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Posterior and anterior tilt

Lateral Shift

Oblique tilt

Pelvic rotation

Pelvic torsion

Shape of Gluteus Maximus muscles:

Observe symmetry. Look at the level of gluteal folds- asymmetry indicates inhibition or weakness of the ipsilateral side, which will be lower.

Slight asymmetry indicate inhibition or weakness-look at the upper external quadrant.In this case it will be flat on palpation as the result of decreased of the muscle tone.

Asymmetry of the pelvis will cause changes to lower back extensors and hamstrings.

Weakness of Gluteus Maximus will lead to lowering of gluteal fold on the same side.

Than look to the lumbar and thoracolumbar area.Look for scoliosis, rotation or kyphosis which may influence the shape of the muscles.

Than compare muscles at the lower lumbar region to the muscles at the thoracolumbar junction. Atrophy at the lower segment of the lumbar muscles will require stabilization and  lead to the hypertrophy of the muscles at the thoracolumbar segment.

Normally, lumbar segment is symmetrical and flatter than thoracolumbar segment which is slightly more prominent but still symmetrical.

Than proceed to the upper part of the body:

Shoulder blades can be protracted, retracted, shifted upward or abducted.

Look at the stabilizers: lower stabilizer (lower trapezius) interplays with upper stabilizers (upper trapezius,m. levator scapulae)

Interscapular region:

This area will be flat in the case of muscular inhibition. Weakness or inhibition of the serratus anterior will lead to winging of the scapulae.

If you see atrophy of the lower stabilizers (lower trapezius) than observe upper stabilizers (upper trapezius and m. levator  scapulae) which will be compensatory hypertrophic, which will lead to abduction and weaning of the scapula.

To look closely to the quality of the upper trapezius and levator scapulae focus on the reference  line  from the occiput/lateral neck and the Acromion . This line normally should have “S” shape.When levator scapulae and trapezius are overactive this line became straight.This called “Gothic shoulders”.

Another example of insufficient scapular stabilization will be protracted scapulae due to inhibition of the medium and lower trapezius, rhomboids and overactive serratus anterior.

Upper trapezius in this cases usually overactive which lead to superior shift of the scapulae.

Observation of the anterior shoulder provide information about humeral control:

flattening of the deltoid abductors indicate deltoid atrophy, altered pattern of the shoulder’s muscles and impaired  proprioception from the shoulder joint.

In the assessment of the lower extremity first view the subject general posture.

E/Rotation of the feet exists  may indicates problem with the muscles or the joint of the hip.

Look at the knee joints: varus , valgus or hyperextension

Correlate limb alignment with calcaneal bone and the position of the forefoot.

Varus leg deformity associated with pronation of the foot and flattening of the foot.

Than estimate the shape of each individual muscle groups.

First, look at the Hamstrings: note if the size of the hamstrings is symmetrical

Usually if gluteal muscle is weaker ipsilateral hamstring compensatory stronger.

Hamstrings best seen in the medium and upper thirds of the thigh.

The second important group of the thighs are ADDUCTORS

In general, there are two groups of adductors: Short (cover upper and middle thigh)and Long(cover entire thigh).

Normally, from posterior view adductors create very shallow letter “S”

If upper adductors are in spasm than upper portion of the “S” will be bulkier. As a compensation of this process lower portion of the “S” will be flat -hypotrophy,-hollow just above the knee.

Than look at the calfs: shape and symmetry. Estimate the tightness of hypotrophy of the m.soleus  muscles in the relation to gastrocnemius muscles

If the solei are tight and short, the muscle belly is evident at the medial border just superior to the Achilles tendon. (The m.soleus is located just underneath the gastrocnemius, and together these two muscles form the Achilles tendon. Since these are the 2 biggest muscles in the calf, they provide the majority of the push off when walking, running, and jumping)

If m.Soleus is tight than Achilles tendon become slightly thicker and shorter.

observation of the heel.

No symmetrical person.No specific norms.

Variation of the muscle

anterior view:

ASIS and umbilicus

Rectus abdominis: Upper quadrants more active than lower quadrants. But left and right are symmetrical.

Observe the groove on the lateral edge of the rectus abdominis: it reflects quality of interplay between m.rectus abdominis and m.obliqus abdominis externus. The more prominent this groove -the stronger m.obliqus abdominis externus and m.Rectus abdominis is inhibited.

Next, look at the lateral edge of the waist, which is normally concave. If it become flat or convex shape- sign of weakness of m.transversus abdominis which stabilize abdominal wall and spine properly.

In the upper trunk look at the symmetry of the muscles and respiratory movement of the chest wall. Focus mainly on the pectoralis major.

Compare muscular folds on both sides.The pectoralis muscle is more prominent on the dominant side. Positions of the nipples. If pectoralis is tighten, nipple will be displaced superiorly and laterally. In female, asymmetry of breasts may indicate m.pectoralis tightness.

Observe neck: SCM muscle, which under normal circumstances will be almost invisible.

Usually we only see insertion in the sternoclavicular region. If the muscle belly is pronounced it indicates muscle hypertrophy.

Groove in the area medial to SCM (between SCM and Scalenus muscles )

The more prominent this groove the weaker (hypoactive)the Scalenus muscle

“Facial scoliosis”-asymmetry of face

4 points:

These points must be symmetrical. Also observe lateral bending and rotation of the head.

Observe hip, knee and feet position.

First look at the tensor fascia latae. normally this muscle is invisible. If muscle is visible it indicate hypertonus of the MTFL.

Than look at the position of the patella: Symmetry, presence of the shift: if quadriceps is tight than patella shifted superiorly

if MTFL is tight patella will shift supero-lateraly and tilt

If vastus medialis is hypertrophied you will see muscle bulk medially to patella

It is usually sign of overstressed knee joint

When proprioception of the knee is altered patella will move in irregular manner from intermittent activity of the m.quadriceps to improve stability of the knee joint.

This vertical translation of the patella is an important sign of poor proprioception of the knee joint.

Look at the lower leg, primarily tibias anterior.

If M.tibialis anterior (anterolateral aspect of the lower leg, just below the knee) is weak than it’s fibers become flat or even they develop groove-early sign of L4-L5 irritation.

Look at the toes.

”Unquiet foot” irregular twitching movement of the tendons of the toes in the different directions-sign of impaired proprioception and the more demanding effort to maintain the balance.

Torso:

Lateral view: Look at the presence of anterior or posterior tilts.

Look at the lumbar, thoracic and cervical curvatures:The interrelationships of which may depend on the balance between  hips flexors and extensors or abdominal muscles and back extensors.

Look at the position of the head, particularly “push forward head position”

Observe line running from the jaw to the hyoid bone: if the supra-hyoid muscles is tight this line become more straight, indicating TMJ problems

Look at the position of the legs, particularly knees (genu recurvatum)

Look at the greater trochanter- MTFL: if groove is present-MTFL is tight

Collagen is the most abundant protein found in mammals, making up about 25 percent of the total proteins in the human body. There are at least 16 types of collagen, but 80 – 90 percent of the collagen in the body consists of types I, II, III and IV. Type I: Makes up the fibers found in connective tissues of the skin, bone, teeth, tendons and ligaments.
Type II: Round fibers found in cartilage.
Type III: Forms connective tissues that give shape and strength to organs, such as the liver, heart, kidneys, etc.
Type IV: Forms sheets that lie between layers of cells in the blood vessels, muscles, and eye.

These collagen molecules pack together to form long thin fibrils of similar structure.  At one time it was thought that all collagens were secreted by fibroblasts in connective tissue, but we now know that numerous epithelial cells make certain types of collagens. The various collagens and the structures they form all serve the same purpose, to help tissues withstand stretching.

The triple-helical structure of collagen arises from an unusual abundance of three amino acids: glycine, proline, and hydroxyproline. These amino acids make up the characteristic, repeating motif Gly-Pro-X, where X can be any amino acid. Each amino acid has a precise function.  Collagen biosynthesis and assembly follows the normal pathway for a secreted protein. The collagen chains are synthesized as longer precursors called procollagens; the growing peptide chains are co-translationally transported into the lumen of the rough endoplasmic reticulum (ER). In the ER, the procollagen chain undergoes a series of processing reactions.

Post-translational modification of procollagen is crucial for the formation of mature collagen molecules and their assembly into fibrils. Defects in this process have serious consequences, as ancient mariners frequently experienced. For example, the activity of hydroxylases requires an essential cofactor, ascorbic acid (vitamin C). In cells deprived of ascorbate, as in the disease scurvy, the procollagen chains are not hydroxylated sufficiently to form stable triple helices at normal body temperature, nor can they form normal fibrils. Consequently, nonhydroxylated procollagen chains are degraded within the cell. Without the structural support of collagen, blood vessels, tendons, and skin become fragile. A supply of fresh fruit provides sufficient vitamin C to process procollagen properly.

The biosynthetic pathway responsible for collagen production is a very complex one. In addition to Vitamin C, collagen crosslinking requires Copper, Iron and Manganese.

Prolyl hydroxylase and lysyl hydroxylase require vitamin C and iron as cofactors. Lysyl oxidase deaminates lysine and hydroxylysine in the first step for collagen crosslinking, and this requires copper (hence the hair and skin signs in Menkes disease).

Linus Pauling

In 1989, the eminent American scientist and two-time Nobel Prize winner, Linus Pauling, announced a breakthrough “A Unified Theory of Human Cardiovascular Disease,” Linus Pauling thought that the deposits of plaque seen in atherosclerosis were not the cause of heart disease, but were actually the result of our bodies trying to repair the damage caused by long-term vitamin C deficiency. In essence, Pauling believed that heart disease is a form of scurvy, and plaque is the body’s attempt to reinforce and patch weakened blood vessels and arteries that would otherwise rupture. Pauling also showed that heart disease can be prevented or treated by taking vitamin C and other supplements.

Plaque Deposits

Pauling based his revolutionary theory on a number of important scientific findings. First was the discovery that plaque deposits found in human aortas are made up of a special form of cholesterol called lipoprotein (a) or Lp(a), not from ordinary LDL cholesterol. Lp(a) is a special form of LDL cholesterol that forms the thick sheets of plaque that obstruct arteries.

Another finding central to Pauling’s theory was the observation that plaque deposits are not formed randomly throughout the circulatory system. This was first reported in the early 1950s when a Canadian doctor, G. C. Willis, MD, observed that plaque always forms nearest the heart, where blood vessels and arteries are constantly being stretched and bent, rather than being spread evenly throughout the entire cardiovascular system. Willis also noted that plaque deposits always occur in regions that are exposed to the highest blood pressures, such as the aorta, where blood is forcefully ejected from the heart.

In 1985, a team of researchers verified that plaque only forms in areas of the artery that become damaged. These small areas of damage expose strands of the amino acid lysine (one of the primary components of collagen) to the blood stream. These strands attract Lp(a). Lp(a) is an especially “sticky” form of cholesterol that is attracted to lysine. Drawn to the break, Lp(a) begins to collect and attach to the exposed strands. As Lp(a) covers the lysine strands, free lysine in the blood is drawn to the growing deposit. Over time, this process continues as lysine and Lp(a) are both drawn from the blood to build ever-larger deposits of plaque. This process gradually reduces the inner diameter of the vessels and restricts its capacity to carry the blood.

Heart Disease as Low-Level Scurvy?

Observing the newly described process of plaque formation, Pauling recognized a similarity to underlying processes seen in scurvy. He also saw similarities between human and animal models of atherosclerosis that pointed to a connection with scurvy. First, cardiovascular disease does not occur in any of the animals that are able to manufacture their own vitamin C. Many animals produce large amounts of vitamin C that are equivalent to human doses ranging from ten to twenty grams per day. Second, the only animals that produce Lp(a) are those which, like man, have also lost the ability to produce their own vitamin C, such as apes and guinea pigs.

Pauling suggested that the ability to form plaque is really the body’s attempt to repair damage caused by a long-term deficiency of vitamin C. Pauling thought that scurvy was one of the greatest threats to humankind’s early survival, and believed that the loss of blood during times of vitamin C deficiency, particularly during the Ice Ages, likely brought humans close to the point of extinction.

Plaque as a Life Saver?

The core of Pauling’s theory is that, over time, the body developed a repair mechanism that allowed it to cope with the damage caused by chronic vitamin C deficiency. When arteries became weak and began to rupture, the body responded by “gluing” the damaged areas together with Lp(a) to prevent a slow death from internal bleeding. In essence, plaque is the body’s attempt to patch blood vessels damaged by low-level scurvy. Accordingly, Pauling believed that conventional “triggers” of plaque formation, such as homocysteine and oxidized cholesterol, are actually just additional symptoms of scurvy.

Collagen Melts Plaque, Keeps Arteries Open

In addition to taking vitamin C to prevent atherosclerosis, Pauling recommended a combination of vitamin C and the amino acids lysine and proline to help remove existing plaque while strengthening weak and damaged arteries. As mentioned previously, the body produces collagen from lysine and proline. Pauling reasoned that by increasing concentrations of lysine and proline in the blood, Lp(a) molecules would bind with the free lysine, rather than with the lysine strands exposed by the cracks in blood vessels.

Pauling Therapy for the Reversal of Heart Disease

1. Vitamin C: to bowel tolerance – as much as you can take without diarrhea. For most people this will be in the range of five to ten grams (5,000-10,000 mg.) each day. Spread this amount into two equal doses 12 hours apart. (Vitamin C prevents further cracking of the blood vessel wall – the beginning of the disease.)
2. L-Proline: 3 grams twice per day (acts to release lipoprotein(a) from plaque formation and prevent further deposition of same).
3. L-Lysine: 3 grams twice each day (acts to release lipoprotein(a) from plaque formation and prevent further deposition of same).
4. Co-enzyme Q10: 90-180 mg. twice per day (strengthens the heart muscle).
5. L-Carnitine: 3 grams twice per day (also strengthens the heart muscle).
6. Niacin: Decreases production of lipoprotein(a) in the liver. Inositol hexanicotinate is a form of niacin which gives less of a problem with flushing and therefore allows for larger therapeutic doses. Begin with 250 mg. at lunch, 500 mg. at dinner and 500 mg. at bedtime the first day; then increase gradually over a few days until you reach four grams per day, or the highest dose under four grams you can tolerate. Be sure to ask your doctor for liver enzyme level tests every two months or less to be sure your liver is able to handle the dose you are taking.
7. Vitamin E: 800-2400 IU per day. (Inhibits proliferation of smooth muscle cells in the walls of arteries undergoing the atherosclerotic changes.)

Dr. Renata Trister DO

The Marshall Protocol is a medical treatment used by physicians worldwide to treat a variety of chronic inflammatory and autoimmune diseases including Chronic Fatigue Syndrome, Fibromyalgia, Crohn’s Disease, Sarcoidosis and Rheumatoid Arthritis.  Dr. Marshall started his research after to being diagnosed with sarcoidosis. After reading studies that demonstrated Rickettsia DNA in sarcoid patients, and by noting that his disease was worsened by sunlight. He developed a hypothesis, and a treatment protocol to treat chronic inflammatory illnesses.

Sarcoidosis is a disease whose etiology is unknown, but is characterized by non-caseating granulomas.  Granulomas are an immunologic response to infections, often fungal or mycobacterial. Sarcoidosis frequently causes dysregulation of vitamin D with increased levels in the blood, the vitamin D being made in the granulomas.

The Marshall Protocol is based on the hypothesis that “chronic diseases (termed T-helper [Th1] illnesses) are the result of infection by an intraphagocytic, metagenomic microbiota of chronic bacterial forms that are often referred to as the Th1 pathogens”. The term intraphagocytic refers to the fact that these bacteria have developed the ability to remain alive and proliferate undetected inside the cytoplasm of the cells they infect. These cells include macrophages (cells of the innate immunity), the very cells that the body uses to kill invading pathogens. Once inside these cells, they cause our own cells to release inflammatory cytokines (proteins that often generate pain and inflammation).

The term metagenomic indicates that there is a tremendous number of different species of these chronic bacterial forms. Finally, the term microbiota refers to the fact that these bacteria are also thought to sustain themselves by grouping into communities called biofilms. The bacteria inside a biofilm produce a protective matrix that allows them to more effectively evade the immune system and develop resistance to antibiotics.

Many of the Th1 pathogens are also postulated to be in a chronic state referred to as the L-form. Under certain conditions, L-form bacteria mutate from classical bacteria and lose their cell walls. Since L-form bacteria lack a cell wall, many antibiotics (that target bacterial cell walls) are not effective, furthermore these pathogens cannot be detected by standard laboratory tests.

The ability of the Th1 pathogens to proliferate in the body is directly related to the vitamin D receptor (VDR). Critically important to the body, the Vitamin D Receptor (VDR) controls the innate immune system – the body’s first line of defense against infection. It’s also responsible for turning on/off a wide array of genes and chemical pathways. One of the VDR’s myriad jobs is to control expression of several families of antimicrobial peptides (AMPs), proteins that kill bacteria, viruses and fungi by a variety of mechanisms including disrupting membranes, interfering with metabolism, and targeting components of the machinery inside the cell.

Although casually referred to as a vitamin by some members of the medical community, molecular biologists have long realized that the precursor form of vitamin D (25-D) is really a secosteroid.  Elevated levels of 25-D can bind and inactivate the VDR, which subsequently shuts down the innate immune system.

Certain species of bacteria also produce substances that can bind and inactivate the VDR in a manner similar to 25-D. Consequently, people who are infected with the Th1 pathogens and consuming vitamin D are no longer able to produce the AMPs or turn on the innate immune response. This allows their bacteria to proliferate and spread.

When the innate immune system can no longer function, people have a very hard time keeping other pathogens under control. They often find that childhood viral infections reactivate, or that they acquire Candida (pathogenic yeast) and Mycoplasma as well.

Unlike its inactive counterpart, 25-D, that inactivates the VDR in healthy individuals, 1,25-D binds and activates the VDR. But in individuals who have 25-D and bacterial proteins blocking the VDR, 1,25-D is forced out of the receptor and into the surrounding environment. Causing 1,25-D to rise to an unnaturally high level.

The nuclear receptors affected by 1,25-D are receptors that regulate the body’s hormones – the glucocorticoid receptor, and the alpha and beta thyroid receptors, the adrenal receptors, and the progesterone receptors, among others.

This means that when 1,25-D is high, it competitively displaces cortisol, T3, and other metabolites from their target nuclear receptors, causing havoc on the body’s hormonal pathways. Thus, most people with chronic disease find they have difficulty tolerating stress, changes in temperature, and a variety of other hormone-related issues. Also, when levels of 1,25-D rise above 42 ng/ml, calcium begins to be leached from the bones, a process that results in osteoporosis and osteopenia.

When 1,25-D rises due to the processes described above, it also binds a receptor called the PXR. The PXR subsequently inhibits conversion of pre-vitamin D to 25-D, causing 25-D levels to drop. This means that low levels of 25-D – the form of vitamin D measured by most doctors – is not a sign of vitamin D deficiency. Instead, low levels of 25-D are a result of the disease process.

The Treatment

Patients on the Marshall Protocol take a medication called olmesartan (Benicar), which is able to bind and activate the VDR by pushing 25-D and bacterial proteins out of the receptor. Patients also lower levels of 25-D in the body by avoiding the kinds of vitamin D present in various foods. These measures renew the body’s ability to turn on the innate immune system and produce the anti microbial peptides. The immune system is then able to kill the Th1 pathogens and is once again able to manage viral and other co-infections.

At the same time, MP patients take pulsed, low-dose antibiotics. Antibiotics taken in this manner are much more effective against bacteria in biofilms and are able to greatly weaken the Th1 pathogens so that the patient’s own immune system is then able to destroy them. The antibiotics weaken the bacteria by blocking their ribosomes, which they need to produce proteins that help them survive and reproduce. It’s important to understand that when the Th1 pathogens die, there is a temporary change in a patient’s immunopathology.

Immunopathology refers to the changes in the immune system that result from bacterial death (another term sometimes used is the Jarisch-Herxheimer or “Herx” reaction). Dying bacteria release toxins into the bloodstream, stimulate the production of inflammatory cytokines, and generate temporary hormonal imbalances. This means that once patients begin the MP, each dose of antibiotic will cause them to feel bad for the period of time it takes their immune system to deal with the consequences of bacterial die-off.

Before starting the MP, many people may feel that they have improved through consuming vitamin D and taking steroids such as prednisone. In reality, these compounds further inactivate the VDR, preventing the immune system from effectively killing the Th1 pathogens. Since it is the death of these forms of bacteria that generates an increase in painful symptoms, people may experience short-term relief when using vitamin D or prednisone as their immune system shuts down and fewer bacteria are killed. However, in reality, this situation allows the bacteria to spread more easily.

Applicable Illnesses

Patients on the MP have dozens of different medical conditions. As evidenced by members’ reported progress on the marshallprotocol.com website, nearly all experience a powerful immunopathological reaction after taking a dose of antibiotics.

Many patients report great improvement, while some are approaching complete recovery.

Some of the diseases patients are currently using the MP to treat include (but are not limited to):

Chronic Fatigue Syndrome

Fibromyalgia

Chronic Lyme disease

Rheumatoid Arthritis

Multiple Chemical Sensitivity (MCS)

Myasthenia gravis

Psoriasis

Osteoarthritis

Sarcoidosis

Hashimoto’s Thyroiditis

Uveitis

Apart from the symptoms or diagnosis indicating Th1 disease, the easiest way to find out if the Marshall Protocol may be applicable to your disease is to get a blood test and check the level of your D Metabolites. This test can detect the elevated level of 1,25-D often seen in patients with chronic disease, but must be done correctly in order to be of any value.

Patients can also use a therapeutic probe to determine whether the MP can be applied to their illness. A therapeutic probe refers to a trial period during which a person tests whether or not the taking the MP medications results in immunopathology or other symptom changes.

Jon Trister , MD.
With this issue of the newsletter, I would like to bring our attention to sacroiliac joint problems and the interrelationship between such as Fascia, Osseous structures, Ligaments, Muscles, Tendons, Neuro-Vascular structures, and Visceral structures.

There are different degrees of sacroiliac joint pathologies-from SIJ dysfunction to SIJ dislocation. What units them is the common element of instability of the supportive structures and a resulting lack of tensegrity. I will focus on the mechanical aspect of SIJ pathology. We will discuss other SIJ problems such as Infectious, Rheumatologic and Malignancy in the future newsletters.

Realizing the difference between dysfunction and dislocation I see similarities between them as well. Different factors and combinations of factors cause Sacroiliac Joint Dysfunction: Connective tissue insufficiency, Ligament laxity, and Muscular imbalance. All of these factors lead to abnormal Sacroiliac movement (hyper or hypo-mobility), joint locking and muscular imbalance.

There are many of variations of SIJ mechanical problems: Up-slip and down-slip are good examples. They develop as a result of acute or chronic injury. They are extreme manifestations of the Sacroiliac Joint instability. Very often underlying mechanism of these injuries are connective tissue insufficiency and ligamental laxity involving multiple ligamentous and musculotendinous structures.

Fryette originally described up-slip in 1914. This lesion (up-slip) is essentially a vertical shear between the sacrum and ilium and most commonly occurs on the left side. This injury shortens the distance between the sacroccygeal attachments of the Sacrotuberous ligament to the ischial tuberosity attachment.  Control of Nutation (forward flexion of the base of the sacrum) becomes insufficient. Secondary stabilizers, such as the Piriformis, Gemellus Superior & Inferior, Quadratus femoris , and Obturator internus muscles are activated to mainatain stability. Significant effort is required on the part of the muscles involved to keep the SI joint stable. Due to this extreme exertion and unnatural forces neuro-muscular pathology eventually evolves such as Piriformis syndrome, Posterior hip pain, buttocks pain, sciatica, peripheral nerve entrapment syndromes and so on.

What happens to the posterior Long and Short Sacroiliac Ligaments? Their orientation and tension will change in response to the structural and functional tensions present, this is turn will affect their control over Counter-nutation (backward movement of the base of the sacrum).  Losing control over nutation and counter-nutation will bring into action Gluteal muscles, Thoracodorsal Fascia, Quadratus Lumborum, the Hamstrings in the immediate area and have far reaching consequences through fascial planes and connections.

Superior displacement of the ilium (up-slip) will shorten the Ligaments running from the transverse processes of L4 and L5 to anterior ilium – the Ilio-Lumbar ligaments. Instability of these ligaments will increase shearing forces on L4-L5-S1 discs and lead to annulus tears, disc protrusion and eventually disc herniation. These forces will also activate contraction of the Quadratus Lumborum, Multifidus muscles, Psoas, Latissimus Dorsi  muscles.

Inferior displacement of the ilium (down-slip)- is a rare condition. To differentiate between the up-slip and the down-slip the physician utilizes thorough clinical examination and Standing x-rays. Sometimes the Iliac crest on the side of the down-slip can be perceived as superior due to activation of the Ipsilateral Quadratus lumborum, which pulls pelvis up and tilts the pelvis to the opposite side.

The pubic symphysis has no strong intrinsic stabilizing structures. Without the stabilizing actions of these muscles: transverse abd. m, oblique abd.  m., rectus abdominis m. and adductor longus m., the pubic symphysis would permit 5-10mm of vertical shear.

Any discussion of Sacrum and pelvis would not be complete without mention of the role of the Psoas muscle.  This muscle is always involved in lumbo-pelvic instability. Having arisen from the sides of the lumbar vertebrae and anterior aspects of the transverse processes, it connects to the respiratory and pelvic diaphragms. It plays an important role in general body support, maintaining body structure and the body’s functional relationships through it’s support of the autonomic lumbar plexus. It exerts it’s major impact through the viscera innervated by this plexus, it can well exert a vital influence on visceral function and bodily well-being.

Therefore, treatment of Sacroiliac Joint Mechanical Pathology should include many of the following treatment options: Osteopathic Manipulative Therapy-to restore normal structural relationships; Regenerative therapy utilizing Prolotherapy, Platelet-Rich Plasma, Stem Cell therapy-to restore structural integrity;  Neural therapy, Neuro-fascial injection therapy-to restore neurologic and autonomic function; Physical therapy-to restore proper biomechanics and neuromuscular re-education; Nutritional and Hormonal treatment-to provide critical elements for healing and repair.

The  following structures should be considered for treatments: Sacroiliac Joint(s), Sacroiliac Ligaments, Sacrotuberous Ligaments, Ilio-Lumbar ligaments, Thoracodorsal Fascia, Thoraco-Lumbar junction, Facets joints, Inter- and Supra-spinous ligaments, Multifidus, Quadratus Lumborum, Piriformis, Psoas muscles and in some cases distal attachments of the hamstrings.

Most cases will require diagnostic imaging studies, such as X-Ray , Ultrasound or MRI.

All of these modalities require a intensive study, reading, and education. Skill does not come after one or two conferences or workshops. The learning of Orthopaedic Medicine is a lifetime affair.

Be patient and persistent. Success will come.

Jon Trister MD

Orthopaedic medicine has a long history and many tools with which to help the patient with musculoskeletal pain. In this Issue I would like to review basic principles regarding Prolotherapy for the benefit of physicians who are developing skills in Prolotherapy (Regenerative Injection Therapy )and PRP and as a review for those already practicing these skills.  In order to achieve the greatest success, the procedure should be performed correctly enhancing safe practices and limiting risk for the patients. Several important elements need attention: practice management (consent, documentation, billing and coding issues), assessment and identification of appropriate candidates for the procedure and safe performance of the procedure itself.

Knowledge of the pathology behind the patient’s complaint.

Identify the problem based on history, physical examination and imaging studies. Look for local tender points, as well as distal referral points. Remember, the initial presentation of pain could be referred pain and not necessarily where the problem is. Learn common patterns of referred pain. Become familiar with the diagnosis of instability of joints based on the clinical symptoms and exam findings. Make the correlation between clinical findings and imaging studies. Remember: Imaging studies do not always correlate with clinical findings and vice versa.

Knowledge of anatomy and function. Do your homework before treating the patient. Read anatomy, so you will know what are you are doing. Proficient prolotherapists are perpetual students of anatomy. Have diagrams, posters and anatomical illustrations readily available in your exam rooms. Show your patients where the problem is and how you will treat it.

Informed Consent

Inform the patient about the procedure in detail. Give them realistic expectations of the treatment and prognosis. Explain to the patient that prolotherapy is a PROCESS and requires multiple treatments and time to see results. Give the patient an option to review other possible treatments: Physical therapy, Surgery, OMT, and especially the options offered as standard of care for their particular diagnosis. Informed consent requires that the patient be presented the standard of care alternatives for their diagnosis.

Documentation of Informed Consent is just as important as the signature. Have the patient sign a detailed consent form, explaining all possible side effects and  complications. The potential side effects and complications should be discussed and outlined to the patient and documented on the consent form. You may wish to have your forms reviewed by your malpractice carrier to be certain they meet the standards. Encourage the patient to contact you before the scheduled procedure and to ask  questions. When examining elderly patients advise them to come with close relatives or friends so that all questions will be answered and not missed. Informed consent must list the standard medical options the patient was informed of and chose not to pursue.

Have the patient sign all medical and financial documents with the co-signature of a witness-your nurse or other office assistant.

Medical Practice/Procedure

Know important medical information pertinent to safe performance of an invasive procedure: Medical history, Medications list, Previous surgeries, Allergies, Presence of prosthesis, hardware, screws and plates. Discuss with referring physician the procedure you are going to perform. If you advise the patient to stop any medications ask the PCP for permission to do so. Do not discontinue  medications ordered by other doctors without consulting with them first. Do not criticize other physicians or previous treatments. You also may not be the last doctor. Strive to create a professional and healing atmosphere in your treatment room.

Never use old solutions. All solutions must be mixed on the day of the procedure. Aseptic technique must be taken very seriously. In some cases you may consider prophylactic antibiotics.  Proper positioning of the patient is very important. It must be safe for the patient and comfortable for physician performing the procedure. Consider IV line and VS monitoring in some cases. Make sure you are ready for medical emergencies. If you chose to use conscious sedation or pre-medicate your patients be sure they have a driver and that you meet the regulations of your state and malpractice carrier for conscious sedation or premedication.

Prepare skin for procedure. If the skin is inflamed in the area the injections are to be performed it is better to postpone the treatment. Again, know your anatomy and be very careful while injecting:

Midline of the vertebrae: direct needle caudate

Avoid cranial direction.

Be careful injecting midline below L3–Interspinal ligaments could be absent and risk for dural perforation is high.

Always touch the bone.

In some cases, aspirate before injecting, especially the transverse processes of cervical spine.

Be very careful around chest/rib/thoracic injections and lower cervical spine – risk for pneumothorax.

Check the function of the treated area after the procedure: ROM, pulsation, lungs sounds and vital signs.

Post Procedure: Offer patients fluids and snacks if necessary. Some patients will be light headed or vasovagal from the sympathetic stimulation of the injections. Give patients time for full recovery. All patients must be instructed to come with a designated driver. Make sure that you will be readily available to the patient after the procedure – give them you mobile phone number. It is a very beneficial practice to call your patient the next morning, especially after the first injection session. This is reassuring to the patient and allows you to evaluate their response to the treatment.

Documentation is a necessary part of the job of the physician. Make it simple, but detailed. Forms with diagrams, flow sheets with check boxes or items to circle can ease the documentation process for procedures. The following should always be present:

General information about Prolotherapy for patients as well as their physicians.

Detailed consent form

Medicare waiver

Financial disclosure and agreement

Preparation for Prolotherapy

Procedure protocols

Patient Response to the procedure

Post-procedure instructions

Taking the time to review these processes and implement safe processes and procedures as you introduce new techniques into your practice will facilitate safe practices for you and good outcomes for your patients.

Article summary   Renata Trister DO

Advances in medicine, science and hygiene have allowed modern man to become the longest living humans in history. As life expectancy lengthened, disorders of the nervous system in the aging population are seen more frequently. Dementia, cerebrovascular disease as well as progressive disorders such as peripheral neuropathy and Alzheimer’s are a growing concern for the aging patient.  Diseases of the nervous system are being diagnosed in record numbers in the United States: up to 6.8 million suffer from dementia; approximately 4 million have Alzheimer’s disease (AD), and roughly 1.5 million may suffer from Parkinson’s disease (PD), with 50,000 newly diagnosed patients every year. These numbers are projected to continue to increase.  Dysfunction in older patients should not be assumed to be the result of the aging process.  Although progressive decline in neurologic functioning is a normal aging process, progression to a neurologic disease is not inevitable.  Early intervention may prevent and delay the deterioration in these disorders.

Research suggests that a cumulative effect of imbalanced biochemical pathways can greatly impact neurologic cellular decline. Four major biochemical pathways are thought to mediate both aging and premature neurologic decline. By maintaining adequate function in these pathways, it may be possible to achieve optimal neurologic health and brain function.

Environmental factors such as poor diet, toxins and oxidative damage can stress biochemical pathways in the body and accelerate the biological aging of tissue.

Four Biochemical Pathways Implicated in Nervous System Decline

I.  Chronic Inflammation—Research suggests that chronic inflammation is a possible mechanism in aging associated neuro-degeneration. Multiple aspects of the inflammatory pathway are capable of propagating premature aging and neuron cell death. Chronic inflammation beyond its protective role, can cause harm to tissue.  Epidemiological evidence indicates that populations taking anti-inflammatory drugs for other conditions have a reduced risk of neurodegenerative conditions.  Inflammation and oxidation are closely linked.  Oxidants serve as signaling agents for the pro-inflammatory factors.  Several natural substances offer safe and effective alternatives to anti-inflammatory drugs, which are known to cause various adverse side effects.

II. Mitochondrial Dysfunction—Tissues with a high-energy requirement, such as the brain and heart, have a greater density of mitochondria—the cell’s energy-producers. Since the brain depends so highly on mitochondrial energy supply, dysfunction of mitochondria can affect the central nervous system (CNS) more severely than other tissues.  Research suggests two methods of supporting mitochondrial health and function: 1) promoting healthy mitochondrial energy production, and 2) combating free radical production and damage by increasing mitochondrial antioxidants.

III. Endocrine Imbalance—Aging is associated with a reduced ability to adapt to stress and chronic elevations of stress hormones called glucocorticoids (e.g., cortisol).Animal and human data suggest that high levels of glucocorticoids can be particularly detrimental to the hippocampus (the brain structure involved in learning and memory). In addition, changes in glucose and insulin handling during the aging process can lead to neuronal degeneration due to negative effects on nerve cell structure and function. Proper diet, exercise, and nutritional interventions may help reduce glucocorticoid levels, enhance the body’s ability to cope with stress, and improve glucose and insulin metabolism.

IV. Hypomethylation—Methylation, the transfer of a methyl group (CH₃) from one molecule to another, is required for numerous biochemical reactions vital to good health. However, insufficient levels of folate and vitamins B6 and B12 can cause reduced methylation, or hypomethylation, which in turn can produce elevated levels of the amino acid homocysteine (Hcy). Elevated Hcy levels are strongly linked to cognitive decline and irreversible dementia.  See tables below.

Nutritional Modulation of the Four Pathways

Fortunately, interventions begun in the initial stages of the disease process may prevent or delay the course of neurologic deterioration, resulting in an overall improvement.  The following nutrients may help prevent and interrupt the damaging cascade that contributes to neurologic decline.

Niacinamide—Niacinamide, a form of the B vitamin niacin, is a potent inhibitor of inflammatory cascade.  In animal models, administration of niacinamide resulted in reduced brain damage and reduced neurologic functional losses.

Essential Fatty Acids—Fish oils, which contain eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), are well known for their anti-inflammatory activity. Furthermore, DHA is required for normal brain function in adults. Decreases in brain DHA content are associated with age-related cognitive decline, dementia, and AD.

Resveratrol—Resveratrol is a polyphenol found in the skins of red grapes and various other plants. In vitro, animal, and epidemiologic research suggests that resveratrol may protect against inflammation and CNS disorders.  It is also a potent antioxidant.

N-Acetylcysteine (NAC)—The protective effect of NAC is likely related its restoration of brain glutathione (GSH) levels.GSH is central to antioxidant defenses in the brain and cellular detoxification of free radicals. In addition, NAC has been shown to support proper mitochondrial function.

Alpha-Lipoic Acid (ALA)—ALA is a cofactor in the synthesis of ATP (energy required for tissue function) and improves overall mitochondrial function. ALA is also an excellent antioxidant agent in neurodegenerative diseases due to the fact that it can interrupt free radical damage at several points. Animal research has shown that ALA supplementation elevates antioxidants in various brain regions and improves memory in aged mice.In addition, ALA supports healthy blood glucose levels and insulin activity.

Acetyl-L-Carnitine (ALC)—ALC is a vitamin-like substance that may improve energy production within brain cells via its effect on mitochondria.An analysis of studies reports that persons with dementia given 1.5 to 3 grams of ALC daily have shown improvement in numerous clinical measures of cognitive function such as memory, depression, and mental deterioration.

Magnesium & Thiamin—Magnesium plays an important role in maintaining the integrity and permeability of the mitochondrial membrane as well as assisting in energy-producing machinery of the mitochondria. Thiamin is a cofactor needed for mitochondrial energy production.

Coenzyme Q10 (CoQ10)—CoQ10 is a mitochondrial antioxidant cofactor that has been shown to be neuro-protective. In addition to being a potent free radical scavenger, CoQ10 is also critical for energy production by the mitochondria. CoQ10 supplementation has proven effective in a wide variety of age-related conditions.

Vitamin E—Vitamin E is the primary antioxidant found in all tissues. Low vitamin E levels are consistently associated with an increased risk and occurrence of neurologic disease, including AD and Parkinson’s. In a study of patients with AD, treatment with 2000 IU of vitamin E per day for 2 years was beneficial in delaying the primary outcome (time to the occurrence of death, institutionalization, loss of ability to perform activities of daily living, and severe dementia) of disease progression.

Ginkgo (Ginkgo biloba)—Ginkgo biloba extract (GBE) is an approved treatment for dementia in Germany, and it is the only nonprescription substance considered a treatment for dementia in Canada. Many clinical studies have demonstrated the effectiveness of GBE in the treatment of patients with dementia, AD, and age-associated memory and cognitive impairment. In addition, GBE may also prevent changes in mitochondrial structure and function associated with aging of the brain.

Adaptogenic herbs—Adaptogens are plants that help to decrease cellular sensitivity to stress. Herbs with adaptogenic properties may be beneficial in ameliorating the decreased ability to handle stress and the increased levels of glucocorticoids associated with aging and neurodegeneration. Ayurvedic herbs such as ashwagandha (Withania somnifera), holy basil (Ocimum sanctum), and brahmi (Bacopa monniera) have a positive influence on stress response, mental function, and cognition.

Mixed Carotenoids—Carotenoids are a class of naturally occurring plant pigments that provide the bright red, orange, and yellow colors of fruits and vegetables. A balanced intake of mixed carotenoids, as found in a healthy diet, provides the best protection against oxidative damage. In addition, the carotenoids lutein and zeaxanthin are found concentrated in the retina of the eye where they offer protection from conditions such as age-related macular degeneration.

Folate, Vitamin B6, and Vitamin B12—Folate and vitamins B6 and B12 are needed for proper methylation and to keep Hcy within a normal range.Insufficiencies of these nutrients may result in forgetfulness, memory loss, confusion, depression, dementia, and mood and sensory changes.

Conclusion

Healthcare professionals and their patients must take a preventative stance against neurologic decline. Due to the great deal of interest and research in this area, information about appropriate nutritional supplementation is constantly evolving. By looking for early warning signs and providing nutritional guidance that simultaneously addresses chronic inflammation, mitochondrial dysfunction, endocrine imbalance, and hypomethylation, perhaps more people can live out their most rewarding years with mind and body intact.