Meanwhile, over on the BIM site, there is a really good discussion led by Neil O’Connell on the recent “back pain as an infection” study (a study that proposed antibiotics could cure 40% of chronic back pain), the media response, and some good links to responses to the study – all worthy reading for clinical scientists to see examples of the kind of questions that would be useful for scientific scrutiny of any research publication.
There is another fallout which has not been mentioned – we are now left with the term “back infection” and it is the clinicians who have to deal with this and somehow mop up the mess until the scientific community sort themselves out. We have struggled with science “gifts” in the past such as “slipped disc”, and “bulging disc” and now we have “infected back”. Is it much different to Frida Kahlo’s cracked column? “Infected” is such a potent word.
I had my first “infected back” last week – A colleague said “I have read about infected backs in the paper and I wonder if mine is infected”. I get sinus infections that come and go and my back pain comes and goes, though not at the same time – should I think about antibiotics? And maybe my tennis elbow is an infection too.”
What does the clinician say in response?
– David Butler
I think that the clinician has to read the papers, discuss the findings with colleagues, do a very good history and physical examination of the patient, discuss imaging results from a specific patient with the appropriate experts, evaluate the data from that exploration, and talk to the patient. I think we, as clinicians, take the information from this study and use it thoughtfully and appropriately just as we would use information from any study whether that study examined physical, biopsychosocial, or (as in this case) potential infectious source of the pain. The infectious model is valid for other forms of joint pain. As someone who is looking at bilateral knee replacements as a result of multiple episodes of Lymes disease, to dismiss the findings of this study, even with its faults, runs the same risks to the patient as those who overly hype its results.
We do our patients no favors if we jump on any clinically biased bandwagon. But we can also do our patients harm if we do not consider all reasonable and reasoned possibilities. I would hope that each clinician would do what we are trained to do: become informed, examine, evaluate alternatives, talk to the patient, and develop a reasoned plan of care. JOhnB
Ah John, would that all health professional do what you suggest – high level reasoning when most of the world indulges in linear reasoning, fails to reason, or follows dogma.
Noone should operate or be operated on with an ongoing infection somewhere in the body, but that is not the issue for me here.
The research (Albert et al. 2013) adds to the body of knowledge and builds on previous research. There are two main issues which I think impact on current clinical practice:
First is the statement in the first paragraph where the authors suggest they have found a specific cause for chronic pain. Chronic pain will never have one cause. Once again we see the relentless search for the holy grail of chronic pain at the end of neurones.
The second is the patient mop up that some clinicians are now doing.– “40% of back pain may be infection curable by antibiotics” thunders The Guardian and host of other papers. Infection means pus, pain and pills for most people.
So here is my attempt to craft a mop up story for my friend.
PATIENT: “Could I have an infected back and will antibiotics help me? I have been reading in the paper about acne infections in the back”.
DAVID: (after seeking out what the patient means by infection) Well maybe, this research is just out and it has had a lot of press. First – I don’t think there is a need to worry too much. You are right – the bacteria responsible for acne is the one they found in disc material in people being operated on. This bacteria is a long term resident on and in our bodies- there are zillions of bacteria and they prefer to hang around pores, ear canal, mouth and gut. They can probably be found anywhere in the body. These and other bacteria are usually very peaceful but sometimes they get activated and can cause problems and multiply. We don’t really know much about how they become activated – science has a way to go here, but we do know, and the recent research helps us here, that they love inflammation and swelling and they can also contribute a make swelling themselves. When you don’t move properly the fluids in your back get a bit stagnant and that encourages a bit of bacterial action. The main thing is that whilst you might have bacteria living in your body and back , it is not like there is any pus and it’s probably not like the image the words “infected back” might give you. They don’t hurt either, but they make help send a few more signals up to the brain saying :hey I am in a bit of danger down here – do something about it and the brain may or may not make pain.
PATIENT: “Well OK, I like bugs rather than bacteria. What about antibiotics? The research suggests it could help?”.
DAVID: That is correct. But I, and many other health professionals would like to see more research on this. It’s also worth knowing that many bacterial infections get better without antibiotics. After all, people got better before antibiotics were introduced in the late 1930s. Why not freshen up your back and try and get rid of the inflammation and stagnant fluids that the bugs play in? The inflammation and swelling is there because your back hasn’t moved properly for a while and it needs movement to disperse the fluid. , Plus swelling can also be caused by nerve irritation ( perhaps go into peripheral neurogenic inflammation if appropriate) and also by fear and worry ( go into discussion on cytokine/cortisol based links to swelling if appropriate). So it can actually be treated, without antibiotics and you can do it yourself. There are also dietary things which can help….etc etc. But there is an option of antibiotics and if you are going nowhere, it would be worth having a chat to a . doctor or pain specialist.
You get the picture – it’s all about dethreatening, giving them something to do about it, using the story to get them moving and certainly not denigrating the actual research itself..
None of this is mentioned in the articles and I have not noted any responses to the media outbursts. The clinician’s job is hard enough already, dealing with people ravaged by fear, anxiety and disgust.
1. Chronic pain will never have just one cause and it’s dangerous to assert that it will.
2. A subset of people may benefit from antibiotic therapy, but please – move, educate, get healthier and get functional. Most won’t need antibiotics.
3. Help manage the press responses. It’s not fair leaving it to the clinicians to mop up!
4. Remember that many patients and clinicians a new language construction – that of infected disc and infected back. We can’t leave patients with that. It must be dethreatened and explained..
I would love some help with the story. I am sure it can be improved.
Albert HB 2013 Eur Spine J 22: 690-696
Of course solid clinical reasoning remains the corner stone of any clinical intervention. The point is that yet another powerful ” Nocebo” has been planted and it will take many, many years to counteract its effect on the fearful patient. Sorry for the core stabilisers out there but the “Myth” of core stability was planted many moons ago and we are still moping up from that one !!!
That is an unfair and clinically unfounded statement. First of all, the research does not create a placebo. We as clinicians and the media do. Should this research not be performed? Should the results of this research not be published for critical comment? Clinical facts or clinical hypotheses do not create placebo’s or nocebo’s. People do in their communications. If this research happens to turn out to be correct, would you still call exploring the possibility of a bacterial nociceptive source of the pain a nocebo? The clinical possibility is real that an infectious agent could be causing back pain. Research will clarify that in the future, but I think that any good clinician who is facing a patient with severe spinal pain has to weigh patient information along with the available research to come up with risk/benefit ratios for all interventions. The use of an antibiotic intervention given the present research would need to be justified by a narrow window of clinical findings to meet an acceptable risk given the present research. But should it be not considered if someone is facing a lumbar fusion? We tend to forget that GMI also has risks associated with it.
I Highly recommend looking at an article in Physiology Reviews 93: 1207-1246, Oct, 2013 ” Placebo the new physiology of the doctor-patient relationship”. We, as clinicians, are the sources of placebo’s and nocebo’s. I also recommend a paper in Eur spin J 6/11 by Hancock and a very distinguished group of spine researchers. “Discussion Paper: what happened to the “bio” in the biopsychosocial model of low back pain?”
Blogs are wonderful things. They provide wonderful outlets to share information, but we need to be careful. We are concerned about producing nocebo’s by the way we present information to patients. I am worried that blogs have the same equivalent in providing “clinician nocebo’s” in the exactly the same way. In my concept of the BPS approach, I have to be pretty darn sure that there are no nociceptive peripheral generators for the pain before I work on convincing a patient that their experience of that existential threat is all a figment of their nervous system. JOhnb
Thanks for your response. I loved and will gladly use much of your wording in the discussion of this with patients. I do have some points to quibble with you.
1. Is number one. I do not think that the authors ever stated that there is one reason for having chronic back pain. Let’s not put words in their mouths or meanings in their paper. I, however, think they would have done themselves a very good service if they would have practiced a little more discipline and either not included or buried deep in their article the first couple of sentences dealing with the percentage of people with chronic pain and modic changes.
2. I highly disagree with you in that it is not the clinicians responsibility to do mop up. As a clinician it is what I do all of the time in multiple ways with multiple issues. It is what I am trained to do. It is absolutely a part of my job. If other clinicians do not feel it is a necessary skill to develop because they don’t want to do it. My answer to them is simple find a new profession because you will not be able to truly address the needs of your patient if you don’t know how to do it. We need to be able to justify what we do in relation to the options and the alternatives out there. A lot of the options out there are crap. GMI and pain education are not the easiest of sells.
3. the ultimate answer to chronic pain is in the neurons but the answer to persistent nociception is removing the offending nociceptive source if possible.
4. I love your explanation of how to get rid of an infection using our inherent physiological coping mechanisms. However, what is the risk benefit ratio in specific patients with evidence of modic change of a trial of antibiotic? What is the risk/benefit ratio of GMI if there is evidence of underlying modic change? I understand that the generalized use of antibiotics posses potential risks for the patient and society/environment. But there are no interventions that we do ( and non-intervention is a clinical choice that has risks/benefits) that do not have risks. In doing the GMI stuff I have run unknowingly into several- undiagnosed or even diagnosed psychiatric problems, missed metastatic disease, and missed orthopedic problems that required other interventions. If I would not have been suspicious of other underlying psychiatric and nociceptive generators, I would have done the patients harm if I had continued.
5. If there is evidence of modic change on MRI, wouldn’t an enhanced placebo effect (antibiotic plus your explanation) be synergistic? ( The IBS studies are examples).
6. I continue to relate back to the Hancock article that I referred to in the last entry. Why are we so quick to throw out the bio in BPS? We need to be careful that we are not being as blind to the bio as the rest of the system is blind to the psychosocial component.
7. In your statement that there will never be one way to treat chronic back pain, it is important to remember that GMI also falls into that category.
David- I love this. Hopefully we can get you to the City of Brotherly Love. Johnb
Hi there John,
Many thanks for the responses. Sorry they have been long, but I have enjoyed the thinking. You have brought up some really important issues and I disagree with some of them as you would expect and I want to convince you otherwise. Should I come to Philly to oversee your rehab post new knees?
The authors (Albert et al 2013) do state that “these finding should not be underestimated as CLBP is universally acknowledged to be extremely difficult to reliably attribute to one cause”, which says to me that they think they have found that one cause, but also makes me think they have a lack of understanding of chronic pain. But let’s leave this and thank them for their useful contribution which also includes getting people like us talking and arguing.
The language construction or I guess it’s a meme now of “infected back” that I believe people may hold is somewhat emergent and non linear. It didn’t come from one place. The infected back notion (and I think there is a reasonably healthy and an unhealthy version) that a person may have will have emerged from the papers, the research, notions of infection, notions of bacteria, germs, experiences of infection, interactions with various health professionals, friends etc etc. I admit being brought up with “germs lose hope when you use soap”. There are plenty of sources of mopping up and it probably adds another 5 minutes of chatting in the clinic. No doubt, perceptions of infected back need researching.
I don’t agree that the answer to persistent nociception is “removing the offending nociceptive source if possible”. That’s just one answer. First there is no such thing as offending nociceptive sources,– it’s up to the brain to decide if they offend but I think that is what you meant. The influence of nociception can be powerfully modulated by the brain. I have been at the computer for 2 hours and haven’t moved. There must be heaps of nociception coming from my old back and bum but I am not experiencing pain as I am enjoying writing this blog so much Thirdly – there are probably multiple sources as the Albert et al. study showed with endplates and disc. The “if possible” you mention is a big if. But you know all that anyway.
Glad you can use a bit of the story. Add to it as its new for me. I have no idea of risk/benefit ratios where modic change occurs. I wonder how much modic change there is neuropathic pain states such as CRPS? That would be interesting. Numbers needed to treat (NNT) for GMI and CRPS are around 3 – maybe the once that don’t shift have significant modic changes. And as for your comment 5 – yes -wouldn’t it be nice and helpful if the authors suggested that explanation and therapeutic movement may be synergistic and worthy of study – It would only take a line!
I read the article which you suggested (Hancock et al 2011 Eur Spine J 20: 2105). These are highly experienced spine researchers who I have a lot of respect for. The article bugged me. They call for more bio in biopsychosocial and the bit of bio they want more of is research into tissue sources of nociception. Nothing wrong with that, but that’s not “bio”. The “bio” in biopsychosocial is big picture biology, not only of the complexity of body tissues but mental processes as well and that includes, for example, neuroplasticity, neuroimmune interaction, extracortical changes and then the two way interaction of these processes with body parts. There was one mention of descending modulation. Its not bio OR psychosocial, its all merged. I was enjoying the Hancock et al paper and then it was “come on guys there is no such thing as a primary source of pain”. Pain is a brain output. If you think there is a primary source of pain in tissues then I ask if you think the primary source of love is in the genitals. I get a bit old and grumpy here but I wish people wouldn’t bastardise the term biopsychosocial, as clumsy as it is.
For me “Infected disc” unless it comes with adequate explanation can be a nocebo. I am sure it was not the intent of the researchers to do this – as I mentioned earlier, the concept of infected disc that members of the public may hold is emergent.
The 100th anniversary of the “slipped disc” is upon us in 2034. Hope I am still alive. For many people the term is scary, it means something out, the disc needs putting back passively and it might happen again.
For “infected disc”, my initial experiences and beliefs are that it’s scary, could mean pus, could mean pills, needs someone to fix it, might happen again.
But this time I am hopeful we can manage the meme much better.
Imagine that thoughts, feelings and emotions were to belong in the Bio, that’s a tough one to get your head around !!!! Could you stretch your fantasy further to include a “Thought virus” as a kind of nociceptive input. Does the understanding of the term nociception – a danger signal – need to be expanded in the light of present day knowledge. Try adding spirituality to the equation, where does that fit in to the equation????? Duality just doesn’t work here does it……However my Mummy always said if you can change just one mind you have won so lets hope this discussion does just that…….
Thanks John and David.
Of course, some injures that may have attracted the diagnosis of “slipped disc” in the past may be absolutely relevant to the disc. John Barbis writes of the need to keep up to date and to reason new science along with what you observe in the clinic, i.e. what is the relevance .
O’Dowd and Casey (2013) in an editorial in the European Journal of Pain suggest that “at the moment, the only patients that should be considered for a course of antibiotics outside the environment of a clinical trial are those with
1. Low back pain of more than 6 months duration and has not responded to exercise therapy.
2. symptomatic disc herniation within the previous year.
3.Modic type 1 changes at the same level as the disc herniation”. They also finish the editorial with “A period of reflective and scientific analysis with further high quality research may well lead to a new treatment for a small subgroup of low back pain patients being established, but it would be very wrong at this stage to give hope to the wider group of patients with chronic disabling low back pain”.
Our readers see large numbers of patients. I am wondering about the pattern of pain that a person reports that should make a clinician consider the possibility of clinically significant modic infection. Obviously disc injury would be one, but perhaps previous spinal surgery, spinal symptoms easing with antibiotics for other problems and perhaps quite widespread pain. I would love to hear more clinical anecdotes and suggestions here.