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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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.
There is an extensive list of differentials in your hand-out, and I am not going to go through all of those, since that’s pretty detailed, but when you see someone with back pain, I think it’s an important aspect of mental discipline. Just to run through a differential and think about some of these things; tumor in particular. An individual over the age of 45, remember that about 10% of patient’s with an unknown primary, will present with back pain as the first symptom of their tumor due to metastatic disease, so it’s probably a good idea, in somebody over the age of 45 coming to you with back pain for the first time, to at least get an x-ray to make sure there is not a lytic lesion there, because that is something you don’t want to miss.
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Of course trauma, infection, very difficult diagnosis to make, and I will finish the talk on that. You really have to think of that, that is a very subtle diagnosis. Mechanical by far, in a way, the most common, and then some of the relatively uncommon entities.
Physical examination. I would just like to run through a few things; the components of that are obviously, you watch the patient’s gait, you check range of motion, you palpate and then do a neurological examination. One of the classic differentials is the hip/spine is actually very, very simple. Flavored kamagra online at discount canadian pharmacy. You don’t even have to read all these areas of referral, posterior, superior, iliac spine or sacroiliac joint, that may be related to the L5 root, and these are basic points of physical examination, buttocks for S1, anterior thigh for L3-4, posterior for L5, calf and foot for L5-S1. It’s a pretty simple differential. Hip is groin pain. Not pain going to the buttock not pain going to the greater trochanter, not pain going to the sacroiliac joint, if you have a bad hip you’re going to have groin pain. Everything else you should think comes from the spine until proven otherwise.
The reason for that is the arrangements of these lamellar fibers. They can’t normalize torsional stress, and that makes this very, very vulnerable to injury. The result of that is the degenerative cascade starts in the third decade, we are all starting to lose water content from our discs in the 30s. The annulus tends to fissure and tear, it become mechanically incompetent and can of course, be a source of pain related to the innervation of that structure, and a very, very common source of pain I would submit to you. Well, if we look at mechanical pain, what does that really mean. There are two types of pain when you are dealing with spinal problems, one is mechanical pain, the other is neuropathic pain. Mechanical pain tends to be back pain or pain radiating not distal to the knees, kind of a Sclerostoma referral pattern. Radicular pain obviously radiates distally, or in the case of a femoral entrapment in L3-4 nerve root, anterior thigh, very different in character. Neuropathic pain tends to be burning, lancinating, stabbing, mechanical pain, kind of a dull, aching, more difficult to localize. They can go together, but often times, different problems that is pure back pain will be mechanical, where as sciatica due to disc herniation will tend to be more neuropathic. If we look at the mechanical side of this, what are the characteristics of mechanical pain? It tends to increase with activity, any activity that tends to raise intradiscal pressure will increase back pain in someone whose disc is the primary pain generator and that’s an important clinical clue. The easiest way to find that out with a patient, is ask them, do you have more pain when you’re sitting or standing? If they say I have more pain when I am sitting, that probably means it’s discogenic because the intradiscal pressure is much higher then you’re sitting than when you’re standing.
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A senior orthopaedist named Nokimsun in Sweden proved that many years ago when he stuck pressure transducers in the discs of normal volunteers, although how normal you would be to volunteer for that would kind of be a point, and found that the intradiscal pressure when you’re sitting, is much, much higher when standing, and the reason for that is in the way the disc is designed. We are supposed to have a nice lumbar lordosis, a nice hollow. If you look at the individual to your right and to your left, look at how they are sitting, tend to sit reversing your lordosis in flexion, intradiscal pressure goes right up through the roof. If you then add a mechanical environment to that, particularly vibration, which also shows to raise intradiscal pressure, the pain should be worse, so another good tip-off for somebody with back pain on the basis of a disc, I have more pain when I am sitting and I can’t stand to ride in a car, that should tip you off to a discogenic source of back pain. Again, mechanical pain can increase with range of motion if you are thinking of disc pain, anything with flexion should be worse, tends to decrease with recumbency, you should very seldom have night pain, that is a red flag to think about, a neoplasm or atypical mechanical behavior.
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The posterior ligaments here, supraspinous and intraspinous which are in between the spinous processes, major resistors of flexion; so if you have any sort of a flexion based injury or posterior element tenderness, you have to worry about disruption of this very important ligamentous complex. Anterior longitudinal ligament is a big, thick structure that attaches to the vertebral bodies and the disc, tends to resist extension but a very, very important auxiliary structure to resist torsion. The main way to resist torsion are in the facets, so any time those structures are compromised, you are going to have relative torsional incompetence. Most of these structures are very, very richly innervated and virtually any structure in the back can be a source of pain contrary to conventional wisdom. Probably the leading offender in that, is the intervertebral disc. If you look in Gray’s anatomy, and not that I would advise you to do that on a regular basis, what you will see, up until the additional before last, I think that’s the 670th edition as far I know, you will see the largest, avascular, neural structure in the body, the L4-5 disc. Well that’s wrong on two levels; number one, it’s L3-4 on population studies, that’s a little bit larger than L4-5. Number two, it’s avascular, but it’s not neural. The outer 50% of the disc is richly innervated with nociceptor fibers and free nerve endings, and in fact, the disc itself can be a source of pain, even in the absence of a disc herniation compressing a nerve root and causing sciatica, and that work has been done in Australia with some very, very elegant histological studies.
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It you notice, there is the nerve root exiting the canal, there is a posterior branch, the facet capsules branch to the supraspinous and intraspinous ligaments, and there are all afferent pathways in here, so all these things are capable of conducting painful impulses centrally, and of course, the disc, you can see the nerve of the vertebral body, the sign of vertebral nerve and don’t forget the sympathetics which are out here as well, which carry some sensory information. What is one of the structures in the back that is probably most vulnerable to injury, and the problem is, it’s the intervertebral disc. If you look at the disc, it does a reasonably good job at resisting axial stress. Here is the jelly-like nucleus and the fibers annulus and circumferential lamella around that. The problem is, it does not do a very good job at resisting torsion, and in fact, if you take a functional spinal unit to the lab which would be the vertebra and adjacent soft tissues, you will see that the disc will fail in torsion long before it fails in any other deflection, flexion, extension, side gliding, lateral bending.
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The diagnosis is frequently made, particular with things like MR, CT myelography, imaging modalities very clear again because of technological advances. The rest is the main stay of treatment, go to bed for six weeks, that kind of thing which was in text books until fairly recently, that surgical indications are very clear and the prognosis is poor. Well, actually, this last part may be a little bit truer than we would like to believe, but with the exception of that, as I mentioned a moment ago, all these things are false, and in fact, as you know from treating this in your own practices, that you seldom make the diagnosis of low back pain. There are a number of diagnostic codes that can be used for low back pain, most of which have very little clinical or anatomic significance, and the problem with that is that back pain is a symptom, it’s not a disease; so what does cause it? If we go back to the medical model where we actually want to make a diagnosis and then create a disease specific treatment plan, how can we do that with back pain, more on that in just a little bit.
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Part of the problem for low back pain, is the etiology is not clear, and the primary cause as identified by an expert, usually to be something within that expert’s realm of interest or clinical specialty.
If you talk to most surgeons, it’s a disc, ever since Mixter and Bard described disc herniations in 1934. If you talk to physiotherapists, it’s fascia and if you talk to just about any body else, it’s psychological, and that of course, is a real danger. There is a problem when you are dealing with a disease, you are giving a patient good care and they are not getting better, it’s easy to sit back and say the patient has psychological problems, what it really means is we haven’t approached it in a very intelligent manner. Well, the anatomy, and I promise this will be mercifully brief or your postprandial somnolence will take over, the slide on the right is from Frank Netter, the things I would like you to keep in mind from this, are the supporting structures of the spinal column.
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