NOTE: For reasons of copyright I cannot publish the figures/images that illustrate this posting – so instead am offering a glimpse of our Corfu garden….. and – to satify his many fans – a recent snap of Dumbo, our highly intelligent, loveable, stubborn, miniature long-haired dachshund

aster has passed, and an intense period of writing and editing is giving way to a brief interlude of travel and teaching.

Among the joys of the past 6 weeks in Corfu – over and above the pleasure of being in a wonderful environment, loaded with flowers, birds and tranquility (in contrast to the economic and personal tragedies afflicting much of Greece and its people) – has been the gradual coming together of a book on chronic pelvic pain – coedited by myself and Ruth Lovegrove PhD.

Our team of brilliant contributors have been providing a steady stream of chapters for editing and collating, while we worked on our own sections.

One of the chapters I have been most involved with (in collaboration with Chris Gilbert PhD) has been one focused on the links between the pelvic floor and the diaphragm – and the functional and dysfunctional two way-traffic of adaptive influences between them.

The material in this post is a small part of that chapter – still “work in progress”, but of possible value for anyone interested in the pelvis and its problems.

There is accumulating evidence for clinical focus on key muscular and fascial structures with the potential to influence pelvic pain and dysfunction.

As Lee, Lee & McLaughlin (2008) have noted : “The abdominal canister is a functional and anatomical construct that synergistically work together [involving] the diaphragm including its crura, and by extension the psoas muscle, whose fascia intimately blends with that of the pelvic floor and the obturator internus muscle, the deep abdominal wall including transversus abdominis, and its associated fascial connections, anteriorly and posteriorly, the deep fibres of multifidus, the intercostals, the thoracolumbar vertebral column (T6-12 and associated ribs, L1–L5) and osseous components of the pelvic girdle (innominates, sacrum and femora).”

The pelvic floor and the respiratory diaphragm are seen to be structurally and functionally bound together by fascial and muscular connections, and just as dysfunctional breathing patterns influence pelvic function, so the reverse is true. Rehabilitation of the functions of the thorax, pelvic girdle, and pelvic floor may be enhanced by more normal physiological breathing patterns, while enhancing these patterns will be aided by pelvic functionality, whether achieved through exercise, breathing retraining, postural reeducation, manual therapy, or other means. (McLaughlin 2009, Chaitow 2007)

Within the patterns of overuse and misuse that characterise chronic and acute insults to the body in general, and the low back and pelvic regions in particular, the evolution of myofascial trigger points is a common feature within a background of hypertonicity, induration and fibrosis. (Travell & Simons 1999, Anderson 2009, Key 2008, Fitzpatrick 2009).

In this same context Anderson et al 2009, Prather (2009,) Cox (2005), Lewit (1999), Janda et al (2007), Fitzgerald (2009), and many others, have implicated dysfunction involving: psoas, iliacus, quadratus lumborum, piriformis, the hip adductors, rectus abdominis, abdominal obliques, scalenes and intercostals.

Focus on these and other adaptive soft tissue, (and inevitably joint) changes, without due regard to etiological features, would offer short-term benefit at most. However it is suggested that postural or other functional rehabilitation, without attention to such changes would offer equally short-term results. (Chaitow et al 2002, Fitzpatrick 2009)

Bialowsky (2009) reports that the effects of soft-tissue-focussed manual therapies includes:

  • Changes of blood levels of b-endorphin serotonin (Degenhardt et al., 2007)
  • Endogenous cannabinoids (McPartland et al., 2005)
  • Improved circulation and drainage
  • Decreased muscle spasm
  • Relaxation
  • Re-alignment of soft tissues
  • Breaking of adhesions
  • Increased range of motion
  • Removal of cellular exudates

In this brief overview of a selection of currently utilised manual therapy approaches that address fascial and myofascial dysfunction, it is taken for granted that there would be simultaneous or subsequent focus on etiological features. The modalities summarised below should not be regarded as definitive, as there are many other variations. However those selected for discussion represent a variety of validated biomechanical approaches, some of them novel and others well-established.

The seven soft-tissue modalities under discussion include:

  • Connective tissue manipulation
  • Fascial Manipulation
  • Muscle Energy Technique
  • Myofascial Induction (or release)
  • Scar Tissue Release
  • StrainCounterstrain
  • Trigger Point Deactivation methods

Connective Tissue Manipulation (CTM)

CTM, as practised in relation to chronic pelvic pain, is a variation on the work of Dicke (1953) and Ebner (1975). Known in Germany where it was developed, as Bindegewebsmassage, it involves direct manual strokes, or forms of vigorous skin rolling, focused on connective tissue. Connective tissue restrictions are thought to emerge from a background of one or other of the following influences:

  • Viscero-Cutaneous Reflex influences
  • In tissues superficial to areas of joint dysfunction
  • In dermatomes of inflamed peripheral nerves
  • In tissues superficial to muscles housing myofascial trigger points

CTM treatment sessions have a number of short and long-term objectives (Prendergast and Rummer 2009):

  • Connective tissue is treated/mobilized until there is: improvement in mobility; decrease in sensitivity; increase in warmth.
  • Goals include: improved circulation, improved tissue integrity; decreased ischemia; reduced nocigenic chemicals in restricted connective tissue; decrease or elimination of visceral pain or dysfunction – possibly involving reflex effects; decrease in adverse neural tension on peripheral nerve branches

Recent CTM study

In 2009, the Urological Pelvic Pain Collaborative Research Network (UPPCRN) concluded that somatic abnormalities, including myofascial trigger points and connective tissue restrictions, were common in women and men with Chronic Pelvic Pain syndrome (CPP). (Fitzgerald et al 2009).

UPPCRN published the outcomes of a feasibility trial comparing connective tissue manipulation (CTM) and myofascial physical therapy, versus global therapeutic massage in patients with CPP. The group receiving skilled CTM and myofascial therapy had a significantly higher response rate than the group receiving massage (Fitzgerald et al 2009).

Muscle Energy Techniques

Muscle energy technique have been defined as “a form of osteopathic manipulative diagnosis and treatment in which the patient’s muscles are actively used on request, from a precisely controlled position, in a specific direction, and against a distinctly executed physician counterforce” (Educational Council on Osteopathic Principles 2009).

Various studies have demonstrated that muscle energy techniques increase muscle extensibility (Ballantyne et al 2003) and range of motion (Burns & Wells 2006) including thoracic rotation (Lenehan et al 2003).

MET and acute LBP Pilot Study (Wilson et al 2003)

16 subjects (8 male, 8 female; ages 19-44) with low back pain (duration 2-9 weeks) were randomized: 1. Control group (n=8) 2. Experimental group (n=8).

Each group received identical supervised re-education and strengthening exercises with the experimental group receiving MET 2 x weekly for 4 weeks = total of 8 visits. There was a statistically significant difference (p

Fascial Manipulation® (FM)

The key premise of FM is that fascia presents a specific organization and relationship with the underlying muscles. In particular, the fascia is seen as:

  • coordinating element for motor units (grouped together in myofascial units)
  • uniting element between unidirectional myofascial units (myofascial sequences) connecting element between body joints via myofascial expansions and retinacula (myofascial spirals).

This model is supported by in-depth studies of fascial anatomy and physiology. Numerous dissections of unembalmed human cadavers have evidenced:

  • muscular fibre insertions directly onto deep fascia (Stecco et al 2007),
  • fibre distribution according to precise motor directions (Stecco et al, 2008 2009),
  • myotendinous expansions that link adjacent segments (Stecco et al 2009).

Extensive histological analysis of deep muscular fascia has also provided evidence for hypotheses concerning fascia’s role in proprioception and tensional force distribution within the fascial system (Stecco et al 2006, 2007).


The aim of a study was to evaluate the time required to modify a palpatory sensation of fibrosis of the fascia in correlation with changes in levels of patient discomfort, in 40 subjects with low back pain utilizing the FM technique. the mean time to halve the pain was 3.24 min; however, in those subjects with symptoms present for less than 3 months (sub-acute) the mean time was less (2.58 min) compared to the chronic patients (3.29 min).

Three small areas over the thoracolumbar fascia that, according to Fascial Manipulation® theory (Stecco and Stecco, 2009), are primarily involved in LBP mechanisms were selected for treatment:

  1. At the level of the first lumbar vertebra, approximately 3 cm lateral to the spinous process of L1 – for the paravertebral muscles.
  2. At the level of the third lumbar vertebra, approximately 5 cm lateral to the spinous process of L3 – for quadratus lomborum.
  3. Immediately below the twelfth rib for latissimus dorsi, posterior inferior serrati and external oblique muscles.

The therapists noted a marked increase in tissue mobility, more or less at the same time the patients perceived a reduction in pain.

The researchers suggest that pain reduction and increase in sliding of the tissue layers, coincides with transformation of the ground substance from its densified state (gel) to fluid (sol) state. (Pedrelli et al 2009, Day et al 2009)

Myofascial Release (MFR) – or – Myofascial Induction

King (2010) notes that myofascial release (MFR) is “a system of diagnosis and treatment first described by AT Still, and his early students, which involves continual palpatory feedback to achieve release of myofascial tissues.”

  • Direct MFR – a myofascial tissue restrictive barrier is engaged for the myofascial tissues and the tissue is loaded with constant force, until tissue release occurs. •
  • Indirect MFR – the dysfunctional tissues are guided along the path of least resistance, until free movement is achieved (Educational Council on Osteopathic Principles 2009).

Myofascial Induction is a simultaneous evaluation and treatment process using tri-dimensional movements of sustained pressures, applied to myofascial structures in order to release restrictions.

The term Induction is preferred to ‘release’ because clinicians do not passively stretch the system, but only apply an initial tension or compression force and follow the facilitating movement.

The aim of the process is the recovery of motion amplitude, force and coordination (Pilat 2009)

Meltzer et al (2009) have demonstrated positive structural and functional changes resulting from simulated MFR (60 seconds) applied to repetitively stressed tissues (8 hours), including reduction in inflammatory products.


Weiss (2001) used myofascial release in patients with CPP and found that 70% had marked or moderate improvement in symptoms after treatment. He found that pelvic floor therapy decreased neurogenic triggers, decreased central nervous system sensitivity, and alleviated pain.

Scar Tissue Release

Kobesova et al (2007) suggest that scars may develop adhesive properties that compromise tissue tensioning, altering proprioceptive input, behaving in much the same way as active myofascial trigger points.

It is suggested that faulty afferent input can result in disturbed efferent output leading to – for example – protective postural patterns, increased neurovascular activity, and pain syndromes.

The term active scar is designated to describe the ongoing additional neural activity associated with adhesive scar formations.

Lewit & Olsanska (2004) reported a series of 51 such cases in which postsurgical scar tissue was found to be the primary pain generator for a multitude of locomotor system pain syndromes. On palpation (light stretching) of dysfunctional tissues the patient commonly reports sensations of “burning, prickling, or lightning-like jabs of pain”.

Valouchova & Lewit (2009) report that active scars in the abdomen and pelvis commonly restrict back flexion, which the patient feels as low back pain. Treatment methods are simple, involving ‘mini-myofascial release’ methods – where skin alongside scars is treated initially, with subsequent attention to deeper layers. Treatment involves “engaging the pathologic barrier and waiting; after a short delay, a release gradually occurs until the normal barrier is restored”

StrainCounterstrain (SCS)

SCS is an osteopathic system of diagnosis and indirect treatment, in which the patient’s somatic dysfunction is treated, using passive positioning, resulting in spontaneous tissue release. (Educational Council on Osteopathic Principles 2009). SCS technique involves shortening myofascial structures to reduce the nociceptive experience arising from firm palpation of a tenderpoint in the dysfunctional tissues.


  1. “A convenience sample included 49 volunteers (15 men, 34 women; 98 limbs), aged 19-38 years, with hip weakness and corresponding TPs [local areas of tenderness]……[after 4 treatments over 2 weeks] ……all groups reported reduced pain and increased strength 2-4 weeks after intervention (p<.001 the results supported hypothesis that scs reduces pain and demonstrated positively affects strength> (Speicher et al 2004).
  2. Standley et al (2008) have described the beneficial effects on fibroblast morphology and actin stress fiber architecture of tissue samples where simulated counterstrain (60 seconds) was applied to samples that had been repetitively strained for 8 hours. Trigger point deactivation (Cox 2005, Travell & Simons1999)

Montenegro et al (2009) insist that myofascial pain syndrome should always be considered as part of the differential diagnosis of chronic pelvic pain.

Systematic reviews have investigated the effectiveness of soft tissue manual intervention for inactivating trigger points (TrPs) (Fernández-de-las-Peñas et al 2005, Rickards 2006, Vernon & Schneider 2009).

Anderson et al (2009) have identified the most common location of TrPs related to pelvic pain:

  • Pubococcygeus (90%)
  • External oblique (80%)
  • Rectus abdominis (75%)
  • Hip adductors (19%)
  • Gluteus medius (18%).
  • Other relevant muscles in which TrPs have been identified that also contribute to pelvic pain are levator ani, iliopsoas, quadratus lumborum, gluteus maximus and thoraco-lumbar extensor muscle (Travell & SImons 1999, FitzGerald & Kotarinos 2003, Chaitow 2007, Montenegro et al 2008; Anderson et al 2009, Fitzgerald 2009)

Travell & Simons described (1999) variations on their basic trigger point release approach:

  1. Ischemic compression : pressure is applied to the point lying in a fully lengthened muscle. The pressure should be sufficient to maintain pain at a level of between 5 and 7 – where 10 is the maximum that can be tolerated, until pain eases by around 50-75% – or for 90 seconds
  2. Trigger point Release : In this version the muscle is partially lengthened and pressure is to the first perception of a tissue barrier, ideally with no sign of discomfort. Pressure is maintained until a sense of a release of the characteristic taut band is noted, or for 90 seconds
  3. Other versions exist including pulsed ischemic compression (Chaitow 1994) in which a trigger point in a partially lengthened muscles received 5 seconds of compression, sufficient to induce pain at level 7 (numerical pain rating scale) – followed by 2 seconds of no pressure – repeated for 90 seconds or until local or referred pain changes are reported or palpated

In these, and all other variants, Travell & Simons (1999) considered it essential to stretch the muscle housing the trigger point towards, or to, its’ normal resting length, subsequent to pressure deactivation.


In a study to assess the value of combined connective tissue manipulation (CTM) and trigger point deactivation, in cases of urologic chronic pelvic pain, Fitzgerald et al (2009) report:

“Patients randomized to the treatment group underwent connective tissue manipulation to all body wall tissues of the abdominal wall, back, buttocks and thighs that clinically were found to contain connective tissue abnormalities and/or painful myofascial trigger points. CTM was applied bilaterally to the patient in the prone position, posteriorly from inferior thoracic level 10 to the popliteal crease. This was done until a texture change was noted in the treated tissue layer. Manual techniques such as trigger point barrier release, with or without active contraction or reciprocal inhibition, manual stretching of the trigger point region, and myofascial release, were used on the identified trigger points”

With such evidence it is not surprising that the European Association of Urology has published guidelines suggesting that TrPs should be considered in the diagnosis of CPP (Fall 2010)


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