
Enacting a coverage policy that would encourage rapid follow-up
procedures (ie, colonoscopy) and that correspondingly would not create
a disincentive for physicians (ie, gastroenterologists) who refer those
procedures.
Reading between the lines, if such conditions are
approved by CMS, then the gastroenterologists will have an unrestrained
ability to perform colonoscopy on any little lump or bump that they
might discover if they or their clinical assistant should be allowed to
read VC exams. It is also the position of many prominent
gastroenterologists to create a split-fee arrangement with radiologists
so that radiologists will be relegated to reading only the extracolonic
portions of a CT scan for a small portion of the professional fee, and,
if radiologists refuse to participate, then they will outsource
radiology services, even to foreign providers![13]
Dispelling Popular Myths
Gastroenterologists frequently try to discredit VC with the following myths:
1. Colonoscopy is the "gold standard."
There are no published studies to validate this claim. In fact, studies
comparing back-to-back colonoscopies on the same patients have reported
OC miss rates of 22% for polyps, even in the hands of expert
endoscopists.[14] Studies such as Pickhardt's[15]
landmark VC study have shown VC to outperform OC. Finally, the accuracy
of screening colonoscopy has been shown to be dependent on how much
time a gastroenterologist spends performing the examination.[16]
2. If VC finds a polyp, then colonoscopy is needed for polyp removal, so why not undergo colonoscopy in the first place?
The vast majority of polyps are benign, hyperplastic polyps, and <5%
of the asymptomatic screening population has a significant adenomatous
polyp.[5] Hence, if OC is the primary screening method, then
>95% of the asymptomatic population would under go OC unnecessarily
with its inherent risks of bowel perforation and anesthesia.
3. The radiation dose associated with VC is prohibitive.
Radiation dose is a valid concern, but researchers are striving to
mitigate this risk by using low-dose techniques, even as low as 10 mAs
(compared with a conventional CT scan that might use a dose of 200 mAs).[17]
Hence, the radiation risk from VC with low-dose techniques can be on
the order of 1 to 2 mSv, which is far below the range that has been
associated with potential cancer and multidetector CT use.[18] Alternatively, VC can be performed using MRI, but the availability of MRI scanners is a temporary hurdle, at least for today.
Actions to Take
Radiologists
are already overworked due to the exponential increase in imaging
studies during the past decade, and as a result, we have become
complacent about the ownership of new technologies. In the meantime,
gastroenterologists are purchasing CT scanners and attending training
programs to get ready for CMS approval of reimbursement for VC
screening.[19] However, if radiologists act quickly and take
certain steps to position ourselves to maintain control of VC, we will
not risk losing this technology, as we have done with cardiac imaging.
Some initiatives include:
1. Taking a stronger, vocal interest in
VC. Radiologists are better trained to read an entire CT examination,
especially when disease crosses organ boundaries to involve both the
colon and adjacent anatomy. We need to establish ourselves as the
imaging experts in order to counter claims that endoscopists and nurse
practitioners are as good as radiologists in reading VC exams.[20]
2.
Beginning a dialogue with community gastroenterologists and primary
care physicians. Radiology practices need to be willing to provide
same-day, on-demand VC services for failed "diagnostic" colonoscopy
examinations in advance of the anticipated reimbursement for screening
VC.
3. Developing practice guidelines for appropriately
working-up extracolonic findings. Perhaps offering immediate but
limited ultrasound evaluation to resolve indeterminate liver and renal
lesions will help to mitigate the gastroenterologists' cry that they
should be the ones performing VC in their offices.
4. Providing
consistent, high-quality reports of VC findings that can be rapidly
delivered to the patient and referring clinician. Utilization of the CT
Colonography Reporting and Data System (C-RADS) and participation in
the ACR's CTC Registry will help to strengthen our position in the
field.[21,22]
5. Challenging any proposals by
gastroenterologists to split the professional fee for reading colonic
and extracolonic portions of a VC CT scan, including legislative
lobbying if necessary. There are many problems with fee-splitting
arrangements, not the least of which is malpractice
liability—radiologists will certainly be held liable when
gastroenterologists fail to make a correct diagnosis if they should be
allowed to interpret only the intraluminal portion of a VC scan.
All is Not Lost, at Least Not Yet
Much
of the rhetoric coming from the gastroenterology community is coming
from a few but very vocal and rabid gastroenterologists. In fact, a
survey of 2400 AGA members regarding their interest in VC resulted in
only 588 responses, of which one third said that they would want to
perform VC, another third said that they would not perform it but would
support their colleagues, and the final third said that
gastroenterologists should not perform VC.[23] In reality,
radiologists and gastroenterologists will need to work together along
with surgeons and oncologists to provide comprehensive CRC screening
and treatment services. If CRC screening really takes off, then there
will not be enough gastroenterologists available in this country to
perform the necessary therapeutic colonoscopies that will be generated.
Although radiologists specializing in VC may eventually become
employees of large, multispecialty clinics specializing in colorectal
disease, it is paramount that the role and expertise of the radiologist
be maintained.
References
|
David J. Vining, MD
is a Professor of Diagnostic Radiology and the Medical Director of the
Image Processing and Visualization Laboratory, University of Texas M.D.
Anderson Cancer Center, Houston, TX
is a Professor of Diagnostic Radiology and the Medical Director of the
Image Processing and Visualization Laboratory, University of Texas M.D.
Anderson Cancer Center, Houston, TX
Disclosure:
Dr. Vining discloses that he has received royalties from Wake Forest
University and Bracco, Inc., for virtual colonoscopyrelated products.
Dr. Vining discloses that he has received royalties from Wake Forest
University and Bracco, Inc., for virtual colonoscopyrelated products.
Tuesday, 11 November 2008
SUPRATENTORIAL BRAIN TUMORS
John R. Hesselink, MD, FACR and Richard J. Hicks, MD
In the diagnostic work-up of intracranial tumors, the primary goals of the imaging studies are to detect the abnormality, localize and determine its extent, characterize the lesion, and provide a list of differential diagnoses or, if possible, the specific diagnosis. Correlative studies have proved that MR is more sensitive than CT for detecting intracranial masses. Moreover, the multiplanar capability of MR is very helpful to determine the anatomic site of origin of lesions and to demarcate extension into adjacent compartments and brain structures. The superior contrast resolution of MR displays the different components of lesions more clearly. MR can assess the vascularity of lesions without contrast infusion. On the other hand, CT detects calcification far better than MR, a useful finding for differential diagnosis. Gradient-echo techniques improve MR detection of calcification by accentuating the diamagnetic susceptibility properties of calcium salts, but the observed low signal on T2-weighted images is nonspecific, in that any accompanying paramagnetic ions would produce the same effect.
Contrast enhancement with gadolinium increases both the sensitivity and specificity of MR. 
CEREBRAL GLIOMAS
Gliomas are malignant tumors of the glial cells of the brain and account for 30-40% of all primary intracranial tumors. They occur predominantly in the cerebral hemispheres, but the brain stem and cerebellum are frequent locations in children, and they are also found in the spinal cord. The peak incidence is during middle adult life, when patients present with seizures or symptoms related to the location of the gliomas and the brain structures involved.
Astrocytomas are graded according to their histologic appearance. Grade 1 astrocytomas have well-differentiated astrocytes and well-defined margins. The clinical course often proceeds over many years and complete cures are possible. The pilocytic variant is a low-grade tumor with a distinct capsule that is commonly found in children. The giant cell astrocytoma is a specialized tumor that develops from pre-existing hamartomas in patients with tuberous sclerosis. Grade 2 astrocytomas are well-differentiated but diffusely infiltrating tumors. The fibrillary type is most common, and although initially benign, they may evolve into a higher grade tumor over time. This changing character of gliomas makes histological classification difficult from sample biopsies, because different parts of the tumor often exhibit varying degrees of malignancy. The higher grade astrocytomas are very cellular and pleomorphic. Anaplastic astrocytomas (Grade 3) are very aggressive tumors, readily infiltrate adjacent brain structures, and have a uniformly poor prognosis. Glioblastoma multiforme (Grade 4) has the added histologic features of endothelial proliferation and necrosis. Multicentric foci of tumor may be seen in 4 to 6% of glioblastomas. Gliomatosis cerebri is an unusual condition with diffuse contiguous involvement of multiple lobes of the brain.
Oligodendrogliomas are the most benign of the gliomas. Calcification is common, and they occur predominantly in the frontal lobes.
The common signal characteristics of intra-axial tumors include high signal intensity on T2-weighted images and low signal on T1-weighted images, unless fat or hemorrhage is present. Fat and subacute hemorrhage (methemoglobin) exhibit high signal on T1-weighted images, and acute hemorrhage (deoxyhemoglobin) and chronic hemorrhage (hemosiderin/ferritin) show low signal intensity on T2-weighted scans. Gliomas have poorly defined margins on plain MR. They infiltrate along white matter fiber tracts, and the deeper lesions have a propensity to extend across the corpus callosum into the opposite hemisphere. They are often quite large by the time of clinical presentation.
The higher grade gliomas, particularly glioblastomas, appear heterogeneous due to central necrosis with cellular debris, fluid, and hemorrhage. Peritumoral edema and mass effect are common features. Following injection of gadolinium, T1-weighted images show irregular ring enhancement, with nodularity and nonenhancing necrotic foci.
The lower grade astrocytomas tend to be more homogeneous without central necrosis. Large cystic components may be present. The cysts have smooth walls, and the fluid is of uniform signal, to distinguish them from necrosis. Enhancement is variable, depending on the integrity of the blood-brain barrier.
Perfusion imaging has shown promise as a technique for determining the grade of intracranial mass lesions. Perfusion imaging relies on a first-pass susceptibility-related signal loss on T2*-weighted images, from which relative cerebral blood flow and volume can be calculated. Several studies have shown a correlation between relative cerebral blood volume and tumor grade, likely due to the relationship of blood volume to vascular proliferation in high-grade gliomas.
MR Spectroscopy
MR spectroscopy provides a measure of brain chemistry and can help characterize tumors and and grade the degree of malignancy. As a general rule, as malignancy increases, NAA and creatine decrease, and choline, lactate, and lipids increase. NAA decreases as tumor growth displaces or destroys neurons. Very malignant tumors have high metabolic activity and deplete the energy stores, resulting in reduced creatine. Very hypercellular tumors with rapid growth elevate choline. Lipids are found in necrotic portions of tumors, and lactate appears when tumors outgrow their blood supply and start utilizing anaerobic glycolysis. To get an accurate assessment of the tumor chemistry, the spectroscopic voxel should be placed over an enhancing region of the tumor, avoiding areas of necrosis, hemorrhage, calcification, or cysts.
Multi-voxel spectroscopy is best to detect infiltration of malignant cells beyond the enhancing margins of tumors. Particularly in the case of cerebral glioma, elevated choline levels are frequently detected in edematous regions of the brain outside the enhancing mass.
A common clinical problem is distinguishing tumor recurrence from radiation effects several months following surgery and radiation therapy. Elevated choline is a marker for recurrent tumor. Radiation change generally exhibits low NAA, creatine, and choline on spectroscopy. If radiation necrosis is present, the spectrum may reveal elevated lipids and lactate.
MRS cannot always distinguish primary and secondary tumors of the brain from one another. As mentioned above, one key feature of gliomas is elevated choline beyond the margin of enhancement due to infiltration of tumor into the adjacent brain tissue. Most non-glial tumors have little or no NAA. Elevated alanine at 1.48 ppm is a signature of meningiomas. They also have no NAA, very low creatine, and elevated glutamates.
LYMPHOMA
Primary malignant lymphoma is a non-Hodgkin's lymphoma that occurs in the brain in the absence of systemic involvement. These tumors are highly cellular and grow rapidly. Favorite sites include the deeper parts of the frontal and parietal lobes, basal ganglia, and hypothalamus. Most occur in patients who are immunocompromised secondary to chemotherapy or acquired immunodeficiency syndrome (AIDS) or in organ transplant recipients who are on immunosuppressant drugs. Cerebral lymphomas are very radiosensitive and respond dramatically to steroid therapy.
Lymphomas typically appear as homogeneous, slightly high signal to isointense masses deep within the brain on T2-weighted images. The observed mild T2 prolongation is probably related to dense cell packing within these tumors, leaving relatively little interstitial space for accumulation of water. They are frequently found in close proximity to the corpus callosum and have a propensity to extend across the corpus callosum into the opposite hemisphere, a feature that mimics glioblastoma. Multiple lesions are present in as many as 50%. Despite their rapid growth, central necrosis is uncommon. They are associated with only a mild or moderate amount of peritumoral edema. By time of presentation they can be quite large and yet produce relatively little mass effect, a feature that sets lymphoma apart from glioblastoma and metastases. Intratumoral cysts and hemorrhage are unusual. Most lymphomas show bright homogeneous contrast enhancement.
The pattern is modified somewhat in AIDS patients. Multiplicity seems to be more common. Moreover, lymphomas exhibit more aggressive behavior and readily outgrow their blood supply. As a result, central necrosis and ring enhancement are often seen in lymphomatous masses in AIDS patients.
METASTATIC DISEASE
Metastases to the brain occur by hematogenous spread, and multiple lesions are found in 70% of cases. The most common primaries are lung, breast, and melanoma, in that order of frequency. Other potential sources include the gastrointestinal tract, kidney, and thyroid. Metastases from other locations are uncommon. Clinical symptoms are nonspecific and no different from primary brain tumors. If a parenchymal lesion breaks through the cortex, tumor can extend and seed along the leptomeninges.
Metastatic lesions can be found anywhere in the brain but a favorite site is near the brain surface at the corticomedullary junction of both the cerebrum and cerebellum. They are hyperintense on plain T2-weighted images. Areas of necrosis are prevalent in the larger lesions, accounting for their heterogeneous internal texture. Peritumoral edema is a prominent feature, but multiplicity is the most helpful sign to suggest metastatic disease as the likely diagnosis. Correlative studies have shown MR to be more sensitive than CT for detecting metastases, particularly lesions near the base of the brain and in the posterior fossa. One limitation of plain MR is the frequency of periventricular white matter hyperintensities found in the same older age group at risk for metastatic disease.
Gadolinium enhanced MR has resulted in improved delineation of metastatic disease compared with nonenhanced scans. Moderate to marked enhancement is the rule, nodular for the smaller lesions and ringlike with central nonenhancing areas for the larger ones.
Hemorrhage is present in 3 to 14% of brain metastases, mainly in melanoma, choriocarcinoma, renal cell carcinoma, bronchogenic carcinoma, and thyroid carcinoma. The presence of nonhemorrhagic tissue and pronounced surrounding vasogenic edema are clues to the underlying neoplasm.
Metastatic melanoma has been a topic of special interest in the MR literature because of the presence of paramagnetic, stable free radicals within melanin. The MR appearance is variable depending on the histology of the melanoma and the components of hemoglobin. Most are hyperintense to white matter on T1-weighted scans and hypointense on T2-weighted scans. Atlas and coworkers
INTRAVENTRICULAR TUMORS
The intraventricular location is unique in that many of the tumor types are more commonly associated with extra-axial locations. Patients often present with obstructive hydrocephalus. Most intraventricular tumors are relatively benign and have well-defined margins. As they grow, the tumors expand the ventricle of origin. With malignant degeneration, extension into the brain parenchymal occurs. The primary blood supply to intraventricular lesions is derived from the choroidal arteries.
MENINGIOMA
Meningiomas account for 15% of all intracranial tumors and are the most common extra-axial tumor. They originate from the dura or arachnoid and occur in middle-aged adults. Women are affected twice as often as men. Meningiomas are well-differentiated, benign, and encapsulated lesions that indent the brain as they enlarge. They grow slowly and may be present for many years before producing symptoms. The histologic picture shows cells of uniform size that tend to form whorls or psammoma bodies.
The parasagittal region is the most frequent site for meningiomas, followed by the sphenoid wings, parasellar region, olfactory groove, cerebello-pontine angle, and rarely the intraventricular region. Meningiomas often induce an osteoblastic reaction in the adjacent bone, resulting in a characteristic focal hyperostosis. They are also hypervascular, receiving their blood supply predominantly from dural vessels.
Most meningiomas are isointense with cortex on T1- and T2-weighted images. A heterogeneous internal texture is found in all but the smallest meningiomas. The mottled pattern is likely due to a combination of flow void from vascularity, focal calcification, small cystic foci, and entrapped CSF spaces. Hemorrhage is not a common feature. An interface between the brain and lesion is often present, representing a CSF cleft, a vascular rim, or a dural margin. MR has special advantages over CT in assessing venous sinus involvement and arterial encasement. Occasionally, a densely calcified meningioma is encountered that is distinctly hypointense on all pulse sequences.
Meningiomas show intense enhancement with gadolinium and are sharply circumscribed.
PINEAL REGION TUMORS
Tumors in the pineal region can be classified into three major groups based on their origin: germ cell, pineal parenchyma, and parapineal. Germinoma is the least differentiated of the germ cell group. It occurs in children and young adults and accounts for more than 50% of all pineal region tumors. The other germ cell tumors include embryonal carcinoma, yolk-sac tumor, and choriocarcinoma. Differentiation along three germ layers results in a teratoma. The true pinealomas consist of pineoblastoma and pineocytoma. Pineoblastoma is an embryonal tumor of neuroectoderm, related to neuroblastoma and medulloblastoma, and is found primarily in young children. Pineocytomas are less cellular and exhibit benign behavior. The parapineal lesions include gliomas of the tectum and posterior third ventricle, meningiomas arising within the quadrigeminal cistern, and developmental cysts (epidermoid, dermoid, arachnoid cyst).
The clinical expression of these tumors is usually related to mass effect upon adjacent brain structures. Hydrocephalus secondary to aqueductal obstruction is a common presentation. Compression of the tectum of the midbrain can produce paralysis of upward gaze, the classic Parinaud's syndrome. Germinomas and gliomas have a propensity to grow into the third ventricle and compress the hypothalamus, resulting in endocrine dysfunction. Dissemination through the CSF pathways is a known complication of pineoblastoma and germinoma.
Pineal germinomas and primary pineal tumors are most often isointense with the brain on T1- and T2-weighted images. A few lesions exhibit long T1 and T2, which may correlate with embryonal cell elements. Despite this relative lack of contrast, with multiplanar imaging plain MR delineates pineal region masses better than CT, showing the relationships of the tumor to the posterior third ventricle, vein of Galen, and aqueduct.
Meningiomas can appear very similar on plain scan, but their intense enhancement may set them apart from other lesions. Gliomas infiltrate the tectum and posterior walls of the third ventricle. They tend to be poorly circumscribed and produce symptoms earlier. Edema is not a consistent finding, and enhancement is variable. Larger gliomas in the splenium of the corpus callosum may present as pineal region masses.
Teratomas are of mixed signal intensity, frequently with calcification. They may also have cystic components and fat. Arachnoid cysts, epidermoid and dermoid tumors can usually be distinguished from other pineal region tumors by their increased signal on T2-weighted images.
Pineal cysts were visualized in 4.3% of normal patients in one MR study.
BENIGN CYSTIC MASSES
Cystic lesions occur most often in the basal cisterns, a midline location or within the ventricular system. They include arachnoid cyst, dermoid, epidermoid, and neuroepithelial cysts, including colloid cyst. These lesions are interesting in that their MR appearance is quite distinct from solid masses. Their signal characteristics depend to a large extent on the cyst contents, but associated solid components may also have specific features.
Arachnoid Cyst
Arachnoid cysts are CSF-containing cysts that are found in the middle fossa, posterior fossa, suprasellar cistern, or near the vertex. They are benign but slowly grow as they accumulate fluid, compressing normal brain structures. Remodeling of the adjacent skull is an important clue for a benign expansile process.
Arachnoid cysts are smoothly marginated and homogeneous. They are not calcified and do not enhance. The multiplanar capability of MR is particularly helpful in establishing the exact location, and the diagnosis is supported by the cyst fluid being isointense with CSF on all pulse sequences.
Epidermoid Cyst
Epidermoid cysts are referred to as "pearly tumors" because of their glistening white appearance at surgery. They arise from epithelial cell rests in the basal cisterns. They are benign and grow slowly along the subarachnoid spaces and into the various crevices found at the base of the brain. Intradural epidermoids are usually quite large with lobulated outer margins and an insinuating pattern of growth. They have a heterogeneous texture and variable signal intensity on MR.
Dermoid Cyst
Dermoid cysts have both dermal and epidermal derivatives, accounting for their more varied histologic and MR appearance. They are primarily midline lesions, occurring in the pineal and suprasellar regions. Dermoids have some distinctive features on MR. They tend to be heterogeneous owing to the multiple cell types within them. Fatty components are common, producing high signal on T1-weighted images. On axial and sagittal scans, a fat-fluid level may be seen, or a level between fat and matted hair within the cyst. Rupture of a dermoid and leakage of cyst contents into a ventricle or subarachnoid space may produce an ependymitis or meningitis, respectively.
Lipomas are also midline lesions and are often associated with partial or complete agenesis of the corpus callosum. Occasionally, an incidental lipoma will be found in the region of the quadrigeminal plate or cerebellopontine angle.
Colloid Cyst
Colloid cysts originate from primitive neuroepithelium within the roof of the anterior third ventricle. They are positioned just posterior to the foramina of Monro between the columns of the fornix. Histologically, they consist of a thin, fibrous capsule with an epithelial lining. The cysts contain a mucinous fluid with variable amounts of proteinaceous debris, blood components, and desquamated cells.
Colloid cysts are smoothly marginated spherical lesions without surrounding brain reaction. Two signal patterns have been reported on MR scans and correlated with their CT features. Those that are low density on CT are isointense on T1-weighted images and hyperintense on T2-weighted images, probably indicating a fluid composition similar to CSF. Most colloid cysts are isodense or slightly hyperdense on CT. The MR counterpart is a high signal capsule and a hypointense center on T2-weighted images. The signal characteristics of the fluid depend on the protein content of the cyst fluid and is similar to that observed in sinonasal secretions.
Dilatation of the lateral ventricles is a common finding, and the enlargement may be unequal owing to asymmetric positioning of the cyst at the foramina of Monro. The expanding cyst also enlarges the anterior third ventricle, but the posterior third, aqueduct, and fourth ventricle should be normal. Following contrast infusion, colloid cysts may show ring enhancement, due to either enhancement of the cyst wall or choroid plexus draped around the cyst.
REFERENCES
Thursday, 6 November 2008
Group I: Monday, February 2, 2009 Day 1
Group II: Tuesday, February 3, 2008 Day 1
08:00 – 08:25 Registration
08:25 – 08:30 Introduction: Presentation of the workshop programme
A. Laghi (Latina/IT)
08:30 – 08:45 Introduction State-of-the-art CT-Colonography
D. Burling (London/UK)
08:45 – 09:10 Polyps and Colorectal Cancer (Gastroenterologist’s view)
James East (London/UK)
09:10 – 10:30 Technical basis of CTC: Preparation, image acquisition, complications
Chairman: S.Taylor (London, UK)
09:10 – 09:30 Bowel preparation and faecal tagging
P. Lefere (Roeselare/BE)
09:30 – 09:50 Practical Issues (technique, insufflation)
J. Stoker (Amsterdam/NL)
09:50 – 10:10 Image acquisition: technical parameters
P. Rogalla (Berlin/DE)
10:10 – 10:30 Complications (Perforation, cardiovascular effects)
S. Taylor (London/UK)
10:30 – 11:00 Coffee
11:00 – 12:40 2D - 3D First approach: face to face
Chairman: S. Halligan (London/UK)
11:00 – 11:20 Basic reading technique, primary 2D and 3D, normal anatomy,
C. Kay (Bradford/UK)
11:20 – 11:40 Pitfalls in interpreting CTC
S. Gryspeerdt (Roeselare/BE)
11:40 – 12:00 Teaching on workstation – easy case (based on ESGAR study)
A. Lowe (Bradford/UK)
12:00 – 12:45 Panel discussion: Q&A
Moderator: A. Laghi (Latina/IT)
Panellists: all speakers of previous three sessions.
12:45 – 14:15 Lunch
14:15 – 16:15 CTC: clinical application
Chairman: R. Frost (Salisbury/UK)
14:15 – 14:35 Study results and indications
A. Laghi (Latina/IT)
14:35 – 14:55 Extra-colonic findings
M. Hellström (Göteborg/SE)
14:55 – 15:15 How to report CTC
E. Neri (Pisa/IT)
15:15 – 15:30 How to set up a CTC service
M. Morrin (Dublin/IRE)
15:30 – 16:15 Panel discussion: Q&A
Moderator: R. Frost (Salisbury/UK)
Panellists: All speakers
16:15 – 17:00 Coffee
17:00 – 18:00 TWO PARALLEL SESSIONS:
17:00 – 18:00 CAD
Moderator: S.Halligan (Harrow/UK)
Technique and results (17:00 – 17:20)
D Regge (Turin/IT)
Integration of CAD in the workflow (17:20 – 17:40)
A. Graser (Munich/DE)
Panel discussion: CAD (17:40 – 17:50)
17:00 – 18:00 Basic teaching on workstation in hands-on workstation room
(in parallel to CAD Session)
Lead: T. Mang (Vienna/AT), A. Gupta (London/UK)
18:00 – 19:00 Moderator: D.Tolan (Leeds/UK)
Workstations are available for participants for individual familiarisation
(Application Specialists are available for questions)
Workstation Room
Group I: Tuesday, February 3, 2009 Day 2
Group II: Wednesday, February 4, 2009 Day 2
08:30 – 09:30 Familiarisation with the different workstations available for the hands-on sessions
Moderator: D.Tolan (Leeds/UK)
Introduction of the tutors and the application specialists
Introduction of each vendor by application specialists. Explanation of workflow
Teaching on workstations
(20 min for cases review on workstation + 10 min for review with faculty)
09:30 – 10:30 Cancer cases
09:30 – 10:15 Cancer cases for review
Participants to review specific cases
10:15 – 10:30 Case review and discussion
D. Hock (Liege/BE)
10:30 – 11:00 Coffee
11:00 – 12:00 Polyp cases
11:00 – 11:45 Polyp cases for review
Participants to review specific cases
11:45 – 12:00 Case review and discussion
F. Iafrate (Rome/IT)
12:00 – 13:00 Difficult cases
12:00 – 12:45 Difficult cases for review
Participants to review specific cases
12:45 – 13:00 Case review and discussion
A. Gupta (London/UK)
13:00 – 14:15 Workstations face to face (Lunch Symposium)
Moderation: G. Maskell (Truro/UK)
14:15 – 15:15 “Blind” case reviews
14:15 – 15:00 “Blinded” Cases
Participants to review specific cases
15:00 – 15:15 Case review and discussion
P. Wylie (London/UK)
15:15 – 16:15 Hands-on session: free
(Participants to use syllabus for findings and to address queries to faculty)
16:15 – 16:45 Coffee
16:45 – 17:15 2 cases prize competition
F.Iafrate/ S.Taylor (Berlin/DE)
17:15 – 17:25 Complete evaluation forms and submit them at the registration desk
Friday, 24 October 2008
Buy homes abroad, save tax here
Wednesday, 29 August , 2007, 08:01
Last Updated: Wednesday, 29 August , 2007, 08:49
Last Updated: Wednesday, 29 August , 2007, 08:49
For
long-term capital gains earned on sale of property, the tax rate is 20
per cent. If the value is above Rs 10 lakh, the tax rate climbs to
22.66 per cent. This applies both to residents as well as non-resident
Indians (NRIs).
Sec. 54 of the Income Tax Act offers a way out of paying such
tax. If the capital gain amount is invested in a residential house
within one year before to two years after the sale, then the capital
gains earned are fully exempted from tax. In case the investor intends
to construct a house, the time limit is extended to within three years
of the date of sale. Of course, if only a part of the capital gain is
used, the exemption would be proportional and the excess will be
chargeable to tax.
So far, so good. Now comes the interesting part, especially for NRIs.
Nowhere does Sec. 54 specify that the new house purchased should
be within India. This means, to save capital gains earned in India, the
NRI can even purchase a house in his or her own host country abroad and
yet claim exemption. Why just NRIs, now even resident Indians can
benefit from this rule. RBI allows an Indian resident up to $1,00,000
per annum to be invested abroad. Such investment could be even in
property.
So far, this was just a theoretical possibility based on a
plain reading of the law. However, in a recent judgment, the Income Tax
Tribunal in the case of Prema P Shah (Citation 282 ITR 211) has ruled
that the exemption offered by Sec. 54 can indeed be extended to a
property purchased in a foreign country.
The brief facts of the case were that the assessee claimed the
capital gains on sale of house property situated in India as exempt. To
support her claim, she filed a photocopy of a lease agreement for a
house in London. The assessing officer disallowed the claim noting that
Sec. 54 speaks of purchase of residential property or construction
thereof. In this case, Shah had purchased only tenancy rights and hence
exemption under Sec. 54 would not be available to her.
This argument was rejected by the Tribunal based on the facts
of the case. In the UK, property belongs to the Sovereign; citizens,
instead of being allowed to purchase, are granted long-term leases. In
the instant case, the lease was valid for 150 years -- in other words,
it was in perpetuity and for all practical purposes, the assessee was
the owner of the property.
It's not even necessary that the same amount of capital gains
be used to buy the property. The assessee can very well buy the
property even on mortgage (housing finance) -- as long as the
conditions specified in Sec. 54 are satisfied, the exemption is
available. This is because, even for properties bought using mortgage,
the borrower instantly becomes the owner of the property.
That he is paying his EMIs (mortgage) on the loan taken is an
agreement between the lender and the borrower inter se. It has no
bearing on the ownership of the property. In other words, as far as
Sec. 54 is concerned, an investment has indeed been made in property.
Whether it's through the mechanism of mortgage or otherwise is
immaterial.
This judgment will have far reaching impact, especially on NRI
investments and taxation. No one is born an NRI. Indian residents
become NRIs when they go abroad for employment or business. More often
than not, such persons own property in India, either the one they left
behind when they went abroad and became NRIs, or one that is inherited.
A number of such persons, who have set up a new life abroad
definitely don't need a new property just to save on tax. Now, such
persons can actually consider buying property abroad and claiming tax
benefits in India.
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