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.
