Thursday, August 27, 2009

MENISCEAL TEAR

There are two menisci in your knee; each rests between the thigh bone (femur) and shin bone (tibia). The menisci are made of tough cartilage and conform to the surfaces of the bones upon which they rest. One meniscus is on the inside of your knee; this is the medial meniscus. The other meniscus rests on the outside of your knee, the lateral meniscus. What does the meniscus do?
These meniscus functions to distribute your body weight across the knee joint. Without the meniscus present, the weight of your body would be unevenly applied to the bones in your legs (the femur and tibia). This uneven weight distribution would cause excessive forces in specific areas of bone leading to early arthritis of knee joint. Therefore, the function of the meniscus is critical to the health of your knee.
The meniscus is C-shaped and has a wedged profile. The wedged profile helps maintain the stability of the joint by keeping the rounded femur surface from sliding off the flat tibial surface. The meniscus is nourished by small blood vessels, but the meniscus also has a large area in the center of that has no direct blood supply (avascular). This presents a problem when there is an injury to the meniscus as the avascular areas tend not to heal. Without the essential nutrients supplied by blood vessels, healing cannot take place.

How does the meniscus work?

The knee joint is very important in allowing people to go about performing almost any activity. The joint is made up of three bones: the femur (thigh bone), the tibia (shin bone), and the patella (knee cap). The surfaces of these bones within the joint are covered with a layer of cartilage. This important surface allows the bones to smoothly glide against each other without causing damage to the bone. The meniscus sits between the cartilage surfaces of the bone to distribute weight and to improve the stability of the joint.

Meniscus Tear or Cartilage Tear?

Both the covering of the bone within the joint and the meniscus are made of cartilage--this makes the issue a little confusing. People often say 'cartilage' to mean the meniscus (the wedges of cartilage between the bone) or to mean the joint surface (so-called articular cartilage which caps the ends of the bone). When people talk about a cartilage tear, they a talking about a meniscus tear. When people talk about arthritis and wear of cartilage, they are talking most often about the articular cartilage on the ends of the bone.
What happens with a meniscus tear (torn cartilage)?
The two most common causes of a meniscus tear are due to traumatic injury (often seen in athletes) and degenerative processes (seen in older patients who have more brittle cartilage). The most common mechanism of a traumatic meniscus tear occurs when the knee joint is bent and the knee is then twisted.
It is not uncommon for the meniscus tear to occur along with injuries to the anterior cruciate ligament (ACL) and the medial collateral ligament (MCL)-these three problems occurring together are known as the "unhappy triad," which is seen in sports such as football when the player is hit on the outside of the knee.

Symptoms of a Meniscus Tear?

Individuals who experience a meniscus tear usually experience pain and swelling as their primary symptoms. Another common complaint is joint locking, or the inability to completely straighten the joint. This is due to a piece of the torn cartilage physically impinging the joint mechanism of the knee. The most common symptoms of a meniscus tear are:
  • Knee pain
  • Swelling of the knee
  • Tenderness when pressing on the meniscus
  • Popping or clicking within the knee
  • Limited motion of the knee joint

Diagnosis of a Meniscus Tear

Any patient who has knee pain will be evaluated for a possible meniscus tear. A careful history and physical examination can help differentiate patients who have a meniscus tear from patients with knee pain from other conditions. Specific tests can be performed by your doctor to detect meniscus tears. X-rays and MRIs are the two tests commonly used in patients who have meniscus tears. An x-ray can be used to determine if there is evidence of degenerative or arthritic changes to the knee joint. The MRI is helpful at actually visualizing the meniscus. However, simply 'seeing' a torn meniscus on MRI does not mean a specific treatment is needed. Treatment of meniscus tears depends on several factors, as not all meniscus tears require surgery.

Treatment of a Meniscus Tear

Treatment of a meniscus tear depends on several factors including the type of tear, the activity level of the patient, and the response to simple treatment measures. When surgical treatment of a meniscus tear is required, the usual treatment is to trim the torn portion of meniscus, a procedure called a meniscectomy. Meniscus repair and meniscal transplantation are also surgical treatment options. Determining the most appropriate meniscus tear treatment is something you can discuss with your doctor.

Wednesday, August 26, 2009

SLAP TEAR SHOULDER JOINT

he shoulder joint is considered a 'ball and socket' joint. However, in bony terms the 'socket' (the glenoid fossa of the scapula) is quite small, covering at most only a third of the 'ball' (the head of the humerus). The socket is somewhat deepened by a circumferential rim of fibrocartilage which is called the glenoidal labrum. Previously there was some argument as to the structure (it is fibrocartilaginous as opposed to the hyaline cartilage found in the remainder of the glenoid fossa) and function (it was considered a redundant evolutionary remnant, but is now considered integral to shoulder stability). Most authorities agree that the tendon of the long head of the biceps brachii muscle proximally becomes fibrocartilaginous prior to attaching to the superior aspect of the glenoid. Similarly the long head of the triceps brachii inserts inferiorly.[1] Together these cartilaginous extensions of the tendon are termed the 'glenoid labrum'. A SLAP tear or lesion occurs when there is damage to the superior or uppermost area of the labrum. SLAP lesions have come into public awareness with their increasing frequency in overhead and particularly throwing athletes. The increased frequency relates to the relatively recent description of labral injuries in throwing athletes [2] and the initial definitions of the 4 SLAP sub-types[3] all happening since the 1990s. The identification and treatment of these injuries continues to evolve, however it is safe to say that a baseball pitcher suffering a 'dead arm' caused by a SLAP lesion today is far more likely to recover such that he can return to the game at its highest level than was the case previously.

Sub-types

At least ten types of this injury are recognized with varying degrees of damage,[4] seven of which are listed here
  1. Degenerative fraying of the superior portion of the labrum, with the labrum remaining firmly attached to the glenoid rim
  2. Separation of the superior portion of the glenoid labrum and tendon of the biceps brachii muscle from the glenoid rim
  3. Bucket-handle tears of the superior portion of the labrum without involvement of the biceps brachii (long head) attachment
  4. Bucket-handle tears of the superior portion of the labrum extending into the biceps tendon
  5. Anteroinferior Bankart lesion that extends upward to include a separation of the biceps tendon
  6. Unstable radial of flap tears associated with separation of the biceps anchor
  7. Anterior extension of the SLAP lesion beneath the middle glenohumeral ligament

MRI OF SHOULDER IMPINGEMENT SYNDROME

 
Fig. 1 20-year-old man with supraspinatus tendinosis. Oblique coronal fast spin-echo T2-weighted MR image shows supraspinatus tendon has increased signal near its insertion on greater tuberosity (arrow). Cystic changes are incidentally noted in humeral head.




Fig. 2 20-year-old man with infraspinatus tendinosis. Oblique coronal fast spin-echo T2-weighted MR image shows infraspinatus tendon has increased signal near it insertion on greater tuberosity (arrow). Cystic changes are incidentally noted in humeral head near attachment of infraspinatus tendon.

Fig. 3 17-year-old girl in abduction external rotation. Fat-suppressed proton density image shows infraspinatus being impinged by posterosuperior glenoid labrum (arrow).


Fig. 4 20-year-old man with cystic changes in humeral head. Axial fast spin-echo T2-weighted MR image shows cystic changes in posterosuperior humeral head near attachment sites of supraspinatus and infraspinatus tendons (arrow).

Monday, August 24, 2009

MR ANGIOGRAPHY

Combining a perfectly timed gadolinium contrast agent injection with three-dimensional (3D) spoiled gradient-echo (SPGR) magnetic resonance (MR) imaging produces high signal-to-noise ratio (S/N) MR angiograms covering extensive regions of vascular anatomy within a breath hold (1, 2, 3, 4, 5, 6, 7, 8, 9, 10). This article provides information for radiologists on

1. Principles of 3D gadolinium-enhanced MR angiography.
2. Patient set-up and positioning.
3. Selection of optimal imaging parameters.
4. Timing of the gadolinium bolus.
5. Reconstruction of images on a computer workstation.
6. Identification of normal variants, postoperative cases, and common pathologic entities.


Principles of 3D Gadolinium-enhanced MR Angiography

Gadolinium is one of the rare earth elements in the transition group IIIb of the periodic table. Actually, it is not rare at all, but a rather common element found throughout the earth's crust. It has eight unpaired electrons in its outer shell, which causes its paramagnetic effects. Gadolinium by itself can cause heavy metal poisoning. However, when bound to a chelator, it is safe for intravenous injection, yet remains paramagnetic. It shortens the T1 of blood in the region of the gadolinium molecule according to the following equation (1):

1/T1=1/1,200 + (R1 × [Gd]),

where R1 is the T1 relaxivity of the gadolinium chelate, [Gd] is the gadolinium concentration in the blood, and 1,200 is the blood T1 (in msec) without gadolinium.


Figure 1. Effect of gadolinium concentration on blood T1. (The graph was calculated with Microsoft Excel 97 [Microsoft, Redmond, Wash] by using the above formula.)

The blood [Gd] must be greater than 1.0 mmol/L for T1 to be less than 270 msec, which is the T1 of fat at 1.5 T (1, 5). This is the property which is important for increasing the MR signal intensity of blood on contrast-enhanced SPGR images. Note that this T1 shortening effect is maximized by using gadolinium chelates with the highest relaxivity and by having a high gadolinium concentration in the blood.

Gadolinium Safety

Gadolinium contrast agents have an extraordinarily favorable safety profile. There is no clinically detectable nephrotoxicity for gadopentetate dimeglumine (Magnevist; Berlex Imaging, Wayne, NJ), gadoteridol (ProHance; Bracco Diagnostics, Princeton, NJ), or gadodiamide (Omniscan; Nycomed Amersham, Princeton, NJ) even at high doses (11). In addition, they have a very low frequency of adverse events. Idiosyncratic reactions are rare, and serious adverse events are extremely rare (1 in 20,000) (12). Note that important contraindications to gadolinium include pregnancy and a history of a life-threatening reaction to gadolinium itself. In patients with poor renal function, there may be delayed excretion of gadolinium contrast agents.

Gadolinium Dose

With intravenous injection, gadolinium is initially in the arm vein, then the pulmonary circulation, then the arteries; eventually it is distributed throughout the circulatory system. Within a few minutes, there is redistribution into the extracellular fluid space. To make blood bright compared with all background tissues, it is necessary to give a sufficient dose of gadolinium. Two or three bottles (20 mL each) of the gadolinium contrast agent (about 0.3 mmol/kg gadolinium) is usually sufficient for an average or heavy person when imaging in the equilibrium phase. However, arteries are best imaged during the arterial phase of gadolinium infusion. This gives a higher arterial S/N and eliminates the confusion caused by overlapping venous enhancement. It may seem that a fast acquisition is necessary to capture the contrast agent bolus during the brief moment when the agent is present in the arteries but not yet in the veins. However, it is possible to take advantage of three important effects that allow the relatively slow MR acquisition to capture an arterial-phase image without having to use large amounts of gadolinium.

K Space

The most important effect is related to how MR data are mapped in k space. K space, or Fourier space, does not map to the image pixel by pixel. Rather, the information within k space determines spatial frequency features of the image. The low spatial frequency information, in the center of k space, dominates image contrast, while the higher spatial frequency data, at the periphery of k space, determines image detail. To obtain an arterial-phase image in which arteries are bright and veins are dark, it is essential that the central k-space data (ie, the low spatial frequency data) are acquired while the gadolinium concentration in the arteries is high but relatively lower in the veins. The presence of contrast agent is not as important for acquisition of peripheral k-space data. This trick allows a relatively long MR acquisition to achieve the image contrast associated with a brief window of time. That brief window of time is the instant when central k-space data are acquired. Therefore, it is critical to time the bolus for maximum arterial [Gd] during acquisition of central k-space data. With perfect bolus timing, high S/N arterial-phase images are possible with smaller doses of gadolinium.

Gadolinium Extraction

A second important effect is the extraction of gadolinium in the systemic capillary beds. This extraction results in venous blood tending to have a lower concentration of gadolinium relative to arterial blood, even for relatively long, sustained infusions lasting several minutes. This effect is not present in the cerebrovascular circulation because of the blood-brain barrier. Consequently, arterial-phase imaging in the central nervous system is more difficult.

Infusion Rate and Cardiac Output

A third effect is the relationship between arterial gadolinium concentration, the infusion rate, and cardiac output as follows:

[Gd]Arterial=Injection Rate/Cardiac Output



Figure 2. T1 versus injection rate at differing cardiac outputs.


This graph is a computer model generated for different cardiac outputs. Note that this graph is for static, nonmoving blood. The actual T1 of moving blood is even less than in the above graph. Notice that an injection rate of 0.2-0.3 mL/sec is required to decrease the blood T1 value to less than 150 msec in a patient with a cardiac output of 5 L/min. This is sufficiently below the T1 of fat (270 msec at 1.5 T) so that only the gadolinium in blood produces high signal intensity on T1-weighted SPGR images.

Arterial [Gd] is maximized by relaxing the patient to reduce cardiac output and by using a high infusion rate. However, fast infusion rates lasting for at least half of the acquisition time require large doses of gadolinium. The dose can be kept to a reasonable level by scanning rapidly. Fast acquisitions (<45 seconds) are possible with high performance gradient systems that allow short repetition and echo times, without having to make the bandwidth too wide. Fast acquisition has the additional benefit of making it possible for the cooperative patient to suspend breathing and to hold perfectly still.

Saline Flush and Intravenous Tubing

It is important to use intravenous (IV) line tubing that allows simultaneous attachment of separate syringes for the contrast agent and saline flush. The SmartSet (TopSpins, Ann Arbor, Mich), developed at the University of Michigan, has one-way valves that allow automatic switching between the contrast agent injection and saline flush so that there will be one continuous bolus with no gaps. By using the same tubing set for all patients receiving dynamic contrast agent injection, the operator becomes familiar with performing the injections and especially with the resistance to injection. It is then easier to concentrate on correctly timing the bolus and instructing the patient to suspend breathing.
Click here to view IV setup and use of SmartSet.



At least 20 mL of saline is recommended to adequately flush the contrast agent through the IV tubing and arm vein. By starting with a 30-mL saline-filled syringe, it is possible to initially prime the SmartSet with 8 mL of saline, test the IV once or twice with a 1-mL saline injection, and still have 20 mL left for the dynamic flush.

Gadolinium Dose

When beginning, we recommend use of two bottles (42 mL) for the average-size patient and three bottles (63 mL) for patients weighing more than 100 kg. Once you learn how to time the contrast agent injections perfectly, you will find it is possible to reduce the dose and still obtain diagnostic images.

Contrast Agent Bolus Timing

Perfect contrast agent bolus timing is crucial to ensure that the maximum arterial [Gd] occurs during the middle of the acquisition, when central k-space data are acquired. It is also essential that [Gd] not change too rapidly, as this will create a "ringing" artifact (13) (click here for example). Minimizing the ringing artifact requires that the contrast agent infusion last for at least half the duration of the 3D image acquisition. Bolus timing is difficult because the time required for the contrast agent bolus to travel from the injection site (typically an antecubital vein) to the artery being imaged is highly variable. For renal arteries, it may be only 10 seconds in a young, healthy person with a central intravenous line, or it may be as long as 50 seconds in an older patient with congestive heart failure and an intravenous line in the hand or wrist.

Timing for Long Acquisitions

For long acquisitions, lasting more than 100 seconds, timing is easy because errors of 10-15 seconds are small relative to the total scan duration. Use sequential ordering of k space, so that the center of k space is collected during the middle of the acquisition. Sequential ordering tends to result in fewer artifacts. Begin injecting the gadolinium just after initiating imaging. Finish the injection just after the midpoint of the acquisition, being careful to maintain the maximum injection rate for the approximately 10-30 seconds prior to the middle of the acquisition. This will ensure a maximum arterial [Gd] during the middle of the acquisition, when central k-space data are collected. To ensure full use of the entire dose of contrast agent, it is useful to flush the IV tubing with 20 mL of normal saline. This can be facilitated by using the SmartSet, which has ports for simultaneous attachment of contrast agent and saline syringes and valves for automatic switching between syringes. In this way, there is no delay between finishing the contrast agent injection and beginning the saline flush.

Timing for Fast (Breath-hold) Scans

For fast scans, less than 45 seconds in duration, contrast agent bolus timing is more critical and challenging. This is because bolus timing errors of 15 seconds can ruin a fast breath-hold scan. There are several approaches to determining the optimal bolus timing for these fast scans. The simplest, although least successful approach, is to guess on the basis of patient age, cardiac status, presence of aortic aneurysmal disease, and IV location. For a typical breath-hold scan duration of 35-45 seconds in a reasonably healthy patient with an IV site in the antecubital vein, a delay of approximately 10-12 seconds is appropriate. Therefore, in this scenario, begin the injection, and then 10 seconds later start imaging while the patient suspends breathing. If there is no convenient clock available to time this delay, take advantage of the natural rhythm of the patient's respiration. One deep breath in followed by a deep breath out takes approximately 4 seconds. Two breaths are eight seconds, followed by a deep breath in, 10 seconds, which represents the optimum delay between start of injection and beginning of scanning. If a patient is older and has a history of cardiac or aortic aneurysmal disease, add one or two extra breaths to the delay. Also, if the IV site is in the wrist, add an extra breath to the delay. Alternatively, if the patient is a marathon runner or you are injecting via a central line, it may be suitable to use only 1½ breaths of delay, or 6 seconds. A firm injection is necessary to keep the contrast agent bolus together. However, if the injection is too vigorous, it may cause rupture of the vein, with resulting extravasation of the contrast agent.

More reliable and precise techniques for determining the contrast travel time are also available. These include using a test bolus (14) to precisely measure the contrast travel time, using an automatic pulse sequence that monitors signal in the aorta and then initiates imaging after contrast is detected arriving in the aorta (Fluoroscopic triggering or MR SmartPrep) (15, 16), or imaging so rapidly that bolus timing is unimportant (10). A typical monitor signal graph is shown below.




Figure 3. Tracking signal versus time.
Blue line - MR signal intensity in volume of interest.
Green line - Level at which signal is 100% above baseline.
Red arrows - Time of injection and optimal time for imaging.


Note that the centric ordering of k space for the triggered acquisitions may create artifacts if the contrast agent bolus is still arriving when the scan is started. Sometimes this artifact may be reduced with sequential ordering. This artifact may also be reduced by delaying 5-8 seconds after detecting the leading edge of the bolus to give the contrast agent time to flow in completely and reach the plateau phase of the bolus.

Postprocessing of MR Data

Substantial improvement in image quality, and especially image contrast, can be attained through postprocessing techniques.

* Zero Padding
Image resolution can be increased with interpolation. One particularly useful interpolation scheme is known as zero padding. This involves filling out peripheral lines of k-space data with zeroes prior to performing the Fourier transform. Although no additional time is required for data collection, the Fourier transform will reconstruct more images with a smaller spacing. For example, with two-fold zero padding, if the partition thickness is 3 mm, the Fourier transform will reconstruct additional images that also have a 3-mm slice thickness but at 1.5-mm spacing with 50% overlap. This helps eliminate volume averaging and creates smooth visualization of small vessels on the reformatted maximum intensity projection (MIP) images. If available, two-fold zero padding in the slice direction is recommended.
* MR Digital Subtraction Angiography (DSA)
Image contrast can be improved by digital subtraction of precontrast image data from dynamic, arterial, or venous phase image data. This subtraction can be performed either slice-by-slice or prior to the Fourier transform by using a complex subtraction method. The improvement in contrast achieved with DSA may reduce the gadolinium dose required. However, there must be no change in the patient position between the precontrast and dynamic contrast-enhanced imaging. This requirement for no motion is easily met in the pelvis and legs, which can be sandbagged and strapped down. It is more difficult to achieve in the chest and abdomen, where respiratory, cardiac, and peristaltic motions are more difficult to avoid. Note that complex subtraction is generally performed automatically by the scanner before creating any of the images.


Multiplanar Reconstructions

Reformations and MIPs are essential for optimal assessment of vascular anatomy. Single-voxel-thick reformations and narrow subvolume MIPs show bifurcations and branch vessels in profile. This is important because atherosclerotic disease tends to be most severe at branch points. By creating subvolume MIPs of the 3D image data, these techniques help unfold tortuous vessels and eliminate the confusing overlap of vascular anatomy.

Creating an MIP Image

One approach to performing a subvolume MIP is to first load the entire 3D volume of arterial phase image data into the computer workstation 3D analysis program. Display a coronal MIP of the entire volume, an axial reformation, and an oblique view. On the coronal view, move the dot (which tracks the location) cranially and caudally while watching the axial reconstruction window to find the renal arteries. Display this subvolume of sagittal data as an MIP. Make this oblique MIP thick enough to encompass most of the aorta. Be certain to align the axis of the subvolume MIP so that it is parallel to the origin of the vessel. Although the entire length of the vessel may not be seen on this image, it will be an accurate representation of the vessel's origin, with no overlap from the aorta. This may then be repeated by moving the tracker dot on the axial image and watching the oblique view to create a sagittal view of the celiac and superior mesenteric arteries. This will show the celiac and superior and inferior mesenteric arteries, as well as the anterior and posterior margins of the aorta to best advantage.

Renal Artery Stenosis

Renal artery stenosis is an important cause of hypertension and renal failure (17, 18, 19, 20). This should be imaged with a comprehensive approach (11) that includes both morphologic and functional assessment of the renal vasculature.Many sequences are available which provide important information (21, 10, 22, 23, 24). We have chosen to do 3D phase contrast because of its simplicity and reliability (2).

Thursday, August 20, 2009

AN INTRODUCTION TO PET

  1. Introduction

    Diagnosing, staging, and re-staging of cancer, as well as the planning and monitoring of cancer treatment, have traditionally relied heavily on anatomic imaging with computed tomography (CT) or magnetic resonance imaging (MRI). These anatomic imaging modalities provide exquisite anatomic detail and are invaluable, especially for guiding surgical intervention and radiotherapy. However, they do have limitations in their ability to characterize tissue reliably as malignant or benign. Anatomic imaging generally has a high sensitivity for the detection of obvious structural alterations (e.g. enlarged structures, abnormal imaging characteristics) but a low specificity for further characterizing these abnormalities as malignant or benign. Necrotic tissue, scar tissue, and inflammatory changes often cannot be differentiated from malignancy based on anatomic imaging alone. In addition, lymph nodes which are not pathologically enlarged by size criteria alone but are harboring malignant cells pose a special diagnostic problem when using traditional cross-sectional imaging.

    Therefore, much effort has been forth in the research and development of molecular imaging techniques to detect abnormal behavior of tissues. The nuclear medicine community has developed positron emission tomography (PET) for imaging the activity of an injected radionuclide labeled glucose analogue, Fluorine-18-deoxyglucose (FDG), as a means to discriminate benign from malignant tissues accurately in many clinical settings. This technique is based on the fact that malignant tissue typically exhibits markedly increased rates of glucose metabolism.

    Just like glucose, FDG is actively transported into cells mediated by a group of structurally related glucose transport proteins. Once intracellular, glucose (and therefore also FDG) are phosphorylated by hexokinase as the first step in the glycolytic metabolism pathway. Normally, after being phosphorylated glucose continues along the glycolytic pathway for energy production. FDG, on the other hand, cannot enter the glycolytic pathway and becomes effectively trapped intracellularly as FDG-6-phosphate. Tumor cells display increased numbers of glucose transporters as well as higher levels of hexokinase. Most tumor cells are highly metabolically active with high mitotic rates that favor the more inefficient anaerobic metabolic pathway which adds to the already increased glucose demands. These combined mechanisms allow tumor cells to take up and retain higher levels of FDG when compared to normal tissues.

    PET provides imaging of the whole body distribution of FDG, thus highlighting the markedly increased metabolic activity of tumor cells. Sites of tumor involvement not obvious from cross-sectional images alone are often found, such as lymph nodes involved by tumor which are not pathologically enlarged by size criterion.

An important concept regarding PET imaging is that FDG is not cancer specific and will accumulate in any areas of high rates of metabolism and glycolysis. Therefore, increased uptake can be expected in all sites of hyperactivity at the time of FDG administration (e.g. muscles and nervous system tissues); at sites of active inflammation or infection (e.g. sarcoidosis, arthritis, pneumonia, etc.); and at sites of active tissue repair (e.g. surgical or traumatic wounds, healing fractures, etc.).

Taking the molecular imaging concept of PET one step further is the combined imaging modality positron emission tomography/computed tomography (PET/CT). PET/CT fuses functional information in the form of PET data and anatomic information in the form of CT data acquired almost simultaneously so that these information sets can be viewed and interpreted together. In PET/CT, both the multidetector CT apparatus and the PET detectors are mounted in the same gantry, one immediately behind the other. Both PET and CT scanning are performed with the patient lying in the same position on the imaging table resulting in optimal correlation of anatomic and metabolic information. For interpretation, the PET data is actually superimposed upon the CT data (co-registration) resulting in improved anatomic localization of normal and abnormal FDG activity. This fusion process has proven beneficial in more exactly localizing tissues involved by tumor. Better co-registration is especially significant in regions of complex anatomy, such as in the abdomen and in the head and neck. More exact localization of the involved tissues results in more accurate staging and more appropriate treatment planning including surgical therapy, radiotherapy, and medical therapy.

GLIOBLASTOMA MULTIFORME


Axial Gd enhanced T1W Image

Axial T2 W Image

WHO Grade IV

Cell of Origin: ASTROCYTE

Synonyms: GBM, glioblastoma multiforme, spongioblastoma multiforme

Common Locations: cerebral hemispheres, occasionally elsewhere (brainstem, cerebellum, cord)

Demographics: peak from 45-60 years

Histology: grossly heterogeneous, degeneration, necrosis and hemorrhage are common

Special Stains: GFAP varies, often present in areas of better differentiation

Progression : Can't get any worse.

Radiology: Glioblastoma is usually seen as a grossly heterogeneous mass. Ring enhancement surrounding a necrotic center is the most common presentation, but there may be multiple rings. Surrounding vasogenic edema can be impressive, and adds significantly to the mass effect. Signs of recent (methemoglobin) and remote (hemosiderin) hemorrhage are common. Despite it’s apparent demarcation on enhanced scans, the lesion may diffusely infiltrate into the brain, crossing the corpus callosum in 50-75% of cases.