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Low Back Pain

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

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.

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.

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.

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.

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.

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? 

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.