Expecting back pain – the possibility of a self-fulfilling prophecy

It seems like years ago now, well, it is years ago now, that I did this study with The Walking Cortex (TWC, Paul Hodges).  This was one of my PhD studies. I think it is quite a groovy study.  We gave supposedly normal healthy volunteers painful electric shocks, through electrodes placed over the back of their pelvis.  We showed that when they are at risk of getting an electric shock AND they move their arm really really quickly (that is the technical term of course), they do something different with their tummy and back muscles.  Just in case you didn’t know – every time you move an arm or leg, your brain thinks ahead and contracts tummy and back muscles and a whole lot of other muscles BEFORE the movement, so that the force of the movement doesn’t throw you across the room.  Anyway, that these postural adjustments in advance of the movement are similar to those we see in people with recurrent back pain was especially interesting because it showed, we think, that when you think your back is about to hurt, your postural adjustments reflect are just like they are when your back does hurt.  So, the argument that we put forward is that, perhaps, the anticipation of back pain induces a protective postural adjustment strategy. This is potentially very important because it is possible that if you keep using this strategy you are putting tissues of the back under excessive load. That is not a problem unless you do it for a long time, in which case it might just cause back pain. Self-fulfilling prophecy perhaps.  We don’t actually know for sure that this is what happens, but our collaborative research led by TWC and his team up at the University of Queensland are trying to untangle it.  Anyway, if you are interested, read the paper.

Does anticipation of back pain predispose to back trouble?

Summary (from the paper)

Limb movement imparts a perturbation to the body. The impact of that perturbation is limited via anticipatory postural adjustments. The strategy by which the CNS controls anticipatory postural adjustments of the trunk muscles during limb movement is altered during acute back pain and in people with recurrent back pain, even when they are pain free. The altered postural strategy probably serves to protect the spine in the short term, but it is associated with a cost and is thought to predispose spinal structures to injury in the long term. It is not known why this protective strategy might occur even when people are pain free, but one possibility is that it is caused by the anticipation of back pain. In eight healthy subjects, recordings of intramuscular EMG were made from the trunk muscles during single and repetitive arm movements. Anticipation of experimental back pain and anticipation of experimental elbow pain were elicited by the threat of painful cutaneous stimulation. There was no effect of anticipated experimental elbow pain on postural adjustments. During anticipated experimental back pain, for single arm movements there was delayed activation of the deep trunk muscles and augmentation of at least one superficial trunk muscle. For repetitive arm movements, there was decreased activity and a shift from biphasic to monophasic activation of the deep trunk muscles and increased activity of superficial trunk muscles during anticipation of back pain. In both instances, the changes were consistent with adoption of an altered strategy for postural control and were similar to those observed in patients with recurrent back pain. We conclude that anticipation of experimental back pain evokes a protective postural strategy that stiffens the spine. This protective strategy is associated with compressive cost and is thought to predispose to spinal injury if maintained long term.



We hypothesized that anticipation of experimental back pain would selectively delay postural activation of the deep trunk muscles during single rapid arm movements and would reduce activation of the deep trunk muscles, and increase the activation of superficial trunk muscles, during repetitive arm movements. The results support both hypotheses and suggest that when people anticipate back pain, there is a change in the strategy by which the CNS attempts to control the spine during the perturbation caused by movement. This change in strategy is not evoked when people anticipate elbow pain, even though the physiological and subjective measures suggested that fear of impending shock, and intensity of expected pain were similar between experimental conditions. Taken together, the results exclude the possibility that the impact on control strategy was caused by the attention requirements of the task or by a generic fear of impending shock.

There are several aspects of the current results that suggest that the strategy for spinal control was altered during anticipation of experimental back pain, even though the arm movements, and therefore the direction and magnitude of the perturbation caused by arm movement, remained constant. In single arm movements, postural activation of the deep trunk muscles was delayed, postural activation of at least one of the superficial trunk muscles was augmented and there was an increase in baseline activity for Sup MF and OE across the group. In repetitive arm movements, there was a decrease in the maximum and mean EMG amplitude of the deep trunk muscles and a reduction in the coherence of deep trunk muscle EMG with arm movement.

In both single and repetitive arm movements, the nature of the change in postural strategy is consistent with a protective response to stiffen the spine by co-contraction of the superficial trunk muscles. Although general spinal splinting may be beneficial in the short term, there is an associated cost. For instance, splinting reduces spinal flexibility, which is important for normal function and dampening of reactive forces (Hodges et al., 1999) and, according to biomechanics, must impart an increased compressive load on spinal structures (Cholewicki and McGill, 1994). Such an increase in loading has been shown to accelerate tissue degeneration (Ching et al., 2003), and sustained increased spinal load is thought to lead to stimulation of nociceptors in spinal structures and predispose to spinal injury (Gardner-Morse and Stokes, 1998). That said, although any increase in superficial trunk muscle co-contraction will impart some compressive load, the minimum change in EMG and the minimum duration of that change in EMG required to injure spinal tissue is yet to be determined. A second aspect of the results suggests increased risk associated with long-term alteration in spinal control. The deep trunk muscles are well suited to control shear (Hodges et al., 2003a) and are important in fine-tuning of spinal control (e.g. Kaigle et al., 1995). Therefore, delayed or reduced activity of the deep trunk muscles is likely to be associated with reduction of fine control, particularly between segments, which further places spinal structures at risk of nociceptive stimulation and injury. Based on the likely consequences of maintaining such a protective postural strategy long term, the current results raise the possibility that anticipation of back pain predisposes to back trouble. Although consistent with previous links between chronic pain-related disability and protective movement patterns (Lethem et al., 1983; Slade et al., 1983; Keefe et al., 1990; Vlaeyen and Linton, 2000, 1995), the current findings make the first link between anticipation of pain and subsequent nociception or injury, or both.

Elbow pain did not impart an alteration in postural strategy. Although anatomical specificity of the effect of anticipated experimental pain on postural responses is a new finding, it corroborates data obtained from patients. For example, when exposed to personally relevant stressors, patients with chronic jaw pain, but not those with chronic back pain, demonstrated increased jaw muscle activity (Flor et al., 1991, 1992). Similar specificity has been shown for frontalis muscle activity in patients with chronic headache (Flor and Turk, 1989), and paraspinal muscle activity in patients with chronic back pain (Flor et al., 1992). Together, those data suggest that the effect on motor output (i.e. increased muscle activity) is anatomically specific to the area of pain, or the anatomical context of expected pain and/or (re)injury. In the current experiment, the effect on motor output (i.e. altered postural response of the deep trunk muscles) only occurred when the impending pain was anatomically specific (i.e. back pain), which is not surprising in light of the potential benefit of the alternative postural strategy, i.e. to stiffen the spine and limit perturbation of the affected part.

The possibility that the changes in postural adjustments observed here could be mediated at a motoneuron or spinal level cannot be excluded. Most data implicating spinal mechanisms in the changes in muscle activity during pain suggest that those mechanisms lead to reduced activity of agonists and increased activity of antagonists (e.g. Graven-Nielsen et al., 1997). That theory would predict, for example, a delay in activation of both superficial and deep extensor muscles and augmentation of superficial and deep abdominal muscles, which was not observed. Rather, we observed a delay in deep trunk muscles and augmentation of superficial trunk muscles. Notably, both Sup MF, an extensor, and OE, a flexor, demonstrated increased baseline activity during single arm movements. As such, the changes observed here are more consistent with an alteration of strategy. Moreover, similar changes have been shown in people with recurrent back trouble, in which they have been shown to reflect changes in postural strategy (Hodges, 2001).

A consideration for the generalizability of the current results is that painful cutaneous stimulation does not accurately simulate non-experimental back pain. We previously have demonstrated a similar change in postural strategy when normal subjects were given experimentally induced low back pain via i.m. injection of hypertonic saline, which more closely simulates non-experimental pain (Hodges et al., 2003b). We have also replicated those findings in a separate study that involved the same subjects as those used here (Moseley et al., 2004). Taken together, this series of studies demonstrates that asymptomatic controls who are anticipating back pain evoked by painful cutaneous stimulation, those who are experiencing back pain induced by i.m. injection of hypertonic saline and patients who suffer chronic recurrent episodes of back pain but who are pain free all demonstrate a similar postural strategy during arm movements. That strategy is different from pain-free controls under normal conditions. Thus, despite the limitations of painful cutaneous shock, it is sufficient to identify that relationship. That said, spinal and cortical projections from cutaneous input differ from those from muscle input, and painful cutaneous stimulation and painful muscle stimulation have different effects on short and long latency motor responses (Zedka et al., 1999), which suggests that experienced and anticipated cutaneous pain and muscle pain may involve distinct mechanisms and impart other distinct effects. It would therefore be valuable to replicate the current findings using a deeper painful stimulus such as i.m. injection of saline. This was not possible in our study because in order to evoke an authentic and sustained anticipation of pain, we considered it important to use a painful stimulus of known intensity and short duration, which permits task performance during expected pain but in the absence of pain. I.m. injection of algesic chemicals does not offer this advantage. We also chose not to use i.m. electrical stimulation because this would evoke a muscle response and it would be impossible to determine whether any effect was consequent to the anticipation of pain or the anticipation of postural perturbation imparted by a muscle response. Nonetheless, differences between experimentally induced pain and non-experimental pain should be remembered.

In summary, the anticipation of experimental back pain changes the strategy by which the CNS controls the spine during perturbation caused by limb movement. The alternative strategy serves to protect the trunk by stiffening the spine. The effect is unlikely to be caused by attention demand due to pain or other generalized effects of stress or fear because it is not present during anticipation of experimental elbow pain. Because this protective strategy is associated with a reduction in fine control and increased loading of spinal structures, it is thought to predispose spinal structures to nociception and injury if maintained long term. The main implications of the current work then, are that the alteration of postural strategy observed in recurrent back pain patients may be caused by the anticipation of back pain, and that anticipation of back pain predisposes the individual to back trouble.

Full free article: Brain 127:2339-2347



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  1. Death, taxes and low pack pain!! Very hard to avoid the first two and high odd’s on the third. Could we expect to go through life without a skin abrasion? Only the obsessive /compulsive would conclude a possibility of septecemia.
    The untangling of mechanisms needs changing perspective of Therapists, Patients, Society and Systems. Watchthis space as the pendulum swings.


  2. Frédéric Wellens, pht says:


    In light of all this, what would then be the ultimate (EBM) best re-education strategy to help correct this altered recruitment pattern in CLBP sufferer ?

    The traditionnal transverse-multifidus conscious contraction progressive regimen begining with the usual attempt at isolated contractions ?

    I sure hope not.