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Herzog R, et al. "Variability in diagnostic error rates in 10 MRI centers performing lumbar spine MRI examinations on the same patient within the three-week period." Spine J 2017; 17:554 –561. [written 6/25/17]

Early in 2017, Hospital for Special Surgery’s, Dr. Richard Herzog, et al., published the results of fascinating study in one of the top Spine Journals in the world, The Spine Journal. Basically, in this first-of-its-kind study, the researchers sent a single chronic low back patient to 10 different MRI centers for a MRI scan, within a very short period of time. Then all the radiology reports were gathered and compared for accuracy and uniformity. Although you would expect that all of these reports would would be similar, that was not the case at all!

Here’s the details: a 63-year-old female, who suffered chronic back and classic radicular pain, underwent magnetic resonance imaging scanning (i.e., had an MRI) at the study’s testing center. Her images were then reviewed by two veteran, board certified radiologists who are specially trained and certified in imaging of the spine. You can consider them as “super-radiologists,” who do not make mistakes when it comes to reading images of the spine. After finishing their analysis of the MRI images, both radiologists independently agreed that the patient had three very common chronic-pain-causing spinal conditions: disc herniation, spondylolisthesis, and severe spinal stenosis. Furthermore, all of these conditions were associated with significant nerve root compression. {There were other more subtle and more complicated MRI findings gleaned by these super radiologists, but I will leave these out of this review in attempts to keep it as simple as possible. However, you should know that the other radiologists screwed up these findings just as badly as they did the big three above!}

Over the next three weeks, this same patient randomly presented to 10 different MRI centers throughout the Greater New York area for the purpose of getting a new MRI and a new radiology report from each one. None of these MRI centers, which were all certified by the American College of radiology, or their radiologists had any idea that the patient was part of this study.  At each center, she gave the same history of injury and other intake information, but she did not reveal that she had previously had MRIs, or that she was part of the study – that was top-secret!

Finally, after the 10 random MRIs/radiology reports had been obtained, she underwent one more MRI back at the original MRI testing center, just to make sure her condition had not changed over that previous three-week period, which it didn’t.

The 10 MRI reports from those random MRI center visits were next compared to the true MRI findings and the shocking results were published.

First the good news: nine out of 10 radiologists (90%) correctly describe the spondylolisthesis that was present. Remember, spondylolisthesis (figure left) is so easy to see that a first-year chiropractors/medical doctor could easily spot it. Pretty sad that one radiologist completely missed it! The overwhelming majority of the radiologists, however, screwed up the associated nerve root compression. (See below)

[Figure left demonstrates a sagittal {from the side} view of a run-of-the-mill spondylolisthesis of L4 on L5. Note the forward slip. Pretty hard to miss this, right? [Note: note: I have used an image for my collection and have not violated the Copyright protection afforded by the Journal.]

Now the bad news: With regard to correctly making the diagnosis for the central spinal stenosis, the “miss-rate (i.e., they screw-up the diagnosis)” was a whopping 45%! In other words, only 55% of the radiologists properly caught and described the central spinal stenosis.

With regard to disc herniation, the miss-rate was 47.5%!

The miss-rate for catching and properly describing the nerve root compression, caused by either disc herniation, spondylolisthesis and central stenosis, was a whopping 72.5%!

Let’s take a more specific example. The patient had severe central stenosis at L2/3, which look like the below picture. (Note: again, I don’t want to violate the Journal’s Copyright protection on this paper/images, so I’ve used images from my own collection that look almost exactly like the images used in the paper. If anything, the image used in the paper demonstrated an even more dramatic difference which really shouldn’t have been missed by anybody! I would speculate that 80% of my eighth quarter chiropractic students would've caught this!)

The image on the below-left shows a normal thecal sac which is not deformed or compressed (always use the image at the pedicle level above the disc that is stenotic). You can see all the nerve roots floating around (black dots) in the cerebral spinal fluid (bright white stuff), happy as can be.  {If you’re having trouble seeing this, please study my Anatomy page, MRI page and Stenosis page to get up to speed.}

The image on the below-right, however, demonstrates a thecal sac that has lost a significant amount of its volume (a 66% loss or more is the definition for severe stenosis) because it’s getting “squished” by ligamentum flavum thickening and a bulging disc. There’s no question that it is significantly smaller than the thecal sac on the left. In fact, the nerve roots of the cauda equina are so squished, that you can’t see any white cerebrospinal fluid around them. This example represents moderate-severe spinal stenosis.













How did the New York radiologists do with regard to identifying this obvious severe stenosis? Shockingly, 40% of them completely missed it! That's right, they didn't even see it! That is completely un-excusable! Of the 60% of radiologists who actually saw it, only one of them actually described it correctly! In other words, only 10% saw it and described it correctly! Again, completely ridiculous.


Who cares about this? Except for spine surgeons and other spine specialists who read their own MRIs, chiropractors, physical therapists, general practitioners, and family docs all typically heavily rely on that radiology report to make their diagnosis, order additional testing and prescribed treatment. Furthermore, insurance claims adjusters and attorneys also rely on these radiology reports to authorize treatment and fight for settlements, respectively. 

So what? Well, as confirmed by the authors, these inaccurate reports may well lead to misdiagnosis; inappropriate treatment and/or lack of treatment; delayed treatment authorization; underpayment or overpayment in court settlements; and, perhaps most importantly, poor clinical outcomes.  For example, we know that the timing for discectomy surgery is crucial for the achievement of a good clinical outcome. If a radiologist misses a compressive disc herniation, this will most likely cause a significant delay in the surgery which in turn, according to research, may significantly decrease the chance for a good clinical outcome. Shouldn’t the radiology center and radiologist be held liable for such a blatant miss, just like they would if they missed a cancer? I absolutely think so.

Anecdotally, I have known for years that many radiologists are really bad at picking out and adequately describing the typical pain generators that may be responsible for the patient’s pain syndrome. Although they are typically very good at picking out things that will kill the patient (fracture, infection, hemorrhage, metastatic disease, etc.) and potentially get them and their clinics sued.  In fact, this phenomenon was the impetus for the development of my coaching service.

The $64,000 question is why are radiologists doing such a terrible job at reading MRI images and then generating a good report? I have some theories:

Reading time: I know several radiologists personally and based on my conversations with them, there is one huge problem: they are not given enough time by the MRI center to properly go through these images! For example, one radiologist I know who works for a prominent MRI center stated that they are only allowed eight minutes per patient! Eight minutes per patient!! That’s absolutely ridiculous, especially on cases that have multiple findings, like the one in the study.

Laziness/burnout: radiologists have to read off a lot of images each day. Therefore, it’s possible that they are just getting burned out and don’t put much effort forth, other than making sure the patient doesn’t have any serious disease. This sort of relates to the reading time problem.

Brainpower?: anecdotally it is known that the smartest medical students “typically” go after and get the more sought after specialties, like neurosurgery. The students who don’t do as well on the USMLE examinations and other testing are typically forced into the subspecialties that most doctors don’t want to go into, one of which is radiology and another is psychiatry. Therefore, perhaps, some of these radiologists don’t have the skill to pick out subtle pain generators other than the obvious spondylolisthesis (although one radiologist even missed that!).

Final Comments: although this is a very small study and needs to be repeated on a much larger scale, I hope that the results of this paper, which are a real slap in the face to the American College of radiology, will be the impetus for change within the radiology industry. Perhaps, akin to the work-hour-limitations placed on truck drivers and airline pilots, limitations should be placed on radiologists with regard to how many scans they are allowed to read in an eight hour day. I would speculate that there are many patients out there with now-chronic pain syndromes which occurred as a direct result of a radiology report which missed a key diagnosis.


Carragee EC et al. 2009 ISSLS Prize Winner: Does Discography Cause Accelerated Progression of Degeneration Changes in the Lumbar Disc: A 10-Year Matched Cohort Study
[written 2/4/17]

In 2009, Carragee et al publisher results of their award-winning study which tested the hypothesis that the “disc needlestick” which occurs normally as part of the discography procedure would not have any deleterious (damaging) long-term sequelae (effects) on that disc. Specifically, they wanted to know whether or not the needlestick would increase the chances of de novo (new) disc herniation and/or accelerated degenerative disc disease, like it does in animals.

What’s the bottom line? Discography, no matter what size needle was used, significantly (p<0.05) increased the rate of accelerated degenerative disc disease and new disc herniation, compared to discs that were not "stabbed" with the discography needle. These findings were actually double confirmed! Keep reading and I will explain below.


Out of a large pool of patients who all had similar diagnoses (i.e., previous symptomatic cervical degenerative disc disease, lumbar disc herniation or somatization disorder), two matched groups of patients were created based on their willingness to undergo provocative discography. Specifically, a discography group (n=75) was created, which was composed of patients who were willing to undergo provocative discography (discography) of the L3, L4, and L5 discs.  Then, a control group (n=75) was created with condition-match patients who were not willing to undergo discography. Both groups were willing to be followed and periodically reevaluated for the next 10 years.

After the groups were created, all 150 patients underwent an MRI of the lumbar spine, as well as standard radiographs. These MRIs were evaluated by two board-certified radiologists and any disagreements between those radiologists were settled by a third radiologist who was only used as a tiebreaker. The patients also completed a self-disability assessment test (the classic Oswestry Disability Index test), the results of which were reported in another paper.


At the 10-year time point, 80.3% of the study group and 74% of the control group were successfully contacted. After the interview, patients were eliminated from the study if it was discovered that they had suffered any type of interval trauma, infection, surgery, or pathology to their lumbar spine, which of course could have con founded the results.  Remember, the only disc injury we are studying is the needlestick injury, so other disc injuries had to be excluded.
After the follow-up exclusion criteria was applied, 52 (69%) subjects were left in the study group and 50 (67%) subjects were left in the control group. Next, new MRIs were performed on most of the remaining group members and reevaluated by the same radiologists.  If the patient had happened to have an MRI that was less than three years old, this was used.


^ With regard to the discs that suffered a needlestick injury during discography (i.e., the L3, L4 and L5 discs of the discography group), there were 55 de novo (new) disc herniations, compared to only 22 new disc herniations in the control group. This difference was very statistically significant: p=0.00003, which is way past the normal statistical threshold of p<0.05! In other words, there is almost no doubt that needlestick injury to the disc increases the chance for de novo herniation.

The discography group also suffered a statistically significant increase in the chance for the development of Modic change (a severe form of degeneration of the disc and vertebral endplate) (p=0.04), which is known to be associated with increased frequency of severe disabling low back pain [Maatta-2014].

The discography group also suffered increased degenerative disc disease (p=0.03) at the needlestick levels, with associated discopathy (disc height loss) (p=0.05).

Furthermore, with regard to the location of the herniations, they typically occurred on the same side and in the vicinity of the original needlestick injury. (p=0.0006).

As a confirmation, they also looked at the L1 and L2 discs of patients only in the discography group. Recall that these two discs were not stuck with the discography needle. Lo and behold, when comparing these two levels with the control group, there was no significant difference between the groups. This confirms that it was the actual needlestick injury to the disc that was causing all the degenerative sequelae.

And finally, they looked at the actual needle size. Some discographers used a 22 gauge (bigger) needle while others use to 25 gauge (smaller) needle. The thought was that the smaller gauge needle would cause less negative sequelae, but it did not. There was no statistically significant difference between the different sized needles, which matches animal studies.


Disc puncture with even a small gauge needle and limited injection pressures appears to be associated with accelerated disc degenerative processes which include disc herniation, loss of the disc height, loss of disc signal (DDD) and the development of reactive endplate changes (Modic change).
We believe careful consideration of risk and benefit should be used [when] recommending procedures involving disc puncture for diagnostic or therapeutic purposes….”


Now it's important to understand that not all of the needle-stuck discs in the study suffered significant pathological degeneration and its sequelae (i.e., Modic change, disc herniation, etc.), for some of them were unchanged, even after 10 years, so the question is, do you feel lucky? [No Clint Eastwood pun intended] According to this study, the odds are against you, for the needlestick disc injury significantly increases the chance of big trouble for that disc. So why take the chance?

I’ve been warning my coaching clients about the dangers of needlestick injury since 2002! The animal research of the 1990s clearly demonstrated that even the tiniest of pricks of the intervertebral disc almost universally doom it to degenerative disc disease (black disc) and the development of a full thickness annular tear and even herniation in some cases. I knew it would only be a matter of time before research would finally prove what seemed so logical to me and others.

Carragee et al. also raised another potential sequelae of discography and fusion outcomes. The phenomenon of adjacent segment disease following interbody fusion (i.e., the Domino effect) may be significantly enhanced if the fusion patient had previously underwent provocative discography. Somebody must do this study as soon as possible. Because it is common practice for a pre-fusion patient to undergo provocative discography which demands that a control disc (one above and/or below the fusion level) be punctured and tested.

I will bet you anything that if someone does a study they will find that patients who underwent provocative discography have a higher rate of adjacent segment disease than those who didn’t. It’s another perfectly logical conclusion which may take another decade or so to be proven by research.

I have decided not to wait, for I stopped recommending that a control disc be used to confirm a concordantly painful disc. Instead, I am recommending that the injectionist use a disc anesthetic to double confirm the concordantly painful disc, which I have learned that many discography practitioners fail to do, which they really should! But now they better.

Another fantastic study produced by Eugene Carragee, M.D., orthopedic surgeon, who is the head of Stanford’s orthopedic spine surgery department.


Two Papers Related to Lateral Lumbar Interbody Fusion [writing date 12/20/16]

Lateral lumbar interbody fusion (LLIF), also known as extreme lateral lumbar interbody fusion (XLIF) or sometimes just a "retroperitoneal transpsoas approach.

LLIF is a minimally invasive surgical procedure that allows surgical access to the lateral intervertebral disc of L1, L2, L3, and (although challenging) L4.

It was first described by Obenchain in 1991 but has only become more mainstream in the last decade. It was hoped that LLIF would become the new gold standard of interbody fusion by eliminating the well-known surgical complications of ALIF (i.e., retrograde ejaculation and great vessel injury) and PLIF/TLIF (i.e., exiting and traversing nerve root injury).

Although LLIF has eliminated the typical complications associated with PLIF, TLIF and ALIF, which is a good thing, it has created a brand new one: a dreaded lumbar plexus injury!

Let me explain. In order to gain access to the lateral portion of the disc, so interbody fusion can be started, the surgeon must "tunnel" or dissect through the psoas major muscle. And as any first year medical/chiropractic student knows, the ventral rami of the lumbar plexus travels right through the center of this muscle and are therefore subject to serious injury by the surgical dissection.

Although neuromonitoring is used and the surgeon is being as careful as possible, these nerves frequently get damaged by instrument trauma or overstretching of the nerve during dilation of the passageway.

Let's take a look at a couple of studies which support my above verbiage:

Cummock et al. (2011) retrospectively reviewed 59 consecutive LLIF surgeries at their institution. After a thorough review of the medical records, they discovered that 62.7 of the patient's had suffered neurological injury to the lumbar plexus which of course presented as anterior thigh and/or groin pain, burning, numbness, and/or weakness. Luckily, 90% of these patients ostensibly had complete resolution of their symptoms by one year, but 10% did not! In other words, 10% of people still suffered radicular pain (sciatica) even one year after the surgery was over.

In an award-winning paper, which was published in a high impact spine Journal, The Spine Journal, Lykissas et al (2013) followed 451 patients for an average of 16 months following their LLIF surgery. Specifically, these patients were separated into two groups: a rhBMP-2 augmentation group (their LLIF was augmented with rhBMP-2 to help ensure bony fusion) and a non-rhBMP-2 group. Immediately after surgery, approximately 47% of all patients suffered neurological injury. By the last evaluation, 40.3% of the BMP group were still suffering! In the non-BMP group, 27.8% were still suffering symptoms of nerve injury secondary to the procedure. Although, the neurological injuries suffered by the patient's who had their procedure augmented by rhBMP-2 was absolutely ridiculous, so was the group that didn't have their procedure augmented with rhBMP-2.

Although some surgeons have published LLIF results showing much less neurological injury, because of the Lykissas et al results, which was published in one of the major spine journals, I am not recommending that patients/clients choose a surgeon who performs this type of surgery.

They must go back to the drawing board on the LLIF (XLIF) technique!

In fact, they already seem to have a replacement that is in its infancy as we speak. It's called oblique lumbar interbody fusion or OLIF. I will not even comment on this yet because there are hardly any papers on, but there probably will be in another few years. The only thing I will say is that it is an approach to the disc that misses the psoas major muscle and its lumbar plexus and still is retroperitoneal (you don't have to open the peritoneum, which is always a good thing).

Desai MJ, et al. A prospective, randomized, multicenter, open-label clinical trial comparing intradiscal biacuplasty to conventional medical management for discogenic lumbar back [spine] pain. SPINE 2016,41:1065-1074. [writing date 9/19/16]

In 2016, Desai et al published the results of their randomized, multi-center clinical trial which compared the results of conservative care against conservative care with the addition of intradiscal biacuplasty, for the treatment of MRI and discography-confirmed discogenic pain.

STUDY DESIGN: using very strict entry criteria (perhaps a little too strict) the team performed provocative discography on 297 patients, all of whom had been tentatively diagnosed with discogenic pain (i.e., low back and/or leg pain secondary to a symptomatic annular tear within the disc). 

Of that large group, only 63 patients met the stringent inclusion/exclusion criteria and were enrolled in the study. Next, these patients were randomly assigned into either a conservative care group (n=34) or a conservative care + intradiscal biacuplasty (n=29) and then followed closely for (only) six months.

Just before they started treatment, at three months, and again at six months, all patients completed a battery of outcome assessment questionnaires, including a visual analog pain scale (VAS), the Oswestry disability index (ODI) and the physical functioning component of the short form SF-36 (SF-36).  Careful, medication usage records were also kept with regard to the amount of daily opioid consumption. There was no patient satisfaction questionnaire, return to work comparison, or minimally clinically important difference assessment, which was quite unfortunate.  Furthermore, there is no follow-up beyond six months.


With regard to the VAS, which was the “primary outcome assessment,” patients in the conservative care + biacuplasty group had a significantly greater drop in the mean VAS score (in other words, they improved more), compared to the conservative care alone group (P=0.02). The authors also looked at patients who obtained ≥ 50% improvement on VAS at six months and discovered that only 7% of the conservative care group reach this level, compared to 42% in the biacuplasty group (P=0.0013).

However, with regard to patient functional disability as demonstrated on the ODI and SF-36, there was no significant difference between the groups with regard to improvement. Furthermore, when they evaluated the opioid usage data, they also found no significant difference between the groups.

So, it seems fair to say that biacuplasty has about a 40% chance that decreasing your pain by 50% within six months. Not an earth shattering outcome!


First of all, I must applaud the authors' effort for designing and pulling off this complex multi-center randomized controlled trial, which is not easy to do.

That said, I was very disappointed that the patients were not followed for the “industry standard” of two years; six months is not nearly enough time to assess the efficacy (efficacy = safety and effectiveness) of any treatment intervention! In fact, I’m not even sure how they got published in SPINE, one of the top spine journals in the world (at least it used to be?) which I know from personal experience is very picky about that two-year mark. Hopefully, they will continue to report outcomes further on down the road.

Secondly, I am very disappointed with the results. Although at first blush I was once hopeful (i.e., based on the randomized placebo-controlled trial results of Kapural et al.) that we finally had a decent intervention for the treatment of chronic discogenic pain, my hopes are now somewhat dashed.  I mean these results demonstrate that only 42% of the patients with single-level discogenic pain got 50% pain reduction, as measured at the six-month time point. Those are not very promising numbers!  Furthermore, with regard to functional disability (the ability of the patient to participate in life), there is no difference between the groups, as measured by the ODI, the SF-36, or opioid pain medication usage.And let's not forget that only single-level symptomatic discs were allowed in the study. It's not uncommon for a patient to have two or even three levels of involvement. Intuitively, it would seem that there's even less of a chance for these multilevel involvement patients.

And what will the long-term consequences be for poking a hole in both sides of the disc? 

Well, we know from the work of Stanford’s Eugene Carragee that a single-sided disc needle puncture has deleterious long-term effects on the health of that disc. (i.e., the stick increases the chance of symptomatic disc herniation and need for surgery). The intradiscal biacuplasty procedure calls for a “double disc needlestick” (one on each side), which can’t bode well for the future of that disc.

What would be very interesting is to follow these same patients for 10 years and see what happens to them. I hypothesize that the group which underwent the biacuplasty would have a much higher rate of interbody fusion surgery (secondary to the development of severe chronic discogenic back pain) and disability, compared to the group that only received conservative care.

How come more people didn’t improve with the intradiscal biacuplasty procedure?

I would speculate that it’s all about the “luck” of needle placement with regard to the location of the annular tear(s). Remember, the needle placement is totally blind. In other words, the doctors can’t see the annular tear during the procedure, so they’re just guessing as to their location. I bet the ones who had good outcomes (got better) also had a needle placement either in or immediately adjacent to the symptomatic annular tear.  The ones who didn’t get better were not lucky enough to have either of the needles close enough to the annular tear to effectively ablate (burn) it into a non-pain generating tissue.

So, is intradiscal biacuplasty worth trying?

Well, in my opinion, if you are scheduled for an interbody fusion for the treatment of discogenic pain, then maybe intradiscal biacuplasty is worth a try as a last-itch-effort to avoid that fusion. However, if your pain and disability are not bad enough to risk having an interbody fusion, then based on the current literature and logic deduced from that literature, I would not recommend it.

BOTTOM LINE: if you have chronic disabling discogenic pain, as confirmed by MRI and provocative discography, then you’ve got less than a 50-50 chance of having your pain decreased by 50% by undergoing the intradiscal biacuplasty procedure. On the downside, based on the work of Carragee, you are most likely increasing your chances of ruining that disc secondary to double-needle-stick-induced degenerative change. Why do I say that?

Carragee followed the long term (10 year) after-effects of a single needlestick injury to the disc which demonstrated a statistically significant proportion of those discs became symptomatic (some to the point of surgery) compared to a control group. Therefore, it seems logical to conclude that the double-stick needle injury necessitated by the intradiscal biacuplasty procedure may doubles the negative effects demonstrated by Carragee.

Forsth et al. “A Randomized, Controlled Trial of Fusion Surgery for Lumbar Spinal Stenosis” 2016, the New England Journal of Medicine; 374:1413-1423. [date written: 8/14/16]

One of the oldest disputes amongst spine surgeons, i.e., whether or not to employ fusion in addition to decompression for the treatment of spinal stenosis, has finally reached the proverbial “Supreme Court” of medical journals: the New England Journal of Medicine.

In April 2016, Forsth et al. published the results of their randomized controlled trial (the so-called, “Swiss Spinal Stenosis Study”) which demonstrated that with regard to 2-year and 5-year clinical outcomes, it made no difference as to whether or not fusion was added to the decompression!


In order to be included in this study, patients had to meet the following inclusion criteria: #1) chronic symptoms of (>6 months) lower back and leg pain; #2) intermittent neurogenic claudication {in Europe they call this “pseudocladication”}; and #3) MRI-confirmed central spinal stenosis at one or two levels, as indicated by a diminished cross-sectional area of the thecal sac to ≤ mm2.  Patients with associated degenerative spondylolisthesis were not excluded! {Not decompressing and fusing a patient with stenosis and degenerative spondylolisthesis is a very uncommon practice!)

The 274 patients (69 of these had spondylolisthesis) ultimately included for the study were next randomly assigned to one of two groups: either a decompression group, or a decompression + fusion group.

Decompression, as described in my stenosis page, is a broad term which typically means that the surgeon employs a laminectomy/laminotomy, foraminotomy, and/or discectomy.

With regard to the exact surgical technique, the nuances were left up to the many different veteran surgeons who participated in the study.

Among other outcome tools, the gold standard Oswestry disability index (ODI) was completed by all patients before the surgery, at the two-year follow-up, and at the five year follow-up.


THERE WAS NO DIFFERENCE BETWEEN THE TWO GROUPS WITH REGARD TO CLINICAL IMPROVEMEN: at two years, the average ODI score had dropped 27 in the decompression + fusion group and 24 in the decompression group, which was not statistically different (P = 0.24). This drop did reach the “minimal clinically-important difference” in both groups: 15 and 17, respectively.

Perhaps the most surprising result was that there was also no difference with regard to clinical improvement between the degenerative spondylolisthesis patients who underwent decompression alone versus the ones who underwent decompression + fusion!

Furthermore, there was “no significant differences between the fusion group and the decompression-alone group in any of the seven patient-reported outcome measures.”


“… Decompression with fusion did not result in clinical outcomes that were superior to those with decompression surgery alone.”

Dr. Gillard’s COMMENTS:

The paper was unclear with regard to what type of spondylolisthesis was allowed into the study. The lead author was gracious enough to answer my email questions to clear this up: specifically, only degenerative spondylolistheses were allowed into the study, and all other types, including isthmic spondylolistheses, were excluded.



Chiropractic manipulation in the treatment of acute back pain and sciatica with disc protrusion: a randomized double-blind clinical trial of active in simulated spinal manipulation. [Spine J 2006; 6:131-137]

OPENING COMMENT: I have been aware of this paper for many years, but never publicly analyzed it because the verbiage in the paper, which includes some of the conclusions, don’t match the actual data presented in table #3 – the two sources are contradictory. I’ve emailed the corresponding author several times over the years (in fact I just emailed him again) but have never gotten an answer to which is actually correct. 

Nevertheless, since this is one of the papers that the New England Journal of Medicine used to support their opinion that the use of side-posture grade 5 manipulation for the treatment of disc-herniation-related back and leg pain is acceptable, I felt compelled to throw my hat in the arena.  So here we go!

In 2006, Santilli et al publish the results of a randomized double-blind clinical trial to assess the efficacy of side-posture chiropractic manipulation for the treatment of acute back and leg pain, which were thought to be secondary to an MRI-confirmed disc protrusion. The study was conducted in Rome, Italy and published in the e-version of The Spine Journal. 

It is important to understand that patients with positive neurological findings (which made them surgical candidates) and patients with the more serious types of disc herniation (i.e., an extrusion or sequestration) were not allowed to participate in the study.


One hundred and two (102) patients, all of whom had MRI-confirmed disc protrusions) with acute back and leg pain were randomly placed into either a side posture manipulation treatment group (n=53) or a sham manipulation treatment group (clinician only touched/very quickly massaged their low back) (n=49).

Patients were evaluated every 30 days with regard to back pain, leg pain, functional status, and non-opioid medication use for six months. MRIs were also taken in all patients at the end of the study (six months after it began) to see if the disc herniations had diminished or worsened in size.

The study was properly powered at 80% (this means it had enough patients to make a determination about the study topic); however, the follow-up period was not nearly long enough; the standard is at least a 24 month follow-up, not 6 months.


During the short follow-up, six patients left the study before its completion: five from the manipulation group, and one from the sham manipulation group.

If these dropouts were counted as treatment failures, then, as admitted by the authors, there would have been no difference with regard to pain intensity, or disability level between the treatment group and the sham group. An adequate explanation of what happened to the patients was not put forth.

However, if you simply remove the six patients from the study, a practice that is customary, then the treatment group patients did do statistically better with regard to back pain improvement when compared to the sham group. In accord with the verbiage of the paper, there was no statistical difference with regard to the intensity of leg pain.

With regard to functional disability (the patient’s ability to go about their normal activities of daily living) as measured by the often-used SF-36 there was no difference between the groups.

Although we don’t know specifically what happened to the five patients who left the treatment group, there were no serious adverse effects found in either group – it seemed like everybody tolerated the manipulation fairly well. Furthermore, although none of the disc protrusions decreased in size, none of them got worse.

The most impressive statistic from this paper, as picked up upon by the New England Journal of Medicine, was with regard to complete pain remission (these patients had no more complaints): at the end of the study (180 days) 28% and 55% of patients in the treatment group reported no back and leg pain, respectively. Only 6% and 20% of the sham treatment group reported no back and leg pain, respectively. This difference easily reached a level of statistical significance (P<0.005 and P<0.0001, respectively)


I’m concerned that the New England Journal of Medicine used this study to support the use of chiropractic grade 5 manipulation (side posture) as a treatment intervention for disc herniations. Why?

Because they failed to disclose that this study did not include patients with the disc extrusion or disc sequestration, two more serious types of herniation. I’m afraid people are going to get confused and think that it’s okay for a chiropractor or other manual therapist to use grade 5 manipulation on a disc extrusion or disc sequestration, which it is not!

Although I applaud the authors for designing and painstakingly carrying out this much-needed study, I don’t know why in the world they didn't continue the study for a longer time interval. I mean you almost always have to have a two-year follow-up, in order to get published in the quality research journals! This study tells us nothing how these patients were doing at at the end of 12, 18, or 24 months.

It’s been 10 years since the study was written; why haven't more results been published? It always makes me wonder that the results were reversed themselves with the passage of more time and therefore the authors decided not to publish. This is something that happens all too frequently in the research world and is called publication bias, or the file drawer effect.

Furthermore, how could a chiropractic grade 5 manipulation (crack of the back) help with disc that has been ripped through and its insides are showing on the outside? Manipulation certainly can’t reduce the size of the herniation, as clearly demonstrated in this study. On the contrary, it is my belief that grade 5 manipulation can potential turn a small disc protrusion into a large disc extrusion or even sequestration, which necessitates spine surgery. Many a chiropractor or other manual therapist has been sued over the latter scenario. So I don’t get it?

So, why did some of these patients in the treatment group get better compared to the fake treatment group? Most likely because their pain generator was not a disc protrusion! Remember, Disc protrusions are very commonly seen in completely asymptomatic (have no pain) people. Specifically, disc protrusions are seen on average in 30% of all people who don’t have low back pain.

Here’s an old analysis I did on this phenomenon:  


So what was causing their pain if it wasn’t a disc protrusion? Most likely something that chiropractors and other manual therapists are very good at treating: an inflammation / fixation of the facet joint! Remember, an irritated facet joint can not only cause severe low back pain, it can also refer pain down the lower extremity, sometimes even past the knee and into the foot (although this is rare).

Anyway, I still strongly disagree with the use of grade 5 manipulation for any type of disc herniation. I think it’s just too risky, isn't supported by research or even logic, and lawsuit inviting!

That said, there are other gentler techniques that chiropractors can use for treating patients with disc protrusions, such as Cox flexion distraction, a Leander table, or, just to make sure it’s not a facet problem, use an activator to mobilize the facet joints safely.

Sorry for the rant!

Kelly-2014: THE BMP STORY CONTINUES [date written: 11/21/15]

Bottom Line: in this very large study of almost 111,000, patients who were exposed to BMP-2 during fusion did not have a greater chance of developing cancer at a ~ 3-year follow-up when compared to patients who didn't have the BMP-2 used during their surgery. In fact, the patients who did not have the BMP-2, actually had a significantly higher rate of cancer development! Perhaps the "sky is not falling" after all.

In 2014, Kelly et al [1] publish the results of their investigation which look at whether or not spinal fusion augmented (accompanied) with recombinant human bone morphogenetic protein-2 (BMP-2) increased the likelihood of new cancer development.  Here’s how the study worked: from Medicare records they pulled out 467,916 patients who had undergone spinal fusion and put them into two groups: a study group (n= 110,808) (all had their fusions augmented with BMP-2) and a control group (none had their fusion augmented with BMP-2). Then they looked at whether or not these patients developed cancer following their fusion.

After crunching the numbers, the team concluded that at three years status-post fusion (that means three years after the fusion happened) the patients who did not have the BMP used during fusion actually had a significantly higher risk (p<0.001) of the development of cancer! Just the opposite of what was anticipated by many (especially the trial lawyers and Dr. Carragee).

Based on these results, the authors concluded, “Recent clinical use of BMP-2 was not associated with a detectable increase in the risk of cancer within the mean 2.9-your time window (following BMP-2 exposure).” And, “In conclusion, this study did not find an association between BMP-2 and cancer within a mean follow-up period of 2.9 years.

*If you don't know the whole BMP-2 story, you can catch up here: (The BMP-2 Drama).


1) Kelly et al. Cancer Risk from Bone Morphogenetic Protein Exposure in Spinal Arthrodesis. J Bone Joint Surg Am 2014;96:1417-1422.

Cribb-2007: Observations on the Natural History of Massive Lumbar Disc Herniation

In 2007, Cribb et al publish the results of their study (in the prestigious Journal of Bone & Joint Surgery {Br}) on the natural history of “massive” lumbar disc herniations. They looked at the common surgeon belief that massive disc extrusions and sequestrations (the largest and most severe types of disc herniations) need to be surgically removed for fear that they will cause cauda equina syndrome (permanent damage to the nerves that control the bladder). Specifically, they followed 15 patients, all in whom had a massive lumbar disc herniation which resulted in painful radiculopathy (sciatica), for two years in order to see how they fared without undergoing the recommended surgical decompression (removal of the disc herniation). The patients were only treated conservatively. All of the herniations were either at L4/5 (n=10) or L5/S1 (n=5) and occupied at least 50% of the volume of the vertebral canal (i.e., at least 10 mm in size).  The reason the patients chose not to have surgery was because #1) they were improving or #2) they were fearful of the surgery.  At an average of 24 months, patients return to the clinic for re-examination and a new MRI.

Natural Resorption: all of the discs significantly reduced in size. The mean resorption percentage was 80% (range 68% to 100%).

Discectomy: one patient needed emergency discectomy because of severe persistent pain (not cauda equina syndrome), notwithstanding a significant decrease in size of the herniation.

Cauda Equina Syndrome: none of the patients developed cauda equina syndrome.

CONCLUSION: “The fear of a missed cauda equina syndrome prompts some surgeons to operate on massive disc [herniations]. This fear may be misplaced.” Although the authors admitted this was a very small study, they concluded that “treating massive disc herniations non-operatively did not result in complications."

My Comments: this was obviously way underpowered (not enough patients to make a strong statistically significant conclusion about)); however, it was very interesting and in fact the first of its kind. So just because that disc herniation of yours is massive, does not always mean that you are forced into surgery. You will, however, be on a very tight leash and need to be closely monitored by your healthcare professional.


Cribb GL, et al. Observations on the Natural History of Massive Lumbar Disc Herniation. J one Joint Surg (Br) 2007;89-B: 782-784.

Seo-2014: Disc Herniation Resorption: Does It Really Occur and is That Resorption Correlated with Clinical Improvement?

Bottom line: this study confirms that approximately two thirds of disc herniations significantly decrease in size within six months via conservative care and mother nature. And if the herniation ruptured the posterior longitudinal ligament (i.e., if the patient has a disc extrusion or transligamentous herniation), then almost 90% of them decreased in size within six months. However, this decrease in size does not correlated with patient improvement.

In 2014, Seo et al published the results of their investigation which looked that whether or not disc herniations spontaneously reabsorbed and at whether positive herniation resorption was correlated with clinical improvement.

Specifically, 43 patients, all in whom had symptomatic MRI-confirm disc herniations at baseline (the beginning of the study), received six months of conservative care which included meds, PT and epidural steroid injections for those that suffered severe radicular pain. A follow-up MRI was performed at six months to assess the size of the herniation and clinical improvement. What was interesting about this study is that this was the first one to use a novel (new) three-dimensional analysis system which determine the volume of the herniation at baseline and then again in six months.

RESULTS: On average there was a statistically significant (p < 0.01) decrease in the size of the herniation at the six month follow-up. However, not all herniated discs decreased in size (volume). In fact, of the 56 disc herniations looked at, 21 of them (38%) actually increased in size (volume). The authors also discovered, as has been previously demonstrated, [Ahn-1996] that the herniation morphology was predictive of reabsorption. That is, patients with a herniation which disrupted the posterior longitudinal ligament (transligamentous herniations) had a greater chance of resorption. Specifically, 88% of the transligamentous-type demonstrated significant reabsorption, compared with only 42% of patients with subligamentus-type herniations.

This study also looked at clinical outcomes and discovered that at the six month follow-up 14% (6/43) of the cohort actually got worse, conservative care notwithstanding, which forced five of them into emergency discectomy. However, volumetric changes in herniated discs were not significantly related to the clinical outcomes of the patients.Therefore, mechanical compression alone does not explain the symptoms of lumbar disc herniation. Other factors must be involved, such as chemical irritation. [26-29] They concluded by saying, "in contrast to prior studies, we found that lumbar disc herniation is a dynamic disease that does not always resolves spontaneously."

Final Comments: although interesting, this study is certainly underpowered so you really can't make any solid conclusion regarding these findings. However, it does support many previous studies and I like the idea of using three-dimensional analysis.


Seo et al (2014) Three-Dimensional Analysis of Volumetric Changes in Herniated Discs of the Lumbar Spine: does spontaneous resorption of the herniated disc always occur? Eur Spine 2014; DOI 10.1007/s00586-014-3587-1