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.
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, 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.
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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Physical examination, and you all know this, this is in the hand-out, just a quick and dirty review of the different levels of 4-5 disc, will pick off the exiting nerve root as shown here, 4-5 picks off L5, 51 picks off S1 because of the arrangement of the cauda equina and you have reflex motor and sensory changes again here, note with the L5 radiculopathy, there is no reflex change, that usually is seen with a 4-5 disc. The thing you don’t want to miss is the cauda equina syndrome which is really the only true spinal emergency and you won’t miss it because these patient’s won’t let you miss it, and that is a massive midline prolapse resulting in many, many nerve roots involved. Remember when you are doing a sensory examination and the dermatomes you can see here, the thigh, medial calf, L4, lateral and dorsal foot L5, lateral foot S1, is that these dermatomes are approximate and if you map out dermatomes precisely in many patient’s, you are not going to see this clean a distribution, so if it’s not as precise a sensory loss in an L5 as you would predict with an L5 disc and an L5 root, don’t necessarily rule that out as the source of symptoms because these are approximations.
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Nerve root tension signs are something that are frequently assessed as well, now this is of utility is somebody with sciatica or referred neuropathic pain from disc prolapse. The sciatic nerve root test was described by Lasegue’s, this is the so-called straight leg raise. You have to remember when you do this, though, you are only testing the L5 and S1 roots, you re not testing the roots farther upstream. Classically, this has been described as positive only if it reproduces leg pain, but if you think about it, if you flex someone all the way up to 90 degrees and they don’t have leg pain, they have back pain, that should tell you something right there as well, because what have you done, you flexed the pelvis, you reversed lordosis, you raised intradiscal pressure and you still could be dealing with a bad disc, even in someone without sciatica. Interestingly too, as you do a passive straight leg raising maneuver, the nerve roots really only start to move at about 30 degrees and then they only move several millimeters, so someone, unless they have a massive disc herniation, you wouldn’t expect to find referred pain in the lower deflection in your physical examination. If you want to test the femoral nerve root for an L3 or L4 prolapse and femoral nerve entrapment, you have to do a femoral stretch and that is trunk flexion with hip extension and knee flexion.
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Low back pain
With gait, when you look at this, this is your quick and dirty neurologic assessment; of you ask a patient with back pain to flex and extend and ask which one hurts more, if they hurt more in flexion you are thinking maybe it’s discogenic because you are raising intradiscal pressure, if they hurt a little bit more in extension where degenerative disc should feel better, then maybe it’s facet or something else, all of a sudden, you are all of a sudden focusing on a mechanical differential, and then you do a quick and dirty neurologic. You check the Trendelenburg maneuver, you have them heel and toe walk, what have you just done, you have tested the neurologic integrity of L4-5 and L5-S1, the three most commonly involved roots. With the Trendelenburg, you check the gluteus medius 5-1, heel walking with the gastrocsoleus, you are checking S1, toe walking you are checking L4-5, so if they can do that, you have already ruled out a catastrophic neurologic deficit and you have a mechanical differential and within 20 seconds, you will have gained more information than most people who are approaching this problem will, and it’s a very, very easy thing to do.
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If we look at the kinematics of the spine, it becomes very, very clear that we were not designed to walk upright. This is clearly a design flaw. If you look at the range of motion of the lumbar spine, 90% of the flexion extension comes from the L4-51 segments, that doesn’t make any sense if you are walking as an upright biped because those support most of the load of the torso, the trunk in an upright posture, so it clearly is rather silly from a point of view mechanical design to have the floppiest segments the most heavily loaded, so that’s one problem. The second problem, if you look at the arrangement of the cauda equina, the only segments that are crossed by multiple extra thecal nerve roots are L4-5 and 51, so if there is posterior protrusion of the disc, you are far more likely to entrap a nerve root there than you would be at more rostral segments, so there are lots of reasons why 90% of the pathology of the low back is at L4-5 and 51. Clearly, it would be better in this particular instance if we weren’t bipedal because this is clearly a design flaw. Now keeping some of those things in mind, you can understand that if someone is a little bit better in extension, you are thinking about a discogenic source of back pain, lordosis is preserved, intradiscal pressure is lower, those people tend to be better standing than sitting.
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If someone is better in flexion, a spondylolysis, spondylolisthesis, something facet mediated, posterior column, or in some body with some sort of nerve root entrapment, usually in the intervertebral foramen. The other differential for flexion is somebody with spinal stenosis, but that is a neurogenic claudication, kind of a different category and we will get to that in just a second.
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