Chaitow's Chat

Breathing Pattern Disorders and Lumbopelvic pain and Dysfunction: An Update

2012-01-23T09:09:00.001+02:00

This post contains a summary of a presentation I will be making at the XXII Physiotherapy Conference, Madrid in March2012, entitled:

Breathing Pattern Disorders and Lumbopelvic Pain and dysfunction : An overview.

It represents an update on my paper written in 2004, on the same theme. (Journal of Osteopathic Medicine 7(1):34-41)

For more on this topic please see my co-authored book (with Dinah Bradley PT and Chris Gilbert PhD): Multidisciplinary Approaches to Breathing Pattern Disorders. (Elsevier 2002)

Also, the newly published, coedited book (with Ruth Lovegrove PhD): Chronic Pelvic Pain and Dysfunction: Practical Physical Medicine.

A second presentation at the Madrid conference will cover a review of indirect manual treatment methods for the lumbopelvic region, and will be posted on this site, in the next few months.

The Figure above represents the myofascial ‘inner stocking’ (or envelope) that involves a prevertebral and intrapelvic myofascial web of support. Among the key structural features of note are the multiple direct myofascial connections between the pelvic floor and the diaphragm.
Reproduced from Key (2010) J. Bodyw. Mov. Ther. 14, 299–301 - with thanks.

Summary

Breathing pattern disorders (BPD) – the most extremeof which is hyperventilation - are surprisingly common in the general population,but more so in women. Despite decades of research BPDs, together with a rangeof the resulting pathophysiological biochemical, psychological andbiomechanical effects, remain commonly under-recognized by health careprofessionals as contributing to pain, fatigue and dysfunction in general andlumbopelvic pain and dysfunction, in particular. These notes focus mainly onone aspect of BPDs potentially negative influence – the contribution towards theevolution, aggravation and maintenance of lumbopelvic pain and dysfunction.

There is also recognition that pain and dysfunctioncontribute significantly to altered breathing patterns, so helping to create areciprocally negative series of adaptations in which pain alters respiration,which in turn amplifies pain.

Definitions
Breathing PatternDisorder (BPD) – also known as Dysfunctional breathing[DB] - is defined as chronic or recurrent changes in the breathing pattern, contributingto respiratory and nonrespiratory complaints. (Thomas et al 2003). Symptoms of BPD includedyspnoea with normal lung function, chest tightness, chest (and othermusculoskeletal) pain, deep sighing, exercise induced breathlessness, frequentyawning and hyperventilation. (de Groot 2011)

Hyperventilation is the statein which breathing occurs in excess of metabolic requirements, leading to anacute reduction in partial pressure of carbon-dioxide (PaCO2) and a prdictableset of physiologic changes. (Lewis 1959, de Groot 2011)

Hypocapnia: Deficiency of Carbon dioxide (CO2) in the bloodresulting from over-breathing/hyperventilation (HVS), resulting in increasedpH, respiratory alkalosis (Naschitz et al 2006)

Respiratory alkalosis: This involvesa rise in pH of the blood, from its normal levels of ~7.4 due to excessive CO2 exhalation duringrapid breathing. An immediate effect is smooth muscle constriction, narrowing of blood vessels, the gut etc, as wellas reduced pain threshold and feelings of anxiety, apprehension.

Respiratory alkalosis leads to decreased levels ofserum calcium ions (Ca²⁺⁾ despite a normal calcium level, due to ashift of Ca²⁺ from the blood to albumin which has become morenegative in the alkalotic state. Hypocalcemia then leads to hyperirritability of nerves– evidenced by Chvostek’s sign (ipsilateral twitch of nose and lips when facialnerve tapped at angle of jaw – an early sign of tetany) (Goljan 2007)

Yee (2010) reports that: “All acid-base disturbances—respiratoryacidosis, respiratory alkalosis, metabolic acidosis, and metabolicalkalosis—have the potential for producing neurologic manifestations”

Bohr effect: In an alkaline environment – such as respiratoryalkalosis - haemoglobin releasesoxygen less efficiently, leading to hypoxia. (Jensen 2004)

Hypoxia: Reduction of oxygen oxygen (O2) supply to tissue, belowphysiological levels.

Etiological and maintaining factorsof BPD include:

· Psychological – for example anxiety (Han et al 1996,Nardi et al 2001)

· Biochemical – for example increased levels ofprogesterone (Ott et al 2006), or altered pH as in acidosis during pregnancy(Jensenet al 2008), or in other states of acidosis (Kellum 2007)

· Habit - “Neurologicalconsiderations leave little doubt that habitually unstable breathing is theprime cause of symptoms” (Lum 1984), or conditioning (van den Burgh et al1997)

· During aerobic exercise (Hammo et al 1999)

· Nixon & Andrews (1996) suggest that deconditionedindividuals utilize anaerobic glycolysis to generate, energy, resulting inrelative lowering of pH, and, consequent homeostatic hyperventilation. Ineffect, lower pH - due todeconditioning - would trigger, hyperventilation, which would furtherencourage, deconditioning.

Epidemiology

In the USA as many as 10% of patients in generalinternal medicine practices are reported to have HVS as their primarydiagnosis. (Lum 1987, Newton 2005) however BPD appears to be far more prevalent(Thomas et al 2005).

Katon & Walker (1998) notedthat patients with the commonest physical symptoms (e.g., abdominal pain, chest pain, headache, back pain),are responsible for half of all primary care visits (USA), and yet only 10%–15%of these are found to be caused by organic illness. All these symptoms are wellrecognised as capable of being the result of BPD.

De Groot (2011) notes that the extreme of BPDs, hyperventilationsyndrome (HVS), is common in adults at between 6% and 10% in different studies,and that is more prevalent in women (14%) than in men (2%).

Special populations, symptoms and BPD

· Perri and Holford (2004) reported that a conveniencesample of 111 patients, attending a chiropractic pain clinic were evaluated forlinks between their health, painhistories and faulty breathing (criteria included evidence of obvious paradoxical –non-diaphragmatic- breathing,or a tendency to raise the upperchest to initiate inhalation). 56.4% demonstrated faulty breathing on relaxedinhalation, increasing to 75% when taking a deep breath. 87% reported a historyof various musculoskeletal pain problems. Based on this self-selectedpopulation, they observe that: “Chancesare 3 in 4 that new patients seen today will have faulty breathing patterns.”

· Cimino et al (2000) found that breathing ratesaccelerate as progesterone levels rise during the luteal phase of the menstrualcycle. This is accompanied by a simultaneous reduction in pain thresholds,suggesting that respiratory changes are at least partially influential inincreased pain perception.

· In a study by Dunnett et al (2007) it was noted thatseveral participants “changed” a diagnosis of fibromyalgia during the course ofa menstrual cycle, fulfilling the diagnostic criteria during the menstrual orluteal phase, but never during the follicular phase.

· Phasic menstrual cycle changes observed inresting minute ventilation and arterial PCO(2) may be due, at least in part, tothe stimulatory effects of progesterone. (Slatkovska et al 2006)

· Premenstrual symptoms (PMS) may be causeddirectly by hyperventilation (HVS). “It has been known formore than 100 years that women hyperventilate during the second half of the menstrualcycle. Symptoms of chronic HVS are remarkably similar to the symptoms observedin some women with PMS.… In women with PMS the sensitivity of the respiratorycenter to CO2 is increased more than normal by progesterone, or some othersecretory product of the corpus luteum, resulting in pronouncedhyperventilation.” (Ott et al 2006)

· Human pregnancy is characterized by significantincreased tendency to hyperventilation largely associated, with increasedcirculating female sex hormone concentrations. (Jensen et al 2008)

· Baranes et al (2005) lists myalgia, back pain andmuscle cramps, as common symptoms associated with overbreathing in children –with the age of onset most commonly between ages 13 and 16.

Painand BPD

· Schleifer et al (2002) outline the way in which painmay be amplified due to BPD. They explain that overbreathing results in a drop in arterial CO2, caused by ventilationthat exceeds metabolic demands for O2, with a consequent rise in blood pH(i.e., respiratory alkalosis). The inevitable resulting disruption in acid-baseequilibrium triggers a series of changes that increase muscle tension, inducemuscle spasm, amplify the responses to catecholamines, producing muscleischemia and hypoxia. Additionally the shift from a diaphragmatic to a thoracicbreathing pattern imposes a range of biomechanical stresses.

· Terekhin and Forster (2006) have used functionalmagnetic resonance imaging (fMRI) involving blood-oxygen-level-dependent(BOLD) contrast, to examine ways inwhich the results of over-breathing impact directly on pain mechanisms. They note that this type of scan maps neural activity in the brain or spinal cord byimaging the change in blood flow (hemodynamic response) related to energy use bybrain cells. Hypocapnia(reduced carbon dioxide in the blood), usually resulting from deep or rapidbreathing such as hyperventilation (HVS) provides various, influences on theBOLD indicating that it may differentially affect the processing of pain inputand motor tasks. “The subtle disturbances of breathing which contribute tohypocapnia should, be considered for functional brain imaging studies, especially,those examining the nociceptive system. The, decrease in BOLD signal by up to 7%, in all regions of the braincortex, indicates a wide spread vasoconstriction in the gray matter as an acutereaction to the hypocapnia."

· Studiesalso indicate that the vasoconstrictory effect of over-breathing, and resultinghypocapnia, leads to cerebral ischemia, while also increasing the affinity, ofhemoglobin for oxygen due to alkalosis (Bohr effect), decreasing oxygen releaseinto the tissue (Clausen et al 2004). The altered neuronal excitability andpotentially affects both pain perception, as well as motor control.

· Diatchencko et al (2006) observed that back pain (as well as chronic neck pain) displays allthe characteristics of central sensitization (Flor 2003), and that associated painprocessing changes in such disorders are affected by breathing patterns.

· Individuals with back pain tend to brace theirsuperficial abdominal muscles and diaphragm as well as having poor core muscleactivation. This negatively influences normal diaphragm function, inhibitingabdominal breathing and encouraging an upper chest pattern. (Radebold etal 2001, O'Sullivan & Beales 2007)

BPD, stability, instability and thenervous system

According to Panjabi (1992) three subsystems worktogether to maintain spinal stability:

1. The centralnervous subsystem (control): sensoryreceptors in the spinal structures, their central connections, and cortical andsubcortical control centers

2. Theosteoligamentous subsystem (passive):vertebrae, intervertebral discs, ligaments, zygapophyseal joints, and passivecomponents of the associated musculotendinous structures

3. The musclesubsystem (active):musculotendinous units attached to, or influencing, the spinal column

These subsystems are interdependent, working together tomaintain spinal stability and intervertebral motion.

There is a great deal of evidence pointing to ways inwhich altered breathing patterns are capable of negatively influencing both thecentral nervous and the active muscle subsystems, thereby contributing to theevolution or maintenance of non-pathological lumbopelvic pain and dysfunction.

· Paillard (2012) reported that hyperventilation, decreases CO2 level and increases pH in body fluidsand tissues and that this provokes vascular changes, possibly responsible, foraugmented postural sway (Sakellari & Bronstein (1997).

· Postural and motor control impairments have beenreported extensively in chronic LBP-patients involving mal-coordination ofpostural and respiratory functions as well as trunk muscles. [Hodges and Mosely 2003, O’Sullivan 2005)

· Janssens et al (2010) have demonstrated that inspiratorymuscles fatigue (IMF) results in “a rigidproprioceptive postural control strategy, rather than the normal"multisegmental" control, which is similar to people with LBP. Thisresults in decreased postural stability. These results suggest that IMF mightbe a factor in the high recurrence rate of LBP.” Janssens et al also notethat in the case of inspiratory muscle fatigue, proprioceptive input fromthe lower back becomes less reliable, disturbing sensory integration andthereby postural control. Overall it appears that BPD/hyperventilation affectsthe interoceptive sensory and motor systems of the postural control mechanism.

· Hodges et al 2005 observed that the diaphragmcontributes to spinal stability in healthy subjects by adding tointra-abdominal pressure and therefore enhanced spinal stiffness. Thisobservation built on earlier studies that indicated that the diaphragm is ableto perform the dual tasks of offering trunk stability, as well as performingrespiratory tasks, when trunk stability is challenged (Hodges et al 2002) - but not when sustained over-breathingis a feature. They found that after approximately 60 seconds of over-breathing,both postural (tonic) and phasic functions of the diaphragm and transversusabdominis were reduced or absent.

· Findings byHodges et al (2001) suggest that “the stabilityof the spine may be compromised in situations in which respiratory demand isincreased, such as exercise and respiratorydisease. …..During strenuous exercise, when the physical stresses to the spine are greater, the physiological vulnerability of thespine to injury is likely to be increased”.

· This supports McGill’s (1995) study that reported thatreduced spinal support is noted during a combined load challenge to the lowback during breathing
challenge (e.g. digging or clearing snow).

· O’Sullivan & Beales (2007 have demonstrated thatSI joint pain and dysfunction, are frequently associated with aberrant pelvicfloor and diaphragm behaviour, and that a program that enhances motor controlvia rehabilitation of pelvic floor control, and a more functional respiratorypattern, improves both pain and disability

· Roussel et al (2009) have reported that more than half of patients with chronic non-specificlow back pain exhibit altered breathing patterns during performances in whichthe trunk-stability muscles are challenged.

BPD,pelvic pain and postural considerations

The pelvic floor and the respiratory diaphragm are,structurally and functionally bound together by fascial, and muscularconnections. (Lee et al 2008).

Gibbons (2001) has described the anatomical linkbetween the diaphragm, psoas and, the pelvic floor: ‘The diaphragm’s medial arcuate ligament, is a tendinous arch in thefascia of the psoas, major. Distally the psoas fascia is continuous withthe pelvic floor fascia, especially the pubococcygeus’. .

Jones (2001) has summarized the integrated structuraland functional thoraco-pelvic unit as follows: “The pelvic floor muscles are part of a multi-structural unit formingthe bottom of a lumbopelvic cylinder with the respiratory diaphragm forming itstop and transversus abdominis the sides. The spinal column is part of thiscylinder and runs through the middle, supported posteriorly by segmental,attachments of lumbar multifidus and anteriorly by segmental attachments ofpsoas to the abdominal muscles.”

With psoas fibres (and those of QL) merging with thediaphragm, and the pelvic floor, any degree of, inappropriate stiffness orweakness in any these muscles is likely, to impact on the ability of either ofthe diaphragms to function normally – compromising spinal stability.

There appears to be a clear connection between respirationand pelvic floor function as well as SIJ stability, an observation thatapplies particularly in women. (Hodges et al 2007)

Having analysed data from over 38,000 telephone interviews,Smith et al (2006) reported that middle-agedand older women had higher odds of having back pain when they experiencedbreathing difficulties, and that disorders of continence and respiration werestrongly related to frequent back pain, possibly explained by physiological limitationsof coordination of postural, respiratory and continence functions of trunk. They note that if pelvic floor muscles are dysfunctional,spinal support may be compromised, increasing external oblique muscle activity,overcoming pelvic floor muscle activity and possibly resulting inincontinence.

Haugstad et al (2006) observed that womenwith chronic pelvic pain “typicallydisplayed upper chest breathingpatterns, with almost no movementof the thorax or the abdominal area”. They also confirmed “a characteristic pattern of standing, sitting, and walking, …..lack of coordination and irregular high costal respiration”… andthat “the highest density, and the highest degree of elasticstiffness [was] found in the iliopsoas muscles”.

Recognising and diagnosing BPD (Courtney et al 2009, van Dixhoorn & Duivenvoorden 1985)

· Restlessness (type A, “neurotic”)
· ‘Air hunger'
· Frequent sighing
· Rapid swallowing rate
· Poor breath-holding times
· Poor lateral expansion oflower thorax on inhalation
· Rise of shoulders on inhalation
· Visible “cord-like” sternomastoidmuscles
· Rapid breathing rate
· Obvious paradoxical breathing
· Positive Nijmegen Test score (23 orhigher)
· Low end-tidal CO2 levels oncapnography assessment (below 35mmHg)
· Reports of a cluster of symptoms such asfatigue, pain (particularly chest, back and neck), anxiety, ‘brain-fog’,irritable bowel or bladder, paresthesia, cold extremities (Chaitow et al 2002)

Rehabilitation

· A randomized controlled study suggested thatpatients with moderate chronic low back pain of an average of one-yearduration, improved significantly (in both pain and functional symptoms) aftereither breathing rehabilitation or physical therapy for 8 weeks. (Mehling et al2005)

· Diaphragmatic breathing, progressive musclerelaxation, exercise, self-visualization, and self-hypnosis have been shown tobe effective in reducing both stress and pain perception. (Whitmore 2002)

· Chronic pelvic pain associated with chronicprostatitis, involving nonbacterial urinary difficulties, has been shown, in astudy at Stanford University School of Medicine, to be capable of being effectivelytreated using trigger point deactivation, together with relaxation and breathing reeducation techniques. (Andersonet al 2005)

· Holloway & West (2007) report that breathingrehabilitation (Papworth Method), as part of a randomized controlled trial, involvinga sequence of integrated breathing and relaxation exercises focused on BPD (includinghyperventilation), led to a clinically relevant improvement in quality of life.

· Musnick (2008) has outlined a protocol that places the role of breathingrehabilitation into context, when managing musculoskeletal pain:

1. Reduce thesynergistic inputs to the pain process (i.e. modify adaptive demands)

2. Deactivate trigger(or tender) points

3. Remove noxious inputfrom scars

4. Enhance spinal andgeneral joint functionality

5. Improve musclerecruitment, strength, flexibility

6. Pay attention toexacerbating factors in diet, lifestyle and habits (sleep, exercise, posture,balance, breathing)

7. Consideremotional/psychological factors

Conclusion

Breathing pattern disorders(BPD) can contribute to, exacerbate, and help maintain, a variety of symptoms,including lumbopelvic pain and dysfunction.

BPDs are relatively easy torecognise and diagnose, and can commonly be improved or normalised by means ofa combination of rehabilitation exercises and manual therapy.

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"Pranotherapy" predecessor of Neuromuscular Technique

2012-01-15T17:37:00.001+02:00

The text below is the Foreword that I prepared for Masterworks International for a book that they recently published entitled Pranotherapy: The Origins of Polarity Therapy and European Neuromuscular Technique, based on the original work : The Human Machine and its Forces by Dr. Dawanchand Varma.

The Foreword explains my tangential connection to Varma, who influenced my Father's cousin Stanley Lief ND DO (photograph above) in his development of NMT. I was unaware of the Polarity Therapy (PT) connection until the publishers explained that Varma and Randolph Stone, developer of PT, had worked together. The really fascinating part of this story is the full circle that emerges (explained towards the end of the Foreword) in which Varma's early descriptions of the target tissues in what he called Pranatherapy (or Pranotherapy) were the subdermal, superficial fascial, structures that are currently receiving so much attention.

I have written extensively of Lief's work in several of my books, for example; Modern Neuromuscular Techniques, 3rd edition 2010 , Clinical Applications of Neuromuscular Techniques (with Judith DeLany) Volumes 1 Upper Body 2nd edition 2009; Volume 2, Lower Body. 2011 (all published by ChurchillLivingstone, Edinburgh)

These notes represent a personal perspective based on the ways inwhich the ideas and the work of Dr Dewanchand Varma became a part of myclinical approach to health management.

When I was studying osteopathy andnaturopathy in London in the late 1950s I was taught Neuromuscular Technique (NMT) as part of our soft-tissue assessmentand treatment course. The version of NMT that I learned had been developed inthe 1930s by my father’s cousin, Stanley Lief ND DC, assisted by his cousin, myuncle Boris Chaitow ND DC.

Lief told us that he had modified atechnique, taught to him by a Dr Varma, an Ayurvedic physician working in Parisin the late 1920s, early 1930s. It may be of interest to know that among thepeople in contact with Varma at that time (according to Lief) was Ida Rolf –although whether she incorporated any of Varma’s work into hers is not known.Lief persuaded Dr.Varma to come to London, where he worked in Lief’s practice(144 Park Lane), for some years, during which time Varma’s book was publishedby Lief’s imprint “Health for All Publications.”

Varma believed that the manualtreatment method he practiced (he called it “Prana-therapy”) and which hetaught to Lief, was capable of identifying and treating local areas ofobstruction to the free flow of energy, using skilful, intelligent, finger orthumb strokes, and applied pressure.

Lief found the subtle techniquesemployed by Varma gentle and efficient – essentially involving as they did a ‘meeting and matching’ of tissue tension,in order to identify – and where necessary modify – freedom, or lack of freedomof motion within these tissues.

Lief used his modifications ofVarma’s approach – which he called NMT - to assess and treat soft-tissuedysfunction, preparing joints for mobilisation or manipulation. And this is whywe were taught NMT in our training at the then British College of Naturopathy and Osteopathy (now renamed as the British College of Osteopathic Medicine).

By the time I was being trained theearly work of Janet Travell MD was available and we began to speak of triggerpoints as one of our targets in NMT assessment and treatment. Simultaneously – in the late1950s/early 1960s the work of Raymond Nimmo DC was becoming more widely known.Nimmo had worked in parallel with Travell (and subsequently another major researcherinto myofascial pain, David Simons MD) in describing localised soft tissuechanges that could generate local and distant pain – myofascial trigger points.When Nimmo came to the UK to teach briefly in the early 1960s, I was privilegedto attend his classes, and found that his terminology was different from thatof Travell, as were his treatment methods (which he called Receptor Tonus Technique) – but that they could usefully beharmonised clinically with Lief’s methods. This is what has happened, as NMThas continued to evolve in both the UK and USA. (Chaitow & DeLany 2011)

Lief’s (European) modified versionof Varma’s approaches, NMT, became a superbly effective soft tissue assessmentand treatment protocol. The delicacy of the finger or thumb strokes allowingfor extremely fine work to be performed – involving intelligent contacts thatdo not overwhelm restrictions, but insinuate (‘melting’) their way into them,teasing and releasing, rather than aggressively forcing change – and it is thisdegree of subtlety that Lief learned almost entirely from Varma.

In the USA Neuromuscular Therapyevolved in a direction that was far more focused on myofascial pain in general(influenced by Travell, Simons and Nimmo), and trigger points in particular.The modalities used in American NMT comprise soft tissue methods developed bypractitioners of massage therapy, osteopathy, chiropractic, physical therapy,manual medicine, naturopathic medicine, and others. (Chaitow & Delany 2011)

Varma’s visionary perspective- connective tissue connections

In his book ‘The Human Machine andIts Forces’ Dr. Dewanchand Varma says:

‘We have discovered that the circulation of thenervous currents, slows down occasionally because of the obstruction caused byadhesions; the muscular fibres harden and the nervous currents can no longerpass through them. We have demonstrated effective and positive methods designedto restore nervous equilibrium which promotes the healthy circulation of blood,so that new tissues begin to be built up again’

In these words Varma seems to bediscussing obstructions in the connective tissue – something that is recognisedtoday as fascia research expands exponentially.

Lief had become interested infascia/connective tissue many years earlier than his introduction to Varma, viathe work of a Scottish physician, Dr Andrea Rabagliati (1843-1930).

In 1916 Rabagliati had published abook “Initis – nutrition and exercise”that advanced the theory that connective tissue congestion played a significantpart in the etiology of dysfunction and disease. Dr. Varma maintained that it was possible, usingwhat he termed ‘pranatherapy’, toboth palpate and normalise soft tissue restrictions that interfered with whathe envisioned as the normal flow of energy (“prana”) around the body.

Osteopathic practitioner andeducator, Tom Dummer DO, who had studied NMT with Lief in the 1950s, has noted(in an unpublished monograph, dated 1991)):

“Lief noticed the similarity between the theories and techniques of DrVarma and Dr Rabagliatti and realized that they were virtually complementary toeach other. It was from the synthesis of the two that neuromuscular techniqueeventually evolved.”

Writing in the 1960s, Brian YoungsND DO – who had studied and worked with Stanley Lief, observed as follows:

“Connective tissue ……was largely ignored until recently, but hasnow been made the subject of close study in regard to its structure andfunctions. The ubiquity ofconnective tissue caused Rabagliatti to compare it to the ether - as the mediumfor, as he termed it, 'the zoodynamic life force'. Through the connective tissues' planes run the trunks andplexuses of veins, arteries, nerves, and lymphatics. Connective tissue is thesupport for the structural and, therefore, functional relationships of thesesystems…… and as (NMT) operates primarily on connective tissue itwill usually be concentrated at those areas where such tissue is most dense,e.g. muscular origins and insertions, especially the broad aponeuroticinsertions …..connective tissue is, after all, ubiquitous”

This brings us right up to date,where research at major institutions is highlighting the role of fascia in bothfunction and dysfunction, much of it echoing the work of Rabagliatti, Varma andLief.

For example, in relation tofunction McCombe (2001) hasobserved:

· “Fascia forms a gliding interface withunderlying muscle [allowing] free excursion of the muscle under the relativelyimmobile skin. A plane of potential movement exists in the form of the areolartissue layer, [apparently] lined with a lubricant, hyaluronic acid.”

While in regard to dysfunction:

· “When fascia isexcessively mechanically stressed, inflamed or immobile, collagen and matrixdeposition becomes disorganized, resulting in fibrosis and adhesions – fascialthickening’ Langevin et al 2008, 2009))

· “Densification occurs, involving distortion of myofascialrelationships, altering muscle balance and proprioception” (Stecco et al 2009)

· “Binding occurs among layers, that shouldstretch, glide and/or shift on each other, potentially impairing motorfunction” (Fourie 2009)

· Chronic tissue loading occurs, forming ‘global soft tissue holdingpatterns’ (Myers 2009)

All of these quotes could have come from Varma – and so I willrequote his observation, which was 80 years ahead of this current research –even though the terminology belongs to a time long gone:

Research

As far as NMT’s efficacy - researchvalidation is slowly appearing– for example:

· Nagrale andcolleagues (2010) demonstrated the efficacy of NMT methods that wereincorporated into a focused trigger point protocol - Integrated NeuromuscularInhibition Technique – INIT (Chaitow 1994).

· Spanishresearchers (Ibáñez-García J et al 2009 ) showed that NMT (Lief’s method) and Strain/counterstrainwere equally effective in the management of latent trigger points inthe masseter muscle.

And of course - in addition to Varma’sinfluence on NMT - there is alsohis connection with Polarity Therapy – about which I know too little tocomment, but which appears to have been just as profound.

There also remains a tantalising possibilitythat Varma may have influenced the work and thinking of Ida Rolf.

We owe Dr Varma our thanks, and therepublication of his book is a fitting tribute.

References

· Chaitow L Delany J 2011 ClinicalApplications of Neuromuscular Techniques. Volume 2: Lower Body (2ndedition). ChurchillLivingstone, Edinburgh

· Chaitow L 1994 Integrated NeuromuscularInhibition Technique British Jnl of Osteopathy 13:17-20

· Dummer T 1991 (unpublished)The Lief Neuromuscular Technique. Maidstone, Kent.

· Fourie W 2009 IN: FascialResearch II: Basic Science and Implications for Conventional and ComplementaryHealth Care Munich: Elsevier Gmbh

· Ibáñez-García J et al 2009Changes in masseter muscle trigger points following strain-counterstrain or neuro-musculartechnique JBMT 13(1): 2-10

· Langevin H 2008.. In: Audette, Bailey(Eds.) Integrative Pain Medicine. Humana

· Langevin H 2009 FascialResearch II: Basic Science and Implications for Conventional and ComplementaryHealth Care Munich: Elsevier GmbH

· McCombe D et al 2001 Jnl. HandSurgery 26B:2: 89-97

· Myers T 2009 Anatomy Trains, 2^ndedition Edinburgh: Churchill Livingstone

· Nagrale et al 2010 Efficacy of anintegrated neuromuscular inhibition technique on upper trapezius trigger pointsin subjects with non-specific neck pain. Jnl Manual & Manipulative Therapy 18(1):37-43

· Rabagliatti A 1930, 2nd Edition. Original 1916) InitisOr Nutrition and Exercises C. W. DanielCompany, London,

· Stecco L Stecco C 2009 Fascial Manipulation:Practical Part. Piccin Italy

· Youngs B. 1963 Thephysiological background of neuromuscular technique. Br Naturopathic Jnl& Osteopathic Rev. 5:176–178

The Role of Fascia in Manipulative Treatment of Soft Tissues

2011-11-30T22:39:00.006+02:00

Fascia provides structural and functional continuity between the body’s hard and soft tissues, as an ubiquitous elastic–plastic, component that invests, supports and separates, connects and divides, wraps and gives cohesion, to the rest of the body – playing an important role in transmitting mechanical forces between muscles (Huijing 2009).

Due to trauma or inflammation fascia may shorten and what was previously a pain free range of motion may become painful and restricted. (Langevin 2008)

“Fascia forms a gliding interface with underlying muscle [allowing] free excursion of the muscle under the relatively immobile skin. A plane of potential movement exists in the form of the areolar tissue layer, [apparently] lined with a lubricant, hyaluronic acid.”

Binding may occur among layers, that should stretch and glide on each other, potentially impairing motor function. (Fourie 2012).

Many therapeutic manual approaches claim to relieve such dysfunctional states, with some hypothesised explanations. “In order to achieve a viscoelastic deformation during manual intervention, without causing tissue damage, … there should be no slow increase in the applied force. Rather it is recommended that a fairly constant force be maintained, for up to 60 seconds, in order to allow for a plastic stress relaxation response of the tissue.” (Chaudhry et al 2008).

Examples include:

· Schleip (In Press) suggests some responses may relate to a sponge-like squeezing and refilling in the semi-liquid ground substance.

· Loose connective tissue and light tissue stretch “may be key to the therapeutic mechanismof treatments using mechanical stimulationof [loose] connective tissue” (Langevin 2005) e.g myofascial release (Pilat 2009)

· Collagen architecture responds to loading (Kjaer et al 2009). Load can be used therapeutically to stimulate tissue repair and remodelling in tendon, muscle, cartilage and bone. Exercise and manual methods stimulate tissue repair and remodelling in tendon, muscle, cartilage and bone.

Mechano-coupling = Physical load (often shear or compression) that perturbs cells, transforming into various chemical signals - within and among cells.

Cell–cell communication = Stimulus in one location leads to a distant cell registering a new signal, despite distant cell receiving no mechanical stimulus.

Effector cell response = Mechanical loading stimulates protein synthesis at the cellular level, promoting tissue repair and remodelling (Kahn & Scott 2009)

· Trigger point release may involve repetition of voluntary isometric contractions that initiate lengthening of the series elastic (fascial) component of sarcomeres. (Simons 2002).

· Active scars restrict movement and produce pain - relieved by treatment (Kobesová, 2007)

· Following visceral mobilization post-operative adhesion severity & number of adhesions were significantly lower, in a rat model (Bove & Chapelle 2012)

· Connective tissue massage (‘skin rolling’) has been shown, via ultrasound imaging, to modify collagen density. (Pohl 2010)

· “Evidence supports the possibility that ligamento-muscular reflexes can have inhibitory effects on muscles associated with that joint.”(Solomonow 2009)

· “Strain direction, frequency and duration, impact important fibroblast functions known to mediate pain, inflammation and ROM” (Standley & Meltzer 2008)

· Fascial Manipulation (FM^®)) studies suggests that fascia involves specific organizational relationships with associated muscles. (Borgini et al 2010)

· Tool assisted treatment (e.g. Graston) produces mechanical deformation that influences extracellular matrix, modulating synthesis of proteoglycans and collagen, apparently influencing connective tissue rehabilitation (Chiquet 2003)

· Klingler (2012) reports that heat in the therapeutic range, relaxes many fascial contractures associated with myofascial dysfunction. (IN PRESS)

REFERENCES
· Bove, G Chapelle S 2012 Visceral mobilization can lyse etc JBMT IN PRESS
· Borgini E et al 2010 How much time is needed to modify fascial fibrosis? JBMT 14(4):318-325
· Chaudhry H et al 2008. Three dimensional model for deformation of human JAOA, 108, 8, August 2008.379.
· Chiquet M et al 2003 Matrix Biol. 2:73-80
· Fourie W 2012 Scar Treatment Methods. IN: Schleip R Findley T Chaitow L Huijing P (Eds) Fascia - The Tensional Network of the Human Body:. Elsevier IN PRESS
· Huijing PA 2009 Journal of Biomechanics. 42(1):9-21
· Khan K M Scott A 2009 Mechanotherapy:. British J Sports Medicine 43:247–251
· Kjaer M, et al 2009 From mechanical loading to collagen synthesis. Scand J Med Sci Sports 19(4):500-510
· Klingler W 2010 IN: Chaitow L Lovegrove R (Eds.) Practical Physical Medicine Approaches to Chronic Pelvic Pain (CPP) & Dysfunction Elsevier IN PRESS
· Kobesova A et al 2007 Jnl. Manipulative & Physiological Therapeutics 30(3):234-238
· Langevin H et al 2005. American Journal of Physiology and Cell Physiology 288: C747-C756
· Langevin H 2008.. In: Audette, Bailey (Eds.) Integrative Pain Medicine. Humana
· McCombe D et al 2001 Jnl. Hand Surgery 26B:2: 89-97
· Pilat A 2009 Myofascial induction approaches for headache. In: Fernández-de-las- Peñas C Arendt-Nielsen L Gerwin RD (ed). Tension Type and Cervicogenic Headache: pathophysiology, diagnosis and treatment. Boston: Jones & Bartlett Publishers
· Pohl H 2010 Changes in structure of collagen distribution in the skin JBMT 14(1):27-34
· Schleip R 2012 Strain hardening of fascia: Static stretching of dense fibrous connective tissues can induce a temporary stiffness increase accompanied by enhanced matrix hydration. JBMT IN PRESS
· Simons D 2002 Understanding effective treatments of myofascial trigger points. Jnl Bodywork and Movement Therapies 6(2):81-88
· Solomonow M 2009 J. Bodywork Movement Therapies 13(2) 136-154
· Standley P Meltzer K 2008 Effects of Repetitive Motion Strain (RMS) & Counter-Strain (CS), on fibroblast morphology and actin stress fiber architecture Jnl.Bodywork & Movement Therapies, 12(3):201-203

Pulsed Muscle Energy Technique (MET): New insights from Fred Mitchell Jr.

2011-10-15T08:13:00.024+03:00

Following the previous blog posting on the use of rhythmic isometric contractions in application of MET, there was a discussion on the topic on facebook.
In that thread of discussion the following postings occurred (Note: some of this selection of posts from that thread have been summarised reduced in length):

Before looking at some of these, and the remarkable insights they led to from Fred Mitchell Jr DO, I will draw attention to a variation on Pulsed MET (as previously described) - deriving from Karel Lewit (2010).

Lewits 1st rib method

Lewit describes the therapist as being active, with the patient resisting....the direct opposite of the way pulsed MET is employed.

In the illustration, above,the therapist stands behind seated patient, stabilizing neck/shoulder region of side to be treated, with one hand. The other hand is placed against side of the patient’s head.

The patient is asked to press her head against this hand, as the therapist rhythmically intensifies and slackens pressure.

Lewit suggests that 20 scalene isometric contractions of this sort (two per second) usually produces mobilization of the 1^st (and sometimes 2^nd) rib.

Ruddy’s model would require all efforts to be by patient - resisted by the practitioner.

The facebook thread

The facebook thread that led to Dr Mitchell's explanations (see later in this posting) begins with my post:
‘Teaching in London this weekend, and I came across this quote from Fred Mitchell Jr. DO, son of the major developer of Muscle Energy Technique.’
"Treating a joint motion restriction as if the cause were tight muscle(s) is one approach that makes possible restoration of normal joint motion. Regardless of the cause of restriction, MET treatment, based on a ‘short muscle’ paradigm, is usually completely effective in eliminating blockage, and restoring normal range of motion, even when the blockage is due to non-muscular factors”
‘What do you think? This approach is usually, but not always successful, and when not - there's always HVLA.’

There then followed a lively discussion between Ben Cormack, Rajam Roose, Zac Laraman and Vijay Gambhir, on the relative value of MET in treating joint dysfunction locally, to which I added:

“When a joint is restricted - particularly a spinal joint - of course it is a part of a chain of other functional and structural features, and seldom an isolated problem (unless the result of recent, direct, trauma).

So if we regard most spinal joint dysfunction as adaptive, we are not dealing with a local problem. The statement by Mitchell that I posted says (to me anyway) that MET is an efficient way of starting the normalisation process, instead of HVLA manipulation aimed at 'correcting' or 'adjusting' that same dysfunction.

That reeducation in patterns of use, posture, breathing etc etc, are all part of what needs to be done is not the issue....only that MET is safer, more efficient (usually - in my experience) and involves more of the involved tissues beneficially, than HVLA. …..Kappler & Jones (2003) observed, relative to what's preventing free motion in joints (commonly, but not always): "As the barrier is engaged, increasing amounts of force are necessary and the distance decreases. The term barrier may be misleading if it is interpreted as a wall or rigid obstacle to be overcome with a push.
As the joint reaches the barrier, restraints in the form of tight muscles and fascia, serve to inhibit further motion. We are pulling against restraints rather than pushing against some anatomic structure.”

It is these soft tissue barriers to free movement that MET addresses most effectively.....however…. I never said that this was all that needs to be done, only that it may be more effective than high velocity methods.”

Following some mild bickering from those engaged in this discussion, Christian Fossum DO entered the thread with this posting:

“I find MET an effective approach, but do chose other techniques when called for. One thought which I now frequently return to when my MET seems to be less effective is one given to me by Ed Stiles, D.O.: "When ineffective, are you treating the patient out of sequence?". Sequencing the treatment added to my success, but didn't exclude the use of other manipulative methods.”

More interchanges followed at which point Nathan Josephs brought in the names of Fred Mitchell (Sr and Jr) as well as Philip Greenman – referring us to his blog.

Hallie Robbins DO then added:

“MET is a blunt or sharp instrument depending on the practitioner's precision. I use MET regularly, but I vary the amount of loading or activating force recruitment in order to address the discrete fiber bundles or larger muscle masses. I also have found that inviting a patient to move in specified directions in short arcs (or sometimes PNF-style larger movements) can help both provider and patient find and target the prime tissue restrictions quickly. This fits with Ed Stiles, DO, Sequencing approach”

I responded:

“The version of MET I use (and teach mainly) is that of TJ Ruddy, who taught his methods to Mitchell (senior). It is what Rudy called "rapid resistive duction" and involved mini-isometric contractions (2 per second) usually towards the restriction barrier in Ruddy's methodology, but in almost any direction in the way I use/teach it. In spinal regions this often involves coaching the patient into producing translation movements against a firm barrier (my hand as a rule) in order to produce mobilisation. I believe we are actually recruiting the intrinsic spinal muscles in this way. I don't know if Drs Mitchell et al teach this marvellous version of MET?”

Hallie replied:

“Your and my interpretations of MET applications seem similar. Jay Sandweiss is the contact person and faculty with Fred's son for Mitchell MET. In March at AAO Convo, Jay , Mickey and I were comparing treatment techniques; Jay calls mine "Flow" as I interweave functional and other modalities into the MET more than "only" setting up planes and working through barriers in the more classic MET version.”

Steve Goldstein offered these thoughts:

“I've found blending modified MET for joints with myofascial sensibility a fine combination. Clearing global restrictions along fascial lines and planes with modified MET for joints using low force extremely effective. Once I got over the hurdle of thing MET was just for muscles, and the load had to be 20%-30%, was when I started being extremely effective. I use low load resistive, as I call it, to free axial and peripheral joints quickly and efficiently. I use 5-10% force for intrinsic muscle and it also effected ligaments. Upon release a slight counter-force in the opposite direction is often enough to open a restricted direction. I agree the preciseness is a major component and contributor to the success of the application.”

I suggested that it might be useful to~: “Try adding mini-pulses instead of even brief, light sustained contractions. Ruddy's magic injunction was to "avoid wobble and bounce" - so a mere pulsing is called for, and 5 to 10% of strength sounds to be at the upper end of what I think is needed. I'd love to know why Ruddy's approach is not more widely taught...perhaps someone can ask Jay to ask Fred....?

To which Hallie responded: “I can check with Jay and Fred Jr-“

What follows in this posting are the words of Fred Mitchell Jr, one of the primary developers and teachers of MET, and the son of the main developer of MET as we know it....with clear reference to the foundational influence of the work of TJ Ruddy DO, on the evolution of this most useful approach.

Ruddy

Thomas Jefferson (T.J.) Ruddy never used the expression “muscle energy,” to my knowledge. His alliterative name for one of his many techniques was “Ruddy’s Rapid Rhythmic Resistive Duction Technique,” (RRRRD)

It is worth noting that Ruddy was already an ophthalmologist (in his day they were called Eye, Ear, Nose, and Throat –EENT – specialists), MD, before he went to Kirksville to study [osteopathy] with Andrew Taylor Still.

When my father, Fred L. Mitchell, Sr., met Ruddy (approximately 1958), he was demonstrating one of his many (actually, over 100 patented) inventions, the “eye finger” – a soft appliance molded to the ovoid contour of the eyeball used on the eyelid for resisting extraocular muscle actions, which were being used to pump

edema from the orbit. The idea of using a patient’s voluntary precisely controlled muscle actions for a focused local therapeutic effect was an epiphany for my father.

Later, Ruddy applied the principle of using striated muscles as venous/lymphatic pumps in the context of the long-lever techniques he had learned from Still for treating osteopathic lesions of the axial skeleton or limbs. I have seen the photograph taken of Ruddy while he is watching A. T. Still demonstrating thoracic spine long lever technique using the arm.

When I saw Ruddy demonstrate a RRRRD procedure for treating an upper thoracic segmental dysfunction, it looked very much like that old photograph. With one hand he palpated the vertebra, with the other he held the patient’s wrist while taking his pulse (to time his oscillating resistance to the (sustained) muscle contraction) and holding the arm in an abducted position, and using the arm lever to control and localize myofascial tension. His instruction to the patient would be the equivalent of, “Try to keep your arm in this position.”

Resist vs. Think

Herein lies a significant difference between RRRRD and MET. Many practitioners who say they are employing Muscle Energy Technique are in the habit of saying to patients the equivalent of “Resist me when I push against you.”

The few who better understand the MET paradigm give their patient instructions that include a target for the patient’s effort. The patient may be instructed to “Make an eight ounce push with your forehead toward your left hip.” These detailed instructions are addressed (through imagery) to the global reflex systems which impact the somatic dysfunction being treated, with the goal of using imagery to re-program spinal cord internuncial neurons involved in the spinal effector mechanisms of core muscle and synergist participants.

Microcirculation

Ruddy had taken to heart Still’s lectures about the importance of microcirculation. He was among the many students who heard Still state his intension to transform all of them into philosophers, and certainly not the only one who understood Still’s goal. He knew that Still was not quoting a bumper sticker when he said, “The rule of the artery is supreme.” He understood the reference to microcirculation. It is possible that Ruddy understood osteopathic lesions to be importantly, if not primarily, abnormal disturbances of circulatory dynamics. Restoring mobility to a joint was accomplished, mainly, by decongesting the tissues around it.

Neurophysiology

Most people understand the fluid pumping effect of a muscle contraction. Many understand in a general way its stretching effect on fascia and that muscle proprioceptive afferents are stimulated when a muscle contracts. Since its original formulation by my father, MET has evolved for me as biochemistry and neurophysiology have shed more light on the quantitative details of these phenomena.

My father’s earliest concept of what we now call MET placed heavy emphasis on Sherrington’s Second “law” (describing how antagonist muscles inhibit each other).

Consequently, his treatments for dysfunctions of the axial skeletal joints called for very forceful patient contractions “to inhibit the tight muscle.”

Sub-maximal recruitment

Such forceful contractions are still commonly used throughout Europe by practitioners of Post-Isometric Relaxation (PIR), especially those trained by Vlad Janda. Janda’s principal mentor, Karel Lewit, after he visited me at MSU, changed his approach to using grams of isometric force instead of kilograms. He confirmed that in a letter to me, and expressed his gratitude to me for my guidance in MET. We had extensive correspondence regarding MET and PIR. The sub-maximal

recruitment idea probably originated with me. At least, I was thinking in terms of precisely controlling which motor units fire for maximum therapeutic effects by how I instructed the patient.

Old MET vs. Modern MET

The current modern MET applications taught in my courses have departed significantly from what my father taught, mostly from my own research. Being a teacher means being frequently confronted with things you know for sure that turn out to be wrong. (Apologies to either Will Rogers or Mark Twain, whose wisdom I may have paraphrased).

Dr Mitchell has offered many other insights in his generous response to Hallie's query about 'pulsed MET', and I hope to post these in a future blog.

For now though it may be time to digest the essence of the information we have been offered....that Ruddy learned from Still, that Fred Mitchell Sr learned from Ruddy....and that we can all learn from these pioneers, and the insightful commentary from Fred Mitchell Jr DO who continues that legacy.

Kappler & Jones 2003 in Foundations of Osteopathic Medicine 2nd edition pp852-880

Lewit K Manipulative Therapy Elsevier 2010 p217
Mitchell F Jr. 1998 Muscle Energy Manual Vol.2: MET Press, East Lansing p1
Ruddy T 1962 Osteopathic rapid rhythmic resistive technic. Academy of Applied Osteopathy Yearbook, Carmel, California

Pulsed Muscle Energy Technique: Ruddy Revisited

2011-09-17T06:36:00.013+03:00

It's been several months since the last blog-post, due to immersion in writing and editing tasks.
I'm currently working on notes for an eventual updating/revision of Muscle Energy Techniques (3rd edition)....abbreviated to MET.
A 4th edition will eventually emerge, in several years time, hence the current need for information gathering....and this post reflects some of the material I am currently working on.

Osteopathic physician Fred Mitchell Sr., was the developer of MET, then called the “muscle energy treatment.”(1958).
Mitchell wrote several papers in which he credited T.J. Ruddy, DO, as a major source of inspiration.
Ruddy (1962), a Los Angeles based practitioner who specialised in osteopathic management of head, neck and particularly eye problems, had developed a method that he had called osteopathic rhythmic resistive duction therapy - that he used to treat head and neck injury and pain.

This method involves the introduction of a series of rapid pulsating (usually patient induced) isometric contractions, against the practitioner's resistance. A shorthand term ‘pulsed muscle energy technique’ (Pulsed-MET) is now applied to Ruddy’s method (Chaitow 2001).

In some texts Ruddy's method is described differently, for example "In resistive duction technique, the patient’s force is constant against a rhythmic pressure applied by the osteopathic physician at a rate approximating the patient’s pulse."
It would seem obvious that were the patient creating the rhythmic pulsation a greater degree of possible proprioceptive reeducation would be taking place, as compared with the patient resisting the operator's pulsed efforts.
Whichever approach is used, a circulatory (lymphatic and venous) as well as a proprioceptive element occurs.
From a manual therapy perspective however, a further major benefit is the rapid normalisation of range of motion of joint restrictions when Pulsed-MET is used.

Joints as a soft-tissue problem?

The paradigm employed in use of MET or Pulsed-MET for joint restriction requires brief explanation.
Kappler & Jones observe that:
“As a [joint] barrier is engaged, increasing amounts of force are necessary and the distance decreases. The term barrier may [therefore] be misleading if it is interpreted as a wall or rigid obstacle to be overcome with a push. As the joint reaches the barrier, restraints in the form of tight muscles and fascia, serve to inhibit further motion. We are pulling against restraints rather than pushing against some anatomic structure.”

Mitchell explains further:

"Treating a joint motion restriction as if the cause were tight muscle(s) is one approach that makes possible restoration of normal joint motion. Regardless of the cause of restriction, MET treatment, based on a ‘short muscle’ paradigm, is usually completely effective in eliminating blockage, and restoring normal range of motion, even when the blockage is due to non-muscular factors”

The simplest use of Pulsed-MET involves the dysfunctional tissue or joint being held at its restriction barrier, at which time the patient (or the practitioner if the patient cannot adequately cooperate with the instructions) introduces a series of rapid (two per second) tiny efforts.
These miniature contractions toward the barrier are ideally practitioner resisted. The barest initiation of effort is called for with (to use Ruddy’s term) ‘no wobble and no bounce’.
The application of this ‘conditioning’ approach involves contractions which are ‘short, rapid and rhythmic, gradually increasing the amplitude and degree of resistance, thus conditioning the proprioceptive system by rapid movements’ (Ruddy 1962).

As mentioned, Ruddy suggests the effects are likely to include improved oxygenation, venous and lymphatic circulation through the area being treated. Furthermore, he
believed that the method influences both static and kinetic posture because of the effects on proprioceptive and interoceptive afferent pathways, so helping to maintain ‘dynamic equilibrium’ which involves ‘a balance in chemical, physical, thermal, electrical and tissue fluid homeostasis’.

The effects of Pulsed-MET might therefore include:
• proprioceptive re-education
• strengthening facilitation of the weak antagonists
• reciprocal inhibition of tense agonists
• enhanced local circulation and drainage
• re-education of movement patterns (enhanced motor control)

Example: Ruddy’s ‘pulsed’ MET and the erector spinae muscles (see illustration above)

To treat the erector spinae the patient should be placed on a fixed stool or chair, in a seated, slumped position, feet flat on the floor and with the head approximating the knees.
The practitioner stands behind and to the side and passes an arm across the anterior upper chest from shoulder to shoulder, while her other hand maintains a contact with the area of the back (that is being treated.

To treat the erector spinae group a restriction barrier is engaged in which the patient is in an easy end-of-range position i.e. a combination of flexion, sidebending and rotation, with the paraspinal muscles close to their end-of-range, but not at stretch.
The patient is coached as to the rhythm as well as the amplitude of the pulsation needed.
This requires initiation of a series of 20 (twice per second for 10 seconds) very slight attempts to move further in the direction of the restriction barrier, pulsing against the firm and totally unyielding, resistance of the practitioner.
After the series of mini-contractions and a brief rest, the barrier is reassessed and reengaged, and the process repeated.
During this painless procedure the patient is rhythmically activating the antagonist muscles to those which are restricted and preventing full range of movement.
The series of pulsing contractions tones the inhibited antagonists while reciprocally inhibiting hypertonic agonists, so increasing the range of motion.

Use of Pulsed-MET is essentially safe, and very effective .

It's easy on the practitioner, and the patient....and it's really difficult to understand why it is not being taught at osteopathic schools any more?

It was the foundation for MET, and deserves to be rehabilitated

REFERENCES

Kappler RE, Jones JM. 2003 Thrust (High-Velocity/Low-Amplitude) techniques. In Ward RC (Ed) Foundations for osteopathic medicine, 2/e. Philadelphia, Lippincott, Williams & Wilkins pp852-880
Burns D Wells M 2006 Gross Range of Motion in the Cervical Spine: The Effects of Osteopathic Muscle Energy Technique in Asymptomatic Subjects JAOA 106(3):137-142
Mitchell FL. 1958 pelvic function. In: Barnes MW, ed. Year Book 1958: Selected
Mitchell F Jr. 1998 Muscle Energy Manual Vol.2: MET Press, East Lansing p1 Osteopathic Papers. Carmel, Calif: Academy of Applied Osteopathy 1958:71–90.
Ruddy T 1961 Osteopathic rhythmic resistive duction therapy. Yearbook of Academy of Applied Osteopathy 1961, Indianapolis, p 58

Isometric Contractions in Pain Management

2011-07-20T11:55:00.005+03:00

These notes summarise some of the many ways in which isometric contractions can be used in clinical practice

Isometric contractions and trigger points.
• Trigger points appear to be self-perpetuating, unless treated correctly.
• Whatever method is used to deactivate a trigger point - manual therapy, injection such as novocaine or xylocaine, coolant spray, dry needling, laser, acupuncture techniques - the muscle housing the trigger point always needs to be restored to its normal resting length
• If this is not achieved, reactivation of the trigger point is more likely (Simons et al 1999). Failure to restore the muscle containing the trigger point to its normal resting length is likely to lead to only short-term relief
• Whatever stretching methods are used it is important that the process should be gradual, gentle and painless
• The recommendation of Lewit (1999) and Simons et al (1999) is that muscle energy technique (MET) be used to achieve safe and (relatively) painless stretching
• This calls for gentle isometric contractions followed by stretch

• An isometric contraction, alone, produces a stretch of part of muscle (series elastic component) while the other part (parallel elastic component/actin-myosin) shortens (see illustrations above)
• Lewit suggests that, in many instances, simply stretching a muscle – with no other treatment - may be sufficient to deactivate trigger point activity

What happens during an isometric contraction?

As mentioned above - isometric contractions introduce a lengthening of the series elastic component (fascial, tendinous), while the parallel elastic (actin/myosin) component shortens – so that the muscle does not change length during the contraction.

Repetitions of isometric contractions effectively lengthen these structures overall – particularly if additional active or passive stretching is added. (Lederman 1997)

Simons (2002) suggests that mild, voluntary, isometric contractions therefore allow lengthened sarcomeres (contractile unit of a myofibril) to exert an effective elongation force on the shortened sarcomeres of the contraction knot of a myofascial trigger point (MTrP). Individual sarcomeres, like balloons are constant-volume structures (see illustrations above).

Adding pressure

The effects of simultaneous application of trigger point pressure release and voluntary isometric contraction are additive (Simons 2002)

Compressing them in the vertical dimension causes an increase in the horizontal dimension.

Thus, finger pressure applied downward onto a MTrP, tends to lengthen sarcomeres that are shortened, for any reason, and that may be responsible for the palpable taut band which is characteristic of MTrPs

Analgesic effects of isometric contractions

Studies show that both high and low-intensity isometric contractions have analgesic effects in healthy adults (Bement et al 2008)

A recent study (Bemant 2011) compared pain ratings and thresholds in men and women with Fibromyalgia syndrome (FMS), before and after isometric contractions, of varying intensity and duration, performed with the elbow flexor muscles:

1/ Maximal voluntary contractions (MVC)

2/ 25% MVC sustained until task failure,

3/ 25% MVC- for 2 minutes

4/ 80% MVC sustained until task failure

RESULTS:

Significant analgesic responses were noted in some FMS patients, with the greatest change noted after the long-duration, low-intensity contraction sustained until failure

Most benefit was experienced by younger women (average age 39) who had the lowest pain thresholds at outset

Staud et al (2005) showed evidence of negative effect following strong sustained isometric contractions in all FMS patients.

The message that emerges is that low intensity, sustained, isometric contractions produce a reduction in pain in most people, including those with fibromyalgia

Possible ‘hydraulic’ effects on fascia of isometric contractions ?

•Klingler & Schleip (2004) examined fresh human fascia, and noted that during light stretching, water is extruded, refilling afterwards.

•As water extrudes, temporary relaxation occurs in the longitudinal arrangement of collagen fibers.

During the reduced hydration period the tissues become far less stiff, more pliable, allowing increased range of movement

•If the stretch is moderate, and there are no micro-injuries, water subsequently soaks back into the tissue until it becomes stiff again

Many effects of manual therapy may relate to sponge-like squeezing and refilling effects in the semi-liquid ground substance, with its water-binding glycosaminoglycans and proteoglycans.

Isometric contractions and muscle energy technique (MET)

MET uses isometric contractions of varying durations and intensities (Chaitow 2006) to facilitate subsequent stretching procedures.

Fryer and Fossum (2009) have formulated a two possible models to explain the usefulness of these contractions:

1/ During the contraction fluid flow is stimulated on a cellular level, at the same time that fibroblasts are being stretched (as discussed above). This increases drainage from interstitial spaces, reducing concentrations of pro-inflammatory cytokines, so reducing the sensitization of peripheral nociceptors.

2/ As a contraction is initiated both muscle and joint mechano-receptors are activated.

This:

a/ , Evokes sympatho-excitation via somatic afferents that produces localized activation of the epriaqueductal grey that plays a role in descending modulation of pain

While:

b/ Encourages gating of nociceptive impulses in the dorsal horn through mechanoreceptor stimulation

These two processes (a & b) encourage nociceptive inhibition “stimulation produced analgesia:

As a result, following isometric contractions, stretching and range of motion are increased, making MET one of the siplest and most effective modalities.

And finally….

Isometric contractions, as well as most manual therapy methods result in upregulation of endogenous pain relieving substances, including endocannabinoids (Degenhardt 2007)

• The endocannabinoid (eCB) system offers 'resilience to allostatic load’ – dampening nociception and pain. It is anxiolytic, decreases inflammation, and plays a role in fibroblast reorganization.

• Two cannabinoid receptors have been identified: CB1 in the nervous system, and CB2 associated with the immune system (and gut)

There are several tools to upregulate eCB activity, including manual therapy, exercise, acupuncture, and diet– increasing a sense of wellbeing and euphoria

McPartland et al (2005) measured Anandamide (AEA) levels pre- and post-osteopathic manipulative treatment (OMT) including Myofascial Release, Muscle Energy Technique, and HVLA – all of which involve fascial load.

It seems that shear and stretching load upregulates AEA, producing analgesic/euphoric cannabimimetic effects.

Pulsed MET

…..and then there is pulsed MET, the use of rhythmic mini-isometric contractions, which deserves a separate discussion……watch this space........

REFERENCES

Bement M et al 2011 Pain Perception After Isometric Exercise in Women With Fibromyalgia Arch Phys Med Rehabil 92:89-95

Bement M et al 2008 Dose response of isometric contractions on pain perception in healthy adults Med Sci Sports Exerc. 40(11):1880-1889

Chaitow L 2006 Muscle Energy Techniques (3^rd edition) Churchill Livingstone, Edinburgh

Degenhardt, B et al 2007. Role of osteopathic manipulative treatment in altering pain biomarkers: a pilot study. Jnl. American Osteopathic Association 107:387–394

Fryer G Fossum C 2009 Therapeutic Mechanisms Underlying Muscle Energy Approaches. In: Physical Therapy for tension type and cervicogenic headache: physical examination, muscle and joint management Fernández de las Peñas C Arendt-Nielsen L Gerwin R (eds): Jones & Bartlett, Boston.

Klingler W Schleip R Zorn A 2004 European Fascia Research Project Report. 5^th World Congress Low Back and Pelvic Pain, Melbourne, November 2004

Lederman E. Fundamentals of manual therapy. London: Churchill Livingstone 1997. p34

Lewit K 1999 Manipulative therapy in rehabilitation of the locomotor system, 3rd edn. Butterworths, London

Simons D 2002 Understanding effective treatments of myofascial trigger points. Journal of Bodywork and Movement Therapies 6(2):81-88
Simons D Travell J Simons L 1999 Myofascial pain and dysfunction: the trigger point manual. Vol. 1, 2nd edition: The upper extremities. Williams and Wilkins, Baltimore, Maryland

Staud R et al 2005 Isometric exercise has opposite effects on central pain mechanisms in fibromyalgia patients compared to normal controls. Pain 118:1-2:176-184

Chronic Pelvic Pain (CPP)

2011-06-04T06:37:00.009+03:00

In the next few months nearly 3 years of focused effort will come to fruition, with the publication of this book (by Elsevier/ChurchillLivingstone) - coedited by Dr Ruth Lovegrove and myself, with input from around 20 experts including:
Rodney Anderson, Andrew Baranowski, Andry Vleeming, Howard Glazer, Christopher Gilbert, Maria Adele Giamberardino, Diane Lee, Linda-Joy Lee, Bill Taylor, Stephanie Prendergast, Elizabeth Rummer, Cesar Fernandez de las Penas, Andrzej Pilat, Maeve Whelan, Michael Seffinger, Melicien Tettambel, Hallie Robbins, Jan Dommerholt, Tracey Adler and Eric Blake

Dr Lovegrove and I start the book with these words - which gives a fair representation of the aims:
"This book has a single primary aim – to offer a one-stop source of relevant information for clinicians – specialists, practitioners and therapists – on the subject of non-malignant chronic pelvic pain (CPP), with particular emphasis on current trends in physical medicine approaches to assessment, treatment, management and care."

Traditional methods have failed
There would be little need for this book, were current treatment strategies that focus on CPP, proving successful.
Anderson (2006) has observed that traditional medical therapy to treat CPP conditions has failed, ‘whether involving antibiotics, anti-androgens, antiinflammatories, a-blockers, thermal or surgical therapies, and virtually all phytoceutical approaches’.
Shoskes & Katz (2005) concur – demonstrating that a series of monotherapies, used to treat hundreds of men with prostatitis, resulted in only 19% reporting any relief of symptoms.

Successful physical therapy approach
In contrast a randomized clinical trial designed to assess the feasibility of conducting a full-scale trial of physical therapy methods in 48 patients with urological CPPS has shown promise (Fitzgerald et al. 2009).
This study compared two methods of manual therapy; myofascial physical therapy and global therapeutic massage. The global response assessment response rate of 57% in the myofascial physical therapy group was significantly higher than the rate of 21% in the global therapeutic massage treatment group (P = 0.03) suggesting a beneficial effect for myofascial physical therapy.

Not all somatic
But a purely somatic approach is also flawed.
Pontari & Ruggieri (2008) note that the symptoms of CP/CPPS appear to result from interplay between psychological factors and dysfunction in the immune, neurological and endocrine systems.
It therefore seems unarguable that therapeutic approaches should adopt strategies that take account of these multiple interacting factors. And this is precisely the approach that this book takes.

Multiple influences
Throughout the book, there is an emphasis on a background of different influences that may accompany the evolution of CPP, and its associated symptoms.
Identifying the particular influences that have caused, maintained and/or exacerbated a CPP patient’s condition is therefore an appropriate clinical ambition.
In the context of this book, a further ambition is the identification of those influences that may be amenable to therapeutic attention involving physical medicine.

Understanding pain
Ideally the patient and therapist can move away from the solely structural pathological model, to one that considers for example, the brain in pain, their beliefs about their pain, nutritional issues, in addition to any pathology or motor control issues.
For example, there is evidence that understanding pain reduces the threat of it, altering patients’ attitudes and beliefs, increasing pain thresholds, and when combined with physiotherapy, reduces pain and disability (Moseley 2007).
It is therefore important to understand what the patient believes the pain means and help explain modern pain biology, thereby reducing the patients’ attitude and beliefs.

Caution
Currently most treatment options for CPP are empirical, so there is a great requirement for careful clinical reasoning when approaching the management of a patient with CPP, if indeed we are to do no harm.
These thoughts have been considered by all the contributors and both editors - with Diane Lee and Linda Joy Lee providing an excellent chapter to guide the reader through the CPP maze towards clearer clinical decision making.
A quote from their chapter offers a flavor of the guidance on offer:
"As clinicians have long recognized, it is now widely accepted that patients with pain do not form homogeneous populations, but consist of multiple subgroups with different combinations of underlying impairments (physical and psychosocial), and these subgroups require different treatment approaches for best outcomes. Furthermore, given that multiple factors contribute to pain, it is also unrealistic to expect that one single type of treatment modality will resolve a patient’s presenting pain and functional limitations.............In our experience, there are no recipes, prediction rules or guidelines for patients presenting with chronic pelvic disability with or without pain and it is likely that a multimodel approach will always be more effective for long-term success."

References
Anderson, R., 2008. The Role of Pelvic Floor Therapies in Chronic Pelvic Pain Syndromes Current Prostate
Reports. 6, 139–144.

Fitzgerald, M.P., Anderson, R., Potts, J., et al., 2009. Randomized multicenter feasibility trial of myofascial physical therapy for the treatment of urological chronic pelvic pain syndromes. J.Urol. 182 (2), 570–580.

Moseley, G.L., 2007. Reconceptualising pain according to modern pain science. Phys. Ther. Rev. 12 (3), 169–178.

Pontari, M., Ruggieri, M., 2008. Mechanisms in prostatitis/chronic pelvic pain syndrome. Urology 179, S61–S67.

Shoskes, D., Katz, E., 2005. Multimodal therapy for chronic prostatitis/chronic pelvic pain syndrome. Curr. Urol. Rep. 6 (4), 296–299.

The explosion of fascia research

2011-02-18T05:16:00.005+02:00

This posting is a modified version of an article I have written for a British cranial osteopathic publication.

Because I am actively involved in the organizational aspects of next year's Fascia Research Congress in Vancouver I have had only a limited amount of time to give to writing for the blog - hence this recycled - but I hope interesting - update on fascia.

When I was studying osteopathy in the late 1950s (BCNO – now BCOM) fascia entered into the lessons and lectures as a somewhat mysterious part of the economy of the body. It featured large in the historical aspects of osteopathy’s evolution, with early pioneers referring to its all-pervading nature – it was everywhere, and there were theories and assertions as to its relevance, but there was very little that was rooted in science. (Still 1902)

So, the question remained - what did fascia do?

Clues were to be found in American osteopathic writing. For example, decades ahead of his time Cathie (1974) described fascia’s potential for contractility as well as its rich neural supply – features that would not be validated by research until very recently. (Schleip 2006, Stecco 2008).

Osteopaths – and others - in the USA (Little 1969, Taylor 1958, Rolf 1962) made it clear that that fascia was not just a background material, with little function apart from its obvious supporting role, but rather a widespread, tenacious, connective tissue involved deeply in almost all of the fundamental processes of the body’s structure, function and metabolism.

In therapeutic terms it became clear there can be little logic in trying to consider muscles and joints as separate structures from fascia, because they are so intimately related. Remove connective tissue from the scene and any muscle left would be a jelly-like structure without form or functional ability, and joints would quite simply fall apart. (Cantu et al 1992)

We now know that there exists a state of structural and functional continuity between all of the body’s hard and soft tissues, with fascia being the ubiquitous elastic–plastic, gluey, component that invests, supports and separates, connects and divides, wraps and gives cohesion, to the rest of the body – the fascial, connective tissue network. (Ingber 2008, Myers 2009)

Any tendency to think of a local dysfunction, as existing in isolation needs to be discouraged as we try to visualize a complex, interrelated, symbiotically functioning assortment of tissues, comprising skin, muscles, ligaments, tendons and bone, as well as the neural structures, blood and lymph channels, and vessels that bisect and invest these tissues – all given shape, form and functional ability by the fascia. (Schleip 2006, Ingber 2008, Solomonow 2009)

Fascial function and dysfunction revealed

Fascia, when healthy, forms a gliding interface with underlying muscle [allowing] free excursion of the muscle under the relatively immobile skin. A plane of potential movement exists in the form of the areolar tissue layer, apparently lined with a lubricant, hyaluronic acid. (McCombe et al 2001)

This process of ‘sliding fascia’ can now be visualised, using real-time ultrasound and elastography – as was demonstrated recently by Langevin (2010b). Dramatic video images demonstrated the free movement of lumbodorsal fascia in pain free individuals, contrasted with that of individuals with low back pain.

Similar images were displayed of myofascial trigger points, during the same panel presentation, that I co-chaired (Shah 2010). Both elastography and ultrasound images show trigger points to be denser than surrounding, normal, tissue.

When fascia is excessively mechanically stressed, inflamed or immobile, collagen and matrix deposition becomes disorganized, resulting in fibrosis and adhesions, and fascial ‘thickening’ (Langevin et al 2009), also described as ‘densification’ (Stecco et al 2009). This process involves distortion of myofascial relationships, altering muscle balance and proprioception. Consequent binding among layers, that should stretch, glide and/or shift on each other, potentially impairs motor function (Fourie 2009), and leads to chronic tissue loading, which contributes to ‘global soft tissue holding patterns’ (Myers 2009).

Cramer et al (2010) in rat studies showed that “hypomobility results in time-dependent adhesion development within the zygapophyseal joints”. Such adhesion development may have relevance to spinal manipulation, which could theoretically break up Z joint intra-articular adhesions”

Some therapeutic implications

A review by Schleip (2003) has documented both myelinated and unmyelinated fibers in fascia, including sympathetic endings. Stecco et al. (2008) found that the outer layers of the deep fascia contained a rich vascular and nerve supply, with intrafascial nerve fibres seen throughout. Some of these were presumed to be stretch receptors.

Bialowski (2008) has hypothesised that mechanical force (soft tissue & manipulative) initiates neurophysiological responses - peripheral and central – possibly evoking and explaining the clinical outcomes of manual therapy. These hypotheses have been expanded on by Simmonds et al (2011) who suggest that HVLA manipulative therapies (i.e. rapid) stimulate fascial tissues (as in the Z-joint example described earlier), while myofascial therapies (such as myofascial release and muscle energy technique) deliberately stimulate fascial tissues

Langevin's in vivo and in vitro studies have shown that loose connective tissue responds to light tissue stretch, which “may be key to the therapeutic mechanismof treatments using mechanical stimulationof connective tissue” (Langevin & Sherman 2006, Langevin 2010a)

Myers (2010) suggests that stretching can be applied not only to ‘length’ problems, but also to ‘stuck layer’ problems, using shear stress to allow the restoration of increased relative movement between the adjacent planes of fascia (Schwind 2004)

In Germany, Pohl (2010) has demonstrated, using real-time ultrasound imaging, changes in collagen density in various layers of skin before and after connective tissue massage (CTM) involving skin rolling

Mechanotransduction and strain transmission

What has now been established is the remarkable degree to which muscular effort depends on the multiple links that muscles have with connective tissue structures.

These connections mean that – for example - a hamstring stretch will produce 240% of the resulting strain in the Iliotibial tract - and 145% in the ipsilateral lumbar fascia - compared with the hamstrings.

The process of strain transmission that occurs during stretching, involves many other tissues beyond the muscle that is being targeted, largely due to fascial connections, making the use of the word ‘isolated’ - together with ‘stretching’ - difficult to justify. (Franklyn-Miller et al 2009)

A fascial hydraulic effect?

Klingler & Schleip (2004), at the University of Ulm, measured wet & dry “freshly harvested” human fascia and found that during an isometric stretch, water is extruded, refilling afterwards. As water extrudes temporary relaxation occurs in the longitudinal arrangement of the affected collagen fibres. If only moderate strain is involved there are no micro-injuries, and water soaks back into the tissue until it swells, becoming stiffer again. It therefore seems that some tissue responses to manual therapy may relate to this sponge-like squeezing and refilling in the semi-liquid ground-substance, with its water binding glycosaminoglycans and proteoglycans.

Fascia related therapeutic approaches

The range of methods and modalities that focus attention on fascial dysfunction are proliferating. A few of those where a degree of supporting validation exists are summarised below :

· Heat in the therapeutic range, relaxes many fascial contractures associated with myofascial dysfunction. External heat has been shown to be beneficial in low back pain (Klingler 2011)

· Graston Technique® (GT) is an instrument-assisted soft tissue assessment and mobilization method delivering load deformation via stainless steel instruments. Mechanical deformation influences the extracellular matrix (ECM,) modulating the synthesis of proteoglycans and collagen by fibroblasts, increasing collagen formation (Hammer 2007)

· Neurologically active scars can restrict back flexion, which the patient feels as low back pain. This can be relieved by treatment of scars on the abdomen and/or below the symphysis (Kobesová, 2007)

· Fryer & Fossum have suggested that apart from the influence of mechanoreceptors on pain (via both ascending and descending pathways), Muscle Energy Techniques induce in-vivo mechanical stretching of fibro-blasts that both alters interstitial osmotic pressure as well as increasing blood flow, so reducing concentrations of pro-inflammatory cytokines, reducing sensitization of peripheral nociceptors.

· Standley & Meltzer (2008) have demonstrated - on a cellular level - the beneficial effects, on fibroblasts, of both myofascial release and positional release (Strain/counterstrain) methods. “……strain direction, frequency and duration, impact important fibroblast physiological functions known to mediate pain, inflammation and ROM….”

· Borgini et al (2010) have demonstrated the influence of direct compressive force on dense fascial restrictions, using the Italian modality developed at the University of Padua, Fascial Manipulation®

· The benefits of Connective Tissue Massage have been demonstrated in a number of clinical trials – notably in relation to chronic pelvic pain (Fitzgerald 2009)

· The methods used in structural integration (Rolfing) are directed mainly at fascia and connective tissue, which are treated with fingers, open hands, clenched fists, and elbows, with pressure directed to release adhesions between what should be freely sliding structures. (Findley & Schleip 2007)

· Fernandez-de-las-Penas and Pilat (2010) have described the successful use of neuromuscular technique (NMT) in treatment of myofascial pain

Much more to learn

What has emerged from the first two Fascia research conferences – Boston 2007 and Amsterdam 2009 – suggests that there is far more yet to learn.

These conferences brought clinicians of all schools, together with scientific researchers, in the hope and expectation that this would lead to a cross-fertilization, in which the clinical needs, confusions and questions of practitioners and therapists would inform researchers, who in turn would help clinicians to better understand the real nature of fascial structure and function, in relation to their patient’s problems and their own therapeutic efforts. It was further hoped that researchers would be spurred to new directions of study fascia.

And this has happened, and continues, with studies emerging at a remarkable pace, that have further clarified the nature and multiple functions and roles of fascia in the body.

The theme of the 3^rd Fascia Research Congress (Vancouver, Canada, March 28 - 30, 2012) will be: Fascia: What do we know? What do we feel? Continuing the Scientist/Clinician Dialogue.

As the organising committee have said : The 2012 Fascia Congress will centre on the latest and best research on human fasciae. Additionally---and recognizing the interests of clinicians in gaining insights that will bear on practical applications---the program will be designed to include more presentation time to relating the research findings to clinical issues, particularly the practical applications of fascial layers.”

The conference proper will be preceded (March 23-27) by a Fascial Dissection Workshop, with a range of additional pre and post-conference workshops, on March 27th and March 31st .

At this early stage the planning for the Vancouver conference is already advanced.

For example, among the confirmed keynote speakers are:

· Cesar Fernandez de las Penas DO PhD : Muscular and fascial aspects of myofascial Pain

· Al Banes PhD : Mechanical Loading and Fascial Changes – Tendon Focus

· Karen Sherman PhD : Existing trials on fascia in the context of manual therapies

· Carla Stecco MD : Fascial Anatomy Overview

· Dr. Rolf K. Reed : Fluid Dynamics and fascia (lymph, circulation etc)

· Mary Francis Barbe : Changes in Fascia Related to Repetitive Motion Disorders

A number of panel sessions are also in the planning stage that will highlight the needs and interests of all clinicians – including exploration of modern imaging methods

· The conference website is http://www.fasciacongress.org/2012/

· A call for Abstracts will soon be displayed on that website

Proceeding books and DVDs from the 2007 and 2009 congresses can be purchased via this link

British Osteopathic representation in fascia research?

There has to date been little evidence of interest from British osteopaths in current fascial research or the Research Congresses. In contrast, senior members of the American osteopathic profession (including Brian Degenhardt, Michael Kuchera, Frank Willard) are active in research as well as promotion of this trend via participation in the organisation of the 3^rd Congress (Vancouver 2012). For example Dr Kuchera is co-chair of the Scientific Committee, of which I am a member, as are several US based chiropractic researchers.

The possibilities for active involvement in the next congress, via submission of abstracts, is something I would encourage British DOs to consider. In my studies of cranial concepts, the intercranial structures (Tentorium cerebelli, Falx cerebri and others) were always central considerations. Has there been any cranial research that could stand scrutiny in the form of an abstract – and/or possible oral presentation? Are there perhaps a series of cases that could be described, written up, presented?

And if not now - when?

References

Bialosky J et al 2009 The mechanisms of manual therapy in the treatment of musculoskeletal pain Manual Therapy 14:531–538

Borgini E et al 2010 How much time is needed to modify fascial fibrosis? Jnl Bodywork & Movement Therapies 14(4):318-325

Cantu R Grodin A 1992 Myofascial Manipulation Gaithersburg Maryland; Aspen Publications

Cathie A 1974 Selected writings. Academy of Applied Osteopathy Yearbook 1974, Colorado Springs

Cramer G et al 2010 Zygapophyseal joint adhesions after induced hypomobility. Journal of Manipulative and Physiological Therapeutics 33:508-518

Fernandez-de-las-Penas C Pilat A 2010 IN: Chaitow L Lovegrove R (Eds.) Practical Physical Medicine Approaches to Chronic Pelvic Pain (CPP) & Dysfunction Elsevier IN PRESS

Findley T Schleip R 2007 Fascia Research. Basic Science and Implication for Conventional and Complementary Health Care vols. 2–3, Elsevier, Germany

FitzGerald, M.P. et al 2009 Randomized Multicenter Feasibility Trial of Myofascial Physical Therapy for the Treatment of Urological Chronic Pelvic Pain Syndromes. Journal of Urology 182(2):570-580

Fourie W 2009 IN: Fascial Research II: Basic Science and Implications for Conventional and Complementary Health Care Munich: Elsevier GmbH

Hammer W 2007 Functional Soft-Tissue Examination & Treatment by Manual Methods 3^rd ed. Sudbury, MA, Jones & Bartlett pp 33-161

Ingber D 2008Tensegrity and mechanotransduction, Jnl Bodywork and Movement Therapies 12(3):198–200, 2008.

Klingler W Schleip R Zorn A 2004 European Fascia Research Project Report. 5^th World Congress Low Back and Pelvic Pain, Melbourne, November 2004

Klingler W 2011 IN: Chaitow L Lovegrove R (Eds.) Practical Physical Medicine Approaches to Chronic Pelvic Pain (CPP) & Dysfunction Elsevier IN PRESS

Kobesova A et al M 2007 Twenty-year-old pathogenic “active” postsurgical scar: a case study of a patient with persistent right lower quadrant pain. Journal of Manipulative and Physiological Therapeutics 30(3):234-238

Langevin H, Sherman K 2006 Pathophysiological model for chronic low back pain integrating connective tissue and nervous system mechanisms. Medical Hypotheses 68(1):74–80

Langevin H 2009 Fibroblast Cytoskeletal Remodeling Contributes to Viscoelastic Response of Areolar Connective Tissue Under Uniaxial Tension, as reported in Fascial Research II, Elsevier GmbH Munich

Langevin H et al 2010a Tissue stretch induces nuclear remodelling in connective tissue fibroblasts. Histochem. Cell Biol. 133(4):405-15

Langevin H 2010b Presentation: Ultrasound Imaging of Connective Tissue Pathology Associated with Chronic Low Back Pain. 7^th Interdisciplinary Congress on Low Back & Pelvic Pain (Los Angeles, November 11 2010)

Little L 1969 Towards more effective manipulative management of chronic myofascial strain and stress syndromes. Jnl American Osteopathic Association 68:675-685

McCombe D et al 2001Jnl. Histochemical structureof the deep fascia and its structural response to surgery. Hand Surgery 26B:2: 89-97

Meltzer K et al 2009 In vitro modelling of repetitive motion injury and Myofascial Release. Jnl Bodywork & Movement Therapies 14:162-171

Myers T 2009 Anatomy Trains, 2nd edition Edinburgh: Churchill Livingstone

Myers T Fascial Stretching. IN: Schleip, Findley, Huijing & Chaitow. Fascia in Manual Therapy. Elsevier, Edinburgh IN PRESS

Pohl H 2010 Changes in structure of collagen distribution in the skin caused by a manual technique J. Bodywork Movement Th. 14(1):27-34

Rolf I 1962 Structural Dynamics. British Academy of Applied Osteopathy Yearbook 1962. BAAO London

Schleip R, Naylor I, Ursu D, et al 2006 Passive muscle stiffness may be influenced by active contractility of intramuscular connective tissue, Med Hypotheses 66(1):71

Schleip R 2003 Journal of Bodywork & Movement Therapies 7:104-116

Schwind P 2006 Fascia and Membrane Technique, Edinburgh: Churchill Livingstone

Shah J 2010 Ultrasound techniques reveal objective abnormalities of myofascial trigger points and surrounding connective tissue. 7^th Interdisciplinary Congress on Low Back & Pelvic Pain (Los Angeles, November 11 2010)

Simmonds N et al 2011 A theoretical framework for the role of fascia in manual therapy. Jnl. Bodywork & Movement Therapies IN PRESS

Solomonow M 2009 Ligaments: A source of musculoskeletal disorders, Journal Bodywork and Movement Therapies 13(2):136-154

Standley PR, Meltzer KR 2008 In vitro modeling of repetitive motion strain and manual medicine treatments: potential roles for pro- and anti-inflammatory cytokines. Journal of Bodywork & Movement Therapies 12:201-203.

Stecco A et al 2009 Anatomical study of myofascial continuity, anterior upper limb. J Bodyw Mov Ther. 13: 53-62

Stecco C et al 2008 The expansions of the pectoral girdle muscles onto the brachial fascia: morphological aspects and spatial disposition. Cells Tissues Organs. 188: 320-9.

Still AT. 1902 Philosophy and mechanical principles of osteopathy. Kansas City, MO: Hudson-Kimberly Pub. Co.

Taylor R 1958 Bioenergetics of man. Academy of Applied Osteopathy Yearbook 1958. Carmel California

Does HVLA manipulation 'break' adhesions in Z joints?

2011-01-09T12:58:00.013+02:00

High Velocity, Low Amplitude (HVLA) spinal manipulation is sometimes dramatically effective in relieving back pain - but not always.
HVLA has been used in physical therapy, chiropractic and osteopathy for round 150 years - and before that by bone-setters (and village blacksmiths) for many centuries.
Why HVLA is effective - and when HVLA is effective - remain a matter for conjecture?

Papers by Evans & Lucas (2010) and by Evans (2009) suggest that the mechanisms involved can commonly be described and summarised as follows:
1) A force is applied to the recipient
2) The line of action of this force is perpendicular to the articular surface of the affected joint
3) The applied force creates motion at a joint
4) This joint motion includes articular surface separation
5) Cavitation occurs within the affected joint.

The question then arises as to why cavitation (the gapping process which leads to the characteristic 'crack' or 'pop') should result in reduced pain, and/or increased range of motion?
This is particularly pertinent since before and after images (x-ray) don't show any change of position?

Cramer et al (2010) have now offered a credible answer to at least some (the majority? all?) such events.
It seems that fibrous adhesions can form between 'Z' (zygapophyseal) joints during periods of relative immobility, and that these may be 'broken' during application of HVLA manipulation to spinal segments.

The studies that support this hypothesis involved temporary fixation of the lumbar regions of rat-spines, during which periods adhesions of varying thickness developed.
The longer the fixation (4, 8, 12, 16 weeks were tested), the larger the adhesions (see photos above).

1. Fibrous adhesions develop in hypomobile zygapophyseal joints restricting motion

2. Spinal adjustment/manipulation (HVLA) separates the articular surfaces of Z-joints by gapping them

3. This process breaks fibrous adhesions

4. Absence of adhesions allows normal motion to be resumed

Photographs of small, medium and large (rat) adhesions, between Z-joint surfaces, are shown above.

The question then arises....what happens when spinal joints are treated using other, less 'aggressive' methods - such as Muscle Energy Technique - where normal function frequently follows treatment?

Evans & Lucas (2010) provide one model - see the chart at the start of this post, while

Simmonds et al (2011) have offered a different - neurophysiological - model that suggests that manipulative therapies (both rapid [HVLA] and slow [MET, NAGS, SNAGS other soft tissue methods]) stimulate neural structures in fascia, and that this initiates neurophysiological responses - peripheral and central – evoking the clinical outcomes of manual therapy. These suggestions are supported by Bialowski et al (2009)

These models all include a focus on, or reference to, fascia - which is a major change from what might have been considered even 5 years ago.

The two major fascia research congresses (Boston 2007, Amsterdam 2009) have changed the landscape for clinicians - and the focus of much research.

For details of these landmark congresses, and the opportunity to purchase the proceedings books or DVDs click on the (green) links above.

For details of the next fascia congress (Vancouver 2012, click here)

As my friend Robert Schleip never tires of saying ---- "fascianating times"

References

Bialowsky J et al 2009 The mechanisms of manual therapy in the treatment of musculoskeletal pain Manual Therapy 14:531–538
Cramer G et al 2010 Zygapophyseal joint adhesions after induced hypomobility. Journal of Manipulative and Physiological Therapeutics 33:508-518
Evans D 2010 Why do spinal manipulation techniques take the form they do? Towards a generalmodel of spinal manipulation Manual Therapy 15(3):212-219
Evans D Lucas N 2010 What is manipulation? Manual Therapy 15(3)(2010) 289-291
Simmonds N et al 2011 A theoretical framework for the role of fascia in manual therapy. Jnl. Bodywork & Movement Therapies IN PRESS

Stone-age posture and diet : A facebook discussion

2010-12-29T21:03:00.006+02:00

I am relatively new to FaceBook but am finding aspects of the interactions on the site fascinating and educational.

Today I posted the following:

“I came across this picture of a neanderthal guy on BBC's news site. It discussed new evidence that these people ate cooked vegetables. Clearly that was a necessity as their posture was awful. Look at those gothic shoulders! I bet he had headaches!”

I am copying some of the more interesting of the 30+ responses (some using pseudonyms) this attracted – as well as a few of the flip ones:

Gil Hedley said:

“Heck, that's my uncle!!”

Sallie Burge-Thurman observed (perhaps speaking with experience?) :

“No neck, squinty eyes, weather-beaten face, mustache that would keep any fly out, and hair everywhere but the belly and shoulder area.. must have rubbed off from all the potato vodka he drank…..falling down on one side all night long will do that to a guy”

I commented:

“To be serious for a moment....imagine this chap came into your office for an appointment and said -"I have this headache, and my neck's stiff, and I should mention my shoulders hurt like hell"
Is there any chance at all of more than symptomatic relief?
Can that dense mass of what used to be muscle ever be restored to elastic efficiency?
Could his crowded cervical joints realistically be mobilised?
We have all probably been faced with this immovable mass of fibrous gristle. So, where would you start?”

Michelle Doyle offered a serious thought:

“Yes, I have noticed how immobile this guy looks...could probably barely move to hunt, which is why they may be contributing Neanderthal extinction to over reliance on meat. Perhaps he was beyond help, unless given treatments early on. 'Movement is life'...which is probably what really lead to their extinction! But today, we can help people with posture and joint dysfunction.”

Pacific Rim Chiro offered specifics:

“Thoracic mobs/manipulation, SCM and Trap MET to start. Then I like to have my patient in a side lying position, mob the scapula in all directions and then using my hand in a knife edge and with the scapula passively pulled into retraction, try to work my hand up in under it, and then cup my hand slightly to create a little space, reduce adhesions etc.”

My daughter Sasha added her thoughts:

“But... they were designed like this weren't they? As far as I know, skeletal evidence has shown that their arms (shoulder & elbow joints) functioned very differently to ours, somewhat more like those of gorillas than of modern humans. Plus...... they used their arms much in the same way as gorillas - in addition to walking upright, though again. as far as I am aware there were anatomical differences. So are you sure that the picture we're looking at is one of pathology at all - because the whole design is different? Unless of course you do actually mean modern folks who actually do look like this! (yep, we've all seen them!)
And btw, they were very effective hunters.... used spears very well and could bring down mammoths when hunting in groups..... extinction ( I think) may well have more to do with brain evolution and climate than anything else.

Liz Baker commented:

“I have met many patient's in the chronic pain center where I work that could make this guy look better in comparison. These patients would fit your description, Leon. Dense mass, crowded joints, fibrous gristle, etc.”

I chipped in again:

If - as Sasha says - they were designed this way - they were destined to have stiff necks, jaws out of alignment, shoulders that were at a mechanical disadvantage (glenoid fossa protracted, putting stress onto rotator cuff muscles), ribs and thoracic cage crowded etc.

In other words their design was not conducive to the sort of activity they would have had to face in harsh environments....perhaps why only a few of their genes are still around?
If they moved around like gorillas do, they would probably have been better off than trying to walk upright.
As for meat eating Michelle...the BBC piece is about traces of cooked vegetable matter (now fossilised) being identified on teeth....so the diet was more varied than previously thought.”

Ed Lark offered cranial thoughts:

This is a great topic! It seems that their skulls also had an occipital bun. Goodness knows how strong their nuchal ligament was. I bet they had tremendous muscular support to hold their heads up! Now I want to look up cervical degradation ...amongst Neanderthals!
Is there a field called Paleo-Osteopathy?

Jason Erikson offered support for Gil’s remark about his uncle:

“A paleoanthropologist on the radio was saying that we now have DNA proof that Neanderthals mated with human ancestors. Up to 5% of the DNA of northern Europeans is of Neanderthal origin.”

Ravensara Travillian launched into analysis of Sasha’s earlier remarks….and went on with more insights:

“Hi, Sasha--I am a little bit confused by what you wrote.
You say: "they were designed like this weren't they?" which sounds like you are about to present an Intelligent Design creationism argument. But then you mention "brain evolution" which... sounds like just the opposite of a creationist argument. And your timeline and use of comparative anatomical evidence certainly does not sound like creationism. So I am not sure what you mean to say.
Would it be fair to reword your statement to say "they evolved like this in response to their environment, didn't they? As far as I know..."(then all the same as you originally wrote up to the following sentence). "So are you sure that the picture we're looking at is one of pathology at all - because the whole baseline is different?"
If I am correctly understanding what you intended to say, then I would agree that you have raised a very important point. Evolution is not the same as design; it doesn't plan in advance, and it doesn't produce optimal results. The results only have to be good enough to function in a particular niche in order to be successful there. Which I think reinforces your point, if I understand it correctly, that what we would call "pathology" comes from our looking at it from our modern context rather than from the point of view of the environment they themselves operated in.

Leon points out:
"If - as Sasha says - they were designed this way - they were destined to have stiff necks, jaws out of alignment, shoulders that were at a mechanical disadvantage (glenoid fossa protracted, putting stress onto rotator cuff muscles), ribs and thoracic cage crowded etc."

That is one of the classic critiques of Intelligent Design creationism--if we are supposed to believe there really is a designer, he/she/it is at best incompetent (knees, lower back, retina), and at worst, sadistic (surrounding the urethra with the prostate).
There was an amusing analysis of this in _Scientific American_ a couple of years back; you can see it at:

If humans really had been designed to avoid those flaws, you would expect us to look more like the improved versions illustrated in the article, which look (to me) more like hobbits.
"In other words their design was not conducive to the sort of activity they would have had to face in harsh environments....perhaps why only a few of their genes are still around?"
To avoid confusion, would it be ok to restate your first sentence as "their anatomy" rather than "their design"?
What you say is true, but it's equally true for us modern Homo sapiens as well. Neither of us lasts as long as we could, because our parts wear out prematurely, or poorly fit our environment in other ways. As you correctly point out, their environment was harsh, and they were poorly suited to it in the long run--but since their lifespan was ~30 or 40 years tops, the long run wasn't really an issue for them. They didn't have to be perfectly suited to their environment; they only had to be good enough to get by in their younger years.

If you think about what American football does to its players, it's similar in a way. It's harsh and damaging, and chews them up only to spit them out, physically used up, at the end of their careers. The only real difference is that the Neanderthals didn't have much longer to live afterwards. So what we, with our longer lifespans and more options would consider "pathology" might have simply been their baseline for normal.”

I responded to this:

Thanks for the detailed analysis Revensara
Clearly we are ill-designed for modern life/or poorly evolved - whichever suits you best.
Thankfully much of modern life has evolved/or been designed to match our inadequacies - so we (or most of us)... no longer have to sprint after antelopes to catch supper, but only need to hobble down to the store for whatever approximation of food we can afford.
But in truth - every now and then - I catch sight of a well designed and functioning body, the owner of which could probably chase antelope, leap over rivers and climb trees... and in those moments perhaps there is a glimpse of what we could be like - one in which a designer seems less improbable, and/or evolution seems to be on the right track.
For the most part however, both seem t have missed the mark.
Our neanderthal example seems to be just such a dead-end kid.

Elan Schacter observed:

“That artist missed some things we see that artists don't. Try this: ignore the head. On that body, where would you expect the head to be? I would expect it to be much more aligned.”

Laura Allen complained:

“My symptoms exactly and I've been hunched over the computer for so long I'm starting to resemble him.”

Stefan Chmelik moved back to the question of diet

“The Paleo diet seems to be the new trend, is there any evidence for it?”

I responded:

· Stefan, around 1985 I wrote a book "Stone Age Diet" based on current (at that time) research into paleolithic eating habits.

· There's good evidence that they were healthy unless oevrtaken by clubs, tigers or bears etc, BUT

· They had lots of exercise

· They ate at dawn and around sunset (read up on effect of timing of eating, Leptin behaviour & syndrome X)

· They slept at night (read up on Leptin again)

· They ate LOTS of green vegetables (not cultivated, but gathered) as well as seeds, nuts, fruit etc

· The meat they ate was lean

· Many lived by oceans and rivers and fish was a major part of the diet
If we could approximate that pattern then having a physique like a gorilla might not matter.....”

Sasha woke up and replied to Ravensara:

“Ravensara - I was certainly not referring to intelligent design/creationist terms- my use of "designed" was entirely figurative. I'll admit my wording was sloppy (but it was 5am this end!), and also in Europe (or at least in my immediate... environment) the creationist-evolutionary debate is a non-issue, so apologies for any confusion.
You are correct that my point was in fact that I think the question is starting from a mistaken premise: clearly they functioned effectively, and even though they died out when they did, they were still highly successful for almost 200000 years. Homo Sapiens hasn't been around for as long as that, so we don't actually know whether our "design" (figuratively meant!) is any more effective than theirs, and since we left Nature behind centuries ago, perhaps we will never know.
Any number of factors could have contributed to the demise of the Neanderthals, though I think that brain capacity/evolution in contrast (and perhaps competition) with Cro Magnon man may well have been a major factor (abstract thought, innovation, complex reqasoning, etc). But I really don't see how we can talk about this as a pathological posture if this is the build that served them best in their natural environment. Many animals are paradoxical with notoriously inefficient systems of one type or another, yet somehow, they survive and continue to exist and function quite nicely.
Would he have had neck pain? Not if the whole skeletal and muscular setup is different to ours,so that even though the position of the head looks out of alignment in comparison to a modern human - perhaps what we consider "normal" would have been entirely unnatural to him. Skeletal studies necessary?”

“PS, as some of you know, I'm actually a bit of an interloper on this thread, since my area is not bodywork at all, but the Humanities.

Being Leon's daughter however, I've been weaned on a good number of these concepts (and it's his own faul...t for explaining what he did as he went along and being a great teacher to boot!) But given that I've gone off in a different direction, my use of language tends to be more figurative in nature.

Just explaining as I won't pretend to be able to get into the fine detail of anatomical issues, but as I have done quite a bit of reading into prehistoric culture fairly recently, that is why I have an objection to the assumption that this was anything other than a reasonably effective anatomical structure for this particular creature at this particular point in evolution - particularly as it's unlikely that this would have been why they died out.”

Ravensara returned to the fray:

No worries, Sasha--I quite understand the 5 AM thing, and I also live in England, where creationism isn't really an issue, although it's a huge problem in the States. And I have to confess that we biologists add to the confusion whenever we use "design", "purpose", or "body plan" as a shorthand. As convenient as it is, I really think it generates more confusion among non-biologists than it's worth.

From the way your argument was proceeding, it didn't sound like you were taking the creationist position overall, so the word was a little jarring. But you cleared up that confusion nicely.
My favourite example of your point is the use of the terms "obese" or "obesity" in reference to bears. Certainly, they (mostly) have higher BMIs than humans do--but is the term "obese" appropriate? To decide that, we would first have to decide whether "obese" means pathological or not, and how it relates to "normal", which is a whole other discussion right there.
Your overall point about applying human standards of health and illness to other species is well-taken, and can be the basis for some fascinating discussion.
Interloper? To the contrary, some of the best discussions are the interdisciplinary ones.

Leon's point is well-taken:
"If we could approximate that pattern then having a physique like a gorilla might not matter....."
Being young and having lots of physical reserves to draw upon, and maintaining that pattern as long as possible can compensate for a multitude of what would otherwise be problems. :)

Eric Beard was also worried about the accuracy of the picture:

“I too wonder about this accuracy of the artist's rendering. I also have enjoyed Sasha's comments. If this person were to walk in to me me today it would take some serious time and $ on his part to start to get "straightened out". I question what sort of permanent changes could even be made. His continued habits outside of the bodywork sessions would be entertaining to hear about. How did he get this way? Nature? Nurture? or both?”

Charles Smith was clearly pro these ancestors (of some of us)

“Has anyone here ever tried to work flint into anything? It is not such a simple task. A heightened sense of smell would have been a requirement. Just foraging and hunting to survive took far more intelligence than we know. This guys head forward posture screams cervical, neck and upper body issues. Hunting mastadons and other large game is both dangerous and physically demanding. All sorts of joint and alignment pain from stalking, exertion or hard blows in assaulting the beasts. They ate whatever they could find in a area between forested and tundra conditions. There is no reason to assume that they only ate meat but probably learned as much from animals as each other. I an animal can eat it and live (particularly small) then a human might also. Russian soldiers actually ate grass rather than give up when under siege as late as WWII. Food from sources not usually tapped often means survival.”

Ferguson John returned to less serious (for some) matters:

“The San Francisco 49er's need a new head coach. Maybe we will see more of this guy.”

Which was responded to by

Charles Smith:

“How about a line backer? Stocky and low to the ground just right for tripping up other linemen.”

"The They Died out Suddenly Theory is in question. A skeleton that had all of the characteristics was found that dates a few thousand years later than the commonly accepted die out date. Interbreeding is most likely the case. The Hittites of Eurasia were highly successful in their empire yet none of Hittite blood is present today as a separate race. Men meet, fight and interbreed as their mode of operation."

….end of day’s play…which reminds me, today England beat Australia in Melbourne (cricket) – actually gave them a lesson to remember.

HAPPY NEW YEAR

The Greatvine project - offering advice at a distance...and the problems of offering advice at a distance

2010-12-19T17:36:00.027+02:00

A couple of years ago I was contacted and asked to become an 'expert' on a new website project - Greatvine.com

The idea was simple but innovative.
Greatvine was recruiting a wide range of 'experts' in a plethora of areas of interest.
Each expert would have a dedicated page to which they could upload articles and information sheets, that could either be downloaded by visitors at no cost, or for a modest fee (determined by the expert).
There would also be a system whereby experts could be contacted by phone - (for a fee set by the expert, per minute) - at prearranged times.
The process had teething problems but these have now been overcome, and the site is operational, with hundreds of experts (areas range from health & wellbeing, to finance, parenting, writing and more, with thousands of articles available to download.

The site carries this particular notification about my presence on Greatvine:

Leon would be pleased to advise individuals on any questions involving osteopathy, naturopathic medicine, soft-tissue manipulation, complementary and alternative medicine, chronic pelvic pain disorders, fibromyalgia or chronic fatigue syndrome.

My contact details for Greatvine are: www.greatvine.com/leon-chaitow and my advice line number (UK only) is 0906 194 9628
This is only 'active' when I switch on my 'availability' button on the site, signifying that I can receive calls to its dedicated number that finds me anywhere in the world. It's easy to see whether I'm available to chat, as a thumbnail picture appears on the right of the home-page under a heading "Experts Available Now"
At present that 'available' button is not switched on much of the time, as I have a variety of writing and editing deadlines to meet.....but given a few spare hours, I will activate it to test out just how many people are interested in actually contacting me for advice ---- at a cost. ----- as distinct from the many who ask for advice for free.

Advice at a distance....?
When I placed the Greatvine information on my Facebook page, I almost instantly started receiving emails asking for health advice - something I actively discourage on my website - www.leonchaitow.com- as there is no way that meaningful, responsible, specific advice can be offered via that medium.
And even offering general advice, and referral information, requires a greater awareness of the individual's background than can be easily gleaned by email correspondence!

One such email, that arrived yesterday, detailed a truly heart-rending catalog of chronic health problems.
I am copying the non-personal sections of my response - see below - as it represents a summary of the philosophical approach I adopt when considering complex chronic health issues (whether at a distance, or in person) - and I hope it is of some interest:?

Thank you for your detailed summary of your history and current health problems One thing I've learned in trying to advise people with complex problems is to avoid trying to 'fix' anything. The way to best deal with complexity is through a lens that evaluates three possible intervention approaches - built on a foundational recognition that self-regulation/homeostasis is constantly operating, and that the most effective role of health intervention is to provide that inbuilt feature (self-regulation) with the best possible chance of manifesting, without creating additional adaptation demands.
An additional lens requires an appreciation of both inherited and acquired features within the orbits of the biochemical, biomechanical and psychosocial aspects of the individuals makeup.

The first way of trying to reduce complexity via simple initiatives, lies in establishing, as best possible, whether functional improvement can be achieved - possibly not in the most obvious or affected areas/system/tissues. For example in many cases, by focusing on breathing function (possibly, not certainly - as this is an example only).
Other broadly influential areas that always require consideration, and sometimes modification, are nutrition, sleep, posture, exercise and mento-emotional balance.

Functional improvement in all and any of these areas can permeate into improved clinical presentations, even though they may not immediately be recognisable as being part of the etiology.

Secondly, there is a need to focus on what obstacles there may be to enhanced function/symptom reduction, that might be modified or modulated. The idea of removal of obstacles to recovery/improvement, works on the principle that health issues represent failed or failing adaptation (based on Selye's General Adaptation Syndrome concepts) - which calls for attention to whatever adaptive demands can be minimised i.e. 'reduce the load'.

Thirdly, there is the strategy that aims at easing symptoms, without adding to the adaptive load.
This is in contrast to methods that:
a/ try to fix something and/or
b/ impose a new set of adaptive demands, that actually make matters worse
This highlights the fallacy of an 'ideal structural state' which some manual practitioners attempt to restore. There are probably as many people who have multiple structural anomalies (as compared to text-book ideals), and yet who have no symptoms whatever, as there are individuals who are text-book ideal - but with multiple symptoms.! Symptom relief is a reasonable approach, when the first and second objectives, listed above, are not achievable (i.e. enhance function and reduce the adaptive load), or are only marginally successful. Easing of symptoms, even though underlying features are unaltered, can contribute significantly to well-being.

So, with that philosophical (but I believe extremely practical) background, my particular advice for people seeking help for complex health conditions (where regular health-care fails) is to broaden perspectives in seeking help. - by paying attention to diet, exercise, sleep, breathing, stress management etc. It also pays to seek professional advice that evaluates the whole complex story, rather than small pieces of it.
Osteopathic and naturopathic (and TCM) practitioners tend towards looking at the big picture, rather than at the obvious.

My best wishes for 2011

The Vitamin D Scandal

2010-12-01T09:51:00.003+02:00

This post is almost entirely pasted from the latest newsletter from the Vitamin D Council

It is in response to frank distortions of the truth by a quasi-U.S. Governmental agency - the Food & Nutrition Board, acting on behalf of the Institute of Medicine.

Please read Dr John Cannell's words - and weep for the unborn millions who will suffer as a result of this failure to tell the truth.

Subscribe to the Newsletter by writing to: newsletter@vitamindcouncil.org

Today, the FNB has failed millions...

3:00 PM PST November 30, 2010

After 13 year of silence, the quasi governmental agency, the Institute of Medicine's (IOM) Food and Nutrition Board (FNB), today recommended that a three-pound premature infant take virtually the same amount of vitamin D as a 300 pound pregnant woman. While that 400 IU/day dose is close to adequate for infants, 600 IU/day in pregnant women will do nothing to help the three childhood epidemics most closely associated with gestational and early childhood vitamin D deficiencies: asthma, auto-immune disorders, and, as recently reported in the largest pediatric journal in the world, autism. Professor Bruce Hollis of the Medical University of South Carolina has shown pregnant and lactating women need at least 5,000 IU/day, not 600.

The FNB also reported that vitamin D toxicity might occur at an intake of 10,000 IU/day (250 micrograms/day), although they could produce no reproducible evidence that 10,000 IU/day has ever caused toxicity in humans and only one poorly conducted study indicating 20,000 IU/day may cause mild elevations in serum calcium, but not clinical toxicity.

Viewed with different measure, this FNB report recommends that an infant should take 10 micrograms/day (400 IU) and a pregnant woman 15 micrograms/day (600 IU). As a single, 30 minute dose of summer sunshine gives adults more than 10,000 IU (250 micrograms), the FNB is apparently also warning that natural vitamin D input - as occurred from the sun before the widespread use of sunscreen - is dangerous. That is, the FNB is implying that God does not know what she is doing.

Disturbingly, this FNB committee focused on bone health, just like they did 14 years ago. They ignored the thousands of studies from the last ten years that showed higher doses of vitamin D helps: heart health, brain health, breast health, prostate health, pancreatic health, muscle health, nerve health, eye health, immune health, colon health, liver health, mood health, skin health, and especially fetal health. Tens of millions of pregnant women and their breast-feeding infants are severely vitamin D deficient, resulting in a great increase in the medieval disease, rickets. The FNB report seems to reason that if so many pregnant women have low vitamin D blood levels then it must be OK because such low levels are so common. However, such circular logic simply represents the cave man existence (never exposed to the light of the sun) of most modern-day pregnant women.

Hence, if you want to optimize your vitamin D levels - not just optimize the bone effect - supplementing is crucial. But it is almost impossible to significantly raise your vitamin D levels when supplementing at only 600 IU/day (15 micrograms). Pregnant women taking 400 IU/day have the same blood levels as pregnant women not taking vitamin D; that is, 400 IU is a meaninglessly small dose for pregnant women. Even taking 2,000 IU/day of vitamin D will only increase the vitamin D levels of most pregnant women by about 10 points, depending mainly on their weight. Professor Bruce Hollis has shown that 2,000 IU/day does not raise vitamin D to healthy or natural levels in either pregnant or lactating women. Therefore supplementing with higher amounts - like 5000 IU/day - is crucial for those women who want their fetus to enjoy optimal vitamin D levels, and the future health benefits that go along with it.

For example, taking only two of the hundreds of recently published studies: Professor Urashima and colleagues in Japan, gave 1,200 IU/day of vitamin D3 for six months to Japanese 10-year-olds in a randomized controlled trial. They found vitamin D dramatically reduced the incidence of influenza A as well as the episodes of asthma attacks in the treated kids while the placebo group was not so fortunate. If Dr. Urashima had followed the newest FNB recommendations, it is unlikely that 400 IU/day treatment arm would have done much of anything and some of the treated young teenagers may have come to serious harm without the vitamin D. Likewise, a randomized controlled prevention trial of adults by Professor Joan Lappe and colleagues at Creighton University, which showed dramatic improvements in the health of internal organs, used more than twice the FNB's new adult recommendations.

Finally, the FNB committee consulted with 14 vitamin D experts and – after reading these 14 different reports – the FNB decided to suppress their reports. Many of these 14 consultants are either famous vitamin D researchers, like Professor Robert Heaney at Creighton or, as in the case of Professor Walter Willett at Harvard, the single best-known nutritionist in the world. So, the FNB will not tell us what Professors Heaney and Willett thought of their new report? Why not?

Today, the Vitamin D Council directed our attorney to file a federal Freedom of Information (FOI) request to the IOM's FNB for the release of these 14 reports.

Most of my friends, hundreds of patients, and thousands of readers of the Vitamin D Council newsletter (not to mention myself), have been taking 5,000 IU/day for up to eight years. Not only have they reported no significant side-effects, indeed, they have reported greatly improved health in multiple organ systems. My advice, especially for pregnant women: continue taking 5,000 IU/day until your 25(OH)D is between 50-80 ng/mL (the vitamin D blood levels obtained by humans who live and work in the sun and the mid-point of the current reference ranges at all American laboratories). Gestational vitamin D deficiency is not only associated with rickets, but a significantly increased risk of neonatal pneumonia, a doubled risk for preeclampsia, a tripled risk for gestational diabetes, and a quadrupled risk for primary cesarean section.

Today, the FNB has failed millions of pregnant women whose as yet unborn babies will pay the price. Let us hope the FNB will comply with the spirit of "transparency" by quickly responding to our Freedom of Information request

John Cannell, MD
The Vitamin D Council

..a brief preliminary report on the 7th World Low Back and Pelvic Pain Congress

2010-11-13T17:48:00.008+02:00

Moshe and Siegfried sorting out pain and other problems

Myself, examining Gary Cooper's hand-prints.....

This is preliminary -
It is not definitive -
I am teaching (Positional Release Techniques) all day today, in a post-congress workshop, and then fly back to the UK, then Greece...at which time, when duly recovered, I'll add more to this brief post.
4 days of lectures and 4 days and evenings of networking, is exhausting - even in the totally artifical sumptuous surroundings of Beverly Hills/Hollywood at its glitziest.
My first impressions:

a consensus seems to be emerging that static assessment is relatively unimportant (positional structural relationships for example) - whereas movement patterns and functional features are where attention should be placed (motor control, cognitive and behavioural features)

A tension has emerged between those who believe that passive treatment should be minimised and - some suggest - be virtually phased out, with most therapeutic effort being towards the broad theme of enhanced motor control, via well designed exercise and movement patterns, alongside cognitive behaviour approaches..
This view is in contrast to those who argue that these objectives can better be achieved if biomechanical/postural eatures are modulated/improved/corrected before the more functional approach....removing obstacles to rehabilitation, creating windows of opportunity for enhanced function.

Mountains of evidence emerged on both sides...I don't think either camp convinced the other
....to be continued.....

The real highlight for me was real-time ultrasound imaging (video evidence) of fascial planes (lumbodorsal fascia) sliding and gliding on each other during normal movement (flexion and extension) in asymptomatic individuals, and how the slide/glide is inhibited/"stuck" in individuals with (in this instance) back pain.
Helen Langevin PhD once more excelled in guiding us towards a better understanding of the reality of human function

Another bonus was a video of fascial motion and behaviour, in the body, taken with mini-cameras inserted during surgery (with patient permission). The film was made by Dr Guimberteau - a plastic surgeon who works on hand reconstruction. This is his 3rd and best movie (Journey under the skin to the muscles, lumbar fasciae and structural architectures)
I admit to having tears running down my cheeks during this, marveling at the sheer beauty of strands of fascia - identical to a spider's web with dew drops glistening and shining as strands detached, moved and reattached in milliseconds, in response to movement.

Unless and until you have seen/or appreciated, the amazing degree of free fascial movement in living human tissue you have actually very little idea of how the body actually works. These fascial planes can get "stuck" and dense as a result of trauma/overuse/inflammation gone wrong/age etc and that corresponds with palpable "densification", pain and limitation of movement.
It appears that much of the work that practitioners do, achieves its results via restoring slide/glide potential to these superficial layers of densely innervated (mechanoreceptors, nociceptors etc) loose connective tissue - whether we are aware of it or not.

Also imaged (presentation by Jay Shah of NIH) were myofascial trigger points - shown as dark masses in colour-coded images, using elastography

High points of some otherwise dull (even if pertinent) presentations, included:
The avuncular presentation by ligament genius Moshe Solomonow (see picture)
The recent research findings of legendary German researcher into pain Siegfried Mense (see picture of him and Moshe), as well as that by Robert Schleip who is rapidly emerging as a superstar in the fascia fermament.
Yesterday a passionate Craig Liebenson DC launched into a detailed blast at misconceptions and 'Holy Cows' in the field of rehabilitation. His passion and detailed analysis was refreshing....I hope he will write this up for JBMT in due course!

I was one of 3 British DOs there - out of 650 delegates - Phil Beach (parallel session presentation) , Matt Wallden (poster presentation) and myself (keynote)..

The next of these jamborees is in Dubai in 2013