Monday, September 15, 1997:
4 Things X-Rays may be used for:
1.Rule in
2.Rule out
3.Monitor
4.Education
X-Ray is for documentation not discovery. Not very much pathology shows up on plain film x-ray
General practitioners role with the x-ray:
Tuesday, September 16, 1997:
Read Imaging Chapter
Today we will go through common modalities
What is it good for?
How did it make its mark in imaging?
Comparisons.
William Conrad Rankin took first x-ray of his wife’s hand.
Plain film radiography
The side of the parallel illeum is the side of the scotty dog.
PLAIN FILM
Advantages:
 Widely available
 Relatively inexpensive
 Minimum risk to the patient
 Looks best at bone but can be used to look at some soft tissue
Disadvantages:
 Lacks sensitivity
CONVENTIONAL TOMOGRAPHY
Forerunner for CT
TEST Q: Be able to pick out what modality is which. Usually will ask CT from MR
Know where cortical bone should be and if cortical bone is white- it is CT.
If cortical bone is black, it is MR
White on CT because it is ionizing radiation jus like plain film. X-Rays are absorbed and makes the film
white. Cortical bone is the most radiographically dense.
Axial sections typically look from their feet towards their head.
Level is how energetic the beam was. Houndsfield units for CT. Goes from –1000 to +1000.
CT is ionizing radiation.
Can enhance soft tissues or bone. Do reformations of images by computers.
This is a huge advantage over MR.
Axial images are the best images of CT.
Some soft tissue can be seen
Very short acquisition time
BONE BASED PROBLEM USE CT
Only contraindication is size. You could be too big to fit into the hole
MRI
No ionizing radiation
Put in strong electromagnetic field.
Lines up 10% or more of mobile protons and lines them up with the field.
This is FM (radio) Energy and we listen electronically and map the realignment images.
Cannot manipulate images besides making it smaller or larger for printing.
This modality is less versatile and more expensive.
This does sagital images better and does good A-P images.
Acquisition time is much greater
Cannot look at chest or abdomen yet because these structures move.
NEUROLOGIC PROBLEMS USE MR
Contraindications to MR
Size constraints
Claustrophobic patients may have a hard time.
Ferrous metal implants are a contraindication.
Titanium does not interfere with magnetic fields. It is much more expensive
Vascular clips do not belong with the scanner although it has been done before with no side effects.
CT and MR need a 1-3% bone loss
BONE SCAN:
1.Injection of a radioactive isotope
3-5% bone loss is all we need to be positive
technicium or dihydrophosphate which has an affinity for bone is the radioactive material
Patient is the emitter of radioactive material, they are the ion source, not the gamma camera.
Give a couple hours for material to move out of the vascular tree and moving into the bone.
Hot spots are increased metabolic rate. This is increased OSTEOBLASTIC activity.
If tumors destroy bone osteoblastic activity repairs, the bone and shows up on bone scan.
Lytic or blastic tumor will show up on bone scan because body is trying to repair bone.
Multiple Myeloma does not produce a hot spot because they suppress the osteoblastic activity. There
is no hot spot because the hot spot is a result of increased osteoblastic activity.
Bone scans are very sensitive studies
Fluoroscopy
Real time moving images.
Lytic Lesions and Blastic Lesions.
Read Pages 568 to 570 for class tomorrow
Wednesday, September 17, 1997: Dr. Kuhn was not here. Dr. Atherton reviewed the X-Rays
Normal mensuration of x-rays
Cella turcica is 12 x 16 for normal adult
Platybasia and basilar impression: flat clivus if angle is <1500. Basilar impression is when bone softens
and occiput goes down on atlas and atlas comes up foramen magnum.
McGregors line: help discover basilar impression. Posterior hard palate to base of occiput
Chamberlin's posterior aspect of hard palate to opistion (posterior of foramen magnum)
Atlanto dental interspace (ADI)
Allowed up to 3 millimeters in adults
Child allowed up to 5 mm.
Trisomy 21 and RA can have an increased atlato-dental interspace. (ADI)
George’s line: straight down the back of the vertebral bodies. Should be smooth alignment and continuity.
Spinal laminar line: more sensitive than George’s line.
Know normal thyroid cartilage vs. calcification of the Cortaid artery.
Discogentic spondylosis
Sacral base angle 47.7 deg.
Scotty dog should have smooth line
Eisensteins method
Klein’s line: parallel line to top of femoral neck
Bohelers angle.
Monday, September 22, 1997:
Into to Rankinometrics last Wednesday with Dr. Matthews.
Format of the radiology report:
Look in the action notes:
Table 7.2
The seven categories of bone disease:
1.Congenital
2.Trauma
3.Arthritis
4.Tumor
5.Infection
6.Hematologic
7.Nutritional, metabolic, endocrine
Table 7.3
Radiological predictor variables
ANALYSIS OF THE LESION:
Skeletal location position within bone site of origin shape
Margination cortical integrity behavior of the lesion matrix
Size periosteal response (ch 7) soft tissue changes joint changes (trauma, inf)
PRELIMINARY ANALYSIS:
Clinical data:
Age: Can expect to see some things with age (statistically)
65 year old woman:
Common: DJD, Dish, less disk angles, osteoporosis or decreased bone density.
Uncommon: Paget’s, Congenital anomalies
License Stealers: Pathologic fractures due to tumors or metastasis
Pulsatile mass in abdomen (AAA)
Infection or immune compromise
65 year old man:
Expect: DJD, normal bone density,
Surprises: Congenital anomalies, fibrous lesions, paget’s disease
License Stealers: Metastasis, Aneurysm, Infection.
25 year old woman
Expect: Normal bone density
Surprise: DJD, osteoporosis, and congenital anomalies
License Stealers: Aneurysm, infections, metastasis
25 year old Male
Expect: Normal bone density
Surprise: infections, fibrous lesions, congenital anomalies
License Stealers: Infections
50-55 year old Male
Expect: Normal bone density with arthritis; Atherosclerosis
Surprise: Paget’s disease, fibrous lesions, and congenital anomalies.
License stealer: Aneurysm, carcinoma, and metastasis of the bone, infection
55 year old female
Expect: athlersclerosis decreased bone mass, arthritis
Surprise: fibrous lesions, congenital anomalies, and Paget’s disease
License Stealer: Aneurysm, metastasis, and infection
LOOK FOR THINGS THAT SEPARATE OR UNITE THESE AGE AND SEX CATEGORIES:
Sex:
Race
History
Tuesday, September 23, 1997:
Bone Physiology
2 ways to produce bone:
1. Intramembranous
No cartilage precursor
Flat bone
Long bones have Intramembranous in the periosteal tissue
2. Enchondral ossification
Long bones
Physis is main location. (growth plate)
Bone Structure:
Epiphysis tissue: has articular cartilage, which helps differentiate it from apophyseal bone.
Can have ischemia and bone will die. Covered with articular cartilage so we can acquire damage and
get arthrotides.
Tumors: Chondrblastoma (chondral tissue) & Giant Cell Tumor.
Physis
This is the growth plate. Composed of layers of increasingly mature bone.
Where the most mature and immature bone?
ZPC (Zone of Provisional Calcification)
Definition:
 Most mature layer of the physis or the most immature layer of metaphysis
Metaphysis
most metabolically active part of the bone
Most prone to infection and tumor due to sinusoidal blood flow beds.
Diaphysis
Convert from red to yellow marrow within the first year
Red marrow regresses into end of bones as we get older
Apophysis – greater trochanter.
Apophysis is an insertion site of ligamentous tissue.
Includes all major bumps on long bones.
Cortex
Crystal matrix. Very strong complex mechanically and very stable chemically.
Shows up as signal void because it is so stable
Medulla
Thin framework for RBC and WBC production.
Periosteum
Endosteum
Bone Metabolism:
Calcium and Phosphorus.
2:1 Ratio.
Less than 1% of all available calcium is in circulation at any one time.
Parathormone Increases serum calcium
- Parathormone levels rise when circulation levels of calcium get too low (sometimes caused by increased
osteoclastic activity).
Reduces bonding energy to make calcium more readily available. Osteolcasts work is made easier.
Increase solubility of bone matrix
Recover nearly 100% of calcium from the kidneys
Enhance uptake of calcium coming from the GI tract.
Pizoelectric effect (pressure creates an electric charge/electric charge causes growth) is important in
stimulating the bone to produce more bone
Calcitonin: Bone in. Puts calcium into the bone.
Comes from thyroid or parathyroid and works in opposition to parathormone.
Decreases serum calcium. Inhibits uptake of calcium of the GI tract. Loose calcium through the tubules.
Glucocorticoids:
Associated with osteonecrosis
Linkage with diabetes is there but not much is know about it.
PRELIMINARY ANALYSIS (CONTINUED from yesterday)
Clinical data: age, sex, race, and history:
Number of lesions:
Symmetry of lesions:
Systems involved:
SUPPLEMENTARY ANALYSIS
Other radiologic procedures:
Laboratory examination:
Biopsy:
KNOW TABLE 7.4 –Yochum (Action Page 11)
Benign lesions do not destroy cortex
Benign lesions tend to be longer than wide. This is due to the path of least resistance. The cortex slows
down the benign lesions and therefore they have to stretch out in the medulla and leave the cortex alone.
Benign do not have soft tissue mass associated with them.
Usually there is no pain in benign lesions.?
Most frequent complications of some of the benign lesions is fracture due to weakening of the bone.
Wednesday, September 24, 1997:
Review benign and aggressive features of tumors.
Table 7.5
Monostotic versus polyostotic bone disease
Monostotic Polyostotic
CONGENITAL Block vertebra Bone dysplasia
Polydactyly Achondroplasia
TRAUMATIC Localized injury Battered child
Severe injury
OSTEOLYTIC BEHAVIOR
Geographic Lesion
Solitary
Greater than 1 cm
Sharp margin
Motheaten lesion
Multiple
2-5 mm
ragged margins and coalescence
imperceptible transition
Permeative lesion
Multiple
Less than 1 mm
Imperceptible transition
OSTEOBLASTIC BEHAVIOR
Diffuse lesion
Homogeneously sclerotic ("ivory")
Obliterated corticomedullary junction
Localized lesion
Single or multiple
Irregular, hazy border
Asymmetrical
MIXED BEHAVIOR
Both osteolytic an osteoblastic features
TABLE 7.9
Radiologic Features of Lesion Matrix
Matrix Lesion
Fat Lipoma
Lucent
Calcification
Cartilage Enchondroma, chondrosarcoma
Lucent
Calcification
(stippled, floccules, arcs and rings)
Osseous Osteosarcoma, osteoma
Dens
Fibrous Fibrous
Hazy (ground glass)
Table 7.10
Radiologic Features of Periosteal Response
Pattern Lesion
Solid
Homogenous, single
Attached layer
Table 7.11
Normal Laboratory Values
Acid Phosphatase and Prostate Metastasis should be a red flag
Alkaline Phosphatase present when liver is compromised. Also an enzyme marker for osteoblastic bone
disease
Calcium: Tumor, destruction or endocrine disease
CBC:
ESR: sensitive but not specific
Serum reactive protein: think inflammation or tumor
Globulin: strongly associated with multiple myeloma
HLA B-27: Anklylosing spondylitis.
Second hour slide presentation:
Lateral skull
Need to do two laterals
Black X residing is Cella Turtica.
Don’t worry about cella turtica being too small. Worry about it getting too big or loosing part of its
margin
Double floor sign is when pituitary gets bigger. A portion will produce pressure erosion and a portion
of it will not
Over 16-19 mm is bad.
Lateral skull and different view (shows C1-3 and skull)
Double floor sign.
Measurement shows 17 x 21 mm
Lateral skull
Line from cella turtica through clivus to anterior portion of foramen magnum = Basilar Angle
Bone softening makes angle bigger = basilar invagination
Acquired, more risk here and likely progressive
Think of it as a rotten pumpkin that starts to sag. It settles and angles increase
Platybasia means flat base.
More likely to be congenital but does not present a problem
What could make this angle smaller? Didn’t catch the answer.
Brachycephalie is a short skull
Scaphocephaly = boat head. Coronal sutures stop growing limiting the vertical dimension.
Lateral Skull
Dot at posterior portion of the hard palate with a tangential line to base of occiput = Mcgregor’s line.
Mcgregor’s line is much more reproducible because the back of the foramen magnum is much harder
to find that the base of the occiput
Odontoid should not be more than 10 mm above the line. If it is then panic.
Could be basilar envagination.
Chamberlains line starts at the same spot but it goes to the back of the foramen magnum. This line is
higher. The odontoid is not as far above the line and the panic number is lower.
Lateral Cervical
Shows ADI (Atlanto Dental Interspace)
Measure being too small is usually not a problem. DJD may cause this and may not be problematic.
Measurement too big is of great concern. This means this area is unstable and the cord at this level is in
danger
Adults up to 3 mm
Children up to 5 mm
What can make the ADI Larger?
RH (rheumatoid arthritis) can do this by eating away the bone or the transverse ligament or both.
It will leave behind the posterior arch
Trauma can make the ADI larger.
Down's Syndrome?
Lateral cervical spine stress view with weight of head forward
ADI turned to 5 mm. We need to worry about integrity of cord at this point.
Unstable patient needs surgical stabilization because a small trauma could kill them.
Lateral cervical extension view with Closed ADI
Lateral cervical flexion with ADI open
Lateral cervical (Neutral)
George’s line or posterior body line (same thing)
Make it a dotted line to ignore the degenerative places at the joints.
C1 is not involved in this line because C1 does not have a body
This line should be smooth. We are looking for abrupt alterations in line
Could be as simple as muscle strain or sprain or as bad a ligamentous damage.
Lateral cervical (Neutral)
Spinal laminar line
All seven vertebras are involved in this line.
Cases: We will have something like this on the exam.
ADI normal but posterior tubercle is anterior = broken dens
ADI normal, spinal laminar disrupted with posterior arch posterior – OS Odontoidion. May be stable or
unstable
ADI big = transverse ligament compromised.
Monday, September 29, 1997:
Most common complications of joint fusion are DJD to segments above and below.
Most serious complication of acquired fusion is increased ADI.
Some ways to make ADI big is transverse ligament compromise in abrupt trauma or small repeated
traumas.
Must do flexion and extension views to assure there is no increased ADI.
Os-Odontoidian: congenital unstable dens. May show up as an anterior atlas with a bad looking
posterior cervical (spinal laminar junction line).
Plain film is absolutely not predictable for central canal stenosis (Sagital Dimension of the cervical
spinal canal: he will not make us remember theses dimensions)
Pus, blood or cells make pre-vertebral space bigger.
Tuesday, September 30, 1997:

Prevertebral Soft Tissue: (lateral view) (Page 155)
What is the normal measurement above C5 = 5
What is the normal measurement below C5 = 20
Tracheal air shadow has been enlarged. What is Quick and easy differential? Pus, blood, cells and
sometimes combination of that.
Looking at an example (radiograph) we see gas and water densities. This is probably pus.
This is up and down the neck so much it is probably an infection, a primary soft tissue infection, not
involving the bone just yet.
To call a convexity a scoliosis it must be more than 12o. In the past, it was 20o, the rate of scoliosis is going
to increase because the standard just went down since the scale has changed.

Cobb Method Of Scoliosis Evaluation:
This is the one used most often.
This is more reliable, more reproducible.
Risser-Ferguson and Cobb cannot even be compared, they are totally different languages.
 Risser-Ferguson Method of Scoliosis Evaluation:
In the past, it was only for curves over 40 o.
Yochum says we should know of this method but we should not use it.
(Not very good interexaminer reliability. )
Look at these two methods in the book. (Page 156)
Sometimes you must re-measure films to see change
You must re-use the same landmarks to get the same results.


Thoracic Kyphosis:
Start with a moderate Kyphosis and goes up as we age.
There are age appropriate averages with kyphosis
Thoracic Cage Dimension:
Normal for men is 13 cm and women are 11 cm.
If there is not enough room, the heart gets shifted
Pectus excavatum: depression in the chest.
We expect physiologic murmurs because we change the hemodynamics
Valvular abnormalities cause pathologic murmurs.
In the AP view, you can see the heart has been shifted to the left.
Lumbar Intervertebral Disk Angles:
Compare to known values
Lumbar Lordosis:
Sacral Base Angle: 55o

Hadley’ "S" Curve: (page 164)
Can be seen in the oblique view and AP-Film.
1. Start at transverse process and follow cortical lines to Pars into lamina.
2. Once you get to articular surface3. move to anterior portion if the superior articulation facet of the joint below
The smoother the transition, the more normal the joint articulation is.
This can even be used on recumbent patient.
Looks for Rostrocaudal migration. Facet imprecation or facet override are synonymous terms

Ferguson’s Gravity Line: Lumber Gravity Line (page 163)

Ullmann’s Line: (page 167)
Use this assessment to see if L5 is behind or touching the line
If L5 is in front of the line, we have an anterior listhesis.
Now determine if is degenerative or trauma (Pars fracture)

Myerding’s Grading Method in Spondylolisthesis: (page 167)
Reference vertebra is divided into 4 quadrants.
If George’s line intersected in 1st quadrant it was a Myerding Grade 1
(Kuhn thinks we should use the percentage measurement. The grade could be the same with the Myerding
system but since there are only four grades, there could be increased displacement while the grade is still
the same.)

Unterpediculate Distance: (page 168)
Check for stenosis

Eisenstein’s Method for Sagittal Canal Measurement:
Recognize this measurement but documentation is only done with advanced imaging
LOWER EXTREMITY

Klein’s Line: (page 179)
Don’t want to see too much head above the line or it means femoral neck fracture.

Slipped Femoral Capital Epiphysis: this is seen in children. This allows the femur head to slide
inferior and medial.
Sometimes referred to trans-cervical fracture because the head is known as the cervical portion of the
bone.

Hip Joint Space Width: (page 173)
1. Superior portion
2. Axial portion
3. Medial most portion: near Kolars tear drop
Degenerative arthritis produces focal joint space loss or asymmetrical joint space loss.
Pan-compartmental joint space narrowing is when the joint space loss is uniform. This is an example of
inflammatory arthrotides. An example is RA.


Symphysis Pubis Width: (page 174)
Gets wider with trauma and/or childbirth
Shenton’s line: (page 177)
The smoother and more regular the line is the more normal the relationship
"Very Useful"



Measurements of Protusio Acetabuli: Acetabular protrusion (page 177)
Femoral Neck Angle: (page 178)
Eyeball it and make your line
Normal range is 120o to 130o
Less than 120o patient is demonstrating coxavera (decreased angle) (make an R shape)
Greater than 130o patient is demonstrating coxavulga (increased angle) (make a V Shape)
These are relatively important numbers to remember
Dysplasia makes angle smaller or larger
Fracture typically makes angle smaller
Kohler’s Teardrop Distance: (page 172)
Teardrop is radiographic distortion phenomenon (tear drop shape)
Cases of DJD the femur head will not get closer to the line
RH is example where femur head can move toward the line.
If spaces get narrow we have inflammatory Arthritide
If space gets bigger, it is accute inflammatory Arthritide in the early part because of swelling. Quickly
the inflammatory process will ravage bone surface and make space narrow.
3. Infection can make space bigger if infection gets implanted inside joint capsule.
4. With trauma, we can have intracapsular bleeding which can make space bigger.
1.
2.
Waldenstrog observed a teardrop measure bigger than 11mm is abnormal. A difference in 2mm or
greater between left and right is abnormal. Now we have to decide which one of the measurements is
abnormal.
UPPER EXTREMITY:

Glenohumeral joint measurements: (page 184)
Take three measurements and divide by three

AcromioHumeral Joint Space: (page 185)
Bigger, subluxations and dislocations
Smaller is rotator cuff tear. This is because of unopposed action of the deltoid.
Know that normal range is 7 – 11 mm for a normal size person.

Acromioclavicular Joint Space: (page 185)
Measure superior and inferior spaces and average the numbers. Compare to normal charts
Smaller space = DJD
Bigger space = ligamentous damage or resorption of the clavicle. (hyperparathyroidism, RH,
backpackers syndrome)
Wednesday, October 01, 1997:
Continue with Acromioclavicular Joint Space from yesterday.
Must average Glenohumeral and Acromioclavicular because the joint has such mobility and is unstable.


Guylilua lines: (Lou Guylilua) NOT IN BOOK
Look for symmetry and smoothness of the contours
Draw smooth line across proximal row of carpals at the ulna and radius
Draw another line at distal portion of proximal row
Draw another line at the proximal portion of the distal row and ignore the pisiform
Look for dislocation, Ischemic necrosis
Boehler’s angle: (page 183)
Useful in chiropractors practice with MVA when foot gets crushed on firewall
Work related injury from falling or jumping from high places.
Calcaneal fractures will cause a decrease in Boehler’s angel.
He went over the landmarks in class.
Compare bilaterally.
4 Trays of normal variants:
Submental vertex view of the skull: Part of the sinus series
Adolescent’s skulls are not pneumatized.
Hypoplastic sinus. Agenesis. The sinus in this film has not developed.
History of opacification secondary to transilumination. Could be sinusitis, osteoma, or Hypoplastic
frontal sinus.
AP Open Mouth:
Bad view with teeth hanging down
Need to raise the chin so the teeth are in line with the EOP
Want to see all four joints, lateral mass and odontoid.
Later Cervical: (flexion view)
Picture of the same patient as the bad AP open mouth.
Compare with mental image of normal, this film is abnormal.
There is too much space between C1 posterior tubercle and C2 spinous process. Anterior tubercle size is
too big.
It looks like there is a hole posterior to C1
The hole is an abnormal foramen within the diploid space of the skull
OccipitoAtlantal Fusion is DDx
Plain tomography or complex motion tomography: (same patient as above)
Blur out everything else around so we can see the OccipitoAtlantal Fusion better.
Tomography has a great role in upper cervical trauma.
Wednesday, October 01, 1997:
Second Hour:
Two different images of the skull with CT
Cortical bone is white. This means there is lots of mobile hydrogen.
Black it is MR (cortical bone)
White it is CT (cortical bone)
He can ask what study this is at any time on any test and differentiate between CT & MR.
The cortex on this view is very thick. Good Example of Hyperostosis Internus. (page 254)
There is a lot of hypertrophy of bone on the inside but the skull on the outside is very smooth.
This is in the back as well as the front
Teeth Up AP open Mouth:
Tomography of the same Teeth Up AP Open Mouth:
Anomalous foramen facing the front
Craniovertebral anomaly. Craniovertebral synostosis or Craniovertebral fusion.
Same Patient with a Lateral Projection: (page 198)
Big space with no organized posterior tubercle
Another example of Craniovertebral synostosis or occipitalization of C1
This condition is congenital. The only way this could happen otherwise is cervical fusion or infection.
Usually there is no complaints or huge symptoms in patient. We need to worry about instability or a
possible VBAI.
Same patient with oblique view:
Didn’t say anything about this one because C1/occiput was projected on ceiling.
Flexion View on different patient with same problem
Anomalous IVF
Disrelationship between size of face and skull (young child)
Altered cranial-facial ratio.
Should see sutures on this film but we do not see any.
This kids face will not grow any more but his face may.
Craniocervical junction: we see platybasia with basilar invagination because of skulls softening process.
Lateral view of upper cervical
Posterior arch of C1 is missing
Hole is spinous of C2
C2 is extremely tall. We are looking at some version of atlantioaxial fusion
AP Open Mouth
Almost unrecognizable with this fusion.
AP Open Mouth with Spinabifida Occulta
Evidence is lack of tubercle between posterior tubercles.
Lateral view of skull:
Internal acoustic meatus of other side
Craniovertebral junction
Cella turcica
Mastoid air cells
The thing that really catches our eye is the hole in the superior part of skull.
Infection can put a hole in the bone. Typically, there is some soft tissue involvement.
Tumor can put a hole in the bone.
AP skull of same person:
There are a series of holes in this view. One on either side of the Sagittal section and one through the
sphenoid sinus
What could make three symmetrical holes in the skull. This is congenital, it just didn’t fill in while
developing.
These are called parietal foramen.
There are no symptoms in this person, the holes are clinically insignificant.
AP Open mouth:
Can see two round densities on the dens. Very hard to see.
Ununited ossification of the anterior tubercle
No clinical significance to this lesion, found it by surprise or accident
Lateral cervical on same person:
Bipartite anterior tubercle on atlas.
This is not a trauma; there is no mechanism.
This is a smooth and well-contoured line and there are no complaints.
This is an ununited ossification of the anterior tubercle.
Later Cervical of C1, Occiput:
Craniovertebral junction, the anterior tubercle is hazy and the posterior tubercle is not there at all.
Spinabifida Occulta in C1, no clinical significance is associated with this
The posterior arches are superimposed over each other to almost look like a posterior tubercle.
Made up View of different patient: (page 204)
Spinabifida Occulta
No anterior or posterior tubercle
Spondyloschisis (page 204)
This person could be at greater risk for atlas fracture.
Lateral upper cervical film:
Major anterior tubercle of C1
No spinallaminar line on posterior tubercle.
This indicates Spinabifida Occulta
Lateral Cervical
Arcuate Foramen
In the past they were a major problem, now we just treat them a little different to reduce the amount of
stress on the vessel passing through there.
Lateral Cervical:
See huge odontoid process.
Cannot tell if it is Os-terminal or anterior tubercle in the wrong spot.
CT of same person:
Odontoid and anterior tubercle are fused together in this view
There is no ADI
MR of same person:
Can see huge odontoid
Form of atlantioaxial fusion.
Monday, October 06, 1997:
Look at slides of anomalies and normal variation.
spina bifida occulta
Lateral X-Ray can see George’s line and spinal laminar lines are not lined up.
Unstable Os Odontoid.
AP open mouth with odontoid missing.
Patterns of intersegmental fusion:
Somite level may never separate.
Rudimentary disks and atypical foramen may be produced.
When you see a congenital anomaly, there may be another
Always think of anomalies as acquired until you know for sure that they are not.
He has never seen vertebral artery calcification on regular plain film X-Ray. He has only seen it on CT.
Juvenile chronic arthritis destroys the cortical bone.
Congenital is a benign history
Cannot be a fracture if there is a sclerotic rim around it. Bone cannot react that fast. It has been there since
the ossification centers formed. This is unossified unification process.
Developmental cleft: these are unusual.
You should see disruptions in cortex or angular cortex
It is not a fracture because the end plates of adjacent vertebrae are roughly parallel.
This is not a fracture.
Pedicle is not there.
Hypoplastic pedicle. This is just a pedicle that is smaller.
Most common cause of missing pedicle is metastasis.
Read ahead on Limbus Vertebrae.
Tuesday, October 07, 1997:
Lateral cervical in extension with ADI at 2mm
Lateral cervical in flexion with ADI at 3.5mm
Have translation because of weakened transverse ligament.
AP Open mouth with spinous of C2 way off to the side with a good film, head is not rotated.
Neutral Lateral cervical. C4,C5,C6 there is not a lot of disk space.
Surgeon stabilized this patient with a fibular strut to the anterior portion of the bodies
AP lower cervical with cylinder anteriorly. This is another view of the fibular strut.
NEW TRAY OF SLIDES: (normal variants)
AP Lower Cervical with a normal variant. This is a un-united ossification center because the edges are
smooth and uncorticated. A fracture would have cortex on the outer portion and the fracture would be
irregular and lucid.
AP upper thoracic & lower cervicals:
TP’s are directed down and out for lower cervicals
TP’s in thoracics should go up and out
This is an example of a cervical rib. This is probably not a cause of TOS. He really had to expose this
one with bright light because it was not easily seen on regular plain film.
AP Thoracic
See a rib that is going superior
Sprangholts syndrome or deformity
Ulnovertebral bone
Look at scapula from the side and you can see how high it is. This is a neutral lateral lower cervical.
AP thoracic/cervical:
G
AP full spine looking at cervical thoracic junction
Have un-corticated ossicle at end of a transverse process. Hard to tell if it is head of rib or an uncorticated process of the transverse process.
AP in the thoracics. T5 is labeled along with 9o later flexion malposition:
There is a definite slant in the body of T5.
This is a hemivertebra. This happened when somites went through vertical separation and part of the
bone went with T4 above.
AP thoracic
See spinabifica occulta
Intersegmental fusion involving the upper thoracics.
End plates don’ look normal above every pedicle, this means it is fused and it is congenital.
Even arthrotides don’t deform bone in this manner and person did not have any arthrotide symptoms so
It can be ruled out with history and observation.
AP Thoracic
Have three pedicles on one vertebra.
AP thoracic (very dark) BUTTERFLY (Page 225 & 226)
Look at articular construction.
It looks like there is a peak or triangles for articular surfaces
This is called the butterfly vertebrae.
Primary ossification centers did not make the body fill out. This is a good example of failure separation
of primary ossification centers.
AP thoracic/cervical
This is a huge well-developed cervical rib on one side and a hypertrophied transverse process on the
other side.
AP thoracic/cervical
Pair of unossified cortical centers at C7/T1
AP Thoracic (page 241)
Intrathoracic rib coursing through the space of the lung.
AP thoracic
Bifurcated rib with no clinical significance
It probably limits range of motion
AP lumbar
T12 has no spinous process.
With close up you can see it better with the vertical line instead of spinous process
Lumbar Lateral
Limbus vertebra has a "beak" coming down
Limbus is through the end plate (look this up)
Lateral thoracic
Straight back syndrome is associated with benign mechanical murmurs.
Statistical relationship with valvular cardiac anomaly.
Second Hour:
AP thoraco/lumbar junction
Small stumpy rib on one side and a longer one on the other side.
Lateral thoracic
Herrington rods in the spine
AP lumbar/thoracic
Benign calcification of costal cartilage.
Physiologic calcification
Pretty bad curve to the right.
AP thoracic
Pedicle that s smaller on one side than the other
AP thoracic
Heart shadow is way to the left of the patient and there is none sticking out to the patients right.
The ribs rise in the back and take a very steep dive anteriorly
With the lateral view, you can see straight back syndrome. The sternum has moved back and moved the
heart over.
The sternum has deflected inward
This is termed Pectus Excavatum
Lateral thoracic
See reverse thoracic or a lordodic thoracic curve.
Lateral Lumbar:
Limbus vertebra
Result of migration from nucleus pulposus while spine is skeletally immature and it goes through the
growth plate
Growth ring is an effective barrier
LOOK UP LIMBUS RING
Lumbosacral joint:
No TP on L5
Lateral Lumbar
Large chunk of bone went posterior with a decreased sacral base angle
AP view shows a very flat sacral base
L4/L5
Tropism: cannot see on plain film. Need CT or MR to see tropism.
Tropism is when facets do not line up, one is vertical and one is horizontal.
AP lumbar
Missing a pedicle. #1 cause is metastasis
Contralateral sclerosis is congenital sclerosis or agenesis or hypoplasia
Worry when you have missing pedicle and a normal contralateral pedicle. This means it was taken
away too quickly for the other side to adapt to the change.
Wednesday, October 08, 1997:
Look at variants that are more normal and congenital anomalies.
2-3 block with anomalous foramen
Joint scar is white line where disk space is supposed to be.
Premature degenerative changes with blocked vertebra in the segment below when congenital.
Most serious complication is ADI instability with blocked vertebrae.
People with acquired blocked vertebra usually have DJD before they get fused.
Surgeons never take the time to do an anterior and posterior fusion so if we see this it is most likely
congenital.
Wasp-waist dimensions PAGE 213 CONGENITAL BLOCKED VERTEBRAE
Congenital fusion may also fuse the spinous together so there will be 7 bodies and 6 spinouses.
Oblique view showing anomalous IVF.
Un-united transverse process.
Discitis: crappy job of fusing two vertebrae. Infections work on both sides of the joint so you can see it
is probably not cancer because both joint surfaces look crappy.
New Slide Tray:
Limbus vertebra are not rare:
Knife clasp deformity is combination of elongted spinous process of L5 and spinabifida of sacrum
(PAGE 239)
Teacup shaped vertebra due to a Schmorals node placed anteriorly years ago.
Oppenheimers nodules.
Lumbosacral transitional segments
Ia: one tp is bigger than 19 mm in vertical dimension
Ib: both tp’s bigger than 19 mm
IIa: accessory joint
IIb: pair of accessory joints
IIIa: a bar of bone with normal contralateral TP
IIIb: a pair of bar of bone. Some people use sacralization but he does not like that term
IV: an accessory joint and a fused side.
It would be impossible for disk damage to occur in IIIa, IIIb and IV because of the bone bar and there is
no movement at this level and no ability for damage.
Can have disk damage at Ia and Ib but it is not any different than a normal vertebrae.
IIa, IIb have over an 80% herniation rate
Missed Class from October 9, 1997 to October 17, 1997:
Monday, October 20, 1997:
Dysplasia’s are not that important.
Can mimmic osteoblastic diseases occasionally
Dysplasia is last stuff for written
Arthritis is for next written exam but it is on this slide exam. We have to study arthritis twice because
we need to be experts in this.
Today’s x-rays be able to describe how they vary from normal but we do not have to name.
Dr Brahe lecture:
Get Notes From Liz for Dr. Brahes lectures:
Engelmanns: diaphysial dysplasia. Medulla is sidened in central portion
These people don’t get anemia even though the medulla is messed with. This is unusual.
More common in males than females.
Complain of extremity pain and muscle weakness
Pyknodysostosis:
Lateral skull view
Very short stature with multiple fractures
Fragile bones with increased bone density.
Everything is sclerotic. It is not strong bone, it is very weak bone
Get transverse pathological fractures.
AP skull view
Humerus
Cortex is thick and denser than it usually is.
Hands are sclerotic and distal epiphysis look flattened and small instead of their normal elongated shape.
Dr. Kuhn Lecture
He went over which Skeletal Dysplasias we need to know for the exam I. Page 585 in book.
Know abnormalities that can be confused with something else
Flabella: accessory ossicle around the knee is easily confused
Agenisis of transverse ligament or dense
Report writing, levels of liability, major modalities, he will have a little bit of everything