Wednesday, August 07, 2013

Melzack & Katz, Pain. Part 19b: Implications of the Neuromatrix concept - low back pain.

The paper, Pain.

Part 18: Multiple determinants of pain Part 19: Implications of the Neuromatrix concept - phantom pain


SEE ALL PREVIOUS BLOGPOSTS IN THIS SERIES LISTED AT THE END

Here is the second of Melzack and Katz' "Implications" section:

2. Low-Back Pain
SOURCE
Can you even FIND much back representation on this image? 

 First, let's observe the fact that backs do not have access to very much real estate in the somatosensory cortex. Sensory-discrimination of backs is very low. That is probably a good thing. Back when only quadrupeds roamed around, it would not have been a good thing to have high-res sensory-discriminative capacity in the skin over the back - think of the rain dripping down on a back that could feel every drop distinctly. Would that not have been annoying and stressful? Lots of creatures jumped on lots of other creatures backs, bit them; those who didn't feel attacks as intensely managed to get away and live to reproduce. The creatures who went, "OW!! OW!! OW!!" and were paralyzed by a pain response from skin nociception, or became too stressed out by insect bites or raindrops on exposed backs, likely didn't survive to reproduce, which is how we ended up with brains that don't represent exteroception from backs very well, .... but somehow, interoception is very well represented. Maybe too well. 

 Anyway, Melzack & Katz: 
"Low back pain is one of the most common types of pain, yet it is poorly understood. It illustrates the complexity of interactions among different contributing factors and the need for multiple approaches to treat it.76"
Yup. The authors can say that again. Reference 76 goes to Long MD. Chronic back pain. In: Melzack R, Wall PD, eds. Handbook of Pain Management. Edinburgh: Churchill Livingstone; 2003, 67–76. Such a short chapter for such a common pain problem. I guess because the medical world still doesn't really know what to make of it. It says back pain is mostly "idiopathic." I have this book open on my lap right now. Classification of back pain is temporal (time-related). 
Here are some notes: 
-  "Transient": this kind is short-lived, treatment usually non-medical and symptomatic, cause remains unknown, is mostly inconsequential. "Acute" falls into this, with or without leg pain. Can last a few days to a few months. Self-limited and resolves spontaneously. Standard treatments (rest, analgesia, local physical measures, watchful waiting) have little influence. If pain is intractable, or is accompanied by significant neurological deficit, surgery. 
- "Persistent": Six months later, the patient still has back pain. The patient adapts, carries on in spite of it. Most have some degree of spondylotic disease. They don't score high on any sort of "illness" index. There is only a 5% incidence of psychological impairment noted overall. They don't respond to standard treatment.  
- "Chronic": The difference between persistent and chronic back pain is in the patients' preoccupation with it and degree of perceived suffering from it. Pain becomes the centre of their existence and the cause of their impairment. Depression and anxiety are accompanying factors. There is a large incidence of psychological impairment. They are disabled by their pain. They misuse, but are not necessarily addicted to, drugs. They use medical resources heavily. 

 Bear in mind, this is the medical model. Melzack and Wall edited this text. I think they were merely surveying the landscape of how the medical model interacts with the pain model it has supported all these centuries. I doubt they wanted it to be some sort of manifesto.

 The medical model apparently classifies things like pain according to how much it feels leaned against or upon by the general population. Apparently. 

 Melzack has always been all about, let's don't blame the patient for their pain or for their response to it. Let's try to look at pain more objectively, not based on its impact on one profession or another, not in a manner biased by impact on societal resources, as viewed by the gate-keepers to those resources.
But I digress. 

The rest of the chapter is about the various medically recognized "causes" for back pain.. metastases, osteoporosis, spondylitis from various arthritides, that vague category known as "musculoskeletal", abdominal and pelvic diseases that "cause" back pain, psychiatric or psychosomatic ("the patient must be crazy"), spondylotic/idiopathic, facet syndrome, stenosis, root compression at the foramen, instability, progressive deformity syndromes, degenerative spondylolisthesis, failed back syndrome (should be "failed back surgery syndrome"..). Then there is another laundry list of post-op complications: inappropriate patient selection, failure to correct the initial pathology, nerve root injury, pseudomeningocele, surgically induced instability, infection, excessive scar formation that deforms the thecal sac, failed fusion, loosened or extruding hardware, hardware that wasn't properly placed, degeneration of the segment next to a fixation, arachnoiditis. 
At the end is a short list of more conservative care: injections, blocks, then all the comp&alt therapies in existence, good mattress and chair support, massage, manipulation, acupuncture. Oddly, exercise or movement therapy is not even mentioned.

The chapter ends with the acknowledgement that really, nothing has been found to really work for back pain. 


Things haven't changed much since 2003, but you do start to feel glimmers of hope when medical bloggers start raising their voices; here is KevinMD - Injections for back pain: the evidence is weak. Also when papers surface that show no good effect from medicalizing back pain. Here are a few (thanks to Kenneth Venere for the compilation):



1. Brox JI, Sørensen R, Friis A, Nygaard Ø, Indahl A, Keller A, Ingebrigtsen T, Eriksen HR, Holm I, Koller AK, Riise R, Reikerås O. Randomized clinical trial of lumbar instrumented fusion and cognitive intervention and exercises in patients with chronic low back pain and disc degeneration. Spine (Phila Pa 1976). 2003 Sep 1;28(17):1913-21. 

Conclusion: equal improvement in patients with chronic low back pain and disc degeneration randomized to cognitive intervention and exercises, or lumbar fusion.



2. Jeremy Fairbank, consultant orthopaedic surgeon, Helen Frost, research fellow, James Wilson-MacDonald, consultant orthopaedic surgeon, Ly-Mee Yu, statistician, Karen Barker, director of physiotherapy research, Rory Collins, professor, and for the Spine Stabilisation trial. Randomised controlled trial to compare surgical stabilisation of the lumbar spine with an intensive rehabilitation programme for patients with chronic low back pain: the MRC spine stabilisation trial. BMJ. 2005 May 28; 330(7502): 1233.doi:* 10.1136/bmj.38441.620417.8F (full text). 

Conclusion: No clear evidence emerged that primary spinal fusion surgery was any more beneficial than intensive rehabilitation.

3. Margaret P Staples, biostatistician, David F Kallmes, professor, Bryan A Comstock, operations director, Jeffrey G Jarvik, professor of radiology and neurological surgery and director, Richard H Osborne, professor of public health and director, Patrick J Heagerty, professor, Rachelle Buchbinder, director and professor. Effectiveness of vertebroplasty using individual patient data from two randomised placebo controlled trials: meta-analysis. BMJ 2011; 343 doi: http://dx.doi.org/10.1136/bmj.d3952 (Published 12 July 2011) (Full text)
Conclusion: Results do not support the hypothesis that selected subgroups [ recent onset fracture or severe pain] would benefit from vertebroplasty [i.e., results no better than placebo]

4. J Bart Staal, Rob de Bie, Henrica CW de Vet, Jan Hildebrandt, Patty Nelemans; Injection therapy for subacute and chronic low-back pain  2008 Jul 16;(3):CD001824. doi: 10.1002/14651858.CD001824.pub3. 
Conclusion: Insufficient evidence to support the use of injection therapy in subacute and chronic low-back pain (specific subgroups of patients may respond to a specific type of injection therapy)

And finally, this: Doctors Increasingly Ignore Evidence In Treating Back Pain, July 30/13, from NPR.

Melzack and Katz continue.. 
"Protruding discs, arthritis of vertebral joints, tumors, and fractures are known to cause low back pain. However, about 60–70% of patients who suffer severe low back pain show no evidence of disc disease, arthritis, or any other symptoms that can be considered the cause of the pain."
60-70%!! No evidence of any mesodermal derivative being wrong or bad or misplaced or ripped or torn. Nada.
"Even when there are clear-cut physical and neurological signs of disc herniation (in which the disc pushes out of its space and presses against nerve roots), surgery produces complete relief of back pain and related sciatic pain in only about 60% of cases."
The amount surgery helps a disc herniation is only slightly better than chance.  Gee. I think I'd hang onto mine, and see if I could find someone non-surgical to help me deal with less pain from it until it gets over itself.
"The rate of success in different reports ranges from 50 to 95%, depending in part on the spatial distribution of the pain."
Kind of a crap shoot.. 
"Furthermore, patients with physical signs such as disc herniation in the lower spine are rarely helped by surgical procedures such as fusion of several vertebrae to provide structural support to the back.76 "
See references above...
"A variety of forms of physical therapy are more likely to help low back pain. The most effective is a regimen of exercises that develops the back muscles. Transcutaneous electrical nerve stimulation, ice massage, and acupuncture may also help some patients." 
So, back to distracting the patient until nature settles itself back down. See Hippocrates.
"Injections of anesthetics into trigger points may be effective as well."
Sorry Melzack and Katz.. see Staal 2008, above.

"Still, despite all of these therapies, many patients continue to suffer severe, unrelenting pain.77"
Yup.
Reference 77 goes to Lehmann JF, de Lateur BJ. Ultrasound, shortwave, microwave, laser, superficial heat and cold in the treatment of pain. In: Melzack R,Wall PD, eds. Handbook of Pain Management. Edinburgh: Churchill Livingstone; 2003, 473–483.

[I could have told them none of that stuff works. Most of my training back in the late 60's was how to be a robot, applying junk like that to patients, safely, as an extension of the medical placebo delivery model. But I digress.]
"A high proportion of cases of chronic back pain may be due to more subtle causes. The perpetual stresses and strains on the vertebral column (at discs and adjacent structures called facet joints) produce an increase in small blood vessels and fibrous tissue in the area.78"
Reference 78 goes to Jayson MIV. Rheumatoid arthritis. In: Melzack R, Wall PD, eds. Handbook of Pain Management. Edinburgh: Churchill Livingstone; 2003, 39–48. 
Maybe, "causes" even "subtler" than that. See the gliopathy paper.
"As a result, there is a release of substances that are known to produce inflammation and pain into local tissues and the blood stream; this whole stress cascade may be triggered repeatedly. The effect of stress-produced substances—such as cortisol and norepinephrine—at sites of minor lesions and inflammation could, if it occurs often and is prolonged, activate a neuromatrix program that anticipates increasingly severe damage and attempts to counteract it."
Yes, that is the whole thing pretty much in a nutshell. The brain will automatically and carefully document and memorize a great big barrage of threat stimuli, and from then on thereafter be on the lookout for any hint of similar "danger." It takes a long time to get over pain, and it can also take a long time to get over having had pain.
"The program to reduce strain and inflammation could include generating the neurosignature for pain—part of a neural program which presumably evolved to induce rest, the repair of injured tissues, and the restoration of homeostasis."
I think what he is saying is that pain is supposed to be protective. Part of what comes with it is that reflexive guarding response, a vetoing of movement generated from deep in the spinal cord. Or is he saying it is generated from higher up? He might be..

I'll lay odds, though, that at first spinal cord mechanisms do their best to deal with the scene, before the situation has become obvious to the person living in there with a nervous system that has slid sideways into the ditch, temporarily we hope...
"As a result of the persistence of low back pain despite all the available therapies, it is not surprising that psychological interventions, such as relaxation therapy, Cognitive-Behavior Therapy, and Acceptance and Commitment Therapy have become an important approach to the problem. But no one therapy is more effective than the others. In fact, clinics often employ several procedures at the same time to get the best results.79"
Reference 79 goes to
Turk DC, Okifuji A. A cognitive-behavioral approach to pain. In: Melzack R, Wall PD, eds. Handbook of Pain Management. Edinburgh: Churchill Livingstone; 2003, 533–541.

Yeah.. when you consider how much shorter one's attention span becomes in a pain situation, and how easily a person in pain will become frustrated, it's kind of important to offer any sort of cognitive evaluative input in as many ways as you can as often as possible in the hope that something will stick and start to grow. 
..........

The implications of the neuromatrix model of pain for back pain are HUGE, mainly because of how utterly ubiquitous back pain is. 
.........


SOURCE

I agree wholeheartedly with NOIgroup. They have been leading the PT world for more than a decade, maybe a couple decades, by emphasizing how important it is to help patients start to think about pain, in ways that open up some space around it : that they are NOT broken or damaged or beyond hope or need to be invasively "fixed" as though they were a train wreck.

Giving people really basic information about life in a body and in a primate brain can cut through a lot of misinformation and dreary catastrophic thinking pretty fast. Of course, this requires good timing and a receptive patient. 

It might not help pain, directly, but then nothing truly does anyway - everything - all input,  has to be assessed then approved by the brain in a conscious aware human, so.. add in some innocuous handling to reduce stress and promote yes-ci-ception, teach people how to feed their nerves by moving them around, and help them see how their unhelpful cognitions might be unhelpful. It can help people be less bothered by pain felt anywhere. Including the back. 

.........

EDIT: AUG 21: From BodyInMind blogpost by Neil O'Connell,

Borenstein DG, O’Mara JW Jr, Boden SD, Lauerman WC, Jacobson A, Platenberg C, Schellinger D, & Wiesel SW (2001). The value of magnetic resonance imaging of the lumbar spine to predict low-back pain in asymptomatic subjects : a seven-year follow-up study. The Journal of bone and joint surgery. American volume, 83-A(9), 1306-11 PMID: 11568190
Conclusion: The findings on magnetic resonance scans were not predictive of the development or duration of low-back pain. Individuals with the longest duration of low-back pain did not have the greatest degree of anatomical abnormality on the original, 1989 scans. Clinical correlation is essential to determine the importance of abnormalities on magnetic resonance images.
Conclusion: The development of serious LBP disability in a cohort of subjects with both structural and psychosocial risk factors was strongly predicted by baseline psychosocial variables. Structural variables on both MRI and discography testing at baseline had only weak association with back pain episodes and no association with disability or future medical care.
Jarvik JG, Hollingworth W, Heagerty PJ, Haynor DR, Boyko EJ, & Deyo RA (2005). Three-year incidence of low back pain in an initially asymptomatic cohort: clinical and imaging risk factors. Spine, 30 (13) PMID: 15990670
Conclusions: Depression is an important predictor of new LBP, with MRI findings likely less important. New imaging findings have a low incidence; disc extrusions and nerve root contact may be the most important of these findings.
Comments appear by the authors of:
Hancock MJ, Maher CG, Laslett M, Hay E, & Koes B (2011). Discussion paper: what happened to the ‘bio’ in the bio-psycho-social model of low back pain? European spine journal PMID: 21706216

Conclusions: We believe the misunderstandings presented in this paper partly explain the lack of investigation into pathology as an important component of the low back pain experience. A better understanding of the biological component of low back pain in relation, and in addition, to psychosocial factors is important for a more rational approach to management of low back pain.

"..structural/pathology issues are not, in my view, the only piece of the puzzle to which we should be attaching the label of ‘bio’. Changes in the response profile of central nervous system cells, change in glial expression, changes in gray matter density, upregulation of endocrine, adrenergic and other mechanisms are all biological factors. Cognitive and contextual issues can only have their effect on pain via biological mechanisms. I think what we mean by biopsychosocial is actually more like anatomopsychosocial, in which case I am definitely an anatomopsychosocialist. I believe there is irrefutable evidence that primary nociceptor activity can modulate pain. I also believe there is irrefutable evidence that primary nociceptor activity is neither sufficient nor necessary for pain, so a tissue cannot, in my view, be a source of pain. I imagine that that does not surprise anyone."
.................

Previous blogposts

Part 1 First two sentences

Part 2 Pain is personal Also Pain is Personal addendum., Neurotags! Pain is Personal, Always.

Part 3a Pain is more than sensation: Backdrop Part 3b Pain is not receptor stimulation Part 3c: Pain depends on everything ever experienced by an individual

Part 4: Pain is a multidimensional experience across time

Part 5: Pain and purpose

Part 6a: Descartes and his era; Part 6b: History of pain - what’s in “Ref 4”?; Part 6c: History of pain, Ref 4, cont.. : There is no pain matrix, only a neuromatrix; Part 6d: History of Pain: Final takedown Part 6e: Pattern theories in the history of pain Part 6f: Evaluation of pain theories Part 6g: History of Pain, the cautionary tale. Part 6h: Gate Control Theory.

Part 7: Gate control theory has stood the test of time: Patrick David Wall;  Part 7b: Gate control: "The theory was a leap of faith but it was right!"

Part 8: Beyond the gate: Self as mayor Part 8b: 3-ring circus of self Part 8c: Getting objective about subjectivity

Part 9: Phantom pain - in the brain! Part 9b: Dawn of the Neuromatrix model Part 9c: Neuromatrix: MORE than just spinal projection areas in thalamus and cortex Part 9d: More about phantom body pain in paraplegics

Part 10: "We don't need a body to feel a body." Part 10b: Conclusion1: The brain generates its own experience of being in a body Part 10c:Conclusion 2: Your brain, not your body, tells you what you're feeling Part 10d: Conclusion 3: The brain's sense of "Self" can INclude missing parts, or EXclude actual parts, of the biological body Part 10e: The neural network that both comprises and moves "Self" is (only)modified by sensory experience

Part 11: We need a new conceptual brain model! Part 11b: Intro to a new conceptual nervous system Part 11c: Older brain models just don't cut it Part 11d: The NEW brain model!

Part 12: Action! 12b: Examining the motor system, first pass. 12c: Motor output and nervous systems - where they EACH came from Part 12d... deeper and deeper into basal ganglia Part 12e: Still awfully deep in basal ganglia Part 12f: Surfacing out of basal ganglia Part 12g: The Action-Neuromatrix

Part 13: Pain and Neuroplasticity Part 13b: Managing neuroplasticity

Part 14: Side trip out to the periphery! Part 14b: Prevention of pain neurotags is WAY easier than cure Part 14c: PW Nathan was an interesting pain researcher  Part 14d: Brain glia are from neuroectoderm and PNS glia are from neural crest Part 14e: The stars in our headsPart 14f: Gleeful about glia Part 14g: ERKs and MAPKs and pain Part 14h: glia-fication of nociceptive input 14i: molecular mediators large and small Part 14j: Neurons, calling glia (over, do you read?) Part 14k: Glia calling glia, over. Do you read? Part 14l: satellite cell and neuron cell body interactions, and we're outta here!

Part 15: Prevention of neurobiological hoarding behaviour by dorsal horn and DRG glia is easier than clutter-busting after the fact

Part 16: Apples are to fruit as cows are to animals as nociceptive input is to pain


Part 17: The stress of it all Part 17b: Stress and adrenals Part 17c: Women, pain, and stress Part 17d: Stress, aging, and pain Part 17e: Stress and aging, keeping hippocampal dendrites fluffed up Part 17f: Chrousos and Gold and stress Part 17g: Stress conceptualization through the agesPart 17h: Phenomenology and physiology of stress Part 17i: Pathophysiology of stress Part 17j: cortisol, good or bad? Sensitivity to pain traumatization.




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