Search my links!

Saturday, 7 May 2011

Technical priciples of doppler US (the basics)


Alternating voltage -> ceramic elements (crystals) -> the elements change Shape and Size -> pressure waves (ultrasound)

Conversly: Sonund waves returning as echos cause crystals to vibrate ->induce voltage -> processed -> image is produced


For determining velocity and direction of blood flow.
The doppler effect:

When a sound source and a reflector are moving towards each other, the sound waves are place closer together (higher frequency, high pitch sound).


Freq. shift = freq of echo (FE) - freq of sound originally emitted (F0)


The sound waves travel in human tissue at a constant speed of about 1540 m/s.
The frequency shift measured strongly depends on the cosine of the beam-vessel angle (alpha angle).

- In the least favourable case the cosine angle is =90` to the vessel, the frequency shift equals to zero, therefore no signal is detected.
- The most favourable case with the most accurate measurement is when the alpha angle is <60`, but <45` is even better.


- The sound is continuously emitted from one piezoelectric crystal and is recieved by another crystal.
- Advantage: can detect very higy velocities
- Disadvantage: can`t tell the depth of echo, range ambiguity
- Note: when using CW you cant use the B mode or CDS in most machine, you will be using a frozen-out image to locate the sample gate.


The sound is alternately transmitted and recieved by the sam crystal. The TE-delay time to recieve the echo can be converted to distance. This is needed to construct a 2D color duplex image. The smaller the color box, the faster the operation and the higher the temporal resolution.


The PRF can only be increased to 1/TE ( can take samples quicker than the echo returns, you have to wait for the echo). PRF decreases as the scanning depth increases (more time needed for echo to return). 1/TE sets the upper limit to the flow velocities that can be accurately measured with PW doppler.

Vessels with high flow velocities => high PRF used
Vessels with lower flow velocities (veins, searching for DVT) => small PRF used


Flow towar the transducer = RED
Flow away from the transducer = BLUE
Slow flow = DARK RED/BLUE


Flow in a curved vessel maybe red in one segment and blue in the other.

! Color brightness also changes in accordance to the alpha angle! So the accuracy of measurment in a curved vessel changes along its curve due to the change of the alpha angle of the vessel !

The 90` alpha angle at the junction of the red-blue segments results in a color void which should not be misinterpreted as a thrombus.

Don`t interpret flow direction after you have used the invert button, it confuses you and can result in many mistakes.

Beam stearing is an option in linear transducer can be used to change the angle of doppler waves.

Angling the color box: can correct a bad alpha angle (>60`). This can make vessel segments that initially show poor flow easier to evaluate.

Manually angling the transducer: if still the alpha angle is not ideal.



Can be aqcuired in PW mode, by using the trackball to position the sample volume (SV) in the area of interest. The insonation angle (alpha) must be determined before the frequency shift data can be converted into a true flow velocity.

The scanner then displays the velocity distribution consisting of a slower and faster flow components.

The time to peak (TTP), is the time it takes for the blood to reach its peak velocity in systole (D->S in the image), the TTP proximal to a stenosis is increased, and the curve becomes less sharp. Normally the TTP almost appears as a vertical upstroke in systole.
Renal artery stenosis PROXIMAL to the sampling site i.e. before the sampling site, note the increased TTP

Severe stenosis of the innominate artery. PW Doppler spectral image of the right CCA shows a tardus-parvus waveform, which is suggestive of a severe stenosis proximal to the point of sampling. A severe stenosis of the innominate artery was subsequently demonstrated at angiography. EDV = end-diastolic velocity.


Near the heart arteries pump blood against a relatively low peripheral resistance resulting in a biphasic wave pattern.

The smaller end-diastolic velocity peak is separated from the systolic peak by a small notch caused by the closure of the AO valve.

The lower the resistance the higher the end-diastolic flow, therefore if you see high diastolic flow then this might be indicating a higher perfusion demand by distal tissues (excercise, or in ischemia)


At greater distances from the heart the arteries loose their winkessel function while the the peripheral resistance increases. As a result the peripheral arteries show a triphasic waveform.

General feature: A rapid upstroke in early systole, which then falls off rapidly with a small notch marking the closure of the AO valve.

Due to high resistance in the peripheral arteries early diastole is normally marked by a period of reverse flow directed back to the heart (second phase), this appears as a deflection below the baseline. This is followed by a small upstroke that flows towards the periphery (3rd phase).


These are not distorted by improper angle selection. They are good in evaluating small arteries.

Pulsatility index (PI) = (Vpeak-Vdiast)/Vmean

Resistance index (RI) = (Vpeak - Vdiast)/Vpeak


The measured frequency shift exceeds the Nyquist limit of the (PRF)/2 at very high flow velocities, the wave will be cut off and displayed on the opposite side of the spectrum. This phenomenon is analogous to the wagon wheel effect in western movies, in which the wheels appear to be rotating in the opposite direction.
In doppler aliasing can be corrected by increasing the PRF shifting the zero baseline.
Aliasing in color flow image is manifested in color reversal.

What to do to avoid aliasing?
- increase PRF
- decrease penetration depth
- shift the baseline
- Use a lower frequency transducer (linear -> convex)
- Increase the alpha angle (to increase the range of error)


Proximal to stenosis: little or no change
Immediately before stenosis: backwash pattern

The areas under the curve in both the positive and negative range are the same in a case of total occlusion, all the blood pumped is returned back.

Intrastenotic waveform shows a very definite increase in flow velocity. The smaller the residual lumen of the artery the faster the blood must travel through it (Vmax increase, wave becomes more peaky).

The intra and post stenotic jet of high velocity blood flow after the stenosis falls off quickly with increasing distance from the stenosis.

In the intrastenotic wave there is filling of the area under the wave (filling of the spectral window), this is a sign of turbulance.

Far past the stenosis: delayed upstroke, and prolonged TTP, there may be relative elevation of the diastolic velocities.

Signs of proximal stenosis:
1- Post stenotic decrease in PSV
2- Post stenotic lengthening of TTP
3- Post stenotic elevation of diastolic waveform (depends on distal ischemia)


- Normal PSV
- Norma TTP
- Normal or slight increase in diastolic flow
- Clear spectral window

- Increased PSV
- Normal TTP
- Normal or increased diastolic flow depending on degree of stenosis & ischemia
- Spectral window maybe filled in.

- Slightly increased PSV
- Increased TTP
- Increased diastolic flow
- Spectral window is filled in due to turbulance

- Decreased PSV
- Increased TTP
- Increased diastolic flow
- Clear spectral window - no more turbulance



1- Angle the probe relative to the vessel axis
2- Place the focal zone to the center of the vessel
3- Set the B-mode gain to a low level

Color flow image (CFM):

4- Use beam stearing to improve the beam-vessel angle
5- Adjust the PRF to the prevailing flow velocity
6- Increase the color gain until blooming occures, the lower the signal until color is only seen intraluminally

Doppler spectrum:

7- Place the SV at the center of the lumen, an adjust its size to be 1/2 - 2/3 of the luminal diameter
8- Adjust the baseline level for spectral components to be above or below the baseline to avoid cutoff at the top or bottom
9- Adjust the velocity range (PRF-in PW), if aliasing still occures:
- Doppler trace too short => decrease PRF => to expand trace vertically
- Doppler trace too high => increase PRF => to compress the trace vertically
10- Adjust the PW gain to obtain good contrast-to-noise ratio:
try to get a dark background without noise pixels, but dont set the gain too low
11- Remember to watch out for the alpha angle

Other related images:

(A) Schematic view of different waveforms was showed according to stenosis location (From third edition of Dignostic Ultrasound by Rumak C. M, et al.). (B) Various types of Doppler waveforms. Type A and B are normal types, but type C patterns called parvus-tardus (From second edition of Dignostic Ultrasound by Rumak C. M, et al.).

**** Very good for carotid examination :



(Text main source: Thieme Teaching manual of CDS )
(Images: )

Thursday, 5 May 2011

Portal vein, inferior vena cava...


• Portal and Hepatic System
The portal vein is formed by the junction of the splenic and superior mesenteric
vein. The portal/splenic confluence is found posterior to the neck of the pancreas. The
inferior mesenteric vein drains into the splenic vein to the left of the portal/splenic
confluence. The left gastric or coronary vein usually joins the splenic vein superiorly
near its junction with the superior mesenteric vein. It courses in a cranio-caudad
plane. From the confluence, the portal vein courses lateral and cephalad in an oblique
plane toward the porta hepatis where it enters the liver. Within the liver, the portal
vein is found posterior to the hepatic artery and common bile duct. These three
structures course together throughout the liver and are known as the portal triad.
The portal vein divides at the porta hepatis into right and left branches. The right
portal vein divides into anterior and posterior branches and the left portal vein divides
into medial and lateral branches. The left portal vein is in contact with the
ligamentum teres.
The branches of the portal vein are intrasegmental, traveling within the segments of
the liver, whereas the branches of the hepatic veins are intersegmental, traveling
between the lobes and segments of the liver.
The portal veins can be differentiated sonographically from the hepatic veins by the
bright echogenic walls that surround them. This is due to the thick collagenous tissue
in the portal vein walls. The hepatic veins do not exhibit echogenic borders.

The cystic vein, which drains the gallbladder, is a branch of the portal vein. Although
it is not usually visualized sonographically, the cystic vein has important implications
in the evaluation of portal hypertension. Impaired drainage of the cystic vein into the
portal vein can result in varices within the gallbladder wall. These are recognizable by
ultrasound imaging.

There are usually three main hepatic veins within the liver. They are the right,
middle and left hepatic veins. The hepatic veins are seen to enlarge toward the
superior aspect of the liver where they drain into the inferior vena cava.

• Function

Understanding the function of the portal venous system is key to understanding the
physiological responses manifested in disease processes.
1. The portal vein is 60% oxygen saturated and provides greater than 50% of
the oxygen requirements to the hepatocytes.
2. It brings nutrient rich blood to the liver from the bowel.
3. The portal vein is the primary collateral route for decompression of the
liver in elevated pressure.
4. In a normal state the portal venous system is a low pressure system with a
normal pressure of 5-10 mm Hg.

Portal hypertension (PV HT):

The luminal diameter of the portal veins corelate poorly to the portal pressure. Therefore to diagnose portal HT we need to analyse the spectral properties of blood flow in the PV.

- Definitive signs of PV HT are:
- ***flow reversal and abscence of flow.
- >11 mm intrahepatic, >15mm extrahepatic diameter
- Caliber variation with respiration <2mm
- Hepatic cirrhosis
- Splenomegaly
- Ascites
- Thickening of GB and stomach wall
- Dilated tributaries (left gastric vein, SMV, splenic vein)

Flow changes in PV HT:
- Flow velocity is slowd down to <10cm/s (normal 15-20 cm/s)
- Bidirectional or abscent flow in PV and its tributaries.

The causes of PV HT can be grouped in to:
- Prehepatic (PV thrombosis)
- Intrahepatic (cirrhosis)
- Posthepatic (Budd-Chiari syndrome)

Intrahepatic causes include liver cirrhosis, and hepatic fibrosis (e.g. due to Wilson's disease, hemochromatosis, or congenital fibrosis). Prehepatic causes include portal vein thrombosis or congenital atresia. Posthepatic obstruction occurs at any level between liver and right heart, including hepatic vein thrombosis, inferior vena cava thrombosis, inferior vena cava congenital malformation, and constrictive pericarditis.

Acute PV or mesenteric vein thrombosis presents with the physical signs/complaints of an acute abdomen, in US you see filling defect, vascular dilation.

Chronic PV or mesenteric vein thrombosis presents in US with little or no luminal dilation, echogenic intraluminal thrombus, no flow with collateral formation.

Signs and symptoms of PV HT:

Caused by blood being forced down alternate channels by the increased resistance to flow through the systemic venous system rather than the portal system. They include:

Congestion and the IVC:

Dilated IVC is an indication of right sided heart failiure.
Clinical presentation: dyspnoe, leg edema, in acute right heart failiure pulsatile flow in hepatic veins.

US presentation:

- >20 mm vena cava, >10 mm hepatic veins
- decreased inspiratory collapse of veins
- decreased compressibility
- abscence of soft double pulsations

Doppler Spectral Analysis

• Portal and Hepatic System

-The portal vein normally exhibits a monophasic, low velocity Doppler signal. The
normal range of flow velocity is wide, but is usually between 20-40 cm/sec. The flow
is continuous and should demonstrate little pulsatility. Flow should not cease or
reverse in the normal individual. Prominent pulsatility of the portal vein is abnormal
and may be indicative of right heart failure, tricuspid regurgitation, hepatic vein/portal
vein fistula or portal hypertension. The flow in the splenic and superior mesenteric
veins is toward the liver and both exhibit a low velocity, monophasic signal.

portal vein with a continuous hepatopetal flow in a healthy adult.

portal vein with minimal pulsatile modulation of the portal flow in a healthy adult.

portal vein with marked pulsatile modulation of the portal flow in a thin, healthy adult.

-Hepatic artery flow is in the same direction as the portal vein (hepatopetal). The
hepatic artery normally demonstrates a low resistance waveform with continuous
forward flow throughout the cardiac cycle.

-The hepatic veins (HV) drain blood from the liver into the inferior vena cava. The
normal Doppler waveform obtained from the HV’s is triphasic. This phasicity is
dependent on variations in central venous pressure during the cardiac cycle.

hepatic vein and portal vein in a patient with heart failure, New York Heart Association Calss III and tricuspid regurgitation (left), having a triphasic flow in the hepatic vein (middle) and a marked pulsatile flow of the portal vein (right)

patient with constrictive pericarditis (arrows) (left). A triphasic flow is seen in the hepatic vein (middle) and pulsatile flow in the portal vein (right). RV, right ventricle.

hepatic vein and portal vein in a patient with mediastinal haematoma. A triphasic flow is seen in the hepatic vein (left) and a pulsatile flow with a reversed component of the portal vein (right).

patient with pericardial effusion (left), and triphasic flow in the liver vein (middle) and pulsatile flow in the portal vein (right).

patient with primary cardial lymphoma with a tumour in the right atrium (left), triphasic flow in the hepatic vein (middle) and pulsatile flow in the portal vein (right).

hepatic vein (LV) and portal vein (VP) in a patient with liver cirrhosis having a monophasic flow in the hepatic vein (left) and a marked pulsatile flow of the portal vein (right).

portal vein (left and middle) in a patient with heart failure, New York Heart Association Calss III, having a marked pulsatile flow with reversed flow during deep inspiration (arrows) (right).

pericardial effusion (PE) (left) and a pulsatile flow in the portal vein with a short reversed flow during deep inspiration (arrow) (right). RV, right ventricle; LV, left ventricle.

Ultrasound Findings of Portal Hypertension

Ultrasound findings associated with portal hypertension include enlarged
diameter of the portal vein, lack of respiratory variation in the portal vein or its
tributaries, hepatofugal (away from liver) portal flow direction, decreased portal velocity (<10 cm/s) or volume, and the presence of collaterals or varices. Splenomegaly is uniformly present with portal hypertension. The spleen is enlarged when its length exceeds 13 cm. This should be measured in a cranio-caudad plane. An abnormal liver texture and ascites
are also commonly seen and are usually related to accompanying cirrhosis. A
sudden onset of ascites should prompt careful examination of the portal vein for

Enlargement of the portal vein >13 mm is indicative of portal hypertension
with a high degree of specificity (100%) but low sensitivity (45-50%). The portal vein
diameter should be measured just above the IVC with the patient in quiet respiration.
With deep inspiration, the normal diameter may increase to about 16 mm resulting in
an overestimation of portal vein diameter. It is important to recognize, however,
that the portal vein is not always enlarged with portal hypertension. In some cases,
portal flow may be primarily diverted through collateral channels resulting in a small
portal vein at the porta hepatis. This can be seen with diversion of flow through a
large coronary vein, splenorenal shunt or other similar channel. Portal vein flow velocity decreases with portal hypertension due to increased resistance to flow. However, in the presence of a recannalized paraumbilical vein, the flow velocity in the main portal vein may be increased.
As pressure increases, portal blood flow may become pulsatile. With late stages of portal hypertension, portal flow direction can reverse and course away from the liver. This is termed hepatofugal flow and is easily assessed with color Doppler. The portal flow direction can be compared with the hepatic artery. When they are in opposing directions, portal flow is reversed.
With decreasing velocity of portal flow, stagnation may lead to thrombus formation.
There are many other causes of portal vein thrombosis. Following thrombosis,
cavernous transformation of the portal vein may develop. It is seen as a tortuous
network of blood vessels located in the porta hepatis and extending into the liver.
Doppler waveforms obtained from this area will primarily show venous signals with
flow direction into the liver. Cavernous transformation most commonly occurs in
patients with otherwise healthy livers

Portal Vein Thrombosis (PVT)

Portal hypertension can cause thrombosis of the portal vein due to stagnation
of flow. Hypercoagulable states can result in thrombosis of the portal vein directly or
indirectly through thrombosis in the splenic or superior mesenteric vein. Biliary atresia/cirrhosis may cause thrombus in the main portal vein or the smaller
branches within the liver. Pancreatitis and other inflammatory processes most commonly cause thrombosis that begins in the splenic or superior mesenteric veins. Portal vein compression by
lymphadenopathy or tumor mass can also result in thrombosis. Increased flow through the hepatic artery with a decrease in resistance is associated with portal vein thrombosis. The hepatic artery may appear enlarged with prominent color Doppler signals. Use of color Doppler alone to evaluate portal flow may result in the mistaken identity of an enlarged hepatic artery for the portal vein especially when portal thrombus is isoechoic to the surrounding liver tissue. This pitfall can be avoided by always obtaining a spectral Doppler signal from the portal vein in addition to color Doppler evaluation. Partial thrombus is not associated with hepatic artery changes.


• Sonographic Window

The best scanning approach to the main portal vein is nearly always intercostal.
Although the portal vein is more easily seen with b-mode imaging in a subcostal
position, this approach commonly results in a poor Doppler angle of incidence. The
intercostal view results in Doppler angles that vary from 0º to about 60º. With color
Doppler in this view, the portal vein is seen as a red vessel adjacent to the red hepatic
artery (if color Doppler invert is not selected).

When a large amount of ascites is present, the depth to the portal and hepatic veins can be quite large. Bowel loops and gas may not allow visualization at all from the subcostal approach. Using an intercostal window will usually allow adequate imaging in these cases. If cirrhosis is severe, sound penetration through the liver will be greatly decreased. It may be necessary to use a lower frequency transducer or the lowest frequency setting on a multifrequency transducer. An anterior sagittal approach usually provides the best view to image the left portal vein, left and middle hepatic veins and ligamentum teres. It is important to image this anatomy to rule out the presence of a paraumbilical vein. A transverse or image can also be used to display the paraumbilical vein. It will be seen as a large vessel exiting the liver from the left portal vein at the level of the ligamentum teres. The right hepatic vein may be seen in this view, but is frequently best seen from an intercostal approach.

• Flow Direction

Flow direction can be very important in abdominal Doppler. Confusion about the direction of flow is a common pitfall. For this reason, it is usually best to avoid use of the color and spectral Doppler invert control. Flow away from the Doppler beam is shown as blue and below the zero baseline and flow toward the Doppler beam is shown as red and above the zero baseline. Anytime the flow direction is in question, it is helpful to check a baseline vessel in which flow direction is known. For example, to rule out hepatofugal flow in the portal vein, compare its flow direction to that of the hepatic artery. When flow direction is normal in the portal vein (toward the liver), it is the same direction as the hepatic artery. If they are on opposite sides of the spectral Doppler baseline or show opposite colors, blood flow is reversed in the portal vein.

Doppler spectrum analysis obtained with a large sample volume simultaneously demonstrates waveforms from the portal vein and hepatic artery. They are on opposite sides of the zero baseline. This finding is consistent with hepatofugal flow in the portal vein.

• Presence or Absence of Flow

Color and spectral Doppler are commonly used to determine the presence or absence of flow in a vessel. Another common pitfall is to mistakenly assume the absence of flow when in fact it is present. This most commonly occurs as a result of poor Doppler angles or inappropriate settings of the Doppler parameters.

The Dopplercontrols should be sensitized for the detection of slow flow whenever thrombosis or occlusion is suspected. This requires adjustment of the PRF and filter controls to very low levels. Additionally, if the Doppler angle is too great, the frequency shift from slow flow may be too small to detect. This may lead the sonographer to mistakenly assume that flow is absent. Since most abdominal Doppler is performed with curved linear arrays, steering of the Doppler beam cannot be performed and it is necessary to heel/toe the probe to achieve a good angle of incidence.

Commonly, the view that gives the best B-Mode image of a vessel is the poorest Doppler approach because the angle of incidence is too great. A common example of this is in evaluation of the portal vein. The portal vein is best seen with B-Mode imaging in a subcostal approach where the angle of incidence is near 90º. Color Doppler evaluation of the portal vein in this view may not demonstrate flow, especially if slow flow states are present. The best view of the portal vein for Doppler evaluation is an intercostal approach. In this view, the Doppler angle is much smaller, allowing demonstration of slower flow states.

Other related images:

IVC thrombosis patient



(Text main source:, US Thieme clinical companion, -Cindy A. Owen, RDMS, RVT-)
(Images: google images, BJR -C Görg, MD, J Riera-Knorrenschild, MD and J Dietrich, MD-, RadioGraphics-September 2003RadioGraphics, 23, 1093-1114.-)

Tuesday, 3 May 2011

Skeletel radiology

Pepperpot skull :
(hungarian -borsszoro),

MM is the most common primary bone tumor in adults

Multiple myeloma must be included in the differential diagnosis of any lytic bone lesion, whether well-defined or ill-defined in age > 40. The most common location is in the axial skeleton (spine, skull, pelvis and ribs) and in the diaphysis of long bones (femur and humerus). Most common presentation: multiple lytic 'punched out' lesions.
Multiple myeloma does not show any uptake on bone scan.

4 main forms:

Four main patterns are recognised :

  1. disseminated form : multiple defined lesions predominantly affecting the axial skeleton
  2. disseminated form : diffuse skeletal osteopaenia
  3. solitary plasmacytoma : single large / expansile lesion most commonly in a vertebral body or in the pelvis
  4. osteosclerosing myeloma

Radiographic features

Disseminated multiple myeloma has two common radiological appearances

1- numerous, well circumscribed lytic bone lesions : more commonpunched out lucencies e.g. pepperpot skull endosteal scalloping
2- generalized osteopaenia : less common often associated with vertebral compression fractures / vertebra plana

Some bones are preferentially involved, with a typical distribution being: vertebrae > ribs > skull > shoulder > pelvis > long bones

Plain film

A skeletal survey is essential in not only the diagnosis of multiple myeloma, but also in assessing response, and pre-empting potential complications (e.g. pathological fracture).

A typical skeletal survey consists of the following films: lateral skull, frontal chest film, cervico-thoraco-lumbar spine, shoulders, pelvis, femurs.

The vast majority of myelomatous lesions are lytic ( ~ 3% being sclerotic)


CT does not have a great role in the diagnosis of disseminated multiple myeloma, however it may be useful to determine the extent of extra-osseous soft tissue component in patients with a large disease burden. It may also better asses the risk of fracture in severely affected bones.


MRI is generally more sensitive in detecting multiple lesions compared to the standard plain film skeletal survey. Infiltration and replacement of bone marrow is exquisitely visualised, and newer scanners are able to perform whole body scans for this purpose.

Nuclear medicine

Bone scintigraphy appearance of patients with disseminated multiple myeloma is variable due to the potential lack of osteoblasitc activity. Larger lesions may be hot or cold. Bone scans may also be normal. Therefore bone scans usually do not contribute significant information in the work-up of patients with suspected or established disseminated multiple myeloma, as the sensitivity of detecting lesions is less than that of a plain film skeletal survey.

PET-CT has a growing role to play in the management of this disease, as it is effective in identifying the distribution of disease. Uptake of the F18-FDG molecule by the myeloma lesions corresponds to areas of bone lysis seen on CT.


Giant cell bone tumor in young female patient destroying the epihysis and parts of the metaphysis.

X-Ray Appearance and Advanced Imaging Findings:
Radiologic findings demonstrate the lesion is most often eccentrically placed to the long axis of the bone. The center is most radiolucent with increasing density towards the periphery. There is a well-defined in defect in the metaphysis and epiphysis, with destruction of the medullary cavity and adjacent cortex. The destruction may stop just short of the joint. Intact borders and a sharp inner margin may be associated with a better prognosis. These tumors often thin the cortex, and may expand into the soft tissues surrounding the bone,or they may expand the the bone extensively, remaining within an eggshell-thin rim of periosteal new bone.


  • Presents as an eccentric lytic lesion with a geographic pattern of bone destruction, but can also have a more aggressive appearance with ill-defined borders.
  • By far most giant cell tumors are seen around the knee. GCT is located in the epiphysis with or without extension to metaphysis and frequently abuts the articular surface.
  • Most common bone tumor in adults aged 25 - 40 y.
  • Differential diagnosis:
    • ABC may have the same radiographic features but is found in a younger age group.
    • Chondroblastoma is also located in the epiphysis, but is seen exclusively in the epiphysis without extention to the metaphysis and is seen in a younger age group.
    • Metastases, especially in older patients.



Negative exam showing an empty, free neuronal foramen

Positive exam, showing a neuronal foramen with an occluded lumen


Sclerotic anterior longitudinal ligament: