Persistent pain is certainly a complex beast and if we are to discuss particular body regions, low back pain would have to be the kraken* of all musculoskeletal disorders. In 2018 it was still the number one cause of disability globally and has dominated the number one spot spanning nearly 3 decades (James et al., 2018).
(Please note this blog is an extensive piece of work)
The question is why?
Chronic Low Back Pain (CLBP) has been described as ‘enigmatic, due to the absence of aetiological (cause) clarity’ and ‘that when we are confronted with an unexplained complaint such as low back pain we should rethink our strategy.’ (Eriksen, Kerry, Mumford, Lie, & Anjum, 2013). As the authors highlight when causal links to pathology cannot be substantiated, reductive biomedical management is often ineffective. However, there are clinical advocates that challenge these propositions, claiming that patho-anatomical structures as a specific cause of back pain can be identified. In particular, the Intervertebral disc (IVD), facet joint and Sacro-iliac joint (SIJ) (M. J. Hancock et al., 2007). Furthermore, there are diagnostic procedures that can confirm that these structures are the source of pain.
So, with respect to the person living with back this can lead to a significant conundrum:
How can something felt so specifically (pain) with respect to location of the body not be correlated with a structure in the same area? This is the challenge faced by all clinicians, particularly with non-specific low back pain, and something I wish to explore and share in this blog.
Back pain can be categorized into two classifications – Specific and non-specific.
- Serious Pathology – This includes infections, trauma, Cancer (inc previous hx of) vascular disease (aneurysm), inflammatory disease, cauda equina etc and warrants immediate onward referral to the medical team.
- Neuropathic or nerve pathology – Any symptoms of nerve involvement that reflects radicular symptoms or radiculopathy. With appropriate diagnosis can be managed conservatively or with interventional pain management or in some cases surgically.
- Non-Specific Low Back Pain (NSLBP)– Defined as low back pain not attributable to a known cause or that the patho-anatomical** cause of the pain cannot be determined. This includes all soft tissue structures in and around the spine (Maher, Underwood, & Buchbinder, 2017).
I have highlighted part of the NSLBP definition as this in particular appears to be a contentious area amongst clinicians.
Therefore, to understand why there is disagreement to the label of NSLBP I want to attempt to explore three areas:
- Appraise a variety of evidence on why low back pain has been labelled non-specific
- The opinions of patients as reflected in qualitative evidence
- The opinions of clinicians from social media and their supporting evidence
- Appraisal of evidence on why NSLBP?
Non-Specific Low Back Pain is a contentious problem (I admit to not ever have used the term directly with patients and won’t intend to in the future). There is a split amongst clinicians that argue that the cause of back pain can be diagnosed. Investigation of the evidence that argues for specificity in back pain will be explored later. Before we explore this division, it is of particular importance to discuss the reasons why the term NSLBP exists.
The agreement of Low Back Pain as a symptom rather than a disease has been argued by many academic papers (Balagué, Mannion, Pellisé, & Cedraschi, 2012; Booth et al., 2017; Hartvigsen et al., 2018; Maher et al., 2017). This suggests that back pain is a result of something that is diseased and leads to the symptoms rather than back pain being the disease itself. Conversely, it has been argued recently that non-specific low back pain along with other persistent pain conditions (FMS, IBS, CFS) is a disease in its own right and part of a subgroup of chronic pain problems called ‘chronic primary pain’. A disease in its own right in that the new pain descriptor ‘nociplastic’ pain is understood to describe some of the underlying mechanisms (Treede et al., 2018).
Since the 1940s through to the 1980s, the ‘dynasty of the disc’ became the target of treatment as a cause of back pain (Allan & Waddell, 1989; Lutz, Butzlaff, & Schultz-venrath, 2003; Maharty, 2012). Technologies such as x-ray, MRI and CT emerged providing clinicians a revolutionary way of looking inside the body to identify pathology, and so the pendulum swayed towards trusting technical diagnostic results over clinical judgment (Allan & Waddell, 1989; Lutz et al., 2003; Maharty, 2012). Despite this ability to see inside the body, clinical trials using diagnostic imaging have identified that people can have asymptomatic pathology (Brinjikji et al., 2015; D. Chou et al., 2011; Nakashima et al., 2015). Even as far back as the 1940s and 1950s research identified asymptomatic pathology in older people (Allan & Waddell, 1989; Lutz et al., 2003). The ideology behind this thinking was understanding the ‘body as machine’ (Loftus, 2011), applying principles of structural orthopaedics and biomechanics to justify a hypothesis of the assumed correlation between pain and pathology (Allan & Waddell, 1989). The failure of the biomedical model to provide causal links between pain and pathology and a concurrent increase in disability and persistent pain rates has resulted in the genesis of nonspecific low back pain.
- Qualitative evidence of low back pain
There is an abundance of research around patho-anatomical mechanisms to back pain, but to understand back pain we need to delve into how it affects the individual. In the previous section I have discussed some of the reasons around the shortcomings of obtaining a specific diagnosis of back pain. Pain is a multi-dimensional phenomenon and to comprehend back pain beyond patho-anatomical reasoning means to consider the experience of those who live with pain. Appraising the evidence would appear to be the logical way to do this. (Note – I appreciate there are limiting factors to all forms of study and will accept arguments for and against the following paragraphs).
Often, in low back pain there is a common agreement that patho-anatomical presentations are presumed to result from an injury or a repeated loaded movement such as lifting.
Posture, bending and lifting are terms closely aligned with back pain. Public opinion from the research literature would indicate that good posture is incredibly important to protect the back (B. Darlow et al., 2014). In Darlow’s study, he makes reference to similar research conducted in other countries on the attitudes of people towards back pain. Participants were interviewed about their attitudes and beliefs towards back pain. Of interest were the following statements and corresponding percentage true scores in agreement with the statement.
The statements “Bending your back is good for it” (true score 59.3) ,“Good posture is important to protect your back” (true score 98.7) and “lifting without bending your knees is not safe for your back” (93.5) demonstrated particularly strong beliefs. Unexpectedly a further statement from Darlow’s study “To effectively treat back pain, you need to know exactly what is wrong (true score 86.2). This naturally makes sense, people want to know what’s wrong with them.
A number of the scores in Darlow’s 2014 paper were similar to those in other countries. This suggests that these beliefs are uniform in global societies.
Interestingly, whilst posture, bending and lifting as indicated by Darlow’s study identify negative views with the back, published evidence (as far back as 1965) suggests that bending your knees over bending your back is no more wholly protective of your spine (Davis, Troup, & Burnard, 1965; Potvin, Norman, & McGill, 1991; Veres, Robertson, & Broom, 2010), when lifting and that by providing an understanding of what historically is understood to be good posture may lead to a belief that lifting with anything other than “good” posture is dangerous (Caneiro et al., 2018; B. Darlow et al., 2014).
In her qualitative synthesis ‘exploring the experience of chronic low back pain (CLBP)’, Samantha Bunzli identified three themes describing the CLBP experience: ‘the social construction of CLBP, the psychosocial impact of unpredictable and omnipresent nature of pain, and the strategies employed to cope with the pain and protect against the assault on the self’ (Bunzli, Watkins, Smith, Schutze, & O’Sullivan, (2013). Her paper continues by discussing the experience of CLBP ‘may be conceptualized as a biographical suspension’meaning that individuals living with CLBP are in a state of suspended animation, their life viewed as if the pause button was pressed on their “life” video tape. Only once they were pain-free would their lives play once again.
With so much emphasis on the correlation between pain and pathology as part of biomedical reasoning, it seems an unfair stance of healthcare professionals to not consider the broader contextual factors of a biopsychosocial framework. There are two brief points I wish to make here. 1) The impact that healthcare professionals can have on LBP patients if orientated towards a more biomedical reasoning model (Ben Darlow et al., 2013; Domenech, Sánchez-Zuriaga, Segura-Ortí, Espejo-Tort, & Lisón, 2011)and 2) The misrepresentation of the biopsychosocial model. Papers have suggested that we have forgotten the bio (Mark J. Hancock, Maher, Laslett, Hay, & Koes, 2011)due to the sway towards psychosocial research or that the BPS approach has been misunderstood and applied (Pincus et al., 2013).
I would argue that there is continual research within the biomedical professions, and that we have made very little head way since Gordon Waddell’s seminal paper titled ‘‘A new clinical model for the treatment of low-back pain’’ (Waddell, 1987). Therefore it would seem reasonable that we should be broadening our perspectives more towards qualitative research, how to communicate with our patients, understand what the “bio” in the BPS model actually represents such as physiology, biobehavioural mechanisms, embodiment, how cognitions can affect the broader spectrum of what behavior represents and vice versa, not just pathology and biomechanics.
- What does social media have to say?
I am sure most who are reading this will agree that back pain is an incredibly popular topic of discussion on social media, I mean huge!. A recent twitter conversation lasted no less that 5 weeks! It also didn’t fail to bring all kinds of opinions, beliefs, biases, ad hominem attacks and just outright trolling.
All in all, the conversation and opinion was reasonably civil and respectful. So, for this final section (and also the largest) I’ve decided to consider parts of the discussion had on social media regarding clinical confidence towards identifying specific structures that are a cause of low back pain.
Let’s cut to the chase, there is a strong argument for being able to identify the patho-anatomical cause of NSLBP (Table 1). Several papers have highlighted the prevalence of specific structures as the source of low back pain. Most commonly these include the Intervertebral disc (IVD), facet joint and SIJ. A selection of papers have been identified below.
|Paper Title||Author(s)||% of prevalence of structure|
|Systematic review of tests to identify the disc, SIJ or facet joint as the source of low back pain||(M. J. Hancock et al., 2007)
|39% = Disc
15% = Facet Joint
13% = Sacro-iliac Joint
|Pain Originating from the Lumbar Facet Joints||(van Kleef et al., 2010)||5% – 15% = Facet Joint|
|Pathomechanisms of discogenic low back pain in humans and animal models||(Ohtori, Inoue, & Miyagi, 2015)||39% – 42% = Disc|
|Mechanisms of low back pain: a guide for diagnosis and therapy||(Allegri et al., 2016)||39% = Disc
30% = Facet Joint
10% – 62% = SIJ dependent on the block selection
|What Is the Source of Chronic Low Back Pain and Does Age Play a Role?||(DePalma, Ketchum, & Saullo, 2011)||42% = Disc
31% = Facet Joint
18% = SIJ
Table 1 – Selection of papers identifying percentage of prevalence of structure.
It is generally accepted academically and clinically that the reliability of identifying painful structures using imaging is poor. Imaging fails to provide the investigating clinician the ability to discriminate between a structure that is a pain generator or asymptomatic (see figure 3).
The issue is that it is harder to explain why people have pain and the relationship it specifically has with the tissue. It has also led to some debates arguing the case that clinicians, (the assumption being those clinicians strongly within the NSLBP camp) are guilty of diagnostic nihilism (DePalma, 2015). My argument in response is that those clinicians in the “NSLBP camp” are not suggesting it is nothing, just that a single cause cannot be substantiated.
So how can we identify tissue structures as a source of pain?
Well the answer is we can’t. We could say the tissues are, at some point, a source of nociception (which is the transmission of noxious information), but pain is a human experience. As previously mentioned, imaging is one method, but not reliable. The current alternatives include joint blocks for facet joints and the SIJ (Bogduk, 2004). For the IVD a procedure called discography is used and will be the main focus of this remaining section.
A discography procedure aims to identify the IVD as the source of pain – referred to as discogenic pain. It’s an invasive procedure meaning that the specialist will insert a needle into the spine of the individual at the level that is presumed to be the source of the symptoms. Once the selected disc is located (the procedure is performed under imaging) a contrast solution is injected into the IVD resulting in an increase in pressure in the IVD. It is this increase in pressure in the IVD that is said to reproduce the individuals pain and then correlate that the IVD is the source of pain. The dye also helps to identify the state of the inside of the IVD, inferring that if the dye spreads to the outer aspects then 1) there is internal disc disruption (IDD) and 2) the nerves that innervate this area have been sensitized due to the injury within the IVD.
Confirmatory information is obtained if the injection of an adjacent IVD provokes no pain, the resulting diagnosis can be made that the affected IVD is the source of the pain (Laslett, Öberg, Aprill, & McDonald, 2005).
In addition to identifying the IVD as the source of pain, conservative care protocols have been developed proposing that if a rapid reduction of peripheral (leg) symptoms associated with back pain move to a more central (spinal) position with repeated or sustained spinal movements, it is assumed that the IVD is the source of pain and symptoms. This clinical phenomenon is referred to as centralization or the centralization phenomenon (CP) (McKenzie & May, 2003). Furthermore, Laslett et al., (2005) found that with application of McKenzie’s movement protocol in relation to agreed reference standards~, if a directional preference^ was identified there was a 90% specificity that the IVD is the source of pain.
As a series of papers make recommendations about the prognostic value of discography (Bogduk, 2004; DePalma et al., 2011; Depalma, Ketchum, Trussell, Saullo, & Slipman, 2011; Laslett, Öberg, et al., 2005)and utilizing Mckenzie’s movement protocol as a determinant of discogenic pain (Donelson, Grant, Kamps, & Medcalf, 1991; Laslett, McDonald, Tropp, Aprill, & Öberg, 2005; Werneke & Hart, 2001; Werneke, Hart, & Cook, 1999)it is appropriate to appraise these assertions in the following areas:
- To appraise the evidence around lumbar discography
- To appraise the evidence around mechanical diagnosis and therapy as a method of identifying discogenic pain.
Is discography a reliable method of determining discogenic pain?
Provocation discography (PD) has been claimed to be the ‘most specific procedure to diagnose discogenic low back pain’ (Manchikanti et al., 2018). The International Spine Society recommends four criteria of discography to define discogenic pain: 1) provocation of the suspect disc induces concordant pain, 2) the pain is at least 7/10 on a numeric rating scale, 3) the pain is provoked by less than 50 psi above opening pressure, and 4) provocation of at least one adjacent disc does not induce concordant pain (Willems, 2014).
However, the criteria have been criticized due to false-positive findings during the procedure such as pain being a subjective experience, or high pressures (above 50psi). It has been shown that pressure above 50psi provoke pain in asymptomatic discs (Willems,2014). In addition, PD has been linked with post-discography discitis (Willems, 2014) and acceleration of degenerative disc disease (Cuellar et al., 2016). Finally, the available reference standards for PD are claimed to be unreliable (Willems, 2014) and reference standards themselves may be subject to significant bias affecting diagnostic accuracy of procedures (Reitsma, Rutjes, Khan, Coomarasamy, & Bossuyt, 2009).
One of the many issues with PD is that whilst it is argued to currently be the most effective way of diagnosing discogenic pain once the procedure has been performed there are a limited number of procedures available to address IDD. Steroid injections have been shown to have little effect in the long-term (Deyo, Mirza, Turner, & Martin, 2009; Staal, de Bie, de Vet, Hildebrandt, & Nelemans, 2009)and spinal fusion surgery has also provided little improvement in back pain (R. Chou, 2013; Deyo et al., 2009; Harris, Traeger, Stanford, Maher, & Buchbinder, 2018; Maher et al., 2017).
Mechanical Diagnosis and Therapy
Mechanical Diagnosis and Therapy (MDT) is a popular method of diagnostic assessment and therapeutic treatment for low back and neck pain amongst physiotherapists. Originally developed by Robin McKenzie the approach classifies patient reported symptoms into subgroups based on assessment findings. As well as a subjective history, clinicians perform neurological tests and assess for motion loss, and essentially symptom modification through repeated motion and sustained posture assessment. The 3 mechanical subgroups for MDT included derangement, dysfunction and postural syndromes. An “other” subgroup considers issues that are of non-mechanical cause, serious pathology, post-surgical problems, Spondylolysis and spondylolisthesis or chronic pain.
The intention of MDT is through the use of repeated movements and/or sustained postures the patient experiences a centralization of symptoms from peripheral to more central locations around the area suspected to be the source of symptoms. Depending on the subjective history and movement assessment if diminishing peripheral symptoms are reported with a specific movement it is said that there is a “directional preference”. Studies have identified that most individuals demonstrate a directional preference (DP) to extension (Donelson et al., 1991; Werneke & Hart, 2003), with one study identifying a DP as high as 83%. Interestingly, some individuals demonstrated a DP to flexion (around 7%).
Moreover, a study by Laslett et al., (2005)identified that with relation to the reference standards of provocation discography ‘centralisation observed during a McKenzie evaluation of repeated movements (which its main aim is to determine DP and achieve CP) has specificity of 89% (in distressed patients), and among patients without severe disability or distress it is 100%’. However, in the presence of severe disability, specificity is reduced to 80%.’Therefore, it could be postulated that a majority of participants in Laslett’s study had a directional preference towards extension. What is not clear is the number of participants in Laslett’s study that were deemed At Risk, Distressed Depressive or Distressed Somatic as indicated by the Distress and Risk Assessment Method (DRAM)(Main, CJ, Wood, 1992), which may have an effect on the outcome as one component relates to somatic perceptions. The Modified Somatic Perceptions Questionnaire (MSPQ) has been widely used in general orthopaedic, rheumatology and neurosurgical clinics and specifically to identify symptoms of a non-organic cause, suggesting evidence of malingering (Bianchini et al, 2014). Therefore, what assumptions can be made about what percentage of participant numbers are classed as malingering or somatisizing if they do not experience resolution of their symptoms? I’m not a fan of the word malingering as I believe we cannot come to such conclusions about a person when there is so little we know about them. In terms of Laslett’s work I would conclude that this is rather black or white thinking, meaning that if symptoms centralise (pain and whatever else is reported) then it is definitely an organic cause (often the disc), if not, the client is essentially faking their pain.
Furthermore, Laslett, McDonald, et al., (2005) investigated if an agreement could be made between a physiotherapist using MDT and a radiologist using various invasive diagnostic procedures. The question effectively asking if a physio using MDT as a diagnostic tool was reliable compared to available reference standards for discography, facet, SIJ, hip joint blocks, epidural injections advanced imaging studies. It is noteworthy to recognize that (according to the evidence) no formal reference standard for discography appears to exist (Bogduk, Aprill, & Derby, 2013).
Based on the reference standard / expert opinion diagnoses, the chance of the physiotherapist correctly guessing the diagnosis was 13%. The results found that overall agreement on the basis of chance was between 32% and 57%. The use of the Cohen Kappa statistic was used to determine the agreement between physiotherapy diagnoses and reference standard diagnoses. Kappa scoring was 0.31 which is considered to range from minimal agreement to fair agreement (McHugh, 2013; Viera & Garrett, 2005).
Whilst there are strong advocates of the McKenzie method I think what this shows is that it can be challenging to identify with real certainty that a specific structure is the source of pain. It was not my intention to be overly critical of Laslett’s work as he does have to be commended for his commitment to a method that has been regarded by a subgroup of devotees to be the cornerstone of musculoskeletal physiotherapy practice for low back pain.
However, there are a number of questions that arise from reading and (hopefully) interpreting this extensive list of research. So, without going into great detail I will close this blog with a series of questions:
- What of the relationship nociception has with mechanosensitivity? A proportion of High-Threshold Mechanoreceptors (respond to mechanical forces) can be described as nociceptors (Dean, Gwilym, & Carr, 2013).
- What of the biochemical changes within sensory neurons at the DRG as a result of prolonged release of inflammatory mediators, resulting in a lowering of firing threshold and increase in hyperexcitability? (Edgar, 2007; Schmid, Coppieters, Ruitenberg, & McLachlan, 2013)
- Is CLBP in relation to degenerative disc a form of visceral pain due to the nociceptive afferents being situated close to and behaving like sympathetic afferents(Edgar, 2007).
- What of the association between mechanoreceptors, proprioceptors and nociceptors? Consider the recent research by Stanton, Moseley, Wong, & Kawchuk, (2017)and topical review by Moseley & Vlaeyen, (2015)
- What of pain behaviours and a high proportion of CLBP demonstrating fear towards flexion based activities. (Vlaeyen., 2013)
- What of recent identification of the nociplastic pain descriptor to reflect change in function of nociceptive pathways? (Eva et al., 2016)
- Where is the context in MDT?
To sum up
Back pain is complicated, whilst there are clinicians that sit in the “specific” camp we must consider that there are multiple factors involved in the therapeutic relationship between clinician and patient that can influence the outcome (Ferreira et al., 2013).
There are challenges with diagnostic imaging as discussed and classification systems such as MDT due to their limitations and the multiple factors associated with CLBP (Rabey, Beales, Slater, & O’Sullivan, 2015). This can also lead to difficulties determining the outcomes for people living with CLBP (Rabey, Smith, Beales, Slater, & O’Sullivan, 2017).
What can be said is that we know so much more about how something as complex as back pain (regardless of its classification) can be managed. For physiotherapists, using the knowledge we have from that of McKenzie and Laslett are likely beneficial and useful at one stage of a person’s journey, however it may not be suitable for all and it may also not prove to be any better than similar treatments (Lam et al., 2018). That is not an attempt to disregard the fact that people want to know why they have pain and what’s wrong with them. Importantly, a question that all clinicians should consider when faced with complicated cases, “Why is the person presenting in this way at this time?”
First of all, if you have read to this point then I congratulate you! I have only discussed some of the literature surrounding the reliability to identify a specific tissue structure (IVD) as a source of pain.
And if this blog doesn’t make you scratch your head and ask a few questions perhaps a quote by Dr Alf Nachemson will help you think differently:
“I’ve been studying LOW BACK PAIN for the last 50 years of my life, and if anyone says they know where PAIN comes from, they are full of sh#t.”
I hope that this blog sparked some thoughts, questions and even a rebuttal as I am always keen to learn.
Thanks for having a read
The Kraken is perhaps the largest monster ever imagined by mankind. In Nordic folklore, it was said to haunt the seas from Norway through Iceland and all the way to Greenland. http://theconversation.com/the-real-life-origins-of-the-legendary-kraken-52058
The term patho-anatomical essentially means that a structure (often an organ or tissue) on the body is diseased and within a musculoskeletal field is presumed to explain the source or cause of the clients pain or dysfunction. Thus, this would also suggest that there is a general consensus of what is deemed a normal appearance of tissue or organs.
Directional preference is defined as the repeated movement that produces centralization, or an abolition or decrease in symptoms, or an increase in restricted range of movement.
researchers use the best available practicable method to determine the presence or absence of the target condition, and such a method is referred to as ‘‘reference standard’’ rather than the ‘‘gold standard’’
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