OSTEOPOD

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This is the discussion towards the end of my dissertation on the efficacy of spinal stabilising exercises for low back pain and the relevance of psychosocial variables. It was part of my MSc in Pain Management from Cardiff University.

Given the widespread use of spinal stabilising exercises (SSE) by physiotherapists, osteopaths, personal trainers and a myriad other healthcare professionals, it is surprising that there have been relatively few studies assessing its efficacy for LBP compared to other treatment  modalities (12 RCTs and 4 systematic reviews). Furthermore, the studies which do exist (chapter 2) show conclusively that SSE is no more effective than general exercise and standard physiotherapy treatment (O’Sullivan et al 1997; Koumantakis et al 2003; Lewis et al 2005; Cairns et al 2006; Critchley et al 2007; Ferreira et al 2007). This unequivocal evidence suggests that SSE’s therapeutic claims have been overstated. The recent evidence based guidelines for LBP management published by NICE (2009), advises amongst other approaches, either group or one-to-one supervised exercise programmes, but does not differentiate between types of exercise. It may matter less what type of movement a LBP patient does than the fact that they do some, or indeed, any movement. This is not to entirely discount the worth of SSE since it is more effective  for LBP than usual medical care without exercise (Hides et al 2001; Moseley et al 2002; Niemisto et al 2003) and is of as much benefit as lumbar spinal fusion (Brox et al 2003). However it seems that the Richardson & Jull (1995) model of SSE makes theoretical sense but is limited in practice.  In his paper critiquing the evidence for SSE, Lederman (2007) claims that:
Weak trunk muscles, weak abdominals and imbalances between trunk muscle groups are not pathological, just a normal variation. The division of the trunk into core and global muscle systems is a reductionist fantasy… (Lederman, 2007, p.17).
 
The biomechanically minded therapist may well indulge in this “reductionist fantasy” and confuse the perceived benefit of SSE with general benefits of movement, not exclusive to SSE and not due to the stabilising effect of the “core” muscles. This obsession with limiting the cause and continuation of LBP to local physical structures obfuscates the wider biopsychosocial issues. 
 
If, as seems evident, general movement is a common factor in improving LBP, it can be assumed that anything which limits or prohibits movement will have an important role in maintaining the individual’s pain. The psychosocial variables of pain catastrophising and kinesiophobia have been identified as relevant in this respect. A cyclical model emerges of the relationship between these factors and the development/continuation of LBP:
 
If it can be accepted that catastrophising and kinesiophobia are relevant to the development/maintenance of LBP, then it is possible to extrapolate further the ways in which they may influence SSE. It is feasible that by learning SSE, patients may be reducing their pain by overcoming fear beliefs and realising that movement and exercise are not making their condition worse as they had feared (Trost et al 2008).  Graded exposure to a feared movement has been shown to be more effective than education about the meaning of pain in reducing kinesiophobia (De Jong et al 2005) and the repetition of SSE movements may well have a similar effect. Patients may reassess their pain related beliefs once they realise the movements are not aggravating their condition. 
 Once SSE has been assimilated by the patient, their dependence on an external source of pain management (e.g. medical experts, medication) may reduce and their self-efficacy increase. Self-efficacy has been shown to mediate the relationship between kinesiophobia and pain intensity and between kinesiophobia and disability and to be a significantly stronger predictor of pain intensity/disability than kinesiophobia (Woby et al 2007b). 
This cognitive/emotional effect of physical exercise on pain levels may be due to the descending influence from higher centres of the CNS involved in affective function. The amygdala has an important role “in emotionality, the emotional evaluation of sensory stimuli, emotional learning, and memory as well as affective disorders” (Neugebauer & Li 2002 p.716) and so is highly relevant to understanding both the depressing and anxiety inducing effect of pain and the reciprocal effect that emotions may have on modulating pain and sensitivity (Wilson et al 2001). Other areas of the brain have also been implicated in pain sensitisation, modulation and neuroplasticity including the cerebral cortex, the limbic system, thalamus and hypothalamic–pituitary–adrenal axis (Ulrich-Lai et al 2006; Heppelmann et al 2001). Although not within the parameters set for this dissertation, these studies linking other higher centres of the central nervous system with the experience of pain indicate that pain involves input and output from diverse structures throughout the brain, some of which may be involved in the emotions and cognitions found in catastrophising and kinesiophobia. Particularly when chronic this may be relevant as a maintaining factor in the centralisation of pain via descending pathways of the CNS and sensitisation within the posterior dorsal horn. 
 
The empowerment to develop self-sufficient means of health maintenance and lessen dependence on external resources is of course not unique to SSE and would in theory be applicable to any form of physical exercise which has a positive cognitive effect. It is worth reiterating that the benefits of SSE for LBP were relatively limited particularly in comparison to general movement. This may be due to SSE not exposing patients to as much gross movement of the lumbar spine as other types of exercise, since its emphasis is on stability rather than mobility. In assessing studies of SSE it is vital to control for these psychosocial variables since they would influence the patients’ base-line pain/disability levels and their subsequent progress. The studies critiqued imply that SSE would have a beneficial effect on catastrophising /kinesiophobia. However it is possible that SSE could increase these variables via patient focus and rumination on their LBP. Furthermore it is possible that SSE could increase LBP by providing the patient with an increased external locus of control, an external fixation of hope and distraction, the SSE being seen as the external answer to their prayers. Higher levels of praying or hoping have been related to greater levels of pain intensity via their effect on catastrophising (Woby et al 2005). As stated previously, these implications are made with an evidence informed leap of faith and although soundly justified one cannot assume them to be conclusive. 
 
This inability to produce evidence specifically identifying the influence of kinesiophobia and catastrophising on SSE is a glaring limitation of this extended literature review. Since there have, as yet, been no published studies on the subject, all assumptions made are speculative and must be treated as such. The assumptions made and the critiquing of studies were carried out by a single person (the author) and may have introduced interpretation bias. Attempts were made to limit this by following generally accepted critiquing guidelines but despite this should be taken into account when assessing the findings and their application in practice. Another limitation is the lack of attention paid to studies assessing functional components of the SSE theory e.g. sequential timing, activation and strength of individual core muscles. It may be that by dismantling the biomechanics underlying the SSE model a greater understanding of the exercise system is acquired. However, the author was more concerned with the pragmatic issue of clinical efficacy and felt justified in this omission. Further limitation, due to space constriction, was the absence of any in-depth neurophysiological inquiry into the descending neurological, cognitive/affective influence on pain, which may occur during catastrophising/kinesiophobia. Finally, the focus on this specific type of SSE is limited and the author acknowledges the existence and widespread use of a multitude of other “stabilising” techniques which vary in both theory and practice from the Richardson & Jull (1995) model. However, for the sake of specificity and in identifying the most commonly used method of stabilising the spine through exercise; this exercise system was thought to be an appropriate focus.

This is the discussion towards the end of my dissertation on the efficacy of spinal stabilising exercises for low back pain and the relevance of psychosocial variables. It was part of my MSc in Pain Management from Cardiff University.


Given the widespread use of spinal stabilising exercises (SSE) by physiotherapists, osteopaths, personal trainers and a myriad other healthcare professionals, it is surprising that there have been relatively few studies assessing its efficacy for LBP compared to other treatment  modalities (12 RCTs and 4 systematic reviews). Furthermore, the studies which do exist (chapter 2) show conclusively that SSE is no more effective than general exercise and standard physiotherapy treatment (O’Sullivan et al 1997; Koumantakis et al 2003; Lewis et al 2005; Cairns et al 2006; Critchley et al 2007; Ferreira et al 2007). This unequivocal evidence suggests that SSE’s therapeutic claims have been overstated. The recent evidence based guidelines for LBP management published by NICE (2009), advises amongst other approaches, either group or one-to-one supervised exercise programmes, but does not differentiate between types of exercise. It may matter less what type of movement a LBP patient does than the fact that they do some, or indeed, any movement. This is not to entirely discount the worth of SSE since it is more effective  for LBP than usual medical care without exercise (Hides et al 2001; Moseley et al 2002; Niemisto et al 2003) and is of as much benefit as lumbar spinal fusion (Brox et al 2003). However it seems that the Richardson & Jull (1995) model of SSE makes theoretical sense but is limited in practice.  In his paper critiquing the evidence for SSE, Lederman (2007) claims that:

Weak trunk muscles, weak abdominals and imbalances between trunk muscle groups are not pathological, just a normal variation. The division of the trunk into core and global muscle systems is a reductionist fantasy… (Lederman, 2007, p.17).

 

The biomechanically minded therapist may well indulge in this “reductionist fantasy” and confuse the perceived benefit of SSE with general benefits of movement, not exclusive to SSE and not due to the stabilising effect of the “core” muscles. This obsession with limiting the cause and continuation of LBP to local physical structures obfuscates the wider biopsychosocial issues. 

 

If, as seems evident, general movement is a common factor in improving LBP, it can be assumed that anything which limits or prohibits movement will have an important role in maintaining the individual’s pain. The psychosocial variables of pain catastrophising and kinesiophobia have been identified as relevant in this respect. A cyclical model emerges of the relationship between these factors and the development/continuation of LBP:

 

If it can be accepted that catastrophising and kinesiophobia are relevant to the development/maintenance of LBP, then it is possible to extrapolate further the ways in which they may influence SSE. It is feasible that by learning SSE, patients may be reducing their pain by overcoming fear beliefs and realising that movement and exercise are not making their condition worse as they had feared (Trost et al 2008).  Graded exposure to a feared movement has been shown to be more effective than education about the meaning of pain in reducing kinesiophobia (De Jong et al 2005) and the repetition of SSE movements may well have a similar effect. Patients may reassess their pain related beliefs once they realise the movements are not aggravating their condition. 

 Once SSE has been assimilated by the patient, their dependence on an external source of pain management (e.g. medical experts, medication) may reduce and their self-efficacy increase. Self-efficacy has been shown to mediate the relationship between kinesiophobia and pain intensity and between kinesiophobia and disability and to be a significantly stronger predictor of pain intensity/disability than kinesiophobia (Woby et al 2007b). 

This cognitive/emotional effect of physical exercise on pain levels may be due to the descending influence from higher centres of the CNS involved in affective function. The amygdala has an important role “in emotionality, the emotional evaluation of sensory stimuli, emotional learning, and memory as well as affective disorders” (Neugebauer & Li 2002 p.716) and so is highly relevant to understanding both the depressing and anxiety inducing effect of pain and the reciprocal effect that emotions may have on modulating pain and sensitivity (Wilson et al 2001). Other areas of the brain have also been implicated in pain sensitisation, modulation and neuroplasticity including the cerebral cortex, the limbic system, thalamus and hypothalamic–pituitary–adrenal axis (Ulrich-Lai et al 2006; Heppelmann et al 2001). Although not within the parameters set for this dissertation, these studies linking other higher centres of the central nervous system with the experience of pain indicate that pain involves input and output from diverse structures throughout the brain, some of which may be involved in the emotions and cognitions found in catastrophising and kinesiophobia. Particularly when chronic this may be relevant as a maintaining factor in the centralisation of pain via descending pathways of the CNS and sensitisation within the posterior dorsal horn. 

 

The empowerment to develop self-sufficient means of health maintenance and lessen dependence on external resources is of course not unique to SSE and would in theory be applicable to any form of physical exercise which has a positive cognitive effect. It is worth reiterating that the benefits of SSE for LBP were relatively limited particularly in comparison to general movement. This may be due to SSE not exposing patients to as much gross movement of the lumbar spine as other types of exercise, since its emphasis is on stability rather than mobility. In assessing studies of SSE it is vital to control for these psychosocial variables since they would influence the patients’ base-line pain/disability levels and their subsequent progress. The studies critiqued imply that SSE would have a beneficial effect on catastrophising /kinesiophobia. However it is possible that SSE could increase these variables via patient focus and rumination on their LBP. Furthermore it is possible that SSE could increase LBP by providing the patient with an increased external locus of control, an external fixation of hope and distraction, the SSE being seen as the external answer to their prayers. Higher levels of praying or hoping have been related to greater levels of pain intensity via their effect on catastrophising (Woby et al 2005). As stated previously, these implications are made with an evidence informed leap of faith and although soundly justified one cannot assume them to be conclusive. 

 

This inability to produce evidence specifically identifying the influence of kinesiophobia and catastrophising on SSE is a glaring limitation of this extended literature review. Since there have, as yet, been no published studies on the subject, all assumptions made are speculative and must be treated as such. The assumptions made and the critiquing of studies were carried out by a single person (the author) and may have introduced interpretation bias. Attempts were made to limit this by following generally accepted critiquing guidelines but despite this should be taken into account when assessing the findings and their application in practice. Another limitation is the lack of attention paid to studies assessing functional components of the SSE theory e.g. sequential timing, activation and strength of individual core muscles. It may be that by dismantling the biomechanics underlying the SSE model a greater understanding of the exercise system is acquired. However, the author was more concerned with the pragmatic issue of clinical efficacy and felt justified in this omission. Further limitation, due to space constriction, was the absence of any in-depth neurophysiological inquiry into the descending neurological, cognitive/affective influence on pain, which may occur during catastrophising/kinesiophobia. Finally, the focus on this specific type of SSE is limited and the author acknowledges the existence and widespread use of a multitude of other “stabilising” techniques which vary in both theory and practice from the Richardson & Jull (1995) model. However, for the sake of specificity and in identifying the most commonly used method of stabilising the spine through exercise; this exercise system was thought to be an appropriate focus.

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Before starting to review specific pieces of research here are a few thoughts about evidence in relation to osteopathic practice.

Evidence based practice has been defined as “the process of systematically finding, appraising and using contemporaneous research findings as the basis for clinical decisions” (Rosenberg & Donald 1995, p.1122). There are, however, difficulties inherent in basing osteopathic clinical decisions on high quality research. For the most part, osteopathy has developed independently of rigorously researched studies and much of its teaching relies heavily on tradition, policy and clinical experience. The profession of osteopathy is starting to tentatively embrace the need for evidence based research despite mistrust within the profession of the methods used to acquire this evidence. Accurately or not, some of this mistrust is due to the belief “that a reductionist research paradigm cannot investigate a holistic patient centred approach” (Lucas & Moran 2006 p.76). This philosophical difference may complicate clinical decision making.

For example there are a few trials which seek to compare the efficacy of non-steroidal anti-inflammatories (NSAID) and spinal manipulation for low back pain. Osteopathic philosophy does not see manipulation as a valid treatment intervention in isolation from the complete osteopathic consultation. As Kuchera & Kuchera (1994 p.2) say, “manipulation is not osteopathic philosophy and technically it is not osteopathy”. To remove manipulation from the context of osteopathic, or for that matter chiropractic, consultation and assess the technique in isolation is therapeutically inappropriate. However, the use of NSAIDs for pain relief is viewed by allopathic medicine as being a valid and complete treatment method in and of itself, within or without professional consultation. 


Using RCTs to compare these groups compounds this difference. Double blinding is not possible in trials assessing manipulation (Andersson et al 1999). Therefore, when trial quality is assessed using scales such as Jadad (1996) or PEDro (1999), which both see blinding as integral to high quality RCTs, NSAID trials will always have an advantage over manipulation trials in quality rating. This raises questions of whether these types of trial and rating systems are appropriate for studies of manipulation and whether more emphasis should be placed on qualitative and not quantitative research. Qualitative methods may be better suited to analysing the subjective nature of pain, its complex bio-psychosocial and behavioural elements, and the relationships between the variables (Faltermaier 1997). 


Designing suitable studies for manipulation/osteopathy is vital if osteopathic practice is to become evidence based. Until good quality studies are provided, little evidence can be shown to those influencing healthcare policy and funding, that osteopathic treatment including spinal manipulation is a viable alternative to treatments such as NSAID use for back pain. 


References:

Andersson, G; Lucente, T; Davis, A; Kappler, R; Lipton, J; Leurgans, S. (1999). A comparison of osteopathic spinal manipulation with standard care for patients with low back pain. The New England Journal of Medicine, Volume 341(19), pp 1426-1431

 Faltermaier, T. (1997) Why public health research needs qualitative approaches: Subjects and methods in change. The European Journal of Public Health  7 (4):357-363;.Jadad A.R, Moore R.A, Carroll D. et al. (1996). Assessing the quality of reports of randomized clinical trials: Is blinding necessary?. Control Clinical Trials 17 pp. 1–12

Lucas N, Moran R. (2006). Is Osteopathy Research Relevant? A Challenge Has Been Made. International Journal of Osteopathic Medicine. Volume 9 number 3  pp 75-76.

 PEDro (Physiotherapy Evidence Database  (1999) [Online] Available from http://www.pedro.fhs.usyd.edu.au/ [Accessed November 25 2006].

Rosenberg W, Donald A. (1995) Evidence-based medicine: an approach to clinical problem-solving. BMJ 310:1122-1126.


 

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The idea of Osteopod is to provide a space to slowly yet steadily critique and review studies which relate in some way to osteopathy.

Evidence production and gathering by osteopaths seems to be a slow process. Many osteopaths arent trained in reviewing evidence, quite a few arent really bothered either way and there’s very little funding for studies specifically into osteopathy.

I thought i’d get stuck in and see what i can come up with.

Im by no means an academic nor an expert in critical reviewing. My time is largely spent treating patients 6 days a week in my East London clinic but I’m interested in what can practically help me to better help my patients. 

Let’s see what comes up…

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