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How to identify the most common cause of Movement Dysfunction

The most common and major cause of movement dysfunction is joint immobilisation accompanied by length-associated changes in tissues

The most common and major cause of movement dysfunction

The most common and major cause of movement dysfunction is joint immobilisation accompanied by length-associated changes in tissues (Grossman et al., 1982; Janda, 1993).  When a joint becomes immobilized, initially there are two categories of muscle state; hypertonia: an excited, overactive and dominant muscle; and hypotonia: weak, inhibited, under-active with reduced feed-forwards capacity. Note the ‘initial’ emphasis in the previous sentence – the ‘effect’ of an injury commonly has phases i.e. phase 1, acute, generally days 1 to 3, phase 2, acute, days 4 through to 3 weeks and so on.

Over the past four decades length-associated change observed in muscle tissue, seen when a joint is immobilised, has been categorized in to two symptomatic states; ‘stretch-weakened’ and ‘adaptive shortened’ (Kendall, McCreary, Provance, Rodgers & Romani, 2005). These two conditions of length-associated change, have an immediate negative influence on the physiological, anatomical, biochemical (Grossman et al., 1982), mechanical and methodological (Smidt & Rogers, 1982) neuromusculoskeletal system – in previous Blogs I have termed this the biological tissues ‘capacity’.

Case Study – Strongman

Right-sided sciatica.


  1. NHS Physiotherapist diagnosed: Under-active glutes (no reason for this given).
  2. MRI diagnosed: Worn discs (unable to remember which ones)

Now read the following, and we’ll come back to this….

Stretch Weakened

Stretch-weakened (SW) is a description of a muscle that has maintained rest in an elongated position, but not beyond normal range (Kendall et al., 2005) and within 24 hours of joint immobilization (Tardieu, Tarbary and Tardieu, 1981) the physiology of the tissue begins to negatively change (Crawford, 1973; Williams & Goldspink, 1978; Goldspink & Williams, 1979; Tardieu et al., 1981; Grossman et al., 1982). Although these changes cause weakness, it has been reported the muscle may test stronger at its new extreme length and weaker in a standard muscle test (Janda, 1993; Kendall et al., 2005). Tardieu et al., (1981). Observed 35% of peak active tension has been observed where the muscle has been immobilised.

Clinical findings

You may find the muscle feels stiff, long, weak, with poor tone.

Adaptive Shortened

Adaptive-shortened (AS) muscle also begins to negatively adapt its physiology due to the joint immobility. Within 24 hours catabolism begins (Holloszy, Booth, Winder & Fitts, 1973; Sohar, Takacs & Guba, 1977) causing breakdown of proteins (Sohar et al., 1977), and inhibiting ‘Sherrington’s Law’ (Janda, 1993). Tardieu et al. (1981) observed a 40% earlier peak force (see Figure 1), with 35% deinnervation within four weeks of joint immobilization, and elasticity is reduced within 48 hours as remodeling of the endomysium and perimysium becomes thicker and more fibrotic (Williams & Goldspink, 1973; Tardieu et al., 1981). Although the majority of muscle biochemistry, anatomy and physiology has been explored on animals, observations remain consistently compatible to the pathomechanical changes within humans (Grossman et al., 1982). Emperical observations strongly imply such modifications do occur and play a considerable role in the ability of an individual to properly utilize the stretch-shorten cycle of muscle contraction (Ettema, 1996; Benn et al., 1998). Muscle activation is an important factor in the control of muscle forces and thus the control of active human body movements (Ettema, 1996; Colby et al, 2000).

Clinical findings

Are likely to be reported as painful by the patient/client, painful to palpate, high tone, albeit weak, short, and tight.

The effects are catastrophic

It is important to consider the long-term effect this biomechanical dysfunction may have on the individual and future research. For the individual, research suggests, this biomechanical dysfunction is not necessarily ‘felt’ and tends to be a secondary issue later on, i.e. overtime it the tissue physiology changes.  An inability to voluntary contract a muscle also exposes tissues to accelerated degeneration and may lead to long-term disability (Goldspink and Williams, 1978; Kennedy et al., 1982; Ellison, Rose & Sahrmann, 1990; Janda, 1993; Hurley, Jones & Newham, 1994).

Case Study – Strongman

Right-sided sciatica.

Event that provoked Sciatica: Strongman competition believes it was a loose yoke.


  1. NHS Physiotherapist diagnosed: Under-active glutes (no reason for this given).
  2. MRI diagnosed: Worn discs (unable to remember which ones)

So, having read all previous 8 Blogs on this subject: you are ‘top-of-the-class’ with the anatomical relationship between deep hip external rotators and the sciatic nerve.  So, what may you begin to think is causing this gentleman’s sciatica?  No answer is a silly answer! You will have 100% of my attention for participating.  What length-associated (physiological) change ‘may’ have occurred to the hip external rotators and/or stabilisers? Look at the event that caused the onset of the pain. Obviously without a hands-on assessment and conversation with this individual we are purely bouncing theories in the air – but lets not forget… all EBM starts with a theory!

Where to intervene?

  1. When observing a person who is demonstrating asymmetrical deficit in a movement task (strength, power or stability) maybe we should be exploring if these length-associated changes in muscles are the mechanism that underpins the asymmetry.  If length-associated change in the tissues was the case, trying to make the ‘asymmetrical muscle’ work harder (appropriate load regards to repetitions, sets, time) would cause more risk to the individual as they ‘attempt’ to give you what you need.  Remember what the EBM has found: the muscle is not the cause of length-associated change, the joint dysfunction is the cause.  Find out why the joint is causing length-associated changes in the muscle tissue – that’s where you intervene. Correcting the deficit driving the length-associated changes and you reduce the risk for the individual.


  • Looking at the ‘tasks’ we use in research like; quiet standing, sitting, gait etc, to understand if things are optimal or are individual traits.
  • The things we have been taught to look at and notice that suggest someone can’t do a specific task.
  • Relative Risk and Dose Exposure – it’s importance for the Patient/Client
  • Why these factors are important, and why they are the first thing we need to understand to fully understand injuries and how to treat them.
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