Low-back pain is costly, debilitating and poorly diagnosed. It affects early everyone, about 80% of the population, at some point during their lives. And thousands of pounds (and billions of dollars and a shed load of Euros etc) have been spent trying to improve clinical outcomes but, incredibly, pain, disability and lost time from work have not improved dramatically over the past several decades.

In about half of all LBP cases have associated leg pain. These cases are the testing ones and they account for a disproportionately large amount of LBP related health care cash. Add to this the fact that LBP with leg pain is an important predictor for chronicity and severity of LBP, so if you have leg pain the problem tends to last longer and be nastier.

But why is the leg hurting?

Several structures are capable of producing referred leg pain. These can range from the neural to the musculoskeletal. And, clearly, a failure to identify the etiology of the referred leg pain can mean that the wrong cause is addressed and the wrong treatment is then, promptly, delivered.

There was an interesting article on this published earlier this year by a Schafer A et al. where they set out an interesting way of thinking about low-back pain with leg pain.

They set out the mechanisms that cause low-back related leg pain as follows:

• Inflammation: Internal disc damage or endplate fractures activate the inflammatory cascade which can cause discogenic referred leg pain or nerve root irritation. Inflammation of the nerve root can also increase the nerve’s sensitivity to mechanical compression and change neural mobility.

• Compression: Mechanical nerve root compression secondary to degenerative changes or a space occupying lesion may result in impaired blood flow to the tissues surrounding the nerve and the nerve itself. This, in turn, can cause increased fluid pressure and mechanical nerve fibre deformation. Nerve root compression can result in sensory and motor dysfunction and radiating pain.

• Central Events: This bit is a tad testing but neural plasticity can occur secondary to continued stimulus from nerve fibres associated with handling pain (nociceptive) input. This may result in a lowered threshold to nociceptive input, changes in subcortical and cortical brain regions, disinhibition and a phenotypic switch of non-nociceptive neurons to nociceptive neurons. This is called central sensitization.

• Musculoskeletal Referral: Pain generators can include the intervertebral disc, facet joint, sacroiliac joint, or a variety of myofascial structures. All of these structures have been sufficiently studied and identified as potential leg pain generators and their pain patterns well mapped by the likes of Travell and Simon.

So the authors of the paper propose that low-back pain with leg pain should be grouped into 4 groups that would be treated differently because their causes are different – sensible really. The groups are:

• Central Sensitization - with thermal and mechanical increased response to pain stimulus (hyperalgesia)/extreme tenderness of the skin (allodynia) and neurological evaluation may reveal altered pin prick thresholds or light touch allodynia (oh yes indeed).

• Denervation - structural nerve damage with altered motor strength, deep tendon reflex, and/or sensation in a dermatomal pattern.

• Musculoskeletal - absence of gross neurological deficits and absence of nerve root tension and positive joint provocation manoeuvres or centralization/peripheralization.

• Peripheral nerve sensitization - absence of gross neurological deficits and presence of nerve root tension – referred leg pain with neural movement during testing.

And of course not forgetting that you can have more than one at once – and this is not uncommon:

• Mixed Pathologies - multiple pathologies may be present at once but the authors think the existence of a primary mechanism responsible for a patient’s symptoms can be determined and therefore tackled.

So at C1 we are looking to make this call and we’ll include in our initial examination a comprehensive assessment of the patient’s subjective complaint. We’ll then carry out a physical evaluation, including a neurological examination, an assessment for nerve root tension, an evaluation of active ROM and joint provocative testing.