So how does one get educated? This is a good place to START - but recall the legal disclaimer. The internet is truly a two edged sword. There are a lot of good sites that educate, but unfortunately there seems to be an equal number designed to fool you. In this day and age, information is readily available- to available, and this can easily lead the most astute of individuals into that land of utter confusion and paralysis. My simple advice is to NOT rely on one source of information- be it the internet or your doctor/surgeon. Yes, that's right, do not trust your doctor blindly- this includes me, and this website. If you hear or read the same information from multiple different sources, it's probably accurate. Very few spine issues are so critical that there is no time to become conversant with the problem. Often that means getting a second opinion-something I routinely recommend to my patients; don't worry about offending your doctor-second opinions are a matter of course to most legitimate physicians. Even if you do offend them, who cares; maintain your perspective, this is about your health not their ego!
One last note. BEFORE you see a health-care provider, sit down with a pen and paper and write out ALL your complaints and questions. Get things straight in your head before you try to communicate it to someone else. Important things to know include:
1. What am I seeking help with- ie what are my symptoms?
2. When did they start? How did it start?
3. Have you had them before, and if so what was it then and how did it go away-or did it go away?
4. If you have pain, where is it? When do you get the pain, ie sitting, standing, walking, laying? Does anything make it better? Does anything make it worse? What type of pain is it, ie burning, tearing, throbbing, deep, superficial, etc.?
5. What have you done to treat the problem, ie medications, therapies, shots ,etc.?
A good number of problems are directly related to poor communication- and I have to be honest, it is generally NOT the healthcare providers fault. It's the patients. It is very common for the minds of patients to suddenly go blank as soon as the exam room door opens. Anticipate this and write out your information and questions! Trust me, the doctor will greatly appreciate it.
Enough preaching, on to some spine pathology. Once again I'll include some hyperlinks so if you want to zoom to a specific section just hit your desired term below.
What can I say about back pain except that I Hate It! Everyone does. From the patients to the primary care clinicians to the specialists. It is the bane of our existence. Fortunately, however, it keeps us busy.
First some definitions. Acute pain-of any kind- is pain that persists for days to a few weeks. Subacute pain lasts for weeks to three months. By definition, pain that persists beyond three months is termed chronic.
More than 85% of patients with low back pain will never get a specific diagnosis- which is one of the main reasons clinicians really hate low back pain. By far, the most commonly asked question is "what's causing the pain in my back?" This causes the clinician to stumble through a rambling explanation that is summed up in three words:"I don't know". It may seem strange, but that is the best case scenario- if a doctor does find the cause of a patient's low back pain it will not be good news. The initial assessment of low back pain is geared towards detecting the "red flags"-listed below- that signal a potentially serious pathology. In the absence of these, imaging studies and further testing is usually not helpful in the first four weeks of back pain.
Alright, that was easy, how about something a little more difficult? Where is the "back"? Sounds like a silly question, but if you ask ten people where their back is, you will get ten different answers- go ahead ask them, I'll wait. Or how about where is the "hip"? If you ask an orthopedic surgeon they will tell you that the hip is the articulation of the femoral head with the acetabulum; if you ask my mother, she will tell you that her hip extends from just above the knee to an area that is just below her ribs (but you can't trust her, she raised seven sons and was declared legally insane decades ago). So, for the purpose of this discussion I am going to label the areas that I refer to as the back, buttock, hip, and knee.
The knee is fairly straight forward. It is a restricted area that does not extend very far up, in, around, or below the knee cap. The buttocks area is also easy- it corresponds to the "gluteus maximus"-the big muscle. Below it is the hamstring region. Above it is the "back". This area extends outward only as far as where the skin turns forward, and only as high as the lowest rib. The "hip" is a little more difficult- pain in the hip is usually "referred" into the groin (inguinal area), but the greater trochanter, the sharp point or bump on the upper portion of the femur (the big leg bone), is a common site for hip pain (the trochanter serves as an insertion site for some of the muscles that move the leg- good site for "bursitis" and is what you lay on when you're on you're side). Alright, that should make our verbiage fairly clear.
This topic is restricted to pain that remains restricted to the back- okay, it can radiate a little into the buttock or hamstring regions, but any further and we have changed the topic to radicular-or nerve pain (that comes latter). By this definition, 80% of Americans experience some form of back pain in their lifetime. Most will recover without any intervention beyond anti-inflammatory agents and activity modification. Unfortunately, 5-10% will develop chronic back pain (again lasting more than 3 months) and about 1-3% will become permanently disabled with back pain. On a yearly basis, 75% of chronic LBP (low back pain) patients will seek medical help; 60% will get a cross-sectional imaging study (CT or MRI), and 10% will have surgery. LBP injuries are by far the most expensive occupational injury, averaging close to $10,000 a claim (this statistic is skewed because it includes the much cheaper acute LBP diagnosis- the majority of the overall financial burden is caused by approximately 5-10% of patients who develop chronic back pain). So I think I have established that low back pain (especially chronic low back pain) is prevalent and problematic. So what's to be done? Let's start with acute low back pain-it's a lot easier.
Acute or short-term low back pain generally lasts from a few days to a few weeks. Most acute back pain is mechanical in nature — the result of trauma to the lower back or a disorder such as arthritis. Pain from trauma may be caused by a sports injury, work around the house or in the garden, or a sudden jolt such as a car accident or other stress on spinal bones and tissues. Symptoms may range from muscle ache to shooting or stabbing pain, limited flexibility and/or range of motion, or an inability to stand straight. Occasionally, pain felt in one part of the body may “radiate” from a disorder or injury elsewhere in the body-ie not all low back pain comes from the back. Let's look at other things that cause acute low back pain that need urgent investigations, and then discuss the more common "benign" low back pain.
B. Unexplained weight loss >10 kg (20 pounds)within 6 months
C. Age over 50 years or under 17 years old
D. Failure to improve with therapy
E. Pain persists for more than 4 to 6 weeks
F. Night pain or pain at rest
Infection Related Red Flags with Low Back Pain
A. Persistent fever (temperature over 100.4 F)
B. History of intravenous Drug Abuse
C. Recent bacterial infection
D. Urinary Tract Infection or Pyelonephritis
G. Immunocompromised states
H. Systemic Corticosteroids
I. Organ transplant
J. Diabetes Mellitus
K. Human Immunodeficiency Virus (HIV)
L. Rest Pain
Cauda Equina Syndrome Related Red Flags with Back Pain
A. Urinary Incontinence or retention
B. Saddle anesthesia
C. Anal sphincter tone decreased or fecal Incontinence
D. Bilateral lower extremity weakness or numbness
E. Progressive neurologic deficit
Significant Herniated nucleus pulposus
A. Major Muscle Weakness(can't move a joint against gravity)
B. Foot drop
Vertebral Fracture related red flags with Low Back Pain
A. Prolonged use of Steroids (Cortisone, Decadron,etc.)
B. Mild trauma over age 50 years
C. Age greater than 70 years
D. History of Osteoporosis
E. Recent significant trauma at any age
F. Ejection from motor vehicle
G. Fall from substantial height
Abdominal Aortic Aneurysm red flags with Low Back Pain
A. Abdominal pulsating mass
B. Atherosclerotic vascular disease
C. Pain at rest or nocturnal pain
D. Age greater than 60 years
As a neurosurgeon I don't see a lot of acute LBP except when a patient has one or more of the signs/symptoms listed above. While all of the above are important -and you should review them- the red-flags that I see the most are: history of cancer (esp prostate and breast), weight loss, rest pain, steroid use (cortisol, prednisone, decadron, etc), any discernible weakness (esp if it is progressive), bladder incontinence,significant trauma, or abdominal mass. If you have LBP and any of these, acute low back pain is no longer your diagnosis, it's a symptom of "something-else".
Acute Mechanical Low Back Pain
About 93% of patients with acute low back pain patients fall into this category- meaning that they don't have any of the red flags listed above. So what's to be done with them? As it turns out, the less-the-better. More than 95% of patients with acute mechanical LBP will have resolution of their symptoms spontaneously- most do so within a week, and most of the remainder within a month. Of course, if 95% get better, that means that 5% don't-we'll talk about chronic back pain in the next section.
The treatment of acute mechanical LBP is centered around maintence of function/activity and pain control. The general measures used to maintain function are fairly intuitive: find positions of comfort, avoid exacerbating activities, and use heat and ice. DO NOT STAY IN BED!!! Bed rest is strongly associated with rapid deconditioning and easily converts a temporary problem into a life-changing condition. STAY MOBILE!!! It may seem contradictory that in one line I say avoid exacerbating activities, and in the next say: stay mobile. The reality is that very few patients are completely immobilized with acute mechanical LBP- if you happen to be in that group, and are reading this flat on your back in bed, stay there for no more than two days-anything more and you need to be seen by a health-care professional. Also understand that you are paying a price for those two days of immobility, and for many it is a high price (explanation: most LBP patients at a baseline are not well conditioned- making them susceptible to LBP- more than 2 days of immobility is usually enough to create a vicious cycle of pain-reduced range-of-motion-spasm-more pain, etc..-with very little effort a chronic back pain patient has been created).
Alright, now that you know what not to do what should be done with acute LBP? Let's break up treatment into general measures-things you can do yourself, pain control, and a word about spinal manipulation.
General Measures to treat Acute Low Back Pain
First, and last, stay active; sorry about harping, but it is a critical point that "flies in the face" of "common-sense", ie what most non-medical people will tell you.
Next, be careful. Don't make it worse by ignoring it or trying to "work-it-out". Move slowly and easily- for a time you have permission to "baby" your back. If your wondering how long to shield your back, recall that 95% of patients will have resolution of their back pain within a month. Once the pain has resolved, gradually restart your daily routine and conditioning excercises, but be careful! It is very common for people recovering from a bout of acute LBP to reinjure themselves. Take at least as long as you had the back pain to get back to regular activities.
Ice and heat applied to your back will also work- pick which ever works best because they use the same mechanism to minimize pain. TANGENT WARNING (skip to the next paragraph if you want): ice and heat work through a mechanism called the "Gated-Theory of Pain". It's a fascinating theory and one that everyone can related to. Basically, there are only so many tracts in the spinal cord that can send information to the brain, so the cord has to prioritize the data. Sensory fibers closest to the skin are number one- which makes sense, because if you are on fire or are being eaten you probably want to know it quickly. So if you flood the cord with cold or heat signals from the skin, it will overwhelm deeper pain signals. This is why when you hurt a body part you instinctively begin to rub it. "Cool" huh?
Stretch in directions that are NON-PAINFUL-you will find that if it hurts to flex your back (ie bend forward to touch your toes) extending your back (looking up) often feels good. If you extend repeatedly your ability to flex will gradually improve as well. Rationale is obvious-if you extend your back repeatedly, half the time you will be activating your flexion muscles/tendons/ligaments so that you can return to the neutral position.
Back braces are BAD. They do not stabilize the spine and they reduce the efficacy of the minimal activity/exercises that you can perform. That being said, braces do improve some peoples ability to return to a sedentary occupation, but NOT to a physically demanding job.
Massage and physical therapy are somewhat plus-minus. Neither changes the ultimate outcome- 95% of patients get better with or without it. So does it improve function or quality of life while you're getting better? The studies are at best conflicting, contradictory, and confusing- basically we don't know. If massage helps, do it. There's really no downside to massage aside from time and cost. The same thing can be said for physical therapy, although the cost is MUCH greater- even the co-pays can be problamatic for some. With this monetary outlay I would like some definitive benefit, and for some we do see it, but for most it's lukewarm positive, and for a few it's wholly ineffective or worse. Most primary care doctors will entertain the idea of PT if a patient has not improved within two to three weeks.
Pain Control for Acute LBP
This is fairly easy.
Non-Steroidal Anti-Inflammatory agents (NSAIDs-remember this term, it's commonly used)such as ibuprofen, Naprosyn, even aspirin are good. Acetaminophen or Tylenol is also good, just not as good-it has little to no anti-inflammatory activity but does minimize acute pain. These meds, NSAIDs and Tylenol have problems so DO NOT ABUSE THEM. NSAIDs will kill your kidneys dead if you exceed the recommended dosage. Further, when you are taking extreme dosages you derive very little if any additional benefit compared to the standard dose- this is NOT a situation where if a little is good, more is better. Tylenol poisoning is one of the most common reasons for liver transplants! Just because it is an over-the-counter (OTC) medications does not make it safe outside the standard doses. Finally, take them for as short a time period as possible.
Muscle relaxants: their name is a misnomer. These are actually sedatives- all work through sedation centers in the brain, and not in the muscles. The sedation turns down the resting tone (all muscles stay partially contracted-this is called tone). Acute LBP increases the tone in the spinal muscles which leads to stiffness, reduced range of motion and pain itself. The greatest benefit maybe in helping you sleep, so take it at night.
Narcotics and steroids have NO place in the treatment of acute LBP. They have no impact on outcome and in the case of narcotics, patients actually improve FASTER without them. JUST SAY NO!
There is a poorly disguised distain amongst some neurosurgeons and spine surgeons for chiropractic care. It's not seen in all, but certainly it is prevalent enough to require comment. I believe that as in most occupations there are good chiropracters and bad ones. Unfortunately we see the results of bad chiropractic management much more than the positive results (otherwise why would they need to see us?). MOST people do well with chiropractic management, and for acute low back pain that does not radiate below the knee, spinal manipulation is a good treatment option for the first 3-4 weeks. Studies find that efficacy after a month falls sharply.
Spinal manipulation is at least as good as physical therapy, plus chiropracters are far more accessible and generally alot cheaper. I do, however, have to strongly disagree with what most chiropracters tell their patients. "Spinal malalignment" is almost universally caused by assymetric muscle spasm (your left back muscles are spasming more than your right, so you "list" to one side). In addition, NO amount of manipulation of your back will change the orientation of your bones, discs, or nerves. You can not "pop" a disc or bone back into place. It just can't be done (when we fix severe spine trauma surgically, long pry bars are needed to move the vertebra even small distances). It is explanations such as this which ultimately leads to the difficulties some neurosurgeons and spine surgeons have with chiropracters.
Enough about acute LBP, and with that I say goodbye to 95% of the readers. For the remaining 5% who have developed chronic low back pain, keep reading.
Before I begin let me make things clear; CLBP is NOT sciatica or any other condition that causes radiating leg symptoms (ie disc herniations, spinal stenosis, spondylolisthesis, etc). If you have pain that radiates on a regular basis below the knee-either knee- skip on, this section is NOT for you. We should also include muscle atrophy (shrinking), weakness of a FOCAL group of muscles, or numbness/tingling in the legs- if you are seeking information on those conditions you will not find it here. Chronic low back pain is in the back. Some radiation to the upper thighs or hamstrings is not unusual, but generally not lower.
So ask yourself, before the doctor asks you, is the pain in the back or the legs? Most people will have a clear definitive answer, ie I have BACK pain, that goes to my thighs (CLBP); conversely, I have LEG pain that's also in my back/butt- or it started in my back, but now it's in my LEG (radicular or nerve pain). Unfortunately there is another group in which the pain is balanced-ie I have BACK pain that then goes into my LEGS; this last group also is excluded from this discussion-see below because you likely have spinal or foraminal stenosis of the lumbar nerve roots. Lastly, we need to exclude those patients who have one or more of the "Red-Flags" mentioned above. Not all back pain comes from the back, and sometimes low back pain is the only symptom a patient will have before their real problem explodes onto the scene.
In summary, if you have leg pain that is significant and consistently radiates below the knee, or is associated with numbness, focal weakness, or atrophy your section comes after this one. Or, if you have any of the "Red-Flags" listed above- get yourself into a doctor before something REALLY BAD happens.
Okay, that should have weeded out everyone who doesn't have chronic low back pain. Unfortunately about 70% of you are left (radicular causes of chronic LBP account for about 25% patients, while extraspinal and malignant/inflammatory conditions split the remainder). Some of you will go on to declare yourselves as having an atypical presentation of spinal stenosis (about 5% of patients with spinal stenosis present with CLBP without radicular/leg symptoms), or disc herniation, or even spondylolisthesis- but the majority will not.
Presentation and Evaluation
Chronic low back pain maybe static, remitting or progressive. "The pain has always been there", is a common phrase for static CLBP. Others have a baseline pain that on occasion flares up-remitting. Finally, there's the group that have had worsening low back pain since inception. The pain varies between patients and flares, ranging from a deep ache that "can't be touched" to tender spots-called "trigger-points"-usually along the pelvic bone (technically the posterior superior iliac crest- which serves as the insertion point for the muscles and fascia of the back). The pain can be in the midline, spread from the midline outward (laterally) or extend into the buttocks, or less commonly up into the mid-back. As I mentioned above, it is not uncommon for a component to extend into the front of the thighs or along the hamstrings posteriorly (from behind) or to the outer upper thighs.
Classically the pain is activity limiting. Actions such as bending, twisting or lifting regularly intensify the pain; consequently the patient alters their activity and becomes more sedentary. A point worth stressing is that mechanical structures (muscles, tendons, ligaments, joints/joint capsules) that do not move become hypersensitive to mechanical stresses and thus pain. Perhaps you've started to put this together: pain prevents movement, and impaired movement causes pain.
The majority of patients who develop chronic low back pain will have already had an imaging study by the time they reach my door, but should they? That answer differs depending on who you are; if you are the patient, after 3+ months of pain, all but the most timid would have already demanded an imaging study-particularly an MRI. However, if you are a health-care provider who has done a careful physical exam and history, and ruled-out any severe pathology, you know that studies have repeatedly shown no benefit to imaging benign chronic low back pain. The focus of the initial evaluation is to look for the signs and symptoms of the more worrisome "Red-Flag" pathologies- this group (again only about 30% of chronic back pain patients) should have a cross-sectional imaging study (MRI or CT scan- this is a good time to return to the Neurosurgical Tests page and review those imaging modalities and their limitations).
Imaging has limited utility because most patients with chronic low back pain have nonspecific findings on imaging studies, and asymptomatic patients often have abnormal findings. In plain English, what we see on an imaging study, no matter what the radiology report says, has a POOR correlation with the patient's complaints (was that plain English?). Just because something on an imaging study is worthy of comment in a radiology report does not mean that it is the cause of the symptoms. In fact, it rarely is the cause. This is VERY,VERY,VERY,VERY important-squared. The thinking that I have "this" on an MRI report has lead to untold medical and more importantly, surgical failures. Once again, what we see on an imaging study RARELY will diagnosis the cause of chronic low back pain (that is unassociated with any of the "Red-Flags"). Why am I stressing this? Because there are (expletive deleted) out there looking for people to convince that their procedure or operation will relieve you of your pain- JUST LOOK AT YOUR MRI REPORT!!! All those (expletive deleted) will do is relieve you of your money, and in almost all cases any chance of a meaningful recovery. Every person over the age of 25 has an "abnormal" MRI- it's called aging, and is almost NEVER the cause of chronic low back pain. PROTECT YOURSELF FROM THE CHARLATANS WHO GRAVITATE TOWARDS THE "TREATMENT" OF CHRONIC PAIN CONDITIONS!!! They will use your MRI against you, so do you still want one?
There are a couple of tests that are occasionally used to help diagnosis the etiology of CLBP that are not mentioned in the neurosurgical testing section. The first is facet joint block; this is a diagnostic and therapeutic study (it helps to figure out what's wrong, and treat it at the same time). A needle is directed under x-ray guidance to what is presumed to be a "painful" facet joint (you should know what a facet joint is by now, if not go to the anatomy section) and some local anesthetic and possibly some steroids are injected to make you feel better and possibly determine whether this facet is the generator of your pain. It is a test that has proponents and alot of detractors. At best the test is inconsistent; up to 30% of patients report that the injection relieved all or most of the pain when local anesthetic agents numb the entire joint, but 30% of patients injected with saline (plain salt water) report the same thing. Further, it does not correlate well with treatments that remove the joint or it's nerves. In addition the relief in most cases is short-lived. Despite this it is a procedure that I do recommend (not very often, but often enough to warrant comment); it is virtually without risk; it is a little expensive (done in an OR with x-ray guidance) but not outrageous, and it has a "shot" of making the patient feel better- at least for a time. I NEVER use it as the sole criterion to decide whether or not to operate on someone however; it may be a piece of the puzzle, but it will be a small piece.
The other study done on a semi-routine basis for CLBP is discography. This is a procedure in which a needle is directed to a point inside of what is felt to be a painful disc. Dye is then injected and images,x-rays and CAT scans, are then obtained. A better version of this test is called a provocative discogram- same procedure but pressures within the disc space are recorded and an attempt to reproduce the pain is made. This is HIGHLY controversial with many studies showing that this test can be quite misleading (most volunteers who have normal discs report pain when the dye is injected). What this test seeks to find is something called an Internal Disc Disruption (basically a tear on the inside of the disc), an entity that is hotly debated and is not universally accepted (not even a majority of clinicians accept it). Others believe that IDD is the cause for up to 40% of CLBP. I strongly disagree with that, and believe that discography and IDD have been used to convince a multitude of patients to undergo futile procedures. However, I do believe that there is a small, very small role for discography in the diagnosis of CLBP. Once again, it should NEVER be the sole reason to operate on someone- please memorize this statement.
Cause of Chronic Low Back Pain
"So if these eight things that the radiologist says are abnormal aren't causing my low back pain, what is?" I hear that question probably ten times a week- over twenty years that's about 10,000 times, and honestly, I don't think I have ever fully answered it. The problem is that we just don't know. Somethings we do know, for instance, nothing happens in isolation. What does that mean? It means that the cause of the CLBP is not just "the disc", or "the alignment of my bones". Refer back to the concept of a motion segment in the anatomy section-sorry you'll have to scroll down, I can't seem to get this hyperlink to work correctly. Basically it includes everything that connects two vertebrae as well as the vertebrae themselves.
Each segment of the motion segment affects the others. Now add in the muscles and tendons that move the motion segment and you have somewhere in this cohort a combination of factors that starts a process that ends in chronic low back pain.
Notice that I said "starts a process", because chronic low back pain IS a process. One that by definition takes 3 months to develop. Once again, let me remind you that this refers to the 70% of chronic low back pain patients without any of the serious "Red-Flag Signs". Maybe you should click this link and review them again. What starts this process is highly individualized, and widely debated (anything that is widely debated is clearly unresolved). It is my belief that in most CLBP patients the process started with a "garden-variety" episode of acute low back pain that went tragically awry, culminating in a self-perpetuating process.
Think of the game dominoes. At first all the pieces are standing tall and beautifully arranged. Then something happens, like for instance some slight injury that mechanically stresses the back/domino (overuse injury, fall, car accident, etc). This causes the first piece to fall.The patient starts to hobble around, stressing other aspects of the motion segment, causing the second piece to fall. The pain gets worse so it's off to bed for a week or two. This causes a rip-roaring case of deconditioning (muscles begin to thin, tendons shorten, cardiovascular reserve diminishes,etc). The immobility causes the remaining elements of the motion segment to become hypersensitive to any mechanical stress, leading to more pain, leading to more immobility, leading to more hypersensitivity, etc.. You get the picture.
Now add in some financial and personal stresses, add a dash or two of depression and pretty soon you have a pile of dominoes, and a life that is hardly recognizable.
Now that we know everything that we can know about CLBP how do we treat it? The first thing to do is look in the mirror. Take a critical appraisal of yourself, because that's what your doctor is going to do. What about you can be changed to minimize your back pain? Think about that for a moment while I go off on a slight tangent-I will circle back to this in a moment.
In writing this section I looked at a fair number of other websites and got very depressed (where are my SRIs?). None of them, from the Mayo Clinic to Web MD to Spine talks about remediable factors. These are the things about you that can be fixed. It is an indication of how far political correctness has seeped into our society. These respected authorities are uncomfortable discussing factors that have a direct bearing on your health for fear of offending you. I am under no such burden. Remember what I said at the beginning of the neurosurgery anatomy section- "an over-arcing theme of this site will be personal responsibility. No one can confer health upon you; no operation, pill, or treatment can "fix you" without your help. Simply put you have to become a participant in your own care." With chronic low back pain that starts with a good hard look at yourself. Further, it means that it is very likely that you are going to be asked to do some difficult things-things that you're NOT going want to do. Let me say this simply: if you want your life back, if you want the pain to go away, you WILL have to do them. Enough said.
So what about you can we change? Let's look at the five "biggies".
You knew this was coming didn't you? More than anything else patients with chronic low back pain are overweight. This statement however, while being very intuitive is very hard to verify for a couple reasons. First is the usual difficulty: definition. What is overweight? What parameter are we using? Typically the Body Mass Index (BMI) is used, and here lies a huge problem . The BMI is absolutely inaccurate a good deal of the time. For example, I am 5'8" tall and weigh 210 pounds, which gives me a BMI of 32.2 making me moderately obese. What this number does not calculate is that I have a percent body fat of 18%, a resting heart rate of 52, and a VO2 max of 57 ml/kg*sec, all of which is on a par with elite athletes (if only this translated into real life). Obviously the BMI has some significant shortcomings (a number of studies have thoroughly repudiated the BMI).
The other problem with the statement above is that we have been unable to fully calculate the additional burden (enjoy the pun)that weight adds to chronic low back pain. Obesity, unfortunately using the notoriously inaccurate BMI, has clearly been associated with CLBP. But what about those who don't reach the lofty realm of obesity? What is the threshold for to much weight? What is a persons ideal weight? Once again, we don't know. What we resort to is the old pornography adage: we know it when we see it.
I think it's fairly obvious how additional weight contributes to CLBP. The motion segments of the back are simple machines (actually for you physics freaks the motion segment is a complex machine), and like all mechanical devices they have limited capacity. Being biologic that capacity can change-exercise increases the capacity, and immobility reduces it, but even that has an end point, beyond which the body can no longer effectively deal with the load. When the load exceeds the capacity "adaptations" or "failures" occur. Anatomically these may be micro muscle or tendon tears, joint capsule strain, annular tears, etc.. The points are that all these components are pain sensitive, and that strain/stress on one component will lead to strain/stress on other components until outright failure occurs.
These is the second most common characteristic amongst CLBP patients. It is also the easiest to study and quantify. Smoking DOUBLES the chances for chronic low back pain, and if you are under 45 the risk increases to 250%. Aside from the fact that some of the inhaled chemicals are among the most potent vasoconstrictors (they cause blood vessels to constrict and reduce blood flow-esp to damaged areas) does anything more need to be said?
Here we get a little into the chicken and the egg conundrum. Are you deconditioned because you have low back pain, or do you have low back pain because you are deconditioned? For most people it is both. Recall the scenario in which an acute episode of low back pain becomes chronic. With no literature or scientific studies to back me up, I believe that the group of people who follow that scenario are different in some respects from the other 75% of Americans who develop acute low back pain that resolves within 3 months. We could label this difference a susceptibility- they are susceptible to the development of chronic low back pain but need something to express that susceptibility- like an injury.
Once again, without any proof I believe that not everyone with the susceptibility develops CLBP because they are the "exercisers" of the group. It is not uncommon for some people to develop chronic low back pain after a prolonged (and usually forced) hiatus from exercise, even when the hiatus was not prompted by back issues. Obviously not everyone who takes a hiatus from regular exercise develops chronic low back pain, so what's happening to those that do? Enter my susceptibility theory-they had been keeping it at bay so long as they exercised regularly. After excess weight and smoking, deconditioning is the most common characteristic of CLBP patients.
Lots of patients tell me that they exercise all the time, for instance they walk around the house a lot, or garden, or lift heavy things at work all day. THIS IS NOT EXERCISE! Paradoxically, those activities will lead to the development of acute low back pain, and in 5% to the development of chronic low back pain. You are the classic "weekend warrior", doing things that require a greater degree of conditioning than you currently possess. Exercise is defined as a sustained physical activity that is done on a repetitive basis. The definition of sustained varies from 30 minutes a day to 90 minutes a day-either 5 days a week or everyday. Generally it is recommended that every adult perform 60 minutes of aerobic activity 5 days a week (with a modest intensity-just to the point of having trouble talking smoothly), and 2 one hour sessions of muscle conditioning (weights or resistance training) a week. In addition, stretches of the neck, back, and all major joints should be done daily.
This is where I begin to walk on thin ice. It is absolutely clear that a workers compensation claim or a litigious situation (ie when lawyers are involved) increases the conversion rate of acute low back pain to chronic low back pain. Both of these "conditions" are an independent predictor of a poor outcome, ie protracted pain and unemployment. I'm going to leave the "why" out of this discussion after 2 words: secondary gain.
Do not misunderstand me, I'm not implying that everyone who gets hurt on the job, or has to hire an attorney is malingering, just that the presence of either of those two conditions adversely impacts improvement in back pain. This is the lens people will be viewing you through. Here are a few facts that partially justify this cynical point of view:
It is unlikely that an employee who misses work for up to two years will ever return to work in any capacity, regardless of treatment.
There is strong evidence that if a person misses work for four to 12 weeks, he or she will have up to a 40 percent chance of missing work for the ensuing year; especially if the worker is older than 50.
There is strong evidence that low work place support is a predictor of chronicity in patients with acute back pain.
If it wasn't for the obvious nature of this problem amongst patients with CLBP I doubt anyone would discuss it. This is where we step all over peoples cherished and usually aberrant beliefs. People are far more offended by the fact that they could have a psychiatric problem as opposed to a physical problem, ie obesity. The stigma is large and persisting. That being said let me start to offend you. If you have chronic low back pain, or chronic pain of any sort you have a psychiatric diagnosis, and if you don't deal with it, you will not get better.
To have a discussion about chronic low back pain without discussing the psychiatric contributions is to discuss only half the problem. Patients with any chronic pain syndrome (like low back pain) develop a heightened awareness of physical symptoms- somatosensory amplification (remember the discussion above about some brain centers amplifying nocioceptive stimulus?). A number of excellent papers have examined chronic low back pain patients and an understanding is beginning to emerge that in this particular disease state the psychological reactions are intense. CLBP impacts function, and through function self-worth (ie who you are as a person). It affects recreation and enjoyment, and as stated above is invariably associated with depression (fatigue, sleep disturbances, changes in appetite, decrease libido and interpersonal relationships, etc). However, in many CLBP patients these symptoms are ascribed not to depression, but to the low back pain. A number of patients emphatically reject the notion that there is anything wrong except for the physical cause of their low back pain. This often warps a patient mentally- "no one believes me", "no one listens to me", "no one understands what I'm going through", and leads to symptom magnification and dramatic behaviors which only intensify the patients isolation as no one wants to deal with a "crazy-person". Other patients become "invalids", seeing themselves incapacitated by their "illness". They spend most of their time in bed, dependent upon anyone who will help them, ultimately straining personal and professional relationships.
For some, pain becomes a convenient focus for all the patient's depression, dependent invalidism, unmet expectations, etc.. Their perceptions have become so altered that they find it hard to relate to anyone and unfortunately can only summon any kind of energy when their core belief-that all their problems are related to the back pain-is challenged. These are the kind of patients I and probable most every other healthcare provider just wants to go away, and so they get worse and worse.
Perhaps before we see any patients maybe we should look in the mirror and ask ourselves what about us can we change.
Okay, now that we know the big "5", what's to be done? I'm going to describe some of the most important aspects of what has been termed a Multidisciplinary Biopsychosocial Rehabilitation Program (from now on I'll simply refer to it as Rehab- that other name takes to long to type). Basically this is an acknowledgment that chronic low back pain has physical, psychological and social (including vocational) ramifications, all of which need to be addressed. There is strong evidence that intensive multidisciplinary biopsychosocial rehabilitation with a functional restoration approach reduces pain and improves function in patients with chronic low back pain. There is also strong evidence that intensive multidisciplinary biopsychosocial interventions are effective in terms of return to work, and work-readiness.
So what is this Rehab program? Obviously it centers on the physical state (Bio-), the psychological state and perception of pain (Psycho-), and the social aspect (family, work). Often times this program will seem somewhat piecemeal, ie "my doctor sent me here, and over there", etc., because only a few places have everything under one roof. If you are fortunate to live close to a center that is truly integrated, use it. If you are like most of us it will be up to your treating doctor to "cobble" together all the requisite pieces.
The first step in this process is a cognitive one; sit down and come up with a list of reasonable and specific goals. I know it sounds silly and somewhat condescending, but think about it for a moment. You are going in and asking your doctor for what exactly?The usual complaint is: "I hurt to much and just want to get back to where I was". Be more specific! Do you want to hurt less? Sounds like a good goal, write it down. Do you want to get back to work? Write it down. What about going back to the same job, or a new job? Think about what exactly you want so that you have specific goals to focus on. This is the first task that is required of you to get better; in essence you are defining what "better" means to you.
The sections below will review how it's done (actually one method, as there are different approaches). I'll conclude with a discussion of common modalities (like injections, therapy, medications) that are used during this Rehab Program, and include some others that are well known but not used/helpful.
Weight and Conditioning
I'm going to start this section off by discussing weight and then seamlessly switch over to a conditioning program that I've been recommending for about 15 years.
Most of this you can do on your own. If you are very inexperienced or uncomfortable it may be reasonable for you to be referred to a physical therapist to get started with the physical aspects, or to a nutritionist for the dietary components (esp if you are diabetic). okay, let's get started.
For weight loss your target goal is 6 pounds a month. You're right, that's not alot. Why set the bar so low? Because any more and your body will push back. There is a center in your hypothalamus (a part of the diencephalon of the brain-you should already know these terms) that maintains your percent body fat. It's an old center, built around 10,000 years ago when food was scarce, and it still thinks in those terms. It's job is to keep you alive and active through the next famine by maintaining fat stores; it will do anything it can to keep those stores high. It's chief weapon is to lower your metabolic rate, burning sugars as opposed to fat- ever wonder why you feel so weak and poor when dieting? It's this guys fault- he's ratcheted down your metabolic rate (the rate at which your body burns calories) because your intake has fallen- you burn fewer calories and feel lousy. Our goal is to slowly drop the percent body fat without alerting this guy.
One pound every 5 days or roughly 650 calories a day. That's the number that you have to reach-you have to burn 650 calories a day more than you take in. That's not alot. So how can this be done? Well if you are a child or adolescent you withhold food- their metabolic rate is as high as it can be-ie their metabolic engines are "red-lined". If you are of the adult version, you need to exercise- there's that four letter word again. ADULTS CAN NOT LOSE WEIGHT BY DIETING !!! Sorry Jenny Craig and NutriSystems (but you guys already knew this). However, don't cancel your subscription yet because not all eating is the same- more on that latter. Back to exercise. THE ONLY WAY ADULTS LOSE WEIGHT IS BY INCREASING THEIR METABOLIC RATE- THE ONLY THING THAT LEGALLY RAISES METABOLIC RATE IS EXERCISE!!!This is a simple irrefutable fact.
But wait? How about the time I lost 15 pounds by using the South Beach Diet (or any diet for that matter)? My question to you is did you refind those 15 pounds? Greater than 98% of diets fail by 2 years-ie all the weight you lost is found again within 2 years. If you are in that 2% who don't regain the weight, congratulations- you're probably exercising aren't you?
Or how about bariatric surgery? I can get a lap band or my stomach stapled and I won't be able to eat as much. True, but without exercise all bariatric surgery fails; this is one of the reasons that patients are extensively tested and educated before such surgeries.
Liposuction? "Liposuction should not be used as a quick fix for weight loss. It should be used only in conjunction with exercise and a healthy diet to encourage long-term weight loss success. Liposuction has always been for contouring, not for weight loss," says researcher Rob Rohrich, MD, professor and chairman of the department of plastic surgery at the University of Texas Southwestern Medical Center in Dallas.
Convinced yet? Good. Now, exercise does not have to be unpleasant- in fact if it is you are doing something wrong. Our goal is 650 calories a day- which is just a little more than what the average adult will burn in one hour of moderate aerobic activity. So that is your goal: one hour of moderate aerobic activity a day. Moderate activity is defined as 150% of your resting heart rate, or if you're of average cardiovascular fitness this comes out to between 120 to 130 beats a minute. This is what's referred to as your aerobic threshold- where you are burning all your calories without producing lactic acid (the muscle burn chemical). This is the exercising "sweet-spot", you are reasonable comfortable, sweating a little, a bit out of breath, but still able to talk, read, watch TV ,etc., all the while working your heart and lungs (cardiovascular conditioning=aerobic conditioning).
All aerobic activity is equal. All your body cares about is intensity (above) and duration. Swim, bike, run (wait, that sounds like a triathlon), do an elliptical, an air-runner, anything, they're all equal. So tailor your activities around two concepts: pre-existing orthopedic issues ( I can't bike because of my ______- insert joint name here) and boredom. Yes, you will get bored as this healthy lifestyle needs to be lifelong. Create a weekly schedule that includes some variety; a good way of doing this would be to find a local gym with a number of different aerobic options (exercise bikes, treadmills, pool, ellipticals, etc,etc). If you confine yourself to one exercise modality you are likely going to grow to hate it.
Easy right? Now comes the hard part; to derive the required benefit from aerobic activity it must be maintained for greater than 30 minutes. The reason is a little protein called atrial natriuretic hormone; this hormone is released by heart cells (yes heart cells) in response to a variety of factors with exercise being one of the most powerful stimulants, but it's only released after 30 minutes of sustained activity at the aerobic threshold. One of the chief functions of atrial natriuretic hormone (ANH) is to "reset" the metabolic rate and get the body to burn fatty acids (the products of fat) instead of sugars. It also raises the bodies endorphin levels (the naturally occurring "narcotics" responsible for your overall sense of well-being and the "runner's high") which causes nocioceptive inputs (pain signals) to be blocked in the spinal cord and brainstem. This is the reason that early on, before any substantial amounts of weight have been lost, exercise causes your back to feel better.
Okay, so if this ANH is released after 30 minutes, why do I have to exercise for at least 60 minutes? The answer is 2-fold. First to get your 650, and the second is the fact that the release of ANH stops when you stop. I have alot of patients complain to me that they are exercising everyday for an hour and nothing is happening- the weight isn't coming off fast enough and the pain persists. On closer questioning I usually find that they are breaking the hour up- sometimes having two 30 minute sessions. Do you see the irony of this-they are putting out a greater than needed effort, getting right to the threshold of ANH release and then stopping before they gain any benefit. It's these little details that regularly hobble people.
Do I have to do this EVERY DAY? No, I firmly believe that this leads to injury- your body does need some time to rest and "solidify" the gains you are making. I recommend one hour of aerobic exercise five days a week with two one hour sessions of resistance/core training a week (more on this below). This is counter to what the NIH recommends (they say 7 days a week), but what do they know?
One more thing before moving on to core strengthening- the key to this conditioning program is low grade activity done consistently. The goal is to make you healthy, not dead. Monitor your heart rate (it's your intensity meter), your breathing, your joints, everything, and if something seems to be awry-stop and get checked out (obviously BEFORE starting a conditioning program see your doctor and get checked out, esp if you are on heart medicine that slows your rate-but you've probably already done that). Further, if after an hour of exercise you're gasping for air and crawling, slowly and painfully, towards the door, you've done something wrong. Your aerobic and weight loss benefit plateaus off beyond the aerobic threshold- ie you get NO MORE benefit by exceeding the 120 to 130 heart rate mark, and if you have exhausted yourself, you've exceeded the mark.
Alright let's get away from aerobics and onto some core training. So what is the core? It's the belly, back, gluteals and upper legs. These are the structures that provide additional support for the lumbar spine (by some estimates up to 40%). To train them fully you're going to have to do 2 things-improve their range of motion, and improve their overall strength.
First range of motion. This means stretching- if you're reading this with CLBP you have probably already had a course of physical therapy . PT is quite good at working on ROM (range of motion); drag out your instructions and relearn them. Here's a video demonstrating a very simple stretching regimen. Do each stretch ten times in a row, and repeat them 3 times a day. Once again please ignore the annoying adds.
One other option is to combine some of these stretches into a single exercise: stand-up and bend from the waist as if you were going to touch your toes-now hold that for 2 seconds and relax; then, arc your back like you were looking into the sky, hold for 2 seconds; then, rotate your shoulders (keeping your hips stationary)to the right, hold for 2 seconds, and the rotate to the left. Go just to the point of tightness- NOT pain, and RELAX. Repeat this 10 times and do the whole set three times a day. Okay, I think that should cover stretching.
Now onto core strengthening. Here's a simple slideshow from the Mayo clinic demonstrating a core strengthening routine. After you're done reviewing it scroll down the page to some of the other topics including videos demonstrating weight and core training.
This routine should be done at least twice a week, and should be a part of a general muscle reconditioning program. I'm not going to go into specifics about that, the Mayo Clinic web site has already posted some excellent videos and examples- just know that I give this section of their site my seal of approval (did you just hear their collective sigh of relief?).
Muscle mass and tone are important aspects of health- think of the muscles as the machinery that burns your calories- the bigger and more active the machines, the more calories are burned. Not only that, but muscles are the bodies "pantry"- think of all that protein and other stuff just sitting around waiting for an emergence. Further, Type II diabetes (often called non-insulin dependent diabetes-which isn't always the case) is caused not by reduced insulin production, but by insulin resistance chiefly in the muscle cells. Insulin normally binds to the cell membrane opening the channels that let glucose (the bodies primary sugar) into the cell. With Type II diabetes it takes more insulin to open up those channels. Increasing muscle bulk makes the muscle cell membranes more sensitive (or less resistant) to insulin. Thus, exercise cures Type II diabetes (okay maybe this is a little exaggerated).
Finally, a last comment. At first this program will increase your pain. Go into this with your eyes open and anticipate more discomfort. It may take a week, it may take a month, but exercise ALWAYS WORKS. Always. Without exception, even you! It is not comfortable (at first), but it is completely reliable. If you don't believe this it is likely that your efforts will be suboptimal and you will create a self-fulfilling prophecy:"see, it didn't work". What you get out of this will be exactly what you put into this. Nothing we, you, or anyone will do will work without weight control and physical reconditioning (NOT physical therapy). NOTHING! If you want to get better, if you truly want your life back, this is the ONLY WAY.
That being said, you are not on your own. The following sections describe modalities that will assist you (notice the word assist) on this journey. But first I have to discuss the other two "biggies".
Talk with your doctor-get hypnotized-start oral medications-do it cold-turkey. I don't care how it's done, it simply MUST be done.
This is a tough one. As I talked about earlier if you have chronic pain, you have at least a degree of depression, and quite possibly more. My advice, because that's all I can give, is for you to accept the possibility that the exposure to chronic pain has changed you, and probably not for the better.
Depending on how bad you are you may simply need to talk to someone and find some hope that there's indeed light at the end of the tunnel, and it's not a train about to run you over. You may need some medications; accept that and take them. You may need to find a reason to get out of bed in the morning. What you certainly need is to talk about this with your treating doctor and quite probably be referred to someone who can provide some real help. All that being said, let's switch gears a little, because there is a whole other side to the psychological aspect of chronic pain that a professional can help with. Pain has two parts the physical, and the emotional response to the pain itself. Think about this for a moment, let's say that you are walking down the street and you hear a man scream: "free money". You look up and find that across the street is Bill Gates waving thousand dollar bills. You sprint into the road at the exact moment that Chris McCormack (winner of the 2009 and 2010 Ironman World Championship) is flying by on his bike and he knocks you to the asphalt. You get scraped up pretty bad, but does that stop you? No! Bill Gates is literally giving his money away, so you pick yourself up and run to the crazy man to collect the cash. So how did you pick yourself up and run across the street with your arms, knees, and face bleeding? Adrenaline? Nope-that system takes 30 to 60 seconds to kick in. Insanity? Nope, that requires long-term exposure to children. The real answer is that while your brain received the same number of pain signals, it refused to process all of them, and the ones that did get through were suppressed to the point that you had no emotional awareness of them. You didn't even know you were bleeding until Bill Gates started using thousand dollar bills as bandages for your arms! This filtering is a learned behavior, and with cognitive and behavioral techniques they can be applied to chronic low back pain. The system is already in place, you just have to strengthen it and learn to use it properly. Perhaps it won't be as effective as in the possibility of sudden riches (perhaps it will be), but it is an important treatment component.
Go back to your list of goals; is getting back to work on that list? What about getting back to the same job? Ask yourself if that's reasonable. Studies have shown that if light duty is an option, the percent of patients returning to full employment is increased. It's possible that return to a previous occupation is no longer feasible. In this situation retraining maybe necessary as well as a functional capacity exam (basically a series of physical tests that determine a persons physical abilities).
Now let's move on to some of the modalities that will help you put this program into action. I'm going to describe a long list of therapies that are commonly used in CLBP. I'll start with the most effective and finish with treatments that just don't work. Most of my discussion will be evidence-based (ie based on clinical studies) but where they conflict I will substitute my own opinion and experience.
Effective Treatments for Chronic Low Back Pain
The page looks better if there is a line here, so here it is.
Obviously this excludes medications, anything with a needle associated with it, and surgery. Not much left, except:
Exercise-covered above Transcutaneous Electrical Nerve Stimulation- a TENS unit is a common treatment for CLBP and one that the literature does NOT support. However, I do and I'm right. TENS units are not perfect, they're messy, inconvenient and take some time getting used to, but once you do most patients swear by them. Spinal Manipulation-Spinal manipulation is defined as a high velocity thrust to a joint beyond its restricted range of movement. Spinal mobilization involves low-velocity, passive movements within or at the limit of joint range. Most people do not make a clear distinction between these two, and in clinical practice these two techniques are part of a “spinal manipulation package” that is often referred to as manual therapy.There is moderate evidence that manipulation is superior to sham manipulation for improving short-term pain and function in CLBP. Read that line carefully; what it says/means is that in ACUTE flair-ups of pain, beyond the normal chronic low back pain, spinal manipulation is effective. What it DOES NOT say is that spinal manipulation is effective in stable chronic low back pain- it works when you have an acute episode on top of the chronic pain. Go back to the acute low back pain treatment section and remind yourself that spinal manipulation is good acutely, but that it's utility falls after about three weeks. Long term use of spinal manipulation is NOT recommended.
Surprisingly most medications have been found to be effective.
NSAIDs-Once again this stands for Non-Steroidal Anti-Inflammatory Drugs. Things like aspirin, Ibuprofen, Celebrex, etc.. These medications are, by definition anti-inflammatory, but also pain relievers (analgesics). There is strong experimental and clinical evidence that NSAIDs are effective for the relief of chronic low back pain. That being said they do have risks and long-term use is discouraged. NSAIDs should only be used for exacerbations or shortterm periods (up to 3 months).
Antidepressants-Once again we have a class of drugs doing double duty. Obviously an antidepressant is going to help treat depression, but they also potentiate (magnify) the benefits of other medications-like NSAIDs and low-grade narcotics. There is strong evidence that noradrenergic and noradrenergic-serotonergic antidepressants are effective in relieving pain in patients with chronic low back pain (remember the discussion about serotonin and norepinephrine neurotransmitters?) .
Muscle Relaxants-The term "muscle relaxants" is very broad and includes a wide range of drugs with different indications and mechanisms of action. Muscle relaxants can be divided into two main categories: antispasmodic and antispasticity medications. Antispasmodics decrease muscle spasm associated with painful conditions such as low back pain and can be subclassified into benzodiazepines and non-benzodiazepines. Benzodiazepines (e.g. Ativan,Xanax,Valium) are used as anxiolytics (anti-anxiety drugs), sedatives, anticonvulsants, and/or muscle relaxants. Non-benzodiazepines (e.g. Flexeril, Biocalm, Zanaflex, Soma) include a variety of drugs that can act at the brain stem or spinal cord level. The mechanisms of action with the central nevous system are still not completely understood. Antispasticity medications (e.g. dantrolene, baclofen) reduce spasticity that interferes with therapy or function, such as cerebral pulsy, multiple sclerosis, and spinal cord injuries. we're not really concerned with the antispasticity medications to much in CLBP.
Opioids- This is the term for narcotics. These medications can be given orally or for sustained release, through the skin. We need to study the use of opioids in greater detail, but with the available information it is safe to say that weak opiods (ie Tramadol) that maintain a patients level of function, without dose escalation (ie the patient is not asking for more and more medication) are safe. The real question is what do we do with the stronger medications? What we do know is that due to the risk of addiction, slow-release opioids are preferable to immediate-release opioids,and should be given regularly (around the clock) rather than as needed; making them ideally sited for transdermal (ie patches) route of administration. The same rules apply, however: no dose escalation, and a patients level of function must be maintained. Last word on narcotics: just like with nocioceptive signals, the body WILL down-regulate narcotic receptors (this is the basis of addiction) making the medications less effective over time. This is why Class II narcotics (the strong ones) should be used as sparingly as possible and for as short a period of time as possible.
Capsaicin-This is actually a neurotransmitter in the spinal cord. Guess what it transmits: PAIN. So what is it doing in this discussion? Remember the Gated theory of pain- that there is a finite number of spinal cord tracts that carry information to the brain, and that superficial stimuli get priority? Capsaicin utilizes that. It is derived from chilli peppers and when rubbed onto the skin binds to nociceptors, causing excitation of the neurons and a period of enhanced sensitivity perceived as itching, pricking, or burning. This is followed by a refractory period with reduced sensitivity and, after repeated applications, persistent desensitization. The desensitizing effect is fully reversible. There is strong evidence that capsicum pain cream is more effective than placebo for the short term (3 weeks) relief of pain. As a bonus it's an over the counter medication.
If you believe the literature there are NO invasive modalities that work for CLBP. To explain this let me go off on a tangent. All studies have limitations, the largest of which is trying to sort through the accumulated data and draw accurate conclusions. Even when you look at a single parameter it is hard to be accurate. So when someone sets out to look at something as simple as the efficacy of trigger point injections, they try to pare the investigation down to just that modality. Add in other aspects, say exercise, antidepressants, etc.. and very quickly any meaningful information is lost. The solution to this is to enroll HUGE numbers of patients into the study so that these differences cancel out. But who has HUGE numbers of patients? No one, so several different centers get together and pool their patients. Only problem is that now we've introduced a couple of biases (different doctors, regional makeups, etc.) that lowers the power of the conclusions. In addition these studies are few and far between because the logistics and money that are involved is prohibitive. Don't misunderstand me, studies are the backbone of medicine, but THEY ARE NOT GOSPEL!!! An experienced clinician is going to "stay-up" with the literature, but balance the findings with his or her experience. So after 20 years here are my conclusions.
Facet Joint Injections-See the above discussion. They do have a limited role, particularly with pain that is made worse with extension (bending backward). They are esp good with acute flairs of chronic pain.
Trigger Point Injections- These are shots right in the Bulls-Eye. "It hurts right here", and the patient touches a sore spot. These are usually localized inflammatory reactions- hot spots if you will, that often prevent a patient from doing the things that are required to improve. As simple 1 minute injection usually allows the patient to walk out of the office better than they walked in.
Sacro-Illiac Injections- The SI joints are the largest in the body and by some exaggerated estimates account for 25% of CLBP. here's a 4 minute video that tells you everything there is to know about SI joint problems. Caution: I DO NOT recommend RF ablation of the SI joint nerves or fusion. Beyond those differences I think it's a good video-although a little long.
Epidural Steroid Injections-This one is way out there as far as the literature goes, and it's wrong. ESIs in isolation stink; ESIs however can alleviate enough pain to get the patient to start exercising and get the ball rolling in the right direction. That's the problem with the literature- we can't evaluate these modalities in a vacuum, or even looking at a few of factors. Simple stated ESIs do not cure CLBP- but they improve a patients function long enough for other modalities to become effective. Since I'm in the "video mood" here's another one-sorry no audio. I like how the nerves change color in the end- they're SOO happy.
Surgery-Yeah, finally, something I can do!!! For obvious reasons I'm going to defer any detailed discussion of surgical treatments for later. So for now let me simply say that there is clinical evidence that in selected patients with severe CLBP and degenerative changes at L4-L5 or L5-S1 level, who have failed to improve with an extended course of conservative treatment, surgery is successful in improving function and pain up to 2 years after treatment when compared to traditional non-specific conservative treatment. So what is an "extended course"? A minimum time frame is 6 months, a more reasonable time frame is one year. What that means is if you have ALL the right findings, meaning personal (ie highly motivated- quit smoking, lost weight, have kept working,etc), medical (no major medical problems, no previous spine surgery, etc), isolated pathology on imaging (for instance like the MRI to the right-notice the single "dark-disc") I might consider a 6 month course-otherwise it needs to be longer.
Ineffective Treatments for Chronic Low Back Pain
In this section I am generally in agreement with the literature. I am going to list them quickly with comment only where needed because my back is starting to hurt.
Modalities that Don't Work
Laser Therapy-Who ever thought of this?
Ultrasound-This MAY work as part of a multimodality physical reconditioning program, but not in isolation.
Back Braces-See above.
Diathermy/Interferential Therapy-Ineffective and strange.
Traction-Oh if only I had a dollar for every time I was asked about traction or it's new "sexy" cousin, decompressive therapy. Different types of traction exist: manual traction (i.e. traction exerted by the therapist,using the patient’s head, arms or legs), motorised traction (i.e. traction exerted by a motorized pulley), suspension (i.e. traction exerted by gravitational forces, through the body weight of the patient), and bed-rest traction (i.e. traction by a pulley and weights).There is no evidence for the effectiveness of lumbar traction compared with other treatments in the treatment of chronic low back pain. It may feel good when you are being stretched, but no matter what anyone tells you about realigning your spine or "sucking" discs back into place, IT DOESN'T WORK!
Intradisc Therapies-Sounds reasonable; if the disc hurts numb it up, right? Sorry, doesn't work, and raises the risk of discitis (inflammatory or infectious process within the avascular-no blood supply-disc space).
Prolotherapy-I love the concept. The ligaments and fascia are loose causing excess strain on the motion segment so let's inject a sclerosing agent to damage them in hopes that they will heal correctly. Did I miss that day in Medical School?
Intradiscal Electrothermal Annuloplasty-IDET-Ahh, the boondoggle of the 90's. This procedure was conceived by 2 brothers; it involves putting a needle that is either heated up or pulsed by a radiofrequency generator to damage the annulus of the disc. This burns all the nerves, and causes the annulus to shrink together theoretically "sealing it". Unfortunately, no one, and I mean NO ONE has been able to reproduce the original findings; at VERY best there maybe a very slight improvement in a small number of patients when compared to sham procedures (wait a moment, isn't IDET a sham procedure?). Suspicious? I think so. What's amazing is that this crap (excuse the expletive) is still being done despite volumes of data refuting it. I am impressed with the skills it must take to convince a patient that by burning a disc their back pain will go away. I must have missed that day in Medical School as well.
Boy, am I tired of low back pain in all it's forms. Let's move on to something fun and interesting (and surgical).
First off, I'm going to assume a basic working knowledge of the anatomy of the disc and motion segment. In the segment below I'll go into more detail, but first review the basics in the anatomy section, it will make things a little easier.
Let's start by reviewing the basic parts of the vertebrae- the images below demonstrate the fundamental components of a vertebrae. The one to the left is in an "axial" view (top down), while the one to the right is a "lateral" view (from the side). Mouse over the images for the names- the lateral view doesn't seem to work as well as the axial view.
Notice that on the lateral view (right) that below the pedicle is a round-ish hole- this is the NERVE FORAMEN, the exit site for the spinal nerves. These nerves leave the spine through the foramen and run into the leg, arm, or any other body part. In all but the cervical area the number of the nerve is identical to the pedicle ABOVE, for instance the L4 nerve runs beneath the L4 pedicle. In the cervical (neck) region the nerves run OVER their respective pedicle- except for the C8 nerve root which runs beneath the C7 pedicle. Does this make sense?
Now, go back to the interactive images above. Notice what's directly in front of the nerve foramen, a disc, and what's behind the nerve foramen, a facet joint (that will be important later). So what is "the disc"? As mentioned earlier it is a structure composed of a few parts, and is more of a "complex". This complex accounts for one-third of an individuals height, and are the largest avascular tissues in the body (discs have no blood flowing into them).
To fully understand the anatomy of the disc complex, it's best to first understand what the disc does. The intervertebral disc has three basic functions: it forms a strong joint between the adjacent vertebral bodies; it allows a small range of motion between them, and acts as a shock absorber. This last function requires some explanation as it has a direct bearing on the anatomy of the disc complex. Weight passing through the spine from top to bottom (or vice-versa) is called axial loading. This weight, or load has to be dissipated by body structures. Bone is ill-suited to dissipate load; it will carry a load and transmit it to another structure- usually another bone, but the load that it transmits is very similar to the load it received. A better way of "carrying" a load would be to create a structure that dissipates or reduces that load- enter the intervertebral disc complex. The disc takes weight that is being transmitted from top down (axially) and redirects it laterally, or radially. Imagine an Oreo cookie; the cookie parts are the vertebra and the disc is the cream filling. When pressure is applied to the top cookie, the cream squeezes out, reducing the amount of pressure that is transmitted to the lower cookie. Try it, and then eat your experiment as a treat for reading this. This redirection of force laterally (actually it's a radial redirection) minimizes repetitive trauma to the vertebra. The disc is capable of handling tremendous forces when applied axially (top down), but its ability to handle asymmetric forces (like bending and twisting) is not nearly as tremendous, and this is a common mechanism for disc complex failure. But before I get into failure let's talk about how well the near-magical intervertebral disc complex is built.
The disc complex is composed of a band of encircling ligaments and three components: the cartilaginous end-plates; the annulus fibrosis; and, the nucleus pulposus. To be completely accurate, there are two types of end-plates, the bony end-plate, and the cartilaginous end-plate. One is made of bone (guess which one) and one of course is made of cartilage; the bony end-plate is the bottom or top of the vertebral body and serves as an attachment site for the outer layers of the annulus fibrosis, BUT NOT the cartilaginous end-plate which sits on top of the bony endplates (there is a loose attachment but no meaningful stability is derived from it- think of a ham and cheese sandwich- the bony endplate is the cheese and the cartilaginous end plate is the ham). The cartilaginous endplate is about 1 mm thick and serves as an attachment point for the other two structures of the disc complex- actually, only the inner layers of the annulus fibrosis are strongly attached to the cartilaginous endplate. It also serves as a conduit for nutrients and water (very important as there is no blood supply into the annulus or nucleus-everything relies on diffusion through and from the endplates). Enough about endplates, lets move on to ligaments.
Below is a drawing I borrowed (without permission) from a fairly informative web site written by a chiropractor (www.chirogeek.com); while I don't agree with some of the material on the web site, it has cool pictures, and for now that's what's important. The drawing is for the most part self-explanatory, but let me emphasize a few points. First is the thin grey layer that encases/encloses the green annulus fibrosis (designated by the number 6). This grey layer is critical to the integrity of the disc complex. It represents the ligamentous support (ligaments hold bones together).
The two most important ligaments are the Anterior Longitudinal Ligament (ALL) and the Posterior Longitudinal Ligament (PLL)- if you want, scroll down a bit there's another interactive diagram that illustrates the two ligaments. The ALL attaches very strongly to the front of the vertebra and their bony end-plates, and even merges with the outer layers of the annulus fibrosis. It is VERY strong and one of the chief structures that prevent over flexion of the spine. It constrains and backs-up the annulus fibrosis (the green structure above-more in a bit) and prevents the nucleus pulposus from herniating through the front of the disc space. The PLL is the ALLs analogue but is applied to the BACK (posterior) part of the vertebral body (or the anterior part of the spinal canal)- it's the blue line in the diagram above (labelled #7). Like the ALL it too extends the length of the spine, allowing movement but preventing excess movement-in this case flexion (ligaments are like rubber bands, they allow a limited amount of stretch and then they recoil). Unlike the ALL the PLL is not as well attached to the vertebral end-plates, despite having lateral extensions at every disc space. Study the image to the right, it's from Grey's Anatomy, the definitive and original anatomy text book (the illustrations are great, but the text is a little like reading Shakespeare in the original Old English); the perspective is from behind looking into the spinal canal and the backs of the vertebral bodies. Notice how the PLL extensions don't completely cover the disc space, leaving the annulus "unbuttressed"- this is the main reason why most disc herniations occur laterally (once again, more later).
Alright, now on to the annulus fibrosis. This structure is relatively straight forward. The annulus is composed of around 20 concentric layers of collagen (proteins that are linked into long chains-the main connective "tissue" in the body) running around the intervertebral space. Each layer is 60 to 90 degrees rotated away from the previous and subsequent layer. Think of a radial tire- the lamellae of the annulus are like the steel belts alternating in direction. This allows for reasonable flexibility, but great strength. The outer layers of the annulus are very much like ligaments, and as mentioned above, actually fuse with the ALL and partially to the PLL. The inner layer, adjacent to the nucleus pulposus is much softer, more hydrated and merges with the nucleus. Despite being heavily invested with protein, ie collagen, the annulus out of necessity is quite well-hydrated (in the healthy state). More on this below.
The nucleus pulposus (NH) is the third and innermost component of the disc complex. It is a remnant of the fetal notochord (review the embryology section in the Chiari section of Congenital Brain Abnormalities). This is the guy who does most of the work in terms of redistributing loads. The NH is mostly water- about 80%, and it is the hydrostatic properties that allow the NH and disc complex to be so successful. The NH cells produce long chains of special molecules that are dumped into the extracellular spaces (proteoglycans-proteins that are complexed with special sugars). These molecules are very hydrophilic (they LOVE water); in addition they have a very negative electrical charge. This charge encourages the flow of water and nutrients through the end plates, the annulus and ultimately to the NH cells. But doesn't standing force the water back out? In fact it does. Your discs become hydrated at night when you are down, and during the day, as the discs lose water content, you can shrink by almost a full inch. This cycle of water flowing in and then being forced out is for lack of a better term the "circulation" of the intervertebral disc. Hydration of the NH maintains its height, which improves the ability of the NH to bear weight and redistribute some of it. Maintenance of NH height also makes the collagen fibers in the annulus "taut", the condition in which they are most effective in constraining the NH (obviously as pressure is applied to the NH it wants to deform and squeeze out, think of the Oreo cookie analogy- the annular fibers keep the NH in place and doing its job).
Okay, I think that's enough anatomy- the interactive diagram below sums up some of what we've been discussing.
Anatomy of a Disc Herniation
Sorry about this, but more definitions. The verbiage of disc disruptions is all over the place and is confusing to all except those of us who use it daily. It is also a source of deception; nefarious, unethical, SOBs will twist the definitions of these terms well passed the breaking point to convince patients of phantom pathology. So let's be consistent:
Colloquial Terms- These are terms that have no agreed upon definition and are rarely/never used, or should be rarely/never used, in clinical situations. Two of the most common terms slipped disc and ruptured disc are in common use and generally refer to the more accurate term Herniated Disc (or Herniated Nucleus Pulposus-HNP).
Annular Tears-Obviously this refers to separations between annular fibers. Please refer to the diagram to the right. The "tears" can be between lamellae of the annulus extending concentrically as it conforms to the actual layers; we call these, oddly enough, concentric tears. Or, more importantly the tears can be radial, extending in a radial line through a number/all layers of the annulus. A ‘high intensity zone’ (HIZ) describes a radial annular tear with high signal within the annulus on lumbar spine MRI. These were once believed to be a major cause of chronic low back pain, but studies in normal individuals find them to be common in people without chronic low back pain. A related finding is something called a "linear tear", which is in fact a radial tear, but what gives it distinction is the fact that it enhances when intravenous contrast is given. Normally, because discs do not have blood supply, they will not enhance immediately ( a disc will slowly accumulate contrast as it diffuses with water through the disc-this is normal); a linear tear is present when a radial tear fills with "granulation tissue" (scar and blood vessels-accounting for the enhancement). Presumable, along with the scar and blood vessels that "invade" the radial tear to heal it, nocioceptive pain nerves follow along. A linear streak of enhancement within a disc is a "possible" sign that the disc is a source of pain. This is NOT universally accepted however. Rim tears in the annulus are commonly seen in older patients and are usually associated with bone spurs at the margins of the vertebra.
Degenerative Disc Disease-I include this term in this discussion to refute it. In the usual sense Degenerative Disc Disease (DDD) does NOT exist. Why? Because it is NOT a disease, any more than aging is a disease. DDD is a constellation of Imaging Abnormalities that are commonly seen but are attributed to clinical complaints of back pain. These are radiographic findings that have somehow "morphed" into a clinical diagnosis and disease. This is an incredible disservice to who ever is told they have DDD because the investigation into their clinical complaints (usually some form of back pain) often stops, and treatment is misdirected at relatively NORMAL findings on an imaging study. With age, comes a progressive dehydration of the nucleus pulposus and annulus (which will often develop fissures/tears as well) with a consequent loss in disc space height. As the disc space height decreases, the orientation of the facet joints begins to change; the bones that make up the facet joint respond by thickening and occasionally twisting. Even the vertebral bodies get into the act by developing marginal/traction bone spurs. This process is in part caused by repetitive injury/activity, with a possible contribution from genetics, and the natural development of ligament laxity (all ligaments weaken with time), etc.. This is the NORMAL EXPECTED progression of the human spine over time. Some progress along this pathway slowly, others more quickly, but EVERYONE will experience these radiographic changes to some degree. Please, in your mind, disconnect these normal findings from ANY clinical condition (ie back pain) unless they have been shown to be causative- by a reputable source.
Disc Bulging-Also a NORMAL finding. All the discs, given enough time will bulge. If you've followed this discussion closely you already know why. As we age the disc space begins to narrow as the nucleus and annulus start to dehydrate. This has the same effect as pressing down on an Oreo cookie (there's that cookie again), the center bulges outward. THIS IS NORMAL and only in the most extreme cases is it symptomatic (you have to have alot of other things wrong with you for disc bulges to be relevant).
Herniation of Nucleus Pulposus-Finally we get to disc herniations. Here still we have some terminology issues. For instance Disc Protrusion. This is a condition in which the nucleus pulposus has worked it's way through tears in the annulus to a position immediately in front of the posterior longitudinal ligament (PLL)and the spinal canal. Some believe that this is the precursor of a Contained Disc Herniation (ie contained only by the PLL-it's already through the annulus making it a herniation). A Disc Extrusion is what most of us in the business refer to as an HNP. Here a piece of the nucleus and shards of the annulus have broken through the last barrier (the PLL) and occupies space within the neural or foraminal canal (the space available for the spinal cord/cauda equina, or for the nerve in the nerve foramen). If these terms are unfamiliar please see above. Once a disc extrudes fully it can lose its connection with the disc it arose from (a sequestered fragment) or migrate upward or downward as a free-fragment.
Schmorl's Node-Very simply this is a piece of nucleus and annulus that has ruptured through the endplates into the vertebral body.Usually an incidental finding on MRI and RARELY problematic.
Enough terminology; let's look at some pathology. An HNP requires a tear in the annulus and PLL. The nucleus is really not to blame. The pressure of axial loading forces the nucleus to push against the annular fibers, and if they are torn the nucleus will squeeze through these tears as the pressure forces it. Now the nucleus is not totally innocent; if it maintains its hydration it will maintain its vertical height and keep the annular fibers taut and strong. When these fibers bulge in response to a dehydrated NP they are a whole lot less effective in containing the nucleus and preventing tears.
Any of the 23 discs can herniate, but the ones that do it most often are the ones exposed to a combination of axial loading (weight passing through them), and movement. For instance, the thoracic spine discs rarely herniate, and when they do they are invariable small and very rarely relevant. Why? They carry more weight than the cervical discs which herniate at a much higher rate? The answer is simple: the ribs. The T-spine is stabilized by the ribs; yes these discs bear weight, but are exposed to very little motion. The low cervical spine, especially the C5 and C6 discs, as well as the low lumbar spine, especially the L4 and L5 discs are exposed to the bad combination of weight and movement.
Enough words, how about some video?
Let's start with this "sample-use-only" video of a cervical disc herniation. Notice that they errantly call a "contained disc herniation" a "disc bulge".
Here's a video for the lumbar region- let's see if you can pick up the mistake on this animation.
Did you notice that they mistakenly labeled the spinous process as the lamina? It's not a big point but this and the cervical video reflect how much misinformation/bad information is out there. At least this one had audio.
So, the rest of this section will concentrate on the poor unfortunates that have clinically relevant symptoms.
Symptoms of a symptomatic herniated disc, hmmmmm. One word: PAIN!!!! The first nine in a list of the top ten symptoms of a herniated nucleus pulposus (HNP) are PAIN. Am I getting through? I have had patients describe the pain as "beautiful" and "all-encompassing". It is second only to renal colic (kidney stone pain) on the pain scale-sorry ladies, but child birth is a distant third. The origin of the pain is two-fold: a minor pain in the back or the neck (depending upon if the HNP is lumbar or cervical)- this arises from damage to the PLL and annulus, and a major pain that courses down the limb (arm or leg) in the distribution of the nerve that is being compressed. All that being said, let's take a closer look.
The location of the pain depends on where the herniation occurs.Let's start with a Cervical HNP. This is a disc herniation in the neck and will affect both the neck and in most cases the arm. It starts with a nagging neck pain:"I slept on it wrong", is a common refrain. The ache in time begins to localize to a spot between the shoulder-blade (scapula) and the spine. Notice on the drawing to the right the patch that is labelled "Medial to the shoulder blade"; this is the infrascapular space and is the first location of pain (the first branch of a cervical nerve root is the dorsal branch which runs into the back to give sensation to the infrascapular area). For many this will be the limit of their symptoms and the infrascapular pain slowly resolves. For the remaining patients, days to a week or two later, this pain yields to what is called radicular pain. Anything involving a nerve root will have the term "radicular" in it: radiculopathy (nerve root pathology), radiculitis (inflammation of a nerve root), etc.. Nerve pain is in the distribution of the nerve, obviously- the nerve hurts only in places where it goes. It won't cause the entire arm to hurt, just a band, similar to the black bands in the image above. The pain is generally constant, ie 24 hours a day. Certain things will ease it, like immersing it in hot water (Gated-Theory of Pain) or draping the arm over the head (this maneuver decreases the "pull" on the pinched nerve), but nothing (not even narcotics) will completely alleviate the pain. There are ALOT of things which will make it worse: coughing, straining, sneezing, turning the head (usually towards the arm that hurts, this is called Spurling's Sign), lifting things, etc. The pain is a deep, boring, achy pain felt in "the-bones". It RARELY is the "shooting" or electrical pain that most people relate to nerves, and it never makes anything tender to touch. This is what is referred to as "referred-pain" (sort of like ghost or phantom pain). Finally the distribution of the pain is different for each nerve root; study the diagram (I had to memorize it) and notice that the upper distribution of pain, ie in the neck and shoulder is very similar for each of the four roots listed. We differentiate them by where the pain ends, or "which fingers it goes into" (C5-shoulder to the elbow, no fingers,C6-thumb, C7-index and great finger, C8-small and ring-finger).
A LUMBAR DISC HERNIATION shares many characteristics of the cervical HNP. Patients often start out with a generalized back pain that begins to localize into the buttock and eventually down the leg in the distribution of the nerve involved. In broad terms L4 pain is referred to the inside ankle, L5 will affect the top of the foot and the big-toe, and S1 will affect the bottom of the foot and the little toe. Like the cervical Spurling's Sign, a compressed nerve root will hurt more when it is mechanically stressed (we call these Nerve Root Tension Signs). Rotation of the low back will accentuate the compression of a nerve, as will straightening out the leg (Straight-Leg Raising Sign), thus patients note that they feel better with a straight back and a slightly stooped posture.
One last not about pain and then I'll move on. The lumbar HNP may be typical or atypical-these are not standard medical terms so let me explain. Most lumbar HNPs occur within the spinal canal (the circle formed by the disc/vertebral body in front, the pedicles to the side, and the lamina/spinous process in the back); see the image above. For simplicity sake let's define a lumbar HNP as having to occur within the space defined by the pedicles. A disc herniation that occurs outside the pedicles is atypical and located in the far lateral area, and therefore a Far Lateral Disc Herniation(there's a version that's even more extreme: Extra-Foraminal HNP). What makes these guys so special? They damage the DORSAL ROOT GANGLION (DRG). The DRG is the home for the nerve cell bodies of all the spinal sensory nerves and is the most mechanically sensitive portion of the nerve. Damage to this structure is usually permanent and can be extremely debilitating. Instead of the dull achy sensation, a compressed DRG gives a horrible BURNING sensation that can exceed the nerve roots distribution and predispose a patient to COMPLEX REGIONAL PAIN SYNDROME.
Weakness is both a symptom (what a person experiences) and a sign (what a doctor finds on an exam). Like the distribution of pain, the distribution of weakness is determined by the nerve involved. Here's a list of myotomes (all the muscles run by a single nerve) of commonly injured nerves.
C5 – The deltoid muscle (lifting of the arm at the shoulder)and the biceps (flexion of the arm at the elbow with the thumb pointed outward, ie "making a muscle")
C6 - The brachioradialis muscle (flexion of the arm at the elbow with the thumb pointed upward)
C7 – The triceps (extension of the arm at the elbow).
C8 – The small muscles of the hand.
L4 – The quadriceps (extension of the leg at the knee).
L5 – The tibialis anterior (upward flexion of the foot at the ankle- walking on your heels).
S1 – The gastrocnemius muscle (downward flexion of the foot at the ankle- walking on your toes).
Here's a video of a motor exam; it shows a normal exam and lists the muscles being tested along with their named nerve as well as the nerve roots. He didn't examine the brachioradialis muscle-C6, so there's a second video that demonstrates that muscle; the first muscle she checks is the brachialis muscle in the arm (sort of a biceps helper muscle), then she demonstrates the brachioradialis muscle.
We label the muscles listed above as "key" because they are excellent indicators of the nerve which activates them. For instance, when we are concerned about a pinched C5 nerve root we look to the biceps and deltoid. For an L5 root problem we look to the anterior tibial muscle- ie walk on your heels. This combined with a distinctive sensory loss and reflex abnormalities help to localize the cause of the problem.
These complaints, like the motor/weakness complaints are both symptoms and signs (patient complaints and what is found on exam), only these changes are a good deal more subjective (intensity varies from person to person).
I categorize the sensory disturbances into two big groups: positive symptoms (things you have, but shouldn't), and negative symptoms (things you don't have, but should). "Tingling" is a positive symptom, and numbness (like you were injected with novacaine) is a negative symptom. The positive symptoms are further characterized by the type of sensation experienced. The descripters used most commonly are "tingling", "going to sleep", and "pins and needles". These lower grade positive symptoms are called Paresthesias (Greek for "abnormal sensation"), and are experienced in everyday life. What makes them worrisome is if they persist. These paresthesias will also conform to the distribution of the nerve, exactly as the distribution of pain conforms to the nerve root distribution. I blew this Wikipedia image up some, which makes it a little blurry, but you still get the picture. You don't need to memorize this, your doctor already has.
Not all positive sensory disturbances are as benign as tingling. There are some who experience a constant burning or electrical sensation that is all together uncomfortable/painful. These sensations are called Dysesthesias (Greek for "bad sensations"), and are NEVER normal. Classically, dyesthesias are NOT related to root compression caused by disc compression. They are more associated with process' that are termed Neuropathies, which are disease states that involve the nerve itself, usually within the limb (ie diabetes). Dysesthesias can be seen with radiculopathies (problems with the nerve root-the topic of this section), but not commonly.
Finally, for completeness sake, some patients will experience pain when non-painful stimulus is applied, ie when the area is lightly touched the person feels a burning or ripping pain. This is termed Allodynia, and is the Major League of pain. Allodynia is never (okay, almost never) seen with a radiculopathy, and is always (okay, almost always) associated with a neuropathy.
There, now you know everything there is to know about sensory changes, unless you're a Neurologist/Neurosurgeon in which case you should be doing something more productive than reading my website.
Aside from pain, weakness and sensory loss, most patients will have some minor complaints of muscle stiffness and a complete lack of energy and reduced exercise tolerance. These aren't the "other symptoms" that warrant comment. Refer back to the Red Flag symptoms listed above because this is what this section is about. If you have any of these take them seriously!!! With regards to disc disease the symptoms of incontinece (loss of bowel or bladder control), progressive symptoms, bilateral symptoms (have problems with either both arms or both legs), inability to control your legs, are especially important. These are good indictators of something compressing ALL the nerves or spinal cord and should be considered an emergency.
Investigations into Disc Disease
Now I need you to refer back to the Neurosurgical Testing section. Recall that most disc herniations are asymptomatic and do not require imaging before about a month (unless of course any of the Red Flags are present). So I'll assume we're a month down the road and a cross-sectional imaging study is now warranted. Our options are an MRI, CT scan, or CT/Myelography.
This is the most popular cross sectional imaging study. BEWARE, however, and recall the first rule of MRIs: MRIs lie! For most significant pathologies MRIs are fine, but anything below a "medium" level of complexity will likely be lost in an MRI. Enough words, lets look at some imaging and play radiologist (it's an easy game). First let's look at normal MRIs, and we'll start with the lumbar region.
I took these pictures off the internet, and while the axial/cross-section view is accurate, there are a couple of mistakes on the lower sagittal image. First off, the color of the discs is completely dependent upon what imaging sequence is used during the MRI- this particular sequence is a T2, where a healthy nucleus and the fluid within the spinal canal appear white. The other issue, which is a personal irritant, is that they discuss cord compression, but you, who has reviewed the anatomy section of this site, know that the spinal cord ends at L1 and from that point on down we have the cauda equina (nerve roots within the spinal canal). Of course this may simply be the author taking some literary license, but I don't think that the anatomy is so difficult that it needs to be "dumbed" down for non-medical people. Anyway, I digress, the focus here is disc herniations, and the images themselves are good examples of normal lumbar spine anatomy as viewed by MRI.
Okay, so that was the normal lumbar spine, let's have a couple of normal cervical spine images. The upper axial image is interactive so just hover your mouse over it for a description.
Look how smooth the spinal canal is on this sagittal image. Not even a hint of a disc bulge-this is obviously a very young spine.
For the sake of completeness here's a sagittal thoracic spine MRI; I won't show the axial or cross-section as it looks pretty much like the cervical axial image.
Okay, that's enough of boring normal anatomy, let's look at the fun stuff. As above let's start with the lumbar spine. Here are an axial and sagittal MRI of a lumbosacral disc herniation (lumbosacral=L5). Once again these are interactive so just place your mouse over the image for descriptions.
Now on to the cervical HNPs. Here we are dealing with the spinal cord, also note that the canal is much smaller. The discs are also smaller, raising a good point, this is not about absolute size of a disc herniation, it's about where that herniation occurs both within the spine, and the spinal canal. Everything is relative.
Now for the pictures; the pair below, axial images, are identical except that in the right image I've colored the disc and cord in. The lower sagittal image hardly needs any more explanation.
Once again, for completeness sake here's a view of a thoracic disc herniation. These are rarely symptomatic. This is also an interactive image. Notice that this thoracic disc herniation is similar in appearance to the cervical HNP.
We don't often use CT by itself for disc problems because the x-ray appearance of a disc and the spinal cord/cauda equina are quite similar. We do occasionally get an idea something is wrong, and in those cases a better study-MRI or CT/Myelography will be done if clinically indicated (ie the patient has the correct symptoms). CT is excellent for looking at the bones- far superior than MRI, and can be done when a fusion is contemplated, or other pathology is of concern. Here's another interactive image of a good CT scan of the lumbar spine.
If you haven't reviewed the Neurosurgical Testing section now would be a good time to do that. Myelography is an invasive study, you get stuck with a needle, but it is the best way of imaging anything within the spinal canal from a surgeons perspective. I use CT/Myelography in any situation in which I have a question whose answer may lead to a surgical recommendation. So let's look at some imaging and get on to the treatment section. First some normals. Here's an axial view (the arrow points to the nerve roots inside the spinal sac), and a sagittal view of a post myelographic CT scan (dye was placed into the spinal canal, this is the myelogram, and then a CAT scan was taken). Looks sort of like an MRI, so why go to all the trouble?.
Because the myelographic portion is a dynamic study. After the dye is placed we can take x-rays of the patient as they stand, flex the back, lay down, etc.. The study shows what happens to the nerves/cord and vertebra as we move. CT and MRIs are done with a patient laying down ("but it doesn't hurt when I lay down"). The image to the right is from a standing myelogram in a patient who had a "normal" MRI. The arrow points to what is called a "nerve-root cut-off". Something is preventing the dye from flowing into the nerve root, but in this case the compression only occurred in the upright position. Below is a CT scan showing a lumbar HNP.
Let's finish up with the cervical region. The image to the left is relatively normal, while the image to the right shows a right sided disc herniation.
Other Evaluations into Disc Disease
The only other appropriate test done with regularity in this setting is an EMG/NCS to assess the integrity of a nerve root and it's intrinsic function . Once again refer to the Neurosurgical Testing section.
One final note, and it is an important one, so I'm going to make it bold. If a surgical recommendation is made, you should have at least two of the following three: a positive (meaning that it shows pathology) imaging study; a positive physical exam; a positive EMG/NCS. In addition, all aspects should correlate (ie your exam should match the positive findings on either imaging or the electrodiagnostic study).
I don't know about you , but I'm getting bored with evaluations, lets treat something.
Treatment of Disc Disease
Now we get to where the rubber mets the road. Once again, this is an extremely controversial topic, but it really shouldn't be.Disc herniations that cause radicular symptoms (ie referable to a nerve root) beyond six weeks are best treated surgically.This statement is the culmination of many very large clinical studies and should NOT be remotely controversial. There are four exceptions to the six week rule: Cauda equina syndrome (symptoms in both legs and bladder); myelopathy (symptoms caused by compression of the spinal cord); MAJOR motor weakness (ie near paralysis of a muscle group); and, intractable pain (resistant to intravenous medications). These exceptions should remind you of the red flag symptoms listed above, and while they are extremely important, they are relatively rare. The majority of patients who reach the six week mark are not so severely afflicted (although it would be unwise to tell some one who has suffered with a radiculopathy for a month and a half that they are not severely afflicted).
So, that means that when I see someone who has a symptomatic disc herniation that is six weeks or older I drag them off to the operating room, right? Of course not! It also does NOT mean that I force a patient to wait 6 weeks before fixing a problem that is clearly debilitating and going to persist. Clinical judgement always outweighs clinical GUIDELINES (these are not rules); this is why surgeons are also physicians, and not just barbers (surgeons use to be barbers).
Now, once again I must stress that the disc herniation has got to be SYMPTOMATIC, and they have to be the correct symptoms. It is not uncommon for a patient with acute or chronic back pain to have a HNP on an imaging study, and it is only natural to associate the two. Unfortunately this is rarely accurate. A truly symptomatic HNP will have limb symptoms, spinal cord symptoms or cauda equina symptoms. It is very rare for a HNP to cause ONLY back or neck pain. This is HUGELY important- most surgical failures are caused NOT by patient or surgeon, but by a BAD diagnosis! To put this in perspective, the CURE rate (in medicine we rarely discuss cure rates) for a lumbar laminectomy (more on that in a bit) for a lumbar radiculopathy (pain, weakness, numbness into the leg) is 96%. The IMPROVEMENT rate (a much lower criteria than cure) for a lumbar laminectomy performed for pure back pain is less than 50%, and I think a good deal of that is placebo effect combined with post operative exercise. Once again, I need to stress that just because you have a HNP and symptoms, does not necessarily mean that they are related.
All that being said let's assume that we have someone with a HNP that has the appropriate symptoms. What is to be done? Let me answer that question in the next two sections divided by duration of symptoms.
Disc Herniation: From Day One to Six Weeks
Before getting started with treatment read the four exceptions listed above. If you have any of these skip this section and go right to the surgical section.
I'm going to lump all disc herniations into one section, ie cervical, lumbar, and the extremely rare, symptomatic thoracic disc herniation. Basically the treatment is expectant- we expect you to get better, so don't screw it up.
There are two phases to most disc herniations; the initial phase that lasts one to two weeks and is defined by very severe pain and little concrete neurologic abnormalities, then a second phase which is defined by an overall reduction in pain, but in some an increase in discernible neurologic abnormalities.
For most patients this is the most memorable phase. Often the HNP is heralded by an aching sensation in the back or the neck followed by a march of pain down into the limb. The pain is deep and suffering in nature and is made worse with almost any movement, but sufferers are compelled to move by the intensity of the pain. Virtually nothing provides relief; not positions or medications. It is in a word, miserable.
The goals of treatment are symptom relief and avoidance of exacerbating behaviors. However, complete relief of symptoms is difficult to achieve. The focus is on trying to reduce the inflammatory reaction that is initiated with compression of the nerve and the tearing of the ligamentous support structures. Inflammation is the bodies "healing-process", but it's a very messy process, one that has the potential to cause injury to uninvolved structures. Anti-inflammatory agents such as ibuprofen, and in more severe situations, steroids are used to "tone-down" the inflammatory reaction. If successful the pain will decrease; if the pain relief is substantial then we have just proven that the majority of the problem is inflammatory, which is a self-limiting process, and that the prognosis for early and complete recovery is good. If pain relief is not as complete then a fair amount of the pain is being generated by physical compression of the nerve root and impairment of the roots blood flow; which means you're in it for the long haul. In these situations steroids can be injected along the course of the involved nerve root (epidural injections or selective nerve root injections) in severe cases.
TANGENT NOTE: IF YOU ARE ONLY A CASUAL READER SKIP DOWN. The Agency for Health Care Policy and Research (AHCPR), a division of the US Department of Health, looked into the treatment options for herniated lumbar discs in 1994. A good deal of the information regarding the treatment of HNP derives from their work. They investigated just about every form of treatment for HNPs and either gave them a recommendation, made them an option for treatment (meaning that the efficacy was debatable), or found them ineffective. Oral steroid use was found to be ineffective. Here is what they concluded: "no difference was found at one year in patients who received a one week course of Decadron (powerful steroid) versus placebo". This single statement encapsulates the difficulty with clinical trials and studies: the use of a weeks worth of steroids is to reduce the symptoms during that immediate HNP phase, it is NOT for treatment. It simply helps you get from Point A to Point B a little more comfortably. Using this same logic narcotics or any pain reliever will not change the clinical outcome at one year, but try and tell someone with radicular pain that they are "not recommended"! Okay enough tangents.
It is not uncommon during this first week or two to see your doctor or go to the ER (sometimes more than once) and just get prescriptions, often pain medicines and anti-inflammatories. This naturally frustrates patients because obviously something is wrong ! Here's my advice, which most don't take: be patient. Unless you have red flag symptoms you do not need an imaging study because it won't change anything we will do for you. In addition, the symptoms, primarily pain, are likely to tone down very quickly. Don't get mad or frustrated because no one is listening to you, they are. They simply know that in all likelihood you will be better very soon.
You should not go to bed rest; keep moving as much as possible to avoid creating a chronic pain situation by becoming deconditioned. You should, however, avoid bending or twisting the involved area (neck or back), and you should NOT lift anything greater than 10 pounds until all symptoms have resolved. This is important so let me repeat it : DO NOT BEND, LIFT OR TWIST UNTIL ALL THE SYMPTOMS HAVE RESOLVED!!!. If you ignore this advice it is likely that you will convert a self-limiting process (ie you'll get better all by yourself) to a surgical situation. Give your body a chance to fix itself, because in most people it will (unless you screw it up).
Chiropracters and Physical Therapy for radicular pain are absolutely CONTRAINDICATED. NOTE: this is for radicular pain (pain that goes into the limb) and not for the more common low back or acute neck pain patients (see the low back pain section above, both these modalities have benefit for PURE BACK or NECK PAIN early on- but that's NOT what this section is about). Do not manipulate your back or neck (depending upon whether your problem is lumbar or cervical) in any way until all symptoms have resolved, and don't let anyone else manipulate your back or neck. It will make the situation worse.
Two more things might help during this acute phase. First, immerse the affected limb in hot water (hot, not scalding) for 10-15 minutes. This will help reduce the pain for an hour or two. Second, and this is aimed more at lumbar radiculopathies, try a short jog or run. That's right, and no I am not insane, a run will increase the blood flow into the damaged area. Blood is nutrient rich and will wash away all that metabolic garbage that your angry nerve root is sitting in. Try it.
Alas, there is nothing else that will help you get through this initial miserable phase of an acute radiculopathy.
This period generally runs from about the second week through the sixth week and is in many ways the most important time period. This is where the radiculopathy will declare itself: patient will either get better or end up in the OR.
Clinically the pain begins to tone down and some patients will begin to note numbness or weakness in the affected limb. It's likely those symptoms have been there all along but with abatement of the pain these "other" symptoms have become more noticable.
The change in symptomology is due to an easing of the inflammatory process. As it begins to wind down we get our first real look at the true extent of nerve root involvement. Symptoms at this point are due to frank compression of the nerve and altered blood flow to the nerve cells and the insulation that envelops them. Both of these cells (nerve and insulating cells) will have been affected by the diminished blood flow and have undergone changes. Some of these changes will begin to reverse as the additional burden of inflammation is lifted, in which case the patient begins to improve. Other changes are more enduring and it is not uncommon for a patient to lose "neurologic" ground for a week or two before things begin to stabilize.
Most patients will have a complete or near complete resolution of their symptoms during this month long phase. Unfortunately,there is very little that will hasten this improvement, but there are are alot of things which will delay or reverse gains already made. So, like in the acute phase, DO NOT BEND, LIFT, OR TWIST THE AFFECTED AREA UNTIL ALL SYMPTOMS HAVE RESOLVED, BUT STAY MOBILE!!!.
For those people who do not see a substantial improvement in their symptoms (roughly one third) we generally will get images towards the end of this month.
One last note, refrain from any activity that prompts the limb pain/symptoms. Also be aware that nerve pain is not immediate; it's not like dropping a hammer on your toe and learning that dropping a hammer on your toe is a painful experience and one that should be avoided in the future. You may very well be able to bend, twist or lift objects without exacerbating the limb pain, only to feel it hours later. Use that structure between your ears to protect your nerves.
(1) Take anti-inflammatories as prescribed
(2) Take pain medicines as prescribed
(3) Stay active-minimize any bedrest
(4) Do not manipulate, or let anyone else manipulate your back or neck
(5) DO NOT BEND, LIFT, OR TWIST THE AFFECTED AREA
(6) Be Patient!
Beyond Six Weeks
Finally we've reached the point where the rubber mets the road (or the scalpel mets the skin?). Patients who have "made-it" this far with radicular symptoms and signs generally are viewed in a surgical light (about 5% of cervical patients and 33% of lumbar patients). Once again several very large studies have found that by this point surgical relief of a radiculopathy is the best medical management. In my mind and anyone who is truly conversant with the medical literature, this statement has been validated again and again, so I will not belabor the point or offer any further discussion. This statement, as far as anything in medicine can be, has been proven.
As stated in the paragraph that started this section not every patient who reaches this point is operated upon. There are exceptions, ie, high surgical/anesthetic risks, minimal symptoms, resolving symptoms, etc.. Like all surgical situations a thoughtful review of each patients condition is warranted, with the overall risk assessment being done by your surgeon, but the "should I" question is left to you. The question I ask every patient is: "can you live with what you have?" This includes the pain, weakness, sensory loss, and the open-ended restrictions that accompany a non-surgical approach. If the answer to these questions is "yes", you're done. Don't have surgery. If the answer is "no", then surgery is your best option.
From this point on I'll assume that the answer to at least one of those questions was "no", and move on to the surgical procedures themselves (this is why you've read this far, Right?). So let's start by seperating the various types of HNPs.
Just to make everything clear, for those of you who did NOT read the required anatomy section, I'm referring to neck and arm symptoms. One other salient point, in the cervical region, unlike the lumbar region, we have to account for the spinal cord. Whether it is directly involved or not, it's relative postition to the HNP will dictate how this is approached surgically. In other words, if the disc herniation is in front of the spinal cord the preferred surgical approach is through the front (the throat), but if the HNP is to the side of the cord, in the lateral recess of the nerve, the preferred approach is from behind. Simple,right? There are exceptions to this rule, but for the most part the relative position of the disc fragment (to the cord) dictates the surgical approach.
TANGENT: the rationale for this rule is that viewed from behind, through a laminectomy approach (explanation in a moment), the spinal cord will prevent access to anything in front of it. So if there is a disc fragment, or bone spur in front, or anterior to the cord, the surgeon will not be able to see it from behind without retracting the spinal cord (spinal cords don't work real well after being retracted).
So let's start with the easier, and unfortunately, less common situation in which the disc herniation is accessible from behind. This approach is called a laminectomy; to be technical it is actually called a hemilaminotomy and medial facetectomy (a true laminectomy involves complete removal of the lamina). The verbiage is not all that important. Basically the lamina is trimmed back to allow entry into the spinal canal and the nerve foramen (exit site for the nerve root). Once there all sorts of things can be done, but in this section we are removing a piece of broken disc that has ruptured into the spinal canal and caused nerve root compression. Here's a video showing the basics.
The procedure takes anywhere from 30 to 60 minutes and is almost always an outpatient procedure (you go home the same day). The neck is sore at first, but the incisional pain is usually controlled with oral pain medicine.
The risk of a cervical laminectomy are small, roughly 1%. Everything that is seen in surgery is at risk for injury, including the nerve being decompressed, and the adjacent spinal cord. This is an extremely RARE event in this very common operation. Numerically the greatest risk is a wound infection. The risk of infection is increased proportionately with the length of the operation and how long a patient stays in the hospital. Of course patient characteristics are also extremely important. Diabetics, those on steroids or immunosuppresion have a much higher risk of infection, and these parameters must be weighed against the benefits of surgery. Smoking is THE greatest modifiable risk; most surgeons, myself included, will NOT operate on someone who continues to smoke- the risk of complications is to great (it is also an indication as to how well the person will participate in their own care). The risk of general anesthesia is VERY, VERY low, unless there have been anesthetic problems in the past or a family history of them. Lastly, the risk of DVT (deep venous thrombosis), or blood clots in the legs, is increased with surgery and immobility. Most patients are asked to wear compression stockings for a week, and walk as much as possible to minimze this risk.
The restrictions post-laminectomy are very similar to the pre-laminectomy restrictions: DO NOT BEND OR TWIST THE NECK, AND DO NOT LIFT ANYTHING HEAVIER THAN TEN POUNDS. Typically these restrictions are in place for six weeks. Note that this does NOT mean you should not be active; in fact, your over all level of activity should increase post-operatively. I ask my patients to walk 30 minutes of each daylight hour. This lowers the risk of wound infections and blood clots in the leg, and minimizes the overall deconditioning effect caused by surgery and general anesthesia. Most people will return to a sedentary occupation within one to two weeks, while those with more damanding occupations will need to wait the entire six week post operative period before returning to work.
Now for the benefits. About 96% of patients have their radicular (arm) pain alleviated or substantially improved (3% are no better, and 1% are worse) with surgery. But, it doesn't happen right away. Anticipate a 50% reduction in pain immediately with the rest slowly resolving over the next 4-6 weeks. In addition, it will NOT be a smooth resolution. Most patients describe good days and bad days as the pain slowly winds down. Sensory disturbances-numbness/tingling takes on the order of 6 MONTHS to improve. That was MONTHS, not days, or even weeks, and even then those with severe sensory involvements rarely get full return of function (recovery is loosely correlated with duration of symptoms pre-operatively and degree of neurologic impairement before the decompression). Motor function (weakness/strength) will improve over a two YEAR time frame. You can help to recover the strength with exercise.
For those patients who fall out of the traditional six week mark, ie a patient who has dealt with a radiculopathy for months, even years, the above time frames need to be extended and hopes of a meaningful recovery have to be tempered. It stands to reason that a nerve that has been compressed for months, as opposed to weeks, will have undergone more substantive changes. Typically I have the patient take the amount of time they have been symptomatic and cut it in half. This is a good time frame for improvement in pain. Sensory disturbances and weakness that have persisted for 6 months or more are unlikely to improve no matter what is done.
Okay, now you have a dowel of cadaver bone in the neck, isn't the body going to reject it? Hopefully! We are tricking the body into growing bone where bone was never intended (this is called a fusion- linking one bone with another, using bone). When we break a bone the fracture fragments are chewed away by the immune system, sort of like little pac men; behind those pac men come a wave of bone making cells that in this case will replace the cadaver bone with the patients own bone. This process takes about two years to be completed, but structural integrity is achieved much sooner. The metal plate holds the bones together during this process of fusion. In the end, the disc space will be replaced with smooth native bone.
Okay, but if a disc space is fused, doesn't that mean that the remaining spaces have to work harder? Yes, again. A fusion of any kind in the spine increases the chances of adjacent level disease (for instance if you fuse C5, the levels at greatest risk are C4 and C6). As we have been fusing the spine for decades now we have a reasonable understanding of the risk, so let me try and simplfy a very complex discussion. THE MAJOR DETERMINANT OF A REPEAT FUSION IS THE ORIGINAL PATHOLOGY. What? In plain English, the thing that caused you to need the first fusion is generally the reason for the second fusion. The fusion itself increases the risk for follow-up surgeries by about 10% (actually it's 9%). Small, but significant.
Alright, now I have a cervical fusion, does that mean I won't be able to turn my head? NO,NO,and NO!!! The majority of the cervical range of motion (ROM) comes from the first three cervical vertebra. If these are involved (rare outside of trauma and rheumatoid arthritis) then there will be a reduction in ROM; if they are not involved, fusing one or even two cervical levels will cause only an imperceptible change in ROM. That is, if the patient is compliant with the post-operative stretching instructions. The people who complain that they can't move their neck because they have had a neck fusion are almost certainly non-compliant.
The risk of an ANTERIOR CERVICAL FUSION and PLATING are for the most part the same as the laminectomy mentioned above. There are some unique risks however. Recall that I said that everything seen during surgery is at risk? In an ACF we expose the trachea and the esophagus. As a result both can be injured, and even if they are not, most patients report an altered, almost whispering voice, and trouble swallowing for about 6 weeks. The risk of neurologic injury is also slightly higher because more of the spinal cord is exposed with this approach. Finally there is the risk that the bone won't fuse in. The body has to "claim" the bone plug as it's own and start to attach it to the rest of the body. In some this does not happen, leading to a painful condition called a "psuedoarthrosis"(false-joint). If there ever was a single reason to be compliant with post-operative instructions (no bending or twisting of the neck, and no lifting greater than 10 pounds) the threat of a psuedoarthrosis would be it.
The time course for improvement is the same as with a cervical laminectomy-6 weeks for pain, 6 months for sensation, and 2 years for return of strength.
The post-operative instructions are also the same. Compression stockings are worn for a week. As mentioned above, the neck is not to be bent or twisted (you walk in the "at-attention" posture), and no lifting greater than 10 pounds all for 6 weeks. At that time x-rays are taken to assess the bodies fusion rate. And lastly, once again, there is NO BED REST. Patients are to walk 30 minutes out of every daylight hour.
Relative to the lumbar spine, treatment of cervical disc herniations is not all that controversial. I think that this is true because the presence of the spinal cord in the cervical region has a tendency to "weed-out" the charlatons, but not entirely, and people still need to protect themselves from these SOBs, but sticking needles into disc spaces, or shooting lasers into bulging discs becomes much more difficult and dangerous when the spinal cord is in the way.
Some of the biggest issues are bone graft from cadavers versus autograft (taking the bone from a patient's hip), minimally invasive approaches versus microscopic approaches. Lastly is the emerging use of the articical disc (arthroplasty).
Most surgeons use allograft (bone from a cadaver)for their surgical fusions for two reasons: it's easier, and taking a graft HURTS. The fusion rates are virtually identical, especially when a plate is used, so the only arguement that can be made is disease transmission. However, with the way the grafts are treated, and the donors cultured the arguement quickly becomes moot.
Minimally invasive surgery is all the rage now. Everything is done through a 14 mm tube. The theoretic advantage is less muscle take down, smaller incisions and shorter operating/hospital time. In theory it sounds great, but as always the devil is in the details. When compared to the standard, traditional open microdiscectomy (clarification note: the anterior cervical fusion IS NOT included in this discussion as there is no minimally invasive approach that is safe through the throat. This discussion pertains ONLY to a laminectomy) the incisions are almost the same size, long term the muscle injury is identical, and the minimally invasive approach actually takes LONGER. All this at a cost of limiting the surgeons view and options. Not to mention that it costs more. All that being said there are surgeons who are quite comfortable with minimally invasive procedures and are quite good at them, but it is a practice choice. THERE IS NO, AND I MEAN NO GREATER BENEFIT TO MINIMALLY INVASIVE PROCEDURES WHEN COMPARED TO THE MICROSOPIC PROCEDURES!!! Recovery time is identical, post-operative restrictions and activities are identical, hospital time is identical, postoperative pain (as measured by narcotic use) is identical, etc.,etc.,etc.. TAKE HOME MESSAGE: NEVER CHOOSE A SURGEON SIMPLY BECAUSE THEY OFFER A "MINIMALLY-INVASIVE" PROCEDURE!!! It is a dirty little secret that these operations have become a haven for some of the worse surgeons and individuals who practice medicine, simply run a web search for minimally invasive spine surgery for a list of them. I will talk a little more about this in the lumbar laminectomy section.
At the time I'm writing this there are three versions of the cervival artificial disc, made by three different manufacturers, approved for use in the US (more are available in Europe). Unlike the ill-fated lumbar artificial disc, cervical arthroplasty ("new joint")makes a good deal of sense. There is not alot of weight passing through the cervical spine (relative to the lumbar spine) so the mechanical device simply has to move and maintain motion. It is placed through an anterior approach, and can be used after a discectomy, or after decompression of the cervical canal in patients with spinal stenosis (see below), or less commonly, without decompressing the spine (ie neck pain patients). A mechanical device is inserted into the disc space instead of the bone graft and plate; otherwise the procedure is identical to the one described above. Arthroplasties may in time replace cervical fusions, but if you have been in this business for any time you have heard this before. Everything we put in the body will eventually fail, and these discs are no exception. As yet we don't have a good idea on the time frame, and our options aren't good once they fail (a posterior fusion). However, theoretically they MAY reduce the rate of failure of adjacent levels- this has not yet been borne out in the literature (in fact, in Europe the rate of reoperations is HIGHER with the artificial disc than with a simple one level fusion- I'm not certain I buy that though, there are alot of confounding factors). I think there is a role for the artificial disc, but we have yet to define it. What I am comfortable saying is that in single level cervical disc herniations,an artificial disc offers no clear advantage over a standard cervical fusion.
To be clear this section ONLY discusses the condition of lumbar disc herniations. The standard surgical procedure for these is a laminectomy, much like what was discussed above in the cervical section. However, a lumbar laminectomy is used to treat other forms of pathology, ie degenerative and traumatic conditions. These will be discussed later, so if you are interested in lumbar disc herniations, read on. If not, skip ahead.
Note that I limited this topic to HERNIATIONS (not bulges, or internal disruptions, or any other pathology that unethical surgeons use to convince patients that they need surgery). To get the most out of this you need to understand what a herniation actually is, and what it is not. If you've been reading along you already know the difference, if you've skipped to this section without reading the parts above you are going to get lost and need to start at the beginning of thischapter; click here and get educated.
As I said above, a lumbar laminectomy is very similar to a cervical laminectomy. We do NOT do an anterior approach for a simple lumbar disc herniation- at least reputable surgeons don't.So here is a short animation that demonstates the procedure. Two points of clarification: first, we do NOT cut out the ligament flavum, and second, we do NOT cut a window into the posterior longitudinal ligament except in rare cases.
The time course for improvement is identical to the cervical HNPs, which is understandable as the pathologies are identical. Pain is reduced about 50% with the surgery, and the rest diminishs over the next 6 weeks. Sensory disturbances (numbness/tingling/pins and needles) slowly resolve over 6 months; the possibility of complete recovery is directly related to length of time the root has been compromised and the degree of pre-operative deficit. Motor function slowly improves over 2 years with little return expected after that time period.
Once again risks are similar to the cervical laminectomy: neurologic injury, infection, blood clots in the legs and anesthesia complications. The total risk for an uncomplicated lumbar laminectomy is about 1%. Some authors like to toss in the risk of "failed-surgery", ie the patient's symptoms don't resolve. This risk is about 3%, but it is only 3% if the strict criteria for lumbar laminectomy are utilized. If the surgical procedure is done predominately for back pain, as opposed to radicular/leg pain, expect a success rate of only about 50%. This is why a laminectomy, OR ANY INVASIVE PROCEDURE (more on this later), should be reserved for radicular/leg symptoms. A disc herniation and back pain is a common situation, and only in an extraordinary situation should a laminectomy be used to treat the back pain. Heed this warning or reap the consequences of an unsuccessful surgical procedure.
Restrictions and instructions are again familiar. Do not bend or twist the back, and do not lift/carry anything heavier than 10 pounds. Walk 30 minutes during each daylight hour. Wound care for my patients is simple: LEAVE THE WOUND ALONE. Do not cover it, clean it or treat it with antibiotic ointments. Let your body treat it. For the first week I allow my patients to shower, after the first week the wound can be immersed in water (bath/pool).
At the end of 6 weeks it is imperative that you start to recondition yourself. This was also covered above, but in broad strokes there are three components of reconditioning: flexibility, cardiovascular conditioning and core strengthening. In addition if you are overweight that will need to be addressed. I would like you to read, hopefully reread, the section above that covers weight loss and reconditioning. I can't stress this necessity enough. The minimal risk of a lumbar disc reherniation is 20%, whether it is operated on or not. Surgery does not increase or decrease the chances of disc reherniation, but excess weight and poor conditioning do. Unless you enjoyed the experience of severe nerve pain and a lumbar laminectomy I would strongly recommend that you attend to all the factors in your control to prevent a reherniation.
I'm often asked if a patient after a lumbar HNP (either with or without surgery) can return to a physically demanding occupation, and the answer is "yes", with one caveat. The actions that stress the disc and ligamentous complex the most are bending, lifting and twisting. Someone who has had a lumbar HNP can return to those activities, but only if they perform them in isolation, ie you should NOT combine them. It is okay to lift objects, just do it with a straight back; it's okay to bend, just make sure that the back is not loaded with weight or twisted, etc.. These actually are the OSHA requirements for safe use of the back.
Lumbar Disc Reherniation
As I just said the risk of reherniation is 20%. After a second disc herniation (any level any side, although most reherniations occur at the original site) that risk more than doubles to roughly 45%. After three herniations the risk of a fourth is about 75%.
Now just because you have had a previous HNP does not mean we treat subsequent herniations any differently. We still have an expectation that most will resolve on their own. A reherniation does not automatically mean surgery- even if you have already had surgery. If you are the unfortunate person who requires a second operation for symptomatic HNP (again, they have to be the right symptoms) a laminectomy is probable all you need. There are some exceptions, ie overt lumbar instability, massive disc rupture with dissolution of the posterior longitudinal ligament, etc., but these are relatively uncommon. I can't fault a surgeon to strenuously if they recommend a fusion following a second disc rupture, there is a modest amount of support, both scientific and empiric for this approach, I prefer to allow the patient to fail a third time before recommending a fusion.
So obviously, if a patient is a three time loser as far as disc herniations, a fusion is universely recommended, unless the herniations all occur at different levels (a situation I have never seen). I'll explain a fusion in the Degenerative Spine section that follows this one.
Oh boy am I going to love this. This is my chance to go on record and address the massive amount of misinformation that exists on the internet, most of which purposely misleads patients. There once was a time when it was felt that advertising by a physician was unethical. When I was a little baby doctor I thought that this prohibition was simply egotistical physicians setting themselves apart from the rest of the consumer world; we wanted to be viewed as above all of that. Perhaps there was a part of that, but I now see that with the advent of the internet and the explosion of misinformation coming directly from physicians I see that we are not only "not above that" we are some of the worst offenders. There are countless videos, articles, websites, blogs, etc. sponsored by physicians, all of whom have sworn an oath to protect patients, that are bald-face lies. There is no better way of saying it, we have physicians staring into cameras attesting to things they know (or should know) are false.
Who is responsible for this? Partly the patients who are swayed by these charlatons. This is an age of information, and the real answers are out there; sometimes those answers aren't what people want to hear so they go shopping for someone who will tell them exactly what they want to hear. As I have said over and over again, do not trust any single source of information (including this website, or even me). Try to find a concensus, and even if it is not something you wanted to hear, entertain it. Please don't search for an opposing opinion beyond the fringes of standard medical practices because you are likely to find one.
I think that the majority of the blame for the proliferation of these cancers in the body of medicine lies with our medical organizations. Our state medical boards and professional societies need to take an active roll in countering the misinformation that is being proffered by this small, but growing group of unethical and vociferous scoundrels. Currently the silence of our medical leaders is deafening, and all the public hears are the lies coming from the miscreants.
Let's start with the two biggest offenders: Minimally invasive spine surgery and Laser spine surgery.
As I said above the concept of minimally invasive anything is appealing at many levels. Professionally if we can do more, or even the same amount of work, with less overall surgical trauma and achieve similar results, I am all for it. Bring it on! Where is the next course? Unfortunately we DO NOT achieve the same results. MISS is an emerging and promising technology, and it frankly is subject to less scrutiny. We as surgeons want this to work so for a time we ignore its inadequacies, and when they can't be ignored statements such as "there is a steep learning curve" are made to excuse them. To a degree this form of intellectual dishonesty is understandable; every surgical advancement had its own "steep learning curve".
What makes this situation different is that you the patient aren't told this. Here is an example from my own professional society, the American Association of Neurologic Surgeons. In April 2008, on the AANS wesite an abstract (a small article) was published that discussed the rate of dural tears (durotomy) during MISS. Here is their conclusion:" The incidence of durotomy in MIS procedures is well within the range of reported rates of open spinal procedures". Sounds good right? Once again, the devil is in the details. Their rate of tearing the dura, the coverings around the nerve and spinal sac, is quoted as 6.8%, and they describe a reported incidence up to 14% in open procedures. What they have compared is apples and oranges; the durotomy rate for an open discectomy (the same procedure) is around 1%. They get the 14% from open, multi-level fusions that have been previously operated upon, a radically different situation. Understand that the authors of the article work at high volume centers, meaning that they do this all the time, and that this is about as good a result as we can hope to achieve. Now the number is still quite low, and in most situations a durotomy is NOT a big deal, but it does represent a nearly 7-fold increase over an open procedure.
Example number two, and here I have to stray into the fusion territory. Same website, AANS, comparing open versus minimally invasive instrumented fusions. They found that operative time was increased with MISS approachs, but that blood loss and hospital stays were lower. The blood loss from the open fusion averaged about 500 ml (about 16 ounces) while the MISS approach was only about 160ml (about 5.5 ounces). Sounds like MISS is much better as far as blood loss, right? The problem is that a 500ml blood loss in a single level instrumented fusion is about 3 times to much. In the real world if a surgeon averages 500ml blood loss in a 2.5 hour case, people are going to start asking questions (I think that the explanation for this significant blood loss is the length of time of the reported surgical procedure: 5.25 hours, which is easily more than double the real world average, and I'm guessing that this means a good deal of the work was done by residents as opposed to the operating surgeon- at least I hope so). One of the big conclusion of the study is that the average hospital stay was 3 days for the MIS group and 4 days for the open group. Once again it sounds like MISS has it all over the open group, right? NOPE. There is no insurance company in the world, including Medicare, that will authorize a 3 or 4 day stay in the hospital after a single level spine fusion, and no hospital in the world can afford to eat that extra cost. Once again in the real world most patients will be up walking the day of surgery and be home the next day; most of my patients will be home within 24 hours. Still think MISS offers an advantage?
There are many more examples, but I think I've made the point that MISS is perhaps not the end and all and be all that many want you to believe. I am not opposed to MISS, I just don't believe that the case for MISS has been made, and I am adamantly opposed to its use as an advertising tool. The rigorous studies that do compare MISS versus open procedures have NEVER found MISS to be superior, at very best it is equal to the more traditional approach in certain situations, making it a treatment option for those surgeons who perform a high volume of both procedures. As far as I am concerned, and back to the original topic, I see NO advantage to MISS in the case of a simple lumbar or cervical laminectomy and discectomy (and quite possibly some disadvantages). Conceptually I do not see the reason to try and minimize a 30 minute outpatient procedure that has withstood the test of time.
Laser Spine Surgery
Search the internet about anything remotely spine related and you will be inundated with adds for "Laser Spine Surgery". This is a situation that needs to be addressed. Simply stated the laser has no place in the treatment of disc disease. I will issue an open challenge to anyone to prove me wrong.
The word laser started as an acronym for "light amplification by stimulated emission of radiation". The laser is light that burns things. That's all it is. It is not magically; it does not reduce scarring; it does not hurt less. You point the laser, turn it on and whatever it is pointed at will burn and vaporize. The laser is a useful surgical tool; just not in disc disease. I use it in brain surgery for a bloodless approach to deep-seated lesions. Others have bastardized its use not because it is the right tool for the job, but because it sounds sexy and state of the art. Please let me assure that the use of lasers in the spine is NOT state of the art, or appropriate. What it is is an advertising ploy, nothing more. It is designed to get you, the patient, to click on their website and read their spiel.
Most medical websites that are used for advertising (I do not include this website as I am NOT soliciting my services) flirt with the truth. They use terms like "experts in the field", "world class", "leaders", etc.; personally I skoff at these claims (how does one know if they are an expert or not, or a leader in the field? Oh, I know, they simply say they are), and I think that the majority of people also look right passed those claims. It's a venial sin; the mortal sin occurs when they start to actively decieve you. Here is an example from one of the most aggressive groups, and one of the greatest offenders: THE LASER SPINE INSTITUTE. The ad focus' on spinal stenosis (a condition I talk about in the next section), insinuating that their treatment involves the use of a laser.
So you click on the website and find that their treatment for spinal stenosis is the same minimally invasive technique offered everywhere. Hey wait a minute, where's the laser?
The laser is used to treatment conditions that should NOT be treated with any procedure, much less a minimally invasive one. Here is a quote from the website, see if after reading the section above, you can detect their prevarication.
"A percutaneous endoscopic laser discectomy is done when the patient's history, physical examination and imaging (such as CT scan or MRI) indicates herniated or bulging disc and the material inside the disc has not ruptured into the spinal canal."
By definition a herniated disc requires rupture into the spinal canal. Further, bulging discs are NORMAL, and are not the etiology of back pain. These are SHAM procedures that rely upon the placebo effect, and the physicians who perform them know this.
Read this article from Bloomberg BusinessWeek exposing the Laser Spine Institute. If you want to skip it, here are the major points: this company (because that's what it is) spends more than $100,000 a MONTH on internet advertising alone; surgeries and procedures cost twice to three times the norm; many insurers will not pay for these procedures because of a lack of efficacy; surgeons contacted by Bloomberg Businessweek agreed that the company is doing surgery that is often unnecessary or inappropriate. The evidence that ablation helps patients is "pretty weak," says Dr. Roger Chou, a physician at the Oregon Health & Science University and director of the American Pain Society's clinical guidelines program. "Even in studies showing some benefit, the benefit is small and doesn't last," Chou says. Finally their malpractice suit rate is more than 6 times the national average for ambulatory surgery centers. These are the people who report to be the "Leader in Endoscopic Spine Surgery".
Laser Spine Institute is not alone; there are dozens of other sites doing and saying the same things. My simple advice is not to choose any surgeon or physician solely because they use the laser for treatment of back or leg pain- in fact I would NOT recommend using anyone who uses the laser for back and/or leg pain except as the butt of jokes.
Enough of this negativity, let's get back to Neurosurgery.
Once again, if you have jumped to this section without reading the basic anatomy section you are going to get lost. Go back and read.
If it is possible, there is more deception in the treatment of degenerative spine disease then there is in the treatment of disk disease. So let us start with getting are facts straight. Degeneration of the spine, both cervical and lumbar, is a natural process. To a degree, everyone's spine will begin to degenerate after the age of 25. Some people have spines that degenerate at a faster rate, while others enjoy a relatively benign course. If you have read the anatomy section above, you know that over time all the disks (cervical, thoracic, and lumbar) began to dehydrate, the facet joints begin to develop bone spurs and begin to twist, the ligaments begin to thicken, and the spinal canal, as well as the nerve foramina, began to narrow. We are designed to do this this, and in and of itself, this is not pathology. Most people with advanced degenerative changes, changes that involved the disks, facets, and even the spinal canal are without symptoms. It is worth emphasis, so one more time: everyone will have some degree of degenerative changes, and almost all of them are asymptomatic. This point can not be over stated, because MOST of the unnecessary (and invariably,unsuccessful) spine surgery and procedures fall into the category of spinal degeneration. I believe that a good deal of these "failures" could have been prevented if this concept had been fully appreciated by all involved.
ALWAYS ASK THE QUESTION: ARE THESE CHANGES CAUSING MY SYMPTOMS? In most cases of isolated back or neck pain, the answer will probably be "NO". There are exceptions,and I'll discuss them below, but for the majority of people, the answer lies elsewhere.
So what if you do not have neck or back pain, or you do but your chief complaint is pain/weakness/numbness in the arms or legs? Could the degenerative changes on the imaging studies be responsible for these symptoms? Absolutely. Even in the presence of axial (meaning midline, back or neck) pain, most symptoms that radiate into the limbs are related to degenerative changes. Note that I said MOST and not ALL; there are other conditions which will cause symptoms in the limbs (diabetes and peripheral vascular disease are two common conditions) that can be combined with axial (back or neck) pain that are NOT related to the spine. In these situations a high index of suspicion must be observed to avoid unnecessary attention directed towards the "innocent degenerative changes" in the spine. It's your doctor's responsibility to sort this out, but as you, the patient will ultimately have to live with the consequences it is in your best interest to be aware of other possibilities.
So, as I have stated a number of times already: IMAGING CHANGES ARE RARELY SYMPTOMATIC, and SYMPTOMS ARE RARELY RELATED TO IMAGING ABNORMALITIES!!!
Degenerative Spine Disease and Chronic Pain
I hate to harp on this, but I have to. Degenerative spine disease is a misnomer that is used to justify thousands maybe tens of thousands of procedures annually. A few will be successful, most will not. Perhaps even more problematic is that this "diagnosis" (or "pseudo-diagnosis") stops all intellectual activity and investigation. Not all back and neck pain is caused by the back or neck, even if an imaging study finds "degenerative changes". ALL patients, even those with "degenerative spine disease" need to be screened and examined for the RED FLAGS.
Once that is done, we are usually left with a patient that has chronic axial (back or neck) pain. I have already covered this topic in the Chronic Low Back Pain Section above, and most of the comments are equally applicable to chronic neck pain. A multi-modality, comprehensive approach is required for successful management. The last step in this process is surgery.
Spondylosis is doctor-talk for arthritis of the spine. So, from reading above, you know that to a degree everyone has some spondylosis, and that it's normal; once again, to a degree. So what happens when it's a little more than a degree? Then you are likely going to see me or someone like me.
Let's refresh your memory with regards to spondylosis. Starting with the cervical spine, here is an image which shows early and mild degenerative changes (spondylosis). Notice the bone spurs (spondylosis) projecting forward into the esophagus and trachea (swallowing tube and breathing tube respectively); suprisingly these almost NEVER cause difficulties with swallowing or breathing. Even monstrous osteophytes (fancy term for bone spurs)that displace the esophagus and trachea almost never cause problems. The other thing to notice is the narrowing of the disc space. From the reading that you have already done you know that disc space narrowing and osteophyte formation are the earliest manifestations of spondylosis and are both NORMAL and NEVER symptomatic (okay maybe 0.0001% are symptomatic). Spodylosis is the bodies reaction to the ligaments (the straps that bind the bones together) loosening with age. Movements that are normally retricted by the flexible ligaments are now checked by bone spurs and narrowed disc spaces (I'm taking some literary license here).
That was early and mild spondylosis, the image to the right is a more advanced state. Despite the impressive changes, I would still hesitate ascribing symptoms to them, unless they were radicular (related to nerve roots-pain weakness, numbness radiating into an arm) or myelopathic (related to the spinal cord itself). Looking beyond the fact that this image is an MRI and the one above is a simple x-ray, I think it's easy to appreciate the differences. In this study we see osteophytes both in front (neck-side), but also inside the spinal canal, bumping the spinal cord. The disc spaces are so collapsed that some of the bones have "settled" either in front or behind the vertebrae it sits upon. Impressive as the image is, unless the patient has NEUROLOGIC signs or symptoms (weakness, numbness, gait problems) it is unlikely that any surgical procedure is indicated.
In the interest of time, space, and repetition, I'm going to skip the lumbar images of spondylosis for now, and move on to the clinical conditions (where I'll show lots of images). Spondylosis has two major presentations: spinal stenosis and spondylolisthesis (anterior-rarely posterior-slippage of one vertebral body on another). A MINOR presentation is chronic low back pain; I'll discuss this, reluctantly, after the two more "solid" conditions.
Stenosis simply means narrowing. Alot of things can become stenotic : blood vessels, esophagus, minds, etc.. Spinal stenosis encompasses both the central canal (where the spinal cord/cauda equina reside) or the nerve foramina (where the nerve roots exit the spine).
Spinal stenosis is usually caused by spondylosis (thickening of the spinal ligaments and facets, narrowing of the disc spaces, and bone spurs). Occasionally a massive disc herniation can cause stenosis, but I dealt with that topic above; there are a couple other causes of stenosis, but the most important is spondylosis. The myelographic CT scan to the right is a good example of lumbar spinal stenosis; the arrows point to massively thickened facet joints. Compare this image to a normal lumbar myelogram.
Cervical spinal stenosis looks similar, and again is caused by the natural degeneration of the discs, thickening of the spinal ligaments and facet joints.Only here we have the spinal CORD to deal with (of course you remember that the spinal cord ends around L1 and is almost never involved with lumbar spinal stenosis).Another difference between lumbar and cervical stenosis is that the disc often plays a greater role in the pathology of cervical stenosis (the spinal ligaments and facet joints are the major offenders in lumbar stenosis).
I skipped thoracic spinal stenosis because outside of congenital or neoplastic conditions, it just doesn't occur. Now on to the clinical presentations.
Once again, stenosis can either be central (involving the spinal cord), foraminal (involving a nerve root), or more commonly both.
I am not going to cover symptomatic foraminal stenosis, because I already did under the heading of cervical disc herniations. Both conditions cause a radiculopathy (pathology of a nerve root) that will manifest as PAIN, weakness, and numbness. For more details look at the cervical radiculopathy section.
So on to a cervical myelopathy. This is the term that describes all the symptoms and signs of spinal cord dysfunction in the neck. The following list describes a "generic" cervical myelopathy:
Vague poorly localized neck pain; not always severe
Pain, weakness, or numbness in the shoulders, arms, and legs
Hand clumsiness-buttoning buttons, writing, using a key, etc
Gait and balance disturbances
Burning sensations, tingling, and pins and needles in the arm(s), including the top of the shoulder, shoulder blade area, upper and lower arm or hand
In advanced cases, bladder and bowel problems
Very late/severe cases can present with paralysis
The symptoms usually develop slowly over many months (about 75% of patients), but it is not uncommon to have a rapid acceleration as the situation progresses. Rarely a patient will develop symptoms over a short period of time (weeks to days), particularly after a traumatic event (often very minor). Unfortunately, because of the slow progression of symptoms, they are often ascribed to something other than the cervical spine, especially in the elderly:"I'm just getting older".However, Cervical spondylosis is the MOST common cause of myelopathy in people older than 55 years. A cervical myelopathy caused by stenosis is rare in those less than 40.
The natural history (what happens if nothing is done) is poor. Greater than 50% of patients continue to deteriorate neurologically with non-surgical management. Once symptoms develop, sustained spontaneous improvement is rare.
Treatment of Cervical Stenosis
Non-surgical management is an option for those with minimal symptoms restricted to the nerve roots (ie no myelopathy). Even with the best non-surgical management the "success" rate is only about 38%, with success being defined as stabilization of symptoms (a fairly low criteria). Treatment is a combination of bracing, anti-inflammatories and nerve blocks. The goal is to stop the movements that aggravate the radiculopathy and exacerbate the stenosis.
Management of a cervical myelopathy caused by cervical stenosis is surgical. Suprisingly, however, there is little support for surgical decompression in the neurosurgical literature if the myelopathy is stable (ie the patient is not getting worse). This is a relatively uncommon situation (remember that the natural history is one of progression), but even with a truly static myelopathy I think VERY few surgeons (myself included) would be comfortable simply watching this patient. So back to the first line: Management of a cervical myelopathy caused by cervical stenosis is surgical.
There are two ways of decompressing the cervical canal: from in front, or from behind. The debate between anterior approaches and posterior approaches dates back to the time when both became widely utilized. General sentiment is to treat anterior disease (ostephytes and disc herniations) with an anterior approach, and to use a posterior approach in all other conditions. A posterior approach is the preferred method because it avoids a fusion (in most cases) and eliminates the risk to the neck structures; unfortunately, most spinal stenosis, like most cervical disc herniations are ventral, or in front of the spinal cord, which limits the utility of the posterior approach. The choice of approach will also be influenced by curvature of the neck (if the neck is naturally bent forward-kyphosis-an anterior approach will not be as successful), and also by how many cervical levels are stenotic (narrowed). We try to limit the number of anterior cervical fusions to two (occasionally three). Lastly, there are disease states that cause spinal stenosis which will also influence the surgical approach (ossification of the posterior longitudinal ligament-OPLL- is one; I'll discuss this later).
For the most part I have already covered this in the cervical disc herniation section. The procedure is modified somewhat, instead of simply taking a disc herniation off of the spinal cord and spinal nerves, bone spurs are removed and a "roto-rooter" job is done at each level. Occasionally a larger graft, not the dowel mentioned in the cervical disc section, will be needed to reconstruct the cervical spine. With multiple levels a larger plate will also be needed, otherwise the procedures are the same. Often times with cervical myelopathy monitoring of the spinal cord activity will be performed during surgery.
As I said above, this is the preferred approach, but unfortunately it is suitable only for a minority of patients. Most of the things that cause cervical spinal stenosis are in front of the cord. Exceptions are when the facet joints are causative; when the patient has a severely "bent" neck; when the posterior ligaments are the problem; when the stenosis extends 3 or more levels (as in congenital spinal stenosis).
The minimum procedure is a laminectomy. This is a term that needs explanation. The lamina has already been well defined- it forms the back of the spinal canal, and removal of a lamina, a laminectomy, opens up the spinal canal. However, the true definition of a laminectomy is COMPLETE removal of the lamina. When we use a posterior approach for a disc herniation (NOT for stenosis) we remove only a portion of the lamina, but still generally call it a laminectomy; this is confusing and inappropriate (to be honest I use the term indiscriminately). Partial removal is actually a LAMINOTOMY (a window in the lamina).
Now that we have our verbiage correct, let's see a video that demonstrates a multi-level bilateral decompressive laminectomy. Once again I've "borrowed" this video, so please don't distribute it.
There are some people who, after a decompression, will become unstable (mechanically, not mentally). This occurs in about one in four patients. Taking off bone and ligaments in most cases will only minimally alter the stability of the cervical spine (if the facet joints are left intact), but what if the stability was less than optimal before surgery? In these cases the decompression of the spinal cord and nerves will have to be supplemented by a fusion (linking one bone to another through bone). Unlike the anterior approach , multiple levels can be fused with a reasonable chance of success. Once more I am going to "borrow" a video from MediLaw.TV, so you'll have to listen to the British narrator one more time.
Success is determined in large part by how long the symptoms have been present, and their severity. Patients with long-standing, severe cervical myelopathies experience only modest improvement with decompression and stabilization. Surgery generally halts the progression of symptoms, but often does not reverse them. Patients with less severe presentations of course do much better (approximately 75% of mild to moderate myelopathic patients improve).
Patients with a radiculopathy as the presenting complaint do very well, with greater than 90% of them recieving a significant benefit from surgery.
Lumbar Spinal Stenosis
Let me start this section by saying that every neurosurgeon loves lumbar spinal stenosis. It is almost exclusively surgical (nonsurgical success rates are about 20%), and it makes us look REALLY good. Almost every patient walks out of the hospital better than they walked in (even with the incisional pain). The only real controversy is whether to fuse or not to fuse.
The predominant symptom of lumbar spinal stenosis is summed up in one word: psuedoclaudication. This is a fancy word that means an inability to walk because of the spine (claudication is an inability to walk because the blood vessels that run to the legs have become stenotic). Lumbar spinal stenosis RARELY causes true back pain; instead, patients feel pain radiating from the upper buttocks into the legs (usually below the knees) when they stand in one place or walk. The only thing that alleviates the pain is sitting down (at least in early cases). Claudication, the blood vessel version of leg pain, is alleviated simply by standing, which allows the blood to "catch-up" to the muscles. Spinal stenosis pain is also partially relieved by leaning forward (again, early on in the disease). Leaning forward opens up the spinal canal a fraction, but often times this is enough to ease the leg pain. The classic story is a patient that states that they can't walk except when they go to the grocery store and drape themselves over the shopping cart. Interesting note: uncomplicated spinal stenosisNEVER involves the L5 level.
In MOST cases there is an inverse relationship between successful treatment and the amount of back pain a patient experiences. By itself, spinal stenosis does not cause back pain. That being said, let me take some of that statement back; in RARE, VERY RARE cases spinal stenosis will present with psuedoclaudication that is restricted to the back/buttock (pain in the back with standing and walking, alleviated by sitting). This is a slippery slope, because most mechanical back pain patients will have some degree of spinal stenosis (remember that these degenerative changes are common), and their pain is worse with movement and weight bearing. What differntiates the two is that the patient with pseudoclaudication does not report increased pain with flexing forward (in fact flexing alleviates some of the pain-to be clear, a patient with symptomatic spinal stenosis will report increased pain when they extend because this maneuver closes the spinal canal), or when carrying things, or with sudden jarring movements. The situation becomes really murky when a patient has spinal stenosis, pseudoclaudication restricted to the back, AND mechanical back pain. These patients make my head hurt. TAKE HOME MESSAGE: IF YOU HAVE MORE BACK THAN LEG PAIN, THE SYMPTOMATIC SPINAL STENOSIS BAR IS SET ALOT HIGHER.
No form of conservative mangement is even close to the efficacy of surgical decompression. Physical therapy, chiropractic management, injections, accupuncture, traction/decompression therapy etc.,etc.,etc. are all FAR inferior to a surgical decompression.
Surgical Management of Lumbar Spinal Stenosis
There are two options: decompression, or decompression followed by fusion. This is a fairly controversial point, and while I think that the question has been answered, it is still debated. This is also a situation where nefarious, unethical SOBs will attempt to take advantage of the uninitiated. Here is the recommendation made by the Spine Section of the American Association of Neurologic Surgeons:
"Fusion is not recommended as a treatment option in patients with lumbar stenosis in whom there is no evidence of preexistingspinal instability or likely iatrogenic instability due tofacetectomy."
What this says in plain English is that if the bones of the back are stable, and surgery doesn't affect that stability, DO NOT FUSE!. What if along with symptomatic spinal stenosis the patient has mechanical back pain? In that case: DO NOT FUSE! The back pain is treated like, BACK PAIN, and the spinal stenosis is treated like SPINAL STENOSIS. In the rare situation in which a patient has both symptomatic spinal stenosis and intractable back pain that has failed to respond to a protracted course of multimodality conservative management, then fusion coupled with decompression becomes an option. This is the ONLY situation, outside of instability, in which a fusion should be done following an appropriate decompression. If you are told that your decompression should be followed by a fusion, ask your surgeon if you are unstable (better yet ask the surgeon if your lumbar spine is unstable).
Unfortunately, lumbar instability caused by degenerative process' is often accompanied by spinal stenosis, so in alot of patients a decompression is followed by a fusion.
This procedure is no different from a cervical decompression. A laminectomy is done to open up the spinal canal. How that laminectomy is done can be debated. The goal of the operation is to take the pressure of the nervous structures while minimizing the damage to the spine. The oldest version of a decompressive laminectomy is to completely unroof the spine, ie take the lamina and spinous process' along with the ligaments, fully openning the spinal canal. This complete decompression is done "open" (ie a real incision is made), and is the gold standard. It is the gold standard because, simply put, it works! However, not everyone needs such a wide decompression. Newer procedures involve creating small "port-holes" in the laminas, and under the microscope the canal and nerves are decompressed. This operation can be done endoscopically (see the above comments on minimally invasive surgery), or it can be done "open". The surgeon will have to decide both how to approach the stenosis, open versus MISS, and whether a "midline sparing" decompression or the more traditional wide decompression is needed.
This procedure addresses two issues, nerve compression and spinal instability. Nerve compression requires no further explanation, but what is instability? Good question, and I wish I had a good answer.
The classic description (from White and Panjabi) describes clinical stability as "the ability of the spine under physiologic loads to limit displacement so as to prevent injury or irritation of the spinal cord and nerve rootsand, to prevent incapacitating deformity or pain due to structural changes". Quite a mouthful. In plain English they say that the spine is stable when it is able to resist movements, under ordinary stress, that cause pain or nerve/cord injury. Sounds pretty reasonable. But what does this mean in the real world?
Maybe x-rays can help. A concensus of x-ray abnormalities showing instability include: angular motion of 20 degrees, translational motion of 5 mm, and intervertebral end-plate angle on the flexion film of −5 degrees. That's helpful, but only for a limited number of patients.
We just don't have a universal concept of lumbar instability. It is a state that is both physiologic and anatomic. For instance, a patient that has herniated the same disc three times may not have any of the radiologic abnormalities listed above, but they certainly have clinical instability. On the other hand, it is not uncommon for someone to have 5mm of motion between flexion and extension (bending forward and then backward, and the involved vertebrae moves 5 mm) and be asymptomatic. So how do we define whether a patient has instability or not?
The real answer is that most surgeons have their own definition or feel for instability. Things like traction spurs (the bird beak lips on the front of the vertebral body), "warped" facet joints, swelling in the vertebral bodies closest to the disc space, etc.. I could go on forever and still not fully describe the process or define the problem. Obviously this introduces a surgeons bias; one surgeon's instability may not be another surgeon's instability. So where does that leave us with all the bold statements about not fusing patients without instability? On shaky ground I'm afraid. So with a quick sleight of hand I am going to make this question go away by saying that we know instability when we see it (sorry).
Lumbar fusions come in different varietiesThe oldest form, and it is still performed today (although it has fallen out of favor), is a posterior lateral fusion, in which bone graft is placed along the transverse process' of the spine. In time the small struts of bone coalesce into bars that fuse, or link the two bones together. Posterior lateral fusions have a lower fusion rate than some of the newer techniques, although the rate is improved with the addition of pedicle screws (more on those in a moment).
The more modern fusions involve putting bone grafts in the disc space. It is more successful for several reasons, chief of which are the facts that the disc space has more cross sectional area than the transverse process', and more weight passes through the disc space than through the back of the spine (weight passing through a fusion site encourages it to grow). There are different versions of interbody fusions. We have posterior interbody fusions (PLIF), transforaminal interbody fusions (TLIF), extreme lateral interbody fusions (XLIF), and finally anterior interbody fusions (ALIF). The first three procedures are somewhat similar, approaching the disc space from behind or from the side. An ALIF however goes through the abdomen requiring moblization of the abdominal contents, great vessels, and the nerves that surround them. Here is a video of a PLIF, which is the procedure I prefer.
The video mentions that the procedure is done for degenerative spine/disc disease, and it is used for recurrent disc herniations, but I use a PLIF more for spinal stenosis associated with that mythical spinal instability.
The TLIF and XLIF are similar procedures, but there are important differences. Both of these procedures are often done using a minimally invasive approach (the XLIF IS a MIS procedure).
The TLIF involves removing the majority of a joint, lifting a nerve out of the way and accessing the disc space through the foramen (ie transFORAMINAL). A single graft is then tapped into the disc space, and like the PLIF the remaining disc space is packed with the patients own bone. Pedicle screws are placed and that's the end of the procedure. Like the XLIF below this procedure is USUALLY done for back pain and only rarely for stenosis. If a minimally invasive approach is taken, additional incisions will need to be created for placement of the pedicle screws and the for the actual decompression. Instead of a single midline incision a number of smaller incisions are made off the midline. The big advantage of a TLIF and an XLIF is minimal exposure of the spinal canal, ie in situations of previous surgery where the risk of neurologic injury is increased. Obviously a TLIF's main advantage is lost when the patient is being operated on for spinal stenosis as the spinal canal will need to be exposed to relieve the stenosis. Here's a nice video demonstrating an open TFIF, but it also has a good demonstration of pedicle screw placement. You can also see how a TLIF can also be used after a laminectomy for spinal stenosis. Of note, I do not use the VALEO implant so there is no conflict of interest in me using their video.
An XLIF is the extreme lateral approach, and is used almost exclusively for back pain (occasionally for single nerve root pain). An incision is created on the side/flank and a graft is placed through a tube into the disc space. This opens the nerve foramina but unfortunately does not fix the central stenosis; this will require further incisions, as do the pedicle screws (unless as the following video demonstrates, lateral screws are used).
The last common fusion technique is an anterior interbody fusion ALIF. This is a procedure that I firmly condemn. I know alot of people will disagree with me, but anything an ALIF can accomplish can be done in a much safer, and cheaper fashion with one of the techniques above. An ALIF involves an abdominal incision, mobilization of the abdominal contents and great vessels along with the nerves that surround them. Then, just like an anterior cervical fusion the disc is removed and bone (or the failed artificial lumbar disc) is inserted into the disc space. The complication rate is high (5-30% impairement of sexual function) and completely unnecessary. Obviously additional incisions are needed to deal with any degree of spinal stenosis or stabilization, so what's the point? I am not going to show an ALIF video because I believe that it is a BAD procedure and I do not want to give it equal footing with the more successful operations.
The choice of a fusion technique is usually made by the surgeon. Anatomy and familiarity are ultimately how that decision is made. I do not see any distinct advatage of one technique over another (with the exception of the posterior lateral fusion and the ALIF-both are inferior to the three mentioned above). I like the open PLIF procedure, but have done the TLIF on occasion. I have never done the XLIF, but two of my partners do these on a regular basis and have similar results (of note, they use the minimally invasive techniques, and my patients use less narcotics and go home sooner- so much for the MIS advantage).
Once again I've covered these. The instructions and restrictions with or without a fusion are the same. In fact, the instructions and restrictions of a fusion are the same as after a simple lumbar laminectomy for disc herniation. There is no bending or twisting of the back, and no lifting greater than ten pounds. There is also NO BEDREST!!! It is critical that movement be maintained- 30 minutes of walking each daylight hour. Once again, patients find very quickly that walking is comfortable and sitting and laying are the positions of greatest discomfort. The wound requires no care and should be left open to the air.
As mentioned above, relief of spinal stenosis pain is the expectation. It is the rule that patients that have not walked comfortably for years are quite literally able to get up and walk shortly after surgery (I'm starting to sound like one of those "laser-spine" surgeons, but it is completely true). Even with a fusion patients after surgery are generally more comfortable than before surgery. Relief of nerve pain is about 96%, with 3% no better and 1% worse.
Fusion rates vary; in fact the definition of fusion also varies, so it's hard/impossible to put a reliable number on this. Outside of huge technical or medical issues, it is the patient that determines whether a fusion will be successful. Six weeks after surgery, a mild to moderate reconditioning MUST begin. This includes range of motion, cardiovascular conditioning, and core-strengthening. Weight must be optimized. Narcotics must be weaned off as soon as possible. NO USE OF TOBACCO. If these details are not attended to the chances of success fall tremendously. Once again, a patient can not be made better without their help, and in a fusion operation the patients level of cooperation is DIRECTLY proportional to their level of success/satisfaction.
I think I've covered this as well. The biggest are:
To fuse or not to fuse
Open or minimally invasive
What type of fusion
Alot of this will be determined by your surgeon, and once again let me have you read the first two paragraphs of this page. Do not trust anyone blindly!!! Get informed, get educated, and even other opinions. This is especially important in this situation where so much remains undefined.
The word spondylolisthesis is derived from the Greek words spondylo, meaning spine, and listhesis, meaning to slip or slide. Spondylolisthesis is a descriptive term referring to slippage (usually forward) of a vertebra and the spine above it relative to the vertebra below it.
There are two big versions of spondylolisthesis (at least) and I'm going to label them congenital and developmental. I'll discuss the congenital version later (to be exact, it is not congenital-meaning from at birth, but a poorly formed vertebrae). The developmental version occurs because of arthritic changes in the facet joints, and is another manifestation of spondylosis (arthritis of the spine). Essentially the joints begin to thicken in response to the loss of ligamentous support as we age. Usually the process goes no further, but in some the joints begin to deform and twist which ultimately leads to a loss of the stability offered by the locking mechanism of the facets, allowing the superior vertebrae to slide forward over the inferior vertebrae. Enough words, how about some pictures. Let's start with a simple diagram.
Now for some images; this first is a typical appearance of slippage of L4 on L5 (one of the most common level). Note that the spinal canal is narrowed; spondylolisthesis is a common cause of spinal stenosis, and unlike the more typical "arthritic" cause of spinal stenosis, this form is USUALLY symptomatic. Note also the severe narrowing of the disc space. While this narrowing contributes to the narrowing of the nerve foramina, ironically it may mean that the process has begun to arrest itself (ie the slippage probably won't get much worse because the narrowed disc space won't allow further movement).
Here's a cross-section view showing the warped facet joints.
We grade spondylolisthesis from Grade 1 to Grade 5, but in the degenerative form we rarely see anything beyond a Grade @, but for completeness sake here's the grading system-essentially we divide the body into quarters: 0-25% is Grade 1; 26-50% is a Grade 2; 51-75% is Grade 3; greater than 75% is a Grade 4; and a Grade 5 is when there is a complete offset of the vertebrae above relative to the vertebrae below.
Presentation of Spondylolisthesis
Basically there are 4 ways a spondylolisthesis can present: incidentally; back pain; nerve symptoms/pain; spinal stenosis. I don't think these need to be expanded upon, but I will, a little.
BACK PAIN: presents as a mixture of mechanical low back pain (worse with any physical activity or movement), and a version of psuedoclaudication- a deep, aching sensation in the upper buttocks that is worse with standing and walking and better with sitting.
NERVE SYMPTOMS: as expected it is related to what level is involved. The most common level is L5 on S1 and we would expect that the L5 nerve root, one or both, would be involved, causing pain to radiate from the buttocks down the leg to the top of the foot. We could also expect numbness in the great toe and top of the foot, along with weakness in the hamstrings and an inability to lift the toes and foot. If the slippage involved L4 on L5 we would expect the L4 nerve roots to be impaired.
Spinal Stenosis: all the symptoms mentioned in the previous section, ie pain radiating down both legs when walking or standing, with prompt relief upon sitting.
The diagnosis is simple to make, an x-ray, often with bending views (flexion and extension), will tell most of the story. An MRI or CT/myelogram will fill in any gaps.
Obviously treatment is predicated upon the presenting symptoms. Those who have no symptoms need no treatment, no matter how bad the films look.
Those with low back pain should be treated non-surgically. Essentially, this is treated as chronic low back pain, only with a diagnosis. Review the treatment for chronic low back pain above. Exercise/reconditioning that involves range of motion, cardiovascular conditioning and core strengthening will effectively treat most low to medium grade spondylolisthesis patients who present only with back pain. Only after an extended trial of non-surgical management should a stabilization procedure be contemplated.
Those presenting with nerve root symptoms or psuedoclaudication (the symptoms of spinal stenosis), are likely going to end up in the OR. We just do not have good nonsurgical treatment for any form of nerve root impingement, much less spinal stenosis. The only questions are "when" and "should a fusion be included"? The when question is probably the easiest to answer: either when the patient has had enough of the pain/symptoms, or they develop motor weakness. Not much more than that.
The fusion question is a bit trickier. once again, it is best NOT to fuse patients, but for some it's the least bad option. How we differentiate who gets fused and who doesn't often boils down to personal opinion (see the section above that tries to define lumbar instability, and fails). Dynamic x-rays (those that are done with the patient flexed and then extended) help in a few patients, but most will come down to less objective factors (disc space height, degree of facet degeneration, severity of stenosis and symptoms, etc., etc.). Once again I would recommend getting educated and even second opinions before a fusion procedure.
The surgical procedure for symptomatic spondylolisthesis are identical to the surgeries for spinal stenosis, so there's no point repeating it here. Most slips are fused in situ, which means "as they are". Reduction of the slippage, especially a higher grade slippage will stretch the nerve roots (something that will already happen to a small degree when the disc space is elevated back to its normal height).
Juxtafacet Cysts/Synovial Cysts
The term juxtafacet cyst (JFC) is used to describe fluid or mucinous filled masses that occur primarily in the lumbar spine. When they are associated with the facet joint, and have a synovial lining they are called synovial cysts; when they are associated with severe degeneration of a ligament (primarily the yellow ligament that "roofs" over the spine between the lamina) they are called juxtafacet cysts. Clinically they are indistinguishable and so I will treat them as the same entity
Patients with lumbar synovial cysts typically present intheir mid-60s with symptoms of radiculopathy and neurogenicclaudication. By themselves, the cysts DO NOT CAUSE back pain, however, the degenerative process' that cause the cyst to form in the first place can cause back pain.
There is also a close relationship between these cysts and spondylolisthesis. The reason for this is clear once you know the etiology of the synovial cyst. First some anatomy. The facet joints are wrapped up inside a strong capsule that holds the two bones together. Inside the joint, where the two bones actually meet, is a super-slick lining that allows the bones to slide smoothly over each other, this is the synovium. When a facet joint degenerates severely the capsule gets torn and some of the synovial lining can peek out of the joint space (often times into the central canal or nerve foramina causing central or foraminal stenosis). Without the constraining effect of the joint capsule, the synovium that has peeked out goes nuts and starts to enlarge squeezing everything in its way. Now you have a synovial cyst. Not all synovial cysts find their way into the spinal canal, they can push their way into the spinal muscles (where they aren't really a problem). So, if synovial cysts are caused by severe facet degeneration, and degenerative spondylolisthesis is caused by severe facet degeneration, it should not suprise anyone to find that the two often coexist. Let's look at some pictures.
Treatment Of JuxtaFacet Cysts
As these cysts present either incidentally (found accidentally), with back pain (again NOT directly related to the cyst), with nerve root pain, or with spinal stenosis symptoms, their treatment is dictated on how they come to attention. Incidental cysts are left alone, especially if they spare the central canal and the nerve foramina. Cysts that are found during the investigation of chronic low back pain are treated like CHRONIC LOW BACK PAIN. This is important as simple removal of a synovial cyst in a patient with only low back pain as a complaint (and NO nerve symptoms) WILL NOT SEE ANY IMPROVEMENT OF THEIR BACK PAIN. Instead they should be treated in the same manner as anyone else with chronic low back pain.
Those presenting with neurologic symptoms, either nerve root pain, or symptoms from spinal stenosis, are generally going to be treated surgically. The natural history of synovial cysts is still debated, but in time, practically all patients end up in the OR. Non surgical management, such as injections into the facet joints (usually steroids), and CT guided needle drainage of the cysts will provide very short term relief if they provide anything at all.
Surgical management revolves around complete resection of the cyst, which sometimes is a tall order, and consideration of a fusion. Complete and safe resection of a synovial cyst is complicated by the fact that the cyst "burrows" into the coverings of the nerves (the dura), and removal of the cyst can mean removal of the dura and leakage of the spinal fluid (risk ranges from 4 to 14%). An experienced surgeon should already know this. The other issue is whether to fuse or not. If no fusion is done, ie the degenerative process that formed the cyst originally is left untreated, can the cyst return or other bad things happen? In the case of a cyst combined with a spondylolisthesis simple resection of the cyst has been shown to worsen the slippage. In addition, even when the cyst occurs in a "stable" spine, complete excision often requires destroying the joint that the cyst originated from. Once again we do not have a strong feeling for when to fuse or when to perform a simple excision. Here is what I do:
Single nerve involvement, with no signs of instability: simple cyst excision through a laminectomy
Spinal stenosis with no signs of instability: simple cyst excision through an open decompressive laminectomy
Cyst and spondylolisthesis, stable or not: Fusion
Any previous lumbar surgery for a degenerative process and a new cyst: Fusion
Surgical Management of Chronic Low Back Pain
Here is where the rubber mets the road, or more appropriately, the crap hits the fan. Back surgery for back pain is an epidemic. I can safely say that the majority of back surgery done today solely for back pain is inappropriate. There is a place for surgical treatment of back pain, but it is lost in a cloud of misguided, good, and usually not so good intentions. This is why the success rate for spine surgery for back pain hovers around 50%. To clarify that statement and to lend credence to what I said above, the only reason that the success rate is that high is because the "good" surgeries are offsetting the "bad" surgeries.
So what is a "good" surgery? Here are the guidelines from the North American Spine Society: "lumbar fusion is recommended for carefully selected patients with disabling LBP due to one-or two-level degenerative disease." In the primary quoted study patients had chronic LBP for 2 or more years and had radiologic evidence of disc degeneration at L4, L5, or both, and had failed best medical management. So the keys are: what is a "carefully selected patient" and what is "best medical management"?
Unfortunately, the definitions for "carefully selected" and "best medical management" have not been agreed upon, and it is through this gap that the majority of inappropriate surgeries slip through.
I've listed my medical management for chronic low back pain above. It's origin is in part what others have done and what I have been found to be effective over the last 20 years. It is a rigorous program, but a successful one. Surgical intervention is NOT A SUBSTITUTE, in fact the same program is used post-operatively. If a patient has clear pathology, limited to one or two levels, has demonstrated an ability to participate in their own care (weight loss, adhering to a conditioning program, smoking cessation, etc.), and continues to experience pain more than a year after starting treatment, I would consider them a surgical candidate.
There are are exceptions in both directions. Patients with "pure" single level pathology, such as the image to the right, in a "good" candidate, could be considered after as little as six months (VERY RARE!!!). Others, who have had partial response to treatment, ie weight loss, perhaps localized injections, would best be served by a more protracted course of non-surgical management. While there is some "wiggle-room" as far as the criteria, it's not much and I personally set the bar fairly high. Why? Because you can't take back a fusion. It is a permenant alteration to the spine that even in the ideal candidate will have long term consequences.
The advice I give my patients is to decide whether they can live the life they want with this problem. Not whether they want to, but whether they can. If the answer is yes, they are non-surgical. If the answer is no, then they have to realize they are signing up for a life altering event. Weight management, range of motion exercises, cardiovascular conditioning, and core strengthening will become aspects of their daily lives, forever. The patients who reach this point and follow these instructions as a rule do very well; those who pay it only lip service uniformly regret their decision. It doesn't take long for people to realize that the surgical procedure was the easy part, and all it has done is set the stage for the patient to fix themselves.
Surgical treatment of chronic low back pain involves a fusion. Theories on chronic low back pain center on two concepts: abnormal/painful movement of a motion segment (segmental instability) or painful discs (discogenic back pain). They are not mutually exclusive, and can coexist in a patient. Either way, removal of the disc and immobilizing the level through a fusion corrects the problem.
I have already discussed spinal fusions above. I would recommend reviewing the entire section. I would also recommend getting a second opinion. It is what I tell all my potential fusion patients, and during those first post-operative nights, when their backs are sore and stiff, and they find it hard to sleep through the night, the reassurance that comes with a consenting second opinion is priceless.
Autoimmune Process' that Involve the Spine
These are systemic diseases that as a part of their pathology affects the spine. I am not a rheumatologist, and I do not treat these pathologies, so I am going to limit the discussion to spine involvement and go quickly. Let's start with a familiar process rheumatoid arthritis.
Rheumatoid arthritis is a disease that causes destruction of joints through out the body by attacking the synovial linings of the joints. As the synovium is destroyed the inflammatory reaction causes pain and deformity in the joints. The disease can occur in any joint in the body and is most commonly symptomatic in the small joints in the hands and feet. When rheumatoid arthritis affects the joints in the spine, it is far more common for the neck (cervical spine) to be affected than for the lower back.
Synovium is not just in joints, it is also located in the linings of the heart and lungs; more pertinent to this discussion it is also located between the dens (the upward tooth-like projection of the second cervical vertebra) and the ring of C1. When the inflammatory reaction is severe it creates a huge knot of material we call a pannus. This pannus can compress the upper spinal cord and even the lower brainstem. The destruction of the connections between C1 and C2 also allows the first cervical bone to slide in front of C2 taking the spinal cord with it. This is a particularly nasty case of RA that has a huge pannus that is causing compression of the cord and brainstem, and dislocation of C1 on C2. This patient will likely need extensive treatment, likely traction followed by complex reconstruction of the C1 and C2 connections.
In some cases the inflammatory reaction involving the joints between C1 and the skull and generalized disability lead to softening of the skull-base, and the dens can "telescope" into the cranium (basilar invagination). This particular patient will likely need cervical traction (possibly for a few weeks) in hopes of "pulling the dens out of the cranium and off of the brainstem. If that can be accomplished a posterior occipitalcervical fusion would follow. If reduction of the malplaced dens can not be achieved, or maintained, it needs to be removed. This is often done through a trans-oral (yes that's right, through the mouth) approach, followed by occipitalcervical fusion.
I'm taking some of this directly from the MayoClinic site, I hope they don't mind.
Ankylosing spondylitis is an inflammatory disease that can cause some of the vertebrae in your spine to fuse together. This fusing makes the spine less flexible and can result in a hunched-forward posture. A severe case of ankylosing spondylitis can make it impossible for you to lift your head high enough to see forward.
Ankylosing spondylitis has no known specific cause, though genetic factors seem to be involved. In particular, people who have a gene called HLA-B27 are at significantly increased risk of developing ankylosing spondylitis.
Ankylosing spondylitis affects men more often than women. Signs and symptoms of ankylosing spondylitis typically begin in early adulthood. Inflammation also can occur in other parts of your body — such as your eyes and bowels.
There is no cure for ankylosing spondylitis, but treatments can decrease your pain and lessen your symptoms.
Early signs and symptoms of ankylosing spondylitis may include pain and stiffness in your lower back and hips, especially in the morning and after periods of inactivity.
These symptoms may come on so gradually that you don't notice them at first. Over time, symptoms may worsen, improve or stop completely at irregular intervals.
The areas most commonly affected are:
The joint between the base of your spine and your pelvis-the sacro-illiac joint
The vertebrae in your lower back
The places where your tendons and ligaments attach to bones, mainly in your spine, but sometimes along the back of your heel
The cartilage between your breastbone and ribs
Your hip and shoulder joints
As ankylosing spondylitis worsens and the inflammation persists, new bone forms as part of the body's attempt to heal. This new bone gradually bridges the gap between vertebrae and eventually fuses sections of vertebrae together. Those parts of your spine become stiff and inflexible. Fusion can also stiffen your rib cage, restricting your lung capacity and function
Basically the underlying process is inflammation of the ligaments which leads to injury and ultimately to calcification, greatly reducing their ability to move. In addition, particularly in the spine, it predisposes them to fracture, but not any type of fracture. Because the spine of a patient with AS is basically a solid tube of bone, when it is stressed it snaps, unlike a normal spine which will bend and accomodate the stress. Look closely at the x-ray above and you can see that instead of individual motion segments the entire spine is solid, even the disc spaces are starting to turn to bone. The reformatted CT image to the right shows it even better, along with the unique "bamboo fracture" associated with AS. Basically the spine breaks like a dry twig, often times seperating the fragments widely (this fracture actually shows good approximation of the fracture). This fracture is GROSSLY UNSTABLE and will need surgery to correct the problem. It is very common for these bamboo fractures to cause neurologic injury.
AS also contributes to osteoporosis which can lead to compression fractures. A compression fracture is when the "box-like" vertebral body collapses on itself. This is not an uncommon event for those with garden-variety osteoporosis, and it is almost always treated non-surgically (in some we would do a vertebroplasty-more on that later). However, in those with AS the fracture contributes to the stooped posture and stresses the integrity of the remaining spine, occasionally requiring surgery for stabilization.
AS also is a cause of mechanical back pain. With time the mobile elements of the spine become more "immobile", and with that immobility comes a hypersensitivity to normal movements/ activities of the spine. This manifests as chronic low back pain. Fusion of the SI joint, a key feature of AS, also contributes to the LBP.
Ossification of the Posterior Longitudinal Ligament
Once again I need to refer you to the anatomy section above, and once again if you do not review it, you will get lost.
OPLL, as ossification of the posterior longitudinal ligament is called, was first described in 1838, but it wasn't until the 1960's that people started to look at this disease seriously. Initially it was felt to be a condition that was mostly restricted to the Asian population, now we know that this is probably more due to under-reporting than an ethnic preference.
OPLL presents at a mean age of 53 (range from 30s to the 80s), and patients usually present with a year or more of symptoms. Typically the symptoms refer to spinal CORD compression (less commonly only nerve roots are involved). Obviously the type of symptoms are determined by the location and severity of the process. Roughly 3 out of four cases involve the cervical canal, with the thoracic canal making up the bulk of the remainder. Let's review a cervical myelopathy (the most common presentation of OPLL):
Vague poorly localized neck pain; not always severe
Pain, weakness, or numbness in the shoulders, arms, and legs
Hand clumsiness-buttoning buttons, writing, using a key, etc
Gait and balance disturbances
Burning sensations, tingling, and pins and needles in the arm(s), including the top of the shoulder, shoulder blade area, upper and lower arm or hand
In advanced cases, bladder and bowel problems
Very late/severe cases can present with paralysis
OPLL usually involves 2-4 levels, but not all OPLL is alike. There are four classic pathologic distributions:
segmental 39%: confined to the space behind the vertebral bodies,does not cross disc spaces
continuous 27%:extends from vertebral body to vertebral body,spanning disc spaces
mixed 30%: combines elements of both above, with skip spaces
localized 4%: rare form confined to the end plates
The underlyoing pathology is unknown, but a hereditary component is likely.
OPLL begins as an inflammatory reaction within the posterior longitudinal ligament. Blood vessels grow into the ligament as the inflammation progresses, with increasing growth of fibroblasts (scar tissue), then cartilaginous cells, and finally bone cells (ossification). The inflammation frequently involves the adjacent dura, and in most cases the dura is indistinguishable from the calcified ligament. Eventually the bone matures to the point of developing bone marrow. Obviously by then the space taken up by the calcified ligament/dura is very great, the spinal cord has become compressed, and it's blood flow significantly reduced.
X-rays are often nonrevealing, and the diagnosis is usually made with MRI. As the process is one of calcification (and you already know that MRI is not very good at detecting the degree of calcification) a CT scan is usually required.
Most patients with OPLL have NO symptoms, and like most asymptomatic conditions, they are generally treated non-surgically. This is the generally concensus, however, there are dissenters, and they have good reasons. Once OPLL becomes symptomatic, patients often DO NOT IMPROVE with surgical decompression. Surgery halts the progression, but unlike most other causes of myelopathy, OPLL patients usually don't get much better.
The surgical complication rate is much higher with OPLL and the improvement rate is much lower, relative to other forms of cervical myelopathies. Still, the natural history of OPLL, particularly after symptoms have appeared, is much worse.