DX. IMAGING – 2/20/08
BONE DEVELOPMENT, PARTS OF THE BONES, HORMONES
Dysplasia = Mal-development
2 Types of Bone Formation
Endochodral vs. Intramembranous
Life long (periosteal and endosteal tissue – they are the same except for location because endosteum is inside the cortex and
covers trabecular bone) vs. endochondral (responsible for lengthening long bones by vertical growth)… Takes up shape as
it is developed…Bone is added one layer at a time…It is like the ―building of a brick wall‖…the wall needs to be built 1
brick at a time. Mostly flat bones are built intramembranously at this stage…A form of growth that adds additional layers
(things grow thicker). Ex.—Femur…We would see the bone get wider/thicker…Increasing load is reacted to by the body
by more bone via intramembranous process
Physis = Epiphyseal growth plate…
Enchondral = Formed in Cartilage…We have a precursor phase that is radiolucent on plain film. We can appreciate the
outline. Enough of the outline is present to visualize the structure. The growth is by length (vertical dimension
An immature growth plate appears black on film...It almost looks like a fracture.
Growth hormone before closure vs. after closure
Determines (gigantism vs. Acromegaly)…After closure (bones widen) vs. before closure (bones lengthen)
Maturation is encouraged by hormones and sex hormones. Excess sex hormones show premature closure of growth plate
and we trap the person in a smaller state. Ideally, we need balance.
Metaphysis, epiphysis, Zone of calcification (ZPC)
ZPC = The most mature layer of the growth plate. It is a dense area that makes it look different than the rest of the growth
plate. It al also called the most immature part of the metaphysis. The ZPC is always on the diaphyseal side of the growth
plate. ZPC is either most mature part of growth plate or least mature part of the metaphysic (can be considered
either one of the two for its definition).
Apophysis vs. Epiphysis
Apophysis = A bone protuberance that grows from a primary ossification center. (Ex. Greater trochanter)…These are
actually endochondral centers at one point in time. 1 has cartilage and 1 doesn’t. 1 is an attachment site and 1 is not.
Apophysis and epiphysis both answer to hormones and mechanical stimulation. Sharpey’s fibers do provide some
attachment sites at the apophysis.
Epiphysis = Epiphysis has chondrocytes and extrudes cartilage precursor cells to surface. This leads to the rejuvenation
and maintenance of cartilage. .
Diaphysis (Shaft) = Structural integrity to the system.
All of the areas of bone can be damaged by trauma, vascular compromise, metastatic processes. The most frequent site of
metastasis is the metaphysic since it is the most physiological area of the bone. This part can be damaged by all 7
bone diseases. The metaphysic is the most metabolically active (important for normal growth and a target for
Growth Hormone, Estrogen, Androgens, Parathyroid, Calcitonin, Erythropoietin, Glucocortidoics
A. PTH: Responds to declining serum calcium levels. PTH controls serum calcium and address deficiencies of circulating
calcium. It uses 3 mechanisms:
1). PTH affects the tubular cells of the kidney to conserve calcium…It reabsorbs (enhances) calcium reabsorption in
the kidney (so we don’t pee it out)
2). It increases the kidneys conversion to vitamin D…PTH encourages the conversion to active vitamin D in the
presence of PTH…Active D goes to all areas and particularly the small intestine (we recover the most from the
3). Stimulation of osteoclasts??? (May be not actually occurring since osteoclasts do not have receptors for
PTH)…The bond strength of calcium in crystal matrix is impacted. This will ultimately lead to liberation of osteoclasts.
PTH increases bone fragility leading to osteopenia.
B. Calcitonin = Works when calcium levels are high. Works in opposition to PTH. Increased Calcitonin prevents the
recovery from urine, production of vitamin D is inhibited, and osteoclasts are suppressed. There is a receptor site on
osteoblasts for calcitonin. PTH and Calcitonin are serum calcium regulators!!
C. Growth Hormone = Lengthens and thickens by enchondral and intramembranous hormones.
D. Estrogen and Androgen = affect maturity of endplates
E. Erythropoietin = Affects Red marrow inside bone. It does not stimulate bone directly. Red marrow is dispersed
throughout the young skeleton. We need to increase the number of red cells as the person’s volume (size) increases. If you
don’t need red marrow, you lose it. The GI tract is a frequent source of loss.
F. Glucocorticoids = Responsible for making available building blocks for growth and development. Glucocorticoids
trigger protein catabolism. Glucocorticoids affect the skeleton by helping to build soft tissue and bone to make the
DX IMAGING -- 2/27/08
PHYSICAL CONDITIONS INCLUDING DYSPLASIAS, NORMAL VARIANTS, AND OTHER PATHOLOGY
1. Achondroplasia (Dwarfs)
Protruding abdomen, prominent buttock, champagne glass pelvis (anteverted pelvis so ASIS rotates down and forward
and pelvis rocks upward), often the olecranon fossa is part of the endochondral system and the process bangs on the floor of
the floss limiting full extension of the elbow, asymmetric radius and ulna (the ulna is usually shorter than normal), they
can have odd carrying angles due to the bone (forearms) abnormality, the fingers hang off (trident hand – not seen in
every example but a classic finding)…The abdomen and buttock features go together
*** Slides of Achondroplasia ***
Interpedicle space should increase as you go down the spine, but the pattern is reversed in Achondroplasia. There is a
greater risk of central canal stenosis. The spinal length is mostly normal ending around L1-L3, but achondroplastic
dwarfs can present with stenosis and possible cauda equinae compression.
Central Canal Stenosis is a big worry with Achondroplastic Dwarfs. Their risk profile is much different. Pregnancy is a
risk. They need a pre-pregnancy work-up. Often, they need C-section. Small foramen magnum may be present in the
children. It can be a cause of death at birth.
*** Slide of Bullet Nose Vertebra (linked with Achondroplasia)
Bullet Nose Vertebra = Too little vertebra on the front (abnormal enchondral growth pattern)…The dotted lines on the
vertebra appear as scalloping. Posterior scalloping brings a different list of possible diagnosis. Often this condition on this
patient is acquired. The central canal pulsing. Dural ectasia (depth of concavity increase) a serious of dilations or widening
that can permanently change the vertebra.
***Slide of Rhisomelia***
Rhisomelia = Length is short and irregularity at both ends of articular surfaces. The width is OK. Premature DJD can be
an issue. The irregular contour of the femur head can lead to wear and tear. The pubic ramus is small in the picture and
underdeveloped. The condition is not brittle bone disease, but heavy loading activities are not indicated.
2. Cleidocranial Dysplasia
***Slide of Missing Clavicles ***
The clavicles are missing and the chest on the slide/film appears too narrow at the top. This is called ―funnel chest.‖
Cleido refers to clavicle. Only 10% of these patients that have achondroplasia miss the clavicle. This dysplasia presents
with drooping shoulder. The scapula is in normal orientation and the humeral-scapula orientation is in normal orientation.
The brachial plexus can be at risk due to the missing clavicle. Mobility of the UE is more than normal. The absence of
the clavicle enhances the mobility and decreases the stability of an already unstable joint. The classic finding is
symmetric abnormalities of the clavicle.
***Picture of the Cranium***
Mid-line Defects – We see cleft palate often…Cleft palates can have projections to the surface with the ―air lip.‖
Wormian bones - -Odd sutures but the skull size and shape is normal.
Pubic body can be missing. This is the pelvis analog of the midline defect of the face. This is not exclusive to the
condition but is often found. Absence of pelvic body is classic.
3. Marphan’s Syndrome
*** Slide of the Feet ***
Feet are narrow and long foot. The foot belongs to a patient over 6 feet. This belongs to those with Marphan’s Syndrome.
The width of the bone is normal but the length is much longer than age matched peers. They can present with
arachnodactyly. This is ―spider hands and toes‖ with long fingers and toes. The width to length ratio is abnormal. The
lengths of the bones are longer than you would expect. The Marphan’s group averages six foot tall
Marphan’s syndrome can present with cardiac problems. A hallmark feature is aortic rupture. This is the highest
pressure area. As the blood comes out of the heart and the pressure increases and changes, there is pathologic stress.
Another finding is pectus excavatum and scoliosis. They tend to have ocular abnormality with lens dislocation.
Clinically the patient has thumb sign, a combination of increased length and flexibility inherent (fold thumb across palm of
hand and make a fist with distal phalanx sticking out the other hand).
You should see the right heart border. The heart shifted to the left. The ribs posteriorly are high arched. The thoracic cage
is altered. Pushing in (pectus excavatum) makes the anterior decline more exaggerated and this raises the posterior portion
of the ribs. Pectus Excavatum can be viewed by observation and on the X-ray. The key is no right heart border. This is
the clue that a mechanical shift is occurring, then you check for the high arched ribs consistent with pectus excavatum.
DX. IMAGING 1 – 3/11/08
REASONS FOR POSTERIOR SCALLOPING
*** Image of Post. Scalloping***…Scalloping can occur with:
1. Achondroplastic Dwarfs,
2. TB (granulation tissue that can pressure erode the bone)
3. Lymphoma (scalloping can occur with enlarged lymph nodes either anterior or posterior)
4. Congenital (normal variant)
The point of the image above is that you can diagnose by exclusion. Only by excluding the detrimental findings, you can
then truly find out what the condition is. The image above was due to congenital reasons.
4. Osteogenesis Imperfecta
*** Picture on Overhead of OI with Density Change ***
There is an angle change. At the apex, there is a callus formation indicating a healing fracture. Callus formation is greater
than normal. Osteogenesis Imperfecta (Brittle Bone Disease). The bone is imperfect bone…Cortex to Trabecular Ratio
should be about 1:1; in the picture the ratio is not 1:1. This means that the expected strength is lower than normal. This
brittle bone disease has thin cortices with altered cortical: medullary ratio. OI also presents with exuberant callus
formation. It is much more pronounced with callus formation. The bone is abnormal in presentation due to cortical:
medullary ratio. Another common feature is the difference in density between callus formation bone and other types of
bone. Trivial trauma is what you need to break a bone with OI (Brittle Bone Disease – ex. Shaking someone’s hand can
break a metacarpal). Before skeletal maturity, the OI patients are very fragile vs. after maturity they are less fragile.
*** Picture on Overhead…Rods a patient with OI. Intramedullary rods are thin and located in the tibia. The patient is near
or just beyond skeletal maturity due to the X-ray appearance. Exuberant callus formation is occurring. The lower legs look
straight because the rods provide mechanical support to the bone. The rods help the body stabilize. ***
OI Congenitoform – Found at birth
OI Tartoform – Found after birth
Fragility of the bone can come from child birth or found upon curiosity with a trivial trauma fracture. Exuberant callus
formation occurs. A hematoma with healing is normal. The hematoma is the matrix that aids healing with healing factors
and platelets that assist with healing the bone fracture.
*** Picture of the same person later in time with OI***
It appears as a big white blur. There is exuberant callus formation in the X-ray. On the outside, there is local
inflammation, but they can’t build a good crystal lattice, to support the skeleton. Even the extra callus formation can’t help
support the bone. Often they have asymmetric enlarging of the legs, are in a wheelchair with cushions, and very
fragile…90% of these patients with OI demonstrate a blue sclera. ***
*** Picture of OI in Young Person’s Hand ***
The hands are long and skinny. Arachnodactyly can present with OI. Do not have them make the fist since they could
break metacarpal. These patients have normal length, but the width of the bone is abnormal. Undertubularization
occurs with the diameter of long bones is much narrower than normal and is a feature of the fragility. Length to width ratio
is altered. We don’t want to test a thumb sign due to risk of fracture. Patients can acquire premature maturation (growth
plates close quickly and limit growth potential of long bones). Arachnodactyly is not an exclusive feature of this condition.
These patients can also have brachodactyly. .Congenital malformation is most often associated with lethal features. We do
want to test for this. We usually want to do a C-section when these children are born since they can acquire multiple
fractures during the normal birthing process. These babies are often found as having OI during ultrasound exam and also
by checking the amniotic fluid for protein markers. Also genetic testing of the parents can occur to help determine the
chances for the fetus and for the family having osteogenesis tartoform.
5. Medullary Ostosis
Adds to outside of the bone and fills in the medullary cavity. This is one dysplasia that actually heals stronger than
before. The classic appearance is a ―dripping wax or candle wax appearance‖ principally affecting the thumb and
radius. They don’t have full range of motion. The contour of the hand and thumb is abnormal. It is not tender to the touch
but the area is sensitive to vascular, lymph and neuro compression. You just want to leave the patients alone. IF surgery is
performed, they can have greater bony regrowth than before. The 1 exception is peripheral entrapments where surgeons try
to create a channel. The dripping wax appearance is classic. Bone is added to both the outside and inside.
*** Picture on Overhead of the Humerus***
We acquire a bigger deltoid tuberosity by development. The distal end of the humerus does not appear as normal medullary
bone. There is an external and internal change in the bone. The condition is progressive nature and relatively benign.
We monitor them for neurovascular and lymphatic compression. If compression occurs, then we find a specialist in
this area to release and replace. Bone filling in inside and outside is a hallmark sign.
*** Picture of Hands on Overhead***
Internal change to the metacarpals and external changes occurs. The change does not hurt. We can do blood work and
additional testing to confirm the diagnosis.
*** Proximal Phalanx of great toe ***
It should not be very dense. Peripheral location of density is not an area of load or attachment site.
6. Sclerosing Dysplasia and BBB (brittle bone disease)—Osteopetrosis
Hallmark X-ray features is bone within a bone. Ex. There is an ilium within an ilium…For this patient they don’t lose
their fetal/primordial skeleton. The body tries to mature forward with adult bone but osteoclasts don’t remove the
primordial bone. They essentially have 2 skeletons. Bone within a bone is an X-ray sign and defines a way to remember
the condition. 2 skeletons coexist and there is less than normal space for bone marrow. The patient in the image is young
due to the appearance of the growth plates. There is great need for RBC’s to supply larger volume required for growth. A
hallmark lab feature is anemia. They make normal RBC’s but they don’t make enough.
DX IMAGING -- 3/12/08
Dx. Imaging – 3/18/08
7. SED (Spondyloepiphyseal Dysplasia)
*** AP view of pelvis overhead ***
There is something going on with the epiphyseal parts of the joints, cysts, subchondral sclerosis (DJD). This is a young
patient in the picture on the overhead. DJD is a classic unilateral process, and when bilateral should be asymmetric. This
picture shows symmetry of DJD (so it is not classic DJD). The vertebral body endplates are the target of the abnormality.
There is also end of long bone DJD. The body’s ability to produce normal long bone is affected. The long bones don’t
have the architecture to keep it fully functional.
*** Picture of the Spine on Overhead ***
Humps on the spine/vertebrae…A classic feature is ―humped vertebra‖. The reason for the hump is because the primary
ossification center didn’t grow. We as normal people don’t have things that stick out. The ring apophysis doesn’t grow
(failure to mature). The patient is skeletally mature.
*** Hip joint – Frog Leg view ***
Decrease in joint space, looks like chambers with holes (mostly with synovial fluid or blood), the cysts penetrate the
acetabulum. Poor quality of articular cartilage participates in the derangement of DJD. The underlying or subchondral
bone is more vulnerable.
Mostly characterized by the change is shape of vertebral bodies (humped or heaped vertebrae). As you get toward
your 20’s, the ring apophysis should be hidden, but it is not in this condition. The center of the body grows fine, but the
maturation doesn’t occur. We named this condition due to the spinal change, but later found other problems (like DJD of
the hips). The pattern was later altered due to bilateral symmetrical DJD. If you find bilateral, symmetrical DJD,
suspect SED. We did not appreciate till later the feature of hip abnormality. SED has both hip and vertebrae changes (we
first found the vertebrae and later the hip changes).
** Picture of another spine (lateral view)
We have an inferior hump on 1 vertebra with a heaped up area or hump. There are 3 humps on this view. There is a
segmental superior and inferior hump with a superior hump at another level.
*** Picture of T spine Lateral ***
Notice the irregular contour of vertebral bodies. These people may have large kyphosis. The hump is biased to the
posterior with the anterior part of the vertebra is shorter (assisting the Hyperkyphosis).
8. Progressive Diaphyseal Dysplasia (PDD)
*** Picture of the Humerus ***
There is a filling in of the humerus. There should be a clean corticomedullary junction. We don’t have a sharp
demarcation. The humerus on the screen appears to have a double density on the inferior part. There should be a clear
demarcation of cortical and trabecular bone (there isn’t clear demarcation in this picture). The cortex appears wavy
on the overhead. Over time the bone completely fills in.
***Picture of the cranium—lateral view***
The mandible angle is messed up. The person’s teeth are not well developed. They have a huge gap between C2 and c1
with posterior fracture of C2. The patient is on both brittle bone and sclerosing dyspolasia list. Facial cranial
ratio…The face isn’t big enough for the amount of skull (low facial: cranial ratio). This person looks quite unusual. There
was a painter called Toulouse Lautrec who had this condition (French Painter).
*** Skull Picture from the posterior ***
There are different densities of the bone on the skull. This condition is both sclerosing dysplasia and BBB.
** Pelvis picture ***
The femur is fractured. The bone is normal in dimension. The intermedullary rod in this patient caused later fracture
*** Both Hands on the overhead ***
The distal phalanges aren’t all there. The bone started out normal in dimension. Over time the patient lost the tip of their
distal phalanx. That process is called acroosteolysis. The bone breaks distally in the hand and foot (in the tips). This
is a classic finding for Picnodisostosis (acroosteolysis).
CONGENITAL ANOMALIES and NORMAL VARIANTS
*** You’ll need to use your textbook…Most of these are clinically insignificant…Make a list of clinically significant
anomalies. Some anomalies mimic other processes and need to be separated from those are significant***
10. Os Odontodeum
Dens is not attached to C2 body. This is a congenital anomaly and can be potentially devastating.
11. Limbus Vertebra
Imitates a fracture but is not clinically significant.
12. Hyperostosis Frontalis Internus
***CT of the skull***
The frontal sinus is filled in with bone. Brain function is normal. The brain adapts (plasticity) despite intrusion into brain
space. The bone is hard, ―hard headed.‖
13. Parietal Foramen
***Picture of the skull/cranium ***
There is a hole on the picture. A hole can come from drills (surgery), bullets, lytic METS (local lucency), infection, etc.
*** Frontal View ***
There are 2 holes on this picture. This is a bilateral symmetrical presentation of a hole. The list of holes (what’s left) is an
anomaly. The anomaly of a hole in the parietal bone is called parietal foramen. The hole is palpable. There is a
meningeal covering over the hole. Paired presentation implies a condition that you are born with. In fever, you can feel
more warmth. You can feel pulsation with increased HR and blood pressure. Other than that, this condition is not
12. Craniovertebral Synostosis
*** Picture of the Lat. C-Spine in Flexion ***
ADI = Upper edge of normal ADI in this picture. The ADI is suspect. The ADI is the upper limit of normal or just above.
The measurement is 3 mm in an adult and 5 mm in children. The picture is of an adult because they are skeletal mature.
There is a bone rim hole in the occiput. There is supposed to be a space-C1 and posterior arch. We are looking at a
blocked vertebra. This is occipitalization of the C1. There is fusion of the base of the skull/occiput and C1. They
move as a unit. The only problem they have is less flexion and extension than normal. The have hypermobility between
C1 and odontoid (C2). The patient as a consequence is that the transverse ligament may have slack in it. We must
document stability with flexion and extension views. We may document this on the first visit and then yearly.
Motion palpation may indicate rigid or a bony end-feel to the region. The 2 bones are not separate. This is a failure of
segmentation at the somite stage during embryological development. This is true for the congenital blocked vertebra at all
There is a huge space between the posterior arch of atlas and posterior tip of C2.
*** Picture of C3-C4 Blocked Vertebra ***
Anterior and posterior counting shows a mismatch. This patient has anterior and posterior block. Sometimes both parts are
blocked and sometimes not. The black area in the front is rudimentary disc. You would expect to find some construction
of the annular fibers, but not organized into a normal disc structure.
We can also have acquired vertebral fusion and as a consequence of disease/infection. Osteomyelitis can present with
Acquired fusion won’t have narrow dimension in the middle. Wasp Waste deformity is with the congenital with has the
narrow dimension in the middle. Wasp-Waste Deformity shows narrowing and tapering of the vertebra in the middle.
13. Agenesis of the Posterior Arch of C1
*** Flexion View of C-spine ***
There is a large space between C2 and occiput. We are missing parts of C1. The posterior arch of C1 is missing. We
find that the bone is distributed in the wrong place. C2 spinous is bigger than normal. There is megaspinous at C2. There
is conservation of bone. There is also failure in segmentation. C1 grew with C2 giving C2 the large size and failure to
segment. C1 is now C-shaped. It is not as mechanically sound as a ring structure. This is clinically significant. If you
have a child with this, your child cannot perform contact sports because you cannot guarantee that C1 holds up under the
rigor of contact. Sports like football, soccer, basketball and even diving may be contraindicated. The musculature that
would attach to the posterior arch would be attached now to C2 (RCPM). The supraspinous and interspinous ligaments
would jump the gap. The anterior arch of this patient will be bigger and thicker. This is likely stress response. The
force is transferred to the lateral masses.
14. Os Odontodeum
*** Extension view of the C-spine ***
Visually draw a Spinal laminar line and follow the curve. Each of the 7 levels of the C-spine shows a normal S-L line.
*** Flexion View ***
Draw your lines…S-L line presents with abnormalities. We have the line in extension but not flexion. There is great
bone density in this view. We do not see a black space for the transverse ligament. This is os odontodeum. The segment
goes so far forward that it indents the retropharyngeal airway. The first thought should be ADI widening (so check the
interspace). If the interspace is normal, a defect in the dens would be indicated (os odontodeum).
The ant. arch pushes forward into the airspace. The SL line is off. The odontoid may be tipped forward.
DIAGNOSTIC IMAGING 1 -- 3/19/08
15. Agenesis of C1 Ring (Ant. and Post.) -- Spondyloschisis
*** Picture on Overhead ***
The patient is missing both anterior and posterior tubercles. The person has two C shaped structures. There are only
ligaments and joint capsules holding the structure together. The patient cannot play football. This condition is the most
extreme example of midline C1 defect. The good news is that the cord is not at risk. The patient is at risk for future
axial loading injuries that may occur with contact/collision sports or automobile accidents.
16. Posterior Ponticle (Ponticus), Arcuate Foramen, Kimmerly Anomaly
Various names for the same condition: Arcuate Foramen, Kimmerly Anomaly, Posticus Ponticus
Hallmark Feature: Calcific bridge between the lateral mass and posterior tubercle…15% of the population has
enough ossification of the ligament so that we can see it on plain. Proper testing for VBAI is recommended.
Approximately 10% of the patients with the arcuate foramen demonstrate signs and symptoms we can attribute to
ligamentous calcification. We worry about VBAI. We used to do George’s Test, but we now prefer flow studies to check
the vertebral artery. We also check the patient’s history for positional changes producing a problem. Ex.—I get dizzy
looking out of my mirrors…These patients may be likely candidates for MRA. The problems would be positional in
*** Picture of Arcuate Foramen on Overhead ***
Calcification of ligament behind post. Arch of atlas.
CALCIFICATION PROCESS/REASONS FOR CALCIFICATION
*** Picture of stylohyoid ligament calcification ***
3 Titles: 1). Physiologic Calcification 2). Dystrophic Calcification 3). Metastatic Calcification
2 Things we keep tract of for predictions: 1). Serum Calcium Levels 2). Health of the Tissue (Global – healthy or
Physiologic and Dystrophic Serum Calcium Levels = NORMAL Vs. Metastatic Serum Calcium = ABNORMAL (high)
Physiologic Calcification and Metastatic tissue integrity = NORMAL vs. Dystrophic = ABNORMAL (Damaged)
1. Physiologic Calcification = Cartilage is 2nd most likely tissue to take up calcium. Arcuate Foramen and the Stylohoid
Ligament = Likely to uptake calcium.
2. Dystrophic Calcification = Calcific tendonitis, bursitis, and myositis ossificans are part of this category.
3. Metastatic Category = Hyperparathyroidism—PTH elevates the calcium. Increased PTH, translates into increased
liberation of calcium. Lytic metastasis is part of this category. Lytic metastasis can be deadly.
17. Developmental Cleft
The X-ray shows parallel end plates. We look at a developmental cleft. The longus colli can attach to the site of the
developmental clef.. An enthesis can develop (enthesis is deep attachment to the bone).
This is a congenital anomaly. If you see this with trauma, it is not a fracture and you begin early treatment.
18. Non-Unification of the Growth Center
*** Picture on Overhead on Lower Cervical and Upper thoracic spine showing the end of the TP is not attached ***
A notch in the TP with a ―puzzle piece‖ appearance. This ossification center hasn’t united with the body of the TP.
This condition is often mistaken for a TP fracture often involving auto accidents. There isn’t a jagged edge on the edge of
the TP, so you can’t call it a new fracture. New fractures need a lucent edge. Check to see if the suspected area is corticated
first. If the suspected area is not corticated and clearly demonstrates trabecular bone, it may be an un-united growth center.
19. Cervical Ribs/Cervical Digit
*** Picture has a joint at C7 ***
The joint at C7 is called a Cervical Digit. We know it is C7 because the TP’s point out and down and out. The TP’s of T1
point up and out (typical for T1). The picture demonstrates a cervical digit on the R side in the picture. The relevance to
cervical rib is that for a long time they got blamed for TOS, but it not very unlikely to produce TOS. In the past,
costectomies (rib removal) were very ineffective. Some patients got worse due to adhesions in the soft tissue. The
adhesions further tractioned the cords and nerves of the brachial patients. The patients that did do better following
costectomies got better because of nerve dennervation (an unintended consequence of surgery).
*** Another picture of Cervical Rib on Overhead ***
CT Transitional Segment…This picture does not have a joint. It does have an elongated TP (hypertrophy of the TP).
DX. IMGAING –3/25/08
NORMAL VARIANTS AND CONGENITAL ANOMALIES
20. Down’s Syndrome – Trisomy 21
Most common autosomal syndrome (1:6000) births…Recognizable at birth: Brachycephaly (small nose with a flat
bridge), slanting eyes, protruding tongue, depressed cerebration.
*** Picture on Overhead of C Spine***
Absence of Transverse Ligament with very large ADI. Behind the dens there is minimal room for the cord. There may
be trouble swallowing on this patient. On this patient, there would be no need for a flexion/extension view since the ADI is
very visible on a normal radiograph.
*** MRI of the same patient ***
The cord area appears narrowed. The post tubercle is prevented from moving forward only by the cord in this patient. The
cord shows some chronic degeneration. 1/5th of all Down’s syndrome patients don’t develop a transverse ligament.
Medical Certification for Participation: Down’s Syndrome patients need a letter to qualify them for participation in sports.
This is due to the irreparable harm they can receive from lack of a transverse ligament. Some of these patients have
underdeveloped ligaments, but some do not have a transverse ligament.
Sometimes Down’s patients require screws inserted into C2-C1 drawing the lateral masses into a good position providing
protection for the cord, allowing the cord room to move. Screws are placed in both sides attempting to create more room for
Review of Os Odontoideum (see above also for more information)
*** Picture on Overhead ***
Ant. Tubercle is too far forward. Spinal-laminar line is interrupted at C1. The S-L laminar line is disrupted by either:
1. dens 2. No AA ligament 3. Congenital Small Posterior Arch C1. On this radiograph, we must rule out more dangerous
things like no AA ligament or dens anomaly. The patient has Os Odontodeum. Unstable os odontodeum has unstable
motion possibly leading to cord compression.
Overall considered uncommon, Un-united ossification centers, Long standing non-union fracture…We find these more
often than MD’s, probably because we deal with the spine more often.
2 major considerations: 1). Un-united ossification center 2). Long standing non-union centers.
This condition does include cost-benefit ratio and is a definitive candidate for MRI.
Discovery of Os Odontoideum warrants some questions to be asked:
Does the patient know? Should the doctor know? Clinical Relevance? Documentation imperatives?
1. Does the patient know? – Should they be looking for other signs and symptoms
2. Should the doctor know? -- Is there anything else you the doctor should uncover during exam.
3. Clinical Relevance – This is significant and relevant due to chance for AA instability. This can also be the
cause of sub-occipital muscle spasm and headache. There is also increased risk for VBAI.
4. Documentation – Follow-up MRI to document cord integrity or to determine damage severity
*** OS odontoideum and Down’s belong on clinically significant list!!! ***
Excess translation forces muscles to do double duty. Muscles fail to hold and become pain generators causing the
―headache‖ and knotty presentation. Muscles are splinting to hold the neck.
Hallmark Features: Sub occipital muscle spasm, headaches, VBAI…Translation of upper cervical vertebrae may
compromise the blood supply. Ex.—Looking over right shoulder may cause nystagmus, problems tracking, etc.
21. Dysplastic posterior elements (X-ray on overhead – Levels C5-C6)
You can tell the patient that structure is abnormal, but function is good. Being aware of this may help treat the patient.
This condition is otherwise not clinically significant.
22. Scrambled Spine
*** Cervicothoracic Shot on the Overhead ***
2 Vertebra without pedicles on one side causing structural scoliosis of the upper thoracic and lower cervical
vertebra. The X-ray shows have multiple hemi vertebrae. Several segments in the CT area are abnormal. You’ll likely
see a high shoulder. There is a distinct curvature. The patient can have some discomfort. You can treat the patient, but
may have to alter your technique and approach. The goal of treatment is to reduce the discomfort.
Hemivertebra is the term most often used over wedged vertebrae since wedge vertebra also implies compression fracture.
23. Sprangle’s Deformity
*** Picture on Overhead of Problematic Clavicle ***
This patient has a pronounced clavicle. The scapula is in the wrong spot (winging). This condition is called Sprangle’s
Deformity (unilateral elevation of the scapula). The scapula was never oriented. There is a vertebral-vertebral bone
bar. There is an articulation/joint that shouldn’t be there forming an omovertebral bone. Sprangle’s can been seen by
itself, but 40-50% has an omovertebral bone. These 2 things are part of a bigger problem (Klippefeil Syndrome). This is
multiple blocked vertebrae (Klippefeil) with decreased motion. Sprangle’s often have prominent trapezius (called
Pterygium coli). Pterygium coli have prominent trapezius and ―web neck.‖
Sprangle’s = Failure of the Scapula to Descend to the right position (Failure of the scapula to descend with pronounced
clavicle). It limits rotation and lateral flexion into the deformity (blocked vertebra).
*** Lat View of C-Spine…We see the bone bar better on this view. We see the upper end of the omovertebral bone on the
lateral view. On the AP view we see the upper end better on this X-ray. ***
24. Spina Bifida Occulta
*** Picture on the Lumbar Spine – AP – There is no spinous process…This is not a dangerous condition. This is T12 spina
bifida occulta. ***
You can find this easily with doing your ABC’s. (T12 – Has the proper amount of pedicles). Spina Bifida Occulta is often
called Spina Bifida ―unimporta‖, in the absence of signs and symptoms. Spine Bifida Occulta is usually not important
except at L5 where there is a higher risk for herniation.
25. Soft Tissue Calcification of Costochondral Cartilage & Review of Physiologic Calcification
*** Picture with Pelvic Rotation and Scoliosis. There is soft tissue calcification above and below the diaphragm.
Costochondral cartilage calcification is taking place. The rib cage works normally with no chest complaint. They exercise
and perform all ADL’s normally ***
3 Subcategories of Soft Tissue Calcification: 1). Physiologic 2). Dystrophic 3). Metastatic
Abnormal Tissue = dystrophic
Metastatic = Serum calcium levels increased
Physiologic = Normal serum calcium…This event can be normal.
Cartilage tissue is the 2nd most likely tissue to take up calcium and does not have clinical consequences. We can treat them
normally and expect them to get better.
26. Pectus Excavatum and Straight Back Syndrome
*** Frontal View of the Chest…Heart silhouette appears displaced to the left more. Anterior rib angles are steeper
(more down and in) and posterior ribs appear to be widened between ribs (more down and out). The rib orientation on
a lateral view presents with a pushed in chest. A deep sternum is called pectus excavatum.
Pectus Recurvatum is pigeon chest.
There is a higher association with pathological murmurs with straight back syndrome. Straight back syndrome is the
combination of Hyperkyphosis, pectus excavatum, and cardiac murmurs. The sternum displaces the normal location
of the heart. Pectus excavatum patients have a greater tendency to have pathological murmurs.
As chiropractors, we are more likely to pay attention to structure. This complication would take a couple films and
listening to the patients’’ chest. It is important to be aware of straight back syndrome with heart murmur. If you have this
patient you may want a cardiac consult.
DX. IMAGING – 3/26/08
Omovertebral Bar: Palpates unusual. It is a bone bar that offers protection to the spine. It often forms in the
cervicothoracic area. It is a common feature associated with Sprangle's and can be seen in Klippefeil Syndrome.
27. Limbus Fracture/Vertebrae
The patient appears to have a fracture. The patient had a motorcycle accident with back pain. The patient is skeletally
mature. This occurred when the patient was immature and then the fracture site sealed off. Nucleus pulposus can protrude
for several reasons: 1). Axial loading coupled with a tear in the annular fibers and the NP leaks out = Herniated NP 2).
Schmorle’s Node 3). NP punches through growth plate of vertebrae = Limbus
Schmorle’s., Limbus, and HNP are acquired deformities with movement on the NP due to an axial load. Axial loading
penetrates the growth plate (that’s how you know it occurred before skeletal maturity). The annular fibers are somewhat
innervated. The end plate and growth plate may not have had remarkable trauma. This condition is often confused with
fracture because of the appearance, but this condition does not have a true fracture plane. Early in life (before skeletal
maturity), you could call this an end plate fracture; however, in adult life it does not show a true fracture plane.
Recognizing that this is not a fracture will speed up care.
28. Winking Owl Sign (Agenesis of the pedicle or hypoplasia of the pedicle)
*** Picture of L1…The left pedicle is not observed. ***
The most common cause of this is lytic metastasis. We don’t want to miss this. This is local lucency (meaning tumor or
ON the other side, check the contralateral pedicle. The pedicle on the other side may be enlarged because it performs the
function of two pedicles. This case is actually good news because on this patient it is an interesting congenital anomaly.
If the other pedicle looks normal, that tells us the pedicle is taken away too quickly for the body to react by building up the
other pedicle (infection or tumor).
***CT Scan of Vertebrae…This is a bone window view of lack of full development of a pedicle (agenesis) ***
We see signs of stress response to the bone. The bone needs more cortex to do the work of 2 pedicles. This lack of a
developed pedicle is called hypoplasia/agenesis/winking owl sign. The picture clearly shows there is a pedicle, but it is
much smaller than the other.
29. Spondylolytic Anterolisthesis
***Picture of L5-S1 ***
The posterior part of L5 looks weird. There is a break in George’s Line. There is an anterolisthesis in the picture. There
is a break in Olman’s Line (???). We can document the anterolisthesis by Myerding’s method (+1-+5). This is a grade 1
(less than 25% ant. slippage). Myerding’s is a qualitative method. We prefer to use the percentage method for
We say the inferior vertebra is the reference vertebrae. Gonstead and Gonstead technique would call this retrolisthesis of
the sacrum and uses the superior vertebrae reference. The technique he developed addressed the spine in a PA manner.
Gonstead called this a posterior base (retro sacrum).
5 Major Categories of Spondylolisthesis
1. Retro 2. Antero 3&4. Latero (both sides) 5. Multi-vector
2 Categories with This
1.Stable 2. Unstable
Distraction View of the Spine
A bar with handgrips is used with the patient hanging while you shoot the lateral lumbar X-rays. This is part of a 3 view
series or 5 vies series. After this we put a backpack on the patient and have them wear it for 5 minutes and re-X-ray with a
lateral lumbar X-ray. In the neutral lateral there can be anterolisthesis. Stable patients are treated like everyone else
Unstable patients have frequent periods of pain and longer periods of pain. Treatment for anterolisthesis patients
includes core strengthening and activity modification. If conservative care fails, surgery is an option.
Unstable Anterolisthesis Example = Distraction view (anterolisthesis goes away)…Compression view (translation over 5
mm) ----- This example would be of an Unstable condition since the distraction view shows the condition going away
and the compression view shows significant translation. The meaning is that the vertebra moves significantly
between shots because it is unstable.
Neutral Lateral, Distraction Lateral, Compression Lateral
Unstable = translation more than 5 mm between distraction and compression views
Degenerative and Spondylytic Spondylolisthesis
These are also 2 other classifications for Spondylolisthesis.
DX. IMAGING 1 – 4/1/08
Classification of Spondylolisthesis
The vertebral body can slip in any direction, it does not have to just be anterior or posterior, but typically, the slippage is
anterior or posterior. L1-L2 is unusual for spondylo, but if it does slip there is a great tendency for L1-L2 to go posterior.
Flexion and extension view of the spine was how we used to do check for this on X-ray. We now do compression and
distraction views. Flexion and extension films gave high rates of false negatives.
You can seat them in a stool without wheels and take a seat belt to strap them to the chair (restricting pelvic motion). Bend
forward and arch (this gave a better image than the flexion and extension view). There were less false negatives. The next
phase (or better film) was the compression and distraction views. The views are pretty simple and much more reliable.
There is still some false -, but there are less. Compression/distraction is how we separate intersegmental stability from
intersegmental instability. Intersegmental stability even with listhesis, have incidence of LBP just like everyone else
and response to care is just like everyone else (relief of pain and improvement with care). Intersegmental instability
often do not respond to care and need to be classified and treated differently than stable conditions of listhesis.
Dr. Cox found it was relevant to separate the two. Dr. Cox found that more than 3 mm of instability between views had
more frequent bouts of exacerbation, more time in treatment, less response to treatment, and they eventually got
worse over time.
***Article On Overhead***--Classifying Spondylolisthesis
The most widely used classification of spondylolisthesis is that described by Wiltse, Neman, and Macnab in which 5
distinct types have been identified.
Type 1 = Dysplastic…The congenital Anomaly falls in this category. This is a rare condition. This type
includes those spondylolisthesis with a congenital abnormality in the upper sacrum or the neural arch of L5
allowing displacement to occur.
The incidence of neonatal spondylolisthesis is 7% in the US. In a study of 2100 neonatal cadavers, we expected about
171, but the study found 0. There is a big, gapping hole in the theory of congenital anomaly. The condition can happen,
yet the incidence is extremely rare and low. There can still be normal function even with this condition.
Type 2 = Isthmus… This type has 3 subtypes that involve alteration to the pars interarticularis as follows:
A). Lytic or stress (fatigue) fractures of the pars B). An elongated but intact pars C). An acute fracture or
the pars (rare and seldom affects the pars only)
A. Pars fracture is the most frequent stress fracture of the body and is also the most common
reason for spondylolisthesis. Originally, we thought the most common fracture was the 2nd metatarsal
fracture (March Fractue or Deutsch Fracture). March fracture is now classified as #2, because we have
found higher incidence or pars fracture.
B. We think the elongated but intact pars was fractured and healed by callus formation.
When the pars break usually other things break as well. It is difficult for a pars fracture to occur in isolation
Type 3 = Degenerative Pseudospondylolisthesis…This type is secondary to long standing degenerative arthrosis
of the lumbar zygoapophyseal joints and discovertebral articulations, without pars separation.
Type 4 = Traumatic… This type is secondary to a fracture of part of the neural arch other than the pars
interarticularis. Neural arch and pedicles can be damaged.
Type 5 = Pathologic: This type occurs in conjuction with generalized or localized bone disease (Paget’s,
metastatic bone disease. Pathologic Spondylolisthesis is called ―blind vertebrae.‖ Metastasis can destroy both
pedicles. Infection or tumor (lytic diseases) allows the vertebral body to slip.
*** May be matching questions on the final ***
7 of every 100 people have this spondylolisthesis.
#1 Stress Fracture of Pars is the most common #2 DJD of Z Joints leading to spondylolisthesis…The best method to
quantify this is the Percentage Method.
*** Inuit people in Alaska may have 45% spondylolisthesis (anterolisthesis). This is an isolated group of American
Indians. Dr. Yochum tracked down on anthropologist who reported this fact. The kicker is that there was a schism in the
population. Some Inuit became ―normal Americans‖ and had a 7% rate. Other Inuit lived like there forefathers. The Inuit
that led there lives as their ancestors did carried their babies in backpacks on the back, placing mothers and children in
extension. Repeated extension was the mechanism for the high incidence of spondylolisthesis ***
Other groups: Female Gymnasts, Football Linemen, Spring Board Divers – All are forced into extension.
Other Studies: Average age of onset was about 18 months-10 years (studies vary). The studies imply that
spondylolisthesis is a youngster problem (below the age of 10).
*** Know bolded stats and the classification system***
Sports activity can be contributing factor. More kids are playing aggressive sports younger. Another thing is the toys
children use, ―Johnny Jump Up.‖ Johnny Jump Up is a toy that puts extension moments into the lumbar spine. Another
associated condition is early walking children. When the muscular strength is ready, the bone strength is ready. Muscles
usually adapt first in childhood. Muscle adaptation can pull on osseous structures causing children to acquire the
condition. Another associated condition is the ―Pratt Fall.‖ Repeated forward falls with the legs coming backward and
trunk into extension can hurt. Landing on your butt does not cause a problem (facets are in open packed positions). The
early childhood walkers that fall on their butt may not be at risk for spondylolisthesis because the fall occurs with slight
flexion. Slight flexion is the open pack position for the facts.
Stable Spondylolisthesis we treat just like everything else. Even with a stable spondylolisthesis the child can play
contact sports. If the condition becomes unstable, that would indicate that there can be sequelae and the children cannot
play contact sports.
*** Slide on Overhead of Distraction View…The patient holds from a bar from the ceiling. The patient grabs onto the bar
and sags from the bar while consciously relaxing the low back. ***
***Slide of Compression View…The backpack must be worn for about 5 minutes…There must be about 10% of there
bodyweight in the backpack. This is done to fatigue the back muscles to cause translation. Too heavy, is better than too
light. After 5 minutes, redo the lateral lumbar shot. Translation above 3 mm from distraction to compression is
30. Transitional Segments (L-S junction)
Type 1a: Asymmetric. Single = TP that is bigger than 19 mm in vertical dimension
Type 1b: Bilateral…2 TP’s 19 mm or bigger in vertical dimension.
Both 1a and b are not clinically significant.
2a Single Joint = The most clinically significant because there is a high rate of HNP at the transitional segments and
not quite as significant but possible HNP above the segment. HNP may be at 80% in these conditions. The patient may
be a candidate for back school.
2b Bilateral Joints…Lower rate of HNP than 2a, but still h higher rate than the normal.
Both 2a and 2b have accessory joints with capsule, cartilage and free nerve joints. You may need to adapt your style of
adjusting to 2a and 2b
3a: Fusion with a single bone bar (unilateral sacralization)
3b. Fusion with a double bone bar (bilateral sacralization)
There is no clinical significance for the disc in type 3. Elimination of movement causes the disc to calcify.
4: Hybrid Condition = We have a bone bar on one side and accessory joint on the other side. We have the risks
associated with bone bar (not clinically significant because there is no movement due to the bone bar).
Types 3 and 4 have no additional risk of injury. Type 2 does have additional risk.
*** Ferguson’s view of Transitional Segment on overhead….2a is present…2a is the most significant one since HNP is
possible at the level and the level above. The annular fibers may not be normal. The joint has asymmetric motion
presenting a torque/rotational moment which can damage the annular fibers. Annular fibers are susceptible in rotation. ***
*** Ferguson’s--Another picture of Transitional Segment…2b…A bilateral transitional segment with two joints ***
*** Ferguson’s -- 3b…Bony fusion is present. An intact cortical margin indicates a fusion at this level. This is a fused
functioning unit ***
***Ferguson’s -- Type 4—Single type 4 picture…Significance, there is no clinical significance to this one, as the joint is
trumped by bone bar ***
*** Lateral lumbo-sacral Spot View (the patient is in slight extension) ***
Extension can be very painful with retros . The S2 tubercle is huge. The patient can be losing posterior disc height
(dehydrating the disc). The posterior part of the disc loses height quicker than the anterior and can bring the
patient’s L5 spinous and S2 tubercle together via extension. This patient may be born with the abnormal S2, but now
feel pain because the disc thins and allows the approximation of L5 and S2 into extension. The situation can be further
complicated by thinning of the meniscoid disc within the facets further allowing extension. The best advice for this patient
will be conservative care including adjusting, modalities, inversion tables, possible traction, and activity modification to
prevent extension. ***
32. Knife Clasp Deformity
***View of the Sacrum***
We see agenesis of posterior elements of S1 and S2. The Spinous Process of L5 is large in dimension. The growth
center may have stayed at L5 and not gone down to s1. This is called ―Knife Clasp Deformity.‖ On an extension view of
the spine, the L5 spinous may even enter the sacral canal. This patient will complain of problems with extension and
―lightning strikes‖ down the leg. This is neurological involvement (indicating missing bony protection with nerve
involvement). To treat, stop extension, induce some lordosis and modify posture, and emphasize disc rehydration to restore
the disc. The thicker the disc, the less symptomatic.
***Missing posterior elements…L5 appears greater on this AP view. ***
*** Lateral View of Lumbar spine….Large L5 spinous appears on this picture***
33. Sacral Agenesis
The sacrum is missing. The spinal weight is distributed from ends of L5 to the ilium. In side lying position, it is
noticeable that the gravity line is way off. Anterior shift of weight bearing occurs. The patient is ambulatory but can be in
34. Coxa Vara/Valga
***Picture of Femur Neck Angle***
The angle is 145 degrees and is too big. This is called Coxa Valga. This picture is off an adult. The diagnosis of coxa
valga can only be made after the closing of the growth plates (at skeletal maturity). Coxa varus diagnosis can be made
before skeletal maturity is completed.
35. Fabella vs. Joint Mouse
*** Lateral View of the femur, tibia and fibula***
There can be joint mice breaking off chondral parts/fragments. The fragment can calcify due to dystrophy. It can be a
fabella. Fabella is an accessory ossicle, imbedded in a tendon. Fabella can be sesamoid bones. The fabella is
specifically found in the tendon of the lateral head of the gastrocnemius in this X-ray. A true lateral view with the ossicle
outside the joint capsule = fabella vs. a true lateral view with the ossicle inside the joint capsule = joint mice
The classic fabella patient won’t have much pain. The classic joint mouse is an athlete running and planting, causing
axial loading with rotation to chip off the articular surface. Fabella ossicles have trabecular interiors with cortical rims
vs. joint mice that show ossified cartilage and unorganized bone.
36. Bipartate Sesamoid
*** Distal end of metatarsal X-ray***
3 bones underneath the 1st met head….The lateral met head is the normal head. The later met head and sesamoid offers
protection and gives power to help give us a toe off. The other 2 sesamoids are abnormal. Bipartate sesamoid is a
congenital anomaly or an acquired condition. Sometimes the other foot may also show the same anomaly. Sesamoid
bones can undergo stress fracture and can split in half. Stress fracture can occur in runner’s whole load the area more than
the normal population (acquired condition).
***X-ray of the Foot and Metatarsals***
There are extra metatarsals on the X-ray. It is a little more difficult to see in the AP view. The foot may be wider in the
midfoot. There may be a huge callus indicating wearing of the skin on the shoe. Most shoes don’t accommodate for this
and cause callus formation. There are 5 toes on this patient, but there is an extra metatarsal. The X-ray in this case,
helped make the diagnosis. This tends to be a bilateral condition.
38. Supracondylar Process
***Picture of Humerus, Radius, Ulna (Elbow Joint)***
There is a bump on the distal end of the humerus. This is called the supracondylar process. Supracondylar process
always occurs on the anterior surface of the humerus, down by the elbow. This condition often has a ligament that crosses
the elbow joint (Strother’s Ligament). Strother’s ligament always points towards the elbow joint. The significance is
trapping of the neurovascular bundle. If the bundle is compromised, it requires treatment and if not, no treatment is
The bony process may also break due avulsion that causes forced extension of the elbow. Most often this is a condition to
see, name, make sure it is not tumorous and forget (not significant).
There is 1 benign bone tumor that can be confused with this (osteochondroma). Osteochondroma is both a bone and
cartilage tumor. Osteochondroma’s can be anywhere in the body. When they are on a long bone, they point away from the
joint and never have a ligament attached to it. Supracondylar process points towards a joint and has a ligament attached to
*** Bilateral pictures of the Hands***
There are missing PIP's and DIP’s. This is synostosis or lack of fusion where there should be a joint. There is no
bending of the middle finger. Synostosis can be anywhere in the body.
DIAGNOSTIC IMAGING – 4/2/08
40 .Bilateral Overhang
*** Open Mouth View of C1 and C2***
The goal is to check the odontoid. On this X-ray, the articular surfaces of the lateral masses of C1 hang out very far in
space. We normally have congruency on the joints (including facets, lateral masses, etc.) This view is of a child. If we
see this as an adult, we think there is an axial load and fracture, because the anterior-posterior arch has been injured. IN
this view of a child, it is normal. The child develops C1 and the lateral masses before they develop C2. We check for a
C1 burst fracture in an adult
41. V-shaped ADI
*** Flexion view of the C-spine and noting the ADI***
There is a V shaped ADI on the X-ray. The ADI actually is 9 mm. This is almost double the ADI for a child, and we
shrink the central canal. This X-ray is of a child. The growth ring has not even began to appear. The ligaments are very
elastic at this age. The ligaments stretch very well. We try to measure the lower ADI for comparison. This child has a
lower ADI of 3mm. ***
***Extension view of the same patient above…We have a normal ADI.***
This condition is a normal variant as a child, but worrisome in an adult. We tend to see parallelism as an adult. If an
adult gaps at the top, then measure the inferior ADI. If above 3 at the inferior ADI, you must consider the problem of the
central canal and the cord.
42. Pseudo tumor
*** View of the pelvis***
It appears that the pubic ramus and ischium has a lack of cortical border. Both sides of the obturator foramens appear
normal. This is the growth center of the inferior pubic ramus. The inferior pubic ramus is one of the last growth centers
to close, next to the iliac crest (Riser’s sign). This appears to be a ―pseudo tumor of the pelvis.‖ This condition has
fooled many people in the past, and all it is, is a growth plate. ***
43. Pseudo cyst of the Humerus/Pseudo tumor of the Humerus
*** View of the GH and humerus***
.It appears there is cyst or tumor. What this really is = the rotator cuff tendon and the Sharpey Fibers giving the
appearance of a cyst or tumor. This is a geographic finding and can occur in the non-skeletally mature. This is perfectly
normal. When you check the baby arm position, the cyst/tumor disappears. The cyst/tumor disappears because it isn’t
there. This has to be the enthysis or the attachment site of the rotator cuff including the Sharpey fibers.
44. Tropism (of facets)
*** View of the lower lumbar spine, pelvis, and sacrum***
There is tropism. This is facet asymmetry. We always have distortion on plain film because we project a 3D object onto
2D plain film. Tropism is a real condition and can impact care. We know by doing CT or MRI (a 3D image). If you try to
adjust in side posture one way and they don’t like it, and you try to do this the other way and it works, it may be indicative
of a facet tropism. You can partially gage by quality of the lockout. In this view, one facet appears more coronal and one
appears more sagittal. Tropism can depend on the image taken, the patient, projectional distortion (3D image on a 2D plain
film). We probably will not be ordering a CT because often it is not a problem and we can use our hands and techniques to
feel the proper lockout.
REVIEW OF SYNOSTOSIS
Synostosis of the Skull/C1 (Occipitalization of C1)
*** Blurry View of the Skull and the Upper Cervical Vertebrae using a tomogram***
We can slightly see the anterior tubercle and arch. We do not see a posterior tubercle . There should be a joint space
between lateral masses and C1, but a joint space is not evident. We have fusion where there should be a joint space.
This called synostosis. This is synostosis of the atlanto-occipital joint. This is called CO-C1 block or occipitalization
of C1. ***
*** Lateral upper cervical view. WE have an anomalous IVF at C1-C2. WE have a C1-C2 block. This block is similar to
the one listed above, but in at a different area. ***
45. Agenesis of Posterior Tubercle of C1
The Spinolaminar line at C1 is absent. The anterior tubercle is also huge. The bigger the anterior tubercle is to the
odontoid, the more likely the odontoid is too big. If the anterior tubercle is bigger, we have to think that either the growth
center never split A-P or we don’t know what happed to the posterior tubercle, but it is not as strong. A C-shaped structure
is not as strong as a ring shaped structure. This child is not a candidate to play football or contact sports.
DIAGNOSTIC IMAGING 1 – 4/8/07
Review of Tropism/Facet Asymmetry
Many people have this condition. It may be as little as 17% of the population. This condition has the aka of ―tropism.‖
Plain film does not give you the best visualization of tropism, since it is 2-D. CT is the gold standard for the condition
of tropism since it is a 3D image. There was a study between radiologists and students attempting to diagnose tropism.
The students used a math model and were better able to diagnose this condition. The radiologists used the plain film X-
rays. The predictions were compared to CT scans (CT scans are the gold standard). We found that CT was best, then
students using the math model and then the plain film diagnosis by radiologists.
Review of Un-united Growth Center
*** Picture on Overhead***
An imitation of a fracture at the C2 spinous. This is an united growth center. The bone did not fill in the space. The
two pieces are both corticated, which indicates that it is not a recent fracture. So is it an old fracture or an un-united
growth center? We don’t know, save by experience. Spinous percussion won’t hurt. Bone scan may help to answer this
question. This will shoot a big whole in the fracture diagnosis. Breaking a posterior element will show a trabecular edge.
We can’t find a trabecular edge and we only find corticated edges = No fracture …This condition is a normal
variant as sometimes ossification centers fuse and sometimes they don’t.
** Picture of CT junction***
There is an un-united growth center at the CT junction. There is a ―puzzle piece appearance.‖ The difference on film is
that there is corticated bone. A bone scan will be negative. An MRI will not show edema. These factors indicate a chronic
condition, implying un-united growth center ***
Review of Transitional Segments
*** Picture of LS Junction….The TP is up and outward. There is a TP with an unusual angle, but it doesn’t form a joint.
On the other side, we have a joint between the TP and the ilium. This is a 2a transitional segment ***
*** Picture on Overhead of LS junction…another example, this time it articulates with the sacral Ala ***
46. Notochordal Persistency
*** There is a bimodal hump of L4-L5. This is called ―Cupid’s Bow.‖ Cupid’s bow has interest to use because it is
nucleus pulposus. The NP (disc material) divided into a shape conforming to the area. This is confused with Schmorle's
node. Notochordal persistency is a normal variant.
*** Lat view of the Spine***
The inferior end plate hump’s inward. In the AP, we get the 2 humps. In the lateral view, we see one hump, but more
prominent inferior humping.
The condition is also called Owl Eyed vertebra. The condition presents with cortical rim. Cortical bone is reactive, and
not explained by recent trauma.
47. Winking Owl Sign of the Sacrum
***L/S Picture on the Overhead***
We have asymmetry of the facet group articulating with the sacrum. There is more bone on one side as we face this
individual. We have to do a CT to further study. The CT would show a robust pedicle on one side and a lack of pedicle
on the other indicating winking owl sign. We worry about infection or tumor with a winking owl. In this condition, the
sacral facet is not connected so it can’t receive weight. The other side posterior arch is now supporting the weight of two
arches. This is the sacral version of the ―winking owl sign‖ in the spine. This is a normal variant, not a MET.
Review of Pectus Excavatum
The finding prompts us to check for cardiac murmur. We should know the risks. We should also check for straight back
syndrome. We should listen with a stethoscope. If there is a murmur present, it warrants a referral to the cardiologist. If
the measurement between sternum and the spine is greater than 10, this may indicate stress.
48. Physiologic Calcifications
A. Calcification of The Thyroid Cartilage
Cartilage tissue is the 2nd most likely to pick up calcium in the body. IN this film, the thyroid cartilage picks up extra
calcium. The function is still OK. This film also shows stylohyoid ligament calcification.
B. Calcification of the Iliolumbar Ligament
Ligamentous tissue has chondral qualities and takes up calcium. There is more potential for dystrophic calcification in the
L/S area, but this one on the film is physiologic. In this area, we need to check for significant injury with protracted
49. Synostosis of the Pubis
*** View of Pelvis and Pubis***
This patient does not have motion at the pubis. The pubis is fused. They will also present with fixation at the SI joint.
50. Hypoplasia of the Patella
*** Sunrise View of the Patella***
There is a space surrounding the patella. This image shows hypoplasia of the patella. This could be clinically significant
in patella tracking problems. The patella will be pulled to one side. They are also more susceptible to dislocation.
The space is too big in this picture. The femur, tibia, and fibular head appear to be normal, but the patella appears small for
the relative size. Because the person in the film is skeletally mature, assume hypoplasia
51. Rocker Bottom Foot
***View of the ankle and Foot***
The talus is hard to find, and the tarsals of the midfoot are hard to find. The big toe passes underneath the second and
third digits. They step on their own toes. This can be quite painful. There may not be an independent navicular (hard to
find on the film). The cuneiforms are also hard to find. The patient may come in with an angulated big toe seeking relief of
pain. Surgery is done to relieve the pain and help provide pain free ambulation.
Review of Bipartate Sesamoids
*** View of the Metatarsals and Phalanges***
We have additional sesamoids on the great toe
Synostosis of the Cuboid/4th Metatarsal
*** View of the Foot***
We are missing the joint. We don’t see separation of the joint. There is a bridging block of bone where we expect to see a
joint space. This person will have distinctive gait.
52. Calcific Tendonitis vs. Os Peronei
*** Picture of the Foot and ankle***
There appears to be an extra bone/part of a bone on the lateral side of the foot. Calcific tendonitis will be very tender
and may appear red. There is a history of prior multiple injuries with calcific tendonitis. Os Peronei will not be tender
and not be red. MRI may help us diagnose between the two. The peronei should appear with a black rim without edema
(high signal on T2). If there is edema and physical presentation of tenderness, think calcific tendonitis. If the MRI appears
normal showing a black rim without edema and absence of tenderness, think Os peronei.
53. Madelung’s Deformity
*** Picture on Overhead of the distal ulna/radius and the wrist***
The articulation between the radius and ulna is messed up. There is a V-shaped arrangement that is typical as
Madelung’s Deformity. The key is the V-shaped cradling of the carpals, changing the position and the visualization of the
carpals. The radius and ulna appears to bow. On the PA view, the articular surfaces are not in the same plane.
Opposing planes form an obtuse angle. On the lateral view, classically the ulna is posterior. The ulna goes posterior and
can be posterior on both PA and lateral view. This is also called Bayonet Wrist. The bump on the ulna is very prominent.
These patients have higher incidence of dislocation, fracture and avascular necrosis. Sometimes these patient also have
carpal coalition (carpal bones don’t separate).
*** Lateral View***
In this shot, the ulna is very posterior to the radius. The lateral often gives a better view of this condition. The diagnosis is
Madelung’s Deformity. Bayonet wrist is also an indicator of the problem. This patient does have choices to make. Trades
involving your arms and hands may not be good for this patient.
Classic Madelung’s is bilateral, but there can be asymmetric presentations.
54. Ulna Minus
*** View of the Distal Radius/Ulna and Wrist***
The styloid process of the ulna doesn’t line up. The styloid of the ulna does provide some mechanical protection against
dislocation . This is called Ulna Minus. The ulna didn’t grow as long on one side in the picture. There is slightly
increased risk of carpal dislocation and avascular necrosis. The risk is still not as high for carpal dislocation or Avascular
necrosis in Ulna Minus as it is for both of these conditions to occur with Madelung’s. Classically, Ulna Minus is
bilateral; however, there can be asymmetric presentation.
You don’t go looking for ulna minus. You find it usually because there is some other type of trauma or decreased function.
55. Un-united Growth Center of Styloid Process
*** 4 Views on Overhead***
The center could have been never united or injured causing premature maturation. The clinical significance of this is
none. There are corticated margins on these X-rays, so it cannot be a fracture.
Review of Hemivertebra
*** Picture of Thoracic Vertebra***
There is a failure of the ossification center. There is a structural scoliosis. This is clinically significant. The spine
cannot be straightened, but functional movement of the segment is important. Conservative care and/or leaving it
alone are the treatments. Surgery would not be a good option. ***
56. Butterfly Vertebra
***Triangle of bone on the screen***
Superior and Inferior ossification centers did not form. The end plate from another level dips down with the other level
protruding up into the gap. This is called Butterfly Vertebra. This is an incidental finding. The bone continues to
grow up into the space from the inferior, while the superior vertebra grows down into the space. This is failure to separate.
There is no matrix, just space in this gap. Over time the above and below vertebra fill in the space.
Review of Cervical Rib and Hypertrophy of C7 TP
*** Picture of Cervical Rib on one side, with an elongated TP on the Other side***
TP is more horizontal belonging to C7 on one side. The film shows transverse process hypertrophy without a joint (bone
projection). On the other side, the joint is present (cervical ribs). Cervical ribs are not a cause for TOS. In the past they
did surgery that had very poor results. Often, these people were worse with surgery because of pos-surgical fibrosis. Most
common cause of TOS is soft tissue (pec minor, scalenus anticus).
57. Bifid Rib
*** Picture of Ribs***
The rib head unifies adjacent to the spine. Have the patient breath in and out, and your finger will not feel separation that is
typical of other ribs. This may be a finding in disease states. Ribs above and below should move. The bifid rib is not
capable of normal motion.
58. Intrathoracic Rib
***Picture of Chest***
There is an intrathoracic rib. The bone goes through lung tissue. Lung tissue normally can slide, and usually there is
no issue. Every now and then lung can collect pneumonia due to the configuration of the rib within the pleural tissue. This
is a see it, name it, and forget about it phenomena. You cannot palpate this condition and often there are no
complaints. This is found incidentally, often with chest films when checking for pneumonia.
59. Reversed Kyphosis/Thoracic Lordosis
*** Picture of the T-spine***
There is no kyphosis. This is reversed kyphosis or thoracic lordosis.
Thoracic Pedicle Hypoplasia (see other info on pedicle hypoplasia)
60. Lumbar Rib
Review of Blocked Vertebra/Lumbar Blocked Vertebra
*** Lower Lumbar Blocked vertebra X-ray on overhead***
There is a solid cortical line. This is the lumbar presentation of wasp waste appearance. Do extension and flexion films.
You should be able to overlay the 2 vertebra. The blocked vertebra will overlay in clear focus. Don’t adjust in this area, it
won’t do any good. Lack of mobility may cause compensatory hypermobility is other segments. It is very important to lift
properly and have proper mechanics.
Review of Spina Bifida Occulta/Spine Bifida Occulta of the Lumbar Spine
L5 Spina Bifida Occulta/Unimporta (most of the time is benign). At L5, there is a higher incidence of disc herniation
(that may be the only clinically significant relevance. The patient may need to go to back school, have lifting limits, and
watch//monitor their activities.
Review of Scrambled Spine
*** Picture of Spina Bifida at L5***
Pedicles are missing, multiple blocked vertebrae and/or hemivertebra present. Oblique views help us image the Scotty
dogs or lack of them. There can be kyphotic arrangement of the lumbar spine.
61. Small Pars Interarticularis
Very thin necks of the Scotty dogs are present. This patient may not benefit from extension positioning. Disc health
becomes very important. Loss of posterior disc height will load posterior elements. They may fail in this patient. You
may never begin a search for this, usually it is found due to other processes.
DX. IMAGING – 4/9/08
*** Suggestion by Dr. Kuhn: Look at normal again in Yochum and Rowe textbook...Final will include material from the
first exam and the second exam. There will be general material from the first exam and more specific questions
from the second exam material ***
Multiple blocked vertebra…Some associated findings often seen are: 1). multiple blocked vertebra 2).Sprangle’s
Deformity -- Failure of the Scapula to Descend with abnormality of the levator and trapezius 3). Unilateral elevation of the
shoulder blade (one clavicle is horizontal and the other is vertical 4). Omovertebral bone (bone bar crossing one or more
segments), 5). High shoulder 6). Scoliosis 7). Prominent Trapezius (pterygium coli). Many times these children have
surgery to help these conditions.
2 Versions of this: 1). Failure to develop (lack of ossified matrix and that is why the vertebra above and below descend into
the butterfly vertebra 2). Lack of growth center migration (leading to the condition of the butterfly vertebra because normal
amount of bone, that is abnormally distributed)
Champagne Glass Appearance of the Pelvic Bowl. The pelvis has this arrangement because the pelvis rotates. The femur
necks can be either varus or valgus, but it is altered. The ASIS tips forward and the PSIS tips up. These patients also tend
to have protruding buttocks and a belly. The belly and buttocks fits with the anterior positioning of the pelvis. You
recognize these patients by their short appearance. Their spinal lengths are relatively normal, but their arms and legs are
short. The long bones are the shortest parts of their body’s. The paired long bones are short (humerus and femur). These
are called the ―root‖ bones. Rhisomelia (―short root‖) is the name for this condition. These people commonly cannot fully
extend their joints. The olecranon runs into the humerus. The end of the bone doesn’t develop properly. The fossa is
shallow. They can have unusual carrying angles of their upper extremity. Scalloping vertebra can develop. The central
canal can be very small (this is the most serious complication – central canal Stenosis occurring 30-40’s). They combine
DDD and canal Stenosis later causing serious problems. The most dangerous complication is a newborn is a small foramen
magnum. The most common cause of lethal Achondroplasia is the small foramen magnum. Prenatal testing or charting the
birth weight of the baby can also be key intrauterine findings. The baby will then be removed by C-section.
Brittle Bone Diseases
Piknodysostosis, Osteopetrosis (Chalk Bone), Osteogenesis Imperfecta
1. OI—bone fragility, blue sclera (90% have this with OI…they miss a layer of the sclera…steel blue/gray tint),
Congenital forma and Tartar Form---Recognition separates the two. Congenital group is short and acquired shortness due
to premature maturation due to early fractures (the growth plate hurries and closes). Arachnodactyly vs. Brachydactyly –
The bones are not normal size. Density is less than normal. Most of the time diameter is normal, pencil thin cortices and
undertubularization occurs. These people heal by exuberant callus formation. There is not a lab marker peculiar to this.
2.Prominent Lab findings are present for osteopetrosis. Both osteopetrosis and piknodysostosis are dysplasias.
Osteopetrosis have bone within a bone. There are 2 bone systems arising from each other. Bone within a bone squeezes
out marrow, so they are anemic. The greater the osteopetrosis (congenital), the greater the chance the patient may not
survive long because of the severity of the anemia. These people have lack of both red and white cells. They die of
infections. They may need many transfusions, hormone therapy (hemopoietin), and oxygen therapy to survive.
Piknodysostosis: A common feature is big head/small face and also Acroosteolysis (missing finger tips or toe tips).
+ Thumb Sign, Tall height…+ Thumb Sign (Arachnodactyly – more length than width and also due to connective tissue
elasticity)…The aorta can also dilate leading to an aneurysm. The heart valve can also prolapse due to the elasticity.
Targets the Epiphysis…Vertebral Bodies are a target. The ring apophysis fails to develop. We have humped/heaped up
vertebra on X-ray. There is less bone in the corners of the vertebra.
Platyspondyly—flat vertebra…Vertebra Plana (below 50% flatness)…Another big joint that is abnormal is this case is the
lumbar spine. The femur heads can mushroom. The epiphyses of the long bones pay a price.
*** Big common dysplasias will be on the exam (with details)…Know definitions for the exam…Big conditions (like
exuberant callus formation….Anemia…Blue Sclera….),things that make dysplasia stand out are important. ***
*** There will be some roentgenometrics applicable to clinical questions and appropriate to the study…Ex. Violation of the
SL line would implicate? **
Puzzle Piece Appearance = Fracture is the most common. Limbus and un-united growth centers also can present with this.