Reasonable2012ParticipantApril 20, 2013 at 11:26 pmPost count: 10
Hi Doctor Corenman.
Kudos to the Steadman Clinic and appreciate you giving back to the public through this forum.
I was injured in a car crash 2.5 years ago. Both the neck and lumbar area were injured, apparently initiating degenerative cascades in both. Of note is there appears to be bilateral fractures or at least pannus tears at L5-S1 (far-lateral sagital MRI “before” crash shows an angle of 109 degrees of I guess it is pars structure relative to bottom edge of vertebral body, versus angle of 129 degrees “after”…the bone has rotated). Indeed in the last 2.5 years I have suffered ever-increasing chronic continuous inflammation in the lower back. Rather than exercise strengthening and resolving it, all I can do is splint it in place with muscle and ligament…and inactivity; that is the only thing that has worked to calm down inflammation…inactivity. Had the neck surgery done 3 weeks ago, and recovering from it. It needed done for safety reasons before the back surgery.
Here is the lumbar issue that has surfaced in the last couple of months. Prior to the neck surgery, Work Comp ordered a DEXA scan to assess if bone density is adequate. Now, I am only 52 and was in robust health (weight-bearing gym exercise, running, etc.) before the crash.
The arm and hip were scanned, and the results were as follows: arm was above-average, in line with my expectation from an active lifestyle, good nutrition, and what-not. Hip was somewhat below average.
Since I am at work to get the lumbar surgery financed (it is far and away the more debilitating of the two by a magnitude, but evidently the neck is the more dangerous injury of the two and had to be corrected first), the bone density issue seems to be relevant to the low back too. Surely it is *more* relevant since the low back bears much more weight and forces.
So, the PCP ordered an additional DEXA scan of the lumbar region. Here is what T-Scores it found: L1 of -1.1; L2 of -1.8; L3 of -2.0; L4 of -2.7. L4 is osteoporosis and L1-L3 ostepenia. My whole lower back has become multiple times more vulnerable to future fractures!!! Yikes!
The pattern that is suggested to me is that the closer one gets to the “Ground Zero” of L5-S1, the lower is the bone density. It would seem reasonable to infer that if the arm was also below average, that one could conclude a genetic predisposition, bad lifestyle or nutrition, etc. It also seems reasonable that apart from any injury, etc., one would expect the hip and lumbar density to be *higher* than the arm, due to the density-increasing effects of weight-bearing exercise, my being a male (no child bearing) and the lumbar region doing far more load bearing than the arms.
1. What is your assessment and characterization of a possible DEXA Scan pattern?
2. Is it possible that a combination of chronic fractures and resulting chronic inflammation borrowed calcium from the surrounding area, thus resulting in this pattern?
3. The DEXA Scan only went from L1-L4. Based on this data, and assuming for the sake of argument chronic fractures, what is your educated guess or *speculation* as to the numbers I might see at L5-S1?
4. Are these numbers poor enough to alter the plan of a single-level TLIF, and if so, in what way? For example, would multiple levels need to be fused to compensate for the poor density? Or would I no longer be a candidate for TLIF?
5. Were it you doing the surgery, would you stick with the one-level plan, go on in and then manually assess to see if the bone density is adequate at L5-S1? If it is not, what would be your on-the-fly options for compensating? Would you close it up and back out, fuse multiple levels, or ?
6. In the remaining two or three months before lumbar surgery, should I be doing anything other than calcium and vitamin D supplements to protect what bone density I have left in that region? (For example, calcitonin, testosterone patch [though my T level is mid-level normal], bisphosphonates.) Note that I can no longer take my anti-inflammatory med diclophenac while the bone is fusing from the neck surgery, and so inflammation is more a problem than ever…I am able to walk one or two blocks per day at most, I ice multiple times on bad days (was doing this every day, but it has settled down some) and can do no exercise that articulates L5-S1.
Thank you in advance for any feedback you will provide on these issues!!!!
RichardDonald Corenman, MD, DCModeratorApril 21, 2013 at 1:35 amPost count: 8455
I don’t understand how the spine is so much lower in T score than the hip or wrist. This is distinctly uncommon. It is even more uncommon to have increasing loss of bone density descending the spine to the sacrum. I would question the machine accuracy.
Nonetheless, if this bone densitometry T score is true, then certain provisions should be considered. Bone healing (fusion) is normally not affected by osteoporosis but the hold of the screws necessary to reduce and secure the two vertebra together can be a weak link. The surgeon has to be prepared to use cement (PMMA) if the screws do not hold well.
The fact of the matter is the isthmic spondylolisthesis at L5-S1 normally puts so much stress on the abnormally loaded segments that Wolfe’s law comes into effect. Wolfe’s law is that bone that has increased load will increase its density (put down thicker bone). These two segments (L5 and S1) are very stressed by the abnormal load. These segments tend to become very sclerotic (very hard bone is produced) and this makes surgery easier as the screws tend to gain great purchase from this sclerotic bone.
It would not hurt to have an internist or endocrinologist look at these studies to see if they believe you need treatment. Treatment can increase the bone deposition and make surgery more effective.
You can use tylenol after your surgery. It does not have the anti-inflammatory properties but does have pain killing properties.
Dr. CorenmanReasonable2012ParticipantApril 21, 2013 at 3:46 amPost count: 10
Thank you for the information Dr. Corenman.
The studies were done at the Harmony Imaging Center in Fort Collins, and I have every confidence in their accuracy.
Indeed, in trying to explain the odd pattern, that is what led to the suggested hypothesis that chronic inflammation and chronic fractures had been borrowing calcium from the area for 2.5 years. The inflammation has been severe; it feels like I am walking around with a broken back. (Though it has calmed down some since I have become an inert lump sitting around the house.)
Will follow up your suggestion to see an endocrinologist or internist. Should any other possible causes of this odd pattern come to mind, your input would be invaluable. Some other disease or condition? I do know there is about 25% of spondylolisthesis and moderate/severe stenosis as of last x-ray, and that the amount of spondylolisthesis increased 38% over a period of 8 months from last standing x-ray. There is complete disc degeneration at L5-S1 (other discs are not degenerated).
RichardDonald Corenman, MD, DCModeratorApril 22, 2013 at 6:16 amPost count: 8455
If you had the L5-S1 region scanned, you would probably find greater bone density at this level due to the aforementioned sclerosis I noted before.
It is quite puzzling to find diminishment of bone density as you travel down the spine. Remember that the spine is loaded with every step, sitting maneuver and impact. You cannot load the upper vertebra without loading the lower vertebra with the same force. Please let the forum know what your endocrinologist thinks. This is interesting.
Dr. CorenmanReasonable2012ParticipantApril 23, 2013 at 12:31 amPost count: 10
Thanks for the response. I concede that without the additional scan we must speculate. As you indicate, the existing pattern (which is consistent to include data points of hip and arm and L1-L4) of reduced density the closer you get to L5-S1, is not something one would have expected sans scan.
No idea why the L5-S1 is not included in the scan; maybe surrounding bone structures interfere with it’s accuracy? Perhaps that would be wise, to have the PCP request an additional scan of L5-S1, if it is possible?
The MRI does suggest one other puzzling thing. It apparently shows evidence of *both* bilateral fractures plus not having bilateral fractures! As mentioned before, there is apparent rotation of the I guess it is neural foramina, relative to the vertebral body, that suggests fracturing. There is also much degeneration of the facet joints, which evidently is not expected in the case of bilateral fractures, because the facets then are not load-bearing.
Am wondering if the degenerative changes occurred *before* the fractures happened. Or possibly, it is some sort of chronic stress fracture that allows the neural foramina to rotate a tiny amount but is held from separating by muscle and ligament. Then, the fracture poorly heals (and so is load-bearing but with less structural integrity due to the splaying out and “play” in the joint), only to fracture again and rotate some more, when put under stress…vicious cycle. In this way, there is some degree of load bearing, plus there is a lot of inflammation and a chronic fracture process.
It sounds from your responses that you are ruling out the calcium borrowing from such a condition as being a significant factor in causing this loss of bone density. In other words, you would expect to see far less impact to density over a 2-year period then for what that could acount, and especially the pathological mechanical forces at L5-S1 would overshadow the density-sapping effects of chronic inflammation and chronic fracturing. Is that correct?
I am working now to set up the endocrinologist consult, and for sure will post the findings. Had another surgeon say that the MRI-indicated stenosis of my lower back was, “impressive.” Can add “puzzling” to the list of adjectives that are both disconcerting and intriguing at the same time, when they come from leading doctors.
*Kudos* for the intellectual honesty and scientific curiosity to want to explore the issue rather than gloss over it for it daring to challenge a standard model.
Note the before-crash MRI showed no spondylolisthesis, mild stenosis, and no disc degeneration. I am working on the current evidence-based model that the crash started a degenerative cascade.
RichardDonald Corenman, MD, DCModeratorMay 12, 2013 at 9:26 amPost count: 8455
As you note, degenerative facet changes are typically inconsistent with pars fractures as pars fractures will unload the facets. There is one situation where pars fractures and degenerative facets can coexist and that is with dysplastic pars fractures. In this case, the pars fractures and heals/fractures and heals again in a cycle that causes elongation of the pars and finally, degenerative changes of the facets.
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