Diseases, Disorders information » Low back pain

Low back pain. Summary

Disorders — Fri, 18 Dec 2009 15:58:30 +0000

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So, in summary, I know it’s a lot of material pretty quickly, but when you take a history, you want to know about the character and the nature of the pain, what makes it better, what makes it worse, what medications have worked, which haven’t, do you have any neurologic findings, is it back pain, leg pain, and do your quick and dirty assessment. Flexion, extension, check the Trendelenburg maneuver, have them heel and toe walk. If it’s mechanical, brief period of bed rest followed by active physical therapy, pretty much as soon as the patient can tolerate it. If it’s disc herniation, sciatica, neuropathic pain, neurologically intact, maybe an epidural, maybe an oral steroid, but certainly off to physical therapy as soon as possible. If there is a neurologic deficit or the acute cauda equina syndrome, that is obviously an emergency and needs to be referred pronto. Deformity – you pretty much refer those when you see them, unless it is a spondylolysis in a gymnast which can be treated with a brief period of bed rest. Spinal stenosis, making the diagnosis on the basis of history, of neurogenic claudication and physical examination showing a flexion preference, again, perhaps epidural therapy, that is the study hot off the presses, maybe physical therapy, flexion distraction which is the new thing that is being evaluated, tumor atypical mechanical features that will be referred, infection, risk factors, atypical features and refer.

The first is metastatic disease

Disorders — Wed, 16 Dec 2009 17:49:53 +0000

In the few minutes that remain, I would like to go over some of the less common, but arguably some of the most important features of the differential, share with you what I hope are some clinical pearls that you will find valuable, and just review the current thought on how to treat these things. The first is metastatic disease, and that is something you certainly don’t want to miss in the differential, remembering that figure of 10% presenting with back pain as their first symptom of metastatic disease due to spinal spread. The spine is the most frequent site of metastatic disease, metastatic disease is the most common tumor in the spine. The site of origin is really not significant, virtually all areas will refer to the spine, there are some predilections of different anatomical regions, and it is almost always anterior. You will almost always find the metastases starts in the body and then will proceed to the pedicle or posterior elements. The reasons for that lie in the arrangement of volvulus plexus which provides a perfect one way highway for metastatic disease to the spine following the reasoning of the seed and soil hypothesis. You will see lumbar vertebrae most frequently involved, neurologic involvement, however, is most frequent in thoracic metastases.
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The blood supply to the thoracic spine is not as extensive as cervical or lumbar, so that is far more at risk for neurologic insult with a thoracic fracture, infection, or certainly a metastatic disease, so you are much more likely to see neurologic involvement in the thoracic spine. Most of the primaries come from these five categories, breasts, thyroid, prostate, kidney and then the hematopoietic. Breasts tend to go to cervicothoracic; lungs cervicothoracic; prostate has a predilection for lumbosacral and pelvis; prostate can be identified with a little bit more facility on plain films because that frequently is a blastic lesion, almost all these others are lytic lesions, so if you see something that’s making bone in a male patient in the lumbar spine, thing about a prostatic metastasis. Most of these present with pain, atypical pain, not mechanical pain, but the pain awakens me at night, it is unremitting, it is unresponsive to nonsteroidals, it is unresponsive to narcotics. Neurologic impairments comparatively rare, under 10%. Deformity, actual collapse with kyphosis, spondylolisthesis, scoliosis due to metastatic disease comparatively rare as well. It is also extremely unreliable. If you look in an elderly patient population, the incidents of some wedging or compression deformities, particularly in the setting of osteoporosis is extremely high, so that is a very, very inaccurate way to determine whether or not metastatic disease is present. Pain thought to be due to the enlarging mass within the body, canal encroachment and then of course neurologic issues as well as instability and cord compression.
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We classify this, according to the matter of Harrington and really, there are five different categories as to whether bone is involved, whether the neurologic structure is involved, or both, the most important thing is just to draw a line right here, and that is basically if there is no evidence of collapse. Those patient’s can be treated nonoperatively, usually with radiation therapy. If there is evidence of vertebral collapse with structural problems, or structural problems and collapse with neurologic involvement, those are the patient’s who usually go to surgery assuming that their survivorship justifies that and they have been appropriately staged. Most of surgery for this is anterior, and that is supported in the literature because again, that’s where the problem is, it’s the Willie Sutton principal, why do you rob banks, because that’s where the money is. Why do you go anteriorly, because that’s where the tumor is. You can see someone here with a clear metastatic lesion at L5, this appears to be kind of a pseudoblastic lesion because of the collapse of the L5 vertebral body, you can see posterior expansion into the canal, this is an individual with known breast disease and metastatic disease, in other aspects of the spine, who presented basically with a cauda equina syndrome, and here you can see the collapse on the AP, you can see the posterior extent of the tumor here virtually obliterating what is left of the cauda equina, metastatic disease elsewhere in the spine, very important thing to think of that with skip areas, that is very, very common. If you have one metastasis, it is pretty likely you will have another, and this patient was managed with an anterior and posterior decompression. Unfortunately at L5, there is really no good anterior instrumentation system. We now have a number, we can do everything from the front, but this patient required a fairly gib operation of front and back, removal of the L5 body, there is a fibular strut and then subsequent posterior instrumentation.

Someone who is refractory to conservative care

Disorders — Tue, 15 Dec 2009 14:08:14 +0000

Here is an example of someone who is refractory to conservative care, rather severe central stenosis, you can see the cauda equina, is just flattened, this is someone who could walk not even half a block before she had to sit and rest, underwent a multilevel decompression as you can see here from L2 south, underwent an instrumented posterolateral fusion concordantly, due to the presence of a spondylolisthesis, which you can see here at L4-5. Female viagra increases sensitivity in women with weak libido. In randomized prospective studies, it has been shown that in the setting of a spondylolisthesis and stenosis, patient will do better with a concomitant fusion. Deformity of spondylolysis, spondylolisthesis, kyphosis and scoliosis, in general, when you see these, you will probable want to refer them because the evaluation of pain generators in deformity can be somewhat confusing, common problem, particularly in younger patient’s spondylolysis, and this is a defect in the pars interarticularis, that can be determined either in plain x-rays or on oblique films, the so-called Scottie dog sign, if you have taken the lamina and twisted it 45 degrees, someone thought this looked like a Scottie dog, where Scotti’s head is the transverse process, his pedicles the eyes, superior articular process, the ear and so forth, if Scottie is wearing a collar, that is a stress fracture commonly seen in female gymnast, particularly in adolescence, that is a spondylolysis, if Scottie is decapitated, then the vertebra is slipped and you’ve got a spondylolisthesis, and that is graded anywhere from 1 to 4, depending on the percentage of slip, grade 125 to 50 and so forth.
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These patient’s can have back pain with or without radicular irritation or neurologic entrapment, these people have a flexion preference because this is the posterior mechanical column, and in attempting to lean forward and flex, interspinous, supraspinous ligaments are getting tightened just like a string of pearls effect and that is relatively stabilizing, so these patient’s again will have a flexion preference or a sitting preference as opposed to someone with degenerative disc disease. Certainly, if the deformity progresses, it is almost invariably a surgical issue. If you pick up a high grade spondylolisthesis, a grade 3 or grade 4, particularly in an adolescent or somebody in their 20s, they will be at a high risk for progression and those patient’s should be referred immediately because that’s the group that will benefit from surgical stabilization of that. So in general, those patient’s should be referred.

Spinal stenosis

Disorders — Fri, 11 Dec 2009 22:54:27 +0000

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Spinal stenosis, something that you will see in an older aged group and as the population ages, this is something we are looking at more and more as far as attempts to define the optimum care of these patients. Remember, with spinal stenosis, the classic symptom is neurogenic claudication, that is bilateral lower extremity pain, heaviness in relation to activity. That is differentiated from vascular claudication in the way that they relieve the pain. Vascular claudication on the basis of aortoiliac disease will present as pain related activity as well. The patient with vascular claudication just has to stop and stand still and the symptoms will get better. The patient with neurogenic claudication actually has to flex and change positions, and that makes sense, because what they are trying to do when they flex, they are trying to open up the canal diameter, by reversing the lordosis, you are trying to increase neural foraminal dimensions in the central canal diameter, so these patient’s will have a flexion preference and a sitting preference.
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The other thing you see is the shopping cart sign, ask somebody if they do their own grocery shopping, they say os yes, I can walk much better as long as I lean over a cart. They have neurogenic claudication until proven otherwise. The neurologic examinations of these individuals is normal as a rule, you are not going to find a motor deficit or a sensory deficit to any degree of regularity. Conservatively, there is an increasing body of circumstantial evidence that epidural steroid therapy may help, there are actually some specific physical therapy protocols for this that have been investigated in the literature, nothing conclusive yet, although intuitively, it’s hard to imagine you are really opening things up in a lasting way in the setting of a degenerative stenosis, perhaps transcutaneous electrical nerve stimulation that has been studied a bit more in the pain literature and then surgical, and of course hallmark of the surgical treatment is a laminectomy to decompress the nerve roots, classically that was thought to be successful in about 85% of people, long term followup studies from Scandinavia have shown the success rate is probably closer to 65 or 70% as far as long term relief of symptoms, the two problems are that many patient’s after laminectomy will complain of back pain, which again is not something a laminectomy is designed to resolve, you are dealing with a nerve compression and the claudication, number two is remember, that degenerative disease is progressive, and five years later, anywhere from 20 to 50% of patient’s may have problems at adjacent levels, so-called junctional syndromes with stenosis at the level at which the decompression was stopped, not because the surgery was done incorrectly, but because the degenerative disease has progressed.

If you don’t have a cauda equina syndrome

Disorders — Wed, 09 Dec 2009 17:04:33 +0000

If you don’t have a cauda equina syndrome and you see someone with sciatica which is a rational way to approach it, a brief period of bed rest, followed by active mobilization and therapy with or without modalities as needed acutely, nonsteroidal, most likely some form of analgesics, epidural or oral steroid therapy, that would certainly seem intuitively to be plausible, but again there are very few studies in the literature that document the efficacy in a statistically valid manner. The exception to that was in the Clinical Orthopaedics and related research, just the last issue of the journal, where the study from Scandinavia showing that epidural steroids in a randomized prospective study, may in fact, have some benefit in this pathology, but that is literally hot off the presses. If you take a patient to surgery to remove the disc and the gold standard for that is the so-called microdiscectomy which is essentially an outpatient procedure, you should be just about 100% successful at relieving the sciatica, assuming you have four of these signs, root pain, root irritation, straight leg raising, root compression signs, motor or sensory deficit and a corresponding myelographic or MRI findings, in other words, what you are seeing in the objective imaging modalities, has got to be precisely concordant with the patient’s symptoms and physical examination, and these are older data, but other studies have verified those. Again, remember we are only treating the leg pain, we are not treating the back pain.
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Here is an example of that, here is a patient who presented with a trunk shift, no neurologic deficit, failed to respond to conservative care after eight weeks, was then referred, and you can see the plain films do show the trunk shift, but not much else. This patient came MRI in hand, courtesy of the referring physician, and in fact, MRI shows this very, very large disc prolapse, it’s a pretty old MRI as you can see, which is just about 40% of the cross section area of the canal, and when you have a prolapse that big, most of the time it’s a free fragment, so-called sequestered fragment, it’s actually broken off and this was the homunculus that was removed at the time of surgery, and you can see that was a very large fragment indeed. Patient’s like this are extremely gratifying to treat surgically because literally they will wake up, and in the recovery room, be pain free, and that is a very, very happy patient and a very happy surgeon.
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About disc herniation

Disorders — Tue, 08 Dec 2009 21:02:07 +0000

How about disc herniation? This is kind of the classic disease that Mixer and Bard described in 1934, with disc herniation and prolapse, we’re thinking about sciatica, referred pain, we’re thinking about neuropathic pain, difference in characteristics, neuropathic pain, remember, tends to respond to membrane stabilizing agents, tends to respond to steroids, will respond to narcotics in extremely high doses, if it’s pure neuropathic pain almost to the point of sedation. Mechanical pain on the other hand, tends to respond to narcotics and nonsteroidal anti-inflammatories, so that’s another important differential point. If someone gets a good deal of relief from a narcotic, you should be thinking a little bit more about mechanical pain than you are neurogenic pain. Well of course, a disc herniation results in sciatica, so the main problem here is not back pain, but leg pain. The sciatica can be caused by disc herniation, subarticular stenosis in the area of the foramen and facet, and those degenerative pictures, lateral recess stenosis, again, is an accompaniment of the degenerative cascade. If one decompresses this with a microdiscectomy or laminotomy discectomy, remember you are treating the leg pain only. You are not going to get the patient’s back pain better, in fact, a recent study from Scandinavia has shown that up to 20% of patient’s after a laminotomy discectomy, will have significant enough back pain so as to require additional care of even in some cases, intervention.
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On physical examination, a patient who presents with a trunk shift, should alert you to the possibility of a disc prolapse and sciatica. If you have a disc prolapse far lateral here, so this is coming down on top of the ganglia, the patient will tend to shift away from that, shifting ipsilaterally with provoke the sciatica like-wise, if the prolapse is in the axilla of the root, a contralateral shift will result in sciatica, ipsilateral shift will tend to decompress that. So if you see a patient with a trunk shift that you really can’t reduce, do think about some form of nerve root entrapment.
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Again, here is the slide from Netter and physical examination, this is in the hand-out, as promised coming back to the acute cauda equina syndrome, and this is really the only the only surgical emergency that you are going to see in spine patient’s. This is usually on the basis of a large central disc herniation entrapping multiple nerve roots as shown at the bottom line, clinically, these patient’s will tell you the diagnosis very clearly because they will be some of the most miserably uncomfortable patient’s that you will see. A typical history, as I was unable to find a comfortable position, I tried to sleep sitting in a chair, tried to sleep in flexion, tried to sleep with a trunk shift to unload the neural compression, the classic triad is bilateral sciatica, GU of GI signs and saddle anesthesia from sacral nerve involvement. The GU sign is retention, not incontinence, very important differential point. You may get overflow incontinence if you have a large distended bladder, but incontinence is more frequently due to stress incontinence and has nothing whatsoever to do with spine pathology, so this is somebody with retention. The GI sign again is constipation, not incontinence and that’s because of the involvement of the sympathetics and the sacral nerve roots. If you see someone with this, an immediate MRI or myelogram, immediate surgery and even if you get these patient’s to the operating room within 24 hours, up to 40% still have some neurologic residual.

Pain generator. Back pain

Disorders — Mon, 07 Dec 2009 19:59:11 +0000

Conservatively, if you see somebody with back pain very rational approach if they are neurologically intact, and you have done your good physical examination and kind of gone the mental calisthenics that I have outlined, and you decide this is mechanical pain, put them to bed for a very brief period of time, nonsteroidal, perhaps a modality in physical therapy if there is a good deal of soft tissue distress such as muscle spasm, a brief course of ionophoresis, ultrasound may help, before you mobilize the patient into an active physical therapy program, hopefully no later than 10 days after the onset of symptoms. If the patient doesn’t improve and the pain is incapacitating after six to twelve weeks, the next step would be to consider an MRI, that is the first line of investigation. Obviously you are going to be able to screen for tumor or infection, although if you would suspect those based on physical examination or constitutional symptoms, I would hope the MRI would be ordered before that time, but really what you are looking at is gathering information on the degenerative pathology and an attempt to localize the pain generator.
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The problem with localizing the pain generator is the MRI, as you know is very, very sensitive, but very nonspecific. There is a high percentage of degenerative change in many asymptomatic individuals, and that percentage increases as the particular sample ages, so that by the time you are looking at individuals in the 60s or 70s, degenerative changes is ubiquitous, even in asymptomatic individuals with ranges of 85 to 90%. So if you suspect that this degeneration may be the culprit, the next step would be to investigate the disc, and unfortunately, that requires an invasive study and this is obviously the point where you would probably consider a referral. One way to look at the disc is a test called discography, intradiscal injection, not without controversy.
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There two sorts of information available from this, one is the morphology, which you really shouldn’t need if you have a good MRI, but the other is the patient’s clinical response. If you pressurize a symptomatic disc and if the test is done correctly in capable hands, it should recreate the patient’s back pain precisely and enable you to localize the level from which the symptoms originate. North American Spine Society, has formulated guide lines for these, the pain, at least four months long, unresponsive to conservative treatment and other noninvasive modalities, unrevealing. Again, hopefully this would occur relatively rarely, as appropriate conservative care should get most patient’s without neuropathic pain better to the tune of 90 or 95%, but this would be the next line. Facet injections, that is one way to look at whether or not the facet is the culprit, that is a fluoroscopically guided injection which is diagnostic and hopefully therapeutic in some instances, whereby the medial branch of the posterior primary ramus is anesthetized. If that is the pain generator, the patient should get better. There are studies looking at duration of relief, depending on the concentration of the drug used in the facet injections and there has been a positive therapeutic effect assigned to that. There is one school that thought that all facet syndromes are secondary, that they accompany the degenerative symptomatic disc, that again, that is somewhat controversial. How can you treat discogenic pain, well in rare instances, you can perform a spinal fusion, and this is our paper from 1994 where we found we were able to successfully treat that in individuals where the fusion healed. Again, though, if you are operating on someone just for back pain without a deformity, without neurologic features, this should be fewer than 5% of the patient’s that come to your door with this diagnosis.

Low back pain. Medications

Disorders — Fri, 04 Dec 2009 21:23:22 +0000

Medications: Good study showing statistical power for nonsteroidals, analgesics and muscle relaxants, the use of those has to be individualized.

Physical Therapy: Absolutely, there was just a publication in the Journal Spine and that is referenced in your hand-out from the Paris Task Force, looking at the superiority of physical therapy to inactivity and shortening symptomatic intervals, particularly active physical therapy, not modality based therapy, manipulation, hot, cold ice packs, but really active physical therapy.
Low back pain medications:
Muscle relaxants: Soma is a muscle relaxant used to treat pain caused by muscle spasms.
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Manipulation: Believe it or not, there is some very compelling evidence to suggest that may help in the acute phase as with any modality, and by that I mean no more than three to four weeks from the time of onset, chronic manipulation has not been shown to impact long-term health care, delivering a positive sense for low back pain, and injections very controversial despite their wide-spread use, and are used in many individuals. There really are very few studies that demonstrate statistical power as far as the ability of injection to shorten the treatment interval.
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Superficial nonanatomic tenderness

Disorders — Thu, 03 Dec 2009 13:55:07 +0000

Superficial nonanatomic tenderness, if you touch the patient very lightly and they have exquisite pain, stimulation rotation, if you basically have the patient stand up and rotate the shoulders and the hips together, you are log-rolling them, you are not putting any torsion movement on the spine, if they say they have back pain, where there’s really not a physiologic reason for that, so that would be a positive simulation rotation; axial compression, you put direct compression down on the head, the patient complains of neck pain, that is fine, they complain of back pain, the really shouldn’t because unless you are extraordinarily strong, you are not putting a load on the lower back by compressing the head. Distraction maneuver, straight leg raising maneuver should produce the same results whether the patient is seated or recumbent, regional motor or sensory dysfunction, that’s the stocking glove loss or over reaction. Now as these things were validated, two of the five are still compatible with organic pathology, and that makes sense because you can get a stocking sensory deficit and a peripheral neuropathy with diabetes, so that makes sense. Three of the five, you start to get a little nervous, four would suggest some somatic overlay, five has theological overtones regarding the second coming and inability to have a cure.
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As we move away from physical examination, the treatment of course, is something in which we are very interested and how would you approach these patient’s initially. Well, the lumbar series, we talked about that, certainly in someone over the age of 45, and again, that’s predominantly the rule at a gross lytic lesion. A brief period of bed rest, the current wisdom in that is no more than 48 to 72 hours, Sam Weasel who is at Georgetown did a study in military recruits 100% compliance in that study population, and found that in fact, 48 hours was the optimum duration to shorten the natural history or the duration of the acute flare-up. Traction absolutely of no value whatsoever. A patient, just to overcome soft tissue restraints at the lumbosacral junction, takes about 40% of body weight and trying to administer that force in a reproducible way is very difficult. There are some instruments that are commercially available now, the so-called Vacs Detraction table which is attempting to deliver the force more accurately, but good prospective data on efficacy are notably lacking in that instance.
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Supports: Very, very limited roll, you have probably seen in your institution these kind of belt-like supports with the shoulder straps, well, guess what, if you did flexion extension x-rays on those patient’s, you would see those supports limit range of motion, so they are biomechanically useless and there are some studies that suggest psychologically it might not be the greatest thing to do because the patient has more of a sense of invincibility with in fact, what is a very token support in the biomechanical sense.

Back pain. Discussion of physical examination

Disorders — Wed, 02 Dec 2009 19:05:06 +0000

A couple of extra things, if you do an active straight leg raising maneuver, that’s just having the patient do a leg lift, hold up both legs at the same time, then do it for 20 seconds, you have ruled out intrathecal pathology because what you’ve done, is you have the patient val salva, you are increasing subarachnoid CSF volume and if the aqua duct is open, no problem, so you have ruled out a tumor. Again, if somebody has back pain with that maneuver, you have reversed the lordosis and you’ve loaded the disc, so that will also give you a clue as to the origin of the back pain.
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Any discussion of physical examination, no matter how brief, would be incomplete without mentioning the nonorganic signs of Waddell. Gordon Waddell who is a Scottish surgeon, described these many years ago and has looked at ways that some of these signs correlate with different aberrations on various psychometric instruments and the way they relate to prognosis. These are thought to be signs of functional or nonorganic or nonorganic pathology. Before we go any further, there is a very important distinction to be made, and that is the distinction between the somatic or hysterical patient, the malingerer. The somatic patient is someone to whom their pain is real. It may not be organically based, but it’s actual, acute distress with pain behavior. The malingerer on the other hand, is someone who is out to consciously defraud the system, and those two people obviously have to be approached very differently, that distinction can be very, very difficult to make, but in fact, in the 12 years I have been doing this, I think I have seen at most really one malinger, so I think that it is fairly uncommon and I would certainly be very, very circumspect before signing that label to any individual. Anyway, what are these nonorganic signs?
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