The Truth About Facet Cysts

One very painful degenerative condition of the spine that I commonly see in my clinic is the facet cyst.   These are also referred to as synovial cysts as they originate from the synovium (lubricating tissue that lines the opposing surfaces of a joint) of the spinal facet joints.  While facet cysts theoretically can originate at any level of the spine, they most commonly occur in the lower lumbar spine (i.e. L4/5 and L5/S1.)   These cysts typically grow from the medial (inner) aspect of the joint were they then begin to compress the traversing nerve root as it passes nearby (see figure 1.)  This compression can be quite severe and, when coupled with the movement of the joint, can lead to excruciating pain (at the time of surgery I’ll often see a dent on the nerve root from the severe pressure of the cyst.)  After far lateral disc herniations, this is probably the most painful non-traumatic pathology that I encounter in my clinic. 

 Sagittal facet cystAxial facet cyst

Figure 1: Sagittal (left) and axial MRI showing large facet cyst (red arrows) emanating from the left L4/5 facet joint.  Note how the cyst originates from the medial (inner) aspect of the joint and severely narrows the right side of the spinal canal.)  

First and foremost, facet cysts are not cancerous. Many patients equate the term “cyst” with cancer so the first thing they want to know is whether or not they have cancer in their spine (reason #146 NOT to read your MRI reports because those terms you don’t understand will FREAK YOU OUT unnecessarily.)   Facet cysts are benign and simply indicate advanced arthritis of the joint from which they emanate.

The treatment of facet cysts is a bit controversial and can provoke colorful discussions at meetings of spine surgeons.  Most of the controversy stems from the question of how aggressive to be with initial surgical treatment of the cysts.  More on that later.   For now, let’s review the treatment options of facet cysts here:

  1. Watchful waiting.  This usually isn’t a good option for patients.  First of all, most patients with this condition are in so much pain when they walk in that they want surgery yesterday.  If I even begin to discuss waiting another 6-8 weeks for spontaneous resolution of their pain they look at me like I’m crazy and immediately begin looking for another doctor to provide another opinion.  The problem with watchful waiting is that unlike a herniated disc fragment which can be reabsorbed by the body, facet cysts typically don’t involute spontaneously. To be fair, though, I have seen cases where the compressed nerve becomes accustomed to the irritation and becomes less painful over time without intervention.  Usually, however, an invasive treatment is needed to take care of the problem.
  2. Interventional pain management. Here’s one of those areas of controversy; even my partner and I don’t always agree on the utility of this treatment for facet cysts.  The thought is that a pain management physician can guide a needle to the cyst using fluoroscopic guidance and then aspirate the fluid within the cyst to decompress it and thus take the pressure off the adjacent nerve.  There are two problems with this approach in my opinion.  First, if you were to come into the OR and watch me resect one of these cysts you’d see that 90% of the time the cyst is filled with a thick gelatinous substance rather than a thin fluid that can be aspirated.  It’s easy to see how this needle aspiration could fail.  Second, cysts that are simply aspirated will often recur.  Without removing the cyst wall the underlying structure of the cyst remains, only to fill up with fluid again later.  Now, I never discourage a patient from trying cyst aspiration or an epidural steroid injection prior to committing to surgery.  I certainly have seen it work.  It’s just important to understand that aspirating the cyst either isn’t possible or doesn’t permanently ablate the cyst so often any symptom improvement achieved with interventional pain management is short lived.
  3. Surgery.  When watchful waiting and/or interventional pain management treatments have been tried unsuccessfully (or if the patient is just too miserable), surgery should be considered.  There is some debate on how aggressive that surgical treatment should be right off the bat, though.  Some surgeons will jump straight to recommending a fusion for a patient with a facet cyst.  The thought is that the presence of a facet cyst suggests that the facet joint is structurally incompetent and that without a fusion these cysts will only recur.  There is some truth to this.  I quote up to a 20-30% rate of recurrence for facet cysts without fusion.  Typically, though, I like to avoid a fusion initially if possible.  Thus, my algorithm for the surgical treatment of facet cysts is as follows (see flow chart):
      1. MRI shows facet cyst that correlates with patient’s pain.  Patient has failed conservative management.
      2. If the facet cyst occurs in the setting of a spondylolisthesis (which they often do) I’ll usually offer a fusion right away (XLIF at L4/5 and above, ALIF at L5/S1.) 
      3. If there is no concurrent spondylolisthesis I’ll check flexion-extension Xrays to evaluate for instability (I may also just do this for the patient WITH spondylolisthesis if for some reason I’m trying to spare them a fusion.)  If the motion segment in question is unstable then the patient gets a fusion. If there is no instability I’ll do a minimally-invasive laminectomy to resect the cyst.
      4. If the cyst recurs after laminectomy the patient gets a fusion. 
Facet cyst algorigth

Lastly, and here’s where it gets really controversial, whenever I do an XLIF or ALIF on a patient with a facet cyst I no longer directly resect the facet cyst.  I rely completely on indirect decompression to take care of the cyst.  By using the appropriately sized spacer to restore disc height and correct spondylolisthesis, the facet cyst is essentially stretched out so that no longer compresses the adjacent nerve (see figure 2.)  It’s also believed that by eliminating the motion at the facet joint with a fusion the facet cyst can then spontaneously resolve.  It’s like magic.  This always makes the patient nervous though.  They always want to know why I’m not cutting that painful cyst out to be sure it’s off the nerve.  What I tell them is that I know, after looking the data on all my patients, that in just about every case the height restoration provided by the spacer is enough to decompress the nerve (there’s less than a 5% chance of failing indirect decompression in our experience.)  Also, these cysts are usually densely adherent to the underlying nerve and dura.  Dissecting these cysts off of the dura can be quite treacherous and the rate of dural tear and cerebrospinal fluid (CSF) leak in these cases is not insignificant (5-10% in our hands).  Thus, why would I subject the patient to the risk of CSF leak (not to mention the risk of spending the extra time under anesthesia that it takes to do the laminectomy) that is greater than the risk of them failing indirect decompression?  As we’ve discussed previously: believe in indirect decompression!  


Figure 2: Preoperative (left) and postoperative MRI images showing a patient with a left L4/5 facet cyst (red arrow) and spondylolisthesis that was treated with XLIF and percutaneous pedicle screw fixation (NO direct cyst resection.)  Patient’s leg pain was relieved immediately after surgery.  Note on the postop MRI (taken about 3 months after surgery) that the facet cyst has disappeared.

Thanks for reading!

J. Alex Thomas, M.D.

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:

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. 

What is Lumbar Stenosis?

Ok, we’ve made it through our discussion of various common neck problems and we will now move our discussion on to pathology of the lumbar spine (a.k.a. the low back.)  The first lumbar spine problem we’ll discuss is lumbar stenosis which is just a fancy medical term for narrowing of the diameter of the spinal canal.    Stenosis can occur at any level in the spine (i.e. in the neck stenosis can cause radicular pain or myelopathy) but in this post we’ll focus on stenosis of the lumbar spine where it is most common (especially in the retired patients who live here in the coastal community where I practice.)  Finally, stenosis can be central or foraminal.  In this post I will focus primarily on central stenosis and I will discuss foraminal stenosis in an upcoming post.

Several times a day in clinic a new patient will present saying that she can only walk a certain distance before she develops severe burning pain in her buttocks and legs.  When she stops and sits down to rest the pain will subside and then she can start walking again.  Down here in eastern North Carolina the patients usually rates themselves by which aisle they can reach in Walmart before they develop pain.  This activity-related pain is called neurogenic claudication and any patient who’s ever had it will tell you that it can be crippling.  I won’t bore you with the specifics of the microanatomy of the blood supply of the nerves of the cauda equina (the bundle of nerve roots at the terminus of the spine after the spinal cord ends at around T12/L1, see figure 1.)  Basically what happens, though, is the patient develops narrowing of the spinal canal because of a variety of degenerative factors (see below.)  This narrowing causes worsening compression of the nerve roots which in turn causes impaired circulation in the microscopic (read: very sensitive to compression) blood vessels that supply the nerve.  This impaired circulation is more apparent during exertion as the starved nerves demand more oxygen and nutrients, hence the searing pain when the patient walks for any distance.

Normal lumbar mri  1Sagittal T2 Lumbar Stenosis jpg

Figure 1: Normal sagittal (side view) MRI of lumbar spine on left and sagittal MRI indicating severe stenosis.  The intervertebral disc (IVD), ligamentum flavum (LF), facet joint (FJ) and cauda equina (CE) are all marked on the normal MRI.  The MRI on the right demonstrates the causes of lumbar stenosis: bulging of the IVD (pink arrow) and ligamentous and facet hypertrophy (yellow arrow).  Clumping of the nerves of the cauda equina (blue arrow) indicates a particularly severe case.

Ax T2 frFSE  5  3 2Ax T2 Lumbar Stenosis jpg

Figure 2: Normal axial MRI of lumbar spine on left and MRI demonstrating severe stenosis on right.  Intervertebral disc (IVD), facet joint (FJ) and ligamentum flavum (LF) are labeled in red on the normal MRI.  The diameter of the spinal canal is indicated in yellow.  Notice on the image on the left how the spinal canal is widely patent (the nerves of the cauda equina are visible within.)  The image on the right demonstrates severe narrowing of the diameter of the spinal canal caused primarily by facet and ligamentous hypertrophy.

So why does the narrowing of the spinal canal occur?  In order to understand this, it’s useful to think of the spinal canal as having four distinct sides (see figure 2, left): in the front of the canal is the intervertebral disc (IVD), the sides of the canal are formed by the facet joints and the back of the canal is formed by the ligamentum flavum.  Stenosis can be caused by an acute change in one of these structures (like a large herniated disc which we’ll discuss in a future post.)  More often, though, stenosis is causes by gradual degeneration of all of these structures in unison.  First, as the IVD dries out and degenerates it collapses and bulges.  As the disc loses its effectiveness as a shock absorber the facet joints then have to absorb more motion.  The facet joint is just like any other joint in the body in that with enough wear and tear it will develop arthritis and become overgrown with bone spurs.  The morphology of the facet joint becomes less compressive as the patient bends forward which is why patients with neurogenic claudication will tell me that they feel better when shopping for groceries when they can bend forward over the shopping cart (or buggy if you’re from The South.)  Finally, we see ligamentous hypertrophy in which the ligamentum flavum thickens.  This thickening is due to a combination of buckling from disc space height loss and fibrosis, or scarring.  Slowly but surely as the patient ages, these factors contribute collectively to the development of lumbar stenosis.

The degenerative changes that cause severe stenosis such as that seen on the MRI in the figures take years to develop.  Stenosis is a structural problem that requires a structural solution.  While physical therapy and core strengthening are excellent for the overall health of your back, no amount of therapy is going to reverse stenosis.  Epidural steroids may provide excellent relief of the pain associated with stenosis.  Unfortunately this relief is usually only temporary as injections don’t address the underlying structural problem of stenosis.  The best treatment for lumbar stenosis is surgery.  This surgery is often done on an outpatient basis and has perhaps the best outcomes of any procedure that I perform.  In the next post we’ll discuss the surgical treatment of lumbar stenosis: lumbar laminectomy.

Thanks for reading!

J. Alex Thomas, M.D.

What is Adjacent Segment Degeneration?

At least once a week a patient will say to me: “I’m not getting spinal surgery because I heard that once you have spinal surgery your spine is never the same and you’ll only need more spinal surgery!”  Well, to some extent there is some truth to this statement.  Whenever a patient undergoes spinal surgery, a well-known long-term side effect is that the level above or below the surgery can degenerate.  This is called adjacent segment degeneration or ASD.  

Why does ASD happen?  ASD can occur whenever the normal anatomy of the spine is disrupted and as a result, a segment of the spine has to handle more stress than it’s used to. This can happen after even the most minor spinal procedure but more commonly happens after fusions. (see figure 1)  Any length of spinal fusion can lead to ASD.  However, there has been some evidence to suggest that the more levels fused, the higher the risk of ASD.  This is because the longer fused segment acts as a longer lever arm and causes more stress on the disc and facet joints above or below the segment fused.  Of course, sometimes long fusion segments are mandatory (as in deformity or trauma surgery) but whenever possible, the number of levels fused should be minimized. 


Figure 1: Image on left shows ASD at L4/5 after an open fusion at L5/S1. The L4/5 disc is now so degenerated that it allows the L4 body to slip forward in relation to L5 (a condition known as spondylolisthesis).  The image on the right is of a patient with severe ASD at L2/3 several years after she underwent an open L3-5 laminectomy.   

 There is some controversy as to what actually causes ASD.  Here’s what we know for certain: ASD is a common long-term complication of spinal fusions. If you look at the rates of ASD across the literature, the rate of symptomatic ASD (i.e. that requiring additional surgery) after anterior cervical discectomy and fusion, or ACDF, is anywhere from 9-25% (Yang et al, 2012).  In the lumbar spine, the rate of symptomatic ASD after fusion is as high as 30% (Cheh et al, 2007). Clearly any patient who undergoes a spinal fusion has to accept the risk that at some point later in their life they may need more spinal surgery.  

ASD (and this is where it gets controversial) may also be seen more commonly after traditional, open spinal surgery vs. after minimally-invasive surgery.  As you have seen in some of my previous posts, open spinal surgery can be quite destructive.  These procedures utilize long midline incisions that strip the supporting muscles and ligaments off of the spine.  I equate these muscles and ligaments to the cables of a suspension bridge: if you disrupt these structures at one level you affect the functional stability at multiple levels.  Minimally-invasive procedures in spinal surgery are still fairly new and only recently has long-term data on these procedures become available.  One recent study (Park et al, 2011) followed patients who underwent minimally-invasive lumbar fusions for an average of 36 months and only 2 out of 66 (3%) patients developed ASD.  Compare that to the 30% rate of ASD for open fusions.  Recall that minimally-invasive procedures spare the normal supporting structures of the spine and theoretically prevent the “collateral damage” that leads the ASD.  In my opinion the Park study is just the first of many studies that will prove that minimally-invasive procedures have a much lower rate of ASD when compared to open spinal procedures.