Logan Class of December 2011



BIOMECHANICS – 1/9/08

STRESS

Surface area affects stress.

Ex….Female on Heels standing on you 100 lb/1/4 inch heel = 400 lb/sq. inch of force would be directed through her heel due to the small surface area the force is applied on.

Whenever you consider force, you must consider the area.

STRAIN

Wherever you have stress, you have strain. Strain occurs when stress is applied. Typically a ligament has a 3% strain rate. Strain can either be expansion (stretch) or compression.

Ex. --The strain rate…10 mm long object stretched to 11 mm = 10% strain.

Stress vs. Strain Curve

As stress is added, strain occurs. This curve begins as a straight line. The straight line is called the elastic range. In the range, the object can return back to original shape. After the elastic range, the curve bends. This zone is called plastic range. Permanent deformation occurs in the plastic range. A ligament is permanently deformed in the plastic range. This is the area of sprain.

Grade 1 = A sprain that occurs in the elastic range

Grade 2 = A sprain that occurs in the plastic range. Deformation occurs with subsequent instability

Grade 3 = The ligament loses function (loses protective value)

Energy is the area underneath the curve. Energy is stored. When the stress is taken off, the stored energy helps bring the tissue back into the elastic zone. Every time stretch occurs less and less energy occurs through the system. This is called hysteresis. The energy is lost as heat.

*** Picture on Blackboard ***

A – More Vertical Line

B – Between A-C

C – More Curvilinear

The slope of the curve is the stiffness. A -- It doesn’t change very much (linear part of graph)…B—Not quite as stiff (midpoint of graph)…C – Not stiff at all (curvilinear portion)

The one that goes up the highest on the graph before it breaks is the strongest. Most ligaments are somewhat stiff

LOADING OF LIVING TISSUE

The faster you load living tissue, the stronger it is. The body tissues are stronger with quicker loading. This is opposite to that of non-living tissue like steel. Steel cannot be loaded quickly or it will break.

Bone Loading Until Fracture

The energy of the bone is given off to the surrounding muscles. The faster you load the bone, the faster you increase the energy that will need to be given off. This mechanism gives us some protection. The greater the force with quick loading, the greater the resistance to fracture due to the dissipation of the force.

Slowly applied forces pose a problem because bone and living tissue cannot dissipate the force as well.

Hysteresis

The energy lost when you put stress/strain into an area. Friction causes some loss of energy and heat. We can restore some of the energy by ATP synthesis.

BIOMECHANICS – 1/11/08

LEVERS

Bones act as levers. Levers produce forces and stresses.

Types of Levels

Type 1 – Seesaw (fulcrum is in the middle)

Type 2 & Type 3 – Fulcrum is at the ends.

Type 1 Joints

Ankle: COG Line should fall slightly anterior to the malleolus. A person normally falls forward when they stand due to built in instability. At the ankle we have built in instability and lean forward (anterior sway). The soleus muscle works as an endurance slow, twitch muscle to keep the posterior sway.

Atlas: Another Type 1 joint is the atlas.

Vertebral Bodies are type 1 levers. The center of gravity is in the middle of the vertebra. Ideally with a type 1 lever like a vertebra, you want the moment arm as small as possible, putting less strain on the body.

Forces at the Head and Neck via a Moment arm

Muscles of the back and neck don’t have a significant moment arm. Adding a larger moment arm will significantly increase the forces through the joint.

Type 2 & 3

These are in long bones with the fulcrum at the end of the bone (joint). 2 & 3 are used for power or speed/ROM.

As humans we are designed mostly for speed and ROM.

Moment arm

Moment Arm = The distance the weight is from the fulcrum. This makes a large difference in the stress on the joint. Forces are due to muscle actions. Muscles that create the most force have the longest moment arm.

Knee Joint as a Lever

The knee has the most stress in the body. The two longest levers and bones of the body (femur and tibia) correspond to the knee. The knee has the highest frequency of injury and has a high incidence of osteoarthritis. The spinal joints are the only joints with higher incidence of osteoarthritis.

BIOMECHANICS – 1/18/08

BONE

2 Types of Bone

There are 2 types of Bone: A).Cancellous B). Cortical. The difference is in the density.

Cortical Bone = Cortical bone is much stronger than trabecular/cancellous bone. Cortical bone is more commonly fractured because it is stiffer.

Anisotrope

Anisotrope = Loading materials in different directions forces the materials to have different properties (resistance to loading will occur in differently). The stress strain diagram will show the same material with different loading forces will have different curves when graphed.

*** Picture of Stress – Strain Diagram ***

*** Picture of Ankle X-ray on Overhead…There is an avulsion fracture…The muscle and tendon pulls the bone. The weakest link is the muscle, followed by the tendon and lastly the bone. Adults should never get an avulsion fracture, except in cases of severe osteoporosis. Children (especially younger athletes) are prone to avulsion fractures as well. Bone disease with avulsion of the greater trochanter is linked to cancer. ***

*** Compression fracture of vertebra on overhead…The end plate buckles…Schmorle’s Node…The back height on the vertebra-disc-endplate is usually normal, and the compression fracture occurs in the middle of the vertebra ***

Appearance of Bone on X-ray

Bone is supposed to be white on X-ray. If it doesn’t appear white, it does not have calcium. Osteoporosis is a condition where the bone does not appear white due to the loss of calcium. Another condition may be multiple myeloma which presents like osteoporosis on an X-ray.

2 Pt or 3 Pt Loading of Bone

Bending the bone from the ends will cause it to break at the weakest point.

A). 2 pt. bending occurs when there is 2 points of contact where the bone is loaded…Ex.—Fibula bent at ankle and knee. The fracture occurs at any point between the ankle and knee, but always occurs at the weakest point.

B).3 pt. bending has 3 contact points with the break occurring at the 3rd point. Ex. -- Getting kicked in the fibula with the foot and leg in a weight bearing position…the bone will break at the 3rd point or the place where it is kicked.

Different Types of Stress

Bone is strongest in compression and worse at everything else

OSTEOPOROSIS

Horizontal Vs. Vertical Trabeculae

We have vertical and horizontal trabeculae. Osteoporosis affects the spacing within the bone causing the vertical lines stand out more, due to less horizontal support. The weak spot of the vertebra is the end point. Compression will fracture the end plate. We protect the end plate via vertical sticks that run from top to bottom to stop the compression force. The long vertical piers when compressed want to bend. The horizontal supports keep the vertical from bending. Less stress is placed on the horizontal support. The horizontal support keeps the vertical from bending and buckling. The horizontal supports are horizontal trabeculae.

The process of osteoporosis affects calcium. Calcium and phosphorus are taken from storage or the part of the bone that is not stressed. The horizontal trabeculae are under the least amount of stress, so calcium is taken from the horizontal trabeculae. The classic finding is that the vertical trabeculae become more prominent than the horizontal trabeculae in osteoporosis.

Disease of Elderly

Osteoporosis is a disease of the elderly (particularly elderly women). Treatment for women over 65 includes bisphosphates. Bisphosphates turn off osteoclasts. The negative is that bisphosphates can induce osteonecrosis of the jaw and cause musculoskeletal pain.

Peak Bone Density

Female Bone Density is at its highest at 26-27 years old. Peak bone age in males occurs later in life than females and is greater in value. The problem is that you develop max bone density between 16-26 or during the time when you stop growing vertically. Women of today have lower peak densities than women of earlier generations. We are seeing that this is due to lack of exercise and activity, and poor diet. They end up at 26 with bone densities that are lower than females of previous generations for the same age. At older ages like 60 years old, they have the density of bone that is comparable to that of an 80 year old. So, osteoporosis is taken care of earlier in life. Strength training can help, but it can fully stop it. The goal is to slow the loss. The only exercise that helps is antigravity exercises like stair climbing and weight training vs. gravity.

Exercise training can also help to improve proprioception and balance. The neuromuscular training can help to limit falls. Another step to prevent injury from fall is to fall proof the home (increase the lighting, put night lights in, move chairs, take off the rugs, live in a 1 story house). Possibly, the best thing to decrease the injury from falls is hip girdle or hip pads. In a research study, a hip pad group had ½ the number of fractures due to absorption of the blow with the same # of falls.

Highest risk for osteoporosis is in the first few decades. It is very important to educate young women to achieve a good peak bone density early in life to minimize the effects of osteoporosis later in life.

Fractures

3 Devastating Types (these are the top 3 for morbidity and mortality):

1). Hip Fractures: 60% of those with hip fractures may need to change their lifestyle

2). Vertebral Fracture

3). Distal Radius – Colle’s Fracture … The most common fracture of elderly between 60-70 is Colle’s. Wrist movement is very important to everyday life and ADL’s (activities of daily living). This is the #1 fracture that causes lawsuits in orthopedic surgeons. The other thing is that with age, falling on the hand can brace the impact and forces to the hip. Some elderly will try to brace the fall with their hand to limit damage from a hip fracture.

*** See end of the chapter reviews and chapter diagrams ***

BONE DAMAGE CHART

Extrinsic Factors

Some Examples of Extrinsic Factors that Damage Bone:

A. Infectious Agents (post surgical patients with a septic process that contract infection of the bone

B. Chemical Factors (Overuse of Steroids – Corticosteroids is bad for bone)…

Corticosteroids: 1). Slow immune response 2). Prevents/Reduce absorption of calcium

3). Affect Osteoblasts – people on steroids have poor bone – RA patients on steroids and asthmatics and transplant patients are at risk for Extrinsic Damage to bone from steroids

C). Radiation Treatment (used for cancer treatment)—Radiation kills small blood vessels in bone…Dosage for cancer patients is between 5,000-7,500 rads vs. X-ray .5-1.0 rads. The rads are given 100 at a time for cancer treatment.

D). Mechanical Factors: Frequency, Rate, Direction of Load, Trauma, and Fatigue

Bone Loss by Immobilization

Bone mass lost in a week is about 1% per week. For each 1% lost, 2% of strength is lost. A classic casting is 8 weeks. This means that 8% is lost and 16% of strength is lost. It takes 3x as long to rebuild the strength of the bone following the fracture. Immobilization is very bad for the body.

Intrinsic Factors

A. Osteoporosis

B. Osteomalacia

C. Ricketts = We don’t see a lot because we don’t look for this…they look the same on X-ray)…Many people are very low on Vit. D. Vit. D is very important for bone health. Vit. D may be more significant than calcium.

D. Osteonecrosis

E. Osteochondrosis

F. Osteochondritis Desicans

G. Mechanical Factors (ex. -- Osgood Schlatter’s)

H. Metabolic Factors

BIOMECHANICS – 1/23/08

CARTILAGE

Hyaline Cartilage, Osteoarthritis and DJD

Hyaline cartilage is located in synovial joints. Adjustments target restoring motion to synovial joints. The #1 MS (musculoskeletal) disorder see in doctor’s offices is LBP caused by osteoarthritis. Osteoarthritis is the pathology of DJD (degenerative joint disease).

Functions of Cartilage

The 2 functions are: 1). Motion 2). Stress Reduction… We want frictionless motion of the joint. We also want the cartilage to slow the delay of shock from one surface to another. The elastic properties of hyaline cartilage allow the force to spread out. As deformation occurs, the force is spread out over a greater surface area to act as a shock absorber for smooth motion.

Composition of Cartilage

Cartilage is made of: 1). Collagen (mostly type 2, but also 5, 7, 9, 11) 2). Water 3). Cells 4). Extracellular Matrix – Proteoglycans

Bone = Bone has type 1 collagen. Type 1 is long and thin and type 2 collagen is short and skinny.

Proteoglycans are really big molecules. A proteoglycan is an aggregan that forms a meshwork and dissociates charge. There is strong repelling of the charge. The charge is 1 x 10 42nd of repelling force. It is very hard to push together. Proteoglycans try to bring in water. The water is about 70-80% composition. Water cannot be compressed under normal means thus giving strength. Water can also provide nutrients.

Glycosaminoglycans are made of chondroitin and keratin sulfate tied to hyaluron.

Cartilage gets nutrition through fluid movement. Moving a joint changes the shape of the cartilage. Compression and relaxation forces water in and out. It takes in nutrients and gives off wastes. Without movement, the cells of cartilage would die.

Collagen gives strength against tension. The cells have holes for bringing food in and letting wastes out. Think of the cells is a water balloon with a sponge in it.

Chondrocytes

Chondrocytes are cells that make cartilage, collagen and proteoglycans. Chondrocytes can also destroy collagen and proteoglycans. The message received by chondrocytes dictates whether creation of material or destruction of material occurs.

There is no nerve supply or blood supply to chondrocytes. A chondrocyte under microscope has a double layer. It seems as though the double layer is a force transducer. The force transducer registers energy transfer (electrochemical transfer) and allows the cell to perform it’s normal function. This quality acts as the message/messenger telling the chondrocyte what to do.

The easiest way to destroy the cartilage is to immobilize the joint. Immobilization shuts off the stimulation to the joint. Cartilage has the least amount of cells per square unit (mm) with a very poor repair capability. Immobilizing the cartilage causes the cell to stop making more cartilage and builds up enzymes to destroy collagen, proteoglycans, and cartilage. This eventually gets rid of the water in the cartilage and joint decreasing the size, motion and load bearing ability.

Measurement of Cartilage

You can measure the amount of cartilage in a joint in your office by X-ray. The X-ray allows visualization of the joint space which is mostly cartilage. There is an average number for each joint. Big joints should be 4-5 mm. The biggest joint and thickest cartilage in the body should be in the knee and behind the patella. There may be about 7 mm behind the patella. There may be only .5 mm or less in the facets of the cervical spine.

OA

Osteoarthritis is measured by comparing the arthritic joint space to the normal joint space measurement. Osteoarthritis is a common condition treated by chiropractors. OA is one of the leading causes of immobilization. 8 weeks of immobilization will lead irreversible damage. Osteoarthritis can be treated with movement/motion.

Synovial Fluid Frictionless Motion

Synovial fluid and synovial joint integrity/function can last up to 120 years. Synovial fluid helps provide lubrication. It is viscous, gooey, and slippery. Synovial fluid is mostly water. There should not be blood cells in synovial fluid. Bleeding into the joint destroys the joint

Synovial fluid is basically “blood without the red cells in there.” It is a filtrate of blood with nutrients and molecules to make it more slippery. The biggest joints have about 5 ccs of fluid. Knuckles or cervical facet joints have very little. There is only enough to coat the surface of the joint. Fluid is exchanged very often. Synovial fluid is like a filter to making a thin coating and allowing the joint to become slippery. Pressure inside the joint capsule should be – pressure. The joint capsule has – pressure to hold the surfaces together.

Lubrication

Electrohydonamic Lubrication = During movement, we generate enough force to squeeze water out of the joint surface with water pooling between the edges of the joint surface. The joint surface is elastic. It bends and moves water between two surfaces. The coefficient of friction is very small. The coefficient of friction is about 10x better than any machine we can design. This allows us not to wear our joint surfaces out.

During immobilization, we try to keep the surfaces from slowly coming together by a compound called lubricin. Lubricin comes form the synovial cells. Lubricin attaches vertically to both surfaces of the cartilage. Lubricin traps small molecules. This trapping of molecules has a mass effect causing adherence of the two surfaces. RA destroys joints by affecting lubricin by a process called boundary layer lubrication.

BIOMECHANICS – 1/25/08

JOINT PRESENTATION

X-Ray Presentation

Thickness of Cartilage is distance between 2 bones on X-ray. You can’t see the capsule very well on an X-ray.

Purpose of – Pressure

There is – pressure in the joint, which helps hold the joint together.

Blood In Joint Space

Blood is bad in the joint space, but good everywhere else.

Synovial Cells

Synovial Cells can make lubricin and help to filter and control fluid.

OA

Osteoarthritis can occur due to immobilization. Immobilization kills cells that make cartilage. Immobilization changes the lubrication system by affecting lubricin. Fluid becomes less viscous through immobilization and increases wear on the joint.

Osteoarthritis can occur by overuse of a joint or a single high impact can trigger osteoarthritis. A change in the biomechanics by disuse or overuse can cause osteoarthritis. Marathoners or super marathoners have no higher risk of osteoarthritis because exercise/movement is one of the best treatments for osteoarthritis.

EFFECTS OF IMMOBILIZATION

1. Kills cells that make cartilage

2. Changes the lubrication by affecting lubricin

3. Fluid is less viscous

4. Increases wear on the joint

5. Is linked to Osteoarthritis

6. Decreased Joint Space (through loss of proteoglycans)

OSTEOARTHRITIS MECHANISM

1. Overuse (affecting biomechanics of the joint)

2. A single traumatic event (affecting the biomechanics of the joint)

Decrease in Joint Space

Leakage of proteoglycans causes a decrease in joint space. The function of the cartilage (shock absorption) decreases when the joint space decreases.

SIGNS OF BONE RESPONSE TO INCREASED STRESS (OSTEOARTHRITIS SIGNS)

1. Reduction in joint space

2. Subchondral Sclerosis

3. Increased bone size and thickness – Osteophytic Development

4. Geode Formation

When bone has more stress to it, bone increases in size and thickness. Decreased joint space will occur (#1). An increase in bone density occurs next to the joint (subchondral sclerosis – 2nd sign). Once you see subchondral sclerosis, you may never be able to get the joint back to the normal bone. #3 Sign is osteophytes. #4 sign are holes in the bone on each side (geodes). Geodes are holes in the bone that are serous fluid filled cysts. We don’t know exactly where the geodes/cysts come from

We can reduce stress (force/surface area) by making osteophytes. This osteophytic development forms all the way across the bone. Osteophytes increase surface area and thus decrease the stress. The capsule can also relax due to the decreased stress. The capsule maintains joint integrity. When the capsule is loose, the joint gets loose. There are 2 theories about osteophytes: 1). Due to laxity of capsule, osteophytes develop and they will stretch the joint out again 2). They grow to increase surface area to reduce stress.

New research points to osteoarthritis as a bone disease and not a cartilage disease like originally thought.

4 Classic X-ray Signs

1. Decreased Joint Space 2. Subchondral Sclerosis 3. Osteophytes 4. Geode Formation

Cold Weather and Geode Irritation

Cold weather can affect the geode. Cold weather with low pressure systems brings storms. The pressure drop can affect the cysts which cause them to expand. This irritates the pain receptors in the bone.

RA

The difference between RA and OA is that RA is a synovial disease vs. OA a soft tissue disease. RA destroys cartilage by different process. RA does not form subchondral sclerosis. Bone density appearance on X-ray is key way to discriminate between OA and RA. OA is more density and RA is less dense on X-ray. OA is not an inflammatory disease but there is an inflammatory component. The cartilage can flake in OA and it can stick into the synovial lining cause inflammation and inflammatory response.

The allopathic treatment for OA was anti-inflammatory medications and pain killers. Pain killers and anti-inflammatory medications can take away pain and allow the patient to move. Movement is one of the only ways the joint can heal itself. The downside of NSAID’s can be GI problems (ulcers and bleeding), and affect chondrocytes. NSAID’s can be counterproductive for repair by making bad proteoglycans. The only proven treatment is low stress exercise (swimming, under water exercise, etc.).

Glucosamine Chondroitin Sulfate Supplementation

Glucosamine Chondroitin Sulfate forms part of proteoglycans. Studies may show that it can provide some assistance. More research needs to be done in this area; however, it appears to be 50/50. 50% show some improvement (especially in dogs) and 50% may have no improvement. Glucosamine –Chondroitin sulfate stops the production of halogenase and collagenase. These are enzymes that stop collagen production sparing cartilage from destruction and allowing chondrocytes the ability to make cartilage.

#1 reason people see a chiropractor is pain (pain from OA).

Ex.—Treatment of Pt. with “Knee Pain”

1. Low Stress Exercise 2. Dietary Modification (Lose Weight) 3. Check Medications (NSAID’s or corticosteroids) 4. Stop Smoking (higher risk for arthritis possibly due to decreased O2 content of blood with less O2 available for joints) 5. Supplementation

JOINT PHYSIOLOGY

Synovial Cells and Fluid in the Joint

Fluid in the joint can be one of 3 things: 1). Blood 2). Synovial Fluid 3). Pus. Blood can be indicative of bone fracture or ligament tear. Blood in the knee may be an ACL or PCL tear which have a good blood supply. Pus can be a sign of an infection causing swelling. Synovial fluid is yellow fluid. The most likely fluid in the joint is synovial fluid.

Role of the Nervous System

Fluid in the capsule in controlled by the nervous system. The sympathetic nervous system controls the amount of fluid in capsule.

Cavitation

Synovial Cells and fatty fibers (meniscoid) help control gapping of the joint. The meniscoid can trap (entrapment/extrapment). Cavitation distracts the joint. This is a – pressure sealed system. Pressure drops when space increases. Surface tension holds the joint together. At a certain point, surface tension breaks. The joint moves beyond the point of surface tension breaking and allows gas out of the soft tissues (mostly CO2). Motion continues beyond this point. We get to a point where the capsule/ligament wall is hit. The noise is not made from the gas, but the end movement is when the cavitation occurs. The “paraphysiologic space” is the point where sufficient breaking of the surface tension occurs. Rapid movement affects the capsular ligament. The paraphysiologic zone is also where the neurological effect occurs with a burst of signals back to the cord. They think this may bombard the cord with a + message (good afferentation). The ROM is increased, but the 2 edges of the joint don’t touch. You must wait 10-20 minutes for the gas to be reabsorbed so that proper stability to be returned to the joint. If the patient does vigorous exercise, they may put them self at risk for injury.

The ligament does not tear as the adjustment should be within the limits of anatomical integrity. The sound comes from the capsule popping. The ligament undergoes rapid stretch but does not tear.

This is “Anti-Newtonian” Physics…Inside the joint friction goes down as the speed goes up. This may be a special property of synovial fluid. The faster you do this, the easier it is to decrease joint friction. Speed is more important for an adjustment than power.

The Capsule sends a lot of information back to the cord.

Can you cavitate a swollen joint?

No, because the joint has + pressure (according to this model). The other side of the joint may have been cavitated and due to the neural network (other changes may occur at other levels Ex.—T7 needs to be adjusted, but can’t due to swelling…changes may occur based the neural network on T6, T5, T4, etc.).

BIOMECHANICS – 1/30/08

BIOMECHANICAL PROPERTIES OF LIGAMENTS AND TENDONS

They are almost identical in composition, but function is completely different. Type 1 collagen constitutes both. It does have some cross-linking. The difference is that the tendon starts out more parallel orientation, as a tendon runs from point A to point B. Ligaments can have many lines of pull; therefore, the orientation is different (less parallel orientation).

Ligaments

Stress-Strain Diagram: ACL ligament – 1). Stretch is placed on the ligament 2). Straight Line portion of graph is hit…Physiological loading is the straight line portion 3). The end of the elastic region we start to tear fibers 4). We have pain with some tearing of the fibers (Grade 1 sprain)

Grade 1 Sprain: IN the elastic range, when the stress is removed the fibers will return to normal. There can be pain. The ligament will snap back into the original length.

Grade 2 Sprain: Enough tearing occurs that when the ligament snaps back into place, it will be longer, longer than original length. Ligaments control excess range of motion and allow the joint to follow a movement pattern. Ligaments don’t have much stretch-ability. The stretch is about 3%. Ligaments should be tight. Grade 2 injuries can be hypermobile. The joints have abnormal biomechanics and forces through the joint. This can lead to osteoarthritis (early onset). The ligament loses some of the diameter and becomes weaker by immobilization. The ligament can get stronger and stiffer with exercise. Grade 2 ligament injuries can never return to normal function.

The ligamentum flavum is the only ligament in the body where the fibers are almost all elastin collagen (very stretchable). This is different than the normal ligament which is mostly collagen.

Grade 3: The ligament can no longer perform its function. Classically, you rebuild the ligament (often surgical management).

Noyes Chart and Noyes Study

The study immobilized normal, healthy monkeys for 8 weeks. The cast was taken off for 8 weeks and compared them to controls. The monkeys lost 39% of strength in 8 weeks of immobilization. After 5 weeks of rehab, the loss was 21%. After 12 months of rehab, the monkeys still had 9% loss.

When you injure a ligament, it takes a long time to rehab. Most athletes will not buy into that wishing to speed back into athletic competition.

Tendons

All tendons are 2-3x stronger than the muscle. When stretched, the tendon should not tear. Achilles tendon is a classic presentation of tendon rupture. A torn tendon under the microscope indicates that it was not a normal tendon. The tendon was overused. There is hemorrhaging, fat tissue and scarring within the damaged tendon, prior to the rupture. The rupture occurs because the tendon is already weaker. The tendon gets weaker by degenerative changes. The muscle should always tear first because it is weaker.

Often, middle aged women have Achilles tendon tearing. Women wear high heels during the week and on the weekends they wear gym shoes and work out. The high heels shrink the tendon and cause degenerative changes. The athletic activity stretches the tendon suddenly. The tendon goes through repetitive Microtrauma. The tendon finally ruptures. Often, surgery is the treatment for the ruptured tendon.

Tendonitis

Tendonitis = Inflammation to the tendon. True tendonitis is quite rare. They find very few inflammatory cell mediators in the area of the tendon. Chronic “tendonapathies” actually is tendinosis. Sharkey’s fibers (the last transition fibers between bone and soft tissue) are torn. Tendinosis requires rehabilitation and takes a long time to heal. Tendonitis requires rest.

Aging

A tendon and ligament in an older person is usually functional.

Pregnancy

Pelvic Ligaments may become lax due to hormonal changes. Elastin, prolaxin, relaxin all can cause changes. When the hormones stop, the stiffness in the ligaments can return.

Diabetes

Diabetic patients can have contractures and stiff joints. We are not sure why this occurs. Problems associated with diabetes relate to length of the problem. The longer the diabetes is uncontrolled, the more chronic the change including contracture and stiffness.

Steroids

Corticosteroid injection into a tendon or ligament will destroy the joint later in life. Tendon injections can lead to later tearing of the tendon.

NSAID’s

They can help tendons and ligaments and may help heal quicker. They think that it can stimulate greater cross linking; so, taking NSAIDS may not be a bad thing.

Function of a Ligament

Function of ligament is to protect joint

Tendon

Tendinosis is very common. It cannot be treated like tendonitis. It will get worse if treated like tendonitis. Eccentric exercises can help heal the tendon during tendinosis conditions.

BIOMECHANICS 2/6/08

MUSCLES

Properties of Skeletal Muscle

1 = Slow Twitch – Slow to Fatigue

2 = Fast Twitch (A and B) – Fast to Fatigue

Every muscle has a different percentage of fibers. The determination of fibers for type is genetics along with nerve supply to the muscle. The musculoskeletal system is based on the nervous system. Exercise creates greater demand on a muscle and on he nervous system causing loose sprouting of neurons (greater nerve supply budding). Atrophy causes loss of budding. We can make type 1 and type 2 more prominent (greater size), but we have a harder time changing the percentage of fibers. We undergo more hypertrophy than hyperplasia.

Neurological changes can occur with exercise. Neurological changes are often the first to occur. You can train and de-train muscles. You detrain very quickly as you can lose 10% per week. It takes longer to train and faster to detrain.

Contraction and Loading

Concentric Contraction = Shortening Contraction

Eccentric Loading = Lengthening (the muscle is told to shorten, but it lengthens)

Concentric is considered + work and eccentric is considered – work.

Isometric = The muscle doesn’t shorten or lengthen. It does not perform work, but it does expend energy.

Eccentric loading is 50-100% more efficient than concentric loading. Stretching a muscle before it fires concentrically shows greater efficiency. Eccentrically loading the muscle before a concentric repetition makes the muscle more efficient. Ex.—Depth Jumps…Depth Jumps are performed as plyometric exercises. Plyometric exercises first eccentrically load a muscle and then concentrically load a muscle. This sequence allows greater athletic performance. The reason is due to efficiency of the muscle.

Stretching

Stretching induces competition of reflexes. As you stretch, the muscle and tendon want to contract stopping the stretch. Stretching should be for 30-60 seconds. We stretch slow in an attempt to make the muscle reflex stop. We want to limit ballistic movement during a stretch. Stretching over a period of time (therapeutic stretching) works by stress relaxation.

During stretching, nothing occurs to the muscle or tendon. The muscle and tendon stay the same length. The change occurs in the joint.

In a normal person/healthy situation, be careful that the ligaments are not stretched. We don’t ever want to stretch a ligament.

Crepe

Crepe = The physiological principle of applying a force for a length of time to a living tissue. Living tissue will lengthen with a sustained, applied force.

Stress Relaxation

Stress-Relaxation = When we stretch and lock something in place the body will attempt to relieve pressure

Contraindications of Stretching

Stretching in many cases is contraindicated. Studies have not shown that stretching prevents injury. Some studies have shown that stretching may even induce injury (in normal situations).

Benefits of Cross Training

When you condition a specific muscle, you decondition other types of muscles. In some training programs, you need to cross train. This helps prevent developing muscle imbalances.

Ex.—Overhead Article – Deconditioning occurs 10-50% per week

Ex.—Overhead Article – Exercise-induced muscle pain, soreness –

Muscle can tear by eccentric loading and direct trauma (ex. Stab wound). They should not tear by concentric loading. When tearing occurs, inflammatory mediators are released. Satellite cells (also called type 2c or type 3 fibers) separate, rebuild and regenerate new muscle. Icing after an eccentric injury may not be a good idea because it can limit the amount of satellite cells sent to the area. The topic of icing following an eccentric injury is controversial.

Cramps

Studies have not proven a singular, specific reason for cramping. Lack of calcium and dehydration are listed as causes but we don’t know for sure. We do know this is a neural problem. We know the problem is not systemic, because only 1 muscle fires. It can’t be dehydration because the effect would be systemic. Our current thought is that the nervous system determines the response of the cramp. We also think that an inflammatory response can’t cause the cramp. The best way to treat the cramp is by facilitation of the antagonist.

Negative Effects of Immobilization

Immobilization Affects:

A). Joints, B). Joint capsules C). Bone D). Muscle E). Ligaments

MS (Musculo-skeletal) Decline

The MS system declines with age. After 40, the decrease is more rapid. The elderly suffer a majority of the MS injuries.

Stretch-Relaxation

The body can become more flexible by stretch-relaxation. The truth is we don’t know why.

Stretching can help to return to normal range of motion in the event of an injured patient, but in a normal situation in a healthy individual it probably doesn’t help. Breaking adhesions is a proven mechanism of stretching in a damaged area.

BIOMECHANICS – 2/8/08

PERIPHERAL NERVES

Can be injured by trauma or pinching…Ex.-- TOS, Carpal tunnel, herniated disc, stingers, plexopathy

Peripheral Nerves

Peripheral nerves require a lot of blood supply. Arteries and veins enter nerves in both directions. You can pinch a nerve and still get normal vascular supply.

Peripheral nerves do not have lymphatics. Lymphatics are designed for when veins can’t handle flow. Lymphatics suck up the excess. There aren’t lymph channels in the nerve to drain.

Putting a hole in the myelin sheath of the nerve would force the neural tissue out due to the change of pressure (+ pressure). When we compress the nerve either by injury or by orthopedic exam (ex. -- TOS), the tests try to compress the NV bundle. In TOS, the problems appear to be mostly neural and not vascular.

Compression of sensory vs. Compression of motor nerve.

The symptoms of nerve entrapment depend on the function of the receptor. The first symptom of sensory nerve entrapment is numbness. Parasthesia and inflammation follow after numbness in a sensory nerve. Pain with TOS as opposed to numbness or paresthesia would indicate a more chronic condition. The first symptom of motor nerve entrapment is weakness.

Signs of Sensory Nerve Damage

1. Numbness (in acute situations)

2. Paresthesia & Inflammation (occurs after numbness)

3. Pain (more chronic conditions)

Sings of Motor Nerve Damage

1. Weakness

Damage to a Nerve by Stretching

Damage to nerves can occur by stretching. Stretching a tube of a nerve increases the pressure. The weak link as pressure increases is the veins. The veins compress and they can’t drain. Blood can’t leave and eventually can’t get in. Ischemia will develop along the stretched area. The classic example is disc herniation.

The herniation stretches the nerve. The fist sign of the herniation is variable. There may pain or no pain. As the nerve stretches, it starts to necrose and may decrease function causing numbness. There may also be a pain response due to inflammation. Inflammation can generate pain. It is believed that inflammation during a herniation contributes to the pain felt during a + SLR test.

Stretching a nerve forces the axons to be weaker than connective tissue. Under a microscope it will appear the same, but there is damage to the axon. The axon cannot function as it normally should despite lack of microscopic presentation of damage.

Damage to a Nerve by Compression

Nerves are also injured by compression. Compression is a more common mechanism for nerve damage than stretch. Ex. – CT Syndrome (Carpal Tunnel)…The only good orthopedic test for CT syndrome is the Tinnel’s tap test. All the other tests are not so good. The cause of CT syndrome is compression of the median nerve. CT is linked to pregnancy, arthritis (rheumatoid – pannus formation can cause compression of median nerve), diabetes, ergonomic problems (repetitive Microtrauma – inflaming the synovial tendon). These conditions all compress the median nerve.

Axoplasmic Flow

Flow with the neuron/nerve goes both ways and has different speeds and direction.

A). Cell body to End of the Neuron – Trophic material…Trophic material (nutrients are sent from the cell body to the terminal ends of the neuron)

B). Back to Cell Body = Information (telling cell body what to do)

The easiest thing and the first thing interrupted with nerve damage is disruption of axoplasmic flow. Parkinson’s Disease (Lou Gehrig’s) presents with changes in axoplasmic flow. Axoplasmic flow is very hard to measure. They are starting to measure this on MRI.

The “silent killer” in public health used to be “subluxation.” Subluxation can cause problems with the autonomic nervous system…Ex. --Animal experiments that induced subluxation…Function of the kidneys in the animals was the same in the subluxation induced groups vs. the controls; however, histologically, the kidney cells were slowly damaged. At the end of the experiment, kidney failure occurred in the subluxation group with evidence finally apparent that function had changed. At that point it was too late to treat the animals with kidney failure. So the conclusion was that the damage from subluxation to the axoplasmic flow was a “silent killer.” The small histological damage took a long time to manifest into a decrease in function. By the time the decreased function presentation occurred, it was too late.

Axoplasmic flow is hard to be studied in a clinical setting. It is more easily studied in a research setting. Axoplasmic flow can be affected in both directions over the course of the nerve, leading to problems in many areas. Problems can occur anywhere the nerve travels.

BIOMECHANICS – 2/13/08

DISC

Purpose of a Disc

We have discs to help allow motion and so that we can transmit forces from one vertebra to another. The primary purpose is not shock absorption, the primary purpose is motion.

Disc Nociception

The substance in the disc (hyaline cartilage and disc tissue) doesn’t have pain fibers. The majority of the disc is not nociceptive. There is some mechanoreception that occurs in the disc. The NP and inner 2/3 of the annular fibers probably does not have nociceptors.

Composition of the NP

Disc is made of NP (nucleus pulposus). The NP is a high percentage of water with some proteoglycans. It doesn’t have a lot cells, but it is active. Type 2 collagen is located in the nucleus, smaller, and lacks tensile strength

Composition of the AF

The annulus fibrosis (AF) has mostly collagen. The annulus is made of water and type 1 collagen. Type 1 collagen has strong tension.

A watery substance like the nucleus has strength advantages, mobility and deformability….Ex.—A water balloon can deform as long as it doesn’t break. Compression of a disc causes the nucleus to expand, but it can’t fully expand because it’s contained. The annular fibers run at an angle and bend very little due to the stiffness of type 1 collagen. Type 1 collagen has a strain rate of 3% (it’s very stiff). The nucleus is not able to change shape due to the stiffness/resistance provided by the AF fibers.

Endplates

The end plates are embryologially part of the disc. Trying to pull the endplates from the disc will result in the endplate staying with the disc. The endplate is made of hyaline and fibrocartilage. The endplate is not very thick (less than 1 mm).

The disc does not have a lot of blood or nerve supply. The endplates serve as a pathway for the disc to exchange nutrients and get rid of wastes. This pathway occurs due to poor blood flow. Poor blood flow does not allow for good oxygenation within the disc. The O2 content of the disc is low due to the acidic and anaerobic nature of the environment with poor blood supply. In the middle of the nucleus it is 5% or less O2. The pH is acidic due to lactic acid. This does not create a problem since we do not have pain sensitive fibers in the nucleus pulposus.

Compression of the Disc with Lateral Bending

Ex. -- Lean to the Right the Compression & Compression is to the Right…Normally compression is in the direction of movement. It is impossible to go any other way with a normal disc. In an injured disc, this process may occur differently.

Orientation of Annular Fibers and Resistance to Movement

The annular fibers run at 60-70 degrees. The fibers overlap, running in different directions. When the fibers are oriented straight up, they all resist tension. The disc is stronger resisting compression and distraction (motions up or down). Pushing straight down provides some resistance, as the nucleus tries to spread out but the fibers of the annulus resist.

Twisting or sliding forward, some fibers resist (those aligned to do so), but other fibers don’t resist. Twisting or sliding the spine is the most common mechanism associated with injury. The primary reason is that fibers are not all oriented to resist the motions of twisting and sliding. This mechanism takes away the fibers that can resist, providing more stress on those that do (compromising these fibers).

Movements of flexion and extension cause 1 mm or so of deformation. Flexion increases internal compression. Rotation places pressure on specific places of the disc. The pressure in the disc comes from the muscles in the back. Muscles of the back have to contract harder and harder to keep you upright with flexion. Muscle tension causes compression of the vertebra.

Aging Process

The disc is mostly water (nucleus)…At birth there is about 90% water in the nucleus…At 80 years old the water is about 65%. There is not a linear decrease between birth to 80 years old. The decrease is rapid in the first decade of life. After 10 years of age, you don’t lose much water. There is a big difference in proteoglycans with aging but not with water content of the disc.

The annulus doesn’t change much with age. The annulus gets thicker and stiffer and loses a little elasticity.

In a young, healthy disc, the nucleus is translucent with the annulus fibers as white. As you age, the color blends together (white/yellowish). In old age, you can’t determine the color.

The most likely age for nuclear herniation is aged 20-40.

Size

The size of the disc increases with age. 5-10% increase in diameter and slight increase in height occur with age. They think thickening of annular fibers with the endplates becoming more convex causes an increase in height. The disc pushes into the endplate increasing the height. Clinically, a shrinking disc is a problem indicating disc pathology. .

Flexibility

Flexibility = How far can you go before the bones touch.

Flexibility and Discs

Children have faster development of the disc than the vertebral column. The discs grow 1st and then the body catches up. By the time you turn 20, the disc height is about ¼ to 1/3 the height of the vertebra.

Cervical Spine

The cervical spine is very flexible. The ratio of the body to disc is greater at C4-C5 and C5-C6 than anywhere else in the spine.

Thoracic Spine

The disc is 1/10th to 1/12th the height of the other discs. Removal of the ribs will not significantly increase motion of the thoracic spine.

Shape of Spine

Curves are influenced by discs.

A. C-Spine: The lordotic curve of the C-spine is due to the discs. Removal of the C-spine discs would cause kyphosis, as the cervical vertebra are smaller in the front and bigger in the back. A reverse curve in the C-spine can possibly indicate pathology.

B. T-Spine: T-spine vertebra are small in front and big in the back. Discs in the T-spine are flat. If we took the discs out of the T-spine, we would still be kyphotic.

C. L-Spine: Vertebrae in the L-spine are transitional. Lumbar vertebra in some cases are bigger in front than in back, while others can be bigger in the back than in the front ((L –spine is built by both). Theoretically, L3 should be transitional zone; however, in most cases it is not! There is a lot of variability. Lumbar curve can be determined by either disc or vertebral size and possibly even both. This variability accounts for differences in couple motion in each person.

Biomechanics – 2/15/08

PATHOLOGICAL DISCS

Herniation and Degeneration

Degeneration = Degeneration is most common (seen in most patients). The amount of degeneration does not correlate well with symptomatic presentation. There can be extreme degeneration with mild symptoms and mild degeneration with major symptoms.

The weak link is the end plate. The end plate is the “Achilles Heel” of the spine. The end plate is thin with holes in it allowing blood flow to chondrocytes and fibroblasts. The end plates are easy to break due to the thinness and holes. The environment of the disc has to be within a specific pH range. The endplates provide the nutrients by exchange of water (imbibition). Immobilizing the disc causes deterioration due to lack of nutrition.

Ankylosing Spondylitis is an example of a condition that fuses the spine. This condition immobilizes the disc and bones. A fused cervical spine can cause paralysis. Don’t adjust a fused joint.

Herniated Discs

Drilling into the nucleus and placing compression on the disc will not force the nucleus to herniate out. The nucleus is not totally liquid, so even with a tear it won’t flow out. To make the tissue more liquid, you must change the pH.

New Theory of Disc Herniation

The current theory of disc herniation states that the 1st step of herniation is an endplate fracture. The fracture may cause blood vessels to run down into the nucleus. Fracturing the endplate changes the permeability of the endplate leading to nutrients not leaving the disc. The nucleus may become more liquid like or slippery due to the change in the environmental pH. The change in environment combined with an annulus tear from pressure exerted by movement makes the nucleus more mobile. A more mobile nucleus protruding through a weakened annulus is the classic herniation.

Current Theory of Disc Herniation

1. End Plate Fracture = Causes blood vessels to run down into the nucleus

2. Permeability and pH Change = Occurs because nutrients cannot enter and wastes cannot leave

3. Nucleus becomes watery/slippery = due to the environmental change

4. Annulus Tear = Annulus tears from change in pressure from movement…Movement places the annulus in a compromised position

5. Disc Herniation = A changed nucleus combined with an annulus tear has led to the herniation.

Degeneration vs. Herniation

The disc eats itself away and degenerates without a pathway for the nucleus to herniate through (annular tear). This eventually causes DDD (degenerative disc disease) presenting as shrinking of the disc.

Fracture with no place to go = degeneration

VS.

Fracture with ability to move (preexisting tear…commonly postero-lateral) = Herniation

Pictures of 4 Discs on Overhead

Normal Disc = Clear Nucleus, Annulus is white…End plate is thin but intact

Degeneration = Yellow, Whitish Color …Endplate is intact but it getting rough

More Degeneration = Yellow, white, red…End plate fracture causing bleeding into the internal disc affecting the nucleus…You have trouble differentiating the nucleus from annulus

Greater Degeneration = Everything appears brown…You cannot differentiate the nucleus from the annulus

Degeneration is not necessarily aging, but it indicates a pathological change.

End Plate Fractures

May not be visible on plain films and CT…May be seen on MRI due to vascular changes. The classic thing is bending and picking something up with a snap or pop and pain. A couple weeks or months later there is back pain with radiation.

Schmorle’s Node

Disc material moves up or down from the end plate to the vertebral body via imbibition. The significance of a Schmorle’s node is that the environment of the disc is changed. It is a common problem. Schmorle’s node may not always be present of plain films. Usually they occur during growth spurts (children 4-5 and teenagers 13-15). In adults, a Schmorle’s node is associated with trauma/fracture.

Herniation

The material in the disc during herniation changes consistency. When disc material leaves the anaerobic low pH environment, it starts to swell. The ESR (sedimentation rate) test is a sign of inflammation (blood marker for inflammation). A + ESR will be present with herniation. The body treats the disc as a foreign object and attacks it.

Macrophages and other body materials will eat up the disc material causing an increase in size and swelling. The herniation can calcify or be completely removed.

Herniation can heal 6 weeks to 6 months. Often times, surgery is not recommended as the first treatment choice for herniation.

A herniation can extrude. Extruding disc has an intact annulus. The tear does not pierce through the annulus fibers. The nucleus can protrude into canal taking with it intact annulus fibers. The big thing with the extrusion is that there are pain fibers in the annulus that are irritated. The fibers are irritated by mechanical and chemical stimuli. This pain can last a long time, since the annular fibers remain intact. In other types of herniation, the breaking of the annulus and the initial insult of pain is severe, but the pain goes away quick to the body’s environment attacking the herniation.

Sciatica

Sciatica from a disc herniation is not the pressure on the nerve. The compression is minimal. The environment and inflammation may irritate the nerve, especially irritating the DRG causing the sensations associated with sciatica.

Criteria for Surgery

The nucleus exiting the canal can heal on its own. The size of the herniation was the criteria for surgery, but they found the smaller herniation hurt more and took longer to resolve. Smaller herniation cannot be attacked aggressively by the body and take longer to remove. Larger herniation had less the pain and less chance for surgery. Larger hernation had more aggressive attacks by the body causing faster resolution.

Disc Herniation Presentation on MRI and Determination of the Disc as a Pain Generator

Disc herniation can be found on many MRI’s in absence of clinical signs/symptoms. The disc may not be generating the pain. A discogram can determine if the disc is a pain generator. The discogram is a test where a needle is inserted into a disc with contrast. The disc is blown up with air to determine if it is the pain generator. This creates mechanical and chemical irritation and severe pain. The discogram can give an idea of the internal arrangement of the disc. It is a very painful exam. You cannot give them an anesthetic because the goal is to find the painful disc which is the pain generator.

Adjustment of the Spine for Bulge and Herniation

Adjustment in a PA position will extend the spine. This brings the ends of the joint together and is theorized to change the internal pressure of the joint forcing some of the material and nutrients to realign. This is the theorized model of how an adjustment may work in a bulge or herniation.

Research has led to the belief, that surgery is a last resort. One of the best options is chiropractic. We don’t know exactly why it works or the mechanism.

Cox Method/Cox Flexion-Distraction

This technique attempts to change the pressure. We are not exactly sure of the mechanism. We do think that the method may be effective due to exchange or pumping of metabolites via the flexion/distraction movements.

Cervical Spine Herniation vs. Lumbar Spine Herniation

Most herniation is posterior. This is due to the uncinate processes serving as protection in the lateral borders of the C-spine. In the lumbar spine, most herniation is postero-lateral. The lumbar spine does not have an uncinate process or mechanism to impede a postero-lateral herniation as the C-spine does.

4 Good Tests for Herniation

1. Valsalva = Increases intrathecal pressure…internal pressure increased so blood backs up and veins become engorged. The build up of pressure forces the tissue into the veins and pain is generated

2. Dejerine’s triad = Coughing, sneezing, bearing down…Laughing may also be added to the triad

3. SLR = Pulls on sciatic nerve

4. Braggard’s = Sitting sciatic test that pulls on the sciatic nerve. This test takes the hip and hamstring out by the patient in a seated position.

Other Good Tests for the Lumbar Spine

Saccard’s: Differentiates between L4 and L5

Turyn’s: Do it first because the test is most sensitive…Most people with herniation may have + test

Milgram's: Lay them flat with the doctor picking the patient’s legs up and pt. holds leg up (+ finding is pain…It is a good test because it checks the psoas…The psoas muscle contracts and pulls on the discs themselves…It tests the disc in compression with hip and trunk flexion movements).

Well Leg Raise: + well raise with +SLR gives you good odds that the problem is a herniation/disc related.

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