What is a Spondylolisthesis?

At this point in our discussion of lumbar pathology we come to one very important topic: spondylolisthesis of the lumbar spine.  First described in the mid-1800s, spondylolisthesis literally means slipping bones.  In this painful condition there is forward slippage of one vertebral body over the body below.  If you want to get academic about it, the severity of this slippage is classified according to the Meyerding Scale:  

  • Grade I: <25% slip
  • Grade II: 25-50% slip
  • Grade III: 50-75% slip
  • Grade IV: 75-100% slip
  • Grade V: >100% slip (the vertebral body above is floating freely in front of the body below.) 

Some patients obsess about grading schemes like these but they’re really not that important for a typical patient with spondylolisthesis.  Grade I is by far the most common grade and if you’ve been told you have a spondylolisthesis this is probably what you have.  I will occasionally operate on a grade II and I can count on one hand the number of times I’ve operated on a grade III.  The higher grades really aren’t seen in adult patients.  They usually require a congenital defect in the bony anatomy of the spine and thus usually are already symptomatic in childhood (which is why, since I’m not a pediatric neurosurgeon, I don’t see these cases.)   A patient with spondylolisthesis may first present with only non-specific back pain.  As the patient ages and their spine degenerates the spondylolisthesis may become unstable and start to progress.  The slip eventually becomes severe enough that the patient develops back and leg pain and they come to see me.  This is the condition for which I most commonly book lumbar fusion procedures.  See figure 1. 

AH L4 5 spondy XLIF pptxIMG 0079

Figure 1: Sagittal MRI showing the forward slip of L4 on L5 in a typical spondylolisthesis.  The image on the right is a schematic of the same process (source: SpinePro III for iPad)

Spondylolisthesis is commonly asymptomatic (radiographic studies on normal volunteers tell us that nearly 10% of us are walking around with this condition yet have no pain.)  In my clinic, though, patients with spondylolisthesis have progressed to the point where they now have pain.  Patients with spondylolisthesis typically present with a combination of two types of pain: mechanical back pain from stress on the facet joints as well leg pain from compression of nerves.  As one vertebral body slips forward over the one below, this puts a tremendous amount of stress on the facet joints at the back of the spine (imagine how your knee would feel if was repeatedly bent outside of its normal range of motion.)  As they struggle to maintain the structural integrity of the spine they get stressed, become inflamed and arthritic and thus cause the back pain associated with spondylolisthesis.  Also, as the vertebral body slips forward, the nerves within are guillotined causing severe pain, numbness, tingling and even weakness.  The condition is especially debilitating because both nerves at the level of the slip can be compressed and injured.  First, there is compression of the exiting nerve because of foraminal stenosis caused by the slip and resultant foraminal height loss.  The traversing nerve (the nerve still within the spinal canal that will exit at the foramen below) also gets crushed in the lateral recess underneath the severely degenerated facet joint as one part of the joint slides forward in relation to the other (see figure 2).   For example a slip at L4/5 can cause compression of both the exiting L4 nerve and the traversing L5 nerve.  Both the back pain and leg pain associated with spondylolisthesis get worse as the patient stands up for even a short period of time.  When the patient is upright this loads the spine, aggravates the slippage and thus causes worsening pain. 

 Spondy foraminal stenosisAH L4 5 spondy XLIF pptx

Figure 2: On the left is a sagittal MRI showing severe foraminal stenosis associated with a spondylolisthesis at L4/5 (red arrow); contrast this with a normal foramen at the level above (green arrow).  On the right is an axial MRI of the same patient.  Note the severe lateral recess stenosis crushing the traversing nerve below the facet joint (red arrow).  Also seen is severe facet arthropathy (blue arrow) as indicated by a displaced joint and fluid within the joint.

There are several types of spondylolisthesis described in the textbooks.   The two most common types by far are degenerative spondylolisthesis (DS) and isthmic spondylolisthesis (IS).  DS, the most common form, occurs, as the name would suggest, as the spine degenerates over time.  As the intervertebral disc degenerates it no longer can properly absorb motion.  The facet joint tries to take up the slack but eventually, after enough time as a defacto shock absorber, becomes arthritic and incompetent (the same thing my wife says is happening to me.)  This incompetent facet joint can no longer maintain the structural integrity of the spine and the spine becomes unstable, allowing slippage to occur.  For reasons that aren’t entirely understood, most people with normal, age-related wear and tear of their spine do NOT develop DS.  A small number of unlucky folks are predisposed to this condition, however, perhaps because of the morphology of their facet joints or a genetic predisposition to accelerated disc and facet degeneration (degenerative conditions like this do run in families.)  DS more commonly occurs in older patients at the L4/5 level.

IS, a.k.a. lytic spondylolisthesis, occurs as a result of a fracture of the pars interarticularis, a small bridge of bone connecting the facet joint at one level to that of the level above (see figure 3).   This condition, also referred to as spondyloLYSIS, is thought to begin as an innocuous stress fracture in young athletes.   Only a small percentage of patients with a pars fracture will ever develop pain and an even smaller number will ever develop a slip.  Again, there seems to be a subset of patients who are predisposed to developing a slip in the setting of a pars fracture.  One theory is that patients with a high pelvic incidence (PI) are more likely to progress, mainly because of the force of gravity pulling the spine forward (PI is a measure of the morphology of one’s pelvis usually associated with a steep downward sloping sacrum.  More on this in a later post.) IS more commonly occurs in younger patients at the L5/S1 level (secondary to pars fractures at L5, see figure 4).  Again, as a patient, don’t get too bogged down in the details of different types of spondylolisthesis here.  If you have a spondylolisthesis it’s probably a degenerative one although it may be an isthmic one.  In the end, though, it doesn’t matter as the treatment is the same. 

Netter Lumbar Spine jpg Spondyolysis

Figure 3: Left, posterior view of lumbar spine at L4/5 level (red line indicates location of a fracture across the pars of L5.)  Image on right shows schematic of slip at L4/5 that has developed as a result of a pars fracture at L4 (yellow arrows.)

L5 S1 spondy Xray

Figure 4: Lateral standing Xray showing spondylolisthesis at L5/S1 associated with pars fracture at L5 (thin red lines).  This patient also has a high pelvic incidence with a steeply sloping sacrum (the top of which is indicated by blue line).  You can imagine how the force of gravity is contributing to the development of the slip in this patient by pulling L5 forward and downward (red arrow.)  

Even today there continues to be a great deal of controversy over the treatment of spondylolisthesis.  As I mentioned previously, spondylolisthesis and spondylolysis are commonly asymptomatic.  Interestingly, several large population studies have failed to show a strong correlation between the presence of spondyolysis/spondylolisthesis and pain, even when the slip progresses.  Patients can have this condition, a structural deformity of their spine, and be just fine. IT raises the question: should these patients even be treated at all?  Ultimately, though, once a spondylolisthesis progresses to the point where it’s now an unstable deformity of the spine, patients usually begin to seek treatment.  

When I first see a patient with a spondylolisthesis I’ll begin by offering conservative treatments such as physical therapy (PT) and epidural steroid injections.  PT will relieve pain in patients with spondylolisthesis, even when the slip is unstable and associated with stenosis.  I’ve been amazed at how some patients, with horrible looking MRIs, will do just fine with regular PT.  If nothing else, even if the patients do progress to surgery, I prefer that the patient has completed a course of PT because it strengthens them for recovery after surgery.  Only when PT and injections fail to provide lasting relief of pain do we consider surgical intervention.

As mentioned in a previous post, instability is one of the clearest indications for spinal fusion.  Indeed, patients with back pain and radiculopathy from an unstable spondylisthesis almost uniformly have excellent outcomes with the proper surgical intervention.  There is some controversy on the best surgical approach to address spondylolisthesis.  In my opinion, though, the best intervention is that which, using minimally-invasive approaches, best restores the structural alignment of the diseased level.  This intervention provides stability to relieve back pain and also, through indirect decompression, relieves nerve root compression and thus relieves leg pain.  More on the surgical treatment of spondylolisthesis in upcoming posts…


Thanks for reading!


J. Alex Thomas, M.D.

Implants in Spinal Fusion, Part I: In-situ Fusions Rarely Fused

As I was writing the previous few posts I realized that I was relying on terms such as pedicle screw and intervertebral spacer to begin the explain techniques used to achieve spinal fusion.  Before we get further into our discussion on these techniques I think it would benefit you, devoted Spinal (con)Fusion reader, if I spent a few posts discussing the various implants used during spinal fusion procedures.   It seems like in my clinic everyone knows someone who didn’t do well after getting “a whole bunch of screws and rods in their back”.  Granted, on their own these sound like medieval torture devices that no sane person would want implanted into their spine.  Hopefully by shining some light on the screws, rods and various other spinal implants used during fusion procedures, I can put prospective patients’ minds at ease if they’re considering a spinal fusion.

In order to appreciate the benefits of today’s spinal instrumentation, you must first understand how terribly inadequate early non-instrumented spinal fusions were.  Recall that we discussed that the main goal of a spinal fusion procedure is to promote bone growth across one or more spinal motion segments.  This bone growth immobilizes what is felt to be an unstable, and thus painful, part of the spine.   While spinal fusions have been done since the early 20th century, the only strategy that early spine surgeons could employ to achieve a bony fusion was to harvest autograft (bone harvested from a site within the patient such as the spinal lamina or the iliac crest) and lay it down over an exposed part of the spine that they wished to fuse.  This primitive in-situ fusion technique, first described by Albee and Hibbs in the early 1900s, was problematic for two reasons.  First, there was no good way to correct spinal deformity while promoting a bony fusion.  Thus, after a long, morbid surgery, patients were often fused with painfully deformed spines and no better than they were prior to surgery.  Second, in order for any bone to fuse together the adjacent pieces of bone have to be immobilized (think of a cast on a broken arm.)  In an in-situ fusion, with the bone graft simply laying on top of a segment of spine, the only way to immobilize a patient’s spine to promote bone growth was to keep them on bedrest, often in full body braces or casts, FOR MONTHS.  UGH!  What’s worse is that because of these inadequate forms of immobilization, in half the cases the new bone wouldn’t grow, the spinal segment wouldn’t fuse and the patient would be left with a painful condition called a non-union, or failed fusion, often requiring subsequent revision surgeries.  It’s no surprise, then, why many at the time considered early spinal fusion procedures to be painfully ineffective.     

Beginning in the mid-20th century, various forms of spinal instrumentation were developed in order to help mitigate the above limitations of early in-situ fusions.  First, spinal implants provide the necessary internal bracing that immobilizes the diseased motion segment so that robust bone growth can occur.  No more full-body casts!   Also, spinal implants, particularly the intervertebral spacers inserted into the disc space at the front of the spine, allow for correction of spinal deformity.  This deformity correction, equally important as correction of instability, restores the spine to its normal form and alignment prior to it being permanently immobilized by the new bone growth of a spinal fusion.  In short, spinal implants create the optimal conditions for new bone to grow to achieve a spinal fusion and thus correct painful spinal instability and deformity. 

In our next post I’ll dive right into the world of spinal implants with a discussion on pedicle screws and other forms of posterior instrumentation. 

Thanks for reading!

J. Alex Thomas, M.D.


What is a lumbar discectomy?

Ok, so at this point all of you know the difference between a bulging and herniated disc.  Ultimately, as we discussed in our last post, the semantics matter less than the fact that either of these conditions can compress a nerve root and cause severe pain, numbness or weakness.  In order to relieve the pressure caused by the bulging or herniated disc a spine surgeon may offer a lumbar discectomy.  

The term discectomy is actually a bit of a misnomer with its suffix –ectomy, meaning to remove.  This term thus implies that the surgeon removes the entire intervertebral disc (IVD).  In fact, in a lumbar discectomy only a small portion, the bulging or herniated portion, of the IVD is removed.

A lumbar discectomy is by no means a mandatory procedure and a trial of non-surgical treatments should be considered prior to surgery.  A large study called the Spine Patients Outcomes Research Trial (SPORT) began enrolling patients in 2000 to try to establish whether surgical treatments were better than non-surgical treatments for some common degenerative spinal conditions.  In 2006 the SPORT authors published a randomized controlled trial of lumbar discectomy versus non-surgical treatment for lumbar disc herniation.   While the study’s methodology was flawed, it was able to illustrate some interesting points about patients with herniated discs.  First, with time, patients improved regardless of which treatment group they were in.  Thus, as long he or she can tolerate it, I typically will encourage a patient with a herniated disc to try a course of non-surgical treatment, including physical therapy, chiropractic manipulation or epidural steroid injections. These therapies buy the patient time while the body heals itself and in many cases the herniated disc fragment is absorbed by the body (contrary to popular belief, no matter what your chiropractor says, the fragment does NOT go back into the disc space.)  While SPORT clearly showed that a trial of non-surgical treatment is a reasonable option, it also showed that patients who underwent surgery for their herniated disc got better faster.  Surgical patients also had improved physical function and had higher satisfaction with their treatment than non-surgical patients.  One of the criticisms of SPORT is that patients with the most severe symptoms could choose surgery immediately rather than being randomized into the study.  This, of course, biases the study in that by eliminating the worst patients from analysis it appears that surgical and non-surgical treatments are more equivalent than they really are.  Ultimately, I interpret SPORT like this: if the patient has mild to moderate symptoms that they are tolerating reasonably well then non-surgical treatments like physical therapy will probably be just fine for them and they can avoid surgery. Patients with severe symptoms, especially if they have weakness (i.e. footdrop), are probably going to recover faster and more fully with surgery.  The speed of recovery is not an insignificant factor for someone who, say, has to miss a lot of work because of his symptoms.  Surgery helps patients like this get back to work and normal life more rapidly. 

Classically, lumbar discectomy (first described in the late 1920s) was performed via long midline incisions.  As we’ve discussed in previous posts these incisions can be quite destructive.  Recently, minimally-invasive techniques were developed to help mitigate some of the problems associated with these midline incisions.  When I perform lumbar discectomy I will make an 18mm incision just off of midline centered over the disc space in question (for an “L4/5” herniation this is the disc space between the 4th and 5th lumbar vertebrae.)  I’ll then use a series of tubular dilators to gently dilate the muscle before a tubular retractor is inserted.  Using an operative microscope, I can perform the entire operation through this small corridor and in turn can avoid damaging the supporting structures of the spine.  Once at the spine I have to drill a small opening through the lamina (a laminotomy) to get into the spinal canal (see figure 1.)  After removing a non-essential ligament, the ligamentum flavum, I’m able to visualize the thecal sac (fluid-filled sac which contains the nerves of the cauda equina) and compressed nerve root.  I then gently move the nerve out of way and can get to the offending piece of disc.  In the case of a herniated disc (a.k.a. a free fragment) the fragment is typically sitting there under the nerve ready to be plucked out.  In the case of a bulging disc (a.k.a. a contained fragment) I have to make a cut in the annulus (an annulotomy) in order to remove the fragments of NP.  After I remove all of the offending pieces of disc I’ll confirm that the nerve is completely decompressed and then will close the incision.  Patients go home immediately after the procedure. Please see the video at the end of the post to see all of these steps during an actual lumbar discectomy. 

SpineLumbar4 5

Figure 1. Orange oval indicates area of bone removed in laminotomy done to gain access to a right L4/5 disc herniation. 

I typically don’t talk about risks of surgeries in this post but it is worth mentioning one risk of lumbar discectomy.  I always tell my patients that for the first two weeks they should do nothing but walk and should avoid any heavy lifting or bending.  This is because for the first few weeks after surgery they are at higher risk of reherniating another disc fragment (I quote a 10% overall risk.)  After the initial fragment is remove the hole in the annulus through which it herniated is still open and takes some time to scar in and close up.  If the patient isn’t careful a new piece can herniate and they’ll be right back where they started.   Surgeons have tried using sutures or small stapling devices to close the annular defect.  Unfortunately this has never been shown to reduce the risk of reherniation so most surgeons leave the defect to heal naturally and advise their patients to be careful in the first few weeks after surgery.  

In our next post we’ll discuss a variation of lumbar discectomy, the far-lateral discectomy.  

Thanks for reading!

J. Alex Thomas, M.D.


Weinstein JN, Tosteson TD, Lurie JD, Tosteson ANA, Hanscom B, Skinner JS, et al.: Surgical vs Nonoperative Treatment for Lumbar Disk Herniation: The Spine Patient Outcomes Research Trial (SPORT): A Randomized Trial. JAMA 296:2441–2450, 2006.

Is my disc bulging, herniated or ruptured?

As I discussed in my last post, when patients read their MRI reports they often become fixated on and perhaps even hysterical about certain terms within the report.  One group of terms that gets patients stirred up like no other pertains to the health of the intervertebral disc (IVD): is the disc bulging, herniated or ruptured

Intervertebral disc cartilage cartilage defect torn cartilage cartilage degeneration sports injury orthopedics arthroscopy cartilage cell implantation chonrocyte implantation

Figure 1: Intervertebral disc with the inner gelatinous nucleus pulposus and outer annulus fibrosus. (Source: http://www.porcpotlas.hu/en/porckorong.html).

First, a herniated disc is the same as a ruptured disc.  For matters of simplicity, I will only use the term “herniated” from this point on in the post.  There are subtle differences between a bulging and a herniated disc as I’ll discuss below.  Ultimately the semantics may not be important as both can cause pain, numbness or weakness when they compress a nearby nerve root. Before we talk about herniated discs, let’s review the anatomy of an IVD (this has also been discussed in a previous post.  The IVD is composed to two primary parts: the inner nucleus pulposus (NP) and the outer annulus fibrosus (AF).  The NP has a soft, gooey consistency (one of my professors in D.C. told patients that it’s like a piece of crab meat and to this day I hesitate for a second before eating a crabcake.)  The AF is taut and strong because of is multiple wound fibrous layers (see figure 1).    As the IVD degenerates the NP loses water content and thus loses its elasticity.  Also, the layers of the AF start to weaken and can begin to develop focal points of weakness called annular tears.  Under repetitive mechanical loads the concentric structure of the IVD is lost and part of the NP begins to escape through damaged layers of AF.  In the cases where the NP is still contained the AF can begin to bulge (the bulging disc.)  In itself, this bulge isn’t problematic unless the bulge becomes prominent enough to start to press on the nerve passing by.  In other cases the annulus rips open and allows a piece of NP to burst out (the ruptured or herniated disc, see figure 2.)  It’s not clear why some patients develop only bulging discs while others completely blow out their NP.  Perhaps these patients are just at different points along the spectrum of degenerative disc disease (DDD)?  On the other hand, I’ve seen several teenage patients with large disc herniations.  Clearly these young patients didn’t progress along the path of AF-weakening DDD prior to herniating a piece of NP.  These unfortunate patients must have some genetic predisposition to more rapid degeneration of the IVD.

Herniated disc netter Google Search

Figure 2: Illustration of herniation of nucleus pulpous (NP) through tear in the annulus fibrosus (AF.)  The herniation causes severe pressure on the nearby nerve root (pink arrow.)

Sometimes a patient can recall lifting something heavy or twisting awkwardly to trigger the disc herniation (these cases almost always involve twisting or bending while carrying a heavy load.)  More commonly, though, the patient just wakes up with leg pain and can’t recall any inciting event that caused the disc herniation.   If this herniation (or bulge) is substantial enough to compress a nearby nerve the patient develops a radiculopathy or nerve root injury.  Usually this is associated with severe pain and perhaps numbness in part of the leg.  In more severe cases the patient may also experience weakness of the muscles supplied by the injured nerve (i.e. a foot drop caused by an L4/5 disc herniation.)  Each nerve root supplies fairly standard muscle groups and sensory distributions in the leg so your surgeon should have an idea of where your problem disc is based on where you say your pain is.  An MRI is usually done to confirm the location of the disc herniation or bulge (see figure 3.)  

Sagittal HNPAxial HNP

Figure 3: Sagittal (left) and axial MRI images illustrating large disc herniation at L5/S1.  Note the large free fragment of NP occupying more than half the diameter of the spinal canal (pink arrow.)  Note how the traversing nerves are being crushed by the fragment (blue arrow.)  

In the vast majority of cases the disc bulge or fragment makes contact with the nerve passing by en route to exiting the spine at the level below (the so-called traversing nerve root.)  This is why a disc herniation at the L4/5 level usually affects the L5 nerve.  In rare cases the piece of disc will herniate in a location on the side of the IVD outside of the spinal canal (a far-lateral disc herniation).  This herniation will affect the exiting nerve root as it exits the spine within the neural foramen (these are also sometimes referred to as foraminal herniations.)  So for a far-lateral L4/5 herniation the nerve that is affected is the L4 nerve.  This may not seem like that big of a deal but don’t tell that to a patient with a far-lateral herniation.  These are typically much more painful than standard herniations because the herniated fragment usually compresses part of the nerve called the ganglion, an important connection center for the nerve that is exquisitely sensitive.  These patients are often crying when I enter the room to meet them.  

The initial treatment for a patient with a herniated disc and radiculopathy should include rest, anti-inflammatories, physical therapy and even epidural steroid injections.  These modalities help provide temporary relief while the body heals itself.  Eventually, with time (and it can take a year or more), the patient will begin to feel better. A common misconception among patients is that the piece of herniated disc “goes back into place” within the IVD.  This isn’t true.  Rather, the body reabsorbs the piece of herniated disc and thus alleviates the pressure on the nerve.  If this doesn’t happen or if the patient desires more rapid relief of his pain, surgery may be considered.  In our next post we’ll discuss the lumbar discectomy, the surgery done to remove a bulging or herniated disc.  

Thank for reading!

J. Alex Thomas, M.D.   

“I have horrible back pain and I was told I have bulging discs. I need surgery.”

I still laugh (internally) when a new patient comes to my office and right off the bat tells me, their neurosurgeon, that they need spinal surgery.  That is a huge red flag for me and typically these are the patients that absolutely do NOT need surgery.  To be fair, most patients are relieved when I explain that they aren’t going to need an operation on their spine.  There are some patients, however, who are legitimately upset with me when I don’t offer surgery!  I get it, they have likely been dealing with severe back pain for quite some time and they’re desperate.  They want a fix.  Ultimately, though, my job is to prevent patients from having a surgery that isn’t going to help them. 

Why does surgery on a bulging disc not fix back pain?  Before we answer this let’s discuss what it means when a disc is bulging.  We’ve talked extensively here at Spinal(con)Fusion about degenerative disc disease.  For quick review, as an intervertebral disc (IVD) ages, a cascade of inflammatory mediators is released that causes degeneration of the disc.  In early phases of disc degeneration the IVD loses water content and becomes dehydrated (this give is a characteristic black appearance on MRI, see figure 1.)  Further inflammatory changes cause a loss of structural integrity of the disc and it starts to collapse resulting in circumferential bulging of the annulus fibrosus-the dreaded bulging disc. So a bulging disc is a disc that is degenerating.  Here’s what’s interesting: this process shouldn’t be painful because the IVD doesn’t have any inherent nerves that carry pain sensation.  It becomes painful because as the disc degenerates the same inflammatory mediators that cause degeneration also recruit new pain fibers to carry pain sensation to the dorsal root ganglion of the nearby nerve.  The degenerating IVD is rewired to perceive pain that it couldn’t perceive before.  After this rewiring process, any movement of the degenerated disc then causes severe pain.    

Bulging black lumbar disc 

Figure 1: T2 MRI shows so-called “black disc” at L5/S1; note the bulging annulus (pink arrow.)  A normal disc is seen at L4/5 with normal water content (as indicated by its brightness) and normal annulus (blue arrow.)

So why not just clean out the degenerated disc and surgically fuse the two vertebral bodies together?  If you eliminate the motion at the degenerated disc then the pain should be relieved right?  I wish it were that simple.  Often when lumbar fusions are done for back pain caused by DDD alone the patient is no better.  We don’t exactly know why immobilizing the diseased motion segment doesn’t relieve the pain but it probably has to do with the way the disc has been rewired to perceive pain.  Once that rewiring occurs the nervous system may learn the pain so that no surgery will ever be able to relieve it.  Unfortunately I think that there are surgeons out there who don’t understand this process and continue to perform lumbar fusions on patients with so-called “black discs.”  I am not one of those surgeons.  In my opinion lumbar fusion surgery should NOT be performed for degenerative disc disease (DDD) alone as often the patient is no better after the procedure.

One caveat: in cases of severe DDD the patient can also develop complete collapse of the disc space, severe arthritis in the corresponding facet joints and Modic changes in the adjacent vertebral bodies (see figure 2.)  These multiple degenerative changes (i.e. not JUST DDD) collectively indicate to me that the entire motion segment has become structurally incompetent.  This structural instability can lead to so-called mechanical back pain.  If a patient has exhausted all conservative measures and is still having severe pain I may offer surgery in these rare cases. 

Modic Changes Rahme R Moussa R The modic vertebral endplate and marrow changes pathologic significance and relation to low back pain and segmental instability of the lumbar spine AJNR Am J Neuroradiol 29 838 42 2008

Figure 2: T1 MRI shows severe DDD at L4/5 with severe disc space collapse (pink arrow) and Modic changes in adjacent vertebral bodies (blue arrows.)  Such severe DDD would also be expected to cause severe arthropathy in the corresponding facet joints. Source: Rahme et al, 2008.

Remember: leg pain is different than back pain.  In our next post we’ll discuss how surgery can be helpful for patients with LEG pain caused by a bulging or herniated disc.

Thanks for reading and Happy Holidays!

J. Alex Thomas, M.D.


1. Rahme R, Moussa R: The modic vertebral endplate and marrow changes: pathologic significance and relation to low back pain and segmental instability of the lumbar spine. AJNR Am J Neuroradiol 29:838–42, 2008.

What is Lumbar Foraminal Stenosis?

In our last post we reviewed how lumbar laminectomy is an effective treatment for central lumbar stenosis causing neurogenic claudication.  Now we turn our attention to foraminal stenosis, or narrowing of the neural foramen.  While lumbar central stenosis causes neurogenic claudication, lumbar foraminal stenosis causes radiculopathy, a.k.a. “a pinched nerve”, and resultant leg pain.

The neural foramen is the opening on the side of the spine through which the exiting nerve root passes.  Its boundaries include the bottom of the pedicle of the vertebral body (VB) above, the back of the intervertebral disc (IVD) in front and the facet joint behind (see figure 1.)  Degenerative changes of these structures can cause narrowing of the foramen, and thus pinching of the exiting nerve, in three main ways.  First, as the IVD degenerates it may bulge or even herniate a piece of disc material into the foramen (a so-called far-lateral disc herniation) causing narrowing of the foramen from the front.  Second, as the facet joint degenerates it can become overgrown with bone spurs causing narrowing of the foramen from behind.  Finally, third, the disc space can become so degenerated that it loses height thereby causing the top and bottom of the foramen to close down on the nerve like the blades of a guillotine (see figure 2.)  Usually the disc height loss occurs symmetrically and both foramina are affected.  Occasionally, however, the height loss only affects one side (this often occurs after someone has had surgery on that side of the spine) resulting in a focal coronal deformity and pain in only one leg (see figure 3.)    (Note: I left out one other cause of foraminal stenosis, spondylolisthesis, which will be discussed in a future post.)


Figure 1: Oblique view of lumbar spine.  Note nerves exiting via the neural foramen bounded by the back of the IVD in the front, the facet joint (FJ) in the back and the pedicles (P) above and below.

Foraminal stenosis

Figure 2: Lateral (side-view) MRI showing nerves exiting foramen.  At the L2/3 level note that the disc space (the boundaries of which are indicated by the yellow lines) is of normal height resulting in normal foraminal volume (outlined in green.)  The black dot in the green circle is the exiting nerve.  At the next level down, the L3/4 level, the disc space is completely collapsed causing severe narrowing (outlined in red.) Note that the exiting nerve, the black dot, is now crushed in the foramen.

 Coronal deformity

Figure 3: Coronal MRI of the lumbar spine demonstrating a focal coronal deformity in which the disc at L3/4 has collapsed to the right (pink arrow.)  This patient had severe right leg pain because of a pinched exiting L3 nerve. (Note that the image is reversed such that the left side of the image is actually the patient’s right side.) 

The first two causes of narrowing discussed above can usually be fixed with a minor outpatient surgical  procedure.  For a example, for a far lateral disc herniation I can usually dock a small tubular retractor on the outside of the neural foramen.  There I find the exiting nerve, move it out of the way and remove the piece of herniated or bulging disc from the foramen.  In the case of an overgrown facet joint a foraminotomy is performed (usually along with a laminectomy and thus the two are sometimes referred to together as a laminoforaminotomy) to decompress the nerve from behind.   The final scenario, disc space height loss from degeneration of the IVD, is a bit more complicated to fix.  In this case the height loss causes circumferential narrowing of the foramen such that a simple foraminotomy usually isn’t sufficient to decompress the nerve.   I could remove the entire facet joint to open up the foramen but this would destabilize the spine and thus would require a spinal fusion (a procedure called a transforaminal interbody fusion, or TLIF, which will be discuss in a later post).  In my opinion the best way to fix foraminal stenosis caused by disc space height loss is to correct the underlying problem: restore disc space height.  This is usually done using a large spacer which is inserted into the disc space as part of an interbody fusion.  There are a variety of ways to achieve this including anterior lumbar interbody fusion (ALIF), extreme lateral interbody fusion (XLIF, which is essentially an ALIF performed via the patient’s flank), TLIF, etc.  All of these procedures achieve the same goal of inserting a spacer into the disc space (note that they all end in -IF for interbody fusion) in order to restore disc space height to decompress the nerve in the foramen (see figure 4).  This is a VERY important take home point here: the difference between direct decompression (i.e. a foraminotomy in which bone is drilled off of the nerve to directly decompress it) versus indirect decompression (in which a spacer in the disc space is used to restore normal disc height and alignment to indirectly decompress the nerve in the foramen.)  Again, in my opinion, if it’s an option I think it’s always best to try to restore the patient’s anatomy to what it once was (i.e. with normal disc height) in order to definitively treat foraminal stenosis.


Figure 4: Image on left shows disc degeneration with loss of disc height; note the compression of the exiting nerve in the foramen.  The image on the right demonstrates restoration of disc height with a large spacer inserted during an XLIF; note the indirect decompression of the exiting nerve.

Thanks for reading!

J. Alex Thomas, M.D.

What is a Lumbar Laminectomy?

In our last post we discussed how lumbar stenosis, or narrowing of the lumbar spinal canal, causes a painful condition called neurogenic claudication.  Patients with this condition report that they can only walk so far or stand for so long before they experience burning pain in their buttocks and legs requiring them to sit and rest.  While all patients should undergo a course of conservative therapy for lumbar stenosis (i.e. physical therapy or epidural steroid injections), ultimately stenosis is a structural problem that is best treated with surgery.  The surgical treatment of lumbar stenosis is a lumbar laminectomy.  

Annotated Netter Lumbar Spine jpgAnnotated normal axial MRI

Figure 1: Image on left demonstrates the elements of the posterior aspect (rear) of the spine.  The pink arrow indicates the lamina, the green arrow indicates the spinous process and the blue arrow indicates the facet joint.  These structures are also seen on the normal axial MRI on the right.  

If you consider the spinal canal to be a bony tunnel, the lamina is the bony roof of the tunnel (see figure 1). The suffix –ectomy is derived from Greek origins meaning “to cut out” (everyone has heard of an appendECTOMY.)  Thus, a laminectomy literally means the cutting out of the lamina.  The lamina itself is rarely the cause of stenosis.  The lamina must be removed, however, so that the surgeon can access the buckled ligamentum flavum and overgrown facet joints that typically cause stenosis.  These structures are then removed in order to decompress the thecal sac (a sac filled with cerebrospinal fluid, CSF, and the nerve roots of the cauda equina) and relieve the stenosis.

Traditionally a laminectomy is done via a long midline incision.  These midline incisions can be quite destructive, however, as they require removal of the spinous process, interspinous ligament and other important structures that support the healthy spinal segments above or below the area of stenosis (see figure 2.)  

Open thoraci lami intraop

Figure 2: Traditional midline incision for laminectomy.  Notice that the spinous process has been removed along with the lamina to expose the thecal sac.  Also note that normal levels above and below must be exposed and may be damaged in the process. 

Rather than using a long midline incision, I perform a minimally-invasive laminectomy using paramedian (off midline) incisions and special tubular retractors to spare the healthy muscles and ligaments of spine (see video 1.)  Once I’ve docked the tubular retractor I use a high-speed drill to drill away the lamina as well as parts of the overgrown facet joints.  This then exposes the underlying ligamentum flavum which is then removed using small instruments called curettes and Kerrison rongeurs.   Removal of the ligamentum flavum is typically adequate to decompress the dura of the thecal sac to relieve the stenosis (see video 2). Occasionally a foraminotomy is also performed to decompress a single nerve root as it leaves the spinal canal (this will be discussed in a later post.)  While the incision is made on one side of the spine I can angle the tubular retractor across midline to undercut the spinous process and decompress the opposite side of the spinal canal as well (see figure 3.)  Thus, in my hands a bilateral two-level laminectomy can be performed through a single 18mm incision.   These tiny incisions allow for less pain, faster recovery and shorter hospital stay (my patients who undergo one- or two-level minimally-invasive laminectomies typically go home the same day) when compared to traditional laminectomy (see figure 4.)

Video 1: Dilation and docking of tubular retractors for lumbar spine surgery.

Bilateral tubular retractor

Figure 3: Using the tubular retractors to decompress both sides of the spinal canal via one incision.  Source: Palmer et al. 

Mendeley Desktop

Figure 4: Pre- (left) and post-operative (right) MRI demonstrating the results of minimally-invasive lumbar laminectomy.  Notice the increase in diameter of the spinal canal after decompression (outlined in blue.)  Source: Alimi et al.

Again, because lumbar stenosis is a structural problem I feel that it is best treated with surgery.  This isn’t just my opinion though: lumbar laminectomy has been proven superior in the literature as a treatment of lumbar stenosis when compared to non-operative treatment.  In a landmark trial published in the New England Journal of Medicine in 2008 Weinstein et al followed 654 patients with lumbar stenosis who were treated with surgery or nonsurgical “usual care” of physical therapy, steroid injection, etc.  The patients who underwent surgery had significant improvement in pain levels and function when compared to nonsurgical patients.  The benefits of surgery were long-lasting and persisted through the two-year follow up period of the study.  Randomized trials such as this one, especially ones that clearly support surgical intervention versus conservative therapy, are almost unheard of in neurosurgery.  Thus, when a patient comes to my office with severe neurogenic claudication caused by lumbar stenosis I won’t waste too much time on conservative therapy before recommending surgery.  

Thanks for reading!
J. Alex Thomas, M.D.

Video 2: Intraoperative video of lumbar laminectomy (with foraminotomy.)


Alimi, M., Hofstetter, C. P., Pyo, S. Y., & Paulo, D. (2015). Minimally invasive laminectomy for lumbar spinal stenosis in patients with and without preoperative spondylolisthesis: clinical outcome and reoperation rates. Journal of Neurosurgery. Spine, 22(April), 339–352. 

Palmer, S., & Davison, L. (2012). Minimally invasive surgical treatment of lumbar spinal stenosis: Two-year follow-up in 54 patients. Surgical Neurology International.

Weinstein, J. N., Tosteson, T. D., Lurie, J. D., Tosteson, A. N. a, Blood, E., Hanscom, B., … An, H. (2008). Surgical versus nonsurgical therapy for lumbar spinal stenosis. The SPORT Authors. The New England Journal of Medicine, 358(8), 794–810.