Diseases, Disorders information

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.