Originally published in Massage Today
November, 2011, Vol. 11, Issue 11
A prospective patient arrives with a problem for you to manage – say a backache (a not uncommon scenario!). Where do you begin? I would suggest you begin by viewing the problem through a broad lens.
The tissues of your (and your patient’s) body respond to applied demands (stressors) deriving from backgrounds of overuse, misuse, abuse (trauma) and disuse, overlaid onto a combination of developmental and maturational experiences of life – the inherited and acquired habits and patterns of use (for example postural or respiratory), ergonomic, work and leisure stresses, as well as the results of injuries, surgeries, emotional burdens and more.
These features and experiences will have blended to create tissues that may gradually have changed from a state of normotonicity to a palpably dysfunctional state, at times involving hypertonicity, and at others hypotonicity, along with altered firing sequences, modified motor control, abnormal postural and/or movement patterns and ultimately dysfunctional chain reactions. What emerges is a picture of impaired or altered function of related components of the somatic framework; skeletal, arthrodial, myofascial, as well as related vascular, lymphatic and neural features, all examples of adaptational overload.
But to the patient, it is simply “a backache.” Such changes almost always demonstrate functional, sometimes visible, often palpable, evidence, that can frequently be assessed in order to guide you towards clinical decision-making, as to what form of management may be most appropriate. What therapeutic and rehabilitation strategies, in the context of acute and chronic somatic dysfunction, may be able to assist in normalization of dysfunction, pain management and rehabilitation? Parsons & Marcer (2005) note that “it is through the summation of both quantitative and qualitative findings that one obtains an indication of the nature and age of the underlying dysfunction”
Repetitive Lumbar Injury: An Example of Adaptation Overload
In discussing a form of low back pain that they describe as Repetitive Lumbar Injury (RLI), Solomonow, et al (2011a), outline the etiology of a complex multi-factorial syndrome that fits the model of adaptive overload. This involves an adaptation sequence, in which prolonged cyclic loading of the low back can be shown to induce a process of creep – defined as continued deformation of a viscoelastic material under constant load over time – in the spinal tissues (Sanchez-Zuriaga 2010), reduced muscular activity, triggering spasms and reduced stability, followed by acute inflammation and tissue degradation (Fung et al 2009), as well as muscular hyperexcitability and hyperstability (Li et al 2007).
These adaptive changes are seen – in animal studies (Solomonow 2011b) and in humans (Solomonow 2003) – to be a response to rapid movement, high loads, numerous repetitions and short rest periods. Behaviours that are not uncommon in many common work and leisure/athletic activities. The conclusion is that viscoelastic tissues ultimately fail via a process involving the triggering of inflammation, due to overuse, a process that appears to initiate the mechanical and neuromuscular characteristic symptoms of the disorder.
In contrast, Solomonow, et al (2011a), found that low magnitude loads, short loading durations, lengthy rest periods, low movement velocity and few repetitions do not constitute significant risk factors, yet nevertheless triggered transient stability deficits and pro-inflammatory tissue degradation. It is suggested that it might be more appropriate to designate these conditions as low risk instead of no risk. In perspective, Repetitive Lumbar Injury – manifesting in your patient with backache – is seen to be a complex multi-factorial syndrome. A clear example of adaptation to imposed demands that exceed the ability of the tissues involved to respond. Repeated bending activities in daily living appear to change both structure (ligaments, discs) and function (protective spinal reflexes).
Therapeutic interventions in such a spectrum of progressive dysfunction (such as myofascial release, muscle energy technique etc) need to offer various potential benefits, for example improving restricted mobility (Lenehan et al 2003), possibly reducing excessive inflammatory responses (Fryer & Fossum 2010), while simultaneously enhancing motor control (Wilson, et al 2003). But, unless the patterns of use that fuelled this degenerative process are modified, the manual interventions will offer short-term symptomatic relief at best.
Grieve’s Decompensation Model
In 1986, Grieve presciently offered a perspective on the evolution of chronic dysfunction. He described the example of a typical patient, presenting with pain, loss of functional movement, or altered patterns of strength, power or endurance and suggested that, all too commonly, this individual would either have suffered major trauma which had overwhelmed the physiological tolerances of relatively healthy tissues or might be displaying “gradual decompensation, demonstrating slow exhaustion of the tissue’s adaptive potential, with or without trauma.” As this process continued, Grieve explained, progressive postural adaptation influenced by time factors and possibly by trauma, would lead to exhaustion of the body’s adaptive potential, resulting in dysfunction and ultimately, symptoms.
Grieve correctly noted that therapeutic attention to the tissues incriminated in producing symptoms often gives excellent short-term results, however “unless treatment is also focused towards restoring function in asymptomatic tissues responsible for the original postural adaptation and subsequent decompensation, the symptoms will recur.”
A Therapeutic Formula: Reduce Adaptive Load And Enhance Function
A therapeutic formula is proposed for the clinician who is confronted with chronic adaptive changes, of the sort highlighted by Solomonow or Grieve, who may well walk into your office with a backache. It is suggested that the focus should be on both reducing adaptive demands; altering the patterns of behaviour that have produced, or which are maintaining, dysfunction, while at the same time focusing on enhancement of function, working with the self-regulatory systems of the body, so that those adaptive demands can be better managed by the body (Chaitow et al 2005). The only other therapeutic possibility would seem to be symptomatic attention.
In simple terms, musculoskeletal tissue absorbs or adapts to forces applied to it and many manual and movement approaches are capable of modifying these changes – for example the use of Muscle Energy Technique (MET) in dysfunctional shoulders of the elderly (Knebl 2002); following sporting injuries (Bolin 2010); hamstring problems (Smith & Fryer 2008), or even in backache (Licciardone et al 2010)! Why do I emphasise MET? Because its track record is excellent (see citations) and because it is safe and easy to use. But I admit to being biased – and acknowledge that other modalities may be equally useful, but not unless underlying stressors are also dealt with.
References
- Bolin, D. 2010. The application of osteopathic treatments to pediatric sports injuries.Pediatric clinics of North America, 57 (3):775-794.
- Chaitow, L. 2005. Muscle Energy Techniques (3rd edition) Churchill Livingstone, Edinburgh.www.leonchaitow.com/muscle.htm
- Fryer G, Fossum C. 2010. Therapeutic Mechanisms underlying muscle energy approaches. In: Fernandez-de-las-Penas C Arendt-Nielsen L Gerwin R (Eds). Tension-type and Cervicogenic Headache: Pathophysiology, Diagnosis, and Management. Sudbury, MA: Jones and Bartlett Publishers, Pp 221-229.
- Fung DT, Wang VM, Laudier DM, et al 2009. Subrupture tendon fatigue damage. J Orthop Res 27(2):264-273.
- Grieve, G. 1986. Modern manual therapy. Churchill Livingstone, London.
- Knebl, J. 2002. J. American Osteopathic Assoc. Improving functional ability in the elderly via the Spencer technique, an osteopathic manipulative treatment.102(7):387-400.
- Lenehan K Fryer G McLaughlin P 2003. Effect of MET on gross trunk range of motion.Journal of Osteopathic Medicine, 6(1): 13-18.
- Li L, Patel N, Solomonow D, Le Pet al 2007. Neuromuscular response to cyclic lumbar twisting. Hum Factors 49(5):820-829.
- Licciardone J Buchanan S Hensel K et al 2010. Osteopathic manipulative treatment of back pain and related symptoms during pregnancy. American Journal of Obstetrics & Gynecology 202:43.e1-8.
- Parsons J Marcer N 2005. (Eds) Osteopathy: Modesls for diagnosis, treatment an practice. Churchill Livingston Edinburgh.
- Sanchez-Zuriaga D, Adams MA, Dolan P et al 2010. Is activation of the back muscles impaired by creep or muscle fatigue? Spine 35(5):517-525.
- Smith M Fryer G 2008. Comparison of two MET techniques for increasing flexibility of the hamstring muscle group. Jnl. Bodywork & Movement Therapies 12(4):312-317.
- Solomonow M Bing He Zhou EE Yun Lu et al 2011a. Acute repetitive lumbar syndrome.Journal Bodywork & Movement Therapies. In Press.
- Solomonow M 2011b. Time dependent spine stability. Clin Biomechanics 26(3):219-228.
- Solomonow M, Baratta RV, Banks A et al 2003. Flexion-relaxation response to static lumbar flexion in males and females. Clin Biomech (Bristol, Avon) 18(4):273-279.
- Wilson E et al 2003. Muscle energy technique in patients with acute low back pain.Journal of Orthopedic and Sports Physical Therapy 33: 502-512.