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.

XLIF: explained

In this post I’m going to give you a step-by-step description of the extreme lateral interbody fusion (XLIF) procedure from patient positioning to skin closure.  While I will occasionally do XLIF as a standalone procedure (when only a spacer is inserted without any posterior instrumentation inserted at the back of the spine) I almost always insert pedicle screws after the XLIF is complete.  The information about XLIF is quite detailed and thus the post gets quite long so I’ll explain the pedicle screw portion of the case in a future post. Keep in mind that this is how I do XLIF in my OR for a standard one-level case.  While the general steps of the procedure are the same no matter where you get your XLIF, some variation may occur so if your surgeon does it a bit differently that doesn’t mean he’s doing it incorrectly. My hope is that this explanation will be helpful to you if you’re considering the procedure or if you’ve already decided to undergo XLIF and want to know what exactly is going to happen to you while you’re asleep.  This is a long, detailed post so hang in there.

Step 1: Induction of anesthesia and placement of neuromonitoring leads.  After you’re brought into the OR you’ll slide off your bed and over to the OR table.  The people who typically will be in the room with you will be myself, my physician assistant Jack, an OR nurse, a surgical technician (the person who handles all of the surgical instruments), the anesthesiologist or nurse anesthetist (CRNA), an X-ray technician (to run the fluoroscopy machine called a C-arm) and a representative from the company who manufactures the spacers and screws that I’ll implant in your spine.  Once you’re on the OR table you’ll be put to sleep and then intubated (when a breathing tube is inserted into your windpipe so that a machine can breathe for your during surgery.)  An extra IV and a Foley catheter (inserted into your bladder to collect urine) may be inserted as well.   After all of this is done we will then insert small needle electrodes into the major muscles of your legs (see figure 1.)  These electrodes are then connected to a computer system that then monitors the status of the nerve signals to these muscles during surgery.  As we’ll discuss in a later post, one of the major complications that may occur during XLIF is an injury to one of the nerves of the lumbar plexus that provides motor and sensory function to your legs.  These electrodes allow me to monitor the function of these muscles, and thus the nerves of the lumbar plexus, so that I know I’m not injuring any of them.  More on this later.  (Some patients occasionally ask me why there are little blood spots on their legs after surgery…the placement of these electrodes is why.)

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Figure 1: small needle electrodes are inserted into the major muscle groups of the legs to allow for monitoring of the nerves of the lumbar plexus.

Step 2: Patient positioning and taping.  Now that you’re all hooked up to the anesthesia machine and the neuromonitoring system we’ll put you into the position that you’ll be in for the entirety of the case.  Several of us will all grab hold of the sheet you’re laying on and then will put you into the lateral decubitus position which basically is how you’d look if you were asleep on your side on a park bench.  Unless there’s something unusual about your anatomy I’ll position you RIGHT side up so that your XLIF incision will be on your RIGHT flank (regardless of which side your leg pain is worse on.)  XLIF surgeons will debate about which side up is best for the procedure.  In my hands I think that right side up is safer (honestly, because that’s what I’m familiar with after hundreds of XLIFs) but a lot of surgeons go left side up because that’s the way that XLIF is classically taught.   In my opinion it really doesn’t matter which side is up as long as it’s the side that your surgeon is comfortable with.  Even though you’re on a heavily padded OR table we’ll pad critical pressure points (like your armpit and knees) so that you don’t get pressure injuries during surgery.  We’ll then flex your knees and hips slightly (to relax the psoas muscle and the nerves of the lumbar plexus within so that they’re easier to navigate during the docking of the retractor.  See below.) and then secure you to the table with tape.  It’s lot of tape actually (see figure 2.)  It’s critical that I maintain a perfectly perpendicular trajectory to the side of spine during the XLIF procedure.  If you’re not secured to the table well enough you may slowly roll to one side or the other which may put you at risk when suddenly you’re not in the position that I expect you to be in. The multiple passes of tape across your hips, legs and chest prevent this rolling.  Of course we’ll also confirm throughout the case that you’re still positioned correctly by checking an image with the C-arm machine. 

IMG 3947\IMG 3959Figure 2: after positioning the patient with the right side up, we then secure the patient to the OR table with multiple passes of 3-inch tape.  Lots of tape.  

Step 3: X-ray confirmation and patient marking. Now that you’re positioned on the OR table with your left side down and your right side up I’ll then obtain an image of your spine using the C-arm machine and then plan an incision on your right flank centered over the level of the spine that we’re treating.  First we’ll shoot an AP X-ray shot (front to back) with the C-arm to confirm that your spine is not rotated at all.  Again I want to be certain that I’m approaching your spine at a 90-degree angle (directly lateral) so we’ll correct any rotation we see on that first X-ray.  Once we’ve ensured that you’re not rotated I’ll then bring the C-arm to a lateral view (side view) to localize the correct level where we’re working and then mark the boundaries of the disc space.  If we’re working at L4/5 for example (where I do in the vast majority of cases) I’ll mark the endplates of the L4 and L5 vertebral bodies as well as the front and back boundaries of the disc space.  I’ll then plan a 3cm incision centered over this marked disc space (see figure 3.)  I’ll then box in the area of the incision, as well as an area over your lumbar area where I’ll eventually make small incisions for the screws, with some preliminary sterile sticky dressings called “10-10s” (see figure 4.)

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Figure 3: Marking the boundaries of the disc space at L4/5.  Note the C-arm monitor in the background. 

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Figure 4: The boundaries of the disc space between the L4 and L5 vertebral bodies.  I’ll typically center my incision right over the disc space. 

Step 4: Patient prepping, draping and time out.  After you’re positioned and we’ve planned our incisions the OR nurse will then use iodine solutions to “scrub and paint” any areas of skin boxed in by the 10-10s (see figure 5.)  During this time I’m scrubbing my own hands and will come in to get my surgical gown and gloves on.  After this Jack (my PA) and I will cover you in drapes so that only your flank and lumbar areas are exposed.  I’m draping not just for the XLIF but also for the placement of pedicle screws (see figure 6.)  At this time we’ll also check to be certain that you have “4 twitches” which indicates how well your muscles respond to stimulus.  We don’t want you to have any muscle relaxing agent on board here so that it doesn’t interfere with the accuracy of the neuromonitoring system.  After all this is done and prior to making an incision we’ll do the OR time out where the entire team confirms that we’ve got everything in the OR ready to do the case correctly (including confirming the identity of the patient as well as the correct level/side of the procedure.). You can never be too careful.

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Figure 5: the OR nurse does a “scrub and paint” prep to remove any skin bacteria or other contaminants. 

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Figure 6: all set up and waiting for the OR time out.

Step 5: Incision and exposure.  After the time out we’re ready to start the case.  The flank incision is made first with the scalpel and then carried down through the underlying fat with Bovie cautery.  I’ll come down with the Bovie until I arrive at the external layer of fascia enveloping the muscular layers of the abdominal wall (the three layers are: external oblique, internal oblique and transversalis muscles, see figure 7). I carefully incise the external fascial layer and then use the scissors to bluntly dissect (not cut) through the muscular walls until I can pop through the inner layer of fascia and into the retroperitoneal space.  This is the space behind the cavity containing your abdominal contents.  I’ll confirm that I’m within the retroperitoneum by palpating the surface of the psoas muscle-it has a very distinctive feel as it rolls under my fingertip. Once I’m certain I’m where I’m supposed to be, in the retroperitoneum and on the surface of the psoas, I’ll proceed with traversing the psoas.

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Figure 7: right flank incision showing the subcutaneous fat, the external fascia of the muscular abdominal wall and the oblique muscles within. 

Step 6: Dilation of psoas muscle and docking of XLIF retractor. Once I can feel the surface of the psoas muscle I’ll take the first of a series of 3 tubular dilators and place it on the surface of the muscle at the level of the spine that I’m targeting (see figure 8.)  Remember those monitoring leads we inserted into the leg muscles prior to the case?  This is where I’m going to need them.  The dilators are electrically stimulated (via a clip at the top) in such a way that they emit a small directional electrical charge.  Thus, when I pass the dilator through the psoas en route to the side of the disc space I will rotate the dilator in order to send out a directional electrical charge to each quadrant of the working area to hunt for the nerves of the lumbar plexus.  If the tip of the dilator is close to a nerve it will stimulate the nerve at a certain threshold and fire the muscles in the leg innervated by that nerve.    My goal is to land on the disc space in front of the nerves of the lumbar plexus so I only want to see stimulation when I’m stimulating towards the back of the patient (see figure 9.)  If I see stimulation when I have the tip of the dilator aiming towards the front of the patient then I know I’m not in the right place.  I know this is complicated and probably more than you need to know for your XLIF.  In my opinion, though, this process of traversing the psoas muscle with the dilators and using them to locate the nerves of the lumbar plexus is the crux of the procedure.  If done properly this makes XLIF one of the safest fusion procedures around and reduces your chance of a nerve injury to near zero. 

Once I’m happy with where I’ve placed the first dilator I’ll insert a K-wire through the dilator and into the disc space to anchor it in place (see figure 10.)  I’ll then use sequentially larger tubular dilators, also stimulated, to gently dilate the psoas muscle.  Once the dilation is complete I’ll insert the specialized MaXcess retractor over the dilators and attach it to a special arm that’s attached to the bed.  I remove the dilators and then insert light sources to illuminate the working area.  Lastly, I’ll use a handheld nerve stimulator to be sure there are no nerves traversing the working area that were somehow missed during the initial dilation.  Once I know the area is free of nerves I’ll insert a shim through the back retractor blade and into the disc space.  This secures the retractor to the disc space so that it won’t shift during the procedure (and also prevents any nerves of the lumbar plexus from creeping into the working area.)  Now the retractor is anchored to the spine, the working area is illuminated and free of any nerves and I’m ready to go (see figure 11.)  Of note, the back blade of the retractor (which should have the nerves of the plexus safely behind it) can also be stimulated.  Throughout the remainder of the case I’ll periodically stimulate this blade to check the health of the nerves behind it.  If it’s taking more and more stimulation to fire the nerve I can assume that the nerve is at risk of injury and I’ll take steps to mitigate these risks (like move more quickly or reposition the retractor.)  The point is that I’m constantly thinking about the nerves of the lumbar plexus for the entire time that the retractor is in place within the psoas muscle. 

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Figure 8: image on left shows insertion of the first of a series of 3 tubular dilators.  Note the cable attached to the dilator.  The tip of the dilator emits a directional electric charge that allows me to search for the nerves of the lumbar plexus.  Image on right shows the tip of the retractor on the side of the spine in front of the nerves of the lumbar plexus.  As the tip gets closer to a motor nerve the monitoring system will turn from green to yellow to red to indicate the proximity of the dilator to the nerve.  

Mendeley Desktop

Figure 9: the nerves of the lumbar plexus shown on the left side of the spine (this patient, unlike the patient in our images, is LEFT side up with the front of the spine at the top of the image and the head of the patient to the right.)  The goal is to dock IN FRONT of the motor nerves of the plexus, particularly the femoral nerve (see the small red circle on the L4/5 disc space.)  Note that the sensory nerves of the plexus, the genitofemoral nerve, the iliohypogastric nerve and the ilioinguinal nerve run on the surface of the psoas muscle or in the soft tissue of the retroperitoneal space and thus aren’t usually at risk while docking on the side of the disc space. (Source: Uribe et al, 2010)

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Figure 10: C-arm image showing the first dilator in place on the center of the L4/5 disc space.  At about this “50-yard line” of the disc space I’m usually far enough forward to be in front of the lumbar plexus.  It’s tough to see but a K-wire has also been inserted into the disc to hold the dilator in place.

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Figure 11: image on left shows C-arm image showing retractor docked over the L4/5 disc space.  A shim is inserted into the disc space to anchor the retractor in place and prevent any migration of the nerves of the lumbar plexus into the working area. Image on right is an illustration of what is seen on the C-arm image (courtesy of Nuvasive.)

Step 7: Discectomy and preparation of disc space.  Now I can look down the retractor at the side of the disc space.  I use surgical loupes to magnify the working area at the base of the retractor (see figure 12.)  I know that the area is free of any nerves so I can start to remove the disc without fear of injury to the nerves of the plexus.  I cut out the annulus of the disc space and then use a “box-cutter” to traverse the disc space and release the contralateral annulus (see figure 13.)  This contralateral release is key to getting maximum height restoration with your spacer later. I’ll then use curettes and other scrapers to clean all of the disc material out of the disc space and off of the vertebral endplates.  This is another key step.  If the endplates aren’t sufficiently debrided of disc material then new bony growth into the spacer and bone graft won’t occur.  Bad disc preparation=no fusion! 

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Figure 12: XLIF is done through a narrow, minimally-invasive corridor so I have to use surgical loupes to magnify the working area at the base of retractor.  

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Figure 13: A “box-cutter” is passed from right-to-left (left-to-right on this AP, or front-view, C-arm image) through the disc space to remove the bulk of the disc material and also to release the contralateral annulus of the disc space (notice how the cutter is protruding just a bit outside the left side of the disc space.)  This contralateral release is critical for getting adequate height restoration from the inserted spacer.

Step 8: Sizing of disc space and insertion of spacer. Ok so now the disc space is completely cleaned out.  I’m ready to insert the properly sized spacer (also known as a cage.)  We will first insert a trial to make sure the spacer is going to sit in the proper location within the disc space (see figure 14.)  I’ve already done measurements on preoperative images so I usually already know what size spacer I’m going to need but if there’s any question the appearance of the trial within the disc space (on the fluoroscopic image) will help me select the spacer size.  Once we’ve decided on the correct spacer height, length, width and lordosis (angulation) we’ll pack it with graft material and get ready to insert it into the prepared disc space.  I could spend an entire post talking about various graft materials.  Usually I use a product called Osteocel which is basically cadaveric bone fragments prepared in a way such that it contains stem cells to promote bone growth (see figure 15.)  I’ll then attach the spacer to an inserter and gently tap it into the disc space with a mallet.  I’ll check the final positioning of the spacer with front and side view fluoroscopic images (see figure 16.) If I’m happy with the placement of the spacer I’ll irrigate, look for any bleeding and then collapse and remove the retractor.  Generally the entire process, from initial docking of the retractor to the time I collapse and remove the retractor takes 10-15 minutes in my hands (see figure 17.)  There is very clear evidence in the literature that suggests that the longer that retractor is place in the psoas the higher the risk of injury to the lumbar plexus.  Speed matters in XLIF! 

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Figure 14: a trial spacer is inserted into the disc space to ensure  a) that the spacer will sit in a good position in the disc space, and b) that we’ve selected the spacer with the appropriate height, width, length and lordosis (usually we do this in advance based on the patient’s MRI but we double check here.)

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Figure 15: a PEEK spacer loaded with Osteocel and ready for insertion. PEEK isn’t visible on X-ray so small metal markers are embedded in the spacer to allow for visualization (notice the small metal bumps on the surface of the spacer.)

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Figure 16: AP C-arm image showing spacer in place, still attached to inserter.  Note the metal markers (black lines) that indicate the outer boundaries as well as the center of the spacer.

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Figure 17: intraoperative view looking down the retractor at spacer in its final position within the disc space.

Step 9: Drain placement and closure. After I remove the retractor I place a small drain into the psoas muscle where I was working.  This is an unusual step that not many surgeons do.  One minor complication that can occur after XLIF is numbness, tingling and even burning on the front of the thigh on the side of the access for XLIF.  Usually this is minor but in some cases it can be quite bothersome and can persist for several months.  This complication usually occurs as a result of stretching of one of the sensory nerves of the lumbar plexus.  When we looked at our data for 50 patients who didn’t have a drain placed versus 50 patients who did have a drain placed, we found that the patients with a drain had a 10x reduction in the incidence of postoperative thigh sensory disturbances (from 40% to 4%!)  Ever since we discovered this in our data we’ve always used drains in the psoas after XLIF.  After the drain is placed (which is removed the next day before the patient goes home) we’ll close the fascia of the muscular abdominal wall and then the dermis (the layer just below the skin) with absorbable sutures.  The skin is closed with small adhesive strips (see figure 18.) 

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Figure 18: we insert a small Blake drain into the psoas muscle where we were working to drain any residual blood and hopefully prevent any postoperative thigh symptoms.  

Step 10: Posterior instrumentation and fusion.  After the spacers are inserted we’ll place bilateral pedicle screws and perform the posterolateral bony fusion.  I think I’ve probably already exhausted you with the very detailed discussion above so I’m going to talk about this second half of the procedure in the next post.  It is worth noting that the two things we typically DON’T do at this point (which most other lateral access surgeons still do) are: 1) perform a laminectomy to directly decompress stenosis; and 2) flip the patient prone to place the pedicle screws.  First, remember I told you about the power of indirect decompression.  Now that you’re a believer in indirect decompression you know that a direct laminectomy is almost never necessary after XLIF.  I know from looking at my XLIF data over the past 5 years that (as of the posting of this post) out of 253 XLIF patients since I started keeping detailed records in 2014 only 3 have had to return to the OR for failure of indirect decompression and none have had to go back in the past two years.  That’s 1.2%.  Why would I subject you to nearly an extra hour of anesthesia time, not to mention the risks of me drilling around your nerve roots (my spinal fluid leak rate is probably 1-2% although I’ve never formally calculated it) when 99% of my patients don’t need direct decompression after XLIF??  Believe in indirect decompression! 

Regarding the placement of pedicle screws, the standard method is to finish the XLIF, take the drapes down, flip the patient face down onto another OR table and then re-prep and drape.  That takes at least 45 minutes with all hands on deck!  Instead, we’ve pioneered a strategy of lateral single-position surgery (LSPS) in which we keep the patient in the lateral position and place the screws that way (see figure 19.)  This has led to massive increases in our OR efficiency that I’m certain will translate into better patient outcomes (I’m involved in several studies to prove this in the literature.)  It seems obvious to just place screws in the lateral position after XLIF but believe it or not a lot of surgeons still feel like they have to reposition the patient prone to place screws safely.  Slowly but surely, through surgeon education and by publishing our data, we’re starting to convince surgeons of the value of LSPS.  More on this in future posts.

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Figure 19: placing pedicle screw fixation (yes, using a power drill) with the patient in the lateral decubitus position (patient is right side up with head towards the left of the image.)  By avoiding having to flip the patient prone and also by allowing members of the surgical team to work concurrently (notice my assistant Jack working in the front of the patient) this strategy of lateral single position surgery saves a tremendous amount of time under anesthesia for the patient. This likely translates into improved patient outcomes. 


Figure 20: pre- and post-operative images of a patient who underwent an L4/5 XLIF and percutaneous pedicle screw fixation for a spondylolisthesis.  This patient had complete resolution of their preoperative symptoms after surgery and went home after less than 24 hours in the hospital. 

Thanks for reading!  I know it was a detailed one!  I just want you to be educated as possible about XLIF if you’re considering it yourself!

J. Alex Thomas, M.D.


1. Uribe JS, Vale FL, Dakwar E: Electromyographic Monitoring and Its Anatomical Implications in Minimally Invasive Spine Surgery. 35:368–374, 2010.

The Big IF: an introduction to the Extreme Lateral Interbody Fusion (XLIF)

Ok up until this point we’ve discussed why a spinal fusion is performed and what makes for an ideal spinal fusion.  We’ve talked about the importance of minimally-invasive techniques to address pathology without the collateral damage of traditional open midline incisions.  We’ve also talked about the importance of large intervertebral spacers to a) achieve fusion, b) restore normal lordosis and c) to achieve indirect decompression of the neural elements.  Lastly, we’ve discussed the importance of restoration of lordosis to a) maximize the chances of a good clinical outcome and b) to prevent adjacent segment degeneration.  In my opinion, the one technique for lumbar fusion that best achieves all of the above goals is the Extreme Lateral Interbody Fusion (XLIF).  First developed in the mid 2000s, this technique allows for the placement of a very large intervertebral spacer at the front of the spine via a small, minimally-invasive incision on the patient’s flank.  

We’re going to talk about the specific steps of XLIF in the next post.  For now, I’d like to just focus on why I think that XLIF is superior to other fusion techniques.  In brief: XLIF is the procedure that allows for the largest possible intervertebral spacer to be inserted via the smallest incision (see figure 1).  There are several ways to achieve an interbody fusion of the spine (these procedures have the suffix -IF as in XLIF, ALIF, OLIF, TLIF, PLIF, etc.) These techniques can generally be thought of as either anterior (XLIF, ALIF, OLIF) or posterior (TLIF, PLIF) approaches.  Believe it or not, spine surgeons still fiercely debate which way is better.  Those in the posterior approach camp say that, through one incision on the patient’s back, they can directly decompress nerves (via laminectomy) and then insert spacers into the disc space and place pedicle screws.  Part of the debate here is whether or not a direct decompression of the nerves is even needed.  I personally believe that indirect decompression is all you need and you can spare the patient the risk and morbidity of removing bone off of compressed nerves.  (I don’t just believe this; I’ve proven it to myself with data from over 300 cases which show that indirect decompression works in greater than 98% of cases.)  This is very controversial though and some surgeons aren’t going to be satisfied until they’ve performed a complete bony decompression and have seen the nerves floating free and decompressed. 

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Figure 1: XLIF spacers have the most “bang for the buck” when comparing the size of the spacer with the length of the incision necessary to insert it.

Here’s the problem with posterior approaches though.  Remember that the disc space, where intervertebral spacers are placed, is at the front of the spine.  In order to place spacers there during posterior fusions the surgeon has to move the thecal sac (fluid-filled sac that contains the nerves) and nerve roots out of the way in order to sneak a spacer around them into the disc space.  There’s only so much space to do this so the surgeon really must compromise in terms of the size of the spacer that can be inserted.  Thus for TLIF and PLIF the surgeon must insert a very small spacer (see figure 2.)  We’ve talked about how important large intervertebral spacers are, the bigger the better in my opinion.  The small spacers inserted via TLIF and PLIF can’t contain much graft material to promote bony fusion, aren’t good at restoring lordosis (in fact, some studies show that patients who undergo TLIF and PLIF actually lose lordosis) and lastly, aren’t good at correcting lost disc space and foraminal height.  Also, because of where these small spacers sit in the disc space (against the soft bone at the center of the vertebral end plates) they often end up subsiding into the vertebral body above and below (see figure 3).  When subsidence occurs the surgeon has failed at achieving one of the main goals of the procedure: restoration of foraminal height and indirect decompression of the neural elements.  This failure can lead to recurrence of nerve compression and leg pain resulting in the need for revision surgery with larger spacers.


Figure 2: Size matters.  Look at the size of an XLIF/ALIF spacer compared to that of the much smaller TLIF or PLIF spacers.

 TLIF subsidence  Acquired foraminal stenosis

Figure 3: First image shows midline sagittal view of a TLIF spacer (red arrow) subsiding nearly 50% into the endplate of the L5 vertebral body below (the endplates are indicated by the thin yellow lines.)  Second image shows severe acquired foraminal stenosis (red arrow) that resulted from the subsidence of the TLIF spacer.

The anterior lumbar interbody fusion (ALIF), in contrast, allows the surgeon to come directly to the front of the spine to insert very large intervertebral spacers without disruption of the posterior elements of the spine. We’ve talked about the benefits of large spacers already so I won’t go into it extensively here.  In brief, though, these large spacers are much better at promoting fusion, restoring lordosis and restoring foraminal height for indirect decompression of the neural elements.  Think of it from a structural standpoint: would you want your house built on a small/narrow foundation or a large/wide one?   The downside to the ALIF, though, is that going through a patient’s abdomen isn’t a benign thing.  There are risks of ileus (when the bowels are “stunned” after manipulation during surgery and don’t move for several days.  Doesn’t sound like a big deal but it can be an awful complication) as well as injury to abdominal organs or the large blood vessels that sit in front of the spine.  Second, the ALIF is usually requires a vascular or general “approach” surgeon who assists in getting the spine surgeon to the spine to do his work.  Lastly, if the surgeon does desire to place pedicle screws or do any other work at the back of the spine he’ll have to close up the abdomen and then flip the patient from the supine position (patient laying on their back) to the prone position (patient laying on their abdomen.) 

XLIF is just a modified ALIF.  Rather than coming through the patient’s abdomen with the patient on their back, the patient is positioned on their side and the surgeon approaches the spine via a small incision on the patient’s flank (see figure 4). You get all of the benefits of a large intervertebral spacer at the front of the spine without the downsides of traditional ALIF.  With an XLIF spacer you get a huge graft window to promote robust fusion.  Also, because the XLIF spacer sits on the hard bone at the periphery of the vertebral endplates (the apophyseal ring) versus the soft bone at the center of the endplate, it resists subsidence and thus is better at correcting lordosis and foraminal height loss than the smaller TLIF and PLIF spacers (see figure 5). In my opinion there is no question that XLIF is superior to TLIF or PLIF and if I needed a lumbar fusion I’d ask for an XLIF.


Figure 4: Oblique view of ALIF and XLIF trajectories into disc space.


Figure 5: Image showing the stronger, more compact bone at the outer apophyseal ring of the vertebral endplates.  XLIF spacers resist subsidence by sitting on the apophyseal ring rather than the softer bone at the center of the endplate.  Source: A.A. White, M.M. Panjabi (Eds.), Clinical biomechanics of the spine, 2nd ed, JB Lippincott, Philadelphia, PA, 1990.

If you’ve gotten one of these posterior fusion surgeries don’t email me asking if you got the wrong procedure (you probably don’t need to hear my opinion any more clearly than it’s presented here.)   To be fair, there are lots of surgeons out there who routinely perform TLIF and PLIF and do them well.  In fact, TLIF is the most common technique for lumbar fusions in the US. These procedures are safe and can be effective.  I don’t do them for a reason though.  At our hospital we have surgeons who perform every one of these techniques so we have a diverse cohort with which to compare immediate outcomes of these various types of fusion procedures.  There’s just something about the immediate structural support and correction afforded by large intervertebral spacers that (again, in my opinion) leads to more rapid and dramatic clinical improvement in patients.  One clear difference: my XLIF patients almost always go home the morning after surgery (average length of stay for nearly 200 1- and 2-level cases since 2013 is 1.2 days) while the TLIF and PLIF patients of other surgeons stay in the hospital at least twice as long if not longer.  If you include training, I’ve been doing the XLIF procedure since 2006 and the clinical outcomes afforded by this technique still amaze me to this day.

So if XLIF is so great why doesn’t every spine surgeon do XLIF and only XLIF for their lumbar fusions?  The answer is that there are some perceived limitations of XLIF that scare some surgeons into not doing this procedure:

  1. Surgeons think that after XLIF you have to close up and then flip the patient prone to place screws (similar to the real limitation described for ALIF.)
  2. Because the iliac crest of the pelvis gets in the way, XLIF can’t be done at L5/S1 (ok, this is a real limitation, not a perceived one.)  So if a surgeon is fusing L4/5 and L5/S1 (which is required quite often actually) you’ll have reposition the patient from the lateral position to some other position to fuse L5/S1 using a different technique. 
  3. XLIF has an unacceptably high risk of nerve injury, especially when done at L4/5.

Over the next few posts I’ll discuss why these are just perceived limitations of XLIF.  In fact, XLIF is a very safe and effective way to perform a lumbar fusion, even at the L4/5 level (greater than 95% of the lumbar fusions that I do involve XLIF at the L4/5 level.)  Also, when XLIF is combined with Lateral ALIF (a minimally-invasive ALIF done with the patient on their side) at L5/S1 and single-position pedicle screw fixation (pedicle screws placed with the patient in the lateral position without flipping prone) a surgeon can perform a robust lumbar fusion from L1 to the sacrum without repositioning the patient.  This strategy of Lateral Single Position Surgery (LSPS) dramatically reduces the anesthesia time for patients, which translates into decreases risk and improves outcomes.  More on this ground-breaking concept in future posts.

Thanks for reading!

J. Alex Thomas, M.D.

Is your spine in line?

Before I talk about the types of spinal fusions that I perform I think it’s very important that we first discuss the concept of spinopelvic balance.  Until recently this was a concept that was only considered by academic spinal deformity surgeons (those spine surgeons who treat scoliosis and other complex spinal pathology.)  Over the past few years, however, data has emerged that suggests that restoration of lumbar lordosis (the normal backwards curvature of the lumbar spine) in order to maintain proper spinopelvic balance is critical even for patients who undergo one- or two-level spinal fusions.   Being sure to consider spinopelvic balance before fusing a patient’s spine will maximize their chance of a good outcome.

What is spinopelvic balance?  Basically, the spine should maintain an upright posture, with the head positioned directly over the pelvis, with minimal energy expenditure.  This notion was elegantly described by the French orthopedic surgeon Jean Dubousset who described a “cone of economy” of an upright patient (see figure 1A).  Neutral spinopelvic alignment keeps the patient at the center of the cone where he has to maintain little energy to stand upright and keep horizontal gaze.  As the spine pitches forward (for a variety of reasons described below) the patient falls to the periphery of the cone and thus has to expend more energy just to stay upright (see figure 1B).  If he falls too far to the periphery he’ll no longer be able to support himself and will need a cane or walker.  This forward pitching of the spine is referred to positive sagittal balance and is the torment of all patients with degenerated spines.  The more severe the imbalance the more disabled the patient.  This was first described in a landmark study in 2005 Glassman et al.  The authors examined full-length standing X-rays on 352 patients and found a direct, linear correlation between increasing positive sagittal balance and worsening patient disability (see figure 2).


Figure 1A: Dubousset’s cone of economy (source: Ames et al). A patient at the center of this cone of economy will have to expend minimal energy to keep their head upright and maintain horizontal gaze.  1B; the King of Pop WAY out of his cone of economy. 

Mendeley Desktop

Figure 2. There is a linear correlation with increasing sagittal balance and poor clinical outcomes.  SF-12 and ODI scores are clinical outcomes (HRQOL) measures used in spine surgery to assess how well a patient is doing.  Lower SF-12 scores and higher ODI scores indicate worse outcomes (Source: Glassman et al.) 

The balance of the spine is assessed using several spinopelvic parameters measured on AP and lateral (front and side) standing X-rays of the patient that include the femoral heads (see figure 3.)  This X-ray is mandatory in my clinic for any patient who is being considered for a spinal fusion.  There are dozens of various spinopelvic parameters that can be measured for a given patient and it can quickly get overwhelming trying to keep track of all of them.  The Glassman study mentioned above used the sagittal vertical axis, SVA, to quantify positive sagittal balance.  SVA is the best measure to describe a patient’s global spinal balance as it assesses the position of the cervical spine over the sacrum (tailbone.)  The problem with SVA, in my opinion, is that it can be difficult to get full-length standing X-rays at most community imaging centers.  In another study by Schwab et al in 2013 the authors prospectively studied dozens of spinopelvic parameters in nearly 500 patients with spinal deformity.  These parameters were correlated with a variety of health-related quality of life (HRQOL) measures.  When they analyzed the data they found that three parameters matter most: 

1)   SVA: which we already discussed

2)   PI-LL mismatch: the amount of discrepancy between the pelvic incidence (PI, a fixed morphological characteristic of your pelvis.  Basically, the way your pelvis is shaped in relation to the hip joints) and the lumbar lordosis (LL, the normal curvature of the lumbar spine as mentioned above.) 

3)   Pelvic tilt (PT): a measure of the extent that the pelvis is tilting backwards to compensate for lost lumbar lordosis. 

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Figure 3: Standing lateral X-ray including femoral heads showing measurements of pelvic tilt (PT), pelvic incidence (PI), lumbar lordosis (LL), PI-LL mismatch and segmental angles.  This X-ray is mandatory for any patients in my clinic being considered for lumbar fusion. 

When the authors did even more in-depth analysis they found that PI-LL mismatch was the variable that most correlated with patient disability (patients with PI-LL mismatch of 11 degrees or greater were more likely to be severely disabled.)   That happens to be very convenient for spine surgeons.  First, both the PI and LL can be easily calculated on standing lumbar xrays that can be done at any imaging facility (full-length films not required!)  Even more important, PI-LL mismatch is the parameter that is most easily addressed with surgery.  Nearly 70% of a patient’s overall LL comes from the angulation at the L4/5 and L5/S1 disc spaces.  So if you’re trying to correct a patient’s PI-LL mismatch you can often do so by restoring LL with large, angled intervertebral spacers placed at one or both of these levels.  I know that was a lot of complicated stuff there but if you take away nothing else, know this: PI and LL should be assessed in all patients being considered for spinal fusion surgery so that PI-LL mismatch can be corrected.

Positive sagittal balance (and remember, “positive” balance is actually a bad thing) can have several causes.  First, pediatric patients can have so-called “idiopathic” scoliosis and other spinal deformities.  These are entirely unique entities and I won’t discuss them here.  In adults, acute changes in spinal structure such as tumor, trauma or infection can cause the spine to lose structural integrity and allow the spine to fall into positive sagittal balance.  Most commonly, however, progressive degeneration of the spine allows for the slow development of sagittal imbalance.   As the intervertebral discs degenerate over a patient’s lifetime, and supporting spinal muscles and ligaments weaken, the spine will lose its normal lordosis  (i.e. it will flatten out, forming a so-called “flat-back” deformity).  In severe cases the spine may even begin to kyphose, or bend forward (see figure 4).  Compounding matters, the spine can also start to buckle under the weight of the torso leading to an S-shaped coronal deformity (see figure 5.)NewImageNewImage 

Figure 4: Image on left shows a normal, healthy lumbar spine with adequate lumbar lordosis (backward curvature of the spine.  Image on right shows a severely degenerated spine with loss or lordosis resulting in “flat back’.  PI-LL mismatch in this patient is 23 degrees.

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Figure 5. AP (front view) Xray of lumbar spine and pelvis demonstrating a severe coronal deformity with a right-sided concavity.  Lumbar spine should be straight up and down on this view.

Perhaps the worst cause of sagittal imbalance is iatrogenic, when a patient is fixed into sagittal imbalance after a spinal fusion.  This is when patients really suffer.  First, we know that patients who are left with positive sagittal balance (as measured by PI-LL mismatch) after spinal fusion surgery have worse clinical outcomes.  Even more concerning, there’s also data to suggest that patients fixed into PI-LL mismatch are more likely to develop adjacent segment degeneration (ASD) after their fusion.  In a 2014 study by Rothenfluh et al, the authors reported a 10x (!) increase in the incidence of ASD when patients had PI-LL mismatch after their initial fusion.  It only makes sense that when a segment of spine is locked into an alignment that is pitched forward, the level above is going to more likely to continue to fall forward! (see figure 6)  (To tell you how much my understanding of this topic has evolved: one of the first articles I wrote on Spinal(con)Fusion, over 5 years ago now, was on ASD and no where in that article did I discuss positive sagittal balance.  I’m now convinced that fusing someone in poor sagittal alignment is the biggest contributor to increased risk of ASD after spinal fusion.)   Thus, one of the main goals of any spinal fusion surgery should be to restore lumbar lordosis to correct PI-LL mismatch.  This will maximize the chances of a good clinical outcome after surgery and may decrease the risk of ASD in the future.

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Figure 6.  Sagittal MRI (side view) showing adjacent segment degeneration at L3/4 in a patient with previous fusion at L4/5.  Notice how L4 is fused into near straight alignment in relation to L5 (there should be 10-20 degrees of angulation there.)  It’s no surprise this patient fell forward above his flat fusion.  

This is really important stuff people.  Spinopelvic parameters should not be ignored.  I will take the time to do these measurements on every patient who undergoes a spinal fusion.  These days it’s easy too.  I can literally snap a picture of a standing X-ray with my iPhone or iPad and an app will basically do the spinopelvic measurements for me (see figure 7).  There’s just no excuse not to check.   If you’re considering a spinal fusion please be certain that your surgeon is taking your spinopelvic parameters into consideration.

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Figure 7.  Nuvaline Pro iPhone app used to measure postoperative spinopelvic parameters in patient who underwent a fusion at L5/S1. 

Thanks for reading! 

J. Alex Thomas, M.D.



  1. Ames CP, Smith JS, Scheer JK, Bess S, Bederman SS, Deviren V, et al.: Impact of spinopelvic alignment on decision making in deformity surgery in adults: A review. J Neurosurg Spine 16:547–64, 2012
  2. Glassman SD, Bridwell K, Dimar JR, Horton W, Berven S, Schwab F: The Impact of Positive Sagittal Balance in Adult Spinal Deformity. Spine (Phila Pa 1976) 30:2024–2029, 2005.
  3. Rothenfluh DA, Mueller DA: Pelvic incidence-lumbar lordosis mismatch predisposes to adjacent segment disease after lumbar spinal fusion. Eur Spine J 24:1251–8, 2014
  4. Schwab FJ, Blondel B, Bess S, Hostin R, Shaffrey CI, Smith JS, et al.: Radiographical Spinopelvic Parameters and Disability in the Setting of Adult Spinal Deformity. Spine (Phila Pa 1976) 38:E803–E812, 2013



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. 

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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.

Lateral ALIF is a true single-position strategy for lumbar fusions

I’m back!  I realize there’s been quite a delay since my last post and for that I apologize.   For over a year now I’ve been busy helping to develop a new retractor system for lumbar spine surgery.  This retractor allows surgeons to perform an anterior lumbar interbody fusion (ALIF) in the lateral position, a procedure we (perhaps not so creatively) call lateral ALIF (see figure 1).  Why does that matter?  In my opinion, an ALIF is the most powerful way to fuse a segment of the lumbar spine and correct spinal deformity (hint: it’s because ALIF allows you to insert the largest spacers!). One drawback of ALIF, though, is that since it’s traditionally performed in the supine position (with the patient laying on his back), if the surgeon wishes to place posterior instrumentation he has to close the incision on the front of the patient and then reposition the patient prone to get access to the back of the spine.  This process of repositioning can add nearly an hour of time to the procedure and may also increase risk to the patient.  By keeping the patient on his side, in a single position, the surgeon can harness the power of ALIF and then immediately be ready to place posterior instrumentation, all without having to stop to reposition the patient (see figure 2).  Now, a so-called 360-degree lumbar fusion that used to take 3 hours to perform can now be done in an hour.  This is good for my OR throughput but it’s GREAT for you, the patient, who will avoid that extra time under anesthesia.  This could potentially be the one of the most important innovations in spine surgery in years. 


Figure 1: The new Lateral ALIF retractor during a recent ALIF at L5/S1.  The patient is in the lateral decubitus position with their left side up.  The patient’s head is at the left of the image.


Figure 2: Lateral ALIF at L5/S1.  This image gives you an idea of the massive increase in efficiency you get without having to reposition the patient.  Here, I’ve already placed wires for insertion of percutaneous pedicle screws while my physician assistant Jack Bagley continues to close the abdominal lateral ALIF incision.  Patient is right side up with head towards the left of the image. 

The ALIF, first described in the 1930s, is the original interbody fusion in which bone graft is inserted into the cleaned out intervertebral disc (IVD) space to promote fusion and correct spinal deformity (in modern ALIF the bone graft is carried in a spacer or cage).  Since then, many other techniques have been developed to place spacers into the disc space via a posterior approach.   These other –IF procedures, such as posterior lumbar interbody fusions (PLIFs) or transforaminal interbody fusions (TLIFs) represent early attempts at a single position strategy.  These procedures allow surgeons to perform the three standard steps of a spinal fusion: 1) neural decompression (laminectomy or discectomy), 2) interbody fusion, and 3) placement of posterior instrumentation with the patient in the prone position.  Thus, traditional spine surgeons may say “Well I’ve been doing ‘single-position’ lumbar fusions for years.”  Indeed, TLIF and PLIF are the most common way to perform lumbar fusions these days.  The problem with TLIF and PLIF, though, is that in order to place spacers from behind, one or more nerves have to be retracted out of the way to sneak the spacer into the disc space.  That means that for PLIF and TLIF the surgeon is forced to use very small spacers (see figure 3).  Because you’ve read recent Spinal (con)Fusion posts, though, you know that I believe in the power of large intervertebral spacers.  Bigger is better and thus ALIF is a much more powerful technique for spinal fusion than PLIF or TLIF.  Now, by doing the ALIF in the lateral position I can have concurrent access to the back of the patient to perform a decompression and place pedicle screws without “flipping” the patient. 

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Figure 3: side-by-side comparison of various intervertebral spacers.  Notice how much larger the XLIF/ALIF spacer  is versus the much smaller TLIF or PLIF spacers. Size matters!

As you can probably tell, I’m very excited about this new retractor and surgical technique (yes, I’m biased.)  In future posts we’ll talk more about the details of a lateral ALIF procedure.  You’ll also see how well lateral ALIF at L5/S1 compliments the extreme lateral interbody fusion (XLIF) at L4/5 and above.  Lots more about single-position lateral surgery to come! 

Thanks for reading!

J. Alex Thomas, M.D.

Believe in Indirect Decompression!

One of the most common procedures that I book patients for is an extreme lateral interbody fusion (XLIF).  This is a minimally-invasive lumbar fusion procedure that has all of the benefits of the classic anterior lumbar interbody fusion (ALIF) without its downsides (all of the bad things that can occur by traversing someone’s abdomen to get to the spine.)   In previous posts we’ve alluded to various types of spinal deformity that can cause pain.  The one constant in all of these types of spinal deformity: stenosis.  Both XLIF and ALIF rely on an old orthopedic principle known as indirect decompression in which properly sized spacers are used to correct spinal deformity and thus correct stenosis. 

Recall from previous discussion that stenosis, or narrowing around nerve roots, typically results after years of spinal degeneration.  The resulting stenosis can be divided into two simplistic types (and these types are just the way that I think about it in my head, don’t go looking for them in textbooks!).  The first type of stenosis is structural stenosis.  Here, the basic anatomical components of the spine are generally unchanged in terms of their shape or volume; it’s just that these parts of the spine have collapsed onto nearby nerve roots thereby causing pain.  I believe that this is the most common form of stenosis by far.  One common example of structural stenosis occurs when the intervertebral disc (IVD) has degenerated and collapsed resulting in loss of foraminal height and foraminal stenosis.  Another example of structural stenosis is seen in spondylolisthesis when one vertebral body slides over the one below it causing a dynamic foraminal stenosis that worsens when the patient stands and loads their spine (more on this topic later.)  Lastly, it is my opinion that the central stenosis that causes neurogenic claudication in the elderly is a form of structural stenosis resulting from buckling of the ligamentum flavum (this is controversial as some believe that the body actually produces reduntant ligamentum flavum which would be more like the reactive stenosis discussed below.) In each of these cases, normal spinal structure and alignment has been lost resulting in stenosis and pain.

The other simplistic type of stenosis is reactive stenosis.  Here, there IS an increase in the shape or volume of a component of the spine, which results in stenosis and compression of nearby nerves. The most common example of this occurs when the facet joint degenerates and becomes larger as it becomes consumed by arthritis.  This leads to osteophyte (fancy word for bone spur) formation, which can cause nerve root compression and radiculopathy. 

To fix reactive stenosis the surgeon must perform a direct decompression procedure, a laminectomy or foraminotomy, to remove all excess bony overgrowth from around the nerves.  In fact, classically this is the way that all nerve compression (regardless of which type of stenosis is causing the compression) is relieved.  The typical neurosurgeon’s mentality (and I can say this because I’m one of them) is that the only way to know that a nerve is decompressed is to remove any overlying bone and actually see the nerve.  But what if this isn’t always necessary?  I believe that in most cases it’s NOT necessary (and trust me, it takes a huge leap of faith on the part of both the surgeon and the patient to come to this realization.)  Because most spinal stenosis is structural and not reactive, restoration of normal structure and alignment of the spine will relieve stenosis and pain without the extra time and risk of a laminectomy.

Recall that loss of normal spinal structure and alignment begins with degeneration and resulting collapse of the IVD.  So, to restore structure and alignment we go to the disc space (remember the post on spacers?)!  Indirect decompression is achieved when a properly sized spacer is inserted into a collapsed disc space to restore the height of the neural foramen (see figures 1 and 2).  This then relieves nerve root compression because the space around the nerve in the foramen is restored; I don’t have to do more work to remove bone that doesn’t need removing!  To be sure, this is a controversial topic.  I know plenty of very good spine surgeons who just don’t believe in indirect decompression and subject their patients to a concurrent laminectomy with every spinal fusion.  They’re paranoid (we surgeons are a VERY paranoid bunch, some are just more so than others) that if they don’t directly decompress the nerve and visually confirm that it’s decompressed then they may not relieve the patient’s pain.  I get it.  Like I said, it’s a leap of faith.  A laminectomy isn’t a benign procedure though.  There’s a 5-10% risk of dural tear and spinal fluid leak for starters.  Typically this is a minor complication but it can be catastrophic.  There’s also the risk of scar tissue formation around exposed nerve roots, which can lead to chronic pain after surgery.  Finally there’s just the risk of being under anesthesia for the extra time needed to perform the laminectomy.  Why would I subject my patients to these risks when I know that the indirect decompression achieved by the spacer will probably suffice?  Believe in indirect decompression!


Figure 1: A, preoperative image showing severe collapse of the IVD resulting in foraminal height loss and nerve root compression; B, postoperative image demonstrating restoration of disc space and foraminal height after insertion of a large intervertebral spacer.

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Figue 2: As above in figure 1, image on left is preoperative image demonstrating severely collapsed IVD at L5/S1 with resultant severe foraminal stenosis (pink outline).  The image on the right is a postoperative image after an L5/S1 anterior lumbar interbody fusion (ALIF) with significant increase in disc space, and thus, foraminal height.  This patient’s leg pain was relieved immediately after surgery WITHOUT laminectomy. 

Of course there are times when relying solely on indirect decompression may not be appropriate.  In cases of severe reactive stenosis in which, say, a nerve root is encased in bone (see figure 3), indirect decompression probably isn’t going to work no matter how large of a spacer you put in.  Also, in cases of large concurrent disc herniations or facet cysts (a type of reactive stenosis, I suppose, which I’ll discuss in a later post) I may also be forced to do a direct decompression.  The more cases I do, though, the more I’m surprised at what I can get away with in terms of avoiding a direct decompression.  These days I’ll typically assume that indirect decompression will work but explain to the patient that there is a very small chance that indirect decompression may fail and that we may have to do a small “second stage” laminectomy later.  How small of a chance you ask?  I went back and looked at the data for every one of my lumbar fusions performed since December 2013.  Of nearly 250 patients only 8 needed reoperation for failure of indirect decompression.  That’s a 3% risk.  I’d say those are pretty good odds in favor of direct decompression. 

Reactive stenosis

Figure 3: Severe “reactive” foraminal stenosis at L4/5 and L5/S1 resulting from severe bony overgrowth around nerve within the neural foramen (red arrows).  This patient failed indirect decompression and required a minimally-invasive foraminotomy a few months after his initial surgery.

Thanks for reading!

J. Alex Thomas, M.D.

Implants in Spinal Surgery Part III: Intervertebral Spacers

In our last post we discussed pedicle screws, the most commonly used form of posterior instrumentation.  Even in the recent past, pedicle screws were the only form of instrumentation used in a spinal fusion.  Unfortunately, these posterior-only fusion constructs didn’t have excellent rates of fusion: nearly 30% of these cases ended up in non-unions.  Today, most spinal fusion constructs utilize pedicle screws at the back of the spine and intervertebral spacers (or cages) in the front of the spine.  These so-called 360-degree constructs (also referred to as interbody fusions) have dramatically decreased the rates of non-union and thus are now the standard way spinal fusions are done.  

Of note, interbody fusion procedures are abbreviated with the suffix –IF. Common examples include the anterior lumbar interbody fusion (ALIF), posterior lumbar interbody fusion (PLIF) and extreme lateral interbody fusion (XLIF).  We’ll highlight the differences between the various –IFs in a future post.  The most commonly used interbody fusion procedure is actually the ACDF which we’ve already discussed here.

In the 1950s anterior interbody fusions were used in the treatment of Pott’s disease, or tuberculosis of the spine.  These anterior fusions proved to be more effective than posterior fusions because they allowed for reconstruction of the front of the spine, which is where most of the destruction of Pott’s disease occurs.  Once the infected vertebral bodies were resected (via a corpectomy), large defects in the front of the spine were reconstructed with pieces of bone fashioned into struts.  These pieces of bone were either harvested from cadavers (allograft), or may have been harvested from somewhere within the patient’s body (autograft) like the fibula or iliac crest.  These bone struts provided immediate support to the front of the spine and also promoted bony fusion.  They were the earliest intervertebral spacers.

While long structural bone struts are important in the reconstruction of the front of the spine after corpectomy for infection, tumor or trauma, the more commonly used intervertebral spacers are smaller spacers inserted into the disc space for fusion for degenerative conditions.  I will be referring to these spacers primarily for the remainder of the post.  The first such anterior interbody fusion utilizing bone inserted into the disc space was reported by Dr. Burns in 1933 for the treatment of lumbar spondylolisthesis (“slipped bones”, to discussed in a future post.)  Unfortunately, in this case, as with early anterior cervical fusions, often only loose shards of bone were packed into the disc space.  While this may have promoted bony fusion across the disc space it certainly didn’t provide any structural support and may have allowed for further collapse of the spinal segment with resultant kyphosis of the spine (see figure 1).  In the subsequent decades since Dr. Burns’ case, intervertebral spacers of various materials and shapes have been developed that are better at providing structural support and are also more readily available than spacers made of bone.  Today most intervertebral spacers are made of a fancy plastic called PEEK (polyetheretherketone) and this is what I use almost exclusively when I perform interbody fusions.  Titanium is also making a comeback (either comprising the entire spacer or as a coating on the surface of a PEEK spacer) as some feel it may be better at incorporating new bone in the early stages of bony fusion (see figure 2).  I could spend multiple posts discussing the merits of different intervertebral spacer materials but that you would likely bore you (and me) to death.  Regardless of what it’s made of, every intervertebral spacer should serve two purposes: a) correct spinal deformity, and b) promote a bony fusion.   

Postoperative Deformity of the Cervical Spine Clinical Gate 

Figure 1: Anterior cervical fusion done with only bone graft and no spacer for structural support.  Note that the fused bones have collapsed somewhat and are now allowing the spine the fall forward  The red line indicates the forward angle of the collapse and should, in fact, be straight (source: Riew et al, 2015).

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Figure 2: Various intervertebral spacers used for lumbar interbody fusion (source: Williams et al, 2005). 

First, let’s talk about the correction of spinal deformity.  In my opinion spinal reconstruction should take place where the degenerative process starts: the disc space.  As we’ve talked about previously, as the intervertebral disc (IVD) degenerates it dries out and collapses.  Without the structural integrity of the IVD the adjacent vertebral bodies fall out of alignment and the spine then becomes deformed.  Spinal deformity is a complicated topic that I won’t delve too far into at this point.  All you need to know now is that a deformed spine causes both back pain and radicular (nerve) pain.  The back pain is caused by the mechanical stress of the deformity.  The radicular pain is caused by foraminal stenosis and the resulting nerve root compression.  Recall that the neural foramen, the hole on the side of the spine where the nerve exits, is an aperture comprised of the top of the pedicle of the vertebral body below and the bottom of the pedicle of the vertebral body above.  As the IVD collapses the diameter of the foramen narrows significantly and the nerve is guillotined within.  An intervertebral spacer inserted into a collapsed disc space corrects deformity by acting like a wedge to a) restore alignment to relieve mechanical stress, and b) restore foraminal height to allow for indirect decompression of compressed nerves.  The concept of indirect decompression is an immensely important one that I’ll get to in an upcoming post.  (See figures 3 and 4.)


Figure 3: Image on left shows collapsed disc with resultant foraminal stenosis and nerve root compression.  Image on right shows the result after a spacer is inserted with restored foraminal height and indirect nerve decompression.   

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Figure 4: Preoperative MRI showing a focal coronal deformity with unilateral foraminal stenosis and nerve root compression resulting in severe R leg pain (the red lines, indicating the vertebral endplates, should be parallel and instead are collapsed to one side.)  Image on right is a postoperative anterior view Xray after a spacer (with plate) is inserted.  Notice that the vertebral endplates (red lines) are now parallel after the deformity has been corrected.  Of note, because it is PEEK the spacer isn’t seen well on Xray and instead the borders of the spacer are indicated by markers within.  

The other important function of the intervertebral spacer is to promote bony fusion.  Recall from previous posts that it’s the bone graft material that is applied between parts of the spine that promotes the new bone growth in a spinal fusion.  There are many types of graft material used in spine surgery that I’ll discuss in a later post.  Most modern intervertebral spacers have large chambers within their structure where bone graft is packed prior to insertion into the disc space (see figure 5).  These chambers then hold the graft material in place, nicely apposed against the adjacent vertebral bodies, in order to promote bony ingrowth (see figure 6).  

 ALIF spacer bone graft Google Search

Figure 5: standard ALIF spacer used in lumbar fusions.  Note the large graft chambers (red arrows) that are packed with bone graft material prior to insertion into the disc space. Source: Globus Medical. 


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Figure 6: Lateral postoperative CAT scan demonstrating robust bone growth (red arrow) across intervertebral spacer (spacer material isn’t seen in this cut of the scan.)  

Lastly, I believe that bigger is better when selecting an intervertebral spacer in an interbody fusion.   Not only do larger spacers provide more structural support for deformity correction but they can also carry more graft material to better promote bony fusion.  THIS is why I prefer anterior procedures such as XLIF or ALIF with their large spacers rather than TLIF or PLIF with their quite puny spacers.  More on that later.

Thanks for reading!

J. Alex Thomas, M.D.


1) Riew et al, 2015, Postoperative Deformity of the Cervical Spine, online access at iKnowledge:

2) Williams et al, 2005, CT Evaluation of Lumbar Interbody Fusion: Current Concepts, ANJR, 20: 2057-2066, September 2005.









Implants in Spinal Surgery Part II: pedicle screws and other (very rarely used) forms of posterior spinal instrumentation

In our last post we discussed how various types of spinal implants help stabilize the spine to promote a more robust bony fusion.  Recall that the main goal of a spinal fusion procedure is to promote bone growth which in turn will stabilize a painful unstable or deformed segment of the spine.  Historically, non-instrumented in-situ fusions had very high rates of non-union in which the spine didn’t fuse despite weeks of bedrest and bracing.  This may have required subsequent revision surgeries and often left the patient severely disabled.

In order to mitigate the problem of non-union, surgeons developed forms of posterior instrumentation (instrumentation applied to the back of the spine) to help stabilize the spine.  These implants also provided surgeons a more powerful way to restore alignment to the spine to correct spinal deformity.  The most primitive form of posterior spinal instrumentation, first described in the late 19th century, was posterior spinal wiring.  Here, various parts of the spine (usually the spinous process or lamina) were wired together for immobilization during spinal fusion.  While useful in the cervical spine (see figure 1), this technique never proved to be effective in the thoracic and lumbar spine, where larger forces prevail, and thus has largely been abandoned today. 


Figure 1: Cahill technique of posterior spinous wiring in the cervical spine.  Source: Omeis et al

In the 1950s Paul Harrington began performing spinal fusions using long rods anchored to the spine with hooks under the lamina (see figure 2).  The rod construct was periodically lengthened to slowly straighten the deformed spines of scoliosis patients. Harrington rod systems were state of the art for decades and I’ll still see patients in clinic today with these long rods in their spine.  Unfortunately, with only a few points of fixation anchoring the long, straight rod in place, these constructs were prone to failure and also predisposed patients to a painful “flat back” deformity.  (When a surgeon fuses a spinal segment without being mindful of its normal degree of curvature he may inadvertently cause more harm by creating spinal deformity.  More on this very important topic in later posts.)  Moving away from Harrington rods, surgeons began to develop new forms of segmental instrumentation in which each segment of the fused section of the spine was anchored with instrumentation (versus the long Harrington rod which spanned multiple non-instrumented segments.)  This segmental instrumentation vastly increased the strength and stability of the fusion construct and therefore further decreased the rate of non-union.  Early forms of segmental instrumentation include variations of trans-facet screws described by King in 1944 and Boucher in 1959 (the latter incorporated part of the pedicle in the screw trajectory and thus is considered by some to be the first pedicle screw.)  In 1970 Roy Camille described the precursor to today’s pedicle screw systems.  In his system he attached screws inserted via the pedicle to a multi-holed plate which would span across two spinal segments from screw to screw.  The screw-plate concept was expanded upon in the U.S. by Dr. Arthur Steffee in the early 1980s with his Steffee Plate/VSP stainless steel pedicle screw system (see figure 3).  Steffee’s company AcroMed was the subject of a 1993 ABC 20/20 expose which profiled several patients who were left disabled after Steffee’s VSP pedicle screws broke (all pedicle screws will eventually break, by the way, if the spinal segment doesn’t fuse properly.)  This prompted hundreds of pedicle screw-related lawsuits around the country in the mid 1990s (part of the issue was that the FDA never cleared the VSP screw for use specifically in the spine).  Ultimately most of the pedicle screw litigation was thrown out.  Today pedicle screws are a mainstay of treatment of a variety of thoracic and lumbar spinal pathology. 


Figure 2: AP (A) and lateral (B) postoperative Xrays demonstrating a single Harrington rod used in correction of a thoracic scoliosis.  Note in image B how flat the fused segment is. 

 Mendeley Desktop

Figure 3: Steffee plate and VSP pedicle screw system in L4-S1 fusion.  Source: Kabins et al.

Today’s pedicle screws are generally made of titanium and have polyaxial heads in which a rod is seated and locked in place using a locking cap.  The rod is used in favor of Camille’s and Steffee’s plates as it allows for easier insertion as well as contouring to correct spinal deformity (see figure 4). Screws vary in size depending on the size of the patients and the part of the spine being instrumented (i.e. smaller screws in the thoracic spine and larger screws for the lumbar spine.)  Typically in lumbar spine fusions I will use screws that are 6.5mm in diameter and 45mm long with a 4.5mm diameter rod.   Once the screws are inserted various attachments can be used to manipulate the screws to rotate, compress or distract across spinal segments in order to correct spinal deformity prior to fusion. 


Figure 4: Modern pedicle screw with polyaxial head and rod locked in place. Source: Zimmer Biomet.

As you can probably guess, a “pedicle” screw traverses part of the vertebral body called the pedicle.  This bridge of bone connects the anterior elements of the spine (i.e. the vertebral body) with the posterior elements (i.e. lamina, facets, spinous process, see figure 5).  In order to properly insert a screw into the pedicle the surgeon must access a starting point at the junction of the transvers process and the facet complex, several centimeters off of midline.  In traditional open spinal surgery via midline incisions the surgeon has to do quite a bit of destructive, bloody dissection to get a wide enough exposure to access this starting point of the pedicle.  Often, in order to gain enough laxity in the tissue to get out to the starting point, the surgeon must also expose the level above and below the level that is being fused.  This “collateral damage” of healthy levels in open spinal surgery is what sets patients up for adjacent segement degeneration and other problems later in life. 

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Figure 5: Axial (left) and lateral (right) views of lumbar spine demonstrating pedicle (outlined in red) bridging the anterior and posterior elements.

Pedicle Screw Incisions

Figure 6: Small stab incisions used to placed 4 percutaneous pedicle screws for an L4/5 spinal fusion.  The red line indicates the length of incision that would have been needed to place the same number of screws using traditional open techniques. 

In order to avoid the increased blood loss and tissue destruction of open spinal surgery, I insert pedicle screws percutaneously with tiny, minimally-invasive incisions off midline (see figure 6.) I’ll first identify the starting point of the pedicle using a fluoroscope (like an xray machine) and then will hammer in a large needle into the pedicle via the starting point.  I can identify the correct starting point not only using imaging but also with the tactile feedback of the hard bone of the pedicle starting point.  Once I’m happy with my position in the pedicle I’ll insert a long, rigid wire called a K-wire into the pedicle and will remove the needle.  The pedicle is tapped to make a pilot hole and the screw is then inserted over the wire (see figure 7.)  The nerve that exits the spine passes just below the pedicle so one potential complication of pedicle screw insertion is nerve injury resulting from improper positioning of the screw within the pedicle. In order to avoid this complication I always use electromyographic (EMG) monitoring in which the insertion needle and tap are stimulated with low-voltage electrical current.  If the screw trajectory is too close to a nerve the current will stimulate the nerve, the corresponding muscles in the leg will twitch and I’ll be alerted to the problem so that I can plan a new trajectory.  After the screws are inserted a rod is passed through the heads of the screw and locked in place.  While some surgeons will try to get away with placing only unilateral screws, I always place bilateral pedicle screws (i.e. on both sides of the spine), as this is the gold standard for maximum spinal stabilization (see figure 8.)  Finally, recall that the screws just serve as an internal brace to allow the bony fusion to occur.  Theoretically we could remove the screws in a year after the fusion has healed but we almost never do this.

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Figure 7: 4 K-wires placed prior to placement of percutaneous pedicle screws for lumbar fusion (red wire).  Note that wires and thus screws can be placed with the patient in the lateral position (in this case patient’s right side is up.) 

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Figure 8: Axial CT image (left) and schematic image (right) demonstrating bilateral pedicle screws traversing the lumbar pedicles. Source for schematic: DePuy Synthes

There are other types of posterior instrumentation that are used in the lumbar spine.  These include interspinous clamps as well as facet screws.  I don’t believe that these implants provide the same amount of stability as a bilateral pedicle screw construct and therefore I never use them.  Not discussed here are specialized screws used in posterior cervical spine fusions called lateral mass screws (named for the part of the cervical vertebral body that they enter.)  These are very similar to thoracic and lumbar pedicle screws (titanium, polyaxial heads, connected by rods passed through the heads) but are much smaller with a typical diameter of 3.5mm and a length of 12-14mm.  

In summary, pedicle screws act as an internal brace to immobilize the spine so that a more robust bony fusion may occur. These screws can be safely inserted into the spine using minimally-invasive percutaneous techniques.

Thanks for reading!

J. Alex Thomas, M.D.


  1. Hasler CC: A brief overview of 100 years of history of surgical treatment for adolescent idiopathic scoliosis. J Child Orthop 7:57–62, 2013.
  2. Omeis I, DeMattia J a, Hillard VH, Murali R, Das K: History of instrumentation for stabilization of the subaxial cervical spine. Neurosurg Focus 16:E10, 2004.
  3. Kabins MB, Weinstein JN: The History of Vertebral Screw and Pedicle Screw Fixation. Iowa Orthop J 11:127–136, 1991.

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.