Modic Changes are an independent risk factor for episodes of severe and disabling low back pain.

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Spine (Phila Pa 1976). 2015 Apr 17. [Epub ahead of print]
Vertebral endplate (Modic) change is an independent risk factor for episodes of severe and disabling low back pain.
Määttä JH1, Wadge S, MacGregor A, Karppinen J, Williams FM.


Abstract
STUDY DESIGN:
Longitudinal cohort study of twins representative of the general population.

OBJECTIVE:
To assess the relationship between Modic change (MC) and severe, disabling low back pain (LBP), features of intervertebral disc degeneration (DD) and incident MC during 10-year follow-up.

SUMMARY OF BACKGROUND DATA:
MC describes vertebral endplate and bone marrow lesions visible on magnetic resonance imaging (MRI). MC has been associated with DD. It remains unclear whether MC causes LBP independently or through association with DD. Moreover, association of MC with severe, disabling LBP is uncertain.

METHODS:
Volunteers were recruited from the TwinsUK register to MRI and interview between 1996 and 2000 with a subset attending for follow-up a decade later. MC, DD (evaluated by loss of disc height and signal intensity, presence of disc bulge and anterior osteophytes) and Schmorl's nodes (SN) were determined on T2-weighted lumbar MR scans.

RESULTS:
Complete data were available for 823 subjects at baseline and 429 at follow-up. Mean age at baseline was 54.0 years (range 32-70) with 96% females. The prevalence of MC was 32.2% at baseline and 48.7% at follow-up. Subjects with MC were older (p<0.001) and more overweight (BMI: p = 0.026, weight: p<0.001). At both baseline and follow-up, more subjects reporting severe LBP demonstrated MC (subjects with MC vs. without MC: 35.0% vs. 16.4% respectively, p<0.001 at baseline; and 35.1% vs. 20.0% respectively, p<0.001 at follow-up). In multivariable analyses, MC was remained significantly associated with episodes of severe, disabling LBP (OR 1.58; 95% CI 1.04-2.41) independently after adjustment for of age, BMI, DD and SN at baseline. Loss of disc height and disc signal intensity were independently associated with prevalent MC at baseline, and disc height and disc bulge with incident MC during follow-up.

CONCLUSIONS:
MC is an independent risk factor for episodes of severe and disabling LBP in middle-aged women. These observations support further work aimed at identifying the precise histology underlying MC.

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Mean age at baseline was 54.0 years (range 32-70) with 96% females. Incidentaloma found in FMS patients.
 
Degenerative Disc Disease in a 30 Year-old Female

David W. Polly, Jr., MD

Professor and Chief of Spine Service
University of Minnesota, Department of Orthopaedic Surgery




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Praveen V. Mummaneni, MD

Professor, Department of Neurosurgery
University of California, San Francisco




Doctor Polly presents a case of a 30 year-old female with axial low back pain with radiation to the thighs. The MRI demonstrates L4-L5 degenerative disc disease (confirmed by discography) and the flexion-extension X-rays demonstrate a minimal retrolisthesis of L4 on L5 in extension. This patient has had symptoms for 6 months.

Prior to offering any surgical treatment, I would recommend maximal conservative management with truncal strengthening, physical therapy and aqua therapy. If the patient is above ideal body weight, I would recommend weight loss. Should the patient fail all conservative measures, I would consider surgery to treat the L4-L5 segment only as a last resort.

My preference is a posterior procedure. The patient is of child-bearing age, and thus I would prefer to avoid an anterior operation (i.e. artificial disc or ALIF) through the abdominal wall musculature.

I would consider 3 surgical options: a direct lateral approach, a posterolateral fusion, or a TLIF. Of these options, I would choose a minimally invasive TLIF. In my hands, this procedure has the least amount of morbidity to the paraspinal musculature, while effectively immobilizing the abnormal segment with a high potential for fusion through the interbody space. The interbody fusion directly addresses the diseased disc and the posterior pedicle fixation addresses the minimal retrolisthesis.

Case Discussion References:

  1. Resnick DK, Choudhri TF, Dailey AT, Groff MW, Khoo L, Matz PG, Mummaneni P, Watters WC, Wang J, Walters BC, Hadley MN: Guidelines for the performance of lumbar fusion for degenerative disease of the lumbar spine. Part 5: correlation between radiographic and functional outcome. Journal of Neurosurgery: Spine. 2005; 2: 656-659.
  2. Resnick DK, Choudhri TF, Dailey AT, Groff MW, Khoo L, Matz PG, Mummaneni P, Watters WC, Wang J, Walters BC, Hadley MN: Guidelines for the performance of lumbar fusion for degenerative disease of the lumbar spine. Part 6: magnetic resonance imaging and discography for patient selection for lumbar fusion. Journal of Neurosurgery: Spine. 2005; 2: 660-667.
  3. Resnick DK, Choudhri TF, Dailey AT, Groff MW, Khoo L, Matz PG, Mummaneni P, Watters WC, Wang J, Walters BC, Hadley MN: Guidelines for the performance of lumbar fusion for degenerative disease of the lumbar spine. Part 7: intractable low back pain without stenosis or spondylolisthesis. Journal of Neurosurgery: Spine. 2005; 2:668-670.
  4. Mummaneni PV, Rodts GE. The Mini-Open Transforaminal Lumbar Interbody Fusion. Neurosurgery. 2005; 57(4 Suppl): 256-261.
  5. Wang J, Mummaneni PV, Haid RW. Current Treatment Strategies for the Painful Lumbar Motion Segment: Posterolateral Fusion Versus Interbody Fusion. Spine. 2005; 30(16 Suppl): S33-43.
  6. Mummaneni PV, Haid RW, Rodts GE: Lumbar Interbody Fusion: State of the Art Technical Advances. Journal of Neurosurgery: Spine. 2004; 1:24-30.
  7. Rodts GE, Mummaneni PV. Discogenic Back Pain: The Case for Surgery. Clinical Neurosurgery. 2004; 51:277-280.


Author's Response

David W. Polly, Jr., MD

Professor and Chief of Spine Service
University of Minnesota, Department of Orthopaedic Surgery




Optimizing nonoperative care is an oft repeated mantra that we all dogmatically espouse, especially in training programs. But what does that really mean? Should patients lose their jobs because they cannot work? Should they sign up for a weight loss program that is pragmatic and doable?

New data is beginning to suggest that after 8-weeks of effort in PT, no significant additional benefit is discernible by Oswestry scores, etc. This patient had done core stabilization, a normal BMI, and was having job Impairment in spite of trying all of the appropriate nonop care. I find it a significant challenge about when to pull the trigger and do the surgery (and then there is the issue of how long does it take to get the person approved, scheduled, and into the OR).




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Dale A. Giessman DC
Chiropractor
Brentwood, CA
Unbelievably there is no mention of manipulative treatment. I have seen over my 25 year career many failed cases of conservative PT which respond and recover with our protocols of manipulation with core stabilization and strengthening.

 
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none of us would send this patient, but PCPs and other orthopods would. this type of scenario happens all the time. young patient, ugly disc on MRI who ends up with a fusion.

manipulative treatment for discogenic pain is ludicrous. if your disc hurts, lets go jostle it up a bit a see if that helps.

if i only believed in GRC blocks......
 
How many would send a 30 y/o to a surveon for fusjon if yhey had axial pain and Modic changes? Does not compute.
I would, if
1) they got no relief from an l/s esi
2) they got no relief from l/s facet joint inj/MBB
3) they had a positive, concordant discogram
4) I knew the spine surgeon took a conservative approach, and fully informed the patient that the likelyhood of success was suboptimal
 
if i only believed in chymopapin...
I do believe in chymopapain, as it is currently used in Europe. It is a shame those who used it in the US did not appropriately assess for allergic reaction to the enzyme
 
So you think a 'positive' discogram effectively rules out central pain.
 
So you think a 'positive' discogram effectively rules out central pain.
I dont discount the posibility that the patient suffers from both. Which is why I also do a modified DRAM on folks I am considering refering for a surgical evaluation.

BTW, what's with the quotes. Are you suggesting that discography s not a reasonable pre-surgical staging tool?
 
I'd suggest that a full 90-99% of discograms are done incorrectly (not per ISIS guidelines) or have no useful purpose other than to benefit the physician.

Lobel's indication for discogram: Patient consented for surgery as a 2 level fusion and surgeon wants to see if he can get away with only a single level fusion.
 
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so a little of the topic but somewhat related. There is a ortho/spine guy in Spain that injected plasma stem cells into Raphael Nadal's spine(tennis player).
The questions I have:
1. where was the material injected, facet vs. disc? diffusely panned-over the facet joints and within?
2. are there places in the USA injecting stem cell/spun plasma in the disc? Colorado the last I heard?
3. what is the status of future injectable stem cell/recombinant therapies. the last I checked, there were some phase III studies.

thanks on any info.
 
I dont discount the posibility that the patient suffers from both. Which is why I also do a modified DRAM on folks I am considering refering for a surgical evaluation.

BTW, what's with the quotes. Are you suggesting that discography s not a reasonable pre-surgical staging tool?

Yes, there is no intervention that reliably predicts the clinical outcome of a fusion. Your DRAM probably is more reliable
than your pressure findings.
 
I'd suggest that a full 90-99% of discograms are done incorrectly (not per ISIS guidelines) or have no useful purpose other than to benefit the physician.

Lobel's indication for discogram: Patient consented for surgery as a 2 level fusion and surgeon wants to see if he can get away with only a single level fusion.
The problem with Lobel's indication is that they assume that the surgeon is sufficiently reasonable and responsible to request discography in the first place.
 
Yes, there is no intervention that reliably predicts the clinical outcome of a fusion. Your DRAM probably is more reliable
than your pressure findings.
Could you provide literature to backstop that assertion?
 
so a little of the topic but somewhat related. There is a ortho/spine guy in Spain that injected plasma stem cells into Raphael Nadal's spine(tennis player).
The questions I have:
1. where was the material injected, facet vs. disc? diffusely panned-over the facet joints and within?
2. are there places in the USA injecting stem cell/spun plasma in the disc? Colorado the last I heard?
3. what is the status of future injectable stem cell/recombinant therapies. the last I checked, there were some phase III studies.

thanks on any info.
This is the last I heard. Which means it didn't work...
http://health.universityofcaliforni...cell-test-aimed-at-regenerating-lumbar-discs/
 
Could you provide literature to backstop that assertion?

Nice try. You are the one making a claim that fusion improves back pain by way of your clinical test. Show me the data.
 
I said no such thing. What I said was I refer patients for surgical evaluation, after first documenting that their pain generator is not improved by ESI/FJI/MBB, but is demonstrable by discography.

If you don't have any data to support your assertion, that's ok. Just curious.
 
You are like a dog chasing cars. So what are you going to do with it when you finally catch one.

You believe you've found a disease - that you bill handsomely for "diagnosing" - and you refer it for an expensive, invasive treatment, that you know
doesn't work. Great job.
 
So I take it you dont have any data? So instead, you resort to name calling. Impressive.
 
You feel that you have a test that is reliable enough to make an accurate diagnosis. But when the diagnosis is put to the test
with the 'gold standard' treatment, the treatment fails to improve the condition. There can be only one conclusion : the diagnosis
was wrong.

You defend discography because you can bill a lot to do it. You are doing a lot of harm to patients with this nonsense.
 
Lots of claims, a little unjustified slander, zero data.
 
Discography False Positives:

1. In vivo discography in degenerate porcine spines revealed pressure transfer to adjacent discs.
Hebelka H, Nilsson A, Ekström L, Hansson T. Spine (Phila Pa 1976). 2013 Dec 1;38(25):E1575-82.
doi: 10.1097/01.brs.0000435141.61593.05.

2.Low-pressure positive Discography in subjects asymptomatic of significant low back pain illness.
Carragee EJ, Alamin TF, Carragee JM. Spine (Phila Pa 1976). 2006 Mar 1;31(5):505-9.

Discography Causes Disc Injury:

1. 2009 ISSLS Prize Winner: Does discography cause accelerated progression of degeneration changes in the lumbar disc: a ten-year matched cohort study.
Carragee EJ, Don AS, Hurwitz EL, Cuellar JM, Carrino JA, Herzog R.

Spine (Phila Pa 1976). 2009 Oct 1;34(21):2338-45. doi: 10.1097/BRS.0b013e3181ab5432. Erratum in: Spine (Phila Pa 1976). 2010 Jun 15;35(14):1414. Carrino, John [corrected to Carrino, John A].

2.Needle puncture injury affects intervertebral disc mechanics and biology in an organ culture model. Korecki CL, Costi JJ, Iatridis JC.
Spine (Phila Pa 1976). 2008 Feb 1;33(3):235-41. doi: 10.1097/BRS.0b013e3181624504.

3. The leakage pathway and effect of needle gauge on degree of disc injury post anular puncture: a comparative study using aged human and adolescent porcine discs.
Wang JL, Tsai YC, Wang YH. Spine (Phila Pa 1976). 2007 Aug 1;32(17):1809-15.

4. Deleterious effects of discography radiocontrast solution on human annulus cell in vitro: changes in cell viability, proliferation, and apoptosis in exposed cells.
Gruber HE, Rhyne AL 3rd, Hansen KJ, Phillips RC, Hoelscher GL, Ingram JA, Norton HJ, Hanley EN Jr. Spine J. 2012 Apr;12(4):329-35. doi: 10.1016/j.spinee.2012.02.003. Epub 2012 Mar 16.

The Expensive, Ineffective, Downstream Treatment of Discography:

1..Meta-analysis of randomized trials comparing fusion surgery to non-surgical treatment for discogenic chronic low back pain.
Wang X, Wanyan P, Tian JH, Hu L. J Back Musculoskelet Rehabil. 2014 Dec 2.

2. Comparison of spinal fusion and nonoperative treatment in patients with chronic low back pain: long-term follow-up of three randomized controlled trials.
Mannion AF, Brox JI, Fairbank JC. Spine J. 2013 Nov;13(11):1438-48.

3. Four-year follow-up of surgical versus non-surgical therapy for chronic low back pain.
Brox JI, Nygaard ØP, Holm I, Keller A, Ingebrigtsen T, Reikerås O. Ann Rheum Dis. 2010 Sep;69(9):1643-8. doi: 10.1136/ard.2009.

4. Surgical stabilisation of the spine compared with a programme of intensive rehabilitation for the management of patients with chronic low back pain: cost utility analysis based on a randomised controlled trial. Rivero-Arias O, Campbell H, Gray A, Fairbank J, Frost H, Wilson-MacDonald J.
BMJ. 2005 May 28;330(7502):1239. Epub 2005 May 23.
 
Throw everything against the wall, and see what sticks? Remarkably, NONE of those articles support your original assertion, "there is no intervention that reliably predicts the clinical outcome of a fusion."

But keep trying. Even a broken clock is right twice a day.
 
Which goes to prove the evidence doesn't change practice, payment does.
 
Really sad that you can't seem to muster a single study regarding your claim, so you feel the need to resort to unsupported vitriolic slander.
 
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:)

Acta Orthop Suppl. 2013 Feb;84(349):1-35. doi: 10.3109/17453674.2012.753565.
Decision making in surgical treatment of chronic low back pain: the performance of prognostic tests to select patients for lumbar spinal fusion.
Willems P1.
Author information

Abstract
Chronic low back pain (CLBP) is one of the main causes of disability in the western world with a huge economic burden to society. As yet, no specific underlying anatomic cause has been identified for CLBP. Imaging often reveals degenerative findings of the disc or facet joints of one or more lumbar motion segments. These findings, however, can also be observed in asymptomatic people. It has been suggested that pain in degenerated discs may be caused by the ingrowth of nerve fibers into tears or clefts of the annulus fibrosus or nucleus pulposus, and by reported high levels of pro-inflammatory mediators. As this so-called discogenic pain is often exacerbated by mechanical loading, the concept of relieving pain by spinal fusion to stabilise a painful spinal segment, has been developed. For some patients lumbar spinal fusion indeed is beneficial, but its results are highly variable and hard to predict for the individual patient. To identify those CLBP patients who will benefit from fusion, many surgeons rely on tests that are assumed to predict the outcome of spinal fusion. The three most commonly used prognostic tests in daily practice are immobilization in a lumbosacral orthosis, provocative discography and trial immobilization by temporary external transpedicular fixation. Aiming for consensus on the indications for lumbar fusion and in order to improve its results by better patient selection, it is essential to know the role and value of these prognostic tests for CLBP patients in clinical practice. The overall aims of the present thesis were: 1) to evaluate whether there is consensus among spine surgeons regarding the use and appreciation of prognostic tests for lumbar spinal fusion; 2) to verify whether a thoracolumbosacral orthosisis (TLSO) truly minimises lumbosacral motion; 3) to verify whether a TLSO can predict the clinical outcome of fusion for CLBP; 4) to assess whether provocative discography of adjacent segments actually predicts the long-term clinical outcome fusion; 5) to determine the incidence of postdiscography discitis, and whether there is a need for routine antibiotic prophylaxis; 6) to assess whether temporary external transpedicular fixation (TETF) can help to predict the outcome of spinal fusion; 7) to determine the prognostic accuracy of the most commonly used tests in clinical practice to predict the outcome of fusion for CLBP. The results of a national survey among spine surgeons in the Netherlands were presented in Study I. The surgeons were questioned about their opinion on prognostic factors and about the use of predictive tests for lumbar fusion in CLBP patients. The comments were compared with findings from the prevailing literature. The survey revealed a considerable lack of uniformity in the use and appreciation of predictive tests. Prognostic factors known from the literature were not consistently incorporated in the surgeons' decision making process either. This heterogeneity in strategy is most probably caused by the lack of sound scientific evidence for current predictive tests and it was concluded that currently there is not enough consensus among spine surgeons in the Netherlands to create national guidelines for surgicaldecision making in CLBP. In Study II, the hypothesized working mechanism of a pantaloon cast (i.e., minimisation of lumbosacral joint mobility) was studied. In patients who were admitted for a temporary external transpedicular fixation test (TETF), infrared light markers were rigidly attached to the protruding ends of Steinman pins that were fixed in two spinal levels. In this way three-dimensional motion between these levels could be analysed opto-electronically. During dynamic test conditions such as walking, a plaster cast, either with or without unilateral hip fixation, did not significantly decrease lumbosacral joint motion. Although not substantiated by sound scientific support, lumbosacral orthoses or pantaloon casts are often used in everyday practice as a predictor for the outcome of fusion. A systematic review of the literature supplemented with a prospective cohort study was performed (Study III) in order to assess the value of a pantaloon cast in surgical decision-making. It appeared that only in CLBP patients with no prior spine surgery, a pantaloon cast test with substantial pain relief suggests a favorable outcome of lumbar fusion compared to conservative treatment. In patients with prior spine surgery the test is of no value. It is believed by many spine surgeons that provocative discography, unlike plain radiographs or magnetic resonance imaging, is a physiologic test that can truly determine whether a disc is painful and relevant in a patient's pain syndrome, irrespective of the morphology of the disc. It has been suggested that in order to achieve a successful clinical outcome of lumbar fusion, suspect discs should be painful and adjacent control discs should elicit no pain on provocative discography. For this reason, a cohort of patients in whom the decision to perform lumbar fusion was based on an external fixation (TETF) trial, was analysed retrospectively in Study IV. The results of preoperative discography of solely the levels adjacent to the fusion were compared with the clinical results after spinal fusion. It appeared that in this select group of patients the discographic status of discs adjacent to a lumbar fusion did not have any effect on the clinical outcome. The most feared complication of lumbar discography is discitis. Although low in incidence, this is a serious complication for a diagnostic procedure and prevention by the use of prophylactic antibiotics has been advocated. In search for clinical guidelines, the risk of postdiscography discitis was assessed in Study V by means of a systematic literature review and a cohort of 200 consecutive patients. Without the use of prophylactic antibiotics, an overall incidence of postdiscography discitis of 0.25% was found. To prove that antibiotics would actually prevent discitis, a randomised trial of 9,000 patients would be needed to reach significance. Given the possible adverse effects of antibiotics, it was concluded that the routine use of prophylactic antibiotics in lumbar discography is not indicated. In Study VI, the middle- and long-term results of external fixation (TETF) as a test to predict the clinical outcome of lumbar fusion were studied in a group of back pain patients for whom there was doubt about the indication for surgery. The test included a placebo trial, in which the patients were unaware whether the lumbar segmental levels were fixed or dynamised. Using strict and objective criteria of pain reduction on a visual analogue scale, the TETF test failed to predict clinical outcome of fusion in this select group of patients. Pin track infection and nerve root irritation were registered as complications of this invasive test. It was concluded that in chronic low back pain patients with a doubtful indication for fusion, TETF is not recommended as a supplemental tool for surgical decision-making. In Study VII, a systematic literature review was performed regarding the prognostic accuracy of tests that are currently used in clinical practice and that are presumed to predict the outcome of lumbar spinal fusion for CLBP. The tests of interest were magnetic resonance imaging (MRI), TLSO immobilisation, TETF, provocative discography and facet joint infiltration. Only 10 studies reporting on three different index tests (discography, TLSO immobilisation and TETF) that truly reported on test qualifiers, such as sensitivity, specificity and likelihood ratios, could be selected. It appeared that the accuracy of all prognostic tests was low, which confirmed that in many clinical practices patients are scheduled for fusion on the basis of tests, of which the accuracy is insufficient or at best unknown. As the overall methodological quality of included studies was poor, higher quality trials that include negatively tested as well as positively tested patients for fusion, will be needed. It was concluded that at present, best evidence does not support the use of any prognostic test in clinical practice. No subset of patients with low back pain could be identified, for whom spinal fusion is a reliable and effective treatment. In literature, several studies have reported that cognitive behavioural therapy or intensive exercise programs have treatment results similar to those of spinal fusion, but with considerably less complications, morbidity and costs. As the findings of the present thesis show that the currently used tests do not improve the results of fusion by better patient selection, these tests should not be recommended for surgical decision making in standard care. Moreover, spinal fusion should not be proposed as a standard treatment for chronic low back pain. Causality of nonspecific spinal pain is complex and CLBP should not be regarded as a diagnosis, but rather as a symptom in patients with different stages of impairment and disability. Patients should be evaluated in a multidisciplinary setting or Spine Centre according to the so-called biopsychosocial model, which aims to identify underlying psychosocial factors as well as biological factors. Treatment should occur in a stepwise fashion starting with the least invasive treatment. The current approach of CLBP, in which emphasis is laid on self-management and empowerment of patients to take an active course of treatment in order to prevent long-term disability and chronicity, is recommended.


Spine (Phila Pa 1976). 2007 May 1;32(10):1094-9; discussion 1100.
Provocative discography and lumbar fusion: is preoperative assessment of adjacent discs useful?
Willems PC1, Elmans L, Anderson PG, van der Schaaf DB, de Kleuver M.
Author information

Abstract
STUDY DESIGN:
A cohort study of clinical outcomes of lumbar fusion patients with preoperative assessment of adjacent levels by provocative discography.

OBJECTIVE:
To evaluate whether the preoperative status of the adjacent discs, as determined by provocative discography, has an impact on the clinical outcome of lumbar fusion in chronic low back pain (LBP) patients.

SUMMARY OF BACKGROUND DATA:
The results of lumbar fusion in chronic LBP patients vary considerably and are hard to predict. It is believed that degenerative levels adjacent to a fused spinal segment may be a cause of continuing pain. In this respect, it is important to know whether preoperative degenerative or symptomatic adjacent levels have an adverse effect on patient outcomes after lumbar fusion.

METHODS:
In 197 patients with an equivocal indication for lumbar fusion (two thirds were patients with prior spine surgery), the decision for either lumbar fusion or conservative management was determined by a temporary external transpedicular fixation trial. During the diagnostic workup, all patients had undergone provocative discography that included the assessment of the discs adjacent to the intended fusion levels. The individual changes in pain on a visual analog scale, assessed before treatment and at follow-up, and patient satisfaction were the measures of outcome.

RESULTS:
In the 82 patients who underwent a lumbar fusion, no difference in outcome was found between those patients with degenerative or symptomatic discs adjacent to the fusion and those with normal adjacent discs.

CONCLUSION:
In this cohort study of chronic LBP patients with an uncertain indication for lumbar fusion, the preoperative status of adjacent levels as assessed by provocative discography did not appear to be related to the clinical outcome after fusion.

J Spinal Disord Tech. 2002 Jun;15(3):245-51.
Does provocative discography screening of discogenic back pain improve surgical outcome?
Madan S1, Gundanna M, Harley JM, Boeree NR, Sampson M.
Author information

Abstract
The value of preoperative provocative discography in the setting of discogenic low back pain was investigated by evaluating surgical outcomes. Seventy-three consecutive patients who underwent posterolateral interbody and posterior spinal arthrodesis for discogenic low back pain refractory to nonoperative management were reviewed. Chronologically, the first 41 patients (group A) were indicated without discography, whereas the remaining 32 (group B) had been indicated only if their pain had been reproduced during disc injection. The two groups were similar in demographic, psychometric, and radiologic parameters. Average follow-up time in group A was 2.8 years and in group B it was 2.4 years, both with a 2-year minimum. Using modified Oswestry scoring, group A and group B patients had satisfactory outcomes of 75.6% and 81.2%, respectively. This difference was neither statistically significant nor suggestive. In this study, provocative discography screening did not improve surgical outcomes after circumferential fusion for lumbar discogenic back pain.
 
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Throw everything against the wall, and see what sticks? Remarkably, NONE of those articles support your original assertion, "there is no intervention that reliably predicts the clinical outcome of a fusion."

But keep trying. Even a broken clock is right twice a day.
Are you really saying, "This works unless you prove me wrong"? The burden of proof is on you.
 
Have to agree. Have to show discography has a clinically significant value/use, and that is more important than saying "nothing says it doesn't help."
 
I was in the Bay Area during the hay day of discography. I did tons myself at Kaiser because
my position was created to take the Derby/O'Neill referrals back inside. We all thought they
were useful back then and - for guys like us - they are fun to do. But, in retrospect they do much,
much, more harm than good.

If you look at the prototypical discography patient they are a working aged adult with normal alignment
and chronic disabling axial pain. Coupled with this are usually a potpourri of : secondary gain, excessive narcotic use, work loss, attorneys, SSDI applications, under-achievement in education, and sad lives with no perceived way out. In retrospect I would argue that the majority of these people have centralized pain that was ignored or misunderstood by us back in the day: http://www.ncbi.nlm.nih.gov/pubmed/23983029

But there is no reason to continue supporting it now. This is technique from the same era - and though leaders -that brought us high dose opioids for CNP.
 
It is pain - or suffering -that is no longer housed in the acute pain's interpretive center in the brain (NPS).(1)
Central pain is pain that cannot be explained through a verifiable peripheral nociceptive source and while it is
"described in terms of such damage" the subjective complaints are vastly disproportionate to physical findings
and typically accompanied by extremes of emotion, rumination, and somatic focus, work disability, compensation
claims, etc.

Note that I am not using the terms 'chronic pain' and 'central pain' interchangeably. An elderly patient with hip OA,
back OA, knee OA, etc probably represents chronic pain as an entity distinct from central pain. Whereas FMS is an example of
central pain. But most experts believe that there is only one central pain syndrome or functional somatic syndrome.(2)
This makes sense if you believe all of the fMRI research that is coalescing around the notion that ALL central pain syndromes
are housed in the brain's emotional circuitry while ALL acute pain is housed in the NPS.

It goes without saying that alot of folks who have built busines models around the treatment of central
pain by way of peripheral procedures and/or opioids will be resistant to the concept of central pain, regardless
of how well it seems to explain the US's pain & opioid epidemic.(5)

Acute Pain Processing:

Acute pain travels from peripheral nociceptors, through the lateral spinal thalamic tracts, to the NPS.(1,2)

Central Pain Processing:
May - or may not - start peripheral nociceptors, and travel from the SLT, but it no longer resides in the NPS,
but in the brain's emotional center. (4)

1. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3691100/
2. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3925165/
3. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3733463/
4. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3754458/
5. https://www.iom.edu/Reports/2011/Re...rming-Prevention-Care-Education-Research.aspx
 
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It is pain - or suffering -that is no longer housed in the acute pain's interpretive center in the brain (NPS).(1)
Central pain is pain that cannot be explained through a verifiable peripheral nociceptive source and while it is
"described in terms of such damage" the subjective complaints are vastly disproportionate to physical findings
and typically accompanied by extremes of emotion, rumination, and somatic focus, work disability, compensation
claims, etc.

Note that I am not using the terms 'chronic pain' and 'central pain' interchangeably. An elderly patient with hip OA,
back OA, knee OA, etc probably represents chronic pain as an entity distinct from central pain. Whereas FMS is an example of
central pain. But most experts believe that there is only one central pain syndrome or functional somatic syndrome.(2)
This makes sense if you believe all of the fMRI research that is coalescing around the notion that ALL central pain syndromes
are housed in the brain's emotional circuitry while ALL acute pain is housed in the NPS.

It goes without saying that alot of folks who have built busines models around the treatment of central
pain by way of peripheral procedures and/or opioids will be resistant to the concept of central pain, regardless
of how well it seems to explain the US's pain & opioid epidemic.(5)

Acute Pain Processing:

Acute pain travels from peripheral nociceptors, through the lateral spinal thalamic tracts, to the NPS.(1,2)

Central Pain Processing:
May - or may not - start peripheral nociceptors, and travel from the SLT, but it no longer resides in the NPS,
but in the brain's emotional center. (4)

1. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3691100/
2. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3925165/
3. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3733463/
4. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3754458/
5. https://www.iom.edu/Reports/2011/Re...rming-Prevention-Care-Education-Research.aspx
Central Pain as classically defined is a very concrete and unambiguous type of pain. Central post stroke pain from thalamic strokes, spinal cord injury, and MS would be a few examples. These are unambiguous pain syndromes caused by definite observable injury to pain centers or pathways in the central nervous system.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2670809/

http://www.practicalpainmanagement.com/classic-central-pain-syndromes-review-neurologic-causes-pain

Lumping those true central nervous system pain syndromes in with fibromyalgia which doesn't even have a definitive cause or pathophysiology at this point, and with other pain syndromes classically thought of as psychosomatic, is very, very questionable, in my opinion. What you're defining is not central pain.

None of your links are even are about true central pain. They reference emotional pain states, which are all over the map as far as understanding or lack thereof.

I disagree, with redefining all chronic pain, under some new definition of "central pain" lumping together diagnoses that likely all have very different pathophysiology.

I disagree completely, in that you repeatedly refuse to differential between types of "low back pain" as if they're all equal and as if "low back pain" is a valid diagnosis. It's not, anymore than "chest pain" is a diagnosis. Chest pain can be an MI, a pulmonary embolism, esophagitis, costochondritis, aortic dissection or other conditions. They all are distinct and have different treatments. I completely disagree with the approach of not taking the thought process beyond a chief complaint as a physician, and especially as a Pain specialist.

Similarly, you can't lump all pain syndromes affecting the lower half of the torso under a single garbage bin term of "back pain." Nor can you lump all pain patients under a single unifying theory of "central pain," which as you use the term, is really "psychosomatic" pain.

You're basically saying, all pain is "in the brain." Therefore, neither opiods nor injections help, and the only thing that will help, is the one thing that is the least likely to ever be funded by any payer, or be desired by patients, which is intensive inpatient cognitive behavioral therapy. If you're anti-opiate and anti-injection, that's fine. But tell me on a diagnosis by diagnosis basis. Don't expect me to equate treatments for fibromyalgia with those for cns pain from a thalamic stroke with those from a chronically crushed L5 nerve root. They are not the same. What treatments work or don't work, and the reasons why, are not the same.

In my opinion, this supposed unifying theory that "all pain is in the brain," though technically true, strips all pain syndromes of any unique pathophysiology and leaves us with essentially no (practical or effective) way to diagnose it, understand it or treat it.

Not all chronic pain is the same, just like not all acute pain is the same. A chronically crushed nerve root does not equal fibromyalgia does not equal post thalamic stroke central pain. Therefore, they should not be viewed the same, diagnosed as the same or treated the same.
 
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Agree with your concerns about terminology. IASP has their work cut out for them.

I don't think ALL disabling CNP in working aged adults is central, just most.

Your belief that you - or anyone- can make a specific diagnosis for back pain is one I shared 20yrs ago, prior to working in Ortho & Neorosurg spine depts. But the fact is that the majority of 'back pain' in working aged adults is nonspecific.
 
I think discography for patient being considered for an adjacent level fusion would be reasonable.

Centrally-mediated pain (thalamic stroke, trigeminal neuralgia, or post-SCI pain) is not the same as "limbic-ly mediated pain." Neither are the same as somatic functional syndromes or "overlap" syndromes (FMS, IBS, CFS). Those are distinct from true psychiatric somatoform disorders and other delusional states (delusional parasitosis and neurotic excoriations).

Headache syndromes, including chronic migraine and trigeminal autonomic cephalgias, are other real "central pain" states.

Finally, there's just good old fashioned medicalized suffering, malingering, and factitious disorders...
 
I think discography for patient being considered for an adjacent level fusion would be reasonable.

Centrally-mediated pain (thalamic stroke, trigeminal neuralgia, or post-SCI pain) is not the same as "limbic-ly mediated pain." Neither are the same as somatic functional syndromes or "overlap" syndromes (FMS, IBS, CFS). Those are distinct from true psychiatric somatoform disorders and other delusional states (delusional parasitosis and neurotic excoriations).

Headache syndromes, including chronic migraine and trigeminal autonomic cephalgias, are other real "central pain" states.

Finally, there's just good old fashioned medicalized suffering, malingering, and factitious disorders...
I agree completely.
 
Your belief that you - or anyone- can make a specific diagnosis for back pain is one I shared 20yrs ago, prior to working in Ortho & Neorosurg spine depts. But the fact is that the majority of 'back pain' in working aged adults is nonspecific.
If you are incapable of distinguishing a facet referral pattern from a radicular pattern, that speaks volumes. If generalized low back pain goes to a VAS of 0 for the duration of the local anesthtic after MBB, a dominant pain generator has been established. If, after first ruling out the posterior elements, a patient hurts when dye is injected into the nucleus of the disc, in a concordant fashion, under appropriate pressure parameters, then you have established the disc as a pain generator. Standard of care is to add Ancef/Gent/Clinda to your contrast material, despite what Dr. Williams' article states. If that same pain is then able to be turned off with lidocaine or marcaine, you have analgesically confirmed your provocation positive disc.
 
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Really sad that you can't seem to muster a single study regarding your claim, so you feel the need to resort to unsupported vitriolic slander.

That's the second time you've used the term 'slander'. I think you mean 'libel'. But hey, I'm not a lawyer....
 
IF you are incapable of distinguishing a facet referral pattern from a radicular pattern, that speaks volumes. If generalized low back pain goes to a VAS of 0 for the duration of the local anesthtic after MBB, a dominant pain generator has been established. If, after first ruling out the posterior elements, a patient hurts when dye is injected into the nucleus of the disc, in a concordant fashion, under appropriate pressure parameters, then you have established the disc as a pain generator. Standard of care is to add Ancef/Gent/Clinda to your contrast material, despite what Dr. Williams' article states. If that same pain is then able to be turned off with lidocaine or marcaine, you have analgesically confirmed your provocation positive disc.

There is always overlap. That's why dipalma's article from a couple years ago was nonsense. You can't use algorithms. Just doesn't work in LBP. We can partially help some types of LBP temporarily.
 
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That's the second time you've used the term 'slander'. I think you mean 'libel'. But hey, I'm not a lawyer....
My bad. Slander is only spoken word.
 
now you are talking 2 different procedures, right?

If, after first ruling out the posterior elements, a patient hurts when dye is injected into the nucleus of the disc, in a concordant fashion, under appropriate pressure parameters, then you have established the disc as a pain generator. Standard of care is to add Ancef/Gent/Clinda to your contrast material, despite what Dr. Williams' article states. If that same pain is then able to be turned off with lidocaine or marcaine, you have analgesically confirmed your provocation positive disc.
the first part is a standard discography, the second part, the anesthetic injection, is a discoblock?


the neurosurgeons do not agree with you regarding discography, but might consider discoblock:

Send to:


J Neurosurg Spine. 2014 Jul;21(1):37-41. doi: 10.3171/2014.4.SPINE14269.
Guideline update for the performance of fusion procedures for degenerative disease of the lumbar spine. Part 6: discography for patient selection.
Eck JC1, Sharan A, Resnick DK, Watters WC 3rd, Ghogawala Z, Dailey AT, Mummaneni PV, Groff MW, Wang JC, Choudhri TF, Dhall SS, Kaiser MG.
Author information
Abstract

Identifying the etiology of pain for patients suffering from chronic low-back pain remains problematic. Noninvasive imaging modalities, used in isolation, have not consistently provided sufficient evidence to support performance of a lumbar fusion. Provocative testing has been used as an adjunct in this assessment, either alone or in combination with other modalities, to enhance the diagnostic capabilities when evaluating patients with low-back pain. There have been a limited number of studies investigating this topic since the publication of the original guidelines. Based primarily on retrospective studies, discography, as a stand-alone test, is not recommended to formulate treatment strategies for patients with low-back pain. A single randomized cohort study demonstrated an improved potential of discoblock over discography as a predictor of success following lumbar fusion. It is therefore recommended that discoblock be considered as a diagnostic option. There is a possibility, based on a matched cohort study, that an association exists between progression of degenerative disc disease and the performance of a provocative discogram. It is therefore recommended that patients be counseled regarding this potential development prior to undergoing discography.
 
Spine J. 2014 Mar 1;14(3):491-8. doi: 10.1016/j.spinee.2013.06.095. Epub 2013 Nov 15.
Cytotoxicity of local anesthetics and nonionic contrast agents on bovine intervertebral disc cells cultured in a three-dimensional culture system.
Chee AV1, Ren J1, Lenart BA1, Chen EY2, Zhang Y3, An HS4.

BACKGROUND CONTEXT:
Carragee et al. reported an accelerated progression of lumbar intervertebral disc (IVD) degeneration after discography in a human trial. Local anesthetics and contrast agents have exhibited toxicity to cardiac, renal, and neuronal cells. We hypothesize that localanesthetics or contrast agents commonly injected into the disc space during discography may result in cytotoxicity in vitro. In this study, we compared the cytotoxicity of these agents, alone or in combination, using nucleus pulposus (NP) and annulus fibrosus (AF) cells in a three-dimensional (3D) culture system.

PURPOSE:
The purpose of this study was to examine the effects of local anesthetics and contrast agents on IVD cells to help guide their usage in future clinical practices.

STUDY DESIGN:
Ours was an in vitro study to assess the cytotoxicity of local anesthetics and contrast agents commonly used in discography, using bovine NP and AF cells cultured in a 3D system.

METHODS:
Bovine NP and AF cells were isolated and encapsulated in alginate beads and cultured in media completed with serum and ascorbic acid. Beads were transferred to a 24-well plate and treated with local anesthetics, nonionic contrast agents, or with saline as a control for 2, 6, and 16 hours. Three different concentrations of local anesthetics, lidocaine and bupivacaine, were tested: 0.25%, 0.125%, and 0.0625%. Two different dilutions (1:2 or 1:4) of nonionic contras agents, iohexol and iopamidol, were tested. In a parallel study, beads were incubated with a combination of local anesthetics at equipotent concentrations and contrast agents for 6 hours. Cells were then examined with the LIVE/DEAD cell assay. Live cells (fluorescing green) and dead cells (fluorescing red) were visualized using fluorescent microscopy. The percentage of live cells after treatment was determined.

RESULTS:
More cell death was observed when NP and AF cells were incubated with anesthetics than contrast agents at the concentrations tested. When tested at equipotent concentrations, 0.125% bupivacaine (N=8) resulted in significantly more cell death than 0.5% lidocaine (N=6) in NP cells (p<.05). In these studies, cell death caused by bupivacaine was both dose and time dependent. When tested at the same dilutions, iopamidol diluted 1:2 caused slightly more cell death than iohexol. When incubating the cells with a combination of contrast and anesthetic agent, the cytotoxic effects of the anesthetics and contrast agent were not synergistic. In this culture system, AF cells were more sensitive to some of the agents than NP cells.

CONCLUSIONS:
Cell death was observed when AF and NP cells were incubated in a dose- and time-dependent manner with local anesthetics and contrast agents commonly used for discography. Relative toxicity of these compounds was noted in the order of bupivacaine, lidocaine, iopamidol, and iohexol. Future studies of the effects of these agents in organ culture or animal models are indicated to predict what happens in vivo.

Copyright © 2014 Elsevier Inc. All rights reserved.
 
Spine (Phila Pa 1976). 2015 Apr 17. [Epub ahead of print]
Vertebral endplate (Modic) change is an independent risk factor for episodes of severe and disabling low back pain.
Määttä JH1, Wadge S, MacGregor A, Karppinen J, Williams FM.


CONCLUSIONS:
MC is an independent risk factor for episodes of severe and disabling LBP in middle-aged women. These observations support further work aimed at identifying the precise histology underlying MC.

Kind of a dumb - pointless article.

It should have been called "If your disc is inflammed enough to cause edema in the adjacent bone, it hurts."

Duh.....
 
I'd suggest that a full 90-99% of discograms are done incorrectly (not per ISIS guidelines) or have no useful purpose other than to benefit the physician.

Lobel's indication for discogram: Patient consented for surgery as a 2 level fusion and surgeon wants to see if he can get away with only a single level fusion.

Steve,

Why are you such a staunch supporter of ISIS? I don't get that. Why are they the be-all masters of the pain universe in your mind?

It is basically the babbling of that very strange and very misguided character Bogduk.

Don't think Bogduk is misguided? Lots of examples I am sure, but I'll give two that I know of. At an ISIS meeting - he tore a female Pain physician a new hole when she was talking about dermatomal patterns - he basically said dermatomal patterns are crap. Does he not practice pain at all? Stick an RF needle on any peripheral nerve/DRG and you will see - dermatomal patterns absolutely can be very defined and clear - to state otherwise begs a review of that persons psyche and education experience. Second, he has publically and in the literature said pusled RF doesn't work. That basically means he either never reads, or he can't read very well, or has alzheimer's.
 
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Define "central pain," please.

We have a guy in-house right now that has severe bilateral lower extremity (feet) CRPS (by budapest criteria). He failed an SCS trial (although it was with medtronic constant voltage so take that with a grain of salt). He was brought in for a week of ketamine and bisphosphonate IV and possible pain holiday.

A spinal was placed. He had no motor movement, and clear sensory changes in legs - however, he had no change in his pain.
 
A classic:

Surgical treatment for primary back pain associated with
disk changes (“discogenic pain”) is the more controversial
and less successful.1,2 When examination of the lumbar spine
reveals only common degenerative changes, the relation-
ship of these findings to a patient’s back pain is unclear. Disk
degeneration, anular fissures, small protrusions, and facet ar-
thritis are commonly found in individuals with little or no
back pain.3-6 Furthermore, many studies have shown that se-
rious disability in this group is associated with abnormal psy-
chological profiles, multiple chronic pain processes, and com-
pensation issues
.7,8Conversely,longitudinal studies have found
that the severity of chronic pain illness in this group appears
to correlate much less well with presence or extent of degen-
erative findings than with these psychosocial or generalized
neurophysiological comorbid conditions
.4,5 Not surpris-
ingly, the surgical treatment of this poorly defined disco-
genic pain illness has been somewhat disappointing.1,9 Ran-
domized trials of lumbar fusion compared with various
nonsurgical strategies have shown neither consistently good
best surgical results, the improvement in pain intensity score
was only 2 points (on a 10-point scale), and the disability im-
provement by Oswestry Disability Index was only 10 to 12
points (on a 100-point scale).11 Furthermore, clinical out-
comes appear to steadily deteriorate after 6 months. In a large
population-based study, approximately 18% of patients who
had spinal fusion for degenerative conditions experienced pro-
cedure-related complications; 20% of these patients went on
to reoperation over the next 5 years.13
 
Kind of a dumb - pointless article.

It should have been called "If your disc is inflammed enough to cause edema in the adjacent bone, it hurts."

Duh.....
Disc's don't get "inflammed" unless they have a vascular supply. Neovasuclarization only occurs after an an anular injury. HIZ's are present in only ~30% of anular injuries. This the presence of modic changes are another objective marker of an acute injury.
 
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