A Tissue Lesion: A worthwhile pursuit….in some cases!

Submitted by: Geoff Schneider, PT, PhD and Ashley Smith, PT, PhD(c)

Clinicians and researchers are often plagued by challenges in making appropriate, evidence-informed decisions when managing their patients with persistent neck pain. As highlighted in a recent article in the Lancet (Murray et al, 2012), neck pain is amongst the leading causes of persistent musculoskeletal pain worldwide. Specifically, road traffic crashes constitute nearly one-third of the world-injury burden and represent the tenth leading cause of disability adjusted life years (Murray et al, 2012). This should not be news to anyone reading this article! Nonetheless, innovative approaches to managing those with persistent neck pain are few and far between.

In 2008, the Neck Pain Task Force reported that 50% of people do not recover after one-year post whiplash injury (Carroll et al, 2008). Of those, a significant proportion have self-reported moderate to severe levels of pain and disability. Interestingly, a subset of these individuals has an identifiable source of nociception stemming from the cervical facet joint. Studies using the reference standard for the diagnosis of facet joint pain (comparative controlled medial branch blocks) in subjects with persistent neck pain secondary to whiplash injury have reported a prevalence of facet joint mediated pain ranging from 36%-67% (Lord et al, 1996; Manchikanti et al 2002; 2008).  Once identified as a primary source of nociception, cervical radiofrequency neurotomy (cRFN) can be performed as an intervention to provide a sustainable relief of pain (Lord et al, 1996; McDonald et al, 1999; Falco et al, 2012). This procedure can be repeated with success if the patients pain returns (Husted et al, 2008; Rambaransingh et al, 2010). Of course, this approach must be taken methodically incorporating a biopsychosocial approach.

The efficiency and effectiveness of the aforementioned approach relies on the ability of health care professionals to identify those with potential facet joint mediated pain. In the late 1980’s, Professor Gwendolen Jull asserted that a physiotherapist could identify the exact spinal level of those with cervical facet joint pain, via a manual examination, with significant accuracy (Jull et al, 1988). Decades later, Jull’s ascertains were seriously questioned by the study results of a fellow Australian group of pain physician’s (King et al, 2007). Recently, we published a clinical decision guide (CDG) for the diagnosis of cervical facet joint pain (Schneider et al, 2014). The CDG followed a pragmatic clinical reasoning approach utilizing the notion that clinicians make diagnostic decisions based on the findings of a cluster of clinical tests, rather than tests used in isolation. Clinical decision guides provide should be reproducible, easy to use, make sense (clinically), and suggest a course of action (Schneider et al, 2012).

In brief, our results showed that common clinical tests used for the diagnosis of potential cervical facet joint pain (extension-rotation test (ERT), manual spinal examination (MSE), palpation for segmental tenderness (PST)) were reliable and relatively predictive when used as a three-test cluster or when used alone (MSE and PST) In particular, sensitivity of the MSE and PST was 92% (88%-97%) and 94% (90%-98%) respectively (Schneider et al, 2013; 2014). Importantly, the negative likelihood ratio associated with the MSE and PST was 0.11 (0.04-0.28) and 0.08 (0.03-0.24) respectively. The specificity and positive likelihood ratio of the three tests used in combination was 84% (77%-90%) and 4.94 (2.80-8.20). From this, one may be confident in ruling out facet joint pain, thus not referring the patient for a facet joint injection, when in fact that may not respond positively. The impact of this could be substantial from a patient centric and healthcare system perspective. Of interest, variables such as age, gender, catastrophization, baseline neck pain and disability, and psychological distress did not alter the predictive capacity of the aforementioned clinical tests. Although, the clinical utility of such a decision guide is promising, one must be cognizant that this CDG has been derived from a single sample and remains to be validated in an independent sample.

The `diagnosis` of facet-mediated neck pain is only useful if a suitable treatment exists.  One randomized clinical trial and various longitudinal cohort studies have demonstrated the efficacy of cRFN for individuals with chronic, trauma-related neck pain Lord et al, 1996; Barnsley et al, 2005; Prushansky et al, 2006) .  Radiofrequency neurotomy is a neuroablative technique, targeting the medial branches of the dorsal rami of the putative facet joint.  It is generally performed by an interventional radiologist or anesthetist.  The effects of radiofrequency neurotomy are finite, with 95% of individuals reporting 7-14 months of neck pain relief post-cRFN (McDonald et al, 1999).  Previous studies demonstrated that cRFN was successful in significantly reducing neck pain and psychological distress, and was cost effective for the management of chronic neck pain (Lord et al, 1996; Wallis et al, 1997; Bogduk et al, 2000).  Few studies had investigated other outcome measures associated with the presence of persistent chronic WAD. 

Studies on individuals transitioning into chronic whiplash have tended to favour heterogeneous inception cohorts for investigation (e.g. WAD II).  Various clinical manifestations in these individuals have been demonstrated in systematic reviews to be predictive of poor prognosis and present during chronicity.  In recent times, high pain and disability levels, high pain catastrophization and post-traumatic stress symptoms are some clinical features which have predicted poor health outcomes in individuals post initial whiplash injury (Walton et al, 2013); whilst individuals with chronic WAD tend to demonstrate the presence of central hyperexcitability (e.g. reduced threshold to elicit the nociceptive flexor reflex, widespread sensory hypersensitivity, restricted bilateral elbow extension range of motion (ROM) during application of the brachial plexus provocation test) (Stone et al, 2013).  Thus, it was uncertain if individuals in studies reported in the literature with chronic WAD included individuals with neck pain attributable to cervical facet joint nociception or were a separate cohort of individuals.  Our initial study revealed that individuals with chronic neck pain attributable to cervical facet joint nociception demonstrated similar clinical manifestations (both physical and psychological features) as individuals in the aforementioned published studies (Smith et al, 2013).  This allowed us to hypothesize as to whether the features evident in chronic WAD could be successfully modulated.  In particular, given that individuals with chronic whiplash symptoms present with psychophysical measures indicative of central hyperexcitability and psychological manifestations, we set out to investigate if these `central processes` could be successfully modulated through effective treatment of a peripheral nociceptive source (i.e. via cRFN of a putative facet joint).  The null hypothesis stated that these `central processes` and psychological manifestations would not be improved with treatment involving modulation of a peripheral nociceptive input.  Our results demonstrated that individuals significantly improved in all physical measures (including psychophysical measures of central hyperexcitability, cervical range of motion and brachial plexus provocation test elbow range of motion), excepting for electromyography (EMG) of the superficial neck muscles.  All measures (including EMG) did not significantly differ from a healthy cohort post-cRFN (Smith et al, 2014).  Pain catastrophization and psychological distress also improved significantly, however no change in post-traumatic stress measures resulted (Smith et al, 2014).  Upon return of pain, 12 months later, all measures returned to original levels.  Thus, the null hypothesis was refuted.  Our results indicated that a peripheral nociceptive input resulted in improvements in `central processes`.  The mechanisms underlying these changes are not fully understood, but varying studies in individuals with post-traumatic headaches, or undergoing joint arthroplasties point to the possibility of structural and adaptive changes occurring in central nociceptive processing within the brain following resolution of nociception.  Much work remains to be performed in this area to fully elucidate the underlying mechanisms involved, and to determine which individuals have a `primary nociceptive focus` that can benefit from such treatment, and for those where this approach is not warranted.       


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