Studio Medico Bassani, dr. Luciano Bassani specialista in terapia fisica e riabilitazione (English NEWS)

Inflammatory Protocol MS format

Jon Trister — Sat, 24 Mar 2012 0:0:0 +01:00

Inflammatory Protocol MS format

Chronic diseases (TH1) are the result of intraphagocytic bacteria. The bacteria have an ability to remain alive and proliferate undetected inside the cytoplasm the cells they infect.
These cells include macrophages, the cells to kill invading pathogens. Once inside, they cause our own cells to release inflammatory cytokines, producing pain and fatigue.
These bacteria sustain themselves by grouping into communities, called biofilms. The bacteria inside the 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 bacteria that have lost their cell wall and called L-form or cell wall deficient (CWD)
Ability of Th1 pathogens to proliferate in the body is related to Vitamin D Receptors (VDR)
VDR controls innate immune system. VDR are also responsible to turning on/off a wide variety of genes and chemical pathways
VDR controls expression of the antimicrobial peptides (AMP), that kills bacterias,viruses and fungi by variety of mechanisms
25d-OH , vitamine D metabolite, in the level above 20 ng/ml can bind and inactivate the VDR, which immobilizes the innate immune system
Some bacteria also produces substances which can bind & inactivate VDR, similar to 25d-OH
People infected with the TH1 pathogens & receiving Vitamin d are no longer able to produce AMP allowing bacterias to proliferate.
When innate immune system no longer functions well, people have a hard time keeping other pathogens under control . Viral infections reactivate, or they acquire Candida or Mycoplasma
Th1 pathogens evolved mechanisms that alter the expression of the genes inside the cells they infect, making it easier for new pathogens to infect the cells.
Evidence is growing that Th1 pathogens can pass the placental barrier, so they can passed from parent to child, so Th1 illnesses run in families
Unlike 25D-OH that inactivate the VDR in healthy individuals, 1,25D-OH binds & activates VDR.
But in individuals who have 25 D 7 bacterial proteins blocking VDR, 1,25D is forced of the VDR & into the surrounding environment
In healthy individuals, the VDR transcribes an enzyme called CYP24, which breaks down excess 1,25D, ensuring a normal level of 1,25D
In chronically ill patients, the VDR, which is blocked by bacterial substances, can no longer transcribe CYP24, & 1,25D becomes elevated.
Another enzyme , CYP27b1 causing more 25D-OH converted to 1,25D-OH.
Making more, & deactivating less, causes 1,25D to rise to unnaturally high level
Unfortunately, when 1,25D-OH levels reach a certain threshold, it bind not just to VDR, but to other nuclear receptors, displacing the metabolites that are meant to be in them.
These receptors regulate the body’s hormones- adrenals, thyroid, sex hormones, etc –causing hormone havoc
When 1,25-OH rises above 42 ng/ml, calcium begins to be leached from the bones, resulting in osteoporosis.
When 1,25D-OH rises, it also binds a receptor called the PXR, which inhibits conversion of pre-vitamine D to 25D-OH,causing 25D levels to drop. So, low 25D-OH level may not be a sign of deficiency, but a result of the disease.
Patients take Olmesartan (Benicar) which is able to bind & activate the VDR, by pushing 25D-OH & bacterial proteins off the receptor.
Patients lower 25D by avoiding Vitamin D
This allows the body’s innate immune system to turn on AMP’s, killing Th1 pathogens & again manage viral & other pathogens.
Patients also take pulsed low dose of bacteriostatic antibiotics which are more effective against bacteriain biofilm
The antibiotics weakened the bacterias by blocking their ribosomes, which they need to produce proteins to help them survive and reproduce.
When Th1 pathogens die, there is a temporary change in patients immunopathology (Herxheimer reaction)
Karl Herxheimer (June 26, 1861 - December 6, 1942) was a German-Jewish dermatologist who was a native of Wiesbaden.
In 1885 he received his doctorate at Würzburg, and later worked with his brother, Salomon Herxheimer (1841-1899) in Frankfurt-am-Main. In 1894 he became director of the dermatology clinic in Frankfurt, and with Paul Ehrlich (1854-1915), was instrumental in founding the University of Frankfurt. In 1914 he became professor for skin and venereal diseases at the new university. In late 1942, at the age of 81, Karl Herxheimer was murdered by the Nazis at Theresienstadt.
Herxheimer is credited with providing an early description of acrodermatitis chronica atrophicans (diffuse idiopathic cutaneous atrophy), which is a dermatological disorder associated the latter stages of Lyme disease. This condition is sometimes referred to as Pick-Herxheimer disease, named along with co-discoverer Philipp Josef Pick (1834-1910). With Austrian dermatologist Adolf Jarisch (1850-1902), the Jarisch-Herxheimer reaction is named, which is an inflammatory reaction to Salvarsan, antibiotics or mercury, when using these agents to treat syphilis.
Dying bacteria release toxins into the bloodstream, which stimulate inflammatory cytokines, which can make patients feel worse
Olmesartan plays a key role in the recovery process, but can have opposite effect- temporary increase in inflammatory symptoms & reduction of some inflammatory symptoms.
Olmesartan activates the dysregulated VDR , so immune system and manufacture antimicrobial peptides (AMP’s) it needs to fight intracellular bacterial pathogens.
VDR, in the nucleus of cells , is key to effective operation of the innate immune system-which attacks intracellular organisms.
Benicar acts as a VDR agonist- dislodging the bacterial proteins to activate the VDR with these agonistic effects.
Upregulates CYP24A1 & CYP 3a$, which deactivates 1,25D , so 1,25D decreases.
Represses transcription of CYP27b1, that hydroxylates 25D to 1,25D, so there is less 1,25D made.
So, making less, & breaking downmore, cansignificantly lower 1,25D
An activated VDR can cause increase symptoms (herxheimer reaction)
Other actions of Benicar can decrease symptoms
It has a modulating effect on the immune system, via the inflammatory pathway: Nuclear Factor Kappa Beta (NF-kappaB), which decreases inflammatory symptoms.
At higher doses Benicar docs into other cellular receptors (opioid) to reduce symptoms
Some pathogens are more affected by one antibiotics than another, & some are more affected by combination of antibiotics
By slowly increasing antibiotics & adding other antibiotics, the whole spectrum of susceptibility may be covered
Process also controls severity of Herx, because it prevents too many pathogens from being killed at one time
This process ensures that the patient suffers minimal damage from secondary inflammation, while the pathogens are slowly killed & all intracellular bacteria are eliminated.
Antibiotic resistance is avoided by using carefully selected antibiotics:
Pulsing low doses- often below minimum inhibitory concentration & avoids suppression of AMP’s
Varying combinations of antibiotics
Regular dosing of Benicar to activate the immune system
All therapy must be individualized
Scripts different than what taken
Always write out specific directions for patients (brain fog)
Generics-pills &capsules
Compounding pharmacies
Controlled Herxheimer’s
Change Benicar-increased frequency, take sublingual
Change Antibiotics Schedule:
Do not take the next dose
Reduce the next dose
Extend the schedule
Take an extra dose
Discontinue antibiotic
Increase antibiotic
Take a lower dose more often
Supplements:
Alpha Lipoic Acis
Diindolymethane
Bromelan
NAC (N-acetylcystein)
Quercetin
Curcumin
Resveratrol
Guaifenesin
Pterostibene
Low Dose Naltrexone
Road Back Foundation
Use of Minocycline and other antibiotics targeted at intracellular organisms, primarily Mycoplasma, to treat Rheumatoid Arthritis and other Autoimmune Rheumatological Diseases
Low Dose Naltrexone
Transiently blocks opiate receptors to stimulate endorphins
Increased endorphins modulate the immune system
Use for a wide variety of autoimmune conditions
Some limited peer reviewed published literature
Decrease Herx
Lyme Disease
3 forms: Cell wall, Intracellular, Cyst
Coinfections-Babesia
Reactivations
Biofilms
Other infections
Viral
Yeast
Parasites

Tensegrity and clinical practice

Jon Trister — Sat, 3 Mar 2012 0:0:0 +01:00

Tensegrity and Clinical Practice
By Jon Trister, M.D.

There are different theories regarding the physiological effects of prolotherapy: stimulation of an inflammatory reaction as a pathway for healing, stimulation of growth factor synthesis and release, stimulation of neuropromodulation, or a combination of these effects. In science we don't have perfect theories and we do just fine with successive approximation.Very often physicians ask me which concentration of Dextrose is the best for Prolotherapy? How do we decide?
Fibroblasts are the major cell–producing collagen. In 1953 Gavriil Ilizarov, a Soviet orthopedic–surgeon, came up with the idea he called "The law of tension". Basically, any mechanical stress acting on fibroblast–like cells will induce proliferation of the various tissues: bones, tendons, ligaments, cartilage, fascia, muscles, vascular structures, nerves, and skin.
This idea was the rationale for the orthopedic method he devised. He utilized mechanical forces via an external device attached to the bones to induce growth in bones and connective tissues which had ceased growing prematurely.
We believe that prolotherapy technique stimulates connective tissue to growth by injecting dextrose solution of various concentrations to areas of deficiency or injury.
Injection of the dextrose induces osmotic forces to act upon the fibroblasts. These forces lead to changes in the volume of the fibroblasts. Depending on the concentration gradient, fibroblast–like cells may swell or shrink.
This leads to changes in membrane tension, which is subsequently transmitted across the cytoplasm to the nucleus via the cytoskeleton, myofibrils and integrins.
The changes in tensile forces affect gene expression in the nucleus, subsequently changing the quality and the quantity of proteins produced by ribosomes – proteoglycans and glycoproteins.
12,5% dextrose may have a stimulatory effect on some functions, while 15% may induce inhibition of the same functions and stimulate others, while 25% may lead to cellular apoptosis.
Concentration of the solution, volume of the solution, vitality of the fibroblasts (they may be infected, or chemically affected) anatomical location (intra-articular, peri–articular, peri–neural etc ), underlying pathology (connective tissue condition), mechanical properties of the extracellular matrix, volume of injected solution, patient's age and gender will produce different responses. There is no linear response: the "more is better" approach does not work in biological systems.
Our predecessors (G.Hackett, G,Hemwall, and those who learned from them) empirically came to these concentrations: 12.5% –15% for extraarticular injections and 25% for intraarticular injections.
When considering the overall practices of prolotherapy practitioners it seems that these formulations are the most effective to date. Choice of the solutions and concentrations are not the only determinant of successful results. Clear understanding of underlying pathology is essential for correct tactics in locating anatomical targets.
For instance, in the treatment of lateral elbow pain: there are different pathologies which contribute to symptoms of lateral elbow pain. What unites all of them is an underlying laxity of the annular radial ligament, which stabilizes the radioulnar joints both, proximal and distal. Neuromuscular symptoms arising from this instability explain compressive neuropathies, muscular symptoms, tendonosis and ligamenthosis.
Stability and coordinated mechanics of distal and proximal radioulnar joints is determined by the local ligaments (radio–ulnar, TFCC, wrists and elbows) and radioulnar interosseous membrane, which controls superior translation of the radius along the ulna. Treatment of these structures very important for successful treatment.

Prolotherapy course day two Verona 04/05/february 2012

Luciano Bassani — Fri, 7 Oct 2011 0:0:0 +01:00

Prolotherapy Course Day Two Verona febrauary 2012ù

For info push here

Trigeminal Neuralgia

Luciano Bassani — Thu, 28 Apr 2011 0:0:0 +01:00

TRIGEMINAL NEURALGIA

The pain and inflammation of the Trigeminal nerves is caused by peptidergic nociceptors. As far as I know there is no anatomical textbook that can give the exact location of all the receptive fields of these peptidergic C-fibers.
Simply because anatomist have never looked for them as they are a recent immune-reactivity and electro-physiological finding. Peptidergic C-fibers (nociceptors) are not nerve fibers one can easily identify with an electron microscope.
They can only be identified by immune reactivity studies for CGRP and SP and electro-physiological transduction studies. Incidentally the receptive field of a peptidergic C-fiber is thought to cover at most 1 cm2 (=100 mm2)

The mechanism of action of the Neural Prolotherapy

John Lyftgt — Mon, 7 Mar 2011 0:0:0 +01:00

The mechanism of action of the Neural Prolotherapy

Subcutaneous prolotherapy’ was targeting the peptidergic sensory nervous system and its effectiveness was directly due to the effect of glucose on the Capsaicin/Vanilloid receptor, now better known as the TRPV1 receptor. I am postulating that Dextrose 5% in sterile water (D5W) is a TRPV1 antagonist.
We now have conclusive scientific evidence that inflammation is under the control of the peptidergic sensory nervous system, not the immune system. In fact it is Substance P released from peptidergic sensory nerves that activates the Immune system, which then results in a positive feedback loop between neurons and immune cells directing the direction of inflammation.
The peptidergic sensory system also directs anti-inflammatory mechanisms through the release of anti-inflammatory neuropeptides Galanin and Somatostatin. All of this is under the control of TRPV1 receptors.
The cloning of the TRPV1 receptor in 1997 by David Julius and his team and published in Nature is a breakthrough of unpredictable magnitude in Medicine and all of us are forced to give a scientific explanation about what we are doing in terms of its effect on TRPV1, as this molecule is the principal mediator of inflammation and pain.
For prolotherapy this means explaining how hypertonic glucose works on TRPV1, how P2G, sodium morrhuate and Sarapin work on TRPV1. The Self-regeneration process is now known to be directed by the same peptidergic sensory nerves, but only during normal physiological conditions through the tonal, non-inflammatory release of CGRP and SP. This means that prolotherapy’s ‘regeneration concept’ has to be explained in terms of peptidergic sensory neurological control.
The cloning of TRPV1 should be a wake up call for all prolotherapist (and all of Medicine) to re-examine our rationale for what we are doing.
George Hackett was always re-examining his rationale and solutions. He introduced the connection between the nervous system and prolotherapy in his 1962 articles. I strongly recommend you read them as it illustrates his brilliance and open-mindedness in a time when there was little of basic science to go on. he was for his time exceptionally up to date with the literature.
If anything my choice of the name ‘neural prolotherapy’ is a primarily a tribute to George Hackett's innovations (Glucose) in the treatment of chronic pain.

John Lyftgt

Prolotherapy solutions

Carl Osborn — Thu, 13 Jan 2011 0:0:0 +01:00

Prolotherapy solutions

I use a number of different prolotherapy solutions and make adjustments based on the individual's tolerance and response to treatment. While I start most patients with a 15% dextrose solution and adjust upward as appropriate, individual factors are important.
For instance, I usually start someone with a diagnosis of congenital hypermobility on a 20% dextrose solution and if that is well tolerated I will increase it to half strength or full strength P2G. Based on my experience, these patients will generally have a better long–term outcome if I provide more stimulation to the tissues for a healing response. In some cases however, going from a dextrose solution to P2G is simply too difficult.
I use a solution that I call "half–strength P2G" that makes a good intermediate solution for injection.The standard stock solution of P2G that is received from the pharmacy is dextrose 25%, phenol 2.5% and glycerin 25%. Before it is injected, this stock solution is diluted by 50% (with something/anything) so that the actual injection solution concentration is dextrose 12.5%, phenol 1.25% and glycerin 12.5%. My intermediate (half-strength) solution is mixed as follows in a 10 cc syringe: P2G 2.5 cc, dextrose 50% 2 cc, lidocaine 1% 2.5 cc and normal saline 3 cc. The solution actually has more dextrose (16.25%) than the standard P2G injection solution but with half as much of the phenol and glycerin (0.625% phenol and 6.25% glycerin). This provides a good option for those patients that seem to need more than just dextrose but have a difficult time tolerating full strength P2G for injection.

Carl Osborn

Psoas Syndrome

Joel Berenbeim D.O. — Tue, 26 Oct 2010 0:0:0 +01:00

PSOAS SYNDROME

By Joel Berenbeim, D.O.

The iliopsoas muscle is one of the longest and thickest muscles in the body. In animals, it is known at the tenderloin. It's importance cannot be understated in the etiology of back and anterior hip pain. The iliopsoas muscle consists of the psoas major, minor and iliacus. Functionally the three muscles act together to flex the lumbar spine and flex the hip. They help to maintain posture while standing and during locomotion and control lumbar lordosis and pelvic tilt. Psoas syndrome may include muscular imbalance, strain, sprain, spasm, tendinosis, and acute or chronic contractures of the iliopsoas muscle and sciatica. A common cause of iliopsoas dysfunction is suddenly resuming an upright position following prolonged muscle shortening, which does not allow the reflexes to reset appropriately resulting in muscle contraction. Examples of this include prolonged sitting, possibly in a soft easy chair, prolonged kneeling when gardening, prolonged crouching, leaning over a table, or bending forward for a prolonged or extended period of time. Strains of the muscle can also occur from forceful contractions; for example, performing straight leg sit–ups, hooking the feet when doing sit–ups, soccer and kicking sports, or forceful running on an incline. There are also organic causes of psoas spasm that need to be ruled out by history and physical. These include femoral bursitis, arthritis of the hip, diverticulosis of the colon, urethral calculi, prostatitis, cancer of the descending or sigmoid colon, salpingitis, appendicitis, abdominal aortic aneurysm, intra–abdominal abscess, inguinal hernia, or Crohn's disease. Pain can present in the groin or can present as painful muscle spasm in the back. In adolescence, avulsion of the lesser trochanter could be seen, and in adults, enthesopathy and tendinosis may be present. It has also been described with inappropriate use of a heel lift.
Anatomy: The psoas major crosses many articulations including T12–L1, lumbar spine, lumbosacral junction, sacroiliac and hip joints. It attaches to the anterior surface of the transverse process and bodies of T12–L4 and inserts on the lesser trochanter of the femur. The psoas minor does not cross the hip joint. It attaches to T12 and L1 and the iliopectineal eminence. Psoas minor is inconsistent and may be absent. The iliacus crosses the sacroiliac and hip joint. It attaches to the iliac fossa and crest, the anterior sacroiliac, lumbosacral and iliolumbar ligaments and ala of the sacrum. It inserts on the tendon of the psoas major, lesser trochanter, hip capsule and femur. Innervation is L2–L3 for psoas major, L1–L2 for psoas minor and motor branch of the femoral for iliacus.
Clinical presentation: Psoas contracture can present either unilaterally or bilaterally. It may be acute or chronic. The patient presenting with bilateral spasm will be forward bent and unable to stand straight up. The usual presentation, however, is a unilateral presentation with pain on walking and standing. The result of psoas contracture will cause L2 to flex, rotate and side–bend to the side of the psoas contracture. This will create a contralateral hip shift and lumbar convexity as it induces rotation and sidebending to the side of the contracture. A sacral dysfunction on an oblique axis will be present on the side of contracture. On the ipsilateral side, the femur will externally rotate due to the connection on the lesser trochanter and the foot will become everted. With prolonged contracture, spasm of the contralateral piriformis muscle will occur. Mechanical and chemical irritation of the sciatic nerve will cause posterior thigh pain above the knee. Gluteal muscles and quadratus lumborum may also become involved. Gluteus maximus may become pseudoparetic. Shortening of the psoas muscle may be diagnosed using the modified Thomas position. The patient is supine with their buttocks at the end of the table. The operator stands at their side. The patient holds their knee flexing it to their chest on the side not being tested. The leg being tested is extended over the end of the table. If the back of the thigh does not contact the table, psoas shortening is present. If the knee flexes to less than 45 degrees, there is shortening of the quadriceps.
Treatment: Treatment of the psoas is directed initially at the dysfunctional flexed, rotated and sidebent L2. Until this is corrected, it is very difficult to treat the rest of the contracture. Stretching should not be done to the psoas if it is in contracture without correcting the accompanying somatic dysfunction or further shortening and contracture can occur. Strengthening should not be initiated until the psoas muscle is back to its normal resting length or else further contraction will also occur. In order to avoid this reflex shortening, osteopathic techniques to turn off this spasm are usually very successfully which include counterstrain. Counterstrain is used to reduce the pain during treatment and allow the full increase back to normal resting length. Other techniques that can be used are facilitated positional release and other indirect techniques. Direct osteopathic techniques such as muscle energy might prove painful in the contracted, shortened iliopsoas and indirect technique until the acute spasm is resolved is preferable. If chronic psoas contracture has progressed to enthesopathy or tendinosis, appropriate regenerative injection techniques can be employed to treat the lesser trochanter and hip capsule.
With appropriate diagnosis including comorbid conditions, treatment of psoas syndrome can be easily recognized and treated in the office setting with good resolution of dysfunction and pain for your patient.

Italin neural prolotherapy seminar 2010

John Lyftogt — Mon, 30 Aug 2010 0:0:0 +01:00

NEURAL PROLOTHERAPY COURSE IN Italy WITH JOHN LYFTOGT, M.D. Jointly sponsored by the Hackett Hemwall Fondation and the Italian Prolotherapy Association. PROGRAM COORDINATOR: STEPHEN CAVALLINO, MD OCTOBER 8-10, 2010 FERRARA, ITALY Reistration Form Neural Prolotherapy has been proposed and advanced by a physician in New Zealand, Dr. John Lyftogt. (Pronounced Lift-off) The workshop will correlate 1) structure 2) function 3) clinical presentation and 4) treatment of neuropathic pain arising from the Peripheral Nervous System. Each module will start with an in depth Power Point presentation of 20 minutes on some aspect of the Biology of the Peripheral Nervous System: Anatomy, Physiology, Pathology, clinical presentation and treatment. Friday Oct. 8, 2010 : DR. JOHN LYFTOGT M.D. 9.00 - 10.00am - Power Point introduction on biology of PNS and History of Neural Prolotherapy. 10.00 -11.00am - Clinical presentations: What can be achieved with Neural Prolotherapy of the upper and lower extremities 11.00 -11.15am - Coffee break 11.15 -12.30pm - Anatomy workshops - group of 5 doctors with neural-prolotherapist 12.30 -13.00pm - Brief introduction of the use and the importance of Vitamine D3 in pain managment and Q/A 13.00 - 14.00pm LUNCH 14.00 - 16.00pm - Clinical Labs - clinical review in chronic pain patients that are in treatment with NP. There will be 2 labs for the afternoon where Dr. John Lyftogt and Dr. Cavallino will demonstrate real injections neural prolotherapy technique. Saturday Oct. 9, 2010 9.00 - 10.00am - Neural Prolotherapy: Power Point on biology of PNS: JOHN LYFTOGT M.D. 10.00 -11.00am - Anatomy Workshops Upper Extremity � group of 5 doctors with neural-prolotherapist 11.00 -11.15am - Coffee break 11.15 -12.30pm - Anatomy Workshops Lower Extremity - group of 5 doctors with neural-prolotherapist. 12.30 -13.00pm - Questions 13.00 - 14.00pm LUNCH 14.00 - 16.00pm - Clinical Labs - clinical review in acute pain new patients with NP - 2 labs for the afternoon where Dr. John Lyftogt and Dr. Cavallino will demonstrate real injections neural prolotherpy in acute pain. All docs will be rotating neural- prolotherapy on patients with their instructors in groups of 5. Sunday , Oct. 10, 2010 9.00 - 10.00am - Neural Prolotherapy Power Point on biology of PNS: JOHN LYFTOGT M.D. 10.00 -11.00am - Anatomy Workshops Lumbar Spine / Hip -group of 5 docs with neural-prolotherapist 11.00 -11.15am - Coffee break 11.15 -12.30pm - Anatomy Workshops Cervical-Dorsal Spine -group of 5 docs with neuralprolotherapist. 12.30 -13.00pm - Questions 13.00 - 14.00pm LUNCH 14.00 - 16.00pm - DOCTOR TREAT DOCTORS WORKSHOP. All doctors will receive a diploma at the conclusion of the course .

Prolotherapy and Baker's cyst

Ross Hauser, M.D. — Sun, 27 Jun 2010 0:0:0 +01:00

Prolotherapy and Baker's cyst

A cyst is a fluid filled sac in any location of the body. One of the more common areas where cysts occur is the back of the knee. These cysts are called popliteal cysts or Baker's cysts. Typically, damage within the knee causes swelling and the fluid is pumped from the knee to this fluid filled sac. This creates swelling and sometimes pain in the back of the knee. This may cause problems achieving full bending or full straightening of the knee.
Typically, draining or cutting out this cyst does not help unless the cause of the fluid accumulation inside the knee is cured. Orthopedic surgeons will recommend that the person get an MRI and subsequent Arthroscopy to 'fix' the problem. For the person who desires not to have a 24 inch probe stuck in their knee and undergo general anesthesia, there is another option: Prolotherapy.
Let's think about it. Someone has a trauma to the knee and eventually a baker's cyst forms. What most likely would be injured to cause instability in the knee so joint fluid accumulates. You got it...ligament damage. In my opinion the best treatment option for a ligament being stretched is Prolotherapy.
Can Arthroscopy fix a ligament that is stretched? No. Prolotherapy to the injured structure will stimulate the body to repair it. Once it is repaired and the joint is stable, no more joint swelling. Once there is no more joint swelling there is no more baker's cyst.
In summary: For those of you with baker's cysts, just draining the cyst doesn't repair anything, it alleviates swelling. Even then the physician will tell you the likelihood is that the cyst will return. Why? Because the damage into and around the knee joint remains. Damage to the following structures could cause a baker's cyst to form: the menisci, ligaments, cartilage, or joint capsule. All of these structures respond to the repair stimulating effects of Prolotherapy. By a person receiving Prolotherapy to the inside of the knee, the joint structure causing the swelling is often repaired. Once it is repaired, the joint swelling stops. Once the joint swelling stops, the baker's cyst ceases to exist. We call this ìceasing to existî a cure. So if you want your baker's cyst cured, get a Prolotherapy evaluation and, if appropriate, Prolo Your Baker's Cyst Away!

Ross Hauser, M.D.

Reflex topognosia of ear points

David Alimi — Thu, 8 Apr 2010 0:0:0 +01:00

REFLEX TOPOGNOSIA OF EAR POINTS

 The somatic representation point.   Areas are three-dimensional (complex neuro vascular) or Voxel neurophysiological and not simple steps, tied to a retinaculum whose shape evolves continuously.
Are constantly adapted, according to the� segmental primary and genera homeostasisl, depending on the variations of the supported disease , may vary in shape but always staying within the perimeter embryological assigned (same value volume).  This volutomo tissue is genetically dedicated to receive information or a physiological or pathological mixage between the 2.
 If cosmetic surgery, the destinated place� don�t change!  It 's a dynamic process active throughout life and genetically determined! In the absence of disease points receive afferents of physiological action potentials (through the reticular formation) from various organs.  If there is a disease, the pathological potentials action� coming from a diseased area, occur with a potential difference between one point and another.
These pathological potentials action� remains mostly trapped in their corresponding somatotopically ear. The reticular do filter , the potentials are developed, settles on the pavilion. This representation of the ear is more intense (and spotter) as the disease is important, significant and durable. There is a descending order of value: the most important representations are those with strong limbic emotional connotation.
They also represents the visceral and somatic disorders (painful) especially during acute diseases disturbing the balance motor postural muscle. The message then disable and shut down� gradually or suddenly if the disease loses its meaning for the homeostatic process management (intregrated and tolerated).  Electrically, there will be gradual reduction of potentials action for habituation, adaptation, compensation ,is a mechanism of economics points topical reflex.  If a chronic process is disabled in the ear and suffers worsening , turn the ear (in proportion to the intensity and duration of aggressive process) and then undergoes the same laws of electrophysiological regression, but may leave place for a� meaning of higher representation.  You can have on the point a puzzle of representation of different powers in the same somatotopically.

REPRESENTATIONS
 PROPORTIONALITY '
 SELECTIVITY '
 POINTS VARIABILITY
ECONOMICS  PLASTICITY '
POINTS EXHAUSTION

Osteoarthritis and Leptins

Carl Osborne — Mon, 22 Mar 2010 0:0:0 +01:00

OSTEOARTHRITIS AND LEPTINS

Carl Osborne AAOM President

Many patients come to my office seeking prolotherapy for "arthritis". There are over 100 different classifications of arthritis, but generally what they mean is "osteoarthritis".We know from various studies that people over 30 have a probability of degenerative spine or joint changes of approximately 50%. If they are over 40 years of age it is closer to 90%. Many of these people don't have pain initially but if they start to hurt and get an x–ray they are told they have osteoarthritis. NSAIDs, physical therapy and cortisone injections are frequently prescribed, but when the pain persists they are commonly told they must "live with it". When we do prolotherapy and the pain resolves do they still have "arthritis" or just degenerative changes that are clinically asymptomatic.
Osteoarthritis is generally considered a "wear and tear" problem, and abuse and injury or ligament damage can clearly destabilize joints, affecting joint health and function. But it is probably more appropriate to think of osteoarthritis as a disease of the whole musculoskeletal system including cartilage, muscle, ligaments, bone and adipose tissue. Research has shown that obesity increases the risk for osteoarthritis in nonweightbearing joints such as fingers as well as the spine and hips or knees. Because osteoarthritis can be a generalized disease, there is more than mechanical force involved in joint destruction.
Adipose tissue secretes leptons which can trigger inflammation and joint instruction. At Duke University, an animal study compared two groups of mice. The first group of normal mice were fed a high fat diet to make them obese, and they subsequently developed arthritic knees. A second group included a breed of obese mice that were leptin deficient. This group showed no signs of joint damage even though they weighed about twice as much as the first group. This suggests a link between leptin signaling in obesity and osteoarthritis. Considering our current epidemic of obesity in the U.S., we are likely to see development of osteoarthritis in a much younger population.

Pain and D vitamin

Archives of internal medicine — Sun, 10 Jan 2010 0:0:0 +01:00

A research letter published in the April 14, 2008 issue of the American Medical Association journal Archives of Internal Medicine reported that vitamin D supplementation reduced pain levels in patients with diabetic neuropathy. The condition occurs when high levels of glucose damage the nerves, and can include burning, tingling, numbness, and throbbing sensations.

Drs Paul Lee and Roger Chen of the Concord Repatriation General Hospital in New South Wales, Australia enrolled 51 type 2 diabetics with neuropathy for the study. Pain severity was rated via two questionnaires and serum 25 hydroxyvitamin D and parathyroid hormone levels were measured at the beginning and end of the treatment period. All participants were found to have insufficient levels of vitamin D at less than 24 nanograms per cubic milliliter at the study’s onset, and were given a mean dose of 2,059 IU of the vitamin for three months.

Lower pain scores were found to be correlated with higher levels of serum vitamin D but not with parathyroid hormone levels. Treatment with vitamin D resulted in a 48.5 percent reduction in pain scores on the first questionnaire and a 39.4 percent reduction on the second by the end of three months. Drs Lee and Chen remark that there is evidence that vitamin D promotes nerve growth and modulates neuromuscular function and neuronal growth and differentiation.

Having inadequate levels of the vitamin could increase nerve damage and impair pain receptor function. They note that vitamin D supplements are unlikely to have harmful effects and may also benefit bone health and glycemic control in diabetic patients. To the authors’ knowledge, the study is the first of its kind to address the effect of vitamin D on patients with diabetic neuropathic pain. “Vitamin D insufficiency is underrecognized and may be a significant contributor to neuropathic pain in type 2 diabetes,” they conclude. “Vitamin D supplementation may be an effective ‘analgesic’ in relieving neuropathic pain.”

Neural Prolotherapy

John Lyftogt — Thu, 7 Jan 2010 0:0:0 +01:00

NEURAL PROLOTHERAPY BY DOCTOR JOHN LYFTOGT MD

INTRODUCTION

Classical Prolotherapy was developed in the 1940s by an American Trauma surgeon Dr George Hackett. He used injections of Sylnasol, a sclerosing agent commonly used at the time for sclerosing varicose veins, haemorrhoids and hernias.

He targeted ‘lax’ or ‘weak’ ligaments with Sylnasol injections to make them stronger. He reasoned that ‘weak’ ligaments were the cause of most joint and ligament pain and that strengthening would resolve the pain. He was certainly most successful and published 16 articles and one textbook. He claimed an 80% success rate for the treatment of low back pain and many other painful conditions. After Sylnasol was taken off the market in the 1950s a number of other sclerosing solutions were used and are still being used in the USA.

One of the solutions developed was P2G containing Glucose, Glycerine and Phenol. This solution was also used in New Zealand by Dr Milne Ongley but caused too many side effects leading to Dr Ongley being struck off the medical register in 1974. It was identified that the Phenol component was responsible for the occasional serious adverse reactions.

Other Doctors in the USA, Australia and elsewhere continued to use glucose injections and no side effects have been recorded from glucose other then temporary and mild irritation. A growing number of prolotherapy studies over the last 40 years have indicated good to excellent results from treatment with glucose injections for painful conditions affecting joints, ligaments and tendons.

With the advent of Evidence Based Medicine in the last 20 years the requirements for scientific research have become intensely demanding and financially well out of reach of most researchers, unless supported by large grants or the Pharmaceutical industry. As a result good high level evidence (level 1&2 out of a scale of 5) research on prolotherapy has been almost impossible to fund, but three researchers, Professor Michael Yelland from Australia and Professors David Rabago and K Dean Reeves from the USA have bucked the trend with some excellent studies published recently.

Doctor John Lyftogt has published six level 4 studies in the Australasian Journal of Musculoskeletal Medicine since 2005 and is a co-author of one level 2 randomised trial published in the British Journal of Sports Medicine in June 2009

SUPERFICIAL PROLOTHERAPY

Dr John Lyftogt has been in General Practice since 1978 and was the senior partner in Parklands Medical Centre, Christchurch until 2008. He has extensive post graduate training and experience in sports medicine and musculoskeletal medicine. He started practising prolotherapy after completing a prolotherapy course with Dr Margaret Taylor in Adelaide in 2003. ù

He has been a full time prolotherapist at Active Health since 2004. Dr Lyftogts early research focussed on the treatment of Achilles tendon problems and he has now treated more then 300 Achilles tendons with a success rate of more than 90%. He has published two level 4 articles on Achilles tendons. The technique developed for the treatment of Achilles tendons differs from classical prolotherapy in that the injections are given immediately under the skin while taking great care avoiding contact with the exquisitely sensitive tendon.

This ‘neural prolotherapy’ or subcutaneous prolotherapy protocol was successfully extended to the treatment of tennis elbow, painful knees, shoulders, neck, hips, ankles, muscle injuries and low back. Results are consistent and two year follow up studies have shown success rates between 80-100%. The treatment is also less invasive than classical prolotherapy.

Because neural prolotherapy does not target tendons, ligaments or joints the question had to be asked what causes the sometimes dramatic decline in pain levels after even a few treatments. A working hypothesis was developed that glucose assists in the repair of connective tissue in the nerve trunks under the skin in a similar way as repairing connective tissue in ligaments and tendons with classical prolotherapy.

These skin nerves are now known to be responsible for painful conditions generally identified as ‘neuralgias’ or ‘peripheral neuropathic pain’. The skin nerve trunks consist for up to 80% of connective tissue and are structurally quite similar to tendons and ligaments.

There is now also compelling scientific evidence that the very small nerves innervating the nerve trunk, known as ‘nervi nervorum’ are responsible for inflammation of the connective tissue of the nerve trunk and surrounding tissues. Interestingly and surprisingly this fact has been known for over 125 years. It is also known that this ‘neurogenic inflammation’ differs from conventional inflammation in that it does not respond to anti-inflammatories or cortisone injections.

This is one of the reasons why these commonly used drugs are proving to be ineffective in many painful conditions in addition to a growing awareness that their use is not without side effects. It is clear from clinical observations on more than three thousand patients and large case series that neural prolotherapy effectively reverses ‘neurogenic inflammation’ and resolves neuralgia pain.

This realisation opens the way for exploring other substances that may have the potential to reverse ‘neurogenic inflammation’ similar to glucose but without having to inject. One such substance has already been identified in Vitamin D in tablet and dermal cream form. Dr John Lyftogt is pursuing other promising drugs and is currently trialling these potential ‘cures’ of debilitating pain and injuries.

Copies of Dr John Lyftogts articles are available on request.

Dr. Samuel Rosen, ear-surgery pioneer

The New YorkTimes — Sun, 6 Dec 2009 0:0:0 +01:00

DR. SAMUEL ROSEN, EAR-SURGERY PIONEER, DIES AT 84 Dr. Samuel Rosen, an ear surgeon who gained worldwide acclaim for developing the ''Rosen stapes'' operation to restore hearing to partly deaf people, died yesterday in Peking. He was 84 years old and lived in Manhattan. Dr. Rosen was completing one of his periodic visits to China as leader of a touring group of American doctors. He and his wife of 52 years, Helen, were visiting friends in Peking when he was stricken with abdominal pains and taken to a hospital, where he died of a massive hemmorhage from a blood clot. In 1952, Dr. Rosen developed, almost by accident, the operation that would bear his name and be performed on hundreds of thousands of patients around the world. A patient suffering from otosclerosis, a disease in which sound waves are unable to reach the auditory nerve, was on the operating table when Dr. Rosen accidentally jarred loose a small, stirrupshaped bone, the stapes, in the middle ear. A Very Delicate Operation The patient regained his hearing immediately. Dr. Rosen concluded that freeing the stapes had restored the bone's ability to vibrate and transmit sound energy from the eardrum to nerve endings in the inner ear. The operation is extremely delicate, in part because the stapes is the smallest bone in the body, measuring slightly more than a tenth of an inch. Nevertheless, Dr. Rosen was able to teach the technique to other surgeons, who in turn taught it around the world. Dr. Rosen and his wife, whom he trained as an audiologist (a specialist in hearing disorders), traveled to many countries, where he lectured and served as a consultant on ear surgery. In the last decade, he visited China at least once a year. Dr. Rosen was the fourth of five children of a peddler of crockery who lived in a poor section of Syracuse. His brothers and sisters paid his tuition at Syracuse University. Originally, he studied law but switched to medicine and received his medical degree in 1921. He was an intern at Mount Sinai Medical Center in New York City, and was affiliated with Mt. Sinai until his death. In recent years, he was clinical professor emeritus of otolaryngology. Received Many Honors Dr. Rosen, who continued an active practice between his trips abroad, was also a consultant at New York Eye and Ear Infirmary and was professor emeritus of otolaryngology at the College of Physicians and Surgeons of Columbia University. In recent years, he received honors from medical groups in China, India and Egypt, as well as in the United States. In 1956, he received the Hektoen Gold Medal from the American Medical Association. He was not always happy with his colleagues, however. After his discovery of the stapes technique, he found associates skeptical. In his autobiography, he said that he believed one reason for the skepticism was that his operation had replaced the standard earfenestration method that took years to master and consequently earned high fees for surgeons. He also accused his colleagues of scorning his liberal stands on political matters. And he wrote in his autobiography: ''I am a Jew, and ours is a racist country, sad to say. Medicine is tainted with this disease just as are the other professions.'' In addition to his wife, the former Helen vanDernoot, Dr. Rosen is survived by a son, Dr. John Rosen; a daughter, Judith Rubin, and five grandchildren. Dr. Rosen's body will be cremated in Peking, and a memorial service there is being planned by the Chinese Medical Association. A memorial service will be held in New York at a later date.

Want to live longer?

Mercola — Thu, 3 Dec 2009 0:0:0 +01:00

Want to live longer?

Try Vitamin D Posted by: Dr. Mercola November 26 2009 | 29,568 views

Writing in the journal Clinical Endocrinology, scientists from the Netherlands, Austria, and the U.S. report that low blood levels of the sunshine vitamin are associated with increased risk of all-cause mortality, and mortality from heart disease, in the elderly. The research follows hot on the heels of similar findings published in Nutrition Research and in the Archives of Internal Medicine.

The new study used data from 614 people participating in the Hoorn Study, a prospective population-based study with men and women with an average age of 69.8. Blood levels of 25(OH)D were measured at the start of the study. After an average of six years of follow-up, 51 deaths had been documented, 20 of which were due to cardiovascular health.

People with the lowest average vitamin D levels were found to be at a 124 and 378 percent increased risk of all-cause mortality and cardiovascular mortality, respectively. Commenting on the potential mechanism, the researchers note: “Apart from the maintenance of muscular and skeletal health, vitamin D may also protect against cancer, infections, autoimmune and vascular diseases, suggesting that vitamin D deficiency might contribute to a reduced life expectancy.” Adults with lower blood levels of vitamin D may also be more likely to die from heart disease or stroke.

Scientists in Finland compared blood levels of vitamin D, and deaths from heart disease or stroke over time in more than 6,000 people. Those with the lowest vitamin D levels had a 25 percent higher risk of dying from heart disease or stroke. In addition, in a study of 166 women undergoing treatment for breast cancer, nearly 70 percent had low levels of vitamin D in their blood, according to a study presented at the American Society of Clinical Oncology’s Breast Cancer Symposium.

The analysis showed women with late-stage disease and non-Caucasian women had even lower levels. Said Luke Peppone, Ph.D., research assistant professor of Radiation Oncology, at Rochester’s James P. Wilmot Cancer Center: “Vitamin D is essential to maintaining bone health and women with breast cancer have accelerated bone loss due to the nature of hormone therapy and chemotherapy. It’s important for women and their doctors to work together to boost their vitamin D intake."

Eye and neck proprioceptive messages

Roll e C. — Sun, 29 Nov 2009 0:0:0 +01:00

Eye and neck proprioceptive messages contribute to the spatial coding of retinal input in visually oriented activities. Roll,-R; Velay,-J-L; Roll,-J-P Exp-Brain-Res. 1991; 85(2): 423-31. The egocentric localization of objects in extrapersonal space requires that the retinal and extraretinal signals specifying the gaze direction be simultaneously processed. The question as to whether the extraretinal signal is of central or peripheral origin is still a matter of controversy, however. Three experiments were carried out to investigate the following hypotheses: 1) that the proprioceptive feedback originating in eye and neck muscles might provide the CNS with some indication about the gaze direction; and 2) that the retinal and proprioceptive extraretinal inputs might be jointly processed depending on whether they are of monocular or binocular origin. Application of low amplitude mechanical vibrations to either the extraocular or neck muscles (or both) of a subject looking monocularly at a small luminous target in darkness resulted in an illusory movement of the target, the direction of which depended on which muscle was stimulated. A slow upward target displacement occurred on vibrating the eye inferior rectus or the neck sterno-cleido-mastoidus muscles, whereas a downward shift was induced when the dorsal neck muscles (trapezius and splenius) were vibrated. The extent of the perceptual effects reported by subjects was measured in an open-loop pointing task in which they were asked to point at the perceived position of the target. These results extend to visually-oriented behavior the role of extraocular and neck proprioceptive inputs previously described in the case of postural regulation, since they clearly show that these messages contribute to specifying the gaze direction. This suggests that the extraretinal signal might include a proprioceptive component.

Strain Counterstrain

Erik Gandino — Tue, 24 Nov 2009 0:0:0 +01:00

Strain Counterstrain Strain Counterstrain technique it's an osteopathic manual approach, developed by an American osteopath Dr. Lawrence H. Jones, in the 1950's. It consists in a passive procedure that places the body in a position of great comfort, which is a mild overstretching applied in a direction opposite to the false and continuing message of strain. This passive position will relieve pain and dysfunction by reduction and arrest of inappropriate proprioceptor activity that maintains the somatic dysfunction in any area of the body. What guides the diagnosis of a Strain Counterstrain (SCS) clinician is the detecting of specific small zones of tense, tender tissue throw out the body, named Tender Points (TP) which will guide the operator in its evaluation and treatment strategy. The ideal position at which there is at least two-thirds reduction of tenderness indicates the correct positioning of the body. Erik Gandino D.O. Jones Institute Europe Director

Research in prolotherapy

Dean Reeves — Wed, 11 Nov 2009 0:0:0 +01:00

Finger osteoarthritis: Injection of chronically painful fingers in osteoarthritis with dextrose proliferant has been studies in randomized controlled fashion with benefit over the control solution. (Reeves 00�1). However, that study has not been repeated. Unless a larger study with randomized design or a larger consecutive patient study demonstrating improvement in objective measure such as finger size and improvement in standard function arthritis outcome measures are performed and confirm benefit, we do not recommend coverage of prolotherapy for finger arthritis.

Golfer's Elbow: A small consecutive patient study on 20 consecutive patients with objective radiographic ultrasound measures was published. (Suresh 2006) Dry needling was performed, followed by autologous blood injection. Although only one injection was significant reduction in pain at 10 months post procedure as well as improvement in echogenicity on ultrasound and a decrease in abnormal (neo) blood vessels. 3 patients failed and opted for surgery but in the remaining 17 VAS for pain improved from 8 to 2.2 and Nirschl score from 6 to 1.vHypoechoic change in the flexor tendon significantly decreased between pre�procedure, when there was a mean (SD) of 6.45 (1.47), and at 10 months, when it was 3.85 (2.37) (p 0.001).

Doppler ultrasound showed that neovascularity decreased between pre�procedure. The measurement of objective tendinosis changes enhanced the power of this study. A larger study with usual treatment or non injection control is recommended prior to insurance coverage consideration.

Groin Pain: Return of elite athletes to full sport after failure with other methods of treatment, as long as there is avoidance of data dropout and a strict consecutive patient design, is a powerful outcome. A study of 24 elite level athletes with chronic groin pain, failure of all standard therapies, and failure to play at high level was reported in 2005. (Topol 2005) 22/24 returned to full play in sustained fashion, with 22 of them to rugged play (rugby). This study was then in essence repeated with 48 additional athletes with identical results. (Topol 2008) IE: 51 more were enrolled, 48 completed a minimum of 2 treatments (average of 3 treatments) and 44/48 returned to full level sustained play, with a variety of sports involved.

This is a remarkable efficacy rate and compares nearly identically to outcome from the best surgically�based studies with many times the expense. This is sufficient evidence to recommend a three treatment trial of prolotherapy in patients with groin pain, although additional studies are recommended in non�elite athletes.

Knee Osteoarthritis: A single randomized controlled trial showed benefit of dextrose injection over simple lidocaine. (Reeves 2000-2) Although this was in knees near or at end stage (3 mm average cartilage and with substantial symptoms), this study has not been reproduced. Prior to consideration of coverage of prolotherapy for knee arthritis it is recommended that a second randomized controlled trial be performed or that an arthroscopically based study demonstrate visual proof of cartilage growth in response to the proliferant utilized.

Low Back Pain: Four randomized controlled trials have been performed. (Ongley 87, Klein 93, Dechow 99, Yelland 04). One was egregioiusly flawed (Dechow 99). The lead author had neither performed prolotherapy, nor learned typical radiation patterns of ligaments. The lead author assigned patients based on incorrect referral pattern assumptions and required the injector to treat areas that had nothing to do with the pain the patient was having without allowing any examination to take place. This was with a strong proliferant and naturally led to pain flare in the proliferant group with a worse outcome than the control group. The other three studies demonstrated long term and substantial reductions in disability in both active and control groups, favoring the proliferant group but not with statistical significance.

This is because even the control groups were not placebo groups. Repetitive needling causes a proliferant effect through several mechanisms. Note that all other consecutive case series of low back pain patients have also confirmed substantial and sustained improvements in pain and function with injection of connective tissue with proliferant in patients with chronic low back pain. (Hooper 04, Wilkinson 05, Cusi 07).

There is no other modality of treatment that has more evidence of long term benefit for low back pain than prolotherapy in such chronic patients. Insurance coverage for low back pain treatment is recommended after another study is published in which a usual treatment control or other non injection control is utilized in the study design to definitively confirm statistically significant improvement in low back pain. It is recommended that the treatment method be clearly described and easily reproducible to allow for clear coverage decisions.

Patellar tendinosis: Two pilot studies have been performed. One used platelet rich plasma with ultrasound guided delivery to areas of tendinosis (Volpi 07) and one used polidocanol with ultrasound guided delivery to areas of neovascularization which is intimately connected to tendinosis. (Alfredson 05) Both were favorable in outcome with excellent pain reduction and improvement in function, although neither emphasized objective followup by ultrasound of changes in neovessels or hypoechoic areas. Prior to coverage consideration a large consecutive patient collection with little or no drop out and long term followup is recommended for either or both of these modalities of treatment.

Plantar fasciosis: There are no no regenerative approach alternatives to proliferant injection except extracorporeal shock wave which has a much higher cost. A consecutive patient study of 20 patients with chronic plantar fasciosis treated with dextrose proliferant injection was reported. (Ryan 09). A mean of 3 treatments were given with a good to excellent results in 16/20. A second and larger study using dextrose proliferant with chronic plantar fasciosis with minimal dropout and long term outcome with more precise measurement tools will merit attention for coverage consideration.

Tennis elbow (Lateral or Extensor tendinosis): A well�designed randomized control trial was published in 2008 in which 24 subjects with chronic elbow pain were assigned to injection with saline or injection with a combination of dextrose and sodium morrhuate. 0, 4 and 8 week injections were performed. (Scarpone 2008) Followup at 16 weeks demonstrated 32% versus 90% improvement, highly significant, favoring the proliferant group. Functional and pain improvement persisted in the proliferant group at 1 year. Another study was reported by Mishra in which 20 surgical candidates were assigned randomly to receive either PRP or bupivicaine injection. Withdrawal of blood in all patients to allow full blinding was not approved by the human subject committee.

Injection was only given once, resulting in a VAS improvement for pain at 8 weeks of 16% (bupivicaine) versus 60% (PRP) improvement. At mean followup of 25.6 months 91% improvement in pain was noted. Both studies represent good pilot outcomes and there are other studies reviewed as well in a a recent review publication. (Rabago 09). Coverage of a treatment trial may merit consideration given the cost and limited efficacy of other approaches (surgical or non surgical in this condition. However it is recommended that another study be conducted using any of the above methods with larger size comparing usual therapy or non injection control to injection of dextrose or PRP with long term outcome measures.

Summary This has been a brief summary of research findings in common conditions and recommendations for reimbursement. It should be noted that all of the above conditions have been shown at least at pilot study level to be successfully treated with a minimum of treatment which would represent considerable cost efficacy. Although insurance reimbursement is recommended only for groin pain at this time, in most areas discussed only one additional high quality study is needed to recommend consideration of insurance coverage. Reimbursement methods are problematic.

It is recommended that at this time that insurance coverage be made according to treatment time at a rate of $400 per hour for non sedation procedures and $600 per hour for treatments that require sedation. The patient would need to pay in addition for proprietary components of treatment (IE PRP) that are not included in usual proliferant injection.

References in Order of Citation Borg�Stein J, Zaremski JL, Hanford MA. New concepts in the assessment and treatment of regional musculoskeletal pain and sports injury. Phys Med Rehabil. 2009. 1(8):744-754. Yelland MJ, Sweeting KR, Lyftogt JA, Ng SK, Scuffham PA, Evans KA. Prolotherapy injections and eccentric loading exercises for painful Achilles tendinosis: a randomised trial [epub ahead of print] Br J Sports Med (England), Jun 22 2009, pages pending. Maxwell NJ, Ryan MB, Taunton JE, Gillies JH, Wong AD. Sonographically guided intratendinous injection of hyperosmolar dextrose to treat chronic tendinosis of the Achilles tendon: a pilot study. JR Am J Roentgenol. 2007 Oct;189(4):W215�20.

Reeves KD Hassanein K Long term effects of dextrose prolotherapy for anterior cruciate ligament laxity: A prospective and consecutive patient study. Alt Ther Hlth Med May�Jun 2003, 9(3): p58�62. Reeves KD, Hassanein K. Randomized prospective placebo controlled double blind study of dextrose prolotherapy for osteoarthritic thumbs and finger (DIP, PIP and Trapeziometacarpal) joints: Evidence of Clinical Efficacy. Jnl Alt Compl Med 2000;6(4):311�320. Suresh SP; Ali KE; Jones H; Connell DA Medial epicondylitis: is ultrasound guided autologous blood injection an effective treatment? Br J Sports Med (England), Nov 2006, 40(11) p935�9. Topol GA, Reeves KD, Hassanein K.

Efficacy of Dextrose Prolotherapy in Elite Male Kicking�Sport Athletes With Chronic Groin Pain. Archives Phys Med Rehabil, 2005;86:697�702. Topol GA, Reeves KD. Regenerative injection of elite athletes with career�altering chronic groin pain who fail conservative treatment: a consecutive case series. Am J Phys Med Rehabil. 2008;87(11):890�902.

�Reeves KD, Hassanein K. Randomized Prospective Double�Blind Placebo�Controlled Study of Dextrose Prolotherapy for Knee Osteoarthritis With or Without ACL laxity. Alt Ther Hlth Med 2000;6(2):68�80. Ongley MJ, Klein RG, Dorman TA, et al: A new approach to the treatment of chronic low back pain. Lancet 2:143, 1987. Klein RG, Bjorn CE, DeLong B, et al: A randomized double�blind trial of dextrose�glycerine�phenol injections for chronic low back pain. J Spinal Disord 6:23, 1993.

Dechow E, Davies RK, Carr AJ, et al: A randomized, double�blind, placebo�controlled trial of sclerosing injections in patients with chronic low back pain. Rheumatology 39:1255, 1999. Yelland MJ, Glasziou PP, Bogduk N, et al: Prolotherapy injections, saline injections, and exercises for chronic low�back pain: A randomized trial. Spine 29(1):9, 2004. Hooper RA; Ding M Retrospective case series on patients with chronic spinal pain treated with dextrose prolotherapy J Altern Complement Med (United States), Aug 2004, 10(4) p670�4. Wilkinson HA Injection therapy for enthesopathies causing axial spine pain and the "failed back syndrome": a single blinded, randomized and cross�over study.: Pain Physician (United States), Apr 2005, 8(2) p167�73. Cusi M; Saunders J; Hungerford B; Wisbey�Roth T; Lucas P; Wilson S.

�The use of prolotherapy in the sacro�iliac joint. [E pub ahead of print] Br J Sports Med (England), Published On line Apr 9 2008. Volpi P, Marinoni L, Bait C, De Girolamo L, Schoenhuber H. Treatment of chronic patellar tendinosis with buffered platelet rich plasma: a preliminary study. Medicina DelloSport. 2007;60(4):595�603. Alfredson H; Ohberg L Neovascularisation in chronic painful patellar tendinosis�promising results after sclerosing neovessels outside the tendon challenge the need for surgery. Knee Surg Sports Traumatol Arthrosc (Germany), Mar 2005, 13(2) p74�80. Scarpone M, Rabago DP, Zgierska A, Arbogast G, Snell E. The efficacy of prolotherapy for lateral epicondylosis: a pilot study. Clin J Sport Med (United States), May 2008, 18(3) p248�54. MIshra A, Pavelko T. Treatment of chronic elbow tendinosis with buffered platelet�rich plasma. American Journal of Sports Medicine Dec 2006 Volume 34: 1774�1778.

Achilles tendinosis

Dean Reeves e coll. — Sun, 25 Oct 2009 0:0:0 +01:00

ACHILLES TENDINOSIS

Dextrose prolotherapy versus eccentric loading exercises or a combination for Achilles tendinosis. Yelland et al 2009

This study used a measure called the VISA-A. The VISA-A score is a measure specifically of Achilles pain and functionality that is an 8 question score graded from 0 to 100 with 100 the best and with questions such as duration of stiffness when first getting up, pain with stretch once warmed up, pain afer walking for 30 minutes, pain with walking downstairs, pain after doing 10 single leg heel raises, how many single leg hops can be done without pain, whether sport is modified or being done, and how long can the athlete train or practice.

Each group has less than 15 so it was not powered sufficiently. In addition the type or prolotherapy here was not intratendinous (Inside the tendon) but rather was a subcutaneous type of prolotherapy which is described on this web site under "options" and has not been tested versus intratendinous types of proliferant injection.

Nevertheless it is of interest that reduction of stiffness and limitation of activity was faster with proliferant injection and that both eccentric loading and proliferant injeciton combined was significantly better than eccentric activity alone.

Yelland MJ, Sweeting KR, Lyftogt JA, Ng SK, Scuffham PA, Evans KA. Prolotherapy injections and eccentric loading exercises for painful Achilles tendinosis: a randomised trial [epub ahead of print] Br J Sports Med (England), Jun 22 2009, pages pending.

ABSTRACT: OBJECTIVE: To compare the effectiveness and cost-effectiveness of eccentric loading exercises (ELE) with prolotherapy injections used singly and in combination for painful Achilles tendinosis. DESIGN: A single-blinded randomised clinical trial. The primary outcome measure was the VISA-A questionnaire with a minimum clinically important change (MCIC) of 20 points on a 100 point scale.

SETTING: Five Australian private primary care centres. PARTICIPANTS: 43 patients with painful mid-portion Achilles tendinosis commenced and 40 completed the treatment protocols. INTERVENTIONS: Participants were randomised to a 12 week program of ELE (n=15), or prolotherapy injections of hypertonic glucose with lignocaine alongside the affected tendon (n=14) or combined treatment (n=14).

Main outcome measurements: VISA-A, pain, stiffness and limitation of activity scores and treatment costs were assessed prospectively over 12 months. RESULTS: At 12 months, the proportions of participants achieving the MCIC for VISA-A scores were 73% for ELE, 79% for prolotherapy and 86% for combined treatment. Mean (95% CI) increases in VISA-A scores at 12 months were 23.7 (15.6 to 31.9) for ELE, 27.5 (12.8 to 42.2) for prolotherapy and 41.1 (29.3 to 52.9) for combined treatment. At 6 weeks and 12 months, these increases were significantly less for ELE than for combined treatment.

Compared with ELE, reductions in stiffness and limitation of activity occurred earlier with prolotherapy and reductions in pain, stiffness and limitation of activity occurred earlier with combined treatment. Combined treatment had the lowest incremental cost per additional responder (AU$1539) compared with ELE.

CONCLUSIONS: For Achilles tendinosis, prolotherapy and particularly ELE combined with prolotherapy give more rapid improvements in symptoms than ELE alone but long term VISA-A scores are similar. Condition Research Home Achilles and Patellar Tendon: Aprotinin injection Orchard et al 2008 Injection of Solutions that block breakdown of tissue may also help healing.

Chronic low back pain

Luciano Bassani — Fri, 16 Oct 2009 0:0:0 +01:00

Chronic low back pain: an integrated diagnostic and therapeutic approach

Dott. Bassani Luciano�

�Introduction

Chronic low back pain is a social problem. 47% of the population suffer from back pain. Third health expense.

13 million missing days at work.93% suffered, suffer� or will suffer� for back pain.The goal is to made a correct clinical diagnosis and to plan an effective treatement.

Chronic low back pain �is the great parodox for modern medicine.� The traditional medical model called by Alf� Nachmeson� � The� dynasty of the disc� can only explain� about 20% of back pain.

This� academical medicine� seems to� have forgotten the power of the two most basic tools of medicine: the history and the physical examination. In the low back the questions of the physician about the pain and the examination of the patient contains� most of the missing� 80%� of the diagnoses.

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�� The objective is to demontrate that� the troubles of the static is the key to explain �constraints, abnormal strain, pains, differents pathologies and that differents kinds of� non surgical treatements can achieve good results.

The large ligamentous and fascial� structures of the low back� and how they work to maintain the stability it is the most important subject in low back pain. When the ligaments� fibers become relaxed, abnormal tension� will then produce a bombardment of afferent somatic� proprioceptive� sensory impulses from the ligament into the spinal posterior root ganglion where some are transmitted to the brain as consciousness of local pain .

Biotensegrity models� shows that the musculoskeletal system mechanically stabilizes itself� by balancing� and distributing� all tension and compression force vectors within it.

The physician who includes painful problems created by joints, muscles, ligaments , fascia, scars, discs, nerve compression �in his diagnostic paradigm should be able to make the correct diagnosis of the cause of low back pain at least 90% of the time.�

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Once a good working diagnosis is made,� applaying the rights treatements the phisician can achieve� 90% of good results.

The treatements included in a conservative approach to chronic� low back pain are various and their use follows a scale depending of� differents elements estimated from the physician: kind of pain, degree of pain, psychological aspect etc.

Once a good working diagnosis is made,� applaying the right global postural reprogramming� (extero-proprioceptive sole, eye�s correction, TMJ correction,scar neutralisation etc.) the phisician try to� rebalance all the postural� system in order to facilitate the action of� the others treatements.

Generally� the physician should� combine� the postural reprogrammation with� neuroauricolotherapy in order to facilitate� the changing� of� abnormals cerebrals patterns. Basically the physician should� use in combine with posture reprogrammation� certains auriculars points as: 1) 01 bilateral which is the rappresentation of �corpus callosus, 2) PMS motor� which is a� general point representing the eye , the associatifs areas and integratives� areas 3)�� cerebellum which is the core of postural system.

Neuroauricolotherpy� is also used in the followings sessions� with the purpose� of reduce the back pain.

The� principals points used in case� of low back pain are all points which corresponds to the same dermatomeric area: disc, muscle, plexus, cord both sensitive and motorial.

In addition it can be usefull to add thalamus, master point of reticular, W2� which is the master mesodermic point, and� cosmonaut point.

In addition to neuroauricolotherapy� in case of ligament, tendon and fascia degeneration,first cause of chronic back pain�� due to insufficient connective tissue,� prolotherapy is very usefull since reduce pain and disability stimulating ligamentous laxity, chronic enthesopaty or thendinosis by provoking an acute infiammatory response by injecting irritants solutions into damaged tissue.

The� patient suffering from chronic low back pain, since his problem is lasting for more than 6 months, has created multiples adaptations�� concerning� specially the muscular system; the muscules during these period have become stiffs and fibrosous� provoking also functional� locked joints.

The purpose of the physician is to� release the locked joints� by manipulations and to recreate a normal muscular play by postural gymnastique.

Conclusions

This� free communication is the synthesis of� several years of experience done directly on the patients which are, each one ,a single person needing a personalized� therapy.

In the field of chronic back pain, more then for others pathology, the physician must try to create a good feeling with the patient and try to riequilibrate both the cerebral patterns and the balance.

A good aid� to this situation comes from postural reprogramming, neuroauricolotherapy, prolotherapy and manual medicine� which, if well managed, can give exellents results.

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