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Oriel Chambers Journal



Wednesday, August 23, 2017


Chris Middleton


 Of the many things which mystify me when dealing with whiplash cases in county courts, one of the most mystifying is how often claimants with ongoing symptoms (often years post-accident) declare themselves “content” to rely on the usual 3 / 6 / 9 / 12 month prognosis contained in their medical reports. The explicit (if not quite coherent) premise of the current “reform” proposals for whiplash cases contained in the Civil Liability Bill is that these people (and just about anyone else with soft tissue injuries following a road accident) are being overcompensated.

However, and much as this may come as a surprise to lawyers in the field (and everyone else), medical studies suggest that between 30 and 50 per cent of patients who suffer whiplash injuries can go on to suffer chronic symptoms of the same type . Does this suggest that a sizeable number of claimants in fact being undercompensated, by a failure to recognise the chronic nature of their injuries, and formulate their claims accordingly ? Against the background of the reform proposals, recent medical developments in relation to chronic pain provide a timely opportunity to consider this issue further.

Central sensitisation:”no thing” rather than “nothing”

Anyone who has dealt with personal injury claims for any length of time is likely to have experience with evidence from “pain experts”, very often instructed by a claimant to try and avoid checkmate when the defendant has wheeled out an orthopod to conclude that only the first 15 minutes (or 20, if s/he is feeling generous) of the claimant’s ongoing symptoms can be attributed to the index accident, rather than the on-the-verge-of-falling apart degenerative spine of which the 23 year old claimant was completely unaware. But in the absence of one of the more clearly understood and demonstrable neurololgical conditions, such as complex regional pain syndrome, judges and lawyers alike can approach such evidence with scepticism. Frequently, in my experience, this is because it is simply very difficult to understand what the expert’s reasoning is, and how s/he links an apparently trivial trauma to a substantial and ongoing condition.

The theory behind central sensitisation is that chronic pain arises from enhanced excitability of the neurons within the central nervous system in response to peripheral nociceptor stimulation . Or in other words, the patient’s central nervous system perceives pain, in a manner out of proportion to the severity of the initial pain-producing stimulus to the peripheral nervous system. Doctors have variously referred to this as the central nervous system’s volume control being turned up too loud, as the body’s warning system becoming hyperactive , or as the “wind-up” phenomenon .

If this premise is accepted, chronic pain could arise in the absence of any, or any significant tissue damage to any apparently relevant body part. Or to put it another way, “[c]linical experience and extensive research suggests it is futile to look for a ‘thing’ in WAD [whiplash associated disorder] which is ‘broken’ to explain chronic symptoms” . The absence of such a “thing”, however, makes it difficult to point to a distinct organic cause for central sensitisation , and harder still to devise a definitive clinical test for it (although it has been theorised that brain changes arising from central sensitisation may be apparent on MRI, PET, and magnetoencephalography scans ).

Inevitably, then, no definitive checklist of clinical signs or symptoms for the presence of central sensitisation exists . Potential diagnosis is therefore based on the following clinical criteria :

1. Pain that is disproportionate to the injury
2. A widespread distribution beyond the injury
3. The use of the Central Sensitisation Inventory questionnaire .

A survey of clinicians has suggested that the following may be characteristic of central sensitisation:

Subjective features:

• Disproportionate, non-mechanical, unpredictable pattern of pain provocation in response to multiple / non-specific aggravating / easing factors.

• Pain persisting beyond expected tissue healing / pathological recovery times.
• Pain disproportionate to the nature and extent of injury or pathology.
• Widespread, non-anatomical distribution of pain.
• History of failed interventions (medical / surgical / therapeutic).
• Strong association with maladaptive psychosocial factors (e.g. negative emotions, poor self-efficacy, maladaptive beliefs, and pain behaviours, altered family / work / social life,
medical conflict).
• Lack of responsitivity to NSAIDs and / or more responsive to anti-epileptics (e.g. Lyrica) / anti-depressants (e.g. Amitriptyline) medication.
• Reports of spontaneous (i.e. stimulus independent) pain and / or paroxysmal pain (i.e. sudden recurrences and intensification of pain).
• Pain in association with high levels of functional disability.
• More constant / unremitting pain.
• Night pain / disturbed sleep. • Pain in association with other dysesthesias (e.g. burning, coldness, crawling). • Hyperpathia or pain of high severity and irritability (i.e. easily provoked, taking a long time to settle).

Clinical features:

• Disproportionate, inconsistent, non-mechanical / non-anatomical pattern of pain provocation in response to movement / mechanical testing.
• Positive findings of hyperalgesia (i.e. increased sensitivity to pain), and / or allodynia (i.e. pain responses triggered by normally non-painful stimuli), and / or hyperpathia within the distribution of pain.
• Diffuse / non-anatomical areas of pain / tenderness on palpation.
• Positive identification of various psychosocial factors (e.g. catastrophisation, fear-avoidance behaviour, distress).

It is worth noting that has been associated not just with whiplash, but with chronic low back and neck pain generally, chronic tension headaches, migraines, rheumatoid arthritis, osteoarthritis of the knee, endometriosis, post-surgical pain, fibromyalgia, irritable bowel syndrome and chronic fatigue syndrome .

From clinic to court room: central sensitisation in legal practice

The mind of a personal injury lawyer representing claimants will, on learning of the concept of central sensitisation, inevitably turn to the eggshell skull rule. The “eggshell central nervous system” posited by the concept of central sensitisation does seem to fit well within the principle that “if it was reasonable to foresee some injury, however slight, to the claimant …. then the defendant is answerable for the full extent of the injury which the claimant may sustain owing to some peculiar susceptibility” , even if the consequences of a relatively trivial initial injury seem out of all proportion, and even if the pathological means by which this has happened are not easy to understand, even for the doctors who specialise in this area.

The mind of a personal injury lawyer representing defendants is not, however, likely to see a case of potential central sensitisation in such simple terms. The absence of a clear medical explanation for what causes central sensitisation presents a defendant with one obvious rhetorical device to use against it. The sheer breadth and vagueness of the clinical signs and symptoms for the condition may provide another, particularly when so many of them seem to be the sorts of things which, in other cases, are often considered signs of false, exaggerated or otherwise “non-organic” injuries (as identified, for example, on Waddell’s checklist). A further problem, as illustrated perhaps by both the signs and symptoms checklist, and by the other conditions associated with central sensitisation, is that the people most likely to suffer from it may well be the sorts of people with long-standing histories of chronic and other medical conditions (and medical records of telephone directory-thickness), who often seem to attract the greatest scepticism when they bring cases of chronic pain, both for reasons of personal presentation, and because of the real causation issues their medical histories can create.

In these circumstances, getting the correct expert medical evidence – from someone who understands the concepts, can apply the diagnostic criteria in a thorough manner, and (perhaps most importantly) comes across as knowing what s/he is talking about - will be of crucial importance for both sides. As in so many other areas, an expert who ploughs dogmatically towards the same condition in every case is unlikely to be as convincing as one who considers the evidence and demonstrates a logical conclusion, particularly if the concept gains traction and the same experts come repeatedly to judge’s attention . Care must be taken to instruct an expert from the correct discipline, bearing in mind just how many disciplines self-styled pain experts can arise from. Much of the research cited in this article has been conducted by consultant orthopaedic surgeons with an interest in chronic pain. This does not, however, mean that every consultant orthopod is likely to be able to deal convincingly with the issues arising from central sensitisation.

It will vital for the expert – and the lawyers - to take proper account of the claimant’s medical history. In particular, it is worth remembering that, even if central sensitisation has been considered a central feature of chronic pain conditions generally (regardless of cause) , the initial cause for the pain giving rise to central sensitisation must still be identified by the expert. In doing so, it is important not to overlook the obvious. If a claimant really does appear to have some pre-existing condition which might be thought to give rise either to the pain suffered, this needs to be taken into account, regardless of whether the subsequent symptoms are magnified by central sensitisation or not (even if central sensitisation might be considered to have amplified whatever percentage or period of symptoms can be attributed to the index accident).

It is also useful to remember that cases of potential central stimulation are no more immune to exaggeration, malingering or downright fakery than any other case involving alleged chronic injury. Lawyers on both sides need to be aware of the multiple weapons in the arsenal which can be used to gather evidence in relation to this – from database checks and having a nose round a claimant’s social media, to cold-calling, surveillance and big data analysis.

A further important factor to consider when obtaining expert evidence is at what stage it should be obtained, and how the case should be managed as a consequence. Although it is well-recognised that, the longer pain persists following a whiplash injury, the more chance there is of chronic symptoms arising, the converse of this is that there is always a certain proportion of patients who will recover even from symptoms which have lasted several years. Accordingly, it is difficult to identify a clear point at which lawyers should be looking at their clients and deciding that pain is present of such chronicity that it is appropriate to begin investigating whether central sensitisation or some other explanation for that chronic pain is present. Again, this may be something best considered in context, for example by keeping informed about any treatment the claimant may be having outside the context of legal proceedings, and the opinions of treating professionals about the potential causes of chronic symptoms.

Conclusions: central sensitisation and “the death of whiplash” ?

If there is one fact worth remembering from this article, it is that 30 and 50 per cent of patients who suffer whiplash injuries can go on to suffer chronic symptoms of the same type. If it is correct that plausible medico-legal evidence may be available to establish a plausible causal link between these chronic symptoms, and the index accident, it may be worth claimant lawyers revising their business models to build in consideration of the potential for chronic injury in every case. In practice, this is likely to mean medical evidence being obtained much longer after instruction than has become the norm , and much more consideration being given to the client’s instructions about the path his or her injuries has taken, and the treatment being provided for it

It is inevitable that, in a legal system where the “overriding objective” seems increasingly to be reinterpreted as a requirement for pile ‘em high, sell ‘em cheap litigation, that cases are being pressed through faster and faster, and with less and less consideration. The whole structure of the portal system, with its interim payment incentives and evidence-lite provisions, has also encouraged a form of speedy justice where speed is perhaps given more emphasis than justice. Ironically, however, in light of its stated intentions, the Civil Liability Bill may be about to change this incentive system dramatically. If a combination of fixed tariff damages for injuries lasting less than 2 years, and a small claims limit bumped up to £5,000.00 is about to make low value whiplash litigation uneconomic for most solicitors, the possibility of scooping out at least a substantial number of cases which would otherwise have disappeared down that particular plug hole may make a new approach to low value personal injury litigation worthwhile for both solicitor and claimant.

Ref 2
R Stace and S Gwilym, “Whiplash associated disorder: a review of current concepts” Bone and Joint, vol 4, issue 1, February 2015
Ref 3

Stace and Gwilym, ibid.

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