I agree that non specific low back pain is a term long past its use-by date. It embeds ignorance into a classification system and implies that there is some value in ignorance. I would argue that back pain is specific whether we know its cause and anatomical source, or not.

It is known that back pain may be caused by any one or a combination of something like 200 different conditions. Presumably many of these will require a specific treatment to address the problem: to reduce or abolish pain, minimise disability, and / or rehabilitate to normal function (if possible). Many of these conditions will have clinical appearances that are similar – one similarity is that they all produce back pain, but will often manifest themselves in ways that do enable differentiation. If the latter were not true, then how would we be able to say that 200 different conditions can cause low back pain? Some of these conditions will have certain features in common and some of these features will logically lead to a treatment. This means that a single treatment may be of benefit for more than one condition. General exercise, NSAIDs, cognitive behavioural therapies are examples of interventions that are of value for a number of discrete conditions. However, general exercise prescription and CBT is of little value when the patient has metastatic cancer of the vertebral body, infection (or any other ‘red flag’ condition), dominant leg pain caused by compression from a disc herniation, or discogenic pain that centralizes after correction of a lateral shift and recovery of extension. These conditions need a specific treatment and it is possible to make a specific diagnosis.

If we can accept that back pain does have, in the great majority of cases, a specific source and cause, whether we know the source and cause or not, then “non-specific” LBP is not appropriate to describe the patient’s complaint. Rather it is a term that is probably best describes the clinician’s state of ignorance. If NSLBP refers to my ignorance of the cause and source of LBP, then this diagnoses my condition, not the patient’s condition. In fact, my colleagues and I have demonstrated that even with the most complex and chronic patient population, clinical diagnosis of the source and cause of back pain is possible for over 50% of cases, which is far better than what would be possible by randomly guessing the diagnosis(Laslett, McDonald, Tropp, Aprill, & Oberg, 2005). This study is by no means definitive and there are many weaknesses which we acknowledge, but it is a starting point from which we can begin to restore clinicians’ confidence in their clinical assessments. Frankly I think that the source and cause of at least 80% of back pains can be identified and most of these do not need more than a history and clinical examination. My interest has been in comparing clinical diagnoses with available reference standards, but there are other clinical manifestations that are of interest others such as those that Paul mentioned. The point here is that most back pains are specific. We can identify sources and causes much more often than is generally accepted by the writers of clinical guidelines. So let’s abandon the NSLBP label and focus on what we can do, not our ignorance.

Reference

Laslett, M., McDonald, B., Tropp, H., Aprill, C. N., & Oberg, B. (2005). Agreement between diagnoses reached by clinical examination and available reference standards: a prospective study of 216 patients with lumbopelvic pain. BMC Musculoskelet Disord. 6[1], 28.

I'd agree that non specific low back pain is a term with a lot of ignorance. It looks like by this diagnosis clinical specialist makes an excuse of non treating patient, or no searching for more thorough diagnosis. I'd like the term functional low back pain more, for it describes a state when the pain has no adequate structural damage or abnormality in the spine.

The terms ‘specific’ and ‘non-specific’ have real meanings which seem to be ignored as soon as spinal pain or musculoskeletal pain is discussed. I don’t think cardiologists and cardiothoracic surgeons would ever be happy with the term ‘non-specific chest pain’. Same goes for ‘non-specific abdominal pain etc. A patient presenting with pain who has not undergone any testing or history taking, by definition has ‘non-specific pain’. This changes to ‘specific’ as soon as a cause of pain can be ascribed to the complaint. For example, a patient presents with leg pain. The doctor looks at the leg and sees a bone sticking out through the skin and the shin looks bent where it should be straight. On taking a history, the patient describes being in a motor vehicle accident. This is not ‘non-specific shin pain’ anymore – the patient has a fractured leg. What follows is an xray that confirms the clinical picture which is followed by open reductive surgery which further confirms the diagnosis and provides the appropriate treatment. Why is back pain different just because some of the diagnoses are harder to make, or because sometimes some patients complain about severe pain but there are not external signs of injury?

What I believed has happened is that after the publication of the Quebec Task Force Report on Activity Related Spinal Disorders in 1987(Spitzer, 1987), clinicians learned that many of their cherished traditional diagnoses had little substance and that the same patient could receive many different diagnoses from different alleged experts. All the experts on the QTF panel could agree upon was that things like cancer, infection, fractures etc – the so-called ‘red flag conditions’, though rarely presenting as back pain, were able to be easily identified after appropriate diagnostic testing. The other group of conditions they could agree on was the diagnosis of disk herniation causing sciatic pain i.e. there did appear to be evidence in support of their claim that this diagnosis was reliable and there was a definitive treatment for it – surgery. Hence, three broad categories were created 1. All the nasty rare conditions 2. Herniated discs (about 5% of all cases) and 3. All other cases which became labelled as ‘non-specific’. Soon after Waddell(Waddell, 1998; Waddell, 1987) supported the biopsychosocial model and recommended that GPs and emergency doctors triage their patients into the three categories. This triaging became the de facto standard and replacement for thinking by most frontline clinicians. It is easy. I can teach my receptionist to do it in half a day’s education, the hardest part of which is to teach the neurologic screening examination. The rest is just a pain drawing and a couple of simple questionnaires to identify red and yellow flags, and a pain drawing to determine the extent and type of pain radiation. As soon as a patient is given the label ‘non-specific’ LBP, it like flipping a switch that make the brain say – there is no diagnosis and none is possible.

Since the timely and appropriate QTF publication, major advances in diagnostic techniques have been made, and there is a much better understanding of the science and mathematics of diagnostics. MRI is now widely available, controlled diagnostic anaesthetic and provocation diagnostic injections have reached a most sophisticated level(Bogduk, 2004), and clinical assessment techniques have been assessed for reliability and validity against reference standards that might not be perfect, but properly used do not deliver too many false positives and negatives. It is common to see criticisms of diagnostic injection procedures, especially provocation discography, because distressed patients respond differently to more normal individuals. Rejecting these diagnostic tests because a subset of patients respond in an inconsistent manner, would be the same as throwing out the stethoscope because it produces unreliable results in a noisy environment. The fact is that, properly used, clinical examination coupled with appropriate use of imaging and controlled diagnostic anaesthetic and provocation injections, can allow the clinician to achieve a diagnosis in the majority of cases. This makes the majority of cases that are not ‘red flag’ conditions, or herniated discs ‘specific’, providing the diagnostic tests are carried out. It may be that the appropriate tests are too expensive, or invasive, or that there is insufficient expertise available to do the tests, but that is quite a different issue. Where these reasons for not pursuing a diagnosis exist, the ‘non-specific’ conclusions has nothing to do with the inherent nature of low back pain. In reality there are no ‘non-specific’ low back pains, only states of knowledge or ignorance about the source and cause of the complaint of pain. If the state of ignorance is caused by clinicians putting their heads in the sand to avoid learning how to make a diagnosis (where that knowledge exists), this is deplorable – but regrettably common. Where a state of ignorance occurs because the examinations and tests are not available, or they cannot be justified for economic or reasons of invasiveness, then this might be reasonable. What must be abandoned is the notion that there is something about LBP that is inherently ‘non-specific’.

References

Bogduk, N. (2004). Practice guidelines: Spinal diagnostic and treatment procedures. San Francisco: International Spine Intervention Society.

Spitzer, W. O. (1987). Scientific approach to the assessment and management of activity-related spinal disorders. A monograph for clinicians. Report of the Quebec Task Force on Spinal Disorders. Spine 12[7S].

Ref Type: Journal (Full)

Waddell, G. (1987). A new clinical model for the treatment of low back pain. 1987 Volvo award in Clinical Sciences. Spine, 12, 632-644.

Waddell, G. (1998). The back pain revolution. Edinburgh: Churchill Livingstone.

Hi Mark and Gunaras,

I totally agree with your point of view and explanation. Gunaras in his response makes a suggestion for functional low back pain. This may lead to the next question: if we decide not to use non-specific, we have to re-define how we name the diagnostic result. In other words, how can we give diagnostic words to what we find. Despite the good attempt of Gunaras, the term functional is to common. It would be an improvement if we could define the cause of the functional problem. I am wondering why it is so difficult to find terms (words). Does this have to do with a lack of knowledge? For example, if we have patient with back pain, hypertone erector and fatty deposits in the multifidus, indicating musltifidus is not working properly. Flexion does not run smoothly but with a tremor. Can we give this a name which can be widely accepted as a diagnose? If not, what is missing to make this possible?

What you’re mentioning Jan-Paul, most probably would be a axial low back pain with the orthopedic cause, usually its loss of sagital balance, with overstretch of spinal muscles while standing and walking, it's really painful, though determination of balance is quite difficult for clinical diagnosis, needs wide X-rays, calculating angles and spino pelvic parameters. What I've meant by functional back pain, is the spine looks OK, with no extensive structural damage, balanced, but it hurts strongly, suggesting the pain in the brain. The reason of this pain might be hypersensitivity of central nervous system with inadequate (small) trigger causing inadequate (extensive) pain, or pain due to socioeconomic factors (patients with yellow (less probable), blue and black flags (most probable)). Every patient has functional component in his disease, the aim would be to separate those structural, who need a help of spine specialist and those functional who need a help of psychologist or psychiatrist or even yoga guru:). That’s my seeing the problem; I don’t expect it to be rules for others.

Hi Paul, there are two points in relation to your response. There is no problem with not knowing the cause and source of a patient's pain. This is not the issue. The issue is using ignorance as an escape clause to avoid effort and cost. As I said earlier, the patient at presentation before assessment is 'non-specific' because assessment has not commenced. As the assessment continues, we gather more and more data and the probability that the patient remains non-specific gets less. This is a right and proper progression. We do know what classification / diagnoses can be gathered easily and what requires more expense and invasion. I think we can answer the question as to how far investigation needs to go and whether or not invasive diagnostics is needed nor not. There are good algorithms for this available, at least at the tertiary level, and to some extent at the primary level. What we do not have is an evidence based algorithm the proceeds from primary contact (GPs and Physiotherapists in our country) through to use of hi tech imaging, invasive diagnostics and invasive treatments like RF and surgery.

The second point is regarding your description of a case scenario - multifidus wasting and fatty infiltration etc. While this scenario is associated with development of chronic pain, it is not diagnostic of anything I think. I do not know of any diagnostic accuracy statistics (sensitivity / specificity etc) for this finding in relation to any specific painful condition - do you know something I don't here? I would call these findings simply data that correlates with persistent pain. Whether it is a pathologic condition causing pain or not I don't know. Is it a secondary phenomenon or a causative one.? I think this matters. If is a consequence of something else - THAT is what needs treating first, then re-hab the muscle afterwards. Otherwise, training the muscle will achieve little of lasting benefit and may actually worsen the patient's pain. On the other hand, if this collection of findings is a primary pathology that cause instability and failure of control, thereby putting stress on structures that cause pain eg the discs, facet joints etc, then obviously directing attention to the deficient muscle is the primary concern. This latter case is the only time I would be happy to call the multifidus dysfunction a diagnosis. In essence, I would say that the term 'diagnosis' should be limited to identification of source and causes of patient's complaints - in this case, pain.

Dear Gunaras and Mark,

This is a very interesting development. I'l try to reflect on what you've written. First Gunaras, you interpret my 'patient' from a structural perspective (x-rays etc). And if that is not the case, then you switch to the psychological side. Mark, your point is that we have do put more effort in the diagnostic process, trying to find (structural?) causes. In the second part of your reply you wander how my representation could be part of diagnostics. And I agree with you there is information missing.

Now I hope you can agree that that this discussion is not about who is right in this patient. It is about how we look at things. I presented this patient because we (our institute) assume there is something going wrong in the patients feedback systems (proprioception). I refer to the studies of Aage Indahl and Hodges etc. The idea is that due to changes in the afferent information the effferent output (motorcontrol) changes, leading to altered motor patterns. You won't find anything on x-rays. It is not primarily psychological. And it is difficult to put your finger on. (Changes in) proprioception cannot be measured.

My point is: we have a patient with non-specific back pain, we all agree this is non-sense because we think we can make this more specific, but next we all choose different ways to specify the complaints.

If we want to abandon the garbage bin 'non-specific' we have to find way's to agree on more specific diagnoses. In doing so we might have to not just stretch, but really leave the paths of structural analysis and diagnosis.

What I fear is that probably our knowledge and ability to point out what specifically is going wrong in these patients is still insufficient (in that I assume it is lack of knowledge more than ignorance, mark) Until that time I think back pain will be frequently labelled 'non-specific'.

Jan-Paul: this is all very rational. I agree. A different perspective does not have to be a challenge representing some sort of Kuhnian battleground. There are, in reality, different perspectives. When we first discover the existence of some phenomenon or object, that discovery is just the beginnings of mapping out its identity. When looked at using different tools, at different times and from different angles, the phenomenon may seem different but it is the same thing. Progress is not just about discovering new entities and phenomena, but also integrating the disparate bits and pieces of knowledge about any given phenomenon or object.

This reminds me of the tale of the blind scientists investigating an elephant:

Where the whole world is talking about a large mammal (non-specific) we all study some aspect (trunk, leg, tail) and try to describe and understand the elephant.

I think the constructive question is: HOW to put this information into one piece.

Of course we can keep on publishing stuff from our own perspective, but it feels like a hard way to come together. Couldn't discussions and exchange of views through research gate be more helpfull?

Interesting discussion. NSLBP - is the catch all. and rules out the limited "specific" cases. Makes efficacy studies difficult to conduct and unless a better system is developed then the future of clinical LBP studies will probably trend towards Clinical Predication Rule models of analysis. i.e. idenitifing responders / non-responders etc.

I think "recurrent episodic LBP" is an under utilised term that may have a place in the rehabilitation strategies particuarly if they attempt to modify behaviours and manage perceived and real risk of the recurrence. (i.e. CBT and Low load training).

I agree Garry. NSLBP should refer only to those to whom a specific cause cannot be ascribed. Thus a person with a 'red flag' is non-specific by definition 'NSLBP' until imaging or other diagnostic test has identified the causative mechanism / pathology. Similarly, if a patient's pain can be made to centralize with a repeated movements examination - low tech, inexpensive and take 10-20 minutes - the pain is highly likely to be discogenic4, If the pain cannot be centralized and three or more pain provocation tests provoke typical pain (a further 2-5 minutes of exam time) , then there is a high probability (80-90%) that the pain is of SIJ origin5. These two classifications account for over 50% and possibly as high as 80% of so-called NSLBP cases. This sort of clinical examination is available at primary care almost everywhere in the developed world. To call 90% of all cases of LBP is, to quote Ron Donelson from his book2, is to ignore the elephant in the room. The use of the tern NSLBP is not only redundant but factually and terminologically incorrect. To my knowledge, the studies our group have carried out and published have never been replicated (excepting the SIJ studies by Peter van der Wurff’s group, and only up to a certain point3;6;7). This is a weakness in the evidence. Attempts to replicate the discography studies have been made by an Australian based group (Mark Hancock and Chris Maher), but funding was rejected on the basis that discography was unreliable and the need for a diagnosis was not seen as a priority. These issues could fill pages of dialog and I apologize in advance to the Aussies and Dutch if it appears that I have given an inaccurate impression in my brief summary here. Despite these obvious weakness, the evidence is strong enough to challenge the idea that the group of patients that do not have ‘red flags’ or evidence of radiculopathy are therefore ‘non-specific’. It is a linguistic dinosaur and should be assigned to history (1980’s – 1990’s) where it once had a role in shattering the scientifically unearned confidence of clinicians regarding diagnosis or the cause of pain.

You are right Garry. Efficacy studies that lump heterogeneous cases together for treatment as if they were homogeneous are useless and produce results that contradict what clinicians world wide feel to be true – that is a high proportion of cases that respond rapidly and predictably to certain treatments. The fact that RCT after RCT that commit this fundamental methodological error find that no treatment is as effective as any other treatment, or that any differences in treatment effects are small and insignificant8. Identification of appropriate subgroups in the NSLBP spectrum became a priority in the late 1990’s1. This call has strengthened, not weakened, so RCTs that commit the error should be ignored, regardless of their otherwise meticulous methodological quality. Clinical prediction rules have their place but there are problems there too. Determining rules for selecting patients for specific treatments is pragmatic but not patient friendly in the sense that it begins with the idea that we have certain treatments available – manipulation, stabilization training, traction etc. Then it proceeds to find out which patients will respond to those interventions. It sounds reasonable, but is it? Shouldn’t we be looking at the patient first? Shouldn’t we be finding out what this individual patient has and needs, rather than selecting patients that suit our treatments? Again, this is a long discussion, but I think we are in agreement that it is time to stop using NSLBP and refer directly to identifiable subgroups that make diagnostic and therapeutic sense and have good evidence in support. RCTs should then focus on these

Reference List

1. Borkan JM, Koes BW, Shmuel R et al. A report from the second International Forum for Primary Care Research on Low Back Pain: Reexamining priorities. Spine 23(18), 1992-1996. 1998.

2. Donelson R. Rapidly reversible low back pain: an evidence-based pathway to widespread recoveries and savings. Hanover, New Hampshire: Selfcare First, LLC, 2007.

3. Kokmeyer DJ, van der Wurff P, Aufdemkampe G et al. The reliability of multitest regimens with sacroiliac pain provocation tests. J.Manipulative.Physiol.Ther. 25(1), 42-48. 2002.

4. Laslett M, Oberg B, Aprill CN et al. Centralization as a predictor of provocation discography results in chronic low back pain, and the influence of disability and distress on diagnostic power. The Spine Journal 5, 370-380. 2005.

5. Laslett M, Young SB, Aprill CN et al. Diagnosing painful sacroiliac joints: a validity study of a McKenzie evaluation and sacroiliac joint provocation tests. Aust J Physiother 49, 89-97. 2003.

6. Szadek KM, van der WP, van Tulder MW et al. Diagnostic validity of criteria for sacroiliac joint pain: a systematic review. J Pain 2009;10:354-68.

7. van der Wurff P, Buijs EJ, Groen GJ. A multitest regimen of pain provocation tests as an aid to reduce unnecessary minimally invasive sacroiliac joint procedures. Arch Phys Med Rehabil 87, 10-14. 2006.

8. van Tulder MW, Koes BW, Bouter LM. Conservative treatment of acute and chronic nonspecific low back pain. A systematic review of randomized controlled trials of the most common interventions [see comments]. Spine. 1997;22:2128-56.

Hi Mark, agree. CPRs are a pathway of investigation to inform diagnosis as

Much as treatment. It is not a service strategy. But may be - yet to be verifed- as good as some of the clinical diagnostic / classification efforts undertaken in clinics around the world. The fundamental issue raised in heterogenous dx in RCTs translates to a parallel problem in justifying specific interventions - many therapists have lols of assessments but limited variability in their treatment choice. Some people advocate a specific intervention for all nslbp ( say stability) this could relate to an lack of DDx as much as efficacy. Cheers

@Garry. Fair enough. Are there really people in the world who would offer stabilization training for cases of LBP? Is it possible that their bag of tricks is so poverty stricken? Have you ever tried to teach a patient with acute LBP how to contract their transverse abs?!!! I shouldn't really be surprised though. There are those that manipulate every case and I do recall in the dim dark ages of my early career that many of my colleagues would give heat and ultrasound to everything including back pain.

I've done a bit of TrAb stuff and underrstand what you are saying. But unless you say it is good for everyone then the question would be if not everyone then who? Back to the DDx question:-) . The flow of conversation has already raised the Blind man and elephant ( used in 'stability' commentaries years ago) the other analogy waiting to be expressed.. is that if you only have a hammer in your toolbox everything you want to treat looks like a nail. Over and out. GTA

This discussion is getting more and more interesting.

One aspect that is highlighted is that diagnostics can be more precise and specific. However this is only a deepening of the old path. The real intriguing question is: what to do with the relatively large group of chronic pain patients where still no structural cause can be pointed out. (it is really to short cut, to make this mainly psychological).

Some previous responders made some somewhat condescending remarks on stability training, however the theme of stability refers to a fundamental underlying question related to non-specific backpain: Could it be that not-optimal function of the spine could lead to pain (without structural findings)? If we agree on that, do we call this physical and lasting dysfunction pathology? If so, how would we describe the diagnose?

If we do not call this pathology, a next question is: could we agree on the notion that physical dysfunction (disturbed or altered motor control) in the end could lead to structural changes (specific back pain!). If so, where does pathology start?

And yes Mark, there are people in the world that provide exercises for chronic back pain patients to improve controll of their spine, and with succes! But you need a very big bag of tricks!

@ Paul. I agree that more precision and specific diagnosis is deepening an old path, but it was very shallow to start with. Also we are finding that the path is both wider and narrower than we expected. Some old diagnoses seem to be little more than fanciful items of poetry - like piriformis syndrome (as it is usually described), SIJ dysfunction (movement and positional anomalies not SIJ pain). I am deeply suspicious of the term "myofascial pain" and "back sprain" is not a diagnosis. NSLBP is not a diagnosis either. So much for narrowing the path. However, back pain can indeed be discogenic but it seems that there are several different types of disc pain. Radicular pain is usually secondary to a disc herniation but can be caused by a variety of other pathologies, like facet joint cysts stenosis and various benign and malignant neoplasms. So the path is widening too.

If I have appeared to be condescending towards stabilization training I apologize, for that was never my intention. As far as I can tell, the only conservative care treatment for confirmed SIJ pain that has ever had any success in my hands is stabilization training. I abandoned manipulation of the joint years ago as it almost always aggravates true intra-articular SIJ pain. There are large numbers of patients with discogenic pain who benefit from stabilization training. In those cases where the pain has been centralized (these are discogenic), part of my management to help reduce recurrence rate, is to initiate stabilization training. We do not have evidence of efficacy in this subgroup yet but it is a good topic for future research. Those patients who have proven discogenic pain (positive provocation discography), but do not centralize, I routinely treat with stabilization training, as the only alternative is quite invasive.

While I have used stabilization training (with a reasonable bag of tricks but not as extensive as others) since the mid 1990's, I still think there are major problems with the DIAGNOSIS of instability. The problem simply comes down to diagnostic criteria. Are they reliable, and against what reference standard are you going to estimate diagnostic accuracy? This is a difficult but perhaps not impossible task. From what I observe, just about everyone that a stabilization enthusiast examines, has problematic motor control. It seems that it is a "disease" like "SIJ dysfunction" (as distinct from "SIJ pain") - the diagnostic tests are highly sensitive but specificity is poor and as yet cannot be subjected to proper diagnostic research because of the lack of a reference standard.

Hi Mark, No hard feelings. Just thought stability training could do with some credits. On the other hand I agree with you that determination of disturbed motor control needs objective diagnostic criteria. I recognize your observation of motor control enthousiasts seeing motor impairment everywhere. I hope the development of objective test will allow us to include motor impairment in the diagnostic process and make non-specific back pain more specific, even without structural findings......

In addition to my previous response I would like to add that supposedly there is a fundamental choice we have to make to get any further. IF we want to incorporate motor control problems in back diagnostics, we have to agree that a diagnosis not necessarily is coupled to some structural finding. This in medical, but even more legal business is a tricky issue. It is very safe to keep saying that functional problems aren/t pathology. It keeps the legal procedures easy. This however is no proper reason to keep disturbed motor control or other function problems out of the diagnostic area.

@ Jan-Paul. Conceptually I have no problems with including motor control problems in a diagnostic / classification schema once the criteria and the target entity have been defined and validated adequately. However the problem I foresee is connecting a particular patients pain to the motor control abnormality. It is a question of specificity. Many patients will have motor control problems that are secondary to or accompany pain arising from a specific structure, but when can you say that the motor control is the initial or even primary pathology? There is no problem for a patient to have more than one diagnosis e.g. discogenic pain and nerve root pain (two anatomic diagnoses), or SIJ pain which is either caused or perpetuated by motor control problems (an anatomical and a biomechanical diagnosis - this is quite common I believe). There is no problem in combining diagnoses from quite different dimensions for a given patient e.g. discogenic pain and psychosocial distress issues perpetuating work disability etc. In fact we do this all the time. However there are problems for the scientific community and other stake holders like insurance companies and government agencies. To transpose the issue to another area like the knee: everyone knows that a fractured patella literally switches off the quadriceps mechanism i.e. the motor control problem is a reflex inhibition of the quads secondary to the painful stimuli from the patellar fracture. Clearly you do not treat the fracture by strengthen the quads – you cant strengthen them anyway because of pain inhibition. However the notion that minor motor control issues could actually cause a knee problem is a different story, and it was very difficult to achieve acceptance of this reverse relationship. Jenny McConnell has fought a long battle in that regard. Orthopaedic surgeons still are divided about that even now - some 30 years later. The same battle will occur in relation to the lumbo pelvic region but even more so because of the much greater anatomical and biomechanical complexity, plus there is a whole sector of back pain researchers who regard back pain as a psychosocial event and reject an anatomical / biomechanical approach entirely.

Do you think that the criteria for this biomechanical diagnosis is close enough to fruition? I have a vested interest in this as Tom Petersen from Denmark, and I are in the early stages of updating our classification system[1-4]

Reference List

[1] Laslett M, Van Wijmen P. Low back and referred pain:diagnosis and a proposed new system of classification. NZ Journal of Physiotherapy, Vol. 27 1999. pp. 5-14.

[2] Petersen T. Non-specific low back pain: Classification and treatment. Doctoral Thesis Lund University, Department of Physical Therapy, 2003.

[3] Petersen T, Laslett M, Thorsen H, Manniche C, Ekdahl C, Jacobsen S. Diagnostic classification on non-specific low back pain. A new system integrating patho-anatomic and clinical categories. Physiotherapy Theory and Practice, Vol. 19 2003. pp. 213-237.

[4] Petersen T, Olsen S, Laslett M, Thorsen H, Manniche C, Ekdahl C, Jacobsen S. Inter-tester reliability of a new diagnostic classification system for patients with non-specific low back pain. Aust J Physio, Vol. 50 2004. pp. 85-91.

The problem with NSBP is that it is a diagnosis of exclusion, as has been mentioned above. Therefore, we should resist labelling people with this, but not abandon this term from our list of differentials. If we were to do this, we would have to abandon a plethora of terms from our diagnosis list, from 'chronic daily headache' to 'atypical chest pain'.

It should also be discussed as to the need for abandoning this diagnosis of exclusion - if there is an extremely rare cause of back pain, with the same treatment as that of NSBP, but requiring a multitude of tests to diagnose, is it in the patient's interests to put them through all of these tests to simply say 'we woul dhave given you this treatment regardless'?

I believe there should be more research into this area, as it consumes a huge proportion of healthcare time, especially in the primary care setting. However, we need to remember to not whet our academic whistles at the expense of exposing out patients to unnecessary and potentially damaging investigations if they do not add to the clinical management.

@David. Quite correct David. The term NSLBP is appropriate when knowledge of the source and cause of back pain is unknown. Your point about rare causes is fair, but the problem, as it seems to me, is that when 90% of cases remain "non specific" just because you have excluded the less common causes (radicular pain / radiculopathy, and those that might have serious illnesses), we cannot rest comfortably there. It is quite clear that this polyglot of cases we call NSLBP is so heterogeneous that well conducted RCTs cannot seem to identify treatments that are much better than doing nothing, despite every back pain clinician observing that some cases do well with one treatment but not with other treatment. There ARE identifiable subgroups that the term NSLBP disguises - to the detriment of patients and great cost to society. Your point about putting patients through unnecessary tests when the treatment is the same regardless is correct in one context but not another. What I mean is that if the tests were expensive and /or invasive, and were applied to large numbers of patients for whom the results did not alter treatment (MRI to all NSLBP cases is a classic example), then this would be wasteful and clinically useless. However, if you had an inexpensive test could be done at primary care level is not invasive / dangerous and will rapidly identify those that respond rapidly to a specific treatment, you would want that rolled out across the country wouldn't you? For this argument, lets say that no such test exists - then you need to do research to try and find that test - if it exists. Paul hints at the possibility of a test which I suspect is a clinical examination issue that will identify those cases where mechanical instability and motor control is the issue. I have mentioned several times that there is a test that has excellent prognostic properties, can be carried out in primary care and is inexpensive and non-invasive. This is McKenzie's testing for the centralization phenomenon and directional preference. The proportion of cases that are identified may be as low as 25% or as high as 75% according to the studies, and the reasons for the uncertainty here is unclear - probably a matter of definition. Why hasn't this test been made as ubiquitous as, say laboratory tests for c reactive protein for infection? Probably because it is not taught in medical schools and is not sexy like lab tests or high tech imaging. However there are very few countries in the developed world where this knowledge and the practitioners skilled in the testing process (takes about 15-20 minutes of time - another problem for GP's), NOT available. Just so you don't think I am some sort of crazy evangelist with a chip on the shoulder, I would like to state up front that I have no vested interest in pushing this testing procedure beyond the academic, and I want to say that this testing procedure is not the only valuable procedure with similar qualities. There are others that identify other subgroups. Its just that there is a huge lag between evidence that is available and uptake at the administrative and public health levels.

Absolutely, I agree, I used the invasive test as an example, but completely agree with your expensive test example as well - why deprive others of important funds for their tests/investigations/treatment by spending this money on tests which do not change management.

I think that the use of other examination techniques or tests, such as the one you mention should be subjected to large-scale trails across multiple centres. With the great number of patients with 'NSLBP' presenting to primary care and being referred on to secondary or tertiary care, the numbers needed to identify whether a test or intervention is worthwhile would be reached in a very short time.

@ David. What sort of trial are you thinking about. There is data, some it of good /excellent quality already.

I would like to see something along the lines of: a real-world trial, whereby patients who get diagnosed with NSBP then get randomised into basic investigations and symptomatic control (as per current treatment) or further investigations to try and identify the exact cause with a tailored treatment. The outcomes and treatment choices for each could then be compared to see if tailoring treatment is a good use of resources and whether it benefits patients, or if it simply panders to our desire to get to the bottom of what is wrong, despite the potential for it to not make any changes to our treatment.

This is an 'off the top of my head' suggestion and is very basic, but I wanted to facilitate/initiate a discussion about this.

The important thing is to not break this down into 'the best treatment for disease X - treatment A vs treatment B' in patients with isolated disease, but to look at real world patients with NSLBP, with all of their comorbidities and different socioeconomic factors etc. (i.e. the opposite of a phase 1 clinical trial for a new medicine) and see how we can create data useful for clinical practice in the real world.

p.s. I completely agree, this is an area with large amounts of high-quality work in the literature, but I think this area lacks something in the practical aspects of whether to investigate and tailor treatment or simply treat the patient symptomatically as the investigations make no changes to management plans as we are unable to provide anything specific to the given diagnosis.

This is not to say I do not think patients with specific diseases should have clinical trials for new treatments of sub-sets of 'NSLBP' but that this should be separate to our work as clinicians who are trying to find the answer to "what is the best management plan for the next patient walking through my door with NSLBP?"

Dear Mark and David,

Your scientific drive is very motivating and stimulating. Finding way's to get NSLBP more specific is good. But I get this idea we are pulled back into the same track again. Mark already pointed out that this track can be broadened and for sure I also believe we can find more specific structural pain causes. On the other hand, the amount of patients where no specific cause is found is so vast, that we really should wonder whether the path of structural diagnose is a fruitful one. The knowledge we have on pain is sufficient to understand that pain does not necessarily have to be caused by some structure. Beware: I am not saying that consequently it has to be psychological. On the contrary. There are many aspects in human function that physically trigger pain sensations without obvious structural change. One very simple one is muscle soreness. This seems to simple to be true, however there are vast amounts of patients who -because of their posture (sleightly flexed)- continuously activate their erector. Due to malnutrition musclesoreness can occur in these patients.

What I realized in an earlier discussion with Mark is that diagnose traditionally is based on finding the specific structure (or pathological process like in cancer). There seems to be a problem with including dysfunction in pathology: when a human body is exhausted, motor patterns can be very distinct from normal. We do not call this pathology. But when motor patterns alter due to changes in proprioceptive feedback for example after an ankle sprain, can we call this pathological? In this case you might say the pathology lies in the altered ankle ligament structure or innervation and we should look for these structural changes. Or is it sufficient to point out the altered motor patterns?

@ Jan-Paul. I think I see where the problem with diagnostic specificity, structural specificity that is, comes from. There are several comments that reveal the issue I think: “..the amount of patients where no specific cause is found is so vast, that we really should wonder whether the path of structural diagnose is a fruitful one.” This is factually incorrect. The proportion of patients for whom a structural diagnosis is not “vast”, it is relatively small actually – even with the most difficult, distressed and chronic case load[11] a patho-anatomical diagnosis is possible for about 50%. In less complex patients, the centralization phenomenon and the related clinical sign, directional preference, is present in at least 50% of cases[1;2;4-10;15-23]. I am sorry for this long (but not exhaustive) list of references but I find I must continually point out that these phenomena are not scientific or bizarre curiosities lacking investigation. They are the most studied clinical phenomena in back pain science and they consistently reveal themselves to be reliable and valid. To return to my argument: If over 50% of cases have signs which point directly to a structural source of pain[12;13...

Are we talking about acute or chronic pain?

@ Jan-Paul. Either. In the severe non - ambulatory acute i.e. Emergency Department presentation, simple triage is all that is possible in many cases. In the ambulatory acute or chronic, the full assessment is possible in the great majority of cases. Where examination is not possible then NSLBP is appropriate until the examination can be done. In the acute and subacute cases, classification / diagnosis as I have characterized it, is possible for 75-80% whereas in the severe chronic about 50% of cases it is possible.

@Mark,

Actually your last figures confirm my expectance. Acute and subacute seem more related to specific lesions and can be identified. In the chronic there will also be patients where a specific lesion can be identified, however there is a vast portion that remains problematic (about 50%).

Now, what I am wondering is to what extend you can agree upon this way of thinking:

The specifc findings in backpain can be considered the tops of the icebergs. People with back trouble mis-use their back for a longer period of time (function problem). (First time ocurrences due to some trauma excepted). The body responds in physiological way to this mis-use and consequently structural changes occur. We focus at these structural changes because they are tangible. But these structural findings are merely a result of the underlying functional problem. What I am trying to say is that structural findings and function problems should not be divided in specific and non specific, because they both belong to and are different aspects of one continuum. From this perspective it can be argued that making the distinction between specific and non specific draws an illegitimate line in our understanding of the human body and its complaints.

Pain has always specific cause so does pain in the low back. Do not understand inventor of this name. Like all sheep following one..?

Low back pain or lumbago is a common disorder involving the muscles and bones of the back which affects about 40% of people at some point in their lives. Low back pain is pain, muscle tension, or stiffness localized below the costal margin and above the inferior gluteal folds, with or without sciatica, and is defined as chronic when it persists for 12 weeks or more. Nonspecific low back pain is pain not attributed to a recognizable pathology (e.g., infection, tumor, osteoporosis, rheumatoid arthritis, fracture, inflammation).

Here I totally agree with Alexia that pain is purely a sensory response which should be always specific to the affecting structures. Unable to locate or identify the pain prodicing structure should not be easily replace by naming it is non-specifi LBA.

Instead of misnomer, I would recommend to improve the method of assessment inorder to identify the pain producing structure (musculoskeletal, referred pain from internal organs, psychosomatic etc...). More over the choice of treatment also would be always specific. Diagnosis as non-specific should not have any specific interventions which may be a questionable whether the LBA will improve or not.

Regards

Ratan

Call it what it is!  It is a subluxation of the sacral axis with an anterior rotation of the innominate bones on the sacrum. 

 DonTigny, RL: Sacroiliac 201; Dysfunction and Management: A biomechanical solution.  Journal of Prolotherapy 3:644-652, 2011

Normally I resist the temptation to post negative comments, but I cannot let Richard Dontigny's post go without immediate comment. Back pain is not caused by a single disorder. It is the symptom experienced with about 200 different known disorders, the great majority of which are quite rare. The terms "back pain", lumbago, "non-specfic low back pain" are terms describing a person's symptomatic complaint. These terms are not diagnoses. A diagnosis is identification of the source and cause of a symptomatic complaint. Richard's fixation on a single cause is regrettable, especially since the disorder he refers to depends entirely on the use of clinical tests known to be unreliable for its diagnosis[12;15]. What evidence that does exist for reliability of measurement of anterior innominate rotation, does not use the tests that Dontigny uses[1]. Furthermore, there are no published data on the validity / diagnostic accuracy of the clinical tests for "subluxation of the sacral axis with and anterior rotation of the innominate bones of the sacrum", though it may be possible to compare Dontigny’s tests with Adhia and Bussey’s reference standard. Even if that were done, there is no demonstrable relationship between anterior innominate subluxation and the experience of back pain despite Dontigny’s claims. It is certainly not appropriate to call back pain a single unproven, purely theoretical mechanical disorder.

There are pathologies of specific structures that are known to cause back pain. The most common tissue sources of back pain are the intervertebral discs, the lumbar zygapophyseal (facet) joints and the sacroiliac joints in order of prevalence (40, 15 and 13% respectively)[2]. Prevalence data provided may well be based on information gleaned from secondary and tertiary care environments, not primary care. These three anatomical sources of pain do have reference standard methods of diagnosis (controlled provocation discography, controlled medial branch blocks, controlled sacroiliac joint blocks)[3-5]. The validation of controlled diagnostic blocks as a reference standard diagnostic tool has been discussed in detail[6]. It must also be noted that clinical tests for discogenic and sacroiliac pain have been assessed for validity against appropriate reference standards[9-11;14]. While clinical tests for facetogenic pain lack validation, there are clinical prediction rules that may be used to select patients for whom more invasive testing with medial branch blocks is appropriate[8]. Clinical testing for discogenic and facetogenic pain need further testing, but provocation tests for sacroiliac joint pain have been validated in independent confirmatory research[7;13;14]. Let’s stick to facts and published data and not indulge in unsupported assertions of opinion.

References

[1] Adhia DB, Bussey MD, Mani R, Jayakaran P, Aldabe D, Milosavljevic S. Inter-tester reliability of non-invasive technique for measurement of innominate motion. Man Ther 2012;17:71-76.

[2] Bogduk N. The anatomical basis for spinal pain syndromes. J.Manipulative.Physiol.Ther., Vol. 18 1995. pp. 603-605.

[3] Bogduk N. On diagnostic blocks for lumbar zygapophysial joint pain. F1000 Med Rep 2010;2:57.

[4] Bogduk N, Aprill C, Derby R. Lumbar discogenic pain: state-of-the-art review. Pain Med 2013;14:813-836.

[5] Bogduk N, Derby R, Aprill CN, Lord S, Schwarzer A. Precision diagnosis of spinal pain., Vol. Comprehensive Musculo-Skeletal Patient Management: McKenzie and Beyond 1998.

[6] Engel A, MacVicar J, Bogduk N. A philosophical foundation for diagnostic blocks, with criteria for their validation. Pain Med 2014;15:998-1006.

[7] Laslett M, Aprill CN, McDonald B. Provocation sacroiliac joint tests have validity in the diagnosis of sacroiliac joint pain. Arch Phys Med Rehabil 2006;87:874-875.

[8] Laslett M, McDonald B, Aprill CN, Tropp H, Oberg B. Clinical predictors of screening lumbar zygapophysial joint blocks: Development of clinical prediction rules. The Spine Journal, Vol. 6 2006. pp. 370-379.

[9] Laslett M, Oberg B, Aprill CN, McDonald B. Centralization as a predictor of provocation discography results in chronic low back pain, and the influence of disability and distress on diagnostic power. The Spine Journal, Vol. 5 2005. pp. 370-380.

[10] Laslett M, Oberg B, Aprill CN, McDonald B. A study of clinical predictors of lumbar discogenic pain as determined by provocation discography. Eur Spine J, Vol. 15 2006. pp. 1473-1484.

[11] Laslett M, Young SB, Aprill CN, McDonald B. Diagnosing painful sacroiliac joints: a validity study of a McKenzie evaluation and sacroiliac joint provocation tests. Aust J Physiother, Vol. 49 2003. pp. 89-97.

[12] Robinson HS, Brox JI, Robinson R, Bjelland E, Solem S, Telje T. The reliability of selected motion- and pain provocation tests for the sacroiliac joint. Man Ther 2007;12:72-79.

[13] Szadek KM, van der WP, van Tulder MW, Zuurmond WW, Perez RS. Diagnostic validity of criteria for sacroiliac joint pain: a systematic review. J Pain 2009;10:354-368.

[14] van der Wurff P, Buijs EJ, Groen GJ. A multitest regimen of pain provocation tests as an aid to reduce unnecessary minimally invasive sacroiliac joint procedures. Arch Phys Med Rehabil, Vol. 87 2006. pp. 10-14.

[15] van der Wurff P, Hagmeijer RH, Meyne W. Clinical tests of the sacroiliac joint. A systemic methodological review. Part 1: reliability. Man Ther 2000;5:30-36.

Mark

You should not jump right in like that without examining the evidence that I have presented.. I have been studying the SIJ for over 50 years.  In 2006 I identified a bony transverse sacral axis at S3 sacral.  This is not an axis of the sacroiliac joint. Several axes have been suggested for the SIJ, but most are impossible because of the overlying iishial tuberosity.  The  sacrum is essentially a non-weight bearing joint with a balanced loading.  You could diagnose 200 different possible causes and still miss it. Jessi Timgren, Finnish physiatrist has been treating  reversible pelvic asymmetries, based on my method for over ten years and found an incidence of 98% in over 500 cases.  He also claims immediate relief of pain in most cases.  If you have a higher incidence of pain relief I might take a look at your stuff, but I sincerely doubt it.  I have had an incidence of total relief of back pain in over 95% of about 8,000 cases over 38 years of practice.  Tell me Mark, what percentage of cases of low back pain do you have free of pain within 10-15 minutes.   I was filmed last year by  Great  Seminars to demonstrate my method.  Everyone on the film crew had back pain and was free of pain with the demonstration.  You  might want to look at my website.

http://www.thelowback.com.  How it works, why it hurts and how to fix it.

http://personal.fimnet.fi/vastaanotto/fysiatri_Timgren/RE-ESTABLISHING%20PELVIC%20SYMMETRY%20.html

http://www.greatseminarsonline.com   Corrections on actual patents with immediate relief of pain.  Five CEUs

Write to me AFTER you examine the evidence.

Richard DonTigny, PT

I am sorry Richard, but any claim to 95% or more cases relieved of pain without presentation of published data from RCT's cannot be taken seriously. Provide the references, upload the papers and I promise to read them. Jessi Timgren needs to present his material for critical review. Even if there are pelvic asymmetries in 98% of 500 back pain cases, it does not mean they have any necessary relationship to the complaint of pain. Perhaps the complaint of pain causes the asymmetry and not the other way around?

I am uninterested in CEUs or watching videos. I have also taught in many places with live unselected patients and know that the success rate on courses is much higher than in the clinic. Have you ever read the book Elmer Gantry by Sinclair Lewis? I certainly do not have a 95% success rate it is true, but then it all depends on how you measure 'success'.

I have just read Jussi Timgren's material accessed from the link you provided. I am sorry but the content is deeply flawed and highly unlikely to be published by any serious scientific journal in its current form. When was the study carried out? Here are just some of the problems a quick scan reveals: retrospective, unblinded, outcome measures not defined or valid, interventions include manipulations of the cervical spine as well as the lumbosacral region without reasonable justification etc. I have reviewed many papers for publication and know that I would recommend a scientific journal to reject the manuscript. Simply not good enough to consider seriously as a contribution to scientific discussion. Just saying something over and over again does not add validity, and the number of advocates of an idea bears no relation to fact or truth. Science is not a matter or opinion and it is not a democracy. There are processes that must be adhered to before ideas can be accepted as adding to the body of knowledge.

In 1964 I had a patient with LBP and after the best treatment I could give her, she was no better- so we made another appointment.  She called the next day to cancel as she was free of pain.  I asked her what she did to get rid of the pain and she reluctantly told me that she fell off of her tractor.  I asked her if I could buy her tractor, but she refused.  I realized that she had a reversible biomechanical problem and that if I could find the nature of that problem I should be able to correct it in my department.  By 1965 I had about 80-90% of consecutive patients free of pain following treatment.  I wrote it up for PTJ and they sent it back...FOUR times.  The last time they just told me their editors were in contention with my findings  and to seek another journal, which I did, but I didn't get published until 1973.  In my great ignorance, if I had any idea that there were 200 different things that could cause back pain, I would not have even begun to analyze the biomechanics. but I did and I am quite happy here, just knowing about biomechanics.

It must take you days to do an examination.  How do you begin to treat it?  Is there any immediate relief?  I have found out some really neat stuff about the SIJ.  Did you know that it is essentially a non-weight bearing joint with a balanced ligamentous loading which functions as two force couples? Or that in the long straddle position the sacrum flexes laterally toward the side of loading to create a force-dependent oblique axis and then rotates on that oblique axis to drive counter rotation of the trunk, which  decreases loading of the femoral head.  The things I could tell you about pathomechanics ...... Did you know the dysfunction in anterior rotation puts a vertical shear on the sacral axis and separates the sacral origin of the piriformis from its ilial origin at the superior margin of the greater sciatic notch. Also separating the sacral origin of the gluteus maximus from its ilial origin on a line from there to the trochanter.  I had a patient whose separated GM used to roll under her trochanter when she sat causing her all manner of grief.   I couldn't get anyone to look at it because of course it was an impossible lesion.      I was a bit brief with my description of back pain.  It is still a subluxation of the sacral axis, from an anterior shearing of the innominates cephalad on the sacrum.   I guess we will just have to agree to disagree. Sorry if I have upset your day a bit.

Be well.

Richard DonTigny, PT

My day is not upset in the least but thanks for your concern!

You continue to provide anecdotal evidence of successes. Reading tea leaves, rubbing on arnica or ingesting a placebo can all claim similar examples. I have seen cases of back pain come and go without apparent cause. Indeed there are countless cases of miraculous cures that bear no relation to the intervention presumed by the provider to have been the active agent. The only way to address this confounding phenomenon is to conduct proper trials and subject the results to peer review. I too have had rejections of papers by good journals - every career researcher has - but in the end the material emerges if it has any merit. That is not to say that all published material has merit. On the contrary, even terrible papers can get published in top journals[1;3]

Your responses effectively hoist you on your own petard. You state that you have been looking at these issues since 1964, and claim to have discovered that the vast majority of cases of back pain are caused by a single easily corrected mechanical fault in the sacroiliac region. In the last 50 years, just about every conceivable idea has been studied to some degree, and many ideas have been pursued endlessly in research only to be found to have limited value. You must seriously ask yourself the question: “If your method is so easy and so effective, why has it been ignored for 50 years by mainstream and peripheral researchers?” Do you think there has been an orchestrated campaign to hide the truth? Could such a successful technique be hidden? It is not as if you have remained in the closet Richard. I have attended several of your lectures over the years and as recently as 2004 attended your course in Reno, so I know that your information is ‘out there’. Furthermore, if you really believe that such an orchestrated campaign exists and has been successful, then why haven’t you found the resources and time to do the quality of research that is required? This latter is probably unfair, as I know that finding the resources for research is not easy and a practitioner in a rural or remote area can often struggle in this regard. However, not a single quality RCT in 50 years? It is hard to believe that if there was a grain of truth in your claims of over 95% success rate in a condition that is acknowledged world wide as very difficult to be able to demonstrate efficacy[2;4-6], someone, somewhere, would have explored your suggestion with sufficient rigour to be published in some journal, somewhere.

Sorry to spoil your day a little.

Reference List

[1] Aprill C, Laslett M, McDonald B. Side of symptomatic annular tear and site of low back pain: is there a correlation? Spine (Phila Pa 1976 ) 2003;28:1347-1348.

[2] Koes BW, van Tulder MW, Thomas S. Diagnosis and treatment of low back pain. BMJ 2006;332:1430-1434.

[3] Slipman CW, Patel RK, Zhang L, Vresilovic E, Lenrow D, Shin C, Herzog R. Side of symptomatic annular tear and site of low back pain: is there a correlation? Spine 2001;26:E165-E169.

[4] van Tulder MW, Koes BW, Bouter LM. Conservative treatment of acute and chronic nonspecific low back pain. A systematic review of randomized controlled trials of the most common interventions. Spine 1997;22:2128-2156.

[5] van TM, Koes B. Low back pain (acute). Clin Evid 2004;1643-1658.

[6] van TM, Koes B. Low back pain (chronic). Clin Evid 2004;1659-1684.

I just spent an hour on   a response and it disappeared.  It was a sign I am too verbose.

Briefly now.  I described a bony transverse  loading axis for the sacrum  at S3ssw, verified by Gracovetsky in Vleemings 2007 book. This has changed my biomechanics somewhat (1,2)   The sacroiliac joint is non-weight bearing.  Primary loading of the sacrum is on the posterior interosseous ligaments.  Secondary loading is on the sacrotuberous ligaments in the opposite direction.  Primary loading equals the secondary loading.

Dysfunction is a subluxation of the sacral axis, not the sacroiiiac joint.  There is a common painful point just below the PSIS from a stretch on the long posterior SI ligament.  There is another common pain point at the PIIS where the innominate puts a vertical shear on the dual origin of the piriformis, which also separates the sacral origin of the glute max from its ilial origin on a line to the trochanter.

See also Murakami and Davis

 DonTigny, RL: Sacroiliac 101; Form and Function; A biomechanical study.

Journal of Prolotherapy  3:561-567, 2011 

  DonTigny, RL: Sacroiliac 201; Dysfunction and Management: A biomechanical solution.  Journal of Prolotherapy 3:644-652, 2011

  Davis P, Lentle BC.  Evidence for sacroiliac disease as a common cause of low backache inwomen.Lancet.1978;2:496-497.

Murakami E. Tanaka Y, Aizawa T. Ishizuka M, Kokubun S. Effect of periarticular and intraarticular lidocaine injections for sacroiliac joint pain: Prospective comparative study. J of OrthopaedicScience.2007;May12(3):274-280.

But none of that answers the question that lbp is multi factorial or all just sij disfunction

This might help.

]  Murakami E. Tanaka Y, Aizawa T. Ishizuka M, Kokubun S. Effect of periarticular and intraarticular lidocaine injections for sacroiliac joint pain: Prospective comparative study. J of OrthopaedicScience.2007;May12(3):274-280.

@ Ralph. There is a proportion of cases where it is known that there are more than one tissue source of pain[2]. In this study of over 200 consecutive patients undergoing reference standard diagnoses (provocation discography, facet joint blocks, SI joint blocks and other guided procedures), 10% of patients had more than one established source of pain. This does not answer your question though since ‘multifactorial’ doesn’t just mean more than one source of pain, but is a broader concept. The broader concept ‘multifactorial’ could also mean that there are other issues affecting the patient with back pain, such as central sensitization, illness behaviours (fear avoidance, anxiety states etc). Indeed, in that study we found that about a third of patients satisfied criteria for clinically relevant depressive symptoms. I believe that paper may be downloaded from Researchgate if you are interested.

With regards to the paper by Murikami et al 2007 et al [3] recommended by Richard Dontigny, it may appear to the uninitiated that since almost all patients responded to SIJ blocks, so SIJ pain is common. This is not correct. The patients (N=50) were already selected as having SIJ pain, and so a high proportion of positive responses is expected. This study was not intended to assess prevalence of SIJ pain. Also, it seems that the injections were not controlled so the potential for false positives can be expected to be 35-40%[1;4]. Here is the abstract from PubMed

BACKGROUND: The sacroiliac joint (SIJ) can be a source of low back pain. Previous studies indicated that SIJ pain could originate from both the joint capsule and the posterior ligamentous tissues. It has not been clarified as to whether an intraarticular or periarticular injection procedure is more effective for this type of pain. The purpose of this study was to evaluate the effect of two injection procedures prospectively. METHODS: After a pain provocation test, an intraarticular injection of local anesthetic (2% lidocaine) was performed on the first 25 consecutive patients with SIJ pain and a periarticular injection on another 25. The periarticular injections were given to one or more sections of the posterior periarticular area of the SIJ and to another section in the extracranial portion. The effect of these injections was assessed using the "restriction of activities of daily life" scoring system from the Japanese Orthopaedic Association. RESULTS: The periarticular injection was effective in all patients, but the intraarticular one was effective in only 9 of 25 patients. An additional periarticular injection was performed in 16 patients who experienced no effect from the initial intraarticular injection and was considered effective in all of them. The injection into the middle of the periarticular area was more effective for SIJ pain. The improvement rate after the periarticular injection was 96%, which was significantly higher than that after the intraarticular injection, which was 62%. CONCLUSIONS: For patients with SIJ pain, periarticular injection is more effective and easier to perform than the intraarticular injection and should be tried initially

Reference List

[1] Dreyfuss P, Schwarzer AC, Lau P, Bogduk N. Specificity of lumbar medial branch and L5 dorsal ramus blocks. A computed tomography study. Spine 1997;22:895-902.

[2] Laslett M, McDonald B, Tropp H, Aprill CN, Oberg B. Agreement between diagnoses reached by clinical examination and available reference standards: a prospective study of 216 patients with lumbopelvic pain. BMC Musculoskelet Disord., Vol. 6 2005. p. 28.

[3] Murakami E, Tanaka Y, Aizawa T, Ishizuka M, Kokubun S. Effect of periarticular and intraarticular lidocaine injections for sacroiliac joint pain: prospective comparative study. J Orthop Sci 2007;12:274-280.

[4] Schwarzer AC, Aprill CN, Derby R, Fortin J, Kine G, Bogduk N. The false-positive rate of uncontrolled diagnostic blocks of the lumbar zygapophysial joints. Pain, Vol. 58 1994. pp. 195-200.

Hi gus, give me a moment to find and read your refs. A link would be useful

instinctively, I'd say, injecting sij will obviously effect/affect the rest of the factors and give the illusion, it all comes from the sij, yet the sij is such a key structure is that evidence that it is vastly the main driver to non spec lbp? Does treatment need to be specific if it's non specific? Do studies separate pts that are from prolonged sitting away from those of high activity?

try to keep personal comments clean, this is RG not the usual forums we debate in

 I have noticed that you can get the same relief in the affected sacroiliac joints by flexing each innominate posteriorly and downward on the sacrum a  couple of times.  This also frequently reverses pelvic asymmetry.

Richard DonTigny, PT. 

DonTigny, RL: Sacroiliac 101; Form and Function; A biomechanical study.

Journal of Prolotherapy  3:561-567, 2011 

 DonTigny, RL: Sacroiliac 201; Dysfunction and Management: A biomechanical solution.  Journal of Prolotherapy 3:644-652, 2011

Hi Ralph.

Nice to see your question getting some responsess from some well-known names in this field of back pain research. I have dissected the presentation of non-specific low back pain using cluster analysis (using Clustan Size & Shape algorhythms) and the results have been summarised in a small booklet called "Low back pain, some real answers"(tfm publishers) which is easily found by checking on Google for that title and my name (Brian Sweetman). The classification using a laptop system has been used on a couple of thousand cases.

At present I have two particular interests following on from that work. Both may well interest Mark Laslett from New Zealand who has given a long answer on your site.

1..........The first has to do with the interpretation of "Downings test" which has long been used falaciously to diagnose Sacroiliac joint problems. However, patients with late stage ankylosing spondylitis have SI joints that have been welded & fused solid but can still get leg lengthening / shortening with this test. Our large database indicated that the problems associated with a "stuck" test have troubles at the thoraco lumbar junction (YES, check it out!!!) suggesting that the hip twisting affects  the psoas muscle origins.

2........ Secondly we hope to publish on the Mackenzie sciatic syndromes which may not need surgery. Our cluster analyses have identified two interesting groups, one seen in younger people and the other in older women. There is much clinical detail describing each group.

               Best wishes

                                  Brian

Sorry, I meant Jan Paul. Also I meant "algorithm" rather than I have got Rhythm (see bit about Clustan & "algorhytm":-). To be pedantic the term "algorism" is even more correct than algorithm!

                        Yours   Brian (not Bryan)

Hi Jan Paul

I was not answering your question!

But it is tautological to ask if "non-specific" can be specified because it implies that we are not clever enough to specify or else there are no differences to be specified (non-specific aka undiagnosed, undiagnosable or nothing to diagnose)

To address this philosophical conundrum, we learnt a lot when learning how to use cluster analysis. Roughly in the order of our learning curve =

1. EXPERTS DIFFER. The first crude analysis showed that there were greater differences between our "experts" than there were between low back pain syndromes. (i.e. our team examined patients differently and believed in different syndromes!) {answer = all to use a fixed examination protocol}.

2."INCIDENT" LITTLE HELP. The causative initial incident was not much diagnostic help. (i.e. each syndrome could be caused several ways, and the same type of incident could cause different syndromes){answer = very crude options of direct lumbar trauma; any other incident; or no obvious incident}

3. PSYCHOLOGGICALS  NO USE. Psycho social factors no use wharso ever!!! (SO pleased to be able to leave this approach to all our colleagues around the world who were obsessed.) {answer =  only patients with "claims" suffered differently!):-(

4. TESTING the TESTS hopeless. To undertake reliability and repeatability testing  of all the tests would have taken centuries! {answer = the cluster analysis would have "failed" to utilise tests that were too flaky because they would have been near random and thususeless}

5. CLUSTER "AMATEURS". Few researcherse tried cluster analysis and then usually only tried once. (They usually tried techniques that only measure severity such as Wards technique which was available early on. This is like lining up a regiment of soldiers by hight with a smooth gradient and no distinct sub groups. It would not have distinguished between the fat and the thin, officers vs regulars, the lame vs the fit et cetera. {answer = tried many algorithms till found those that distinguished "shape" from "size".

6. SYNDROMES WORSE if BAD. Problem 5 aoove requires "standardisation" to allow for differences caused by severity. {answer = mild cases had fewer symptoms, signs, disability, hadicap and emotional response (see "3")

7. WHICH TESTS TO USE?? If you dont know how to tell different specific syndromes, how can you know which tests distinguish them. (i.e. use as many tests as possible within practical limits). {answer = eliminate tests that serve no use as you go along and add in others people recommend}

8.HOW MANY "SPECIFIC" SYNDROMES ARE THERE? There are some mathematical/statistical measures which change abruptly when you hit the right number (but they were of only marginal help) {answer = check a wide range of options; we checked from 2 to 15. Clinical aspects ruled out the extremes} [caveat ~ every case is different to a certain extent]

9. PROBABILITY INDEX (Pi). Our system supplied a probability index. If this is high it suggests the diagnosis is correct for that particular case. If it is low and below 1.0 it implies that important features are missing or possibly that they patient has two conditions with perhaps one occurring long before the other but leaving residual confounding evidence to confuse matters. Alternatively it may be a syndrome that has not been recognised in the system). [so study the cases with a low probability index]

10.VALIDITY ONLY AS GOOD AS YOUR TESTS. Regarding the above problem (9), the system cannot recognise a syndrome if you have not included an appropriate test. {answer = keep on trying!}

11. THE KNOWN HELPS. To include some syndromes/cases that you know exist such as a prolapsed intervertebral disk with nerve root compression. If the cluster analysis cannot distinguish these cases, please change tack!!!

12. much moree, but enough.

13. RED FLAGS not included in these exercises

14. Best wishes, Brian

Happy Christmas. .....  the big NSLBP Question is = to split or not to split? (and how to split?)

Summary =  I have now had a chance to review all the correspondence. 1367 hits and 48 posts. Splendid! A lot of detail but what is the main underlying theme of the dialogue? And does it answer the NSLBP question?

the Answer is = Yes or No depending on the purpose. (and do the3 splitting by finding the best diagnostic tests)

Introduction = Virtually any test can be of some use in splitting up the back pain picture, but some tests are "better" than others. The relative effectiveness ("better") of such tests can be identified statistically (see elsewhere) so that they are lined up from best to worst to useless. Afterwards you can try and find out how and why each test does its hatchet job. Even response to treatment is a sort of test!

To try and tackle the problem from the other way round is almost an impossible task unless you are very very lucky to hit on the perfect set of tests  at the outset. There are endless theories (spellcheck = fairies) and hypotheses and expert opinions imaginable. This is possibly why there has been so little progress in this field of research.

So, what is the practical answer?

Method = Do as many therapeutic trials as you like (preferably with several single mode treatment groups and even a control group). But ensure you have the best set of diagnostic tests you can muster for every patient at the outset (i.e. complete data set) and try and ensure that some of those tests are used in common with all the other studies researchers undertake. If you can also make sub diagnoses according to several different systems the collaborative effort will hopefully yield results eventually. If not, you will at least learn how incompatible the various paradigms really are, and then better research strategy may emerge.

Result = the term NSLBP will it come extinct.

Conclusion = Happy New Year.  Yours, Brian.

Have you been to www.thelowback.com.  How it works, why it hurts and how to fix it. ? Briefly, the sacrum moves to drive counter rotation of the trunk, which decreases loading to the femoral head.  Dysfunction comes with an anterior shift in the line of gravity with lifting, bending, lowering, etc. The innominate(s) rotate anteriorly on the sacrum and put a vertical shear on the sacral axis at the PIIS. This puts  a measurable vertical movement on the PSIS.(1)  This movement will separate the sacral origin of the  g, max from it's ilial origin and the sacral origin of the piriformis from it's ilial origin.   The g. max muscle separation can go from the PIIS to the trochanter. . Much more on line.

. DonTigny, RL:  Measuring PSIS movement. Clinical Management 10:43-44, 1990

It’s non-specific for a good reason.

First off, there is no “back pain”, ALL pain is in the brain, ALL pain is a perception, an interpretation, a guess. There is a tissue issue which sends a signal via nociceptors to the receptors in the brain to make a determination of potential harm. An important point, as harm could effect function and therefore survival. But and this is the important bit, a tissue issue does not necessarily cause a pain issue and a pain issue does not necessarily come from a tissue issue. Correlation is not causation, but we get fooled the relationship must mean cause and so non-specific is the only reasonable diagnosis. If a brick hit you, that’s specific the rest is all guesswork.

We’ve been subtly brainwash over the years through how we use language to be very Binary in our thinking; Good verses Evil, Heaven verses Hell, Communism verses Capitalism, Democrat verses Republican, Muslim verses Christian. And good posture verses bad posture. Most clinical problems have multifactorial causations rather than specific ones but we like to blame something rather than except the obvious, the shear randomness of complex probability chaos, (known as, shit happens).

Second, there is no good or bad, only human thinking makes it so. A Tsunami, an earthquake or meteor is neither good nor bad, it’s the human devastation it may cause that is bad. The only reason a plague pathogen is so bad, is it doesn’t know it’s in a human, the pathogen is relatively harmless in a cow and assumes it’s in a cow, it doesn’t serve the pathogen to kill of the host, otherwise it can’t pass on to another host. But we are human centric, we like to anthropometries everything. We really do think we are the center of the Universe. A good example of this, is the belief in hot and cold, actually there is no such thing, it’s just hot or cold in relation to us. For silly example, a Venusian visiting our planet would die of the cold in our desert, because they are so used to being near the Sun, and conversely, a Plutonian would die of heat exposure in the north pole.

Ever had a pt. who’s back is so bad they are locked upright where they daren’t bend forward or back or sideways or even rotate? Looks like good posture and it is…it’s the only place where they aren’t in pain or least pain. In fact, they are in a posture that is least threatening to the stressed tissue. So there is no specific thing as bad posture and such no such thing as back pain so…

Thirdly, mechanical loading does not cause pain. We mechanically load our backs all the time, that’s what it’s there for. An increase of stress possibly via mechanical loading on an articular structure that the nociceptors affect as a potential tissue threat can be interpreted as pain. Tissue threat causes pain, mostly. One can be bitten by a snake and not feel a thing or we can have a paper-cut that goes through the VAS scale roof.

What causes tissue threat are found design limits, those limits can be high, in elite athletes or low, in academics who are chained to the desk 24/7. First, stress a tissue design limit, then cause a tissue threat, cause a nociception, cause perception of harm, cause pain, cause protective spasm, cause postural distortion. That chain does not start with a postural distortion but… postural distortions or foot anomalies mean the design limit is easily found.

This explains why, “treating lbp specific or not according to the response to movement has been proven successful”. Create movement without tissue threat, no pain, create movement with tissue threat, yes pain. Or restrict movement toward the threat area, no pain. No movement, no threat and slower healing and maladaptation through atrophy, maladaptation through mal-believed limits etc. etc. and these lead to postural distortions. Postural distortions don’t lead to pain in any gymnasts, acrobats, contortionists and dancers I treat, because those postural distortions they do for a living, don’t cause any tissue threat. Dysfunction doesn’t come with an anterior shift in the line of gravity with lifting, bending, lowering, im doing it right now as I type; strange, no pain. Now if my tissue design limit is found whilst doing those moves, then dysfunction, YES. Adverse shearing causes tissue threat, movement doesn’t.

With my colleagues that interpret MRI’s for a living, they have a term called VOMIT, (victim of over medical imaging technique) because they know, pts can have major structural tissue issues and no pain or loss of function, and conversely one can MRI a pts brain and know they are in pain yet not find any tissue damage at all. There is no way at all of knowing, what we see on the MRI is specifically causing the pain.

Because of binary thinking, we need to know who or what to blame and with binary thinking we can take credit for fixing the pt. Even the term, “Fix a bad back” is a poor term, do we really want to create a fixation in a back, I’d have thought our job is to unfixate a locked joint or muscle etc.? Personally I think it’s the million generations of our families that pass on that genetic success, we need to thank. We are abnormally normal, and normally abnormal, a long line of successful mutations. This explains why lbp is “a poorly defined syndrome”, it can’t be defined and explains why we get a lot of negative results, as well as false positives and false negatives.

We all are and want to be unique, just like everyone else. We have all the vestigial, asymmetrical, anomalies running around our bodies, and they on the whole work fine, for the vast majority of us. Usain Bolt was born with scoliosis. Why would the vast majority purposely run around consistently making things immediately not work for themselves? The vast majority work on self interest.

Hi.    On the topic of splitting up NSLBP into "ultimate truth" syndromes I would add  some commentary on how to show how good or bad the various tests (symptoms, signs, investigations etc) are using analysis of variance.

F Ratio.   The F ratio can help show the usefulness of the variables for diagnostic purposes. The variance ratio (6, 293) is a result of invariate variance, being the ratio between group variance to within group variance. In this instance the number 6 refers to a 7 sub group solution (n-1), and the 293 stands for a clinical sample of 301 cases (301-7-1). The greater the figure, the more useful the variable. T values and principal components and factors  show other things. 

For example, from a shortlist of 25 variables;-

An unilateral absent ankle reflex helps diagnose an S1 nerve root compromise due to prolapsed intervertebral disc and scores a massive 118. However it could have done better. There are still some problems. Some people would not include this in NSLBP though it does serve as a reference point diagnosis accepted by most; and there are of course other causes for a lost ankle reflex and even this test is subject to observer error. And should one distinguish an S1 from an L5 or L4 nerve root compromise if one is simply classifying  different sorts of back problem.?

Pain switching sides between episodes scores 65 which is indicative of  inflammatory sacroilitis.

Posterior column painful features as an index scores 38.

Leg pain (sciatica loosely defined) only scores 16.

Age at onset of back pain scores 6.

Anterior osteophytes on x-ray schools 5.

Gender scores 1That is almost zilch.

These were whittled  down from a starting selection of nearly 400 variables. Sadly we could not include "all" tests and did not include "centralisation and peripheralisation". This was in part due to starting work on the studies before those McK concepts were readily available. Response to the extension exercise regimen was not that much help. Furthermore we cannot make guestimates concerning  centralisation as we recorded exacerbation but not amelioration with the various anterior and posterior column tests (nearly did, but had to make the system shorter and more practical for routine use). Nor have I found statistical data even showing weak correlations of centralisation with other single one off tests that could have been linked via group identities.  ? Any help here please? I know that single tests do not  work so well as the full centralisation testing but we hope to publish on two "McK type syndromes" in the  near future from very unexpected indirect statistical Clustan analysis findings.

But if researchers for the different paradigms could show how their specific tests compared with other commonly used tests some progress might be made.

Also I recommend cluster analysis. I was talking on the train to a university student whose department had discovered a new type of Sabre tooth Tiger, They did  not publish this when they found out from where the bones were found  that the two "species" lived in the same area, though type  one was bigger than the other and realised that this was merely one species but they had simply found the differences between the males and the females of the one species! So all the understandings came after making the appropriate findings. I did not get round to asking about the fossil  lumbar vertebral  evidence for back ache with a bite.

Happy New Year, Brian

When pain is predictably provoked by mechanical stress, and eased by its alleviation, we quickly implicate a mechanical, or at least peripheral, nociceptive mechanism, and apply diagnoses like mechanical low-back pain that justify our favoured peripherally directed interventions. While the logic is attractive, what if central processes could mediate this presentation? Centrally mediated pain masquerading as peripheral.

Harvie recently investigated the idea of centrally-mediated mechanical symptoms (Harvie et. al 2015). The study involved twenty-four people with the type of persistent neck pain problems seen in everyday practice, and all with pain on rotation. They performed head rotation to their first onset of pain (P1), in three virtual-reality conditions where the amount of rotation that they saw did not match reality. Instead, the viewed rotation was more or less than was actually occurring, creating an illusion of movement that was different to actual movement. Remarkably, pain with movement depended not only on how far people actually moved, but how far it appeared they had moved.

“Mean (circle) and 95% confidence interval (error bars) for the range of motion to first onset of pain presented as a proportion of the mean range of rotation for the neutral condition. When the visual feedback suggested less movement, the first onset of pain (P1) was delayed by 6%, when the visual feedback suggested more movement, P1 7% sooner.

That pain with movement can be reliably modulated by the (visual) suggestion of more or less movement (i.e. by a non-mechanical input) is significant, and prompts us to reconsider the mechanical presentation.

In the past, perceptions such as pain were simply considered a read-out of incoming information. However, it has become clear that we could not make sense of the world if sensory information was not first filtered and arranged by our subconscious. In the case of visual perception, for example, the infinite array of colours, edges and shapes are arranged by our subconscious into the meaningful objects that we see and understand. Certain rules seem to govern this process — such as the way objects are arranged according to continuity of lines, colour and motion. The rules that govern the construction of pain, while only recently receiving attention, appear to involve the brains analysis of information relating to bodily danger. Nociception is the most obvious signal of danger to the body — but not the only one. Specific movements for example, might also become signals of bodily danger because of their meaning derived from association with injury. This would explain how (visual) signals of movement may have come to be a contributor to pain in these people with neck pain.

While ample research supports the idea that signals of threat influence pain, this study suggests specifically that information about the body in space (whether visual, proprioceptive or vestibular) that has been associated with an injury, might be relevant signals of threat. Indeed their influence may even result in a clinical pattern that appears mechanical, but is in fact centrally driven.

The treatment of threatening pain-associations is an ongoing field of study. In the meantime I think that there are a few things we can do to better align clinical practice with the threat-based understanding of pain that this finding aligns with. Firstly, we can expand our minds and clinical assessments to identify both nociceptive and non-nociceptive sources of threat (guaranteed we wont treat something we don’t assess!). Secondly, we can leverage our skills in education and behaviour therapy to encourage thoughts and actions that counter threat.

So, why diagnostic uncertainty?  In the majority of patients a definitive cause for LBP cannot be established (Krismer & van Tulder, 2007) and many patients report feeling uncertain about their diagnosis. Diagnostic uncertainty may impact how patients feel and cope with their pain and they may continue searching for the causes of their back pain instead of focusing on other important aspects of their lives. But – here comes the interesting part about this construct – research (Serbic & Pincus, 2014a) has shown that patients’ perception of their diagnosis is not clearly related to the diagnostic labels received from their health care providers, even when patients agree with the label. For example, many patients who believe that there is something wrong (structurally) with their backs, yet undetected, also report having agreed with their diagnosis and/or explanation. This might reflect patients’ belief that the diagnosis is correct but does not capture the true severity of their condition; that it fails to capture other factors beyond the, or possibly that they believe the diagnosis is inaccurate, but are not comfortable disagreeing with their provider. As a consequence of this, in the current study we assessed ‘perceived’ diagnostic uncertainty.

Why pain-related guilt? In the absence of a clear cause for their pain patients may feel that their pain is not legitimized and may feel guilty about this. Feeling guilty about their pain may not only increase depression, but may result in increased disability-related behaviours. Previous research (Rhodes et al., 1999; Serbic & Pincus, 2013; Serbic & Pincus, 2014b) has shown that pain-related guilt is a common experience among LBP patients and that it includes several aspects.

 Therefore, one hypothesised mechanism via which diagnostic uncertainty might be linked to disability and mood is through feelings of guilt. We wanted to examine this hypothesized pathway, and alternative models in which pathways between these variables were reversed (e.g. in one of them mood preceded guilt, rather than the other way round, which in turn lead to diagnostic uncertainty and disability).

 Our results showed that all tested models were viable, which may suggest a cyclical relationship between diagnostic uncertainty, guilt, mood and disability, but further (longitudinal) research is needed to confirm and clarify this.   Overall, in all tested models, guilt, and especially social guilt, was associated with disability. Diagnostic uncertainty was associated with guilt, but only moderately. mood (increased anxiety and depression) was also associated with guilt.

 As previously indicated, there is a need to identify and intervene on additional factors; our findings suggest that two of these factors may be diagnostic uncertainty and in particular pain-related guilt. Available interventions only partly address diagnostic uncertainty in that they include elements of education about LBP, and there is no explicit goal or method of intervening on pain-related guilt.

 In addition, it is important to examine how practitioners can effectively reassure patients, for example by targeting diagnostic uncertainty through validation/legitimization of patients’ suffering.

 Dr Danijela Serbic and Professor Tamar Pincus

Etiology:  This is a pathological shift of the force dependent sacral x axis and of the innominates on the sacrum in anterior innominate rotation vertically as a result of a loosening of the sacrotuberous ligaments during, lifting, bending, lowering, pregnancy or a postural forward head.

Dysfunction occurs with an anterior shift in the line of gravity when lifting, bending, lowering, pregnancy, a postural forward head or a pendulous abdomen.  The resultant anterior innominate rotation loosens the sacrotuberous ligaments slightly, interrupting the function of the force couple.  The innominates rotate caudad anteriorly on the sacrum at the sacral axis making the legs appear longer and creating a diastasis or a subluxation of the axis at S3.  The PSIS move cephalad on the sacrum, stretching the long posterior SI ligament and putting a vertical shear on the sacral axis at the PIIS.  The ilial origin of the piriformis muscle is separated from its sacral origin causing piriformis syndrome and sciatica.  The sacral origin of the gluteus maximus is separated from its ilial origin on a palpable painful line from just below the PSIS across the buttock to the trochanter.  Note how the sacral origin of the piriformis and the gluteus maximus both stabilize the sacrum as the innominates rotate anteriorly forcing the separation. (Fig. 4)  Anteriorly the acetabular axis rotates downward and posteriorly causing the legs to appear to increase in length.  The effect is a false multifactorial etiology. 

Correction of the subluxation is a simple manual posterior rotation of each innominate on the sacrum. The legs will get shorter with correction and the muscle separations will approximate.  The immediate relief of pain in all affected areas with the posterior innominate rotation proves the existence of the subluxation, If this were any other type of injury, relief would not be so rapid or complete.

Incidence:  Shaw, orthopedic surgeon at the Topeka Back and Neck Center, did a study of 1,000 consecutive patients with low back pain and found that 98% had this dysfunction.  His surgical rate for herniated discs dropped to 0.2%. 

Richard L. DonTigny, PT

Independent Researcher

81 North Shore Drive #10

Belgrade, MT 59714

USA

[email protected]

Submitted to Researchgate June 12 2016

I am responding to Brian John Sweetman · 27.63 · 187.69 · Researcher

And to some extent Ralph Samwell.

John states “..Nor have I found statistical data even showing weak correlations of centralisation with other single one off tests that could have been linked via group identities.  ? Any help here please?” I am not sure what sort of correlation you are seeking John, but relationships between variables acquired in a patient’s history or physical examination and data about what painful pathologies that patient has or does not have, are certainly available. In fact this was precisely what we attempted to do in a number of studies which were designed in accordance with recommended STARD guidelines. [1;10] The statistical values of sensitivity, specificity, positive and negative predictive values, and the summary statistics: positive and likelihood ratios are recommended. We also examined a large number of clinical variables including centralization, and as you also found, most had a poor relationship to reference standards for discogenic pain, facet joint pain, sacroiliac joint pain and radicular pain. The results have been published and are in the public domain[3-9]. In the case of clinical examination variables being able to identify sacroiliac joint pain, our results have been replicated in part, a different sample, in a different country, using different examiners. [11] The results achieved by these latter researchers are remarkably similar[2]. I believe that these studies (and there are others I have not included here) actually do seek a relevant and diagnostic relationship between clinical tests and diagnoses of subgroups of the low back pain population. The subgroups are diagnostic ones and do reflect tissue and structural sources of pain. No doubt there will be many who will argue that the reference standards in the studies lack perfection, but that is why they are called reference standards, not ‘gold standards’. One can be sure that the best reference standards available for facet joint pain (controlled and guided medial branch blocks), discogenic pain (controlled provocation discography), and sacroiliac joint pain (controlled and guided intra-articular blocks), are not perfect, but then, what is? These reference standards are the best we have – and they are actually rather good. Comparing clinical test results with the results from these reference standards can be done, has been done and the outcomes have been published. To argue that low back pain is non-specific is simply an ostrich-like denial. People can have discogenic pain, facet joint pain, sacroiliac joint and nerve root pain. We know it because the reference standards exist. We know the approximate or estimated prevalence of these pain sources. We also know that psychosocial distress and other issues not only confound our ability to treat patients, but to diagnose their tissue source of pain as well[7]. Do central nervous system issues have an important role to play in the pain experience. Absolutely. There is abundant evidence of such that many others have commented on. Is it either patho-anatomic or CNS issues, or are we able to see back pain patients as having a tissue source of pain with greater or lesser amounts of CNS modulation and psychosocial modulation issues influence the clarity with which we can see the patho-anatomic origin? The biopsychosocial model was intended to reflect this accepted complexity.

With regards to the central question here, I reiterate something I believe I have said before in this discussion: All patients start off being ‘non-specific’ before a history or physical examination is undertaken. Even determining a patient’s gender changes to odds of he or she having certain disorders. Ask yourself this? If male, what is the probability of the patient having pelvic girdle pain? How about this? If the patient with back pain is aged less than 20 years, what is the probability of him or her having spinal stenosis?  All patients have a specific problem or combination of problems and our task is to identify, as best we can, why they hurt, what can be done about that, and how can we achieve the best outcome with the least amount of intervention as possible. To steadfastly stomp one’s foot and bemoan the non-specificity of back pain is to remove oneself from inclusion in the task ahead. If back pain is truly non-specific, then we know literally nothing about it. That is simply not the case. As soon as we know something about the issue, that part at least, becomes specific.

Reference List

     [1]   Bossuyt PM, Reitsma JB, Bruns DE, Gatsonis CA, Glasziou PP, Irwig LM, Lijmer JG, Moher D, Rennie D, de Vet HCW. Towards complete and accurate reporting of studies of diagnostic accuracy: the STARD initiative. BMJ, Vol. 326 2003. pp. 41-44.

     [2]   Laslett M, Aprill CN, McDonald B. Provocation sacroiliac joint tests have validity in the diagnosis of sacroiliac joint pain. Arch Phys Med Rehabil 2006;87:874-875.

     [3]   Laslett M, Aprill CN, McDonald B, Young SB. Diagnosis of sacroiliac joint pain: validity of individual provocation tests and composites of tests. Manual Therapy, Vol. 10 2005. pp. 207-218.

     [4]   Laslett M, McDonald B, Aprill CN, Tropp H, Oberg B. Clinical predictors of screening lumbar zygapophysial joint blocks: Development of clinical prediction rules. The Spine Journal, Vol. 6 2006. pp. 370-379.

     [5]   Laslett M, McDonald B, Tropp H, Aprill CN, Oberg B. Agreement between diagnoses reached by clinical examination and available reference standards: a prospective study of 216 patients with lumbopelvic pain. BMC Musculoskelet Disord., Vol. 6 2005. p. 28.

     [6]   Laslett M, Oberg B, Aprill CN, McDonald B. Zygapophysial joint blocks in chronic low back pain: A test of Revel's model as a screening test. BMC Musculoskeletal Disorders, Vol. 5 2004. p. 43.

     [7]   Laslett M, Oberg B, Aprill CN, McDonald B. Centralization as a predictor of provocation discography results in chronic low back pain, and the influence of disability and distress on diagnostic power. The Spine Journal, Vol. 5 2005. pp. 370-380.

     [8]   Laslett M, Oberg B, Aprill CN, McDonald B. A study of clinical predictors of lumbar discogenic pain as determined by provocation discography. Eur Spine J, Vol. 15 2006. pp. 1473-1484.

     [9]   Laslett M, Young SB, Aprill CN, McDonald B. Diagnosing painful sacroiliac joints: a validity study of a McKenzie evaluation and sacroiliac joint provocation tests. Aust J Physiother, Vol. 49 2003. pp. 89-97.

   [10]   The STARD group. Towards complete and accurate reporting of studies on diagnostic accuracy: The STARD initiative. In: Reitsma H, editor. Amsterdam: The STARD group, 2001.

   [11]   van der Wurff P, Buijs EJ, Groen GJ. A multitest regimen of pain provocation tests as an aid to reduce unnecessary minimally invasive sacroiliac joint procedures. Arch Phys Med Rehabil, Vol. 87 2006. pp. 10-14.

i'm happy with all you said, and by the same logic, we can't abandon the term non-specific entirely.

regards 

Dear everyone that replied to this questions.

I never would have guessed that this 'simple' question would provoke so much discussion. Although this question can be (and is) replied to with several technical answers, its intention was more philosophical.

If we want to treat any kind of complaint (pain, disfunction) shouldn't we at least have a clue or concept on what is wrong? If we do have a notion of what is going on (in disregard of the question whether this notion is right of wrong) the complaint is NOT non-specific. 

If we do NOT have a notion, the complaint might be called non-specific, but then we admit that we don't have anything to treat (as in cure).

As a consequence: rendering back pain non-specific automically leads to treating only  symptoms. Not curing the disease. 

So before we step to any discussion on which concept should be applied. I wonder whether we can agree on the above logic.

totally agree

Agreed entirely

Maybe if we all study the role of the lumbar fibro-fatty tissue disfunction we finally will make the “non specific low back pain”, less unespecific.

Please take in consideration the studies of the reumatologist and surgeons on the 50’s. Work that was eclipsed by the “discopathy fever”. I am currently studying them and I am surprised how all their work somehow became buried. Check in www.backmice.info.

Fat tissue is metabolically active and that can explain certain recurrent and non traumatic low back pain.