What underlies fear for movement in people with low back pain?

“I would never bend over to pick something up. I try to brace myself on any move. Because every time time it hurts I think that I’m doing more damage. Every time it hurts I think it is getting worse and I am breaking down, I am killing myself…” (John, a 42 year old school teacher who has experienced back pain for 2 years).

“I don’t think that picking up that pen is going to damage my spine. But I know if I bend over and pick up that pen, that pen is going to irritate me for the next half an hour. Why would I do that when I could have half an hour pain-free? I can achieve a lot in half an hour if I am not in agony” (Emma, a 48 year old caterer who has experienced back pain for 1 year).

The Tampa Scale of Kinesiophobia (TSK) is a widely used tool to assess “fear of movement and physical activity that is (wrongfully) assumed to cause (re)injury” in people with low back pain (Vlaeyen et al. 1995). It is thought to comprise of two subscales (Clark et al. 1997). The Somatic Focus subscale describes the belief that pain is a sign of bodily harm. It includes items such as “My body is telling me I have something dangerously wrong”. The Activity Avoidance subscale describes the belief that activity may result in (re)injury or increased pain. It includes items such as “I am afraid that I might injure myself if I exercise”

High scores on the TSK (≥37/68) are used to identify candidates for fear reduction interventions, which target the belief that pain is a sign of damage. However these interventions have had modest results: some people respond well, others respond less well, and high drop out rates have been reported (Linton et al. 2008)

To better understand the construct of pain-related fear in people with chronic non-specific low back pain, and who score high on the TSK (>40/68), we conducted qualitative interviews with 36 individuals who met these criteria. Early in the interview process it became apparent that not all high scoring individuals were “fearful of movement and physical activity that they (wrongfully) assumed to cause (re)injury”. This raised the question ‘What construct does the TSK actually measure?’. We explored this in our recent publication in the Clinical Journal of Pain (Bunzli et al. 2014).

Two main beliefs that underly high scores on the TSK were identified. John (above) illustrates ‘damage beliefs’ – he believes painful activity could cause damage to his spine. Emma illustrates ‘suffering/functional loss beliefs’ – she believes painful activity will impact on suffering and/or subsequent function. A few people had mixed beliefs.

Through a process of ‘quantitization’ we then placed individuals into a ‘damage beliefs’ group or ‘suffering/functional loss beliefs’ group according to their predominant underlying belief, and then analysed associations between groups and itemized scores on the TSK.

We found that individuals in the ‘damage beliefs’ group agreed more significantly with items on the TSK- Somatic Focus subscale than individuals in the ‘suffering/functional loss beliefs’ group. This lends ‘construct validity’ to the TSK- Somatic Focus subscale. The TSK- Activity Avoidance subscale did not discriminate between groups, possibly due to the inclusion of the word ‘injure’ that was ambiguously interpreted by the two groups.

While the TSK may be a useful clinical tool to identify individuals who fear the consequences of painful activity, it does not seem to discriminate between these 2 beliefs. We think identifying people with these beliefs may be important for targeted interventions. We suggest that clinicians consider including simple questions in their clinical assessment of patients presenting with low back pain and high scores on the TSK such as:

Do you worry that performing a painful activity will cause damage to your spine?

Do you worry that performing a painful activity will impact on all the other things you need to get done in your day?

About Sam Bunzli

Sam BunzliSam worked for 10 years in musculoskeletal physiotherapy and is now a PhD Candidate at Curtin University conducting her research under the supervision of Professor Peter O’Sullivan and Dr Anne Smith. She likes talking to patients, likes transcribing less, no longer prefers tea to coffee, but is passionate about clinically orientated qualitative research.


Vlaeyen J, Kole-Snijders A, Boeren R, van Eek H. Fear of movement/(re)injury in chronic low back pain and its relation to behavioral performance. Pain 1995; 62:363-372.

Clark M, Kori S, Brockel J: Kinesiophobia and chronic pain: Psychometric characteristics and factor analysis of the Tampa Scale. 15th APS Annual Scientific Meeting, American Pain Society, 1996.

Linton S, Boersma K, Jansson M, Overmeer T, Lindblom K, Vlaeyen J. A randomized controlled trial of exposure in vivo for patients with spinal pain reporting fear of work-related activities. European Journal of Pain 2008; 12:722-730.

Bunzli S, Watkins R, Smith A, Schutze R, O’Sullivan P. What do people who score highly on the Tampa Scale of Kinesiophobia really believe?. The Clinical Journal of Pain 2014. DOI: 10.1097/AJP.0000000000000143

Bunzli S, Smith A, Watkins R, Schütze R, & O’Sullivan P (2014). “What Do People who Score Highly on the Tampa Scale of Kinesiophobia Really Believe? A Mixed Methods Investigation in People with Chronic Non Specific Low Back Pain. The Clinical journal of pain PMID: 25167327


  1. In response to Jill WW’s query:
    “In conditions of spinal cord injury, peripheral nerve injury, or inflammation, spinal microglia and astrocytes are activated by neurotransmitters and mediators [such as glutamate (Glut), substance P (SP), ATP or fractalkine] released from sensitized primary afferent terminals. Glia can also be activated by stress, via direct or indirect GCs-mediated pathways or neural-mediated signals. Activated glia in turn, release a variety of mediators, which act on neurons or glial cells generating a neuro-glial amplification loop. Pro-inflammatory cytokines can act directly on postsynaptic neurons affecting their excitability and are also involved in the modulation of various genes expression including genes for NMDA receptors (NMDAR) or GLT1. The confluence of excessive release of neurotransmitters and pro-inflammatory mediators, the downregulation of glutamate transporters, the compromised glutamate reuptake by astrocytes ultimately lead to postsynaptic hyperexcitability and exacerbation of the pain signaling.” (from: Bradesi S. Role of spinal cord glia in the central processing of peripheral pain perception. Neurogastroenterology And Motility: The Official Journal Of The European Gastrointestinal Motility Society. 2010;22(5):499-511)

    Notwithstanding the rather annoying reference to “pain signaling” there at the end, I think there’s a consensus building among neurobiologists that the stress response can activate spinal cord microglia into doing their nasty business. So, John, as Lorimer is wont to mention from time to time, humans are complex. Rarely does it seem that any pathway in the human alarm system apparatus operates in just one direction. When in doubt, I’m going to place my bets on the role- and power- of the brain and the benefits of movement.

  2. Interesting comment John Barbis. What is the current thinking on the effect of stress/fear on glial cell activation?

  3. John Barbis says:

    Excellent blog. I am in whole hearted agreement that pain can be maintained by cortical and subcortical process that are maintained by fallacious beliefs, non-relevant past experience, conditioning, and inappropriate educational sources. There is too much good research out there to deny that association and the work of Apkarian and others looking at brain imaging of back pain patients is very compelling. Let’s, however, not oversimplify what may be gray areas in this discussion. There are studies demonstrating that abnormal psychometric findings are normalized after successful surgery or other invasive interventions for back pain. Mechanical nociceptive generators can produce behavioral effects and their removal can produce profound changes in behavioral testing results. Some may argue that these results are placebo related but I do not believe any fair thinker would completely rule out the finding that at least some of the good responses of these patients are due to an appropriate intervention for a mechanical nociceptive generator. In addition there is growing body of research on the influence of microglia on pain and the functioning of the nervous system in broader pathological terms. Overly active glia can have pathological consequences. Glia activation and influences on the nervous system are emerging areas of pain maintenance, distribution, and elevation outside of their growing implications in neurological pathology. Can glial cell activation exist outside of ongoing mechanical or neuropathic nociceptive stimulation? The science says yes. Would the types of sensory experiences produced by glial cell activation produce movement and behavioral impairments that would be seen as abnormal on psychometric testing? Animal models would tend to support that finding. Can the cytokine and other chemical substances produced by glial cells damage neural tissue? The growing evidence is yes.
    Up until the last year or so, I had completely accepted that non-mechanically triggered low back pain was not dangerous. I am gaining an appreciation and a concern that that concept may not be totally correct. As the science of pain progresses, I think that we may have to be open to the possibility that that statement may not be totally correct. There may be a cohort of non-mechanical nociceptive back pain patients whose symptoms not solely cortical /sub-cortically maintained, but may be maintained by glial cell activation. In that cohort- is pain potentially dangerous? The jury is out, but the literature is tending to show that there is danger there. I believe that glial cell activation may be the cause of those difficult CRPS and other serious pain patients who do not appear to respond to anything and are exacerbated by everything. It will be an interesting time. We need to keep open minds.