Diseases, Disorders information

Osteoarthritis:This is a disease mainly of the cartilage

Disorders — Wed, 03 Mar 2010 14:11:37 +0000

This is a disease mainly of the cartilage, but also the subchondral bone. If you look at the joint, and some like to think of osteoarthritis as a total joint failure. Again, it’s not a real synovial process but it probably starts in the cartilage. The cartilage is made up of chondrocytes, which are these little circles, then you have your proteoglycans which are very hygroscopic. They hold water in a gel state and give the cartilage its resiliency. And cartilage would expand even more if it wasn’t for this sort of retaining collagen framework that laces back and forth through the cartilage to give it some structure. It’s believed that the initial insult is some kind of damage to this collagen. Maybe what happens then is that when the collagen starts to break down these proteoglycans start to absorb more and more water, the cartilage begins to swell and it loses its typical helpful resilience. Once that is out of balance then the chondrocytes become injured and the cartilage does start to finally degrade. But often these patients have abnormalities of the subchondral bone, probably initially starting in the cartilage. The subchondral bone is not exactly like the rest of the bony structures. It’s designed to absorb some impact and if it starts to sclerose it’s not going to do a very good job of that. The last thing, that’s not shown in this slide, are these neurologic and mechanical factors. Any abnormalities of the ligaments, any alteration of the biomechanics of the joint because of muscle weakness or neurologic impairment, albeit subtle, may actually aggravate the pressure on the cartilage, accelerating the damage. Occasionally patients will have osteoarthritis and then they’ll sprain an ankle or twist a knee, nothing bad enough to require a cast or surgery, but then what you may notice is in that joint the osteoarthritis accelerates because of these probably subtle biomechanical changes.

If you look at it just in a schematic way, abnormalities of the collagen network, for whatever reason, swelling of the cartilage resulting in chondrocyte injury. Like most cells in the body, if the cells become injured, they try to somehow repair. So they actually have what we call “synthetic response”. They produce more of the matrix proteins. They also start to produce more of the proteolytic enzymes. There’s a balance between production of these matrix proteins and destruction. What may also be part of the picture, is that eventually when the chondrocytes can’t keep up the destructive enzymes start to get the upper hand, and finally when the cartilage breaks down you lose your chondrocytes. It’s not the kind of tissue that can repair itself. It’s not like skin or liver. Once it’s damaged to a certain point it does not recover. It doesn’t have any vascular supply. All its nutrients come from blood vessels or synovium so it really has a limited ability to repair. Again, you see that once the cartilage breaks down, that may lead to changes in biomechanical factors but the biomechanical factors may also have an initiating role, or aggravating role, so it becomes a vicious cycle and ultimately the patients develop osteophytes and the like.

Probably about 60 million people have x-ray evidence of osteoarthritis in this county. Any country that has a significant older population, it’s a significant problem. Obviously if you go to a country where the average life span is 45, I don’t think osteoarthritis is going to be on the top of their list of things to treat. But in this country it is a very significant medical problem. It’s not life-threatening, in a sense, but it certainly can be very disabling. I think 500 years ago osteoarthritis probably was a cause of death. People couldn’t keep up, they couldn’t work in the fields or whatever it is that they did, and basically if you didn’t work you didn’t eat and you were just sort of left to die if the culture you were in didn’t have the ability to care for you. In our culture we do, but it is a major health problem, major expense. Over half a million joint replacements are done every year and probably better than 90% of those are done for osteoarthritis. If you think how much these things cost – and also there is some morbidity, occasionally mortality, it’s not a benign procedure – but I’ll tell you the surgeons are getting really good. Most of the patients I see are out in two or three days unless they have a lot of other medical or arthritis problems to go on with it. They just get all their stuff at home, their low molecular heparin and physical therapy all at home. A lot of these patients, of the 60 million that I quoted, may just have x-ray evidence. If you do x-rays of people that are 80 years or older you are going to see a lot of osteophytes, maybe you’ll see some cartilage loss. A lot of these patients really won’t have many symptoms. I’m sure you all have done a flat plate of the abdomen or a chest x-ray, or an x-ray of a knee that got banged up, and you see a little bit of osteoarthritis that is really of no clinical significance. It would be of clinical significance if we had some kind of therapy to prevent progression. But since we don’t, it’s of little importance.

Osteoarthritis:Metabolic and neurologic factors

Disorders — Fri, 25 Dec 2009 09:50:49 +0000

Metabolic factors: certain metabolic diseases are associated with an increased incidence of osteoarthritis. Acromegaly, for instance. Obviously this is very uncommon but there may be more common subtle metabolic factors that play a role in the development of primary osteoarthritis.
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Neurologic factors: this is a disease of older patients. It’s unusual to see a primary osteoarthritis in patients under age 50. What happens when people age is that things just don’t work as well as they used to, in general, and the neurologic system is no different. This is becoming an area of great interest to several of the major centers studying osteoarthritis. Actually, if you look at the number of centers studying osteoarthritis it is much less common. So unfortunately it’s not a disease that rheumatologists and orthopedists are always that interested in, even though it is much more common. But these neurologic factors may be a subtle loss of proprioception or some weakness of some muscles that help support the joint, and people have shown that these things do occur and certain measures can affect that and make the patients symptomatically better. Aging and obesity, clearly osteoarthritis is associated with aging, but whether it is the cause of it is not clear. And obesity; there have been a number of studies. It’s hard to show that obesity actually causes osteoarthritis but certainly if someone weighs 450 pounds there is going to be a lot more stress on their knees, and especially their hips. So it does appear to be an aggravating factor but whether or not it’s a primary cause is not clear.
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Of course osteoarthritis can occur secondarily to other diseases. Trauma. Someone who had a broken hip or a torn anterior cruciate ligament may be predisposed to develop osteoarthritis in that joint later. Inflammation, either chronic inflammation as in rheumatoid disease or acute inflammation, as in a patient with septic arthritis that just didn’t respond well or get treated adequately. Again, metabolic factors, AVN, avascular necrosis, sometimes by the time you see the patient you can’t tell what the cause was in a single joint, but maybe they have a history of AVN in another joint. Of course if you follow a patient with AVN that is very early in the course and you don’t operate right away, they will eventually develop osteoarthritis in that joint. Neurologic disorders, less subtle, such as syringomyelia where you get neuropathic joints, which is just basically a very severe degenerative process. Obviously, congenital or developmental defects. We followed one patient with spondylo-epiphyseal dysplasia, or something like that, and she has abnormalities in the structure of many of her joints, particularly the hip and the back, and I think the knees, and she’s had several joint replacements because this disorder that she was basically born with basically leads to premature osteoarthritis. There are a number of other rarer diseases that can occur and then predispose to osteoarthritis. I think one common thing that pediatricians may see is hip dysplasia, and if that’s not treated properly, those patients get an osteoarthritic joint. If it’s treated properly then the acetabular cup forms normally and the children do much better.

Osteoarthritis

Disorders — Wed, 23 Dec 2009 17:08:11 +0000

Osteoarthritis is one of the most common rheumatic diseases in this country. Actually, for most rheumatologists it may not be the biggest part of their practice -probably rheumatoid arthritis is – because often these patients have mild disease or it’s treated either by the primary care physician or they end up going directly to the orthopedic surgeon who can, in some instances, cure the disease. It’s a slowly progressive, usually polyarticular disease, involving certain joints. Usually weight-bearing joints and certain joints in the hand, especially the DIP joints, PIP joints and also the first carpometacarpal or CMC joint. This is a woman who actually had giant cell arteritis and I was following her for that and she really never complained about any articular manifestations, unless her associated polymyalgia rheumatica flared up. So she had had these little nodules, Heberden’s nodes, for a number of years, thought they were ugly but other than that didn’t seem to care too much about them. I always wondered, why, if it involves weight-bearing joints, would it involve the DIP joints particularly. Evidently there is quite a bit of force because of the tendons crossing these joints, that there is actually quite a bit of force generated across these joints and that’s probably why the arthritis is predisposed to occur in this area.
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As opposed to rheumatoid arthritis, this is the disease that basically starts in the cartilage, whereas rheumatoid arthritis is a synovitis and then secondarily involves the cartilage. With osteoarthritis, for whatever reason, you have a breakdown of this cartilage and the cartilage is lost in a non-uniform fashion. Focal areas wear out first, and in this instance you also have these little bony outgrowths which clinically you can palpate, and these are osteophytes. Presumably these osteophytes are some halfhearted attempt at repair of the joint. Some of the major hallmarks are this focal loss of cartilage and osteophyte formation. Sometimes you also get subchondral cysts, which can also occur in other types of arthritis but they are particularly prominent in osteoarthritis. What happens is when you have a severe loss of cartilage in an area, sometimes a subchondral bone cracks and synovial fluid is literally forced into this area. When you take an x-ray it looks just like a lucency. That’s all it is, just a little bit of synovial fluid that’s been forced into the subchondral bone.
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There’s a lot of etiologic factors in primary osteoarthritis. Hereditary factors do appear to be important. Maybe some sort of abnormality of collagen production in the cartilage. Certainly the type of osteoarthritis involving the hands, if you talk to a patient a lot of times they will tell you that their parents and grandparents may have had the same thing. Stress from impact loading. This is probably more of an aggravating factor. They’ve actually done studies looking at professional basketball players and showing that they didn’t have an increased incidence of osteoarthritis later in life, unless they had had a major knee injury, like a torn ACL.

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.