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Orthopedics10-21-02

Bakody’s Maneuver – this will relieve the pain from nerve root compression – hand on top of head.

TOS

Reverse Bakody Maneuver – hand on top of the head will increase the pain due to interscalene compression – so elbow is at 90 degrees but hand is just hanging there. Indicates TOS.

Allan Maneuver – palpate radial pulse, patient rotates head to opposite side, reproduces chief complaint, decrease in pulse.

Adson’s Test – palpate pulse, patient faces toward side of test slightly extended and then the patient takes a deep breath. Arm is at 45 to the body, interscalene problem, middle scalene.

A modified Adson’s – patient looks to the other side.

Can involve ribs, cervical ribs, etc. so don’t get locked into this.

Costoclavicular Maneuver – bilaterally done at the same time, patient flexes neck forward and Dr. (stands behind) monitors pulse, brings the scapula back (winging) – if complaint is reproduced on one side, and pulse is reduced in that side, think TOS. Made worse with shoulder bags, book bags, seat belts, etc.

Halstead Maneuver – palpate radial pulse, traction arm downward, patient puts neck into cervical extension (some texts say deep inspiration too.)

Traction test – for TOS or NR irritation – traction arm, similar to straight leg raise.

Roos test – aka AER – Abduction External Rotation – patient pumps hands for up to 3 minutes (usually happens fairly quickly – arms up at 90 degrees, fingers toward ceiling.

Shoulder compression – corocoid process, anterior aspect of the scapula – follow clavicle – hypothenar contact pushes straight to the floor for complaint reproduction.

Wright’s test – hyperabduction of arm – 180 degrees – note the angle of complaint reproduction and pulse reduction.

Allen’s Test – not a TOS test – a peripheral vascular test – informatio about the rofusion of the upper extremity. Dr. holds both the radial and the ulnar artery, raises pt. arm above their head and pumps fist, bring arm down and let pressure off the ulnar artery, raise arm again, pump again, bring arm down and let go of the radial artery. Watch for differences bilaterally. Refill should be within 5-11 seconds (Evans says 5 seconds) Anything that has a vasoconstrictive type of affect can affect the test.

Subclavian artery compression – review of anatomy – cervical rib will compress it. Sometimes there are anomolies in the attachment of the scalenes that can cause problems too (middle attaches in front of the anterior, etc.) so if they get injured it can aggravate the situation.

Four categories – counting cervical rib – of TOS KNOW THESE

Scapulaohumeral rhythm – apex of scapular will rotate 60 degrees, 120 degrees of glenohumeral joint – in abdcuction. (30 from the SC and 30 from AC joints)

“Linda’s Notes” by Linda Hite – These notes are not guaranteed to be complete or without errors – they are meant to be a supplement to help you study.


Apley’s Test – this is an active clearing test – for an asymtopatic patient – ask patient to reach behind head and touch back as low down on the spine as possible. (Look for limitations in range and pain) – Apley’s scratch inferior comes from the waist up to the middle of the back. Mark the level and put in your notes – compare as treatment proceeds. Pain in shoulder reproduced look at supraspinatus.

Orthopedics10-23-02

Rheumatoid arthritis – inflammation of the joint (arthritis) – however this one is systemic – presents mostly in synovial joints, often presents bilaterally, increased in females in 30-50 age group (?) Page 157 – Ceba Book (??)

Progressive stages in joint pathology – potential progression – not everyone will go through all these stagesAcute inflammation of synovial membrane (synovitis) and beginning proliferative changes.Periarticular osteoporosis. Pannus – villi (fingerlike projection) proliferate into joint (synovioal tissue) with infiltration of lymphoid cells – soft tissue. (SEE BOOK) – it’s destructive and erodes the normal joint tissue.Subsidence of inflammation, fibrous ankylosisBony ankylosis; advanced osteoporosis

HVLA is contraindicated – in stage 2 the joint is hypermobile, stage 4 is hypomobile – other techniques are OK.

C1/C2 is also a joint that this happens to in addition to the knee. Always check joint for stability before adjusting. Reiters disease and Down’s syndrome are also at risk patients. Inflammatory arthritis needs to be checked before doing it.

Stills disease – Junior Rheumatoid arthritis is different – less common, very debilitating – not on the test.

Rheumatoid arthritis – etiopathic – some factors are genetic, autoimmune component, reaction to previous illness or vaccination.

ADI – measurement from back of atlas to front of odontoid.

Once they are at stage 3 or 4 – you can’t adjust that area HVLA – you can do all sorts of soft tissue/energy work but nothing hard.

Look at the pictures in the book regarding this disease – very interesting. In RA the tendons end up not being attached so the body part can’t move anymore.

PIP, MCP, C1/C2 and wrist joints are the ones that are most affected. Ulnar deviation, swan-neck defomity of many fingers, boutonneire deformity of thumbs (hyperextension at the PIP and flexion at the MCP) and subcutaneous nodules.********Board questions – probably her questions too.

Pannus formation causes the joint pain because the synovial tissue is very pain sensitive.



Typical case on boards – they give you a case history that you have to put totogether clinical findings.

Tendons rupture because the tendons are in synovial fluid and tissue.

This can also affect the lower extremities – feet, knees, hips (flexure contracture) – the body’s attempt to stabilize a hypermobile area.

Subcutaneous nodules around joint – synovial tissue lines the bursa so we can get the nodules due to the inflammation of the synovial tissue of the bursa.

Can appear on a chest film but is not diagnostic without a biopsy.

Synovial cysts – presentation behind the knee it is called a Baker’s Cyst – can be due to trauma or etiopathic. Fluid filled sac that can get pretty big. Can happen in the elbow – no special name. At the wrist it is called a ganglionic cyst – synovitis in the tendons (tendon sheaths) – this DOES NOT mean the patient has RA but if the patient has RA they can develop synovial cysts.

Treatment options – next time. In the erosive, destructive, hypermobile stage HVLA is contraindicated.

Orthopedics10-25-02

Third party billing, self-help stuff, lots more in the library than just histology and gross anatomy stuff. Check it out.

Rheumatoid Arthritis and Osteoarthiritis – handout in library folderGeographic Distribution, Family history, Past History,

Age at onset – RA over 80% between 20-50, OA rare before 40 Mode of onset – OA well nourished, frequently obese, not anemic, no fever, no leukocytosisGeneral condition – RA, the PIP is usually affected. OA usually weight-bearing joints, spine, hips, knees; distal joints of fingers (DIP – Heberden’s nodes) Involvement of joints – RA muscular atrophy, cutaneous changes, subcutaneous nodules.

THIS IS NOT A COMPLETE LIST – SEE THE LIBRARY FOLDER

Partly it is the joint that is being destroyed and partly it is the soft tissue.

RA – lots of “catch” phrases – pay attention to these as we go through the class. The Boards love these kinds of things.

DJD or OA is aggravated by barometric pressure dropped (also old fracture sites). More characteristic in DJD than RA. (Internal vs. external pressure). Lupus is systemic but has an arthritic component also.

DJD – aka osteoarthritis, or osteoarthrosis – “itis” = inflammation (bone-joint inflammation), “osis” = morbid condition of – implies a loss of function (bone-joint loss of function). OA inflammation is somewhat secondary.

Progression – change in instantaneous axis of rotation. Body attempts to stabilize the bone by developing osteophytes. This is a specific sign of OA. It is a boney change, joint space narrowing on x-rays is also a sign. As the cartilage becomes smaller (worn, dehydrated), the bones get closer and the ligaments get slack (which increases the instability of the joint).



Initial stages – increased mobility, decreased in stability – as the body makes it more stabile it becomes less mobile. This isn’t destruction of the joint like RA. This is histologic changes in the cartilage, structure follows function.

From the book1. Early degenerative changes with surface fraying of articular cartilages. 2. Further erosion of cartilages, pitting and clef formation. Hypertropic changes of bone at joint margins.Cartilages almost completely destroyed and joint space narrowed. Subchondral bone irregular and eburnated; spur formation at margins. Fibrosis of joint capsule.

Trauma, immobilization can begin this process.

Geodes in the bone also happen – a subchondral cyst formation.

Increased density in the bone. Weight bearing stress is essential for bone strength, motion is necessary for joint strength.

Carbonation (in soda) in growing children is not good – can set the stage for osteopenia. Orthopedics10-28-02

ROM for shoulder – review today and do in lab tomorrow – bring goniometers

Arm in neutral position – abduction without internal rotation – should be about 150. Painful range of active motion won’t tell us what tissue this is. Passive and resisted have to be assessed. Ligaments involved if pain in ???? – in this case it would be the joint capsule.

Adduction – arm across the body – sometimes this is impossible – large abdomen, large breast tissue – has to have some flexion to get it across the trunk.

Flexion – goniometer at the side – axis of humeral rotation – up over head – usually close to 180.

Extension – patient prone – arm brought up behind back – isolates motion of glenohumeral joint – takes out the thoracic involvement.

External and internal rotation also.

TESTS

Dawbarn’s test – involvement of bursa – tenderness in shoulder – palpate under the acromion process anterior to posterior. Actively abducts shoulder, decrease = bursa involvement.

Ludington’s Test – palpate the contour of the biceps muscle, patient puts hands on head which contracts the biceps muscle.

Supraspinatus Press Test – patient abducts shoulders to 90 degrees, resist looking for weakness and/or pain, then they flex shoulders slightly rotate so thumbs are down and retest. Abducts the first 20-30 degrees. To grade the supraspinatus, arms should be lower.

Muscles Testing by Kendall and McCleary. Good book to get.

Codman’s Sign – aka Codman’s droparm. Dr. passively abducts patients arm above 90 degrees, Dr lets go and ask the patient to hold it up. Checks the stability in the joint to catch the arm.



Deltoid is the functionally active muscle in this range but the supraspinatus has to be active to help here.

Impingement Sign – patients arm is passively taken through flexion looking for pain reproduction under the acromion process – affects long head of the biceps or the supraspinatus tendon. Also can be done in abduction.

Abbott Saunders - Shoulder in internal rotation – palpating the long head tendon. Abduct the shoulder, at the top externally rotate and bring it back down

Transverse humeral ligament test – holds biceps tendon in place – as the muscle contracts, it moves in the tendonous sheaths. Patient is seated, palpate on humerus, passively internal rotate and then externally rotate – looking for snapping or clicking. Noise could be coming from many joints in the area – helps determine which one. Elongation of the humeral ligament allows the biceps tendon to be sloppy. Can involve the biceps muscle.

Speeds Test – palpate of long head tendon, patient flexes shoulder while they supinate, resisted against the Dr. Looking for reproduction of the chief complaint. Bicepital tendonitis.

Yergason’s Test – elbow flexion with supination, supinate against the Dr.s resistance (like arm wrestling), and Dr. tries to extend elbow. Resisted – tests the functional component of the muscle. Yerguson’s reproduced pain at….. – describe where the pain was.

SHOULDER DISLOCATION – joint is dysfunctional and painful, trauma induced, usually not within our scope of practice. Potential vascular and neurological complications. The labrum of the joint can become invaginated and this causes permanent biomechanical changes.

These tests may be on the boards – that’s why we go over them.

Bryant’s Sign – patient in neutral position, axillary fold will be lower on the dislocated side.

Hamilton’s Test – a straight edge can connect the lateral epicondyle to the acromion, normally the humerus is in the way.

Calloway’s – measure the girth from the axillary fold to the top of the humerus (the acromion process) – if it is dislocated, the measurement will be greater.

Circumferential measures – increased due to swelling, tumor, development of tissue; decreases due to atrophy.

Dugas Test – reach across to the contralateral shoulder and bring elbow down to chest – if dislocated you can’t accomplish the elbow thing, and maybe not even the contralateral shoulder contact.

Mazion Shoulder Maneuver – evidence of pain – start with hand on contralateral shoulder, raise elbow to chest level and then to eye level, keeping the hand on the contralateral shoulder.

Apprehension Test – previous history of dislocation, has instability – manually stress the joint, facing the patient look for signs of apprehension. The can also recruit additional muscles to keep it from happening. Abduct elbow to 90 degrees, Dr. hand on shoulder and forearm goes backwards slightly – look for end fell – DON’T FORCE THIS.

Done anterior and posterior test – anterior is done from the front with patient seated, posterior is done with patient supine, Dr. hand on posterior of head of humerus, arm across chest to contralateral shoulder, apply pressure to the posterior.



Orthopedics10-30-02

DJD – OsteoarthritisDeep achy nauseating type of painJoint space decreased due to loss of cartilageOsteophytes form (bone growth)Pain is not correlated to the degree of the degeneration – function will change in correlation.

She went through the differences between OA and RA – she went too fast for me to get it down.

Don’t rely strictly on the x-ray for diagnosis.

RA – PIP is affected (preferred)

OA – Heberden’s nodes – affects DIP, hypertrophy of ligaments and osteophyte formation. PIP can also be involved – this is Bouchards Nodes. Carpal-Metacarpal joint is also a problem.

DJD can affect weight bearing joints – head of the femur and the acetabulum. Hip joint is a major weight-bearing joint. Changes in posture and gait will result.

Changes in the spine – bony hypertrophy of facet joints and the vertebral body, creates a space-occupying lesion, will appear in the x-ray as white, disc shrinks in vertical dimension, IVF gets smaller (lateral recess stenosis results in possible NR compression or congestion of the vascular and lymphatic chains). Central stenosis can happen on the posterior portion of the vertebral body causing problems in the cord – like cauda equina syndrome.

Decreased joint spaced, osteophyte formation (bony hypertrophy), subchondral cyst formation, bony sclerosis.

SCOLEOSIS

Nonsctructural scoliosis – can be straightened out right awayPostural Scoliosis – usually noted in later years of first decade. Curves are always slight

and disappear on lying down.Compensatory Scoliosis – usually a result of leg length discrepancy. Pelvis dips down on

the short side.

Transient Structural Scoliosis- can be straightened out over timeSciatic Scoliosis – not true scoliosis; an irritative form caused by pressure on nerve roots

from a herniated disc (antalgia)Hysterical Scoliosis – rare, usually requires psychiatric treatmentInflammatory Scoliosis – seen with perinephric abcess or similar infection

Structural ScoliosisIdiopathic (Genetic) Scoliosis – about 70% of all cases of scoliosis. Classified by age of

onset (age of detection according to Dr. B)Infantile – before 3 years of ageJuvenile – age 3 to onset of puberty, usually age 10Adolescent – from age 10 until maturity MOST COMMONCongenital Scoliosis – probably not geneticVertebralOpen – with posterior spinal defectWith neurologic deficit (e.g. myelomeningocele)Without neurologic deficit (e.g. spina bifida occulta)Closed – no posterior element defect



with neurologic deficit (e.g. diastematomyelia with spina bifida)without neurologic deficit (e.g. hemivertebra, unilateral unsegmented bar)2. Extravertebral (e.g. congenital rib fusions)

Neuromuscular Scoliosis - had something to do with café-au-lait spots – WAS IMPORTANTMesenchymal DisordersCongenital (e.g. Marfan’s syndrome, Morquio’s disease, amyoplasia congenita, various types of dwarfismAcquired (e.g. rheumatoid arthritis, Still’s disease)Others (e.g. Scheuermann’s disease, osteogenesis imperfecta)TraumaVertebral????

THIS IS SUPPOSED TO BE IN THE LIBRARY – get a copy for reference – I didn’t get it all down.

TERMINOLOGY – any lateral deviation, 10 degrees or more, apex of curve names it, includes direction (L or R) and location (thoracic or thoracolumbar). Can be a “double-major” – two curves of equal magnitude.

R thoracic curve is THE MOST COMMON type.

Scottie dog information – if you can see a Scottie Dog on AP films, the patient has a bad curve (45 degrees).

Paralytic Scoliosis (scoliosis results from paralytic condition) – heart was resisting sideways on the diaphragm, blood ejected sideways – the reason people go to surgery to correct scoliosis is because the heart problems that can result. This can also happen without it being a paralytic scoliosis.

Clinically – Postural analysis, T1 to Sacrum for balance. The righting reflex will want to get the head back over the sacrum so the body will want to continue to increase the curve to get the head back to center. We can stop the progress and reverse the curve.

A scoliometer measures the hump in Adams position – has a plumb bubble in.Orthopedics 11-01-02

At 10 years or later is the onset of Juvenile Scoliosis – by 7th grade a female may be her adult height – most boys wait until later. (High school or college) This (for females) is about the start of menarche.

Never put lemon in your tea in a styrofoam cup (it will “etch” the cup). Type I plastics simulate hormones (estrogen). Cats can eat chocolate but will kill dogs, dogs can take aspirin but will kill cats. Non-microwave plastic can “melt” into the food and you end up eating the plastic (vice versa – spaghetti stains in plastic – don’t use it – the best to use is stoneware, ceramic, non-lead based covering).

ADHD, ADD and other behavioral problems could possibly be due to lead poisoning, formaldehyde, etc. It is totally within our scope of practice to order a blood test for stuff like this. It is called “off-gassing” – comes from particle board, synthetic fibers in rugs, pads, etc.

There is an epidemic of ADD/ADHD – it is a functional problem in the minds of our children which will change the way we function as a society – 6-20% are diagnosable with this. Boys are more likely to be “classified” with this. Ritalin – very similar to cocaine – being pushed on the playgrounds as a “fun” drug. Drug companies are trying to make a time-released formula so



there is better adult control of the drug. Dietary influences in ADHD – studies are not solid at this point – “sugar doesn’t increase hyperactivity, it just impairs concentration” When a child gets diagnosed with ADHD, the school gets money!!!!!!!!!!!!!

Fpinegold diet – Yellow 6 and Red 4 – salicilates (aspirin) but it is in other things like toothpaste and shampoo – also in grapes, cherries, apricots – can trigger the reactions. (Raisins too – anything with pits)

Many times there is a cranial component also – as DCs we can deal with this stuff – cranial and diet.

BACK TO SCOLIOSIS

Paralytic scoliosis – we probably won’t see this in our office. The heart is rotated 60-70 degrees so the blood has to be pumped horizontally.

Most common will be R PAIS (Progressive Adolescent Idiopathic Scoliosis) – ribs are spread apart on R side (convex side) and on the concave side the ribs are approximated – therefore neither side can the muscles function so we respiratory problems. The “rib hump” is actually a protruding scapula with the ribs under it.

The scoliometer is about $40-50 – a great non-invasive way of measuring the degree of scoliosis.

The vertebral body rotates extremely to the side of convexity. The pedicles are lengthened – determines the size of the IVF. Everything is displaced. Decreased vertebral height and disc thickness on the concave side.

Sometimes this can be determined in utero (hemivertebra).

The canal will be asymmetrical, the ribs will be asymmetrical. If they come into the office with the structural changes already in place – our goal should not be to straighten the spine, they are probably asymptomatic - our goal should be to keep them from getting worse (second), keep them functional now and in the future (first goal)Orthopedics11-04-02

Possible pop quiz on Wednesday for the tests on the shoulder.

ELBOW

Tennis ElbowLateral Epicondylisit – inflammation at the epicondyl, distal humeral pain, proximal to the

elbow, reproducable on palpationCommon Extensor TendonitisAffects the tendonous attachments of the extensors ar the lateral humeral condyle and

may have a myofascial component affecting the extensor region of the forearm. (Myofascial Compartment Syndrome is a separate disease)

Pain for true tennis elbow it will be on the distal humerus, lateral epicondyle.

Splints are sometimes recommended for this – a compressive elastic band is wrapped around the forearm just distal to the elbow. This redirects the long axis force of the contraction of the muscle to the bone. (Divide the compression about halfway on the tendon)

Triceps tendonitis is different than tennis elbow – that comes from the top down.



This is a common injury for DCs and DC students.

Head of the radius comes into the radial notch, surrounded by the annular ligament. The “Nursemaid’s elbow” injury – the child’s radius gets dislocated due to pulling on the arm (either by the child or by the parent – the kid will sit down while the parent is holding on to their hand or the parent pulls the child along)

Nerve distribution – Not dermatome but peripheral nerve patternsRadial nerve distribution into thumb and hand for motor control – sensory area is small –

medial and proximal thumb.Median nerve – large part of hand – thumb, index, middle and ½ of ringUlnar nerve – ½ of ring finger, little finger, dorsal hand and ventral for sensory – know the

motor sections. LOOK IN NETTERS FOR THIS INFO

KNOW THIS ANATOMY

Orthopedics tests –Cozen’s Test – looking for reproduction of pain. Patient performs resisted extension at the wrist, stabilize higher than the tendon. Pain at the condyle = tennis elbow. Pain in forearm = muscle (extensor) strain. Pain in distal end = pain in wrist.

Mill’s test – not an adjustment – elbow flexed, hand and fingers flexed, extend elbow maximally and pronate the elbow when arm is fully extended. Looking to reproduce pain at the epicondyle, passive motion. Elbow strain is pain in the elbow joint. Stretch pain = from ligament; contraction pain = from tendon/muscle.

Medial epicondylitis – Golfers Elbow – involves flexorsGolfers Elbow Test – resisted wrist flexion in an attempt to reproduce the pain at the

medial epicondyle of the elbow.True epicondylitis – pain in condyle

Ligamentous Instability Test – aka Valgus and Varus – Joint motion – (Knees toward the midline – motion relative to knee joint is abduction or Valgus – lateral deviation of body part distal to the joint. Varus – medial deviation of the body part distal to the joint, adduction.

Joint is extended and supinated – medial collarteral ligament is what we are challenging in Valgus; Varus would challenge the lateral collateral ligament.

With elbow flexed about 20 degrees. (Closed packed position is closed – in the elbow it is pure extension). Test moving the joint. (??) We are looking for pain. A sprain will be above and/or below the joint.

Do well side first to get a sense of how the person moves.

Tinel’s Sign at the Wrist – Clinical Pearl in Evans – you can get a lot of false positives using this test. Chief complaint of a peripheral nerve compression – if you tap on the nerve and reproduce the complaint, then Tinels is a possibility. Tap on the appropriate nerve (radial, ulnar or medial).

Elbow Flexion test – for ulnar neuropathy – maximally flex the elbow and drop hand onto shoulder for 5 minutes. Paresthesia is a positive test.

Phalen’s – and Reversed Prayer Position with hands, with arms in front, keeping the shoulder at a 90 degree angle. See Evans. Bring reflex hammers and goniometers to lab tomorrow.

Orthopedics11-06-02



Adams Position variation – evaluate the spine – estimation of rib hump, patient bends forward and then laterally bends L and R.

If they have a L lumbar curve and a R thoracic curve and bend L and the Lumber curve straightens out, there is flexibility in the lumbar spine. When they bend R and the thoracic curve doesn’t straighten out, this is the fixed area. A couple of schools of thought – one says that the thoracic is a compensation, others say this is where you should adjust (apex of the curve). Goal is to make the patient maximally comfortable if the curve is beyond correction.

If T1 isn’t over the sacrum, the spine will continue to curve until that happens.

Progression – an increase in the curvature of 3 degrees or more per year. Cobb’s method is commonly used in the office. The factor of error is 5 degrees – this presents a technical problem.

Find the apex, the most inferior and the most superior inclined into the curve. Draw a line from the endplate of the inferior and then 90 degrees to that and one from the superior vertebra endplate and 90 degrees – they will intersect – measure the angle – that is the angle of the scoleosis.

You can have a primary and secondary (or compensatory) aka major and minor. Major describes the degree (structural), minor is functional.

Named for the apex of the curve. R thoracic is the most common; thoracolumbar curve is the most progressive (statistically)

Scoliosis is a tower but not all towers are scoliosis. Has to be 10 degrees or more to be considered a scoliosis.

Cobbs method – done in the office. Films you need – Full spine PA – this gives you more distortion of the image but it avoids scatter radiation to the anterior chest wall and the eyes and gonads (be sure to use shields); don’t over-collimate or you could miss some of the anatomy. If you do it the same way each time, you will be able to compare apples to apples.

Full spine lateral or sectional laterals if the patient is large or you suspect any problems in a particular area. X-raying children isn’t bad if clinically indicated. Don’t do it frivolously and do it well.

Film of L wrist and hand – used to determine developmental age of the bones. Greulich and Pyle atlas of developmental anatomy comparison: When distal radial epiphysis unites, maturation is complete. Have the radiologist read it to determine the age – we aren’t trained to do this. (Know this information for boards – probably her test too.)

In general, have pediatric films read by someone else that has more experience.

Scoliosis can progress after maturation but not as fast; pregnancy can also increase the progression rate.

Skeletal immaturity indications – Hazy ring (ring epiphysis) at the top and bottom of the vertibra – growth plate is in formation.Ring epiphysis is complete but not united – halo affectGrowth plate united to vertebral body; maturation completeEasier to see on a 40” spot shot

Apophysis – growth center – of iliac crest – Risser sign – growth starts at the ASIS and works it’s way back. If the plate goes back ¼, it’s Risser +1; ½ is Risser +2; ¾ is Risser +3, all the way back is Risser +4, Risser +5 is completely ossified to the crest.



Siblings – statistically there is an increase in scoliosis in families – can skip a generation – seems to be X linked. Genetic etiology in about 33% - mom can pass to either child, dad can only pass it to daughter.

Less than 10 degrees the incidence is about equal; 20-25 degrees is 5-8 times more common in girls; above that is comes back to equal.

ROTATION – Scottie dog can be seen on AP film, that indicates a 45 degree scoliosis. WE can also look at the pedicles – we should 2 two owl eyes if normal. If you are seeing just one pedicle, there is some serious scoliosis going on.

TREATMENT – Milwaukee brace – in principle it works it that it produces an irritation and the patient tries to pull away from the irritation which helps straighten it. This is the Gold standard in controlling or halting the curve. The Boston brace is a lighter weight polymer but the same principle.

Protocol for bracing – 23 hours/day until skeletal maturity or until such time that it has been determined that the brace has failed.

************Linda was not here – notes from Scott (I can guarantee they’re not as good as Linda’s!)

ScoliosisFigure 4 – Decision Making Flow Chart for Treating ScoliosisBrace after 3-6 monthsSurgery if >50 degrees – Herrington rod – lamina shaved, SP clipped off, bone fragments taken from ilium – distraction rod used in concavity will reduce angle. Spine is fused and reinforced with the rod. Compression rod used above and below apex on opposite side. No more spinal motion. Sometimes rod slips or breaks and additional surgery necessary.

Chiropractic literature on scoliosis is sketchy – hard to do studies ethically. Aspegren in CO worked on derotating area of lateral bending with very good results but his study population was only 3 people.

Moe’s textbook of Scoliosis – standard text on this subject

LESS – lateral electric surface stimulation – (unit called Solitron made by EBI in NJ) – not a TENS unit, it’s a muscle stimulator worn for 8 hours/ day usually at night doesn’t have to be worn in public, more socially acceptable than Milwaukee brace. Found to be as effective as Milwaukee brace originally after research stage results have not been as good. Pads are placed above and below apex of curve on convex side, midaxillary placement.

Exercise – studies compared Milwaukee brace to exercise and exercise didn’t do as well so for years exercise was eliminated from treatment. But there are some protocols. Also don’t neglect the rib involvement in scoliolsis.

Home care – traction therapy chin up bar tractions spine. Inversion therapy contraindicated from pt w cardio involvement (Dr B recommends about 15 degrees). You can also incline bottom feet of bed frame a few inches.Balance beam and wobble boards – proprioception – important to brace pt somehow when starting to use. Avoid backpacks. Feldentraus or Alexander techniques also helpful.

Wobble boards also good for ankle sprain and diabetes, learning disabilities.

Orthopedics



11-08-02 (Erica’s notes)

Scoleosis (continued)20-40 degrees – the medical model would brace>50 degrees – the medical model would do surgery

LESS – Lateral Electric Surface StimulationHas been shown to slow or halt the progression of the curvePatient does it for 8 hours a day in the privacy of their homeUsually paid for by insuranceUsually used at night while sleepingHas been shown to work as well as a braceIs NOT a TENS unitIs specifically designed for scoleosisPads placed above and below apex of curve on the convex side near the midaxillary lineForces the patient into laterally bending to try to change the curve

Orthopedics11-11-02 (Erica’s notes)

Legg-Calve’-Perthes Disease1st and 2nd stage lead to true LCPD; give (+) ortho test; avascular necrosis1st stage – blood supply to head of femur is lost, osteocytes are gone (dead), bone dies2nd stage – re-vascularization, osteocytes return and osteoclasts destroy dead bone3rd stage – subchondral fracture; true Legg-Calve’-Perthes Disease

Hip Tests – hip joint pain tends to present anteriorly in the groin/inguinal area

Thomas Sign – patient supine; patient flexes hip and pulls knee to chest; (+) if contralateral hip flexes simultaneously (this demonstrates a shortening of the iliopsoas)

Trendelenburg’s Test – evaluates the gluteus medius; patient flexes the leg slightly while standing; watch for hip (crest) drop on side of flexed leg; (+)if crest drop occurs and is due to contralateral gluteus medius weakness.

Ortolani’s Test – looks for congenital hip displacement on newborns. If the hip is dislocated, you’ll hear a “clunk” as the hip moves into place

Barlow’s Test – reverse of Ortolani’s; reduction test

Jansen’s Test – patient supine, have them abduct leg passively while it’s flexed over the opposite knee

Patrick’s Test – similar to Jansen’s but the Dr. places force on the knee and stabilizes the contralateral ASIS

Hibb’s – patient prone, heel to butt with internal rotation of femur by externally rotating the leg

Apparent Leg-Length TestActual Leg Length – measures ASIS to medial malleolusApparent Leg Length – umbilicus to medial malleolus3 measurements taken and they should be within 10%Compare L to R

Scanogram – should be weight-bearing x-raysSpot shot of hip, knees and ankles – all on one 36” film



Radio-opaque ruler next to each shot x-ray so you can determine the differences from L to RNot used to assess pathologyOnly used to determine leg length inequality

Allis’ Test – patient supine with hips flexed and knees bent. Look for queal height of knees and parallel from side

Hip Telescoping Test – patient supine, flex hip 90 degrees and knee 90 degrees. Dr. tractions leg.

Anvil Test – patient supine; Dr. elevates leg (extended) and thumps bottom of heel gently; assesses fracture; (+) = pain at fracture site.

Ober’s Test – patient lies on side; checks for hip to adduct and internally rotate (this would be normal); if hip remains stationary, test is (+) (abnormal)

Orthopedics11-13-02

Recognition of Congenital Hip Dislocation – occurs in 10 out of 1000 live births. 96% it resolves completely – the longer it remains undetected and untreated the more likely it will be permanent.

Ortolani’s and Barlow’s test

Knee and pelvis difference in length when legs are held up – hip is dislocated.

Telescoping or pistoning sign – move femur head anterior and posterior

Allis’ or Galeazzi’s sign

Trendelenburg’s test – weight bearing left, drop on right, L G medius isn’t doing it’s job.

Predisposing factors to congenital hip dislocation – 60% are first born children (intrauterine constraint), breech presentation (1/3 – ½ of births), L side is more common than the R (usually the side against the mom)

Pediatrics file in library has much information on helping turn a breech baby and checking for intrauterine constraint.

Hormonal factors – 6 times more common in female offspring – they think it responds to the mom’s hormones (relaxin, etc.). This is self-limiting depending on how long it takes the baby to process out the mom’s hormones.

Limitation of abduction – splay the baby’s legs up and open – don’t cause pain

Infants double in size the first ½ year and triple by age 1 – 7 pounds when born, 14 at 6 months, 21 at age one. This is a great time to make these kinds of corrections.

Iliopsoas contracts and provides the inferior support for the femur in the case of a femur head dislocated.

Pseudoacetabulum can also be created outside the acetabulum – the pressure of the femur against the bone will create a growth. The labrum will create a physical barrier to keep from replacing the femur head into the actebaulum properly.



Pulvinar – the fatty stuff in the acetabulum when the femur head isn’t there anymore.

Shenton’s line – inferior pubic ramus to the head of the femur.

Acetabular index should be <30 degrees – in hip dislocation it will be greater than 30 degrees. This is clinical indication for referral for x-rays or to do films in your office.

Positioning is important – this condition can be reduced. Triple diapering and/or bracing can be used. The goal is to keep the head of the femur in the acetabulum. Bone responds to stress (movement, etc.) so this bracing has the type of stimulation they each needs to help mold them both.

A pediatric orthopedist would be good to contact a co-manage with regarding this situation. Referring doesn’t mean you release the patient.

Adjusting these patients is important. HVLA into a hypermobile hip is contraindicated – use Basic, upper cervical, etc. If you balance the pelvis you will help the situation.

Safe zone of Ramsey – a position of flexion and abduction that will retain the normal relationship between the acetabulum and the femur head and keeps the blood supply intact.

Too far abducted will compromise the blood flow; too far adducted will redislocate the femur head.

If the baby has tight adductors, the zones will be smaller.

Compression of medial circumflex femoral artery can happen in extreme abduction, internal rotation and flexion. Can cause ischemic necrosis.

Legg-Calve-Perthes – mean age is 7, usually in boys, can present as anterior thigh pain possibly to the knee (not always hip pain)

Episode of ischemic necrosis and then you have a subchondral fracture and a second episode of ischemic necrosis.

Do Thomas’ sign to help determine this.Circumference of the upper thigh – a difference could help indicate this.Roll hip in internal and external rotation – hip joint resistance would indicate a hip problem.Apprehension sign – watch for that

Orthopedics11-15-02

Wobble Boards – different kinds – one she brought information in about was for young children with a “target” game in the middle – the object being that the child has to move a marble around in the target – restores proprioception.

Legg-Calve’-Perthes Disease – ClassificationIn all that she showed us, the AP view you couldn’t see much, but the frogleg view you

could see it. The second set of films was several months after the injury. Pages 62-65 in the CIBA book – look at these pictures – it gives the classifications in there – she went way too fast for me to type anything from the book.

What will allow the head to heal? Molding by the acetabulum – bed rest is minimal. They use splints and braces. Shriner’s Hospital is a very good place to refer these types of problems to.



This can result in an anatomically shorter leg. Also early degenerative changes in the hip can happen.

Doesn’t usually happen bilaterally (if it does happen bilaterally, usually one side happens first and then the other side happens a year or so later). The kids tend to have immature bone in relation to their chronological age.

Prognosis – deformity of the Femoral head – less favorable outcome in girls; age of clinical onset; extent of epiphyseal involvement; containment of femoral head; persistent loss of motion (adductors, iliopsoas); premature closure of the growth plate.

Repeated ultrasound is contraindicated because it increases blood flow and will stimulate early closure of the growth plate.

Flattening of the femoral head – aka coxa plana – results in short leg on that side.

No HVLA into hip joint. Basic piriformis contact for lower extremities is really good to help adjust this. Piriformis is a major mover of the hip joint. Adductors attach to the pubes and the femur – working with this will help the area. Any muscles that control hip motion will be beneficial. Adjusting the SI joint is not contraindicated.

Slipped Capital Femoral Epiphysis – most common in boys 10-17, mean age of 12. Bilateral component 1/3 of the time. Take both the AP and frogleg views. Grade I is less than 33% (femoral head is in the acetabulum); Grade II – 33-50% slippage; Grade III >50% - very abnormal growth, prognosis is not good for this last classification.

Trochanters will be level, the whole pelvis will have dropped, unilateral in the absence of leg deficiency. May or may not have hip pain.

Orthopedic test - with patient supine as thigh is flexed it rolls into external rotation and abduction.

Orthopedics11-18-02

Meniscus – normally it is crescent shaped aka semilunar cartilage. Travels with the tibia. More firmly attached on the medial side than the lateral.

Functions – Serve as important secondary restraints (primary are the capsule and the collateral

ligamnets) – Contributes to joint stabilityAssists in load transmission – enlarges surface area, makes the socket in which the

condyles of the femur fit.Functions as major shock absorberAids in lubrication of jointAids in nutrition of jointHelps control joint motion

Variations – Vertical tear, deep into the tissueRadial tear – condyle of femur will be rubbing across both edgesHorizontal tear - splitting through the fibersBucket-handle teat – tissue is not even approximated, doesn’t heal well conservatively.

Looks similar to Ring Meniscus (a rare congenital anomaly).



Cleavage ear – cartilage will do damage to the femur. Meniscus isn’t pain sensitive, but all the other tissue is very sensitive to pain. It is directly attached to bone so it will pull on these receptors. Patient will present with pain. You can palpate tenderness along the joint line – in a ligament strain it would be above and/or below the joint line.

Joint locking – patient is loading the joint, when they go to pick it up it gets stuck. This happens due to a physical barrier of the meniscus stuck between the femur and the tibia.

Joint giving way – patient is loading the joint, knee buckles, patient falls. They feel (proprioceptively) they are stable, but the meniscus is in the way again and the muscles don’t respond properly. Usually when the quads are being relied on – climbing stairs.

Synovial fluid hypersecretes – joint effusion – associated with meniscal tear, not always indicative but sometimes.

A good sign is noise – femur rides across the meniscus – clicking or snapping sound. You can use the stethoscope to hear it also. Quadriceps atrophy on the injured side would be a good indicator of a meniscal problem.

Menisci are most firmly compressed in flexion.

Meniscus – attached to the medial collateral ligament, the tibia and the capsule. Because they are functionally related

ACL, medial meniscus, MCL – unhappy triad – typical injury is “clipping” in football. Internal femur rotation on the tibia (external rotation of the tibia) will stress the medial compartment.

TESTS

Q-angle test – Q = quadriceps. Draw line from ASIS to midpoint of patella – this will be the axis of the femur; then from the midpoint of patella to the tibial tubercle – measure the angle formed – it should be less than 18 degrees – Valgus angle (tibia goes lateral = Valgus angulation). Patient’s knee should be extended with hip in neutral position. Should be done on every patient with a hip or knee complaint.

Apley’s Compression Test – for the meniscus – patient prone on table, flex knee, push tibia down to the femoral condyle. Tibia external rotation tests the medial meniscus, internal rotation tests the lateral meniscus

McMurray’s – patient supine, knee flexed to 90, a positive response is a clicking or popping. Palpate the “eyes” of the knee, internally and externally rotate the leg as we pull the leg into extension (internal then external).

Steinmann’s Sign (aka Steinmann’s tenderness displacement) – patient supine with knee extended, pain is inferior to femur, flexion causes the pain to go posterior to the femoral condyle.

Bounce Home test – knee in flexion, support the leg, remove hand and knee will drop. In a normal knee it will fall into extension – closed packed position. With a meniscus problem, there will be a bounce. DO NOT traction the leg or snap the joint.

Stress test (at knee) – Abduction (Valgus) Stress Test – medial collateral ligament, be above the joint; adduction (varus) stress test – lateral collateral ligament (then check Ober’s sign if lateral is +) HVLA is contrandicated in this instance – it’s an unstable joint.



Apley’s Distraction Test – same position, Dr. knee on patient’s thigh, Dr. pulls tibia to ceiling and externally rotate – medial collateral ligament; internally rotate – lateral collateral ligament. Traction, rotate, release, traction, rotate, release.

Drawer Test – ligaments – ACL and PCL – produces sloppy motion from the knee. Hip flexed at 45, knee flexed at 45, Dr. sits on foot, pull tibia anterior (thumbs on eye of knee) – anterior drawer is damage to the ACL; broad contact on front of knee and push posterior – posterior drawer is PCL damage.

Lockmans Test (Maneuver) – similar to anterior/posterior drawer, but lifting the tibia and pushing the tibia back

Clarks sign – patellofemoral arthralgia – chondromalacia patellae – softening of the posterior cartilage. Patient supine, patient contract quads against resistance from the Dr. against the patella to keep it from riding up. Tell the patient what you are doing. Retropatellar pain.

Fouchet’s Sign – retropatellar pain – knee should be extended, Dr. broad contact over the patella, Dr. compresses downward and then assess movement (all around) A positive test is a grinding sound as you move it around in the compressed state.

Patellar apprehension – patella should move; a reflex sign is a quick quad contraction to keep it in place.

Meniscal Effusion – tap on the patella, it will displace the fluid and bounce back up – not normal.

Orthopedics11-20-02

John’s Presentation – muscles that attach to the scapula – no notes

Meniscus in the transverse plane - taller, which produces the socket that the condyles ride in.

Synovial Plica – plica refers to remnants of embyrologic components in the knee. This is a synovial partition – clinically insignificant. They are very elastic and mobile. Most common is the medial femoral plica aka the shelf plica. It comes partially across the femur in proximity to the medial meniscus.

Other plica and locations – lateral plica, suprpatellar plica.

Noise from the knee joint – Extended – plica doesn’t touch – at 15 degrees the plica contacts the femoral condyle, by

30 degrees it has rubbed across the femur – if it is inelastic tissue, you may get a snap – then ROM is free.

Meniscal noise will be at about 90 degrees – a patient can have both.

Defect in the cartilage of the bone will heal with fibrocartilage.

OSTEOCHONDRITIS DISSECANSInflammation of the bone and cartilage – coming apart, separates.Affects primary or secondary growth centers.Most common is medial femoral condyle, also can affect the shoulder, ankle and elbow3 different stages

1. cartilage remains intact, on x-ray you can see a line of separation – affects bone only

2. Bone and cartilage damage – will heal - separation



3. Bone and cartilage involve with separation and migration of a piece, a loose body – aka a joint mouse – joint locking, joint gives away, joint noise. Won’t heal because it isn’t attached –it may find a spot and rest, then move around again. Prognosis here is surgery. Using pins is a short-term thing. Bone stimulators are also used.

Obesity can be a predisposing factor; MRI good for diagnosis

OSGOOD-SCHLATTER LESIONConsidered partial avulsion of the tibial tuberosity – trauma, growth spurt, tight quads.Normal growth plate, fibrotic tissue within the growth of bone – this can create problems

at a later time in life. – Soccer, football, basketball. Problems with kids that are Catholic due to kneeling so much.

Tight quads – Ober’s test (tensor fascia lata and iliotibial band – attaches to vastus lateralis, affects the patellar tracking which affects the tibial tuberosity)Leg should be able to go to 90 degrees (SLR), flex leg – thigh should be able to lay on chest. Prone – heel should be able to go to the buttock. If it shifts to the midline or out lateral – one or the other of the quads (lateral or medial) may be tighter than the other. Can also involve iliopsoas and hamstrings.

A brace, just below the patella, pulls the ligament back to the bone – redirects the force. Use ice to decrease the inflammation. Anecdotally – adjust this – you are dealing with an avulsion so be VERY careful – using a tongue blade (depressor) and adjust – adjust knee too.

Orthopedics11-22-02

Chondromalacia – cartilage softening – should be a physiologic diagnosis (biopsy) – clinically it would be pain in the anterior knee (patellofemoral) aggravated by ascending motion (upstairs) and sitting. When the knee is flexed, the patella is up against the femur so it loads the surface. *******

Osteochondritis dessicans – a circumscribed area of defect, a large portion (medial femoral condyle is the most common place – can also affect the shoulder joint) of the retropatellar surface. Patellofemoral arthrosis – very slow and gradual.

Falls under PFA – patellofemoral arthralgia – not the tibiofemoral. Most patients will be referring to the patella rather than the tibiofemoral.

DJD can affect the patella also – hypertrophy changes the way the patella tracks.

Chondromalacia – there will be noise because the cartilage is gone or fissured. They will have swelling and probably have pain.

Degenerative changes are different and the patient can have both.

Treated as a patellar tracking disorder – strengthening of vastus medialis is the treatment. Quads extend the knee – the vastus lateralis pulls laterally, medialis pulls medially, rectus femoris and vastus intermedius should be in the center.

If the patella is tracking laterally, it’s not in the groove. Vastus medialis could be weak or vastus lateralis is over-developed. Kendall and McCleary – muscle testing book. Internally rotate the tibia and extend the knee = vastus lateralis. Externally rotate the tibia and extend the knee = vastus medialis.



Avoid the last part of extension while you are trying to rehab them. Tie a weight to the foot and have them externally rotate the tibia and slightly extend the knee for lots of repetitions throughout the day.

Dislocation of the patella most common is lateral.

Most of us have a fairly deep groove that the patella rests in (between the femoral condyles).

Tension of lateral muscles and/or retinaculum plus weak vastus medialis muscle can cause the patella to deviate laterally.

Sometimes it can be a development disorder – the lateral condyle isn’t developed enough to hold the patella in the groove.

Dreyer’s sign – extended knee, try to flex hip. Dr. squeezes hand around the quads and they can flex the hip more easily. This would be evidence of a patellar fracture.

Congenital Bipartite patella or congenital tripartite patella – they function as one bone. The patella ossifies from several centers of ossification – the lines on the x-rays aren’t fractures, but the growth lines haven’t solidified. Cortical bone line around the line also indicates that it’s not a fracture – a fracture would be a jagged line.

Patellar dislocation – not in the groove at all.

“Owl-eye” (squinting) – patellae face laterally. Femurs are exactly parallel, the patellae should be facing forward – in squinting, they aren’t. (Feet point out = tibial torsion). If you have a “toe-out” situation (or “toe-in”), you need to trace it up to find the source. It could be the ankles, the knees, the tibia, the femur, the pelvis, the SI joint.

Internal tibial torsion – toe in – they will be pigeon-toed or they will force external rotation above the tibia when they walk.

Orthopedics11-25-02

ROM for extremities packets – won’t be on the final – either the written or the practical. This is just for our own information.

FOR THE TEST Check her file in the library – the cervical and lumbar ROM is testable for the practical. ROM and neurological exams for cervical and lumbar areas (sensory, motor), shoulder, knee. Bullet charts in the book to help break this down for other associated tests.

NOTESRotational effects in the lower extremities – can be compounded by more than one place or compensated in more than one place. Look at the patient in multiple postures. (i.e. internal tibial torsion)

External rotation of the femurs –Spread-eagle or frog sleeping position may contribute to external rotation of hips.Reversed tailor position places internal torsional stress on femurs and external torsion on

tibias. May retard correction of torsionsal deformities (TV posture). Forces the femur into internal rotation and stresses the knee.

Valgus and varus



Varus angulation at the knee is normal in infancy and early childhood. After 1 year old through the toddler stage, they become knock-kneed – feet give them a wide lateral support – this happens after they learn to walk. After age 2, this should also diminish. Evans says less than 18 degrees. Children do not develop an adult-style of gait until they are about school age. They have a lateral shifting (waddle side to side) until they get the adult motion of counter rotation (swinging the R arm forward as you step with the L leg). Cross-crawl (marching) will help with the neurological intergration.

Blount’s Disease – Bowleg – called tibia vara – unilateral or bilateral – effects gait, posture. Idiopathic, ischemic necrosis. Juvenile form is between 6-14 years. Resorption of the bone, causes the bone to shift, can’t support the femur properly.

Torsions can be in the feet – they can be pigeon-toed – adduction of the foot aka metatarsus adductus. Can be bilateral or unilateral. Not club foot. All the bones have formed normal, just excessive force pulling/pushing the foot into adduction. Can be corrected with adjustment and taping the foot into abduction. Do x-rays to make sure the structure is OK. Can also be contributed to by uterine positioning.

Club foot – bilateral or unilateral. Can also be contributed to by uterine positioning. Aka Congenital equinovarus. The entire foot is plantar flexed (equine component) and inverted forefoot and hindfoot. Occurs in 1 of 800. 3 kinds – postural club foot, true club foot, teratologic club foot.

Normal structure with real short tendons – requires serial surgeries to correct it.

Effects the tendons, the ligaments and possibly the structure of the tarsal bones.

AS a DC we will probably see adults that had clubfoot surgery as a child. We can adjust and support them. If they are under 23, get a copy of the surgical records. If over 23, try anyway. It will help you understand where their body is at the time you see them.

Orthopedics12-02-02

Fibromyalgia – Leon Chaitow – Fibromyalgia Syndrome, a Practitioner’s Guide to Treatment

Diagnostic Criteria – she will make a copy for the library folderPain (with the patient reporting ‘pain’ and not just ‘tenderness’) in 11 0f 18 tender point

sites on digital pressure involving 4K of pressure. The sites are all bilateral and situated:1. Posterior suboccipital insertion2. Anterior aspects of the inter-transverse spaces3. Midpoint of the upper border of the upper trap muscle4. Origins of supraspinatus muscle above the scapula spines5. The second costochondral junctions on the upper surface, just lateral to the junctions6. 2 cm distal to the lateral epicondyles of the elbows 7. In the upper outer quadrants of the buttocks in the anterior fold of gluteus medius8. Posterior to the prominence of the greater trochanter (piriformis insertion)9. On the medial aspect of the knees, on the fatty pad, proximal to the joint line.

History of widespread pain for at least 3 months – pain in the left side, the right side, above the waist and below the waist. Axial pain – cervical spine or anterior chest or thoracic spine or low back.

The points in this are called “tender points” – not trigger points.



Mind Issues – psychological components – in the book – also includes Chronic fatigue syndrome (CFS)

Many things can be involved here – see the book – Interaction between stressors and gut dysfunction – an avalanche of symptoms with

particular implications in FMS. Additional stress, biochmeical and emotional stresses.Central sensitization or impaired central gating Enzyme and/or HCl deficiency (HCl is zinc dependent)Hyperventilation influencesStress-related influences – produces a neurobiological affectFood intolerances, allergies, toxinsSerotonin (keeps it bioavailable) – T3 function, Substance PInfection – fungal, bacterial, viral, protozoalAntibiotic after-effects

Trauma – whiplash – can trigger fibromyalgia. Even if it is regional it can cause a systemic problem.

Sleep patterns are disrupted –Normal restorative sleep –

1. Increased protein synthesis, tissue repair2. Increased growth hormone secretion3. Enhanced immune activity – e.g. interleukin-1

This is an important thing regarding health. Documented that pain will interfere with sleep, even if the patient isn’t aware of it – the sleep cycles are off, the quality of the sleep suffers. This can produce neurosymptomatic problems (irritable bowel syndrome, fibromyalgia, etc.) More non-REM sleep.

Sleep abnormalities – confirmed clinically but not necessarily explained by EEG evidence of alpha intrusion into NREM sleep as previously postulated

Increase in all painful symptomesReduced protein synthesis, tissue repairDecreased growth hormone secretionReduced immune activityOvernight falls in OS hemoglobin satuarionIncrease in tender point sensitivityGeneral malaise and fatigue, deconditioningPerturbed hypothalamic, pituitary, adrenal axis.Low 24 hour cortisaol levelsElevated evening cortisol (normal is low)Pituitary hyper-responsiveness corticotropin releasing hormone and insulin induced hypoglycemiaAdrenal hypo-responsiveness to stimulated ACTH

NMS standpoint – trigger point referral patternsSCM – anterior border, refers pain to angle of the jaw, forehead, suboccipital, etc.Upper traps – refers over top of the head to the face; temporal arteritisLevator – around the scapula, concerned about having a heart attacke, neck, deltoid

regionPosterior cervical – across the traps. ScapulaScalenes – deltoid, C6 dermatome area, not a NR, scleratongenous (no sensory or reflex

change)Multifidus – lumbosacral pain, diffuse back pain, pain referred to the anteriorG minimus – buttocks, TFL down lateral leg, lateral leg, posterior thigh, posterior legSerratus anterior – pain in the chest wall



Sternalis – across front of shouldersPec major – chest pain

Many more – see the book

Metabolic rehabilitation of a fibromyalgia patient – see the book

“The way up from down” – Slagle – MD – in addition to antidepressants, amino acid supplementation can help re-establish the pathways. Read the book.

Orthopedics12-04-02

Clarification – neurological levels – refer to Hoppenfeld for national boards (biceps – Hoppenfeld says it is C5 and C6 – it is primarily C5)

Names can be a big deal in Part IV – if they say to do a particular move and you know all the moves but don’t know the name ou could have a problem.

For the test:

Legg Calves PerthesAvascular NecrosisDistribution of peripheral nerves – especially the upper extremities; contrast with

dermatomesCongenital Hip Dislocation – know how to diagnosis thisDeQuivaranes – abductor pollicus longus and extensor pollicus brevis?? – she likes thisNodes – Heberdens and BouchardsPatellar Tracking disorders – muscle for rehab?? – vastus medialisKnee – know the meniscus and how it interferes with the mechanics within the joint

(locking, clinical presentation, etc. – McMurray’s – noisy knee will only be evident as the patellar grinds against the femur in extension; meniscal noise will only happen with the knee in flexion; plica at 15-30 degrees flexion)

Blount’s disease – medial tibial plateauMuscle and DTR gradingObers test – KNOW THIS – She likes thisThomas testClarke’s test – possibly – she likes this – also Bowstring’s also but not on this testNR levels when testing extremitiesPathological reflexes – Babinski’s, Boutineer and Swan neck deformities – RAScoliosis – what’s your goal for treatment – know how the patient presents and what you

would do at varying degreesTransverse humeral ligament – long head of the bicepsTOS – know the sites of compression – positional alteration of the symptoms – scapula

and parts, ribs (anterior and posterior), C3 to T6VBAI – 5 B’s and 3 N’sMaximal cervical compression is IVF testQuestions – 25-40 for the test.

Fibromyalgia, Kendal and McCleary Muscle testing book, Orthopedic terminology – books to refer to.


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