These illustrations show variations on the theme of ‘crossed syndromes’ where
muscle groups alternately short/tighten, or are inhibited/lengthen, with
negative effects on functionality
The central figure above shows a lower crossed syndrome with weak abdominals and gluteals, as well as short tight hip flexors and erector spinae

On the left, this individual has:
Short tight : pectorals, upper trapezius, neck extensors
Inhibited/lengthened/weak : deep neck flexors, lower shoulder stabilisers

The figures below illustrate variations on
lower crossed syndromes….neither of these are
likely to have normal respiratory or pelvic

For the past 3 months I have been immersed in putting together a team of writers, in order to compile a book on the physical medicine approaches to management of chronic pelvic pain – CPP (for Elsevier).
These efforts are now virtually complete, with 20 superb researchers, practitioners, therapists now assembled
They will be collaborating on this project over the next year or so – after which my co-editor and I will have several months to stitch the 20 chapters (some of which we will write ourselves) together, with bridging sections to hopefully create a coherent story.

As I reflect on the multiple influences that can result in CPP, a theme keeps repeating itself – that these particular (and indeed almost all) health problems, can be seen to be the result of processes of failed adaptation – of ‘decompensation’ – the result of repetitive adaptive loads, involving biochemical, biomechanical or psychosocial (or combination of these) stressors, interacting with the unique cocktail of acquired and inherited characteristics of the person involved.

That model leads logically to the conclusion that ‘treatment’ should firstly not add to the adaptive melt-down, and should not just mask the symptoms, but should ideally be directed at reducing the stressor load, and enhancing the normal self-regulating functions of the individual.
biomechanics (posture and the way we use, abuse and overuse the structures of the body) are concerned, my mind turns to some great observers of the human condition.
For example:

The first comprehensive discussion, that I was aware of, as to how biomechanical alignment – posture – influences visceral function, was by the orthopedic surgeon Joel E. Goldthwait (and colleagues), in the book Essentials of Body Mechanics in Health & Disease (1945).

The concepts described by Goldthwait are still extremely relevant today….see the illustrative figures above (taken from an insightful paper written by Australian physiotheapist Josphine Key, and her associates, and published in The Journal of Bodywork & Movement Therapies in 2007)

According to Goldthwait, they demonstrate the normal progression as tissues adapt to postural imbalance, with the influences of aging and gravity adding to the picture:
The main factors which determine the maintenance of the abdominal viscera in position are the diaphragm and the abdominal muscles, both of which are relaxed and cease to support in faulty posture. The disturbances of circulation resulting from a low diaphragm and ptosis may give rise to chronic passive congestion in one or all of the organs of the abdomen and pelvis, since the local as well as general venous drainage may be impeded by the failure of the diaphragmatic pump to do its full work in the drooped body.
Furthermore, the drag of these congested organs on their nerve supply, as well as the pressure on the sympathetic ganglia and plexuses, probably causes many irregularities in their function, varying from partial paralysis to overstimulation. All these organs receive fibers from both the vagus and sympathetic systems, either one of which may be disturbed. It is probable that one or all of these factors are active at various times in both the stocky and the slender anatomic types, and are responsible for many functional digestive disturbances. These disturbances, if continued long enough, may lead to diseases later in life. Faulty body mechanics in early life, then, becomes a vital factor in the production of the vicious cycle of chronic diseases and presents a chief point of attack in its prevention . . . In this upright position, as one becomes older, the tendency is for the abdomen to relax and sag more and more, allowing a ptosic condition of the abdominal and pelvic organs unless the supporting lower abdominal muscles are taught to contract properly. As the abdomen relaxes, there is a great tendency towards a drooped chest, with narrow rib angle, forward shoulders, prominent shoulder blades, a forward position of the head, and probably pronated feet. When the human machine is out of balance, physiological function cannot be perfect; muscles and ligaments are in an abnormal state of tension and strain. A well-poised body means a machine working perfectly, with the least amount of muscular effort, and therefore better health and strength for daily life.”

Some 70 years later Schamberger’s malalignment model (2002) has offered important messages for consideration, as he follows Goldthwait and takes the discussion of postural imbalance beyond the biomechanical towards body-wide adaptational influences. He describes some of the inevitable changes that are associated with common asymmetries, as follows.
“Malalignment of the pelvis, spine and extremities remains one of the frontiers of medicine . . . the associated biomechanical changes – especially the shift in weight-bearing and asymmetries of muscle tension, strength, joint ranges of motion – affect soft tissues, joints and organ systems throughout the body and therefore have implications for general practice and most medical sub-speciality areas.”

Schamberger offers examples of visceral problems emerging from malalignment of the pelvis, resulting in pelvic floor dysfunction:
“Typical visceral problems that have been attributed to pelvic floor dysfunction include:

  • Incontinence of bowel and bladder attributed to a lax floor
  • Constipation and incomplete voiding with excessive tension
  • Dysmenorrhoea, dyspareunia, impotence and sexual dysfunction
  • Recurrent cystitis and urinary tract infection.”

In more recent years Vladimir Janda developed his extremely useful overview of the adaptations that evolve when posture and use patterns are less than optimal, in his ‘crossed syndrome’ model (see figures at the start of the posting).
Over time, adaptational changes, as listed by Goldthwait, Schamberger and Janda, may progress from the production of dysfunction (e.g. low back pain) to the development of actual pathological changes.

For example Gofton & Trueman (1971) found a strong association between leg length and unilateral osteoarthritis on the side of the anatomically long leg.
They noted that all subjects with this type of OA ‘had led healthy active lives prior to the onset of hip pain’, and few subjects were aware of any difference in leg length.

They also point out that this form of OA has its onset around the age of 53, but acknowledge that many people with precisely this anatomic asymmetry failed to develop an arthritic hip, suggesting that factors other than the leg length disparity are also important.

This underscores the importance of the context in which this mechanical adaptation was being processed by the tissues under stress – with some joints becoming arthritic and others not.
What were the other variables? Nutritional? Genetic? Gender? Weight? Occupation? Other . . . ?

Holistic perspectives require evaluation of the obvious anatomic and biomechanical, as well as identifiable contextual (e.g. environmental, psychological, nutritional, etc.) etiological features.

Gofton J, Trueman G 1971 Studies in osteoarthritis of the hip: Part II. Osteoarthritis of the hip and leg-length disparity. CMA Journal 104:791–799
Goldthwait J et al 1945 Essentials of body mechanics in health and disease. Lippincott, Philadelphia
Janda V 1986 Muscle weakness and inhibition (pseudoparesis) in back pain syndromes. In : Grieve G (ed) Modern Manual Therapy of the Vertebral Column. Churchill Livingstone, Edinburgh

Schamberger W 2002 The malalignment syndrome. Churchill Livingstone, Edinburgh, p 238–239