Facet syndrome

[PMR2008]

I am a little confused about facet mediated pain.
If there are no examination maneuvers with high specificity or sensitivity how do you determine if someone is appropriate for a facet block?
How do you choose whether to block the facet joint vs. do a steroid injection?
If patient has good relief from block do they always have good relief from RFA?
Thanks

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[Aether2000]

Pure facet disease is probably uncommon- less than 15% of patients. Pathophysiology involves structural changes such as cartilage degeneration (due to spondylolisthesis or weight transfer from a collapsing disc to the facets), subluxation, locking facets (hyperdistraction), traction osteophytes, trophism, capsular tears due to trauma, fracture or fracture/dislocation, hematoma, and subchondral hemarthrosis. Physical exam will be positive depending on the pathology. Capsular tears appear to be more commonly associated with contralateral flexion pain whereas intra-articular processes tend to be associated more with extension plus ipsilateral rotation. However studies tend not to support any specific diagnostic criteria.
In my practice, patients that bend slightly forward at the sink or over the oven and have significant severe low back pain or have more pain on getting up from sitting than from standing or walking have a greater likelihood of having facet pathology.
Selection for RF: depends. The validated studies are for medial branch blocks, and if one does these carefully with low volumes, precision placement, and has a time concordant threshhold of 90%+ pain relief with functional improvement, then there is an 85% chance of having an excellent outcome from RF. Use of 50% relief results in much lower RF efficacy. Use of sloppy blocks, 1-2cc per medial branch and not using either confirmatory views or contrast increases the false positives on the diagnostic block.

 

[facetguy]

Do insurance companies hassle you guys if an injection has more of a diagnostic rather than therapeutic purpose? As PMR2008 suggests, there often isn't a foolproof way of determining exactly the source of a patient's pain, particularly LBP, so I would think that injections are often directed at gaining diagnostic info.

 

[olafa]

Do insurance companies hassle you guys if an injection has more of a diagnostic rather than therapeutic purpose? As PMR2008 suggests, there often isn't a foolproof way of determining exactly the source of a patient's pain, particularly LBP, so I would think that injections are often directed at gaining diagnostic info.

Blocks prior to RFA are standard of care, blocks are just that --> diagnostic. In fact insurances are pushing back on facet injections, which honestly are not a majority of what people do to treat facetogenic pain. You are going to want to RFA for long term relief. Although there are some studies that show repeated blocks giveing long term relief - I dont buy it!

 

[willabeast]

Pure facet disease is probably uncommon- less than 15% of patients. Pathophysiology involves structural changes such as cartilage degeneration (due to spondylolisthesis or weight transfer from a collapsing disc to the facets), subluxation, locking facets (hyperdistraction), traction osteophytes, trophism, capsular tears due to trauma, fracture or fracture/dislocation, hematoma, and subchondral hemarthrosis. Physical exam will be positive depending on the pathology. Capsular tears appear to be more commonly associated with contralateral flexion pain whereas intra-articular processes tend to be associated more with extension plus ipsilateral rotation. However studies tend not to support any specific diagnostic criteria.
In my practice, patients that bend slightly forward at the sink or over the oven and have significant severe low back pain or have more pain on getting up from sitting than from standing or walking have a greater likelihood of having facet pathology.
Selection for RF: depends. The validated studies are for medial branch blocks, and if one does these carefully with low volumes, precision placement, and has a time concordant threshhold of 90%+ pain relief with functional improvement, then there is an 85% chance of having an excellent outcome from RF. Use of 50% relief results in much lower RF efficacy. Use of sloppy blocks, 1-2cc per medial branch and not using either confirmatory views or contrast increases the false positives on the diagnostic block.

would you worry about increasing a grade 2 spondylo by denervating multifidus doing a RF procedure on someone with a stable grade 2 spondylo?
thank you.😕

 

[Aether2000]

No....the multifidus is not completely denervated and the anterior abdominal oblique is the major support for the lumbar spine. The multifidus are actually relatively small muscles....

 

[facetguy]

No....the multifidus is not completely denervated and the anterior abdominal oblique is the major support for the lumbar spine. The multifidus are actually relatively small muscles....

Gotta disagree. Multifidus is critical for lumbar stabilization. Not that other muscles don't play a role, but multifidus is a major key. The lumbar multifidus gets thicker as you go caudally such that it is thicker at the L/S junction than the erector muscles (which thin caudally). Many movements require the transversus abdominus and internal oblique to fire first though, which is perhaps what you meant. LBP patients tend not to fire any of these muscles well.

As an aside, an interesting thing to do is to check the size of and amount of fatty infiltration of the multifidus on your patients' MRIs. Atrophy and fatty infiltration is a pretty good indicator for at least mechanical dysfunction/instability and often pain as well.

 

[Mister Mxyzptlk]

Atrophy and fatty infiltration is a pretty good indicator for at least mechanical dysfunction/instability and often pain as well.

Interesting. This was the conclusion on my brain MRI. No wonder I'm unstable.

 

[lobelsteve]

As an aside, an interesting thing to do is to check the size of and amount of fatty infiltration of the multifidus on your patients' MRIs. Atrophy and fatty infiltration is a pretty good indicator for at least mechanical dysfunction/instability and often pain as well.

I'm not buying it. And instability in allopathic terms typically means greater than 4mm movement on flexion and extension.

I don't believe in subluxations, palpable instability without neurologic compromise, or the Easter bunny.

 

[Aether2000]

PM R. 2009 Aug;1(8):719-22.
The significance of multifidus atrophy after successful radiofrequency neurotomy for low back pain.
Dreyfuss P, Stout A, Aprill C, Pollei S, Johnson B, Bogduk N.
SourceDepartment of Rehabilitation Medicine, University of Washington, 21108 NE 129th CT, Woodinville, WA 98077, USA. [email protected]

Abstract
OBJECTIVE: To determine the presence of lumbar multifidus atrophy and pain after successful lumbar medial branch radiofrequency neurotomy for zygapophysial joint mediated pain.

DESIGN: A prospective observational analysis of 5 patients who had undergone successful unilateral radiofrequency neurotomy (RFN) of the lumbar medial branch divisions of the lumbar dorsal rami. At 17 to 26 months after RFN, 3 blinded radiologists evaluated the relative composition and size of the multifidus muscle at different segmental levels on lumbar magnetic resonance imaging (MRI). They were asked to determine the lesioned levels by evidence of multifidus atrophy. The accuracy of predicting the correct side and level lesioned was evaluated.

SETTING: Private spine practice in Tyler, Texas.

PATIENTS: Five patients who had unilateral lumbar medial branch RFN for proven lumbar zygapophysial joint-mediated pain were selected.

INTERVENTIONS: MRI of the lumbar spine at a mean of 21 months (range, 17-26) after successful lumbar RFN.

OUTCOME MEASURES: Multifidus atrophy on a lumbar MRI, pain assessment and use of cointerventions.

RESULTS: Diffuse lumbar multifidus atrophy was detectable with MRI. However, radiologists could not reliably predict the side and segments lesioned. Despite denervation of the multifidus, at 12 months after RFN all subjects had ongoing pain relief and did not require or request additional treatment.

CONCLUSIONS: This preliminary study provides evidence that successful medial branch RFN for lumbar zygapophysial-mediated pain does cause initial denervation but no discernable segmental atrophy of the multifidus at long-term follow-up. Previous denervation and diffuse atrophy in these subjects was not associated with pain.

 

[mille125]

Gotta disagree. Multifidus is critical for lumbar stabilization. Not that other muscles don't play a role, but multifidus is a major key. The lumbar multifidus gets thicker as you go caudally such that it is thicker at the L/S junction than the erector muscles (which thin caudally). Many movements require the transversus abdominus and internal oblique to fire first though, which is perhaps what you meant. LBP patients tend not to fire any of these muscles well.

As an aside, an interesting thing to do is to check the size of and amount of fatty infiltration of the multifidus on your patients' MRIs. Atrophy and fatty infiltration is a pretty good indicator for at least mechanical dysfunction/instability and often pain as well.

sorry facet guy but I gotta agree with steve on this one...

 

[facetguy]

I'm not buying it. And instability in allopathic terms typically means greater than 4mm movement on flexion and extension.

I don't believe in subluxations, palpable instability without neurologic compromise, or the Easter bunny.

You're right about the classic allopathic definition of instability. The instability that I was referring to is the abnormal forces and loads placed upon the facet joint capsules when muscles, such as the multifidus, do not fire appropriately to stabilize the motion segment. Why don't the multifidi fire appropriately? One reason is because the mechanoreceptors, embedded in the spinal ligaments and small intersegmental spinal muscles, become damaged by either a macrotrauma, a repetitive microtrauma, or fatigue (e.g., prolonged flexion leading to ligamentous creep and subsequent alteration of the 'neutral zone'). Without correct mechanoreceptor input, the motor response (from, say, the multifidi) is "corrupted" as they say. Without muscular stabilization (which I technically incorrectly referred to as "instability"), the joints are exposed and injured, leading to pain.

No Easter Bunny here. But I agree that we aren't talking about the type of instability for which we'd think spinal fusion.

 

[facetguy]

As far as multifidus atrophy and fatty infiltration being associated with low back pain, it makes sense. There's been some study into this:

http://www.ncbi.nlm.nih.gov/pubmed/17254322
"Fat infiltration in the LMM (lumbar multifidus) is strongly associated with LBP" in adults but not adolescents.

http://www.ncbi.nlm.nih.gov/pubmed/21289551
This one showed no association in young adults (avg. age 21), which is more or less consistent with the first study.

http://www.ncbi.nlm.nih.gov/pubmed/10657162
Recommends radiologists report multifidus atrophy seen on MRI.

http://www.ncbi.nlm.nih.gov/pubmed/15543053
Multif and psoas atrophy correlate with unilateral LBP.

I don't think it's everything but may be something to take note of when looking at MRIs.

 

[SSdoc33]

the importance of the multifidi is way underestimated in the pain literature IMHO. if you have an older/painful back that is not moving all that well, then an RF is definitely the way to go. the literature is way behind in this regard.

the multifidi are important not solely for "stability", but also for appropriate movement patterns. dare i say that most pain docs dont give a second thought to biomechanics.

i really try to avoid RF in "younger" patients. i dont know about you, but i dont want a portion of my spine turning into fatty goo. i have enough of the rest of me that already looks like that

 

[willabeast]

would you worry about increasing a grade 2 spondylo by denervating multifidus doing a RF procedure on someone with a stable grade 2 spondylo?
thank you.😕

OK so what do you all think about the above question i posed earlier?😕

 

[101N]

OK so what do you all think about the above question i posed earlier?😕

The mutifidus is a little wussy of a muscle, it cant possibly stabilize a grade II spondy. More important are the supporting ligamentus structures which you arn't affecting.

My question would be: Do you really think it's dorsal column pain in the face of significant anterior column disease?

 

[101N]

As far as multifidus atrophy and fatty infiltration being associated with low back pain, it makes sense. There's been some study into this:

http://www.ncbi.nlm.nih.gov/pubmed/17254322
"Fat infiltration in the LMM (lumbar multifidus) is strongly associated with LBP" in adults but not adolescents.

http://www.ncbi.nlm.nih.gov/pubmed/21289551
This one showed no association in young adults (avg. age 21), which is more or less consistent with the first study.

http://www.ncbi.nlm.nih.gov/pubmed/10657162
Recommends radiologists report multifidus atrophy seen on MRI.

http://www.ncbi.nlm.nih.gov/pubmed/15543053
Multif and psoas atrophy correlate with unilateral LBP.

I don't think it's everything but may be something to take note of when looking at MRIs.

I agree with assessing the paraspinal and iliopsoas bulk as a routine part of your MRI screens. This was how I was taught during fellowship. And now an example:

70y/o healthy male retiree sent to me by a local NS for consideration of vertebroplasty. Patient presents with atraumatic L3 & L4 anterior wedge compression fx's while gardening. With the NEJM articles on efficacy I balk and decide to work him up instead. PMH sig for orchiectomy in the distant past and I tentatively dx andropause related osteoporosis, get a dexa & testosterone levels. Surprisingly, both are normal.

So I take another look at the axial MRI's. Complete fatty replacement of the paraspinals. EMG shows fatty replacement, bx shows fatty replacement. The guy experienced anterior column failure - akin to post-laminectomy kyphosis - due to loss of his dorsal stabilizers. If I weren't so lazy this is a case report. Ran it by Andy Haig who has an interest in this entity.(1)

As Charlie always says: Ya see what you look for and ya look for what you know.

1. The bent spine syndrome: myopathy + biomechanics = symptoms.
Haig AJ, Tong HC, Kendall R. Spine J. 2006 Mar-Apr;6(2):190-4. Epub 2006 Feb 3.

 

[powermd]

In my experience axial pain almost always responds to MBBs with >50% relief if it can be provoked with extension maneuvers. Pain while laying flat on the exam table in front of me and/or low back pain with Patrick's seems to increase the sensitivity. Axial pain provoked with flexion almost never responds. Except in young people who have suffered some kind of traumatic injury.

Of the second group of non-MBB-responders, TPs almost always knock out the pain, at least temporarily, suggesting that the generator is myofascial.

Very rarely, I see someone who seems purely discogenic. Pain with flexion. Nontender paraspinals. Better with extension. Worse with sitting, standing, Valsalva, etc.

 

[bedrock]

TPs almost always knock out the pain, at least temporarily, suggesting that the generator is myofascial.

As long as those TP are done with ultrasound......😀

 

[willabeast]

The mutifidus is a little wussy of a muscle, it cant possibly stabilize a grade II spondy. More important are the supporting ligamentus structures which you arn't affecting.

My question would be: Do you really think it's dorsal column pain in the face of significant anterior column disease?

i never thought too much about this until i did a bilateral RF L345 on a 70 + yo female, did not work that great, became unstable, wound up having fusion. it could have been a coincidence but it definitely increased my paranoia about denervating multifidi.

 

[101N]

i never thought too much about this until i did a bilateral RF L345 on a 70 + yo female, did not work that great, became unstable, wound up having fusion. it could have been a coincidence but it definitely increased my paranoia about denervating multifidi.

You are conscientious and that's good. But you didn't cause the instability if there was any.

"Instability" is more often a pseudo-diagnosis which roughly translates to: I want to fuse you. As someone suggested earlier in this thread, we see the term a lot more than we see the real deal.

 

[PinchandBurn]

extension of spine--likely culprit=mbb

flexion of spine causing pain= discogenic, usually. You can do a discography to confirm Question is what can we really do about it since there's not more IDET. I guess there's biaculoplasty and intradiscal steroids....Alas, there's always fusion.

 

[facetguy]

extension of spine--likely culprit=mbb

flexion of spine causing pain= discogenic, usually. You can do a discography to confirm Question is what can we really do about it since there's not more IDET. I guess there's biaculoplasty and intradiscal steroids....Alas, there's always fusion.

Hey, that made me think of methylene blue. Any updates on that in the literature since that last paper (the one that made methylene blue sound like a miracle)?

 

[101N]

Hey, that made me think of methylene blue. Any updates on that in the literature since that last paper (the one that made methylene blue sound like a miracle)?

Yes, there has been another miracle out of China...

Spine J. 2011 Feb;11(2):100-6. Epub 2010 Sep 20.
Intradiscal injection therapy for degenerative chronic discogenic low back pain with end plate Modic changes.
Cao P, Jiang L, Zhuang C, Yang Y, Zhang Z, Chen W, Zheng T.
Source
Department of Orthopaedics, Shanghai Institute of Traumatology and Orthopaedics, Rui Jin Hospital, The School of Medicine, Jiao Tong University, Shanghai 200025, China.
Abstract
BACKGROUND CONTEXT:
The effect of intradiscal steroid therapy for patients with degenerative chronic discogenic low back pain remains an issue of debate.
PURPOSE:
To evaluate the effect of various intradiscal injection regimens for patients with degenerative chronic discogenic low back pain and end plate Modic changes.
STUDY DESIGN:
Double-blind, randomized, controlled, prospective clinical study.
PATIENT SAMPLE:
One hundred twenty patients with discogenic low back pain and end plate Modic changes on magnetic resonance imaging (MRI) who received discography but were unwilling to accept surgical operation.
OUTCOME MEASURES:
Pain and function were determined by the visual analog scale (VAS) and the Oswestry Disability Index (ODI) assessment.
METHODS:
Patients who received diagnostic discography for suspected degenerative discogenic low back pain were recruited. A total of 120 patients with positive discography and end plate Modic changes at a single level were enrolled in the study and allocated into Groups A and B according to the type of Modic changes on MRI. Then, the patients in Groups A and B were randomized into three subgroups, respectively. Intradiscal injection of normal saline was performed in Subgroups A1 and B1, intradiscal injection of diprospan was performed in Subgroups A2 and B2, and intradiscal injection of a mixed solution of diprospan+songmeile (cervus and cucumis polypeptide) was performed in Subgroups A3 and B3. The clinical outcome of each patient was evaluated and recorded by using the VAS and ODI at 3 and 6 months after the procedure.
RESULTS:
The subgroups were comparable with respect to gender, age, pain, and percentage disability. Neither VAS pain scores nor Oswestry function scores of the patients within Group A had any improvement at 3 or 6 months after saline injection, but both of them improved significantly at the two time points after diprospan and diprospan+songmeile injection, respectively. Meanwhile, the latter two injection protocols led to no significant difference in pain relief and functional recovery. Similar results were obtained in patients within Group B. Furthermore, no difference of the improvement of VAS pain scores or Oswestry function scores was found between the patients within Group A and within Group B at different time points after various interventions.
CONCLUSION:
Intradiscal injection of corticosteroids could be a short-term efficient alternative for discogenic low back pain patients with end plate Modic changes on MRI who were still unwilling to accept surgical operation when conservative treatment failed.
Copyright © 2011 Elsevier Inc. All rights reserved.

 

[powermd]

As long as those TP are done with ultrasound......😀

The only way bro... 😀

To be fair, I do put steroids in these injections. So how is it different from the well accepted piriformis injection? You're putting local and steroid into a muscle you believe is causing pain. Did this four weeks ago for a guy with gluteal pain, came back yesterday- still 99% relief. I need an infomercial.

 

[facetguy]

The only way bro... 😀

To be fair, I do put steroids in these injections. So how is it different from the well accepted piriformis injection? You're putting local and steroid into a muscle you believe is causing pain. Did this four weeks ago for a guy with gluteal pain, came back yesterday- still 99% relief. I need an infomercial.

Speaking of piriformis injections, would there ever be an indication to inject the sacrotuberous ligament?