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. 

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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.


True spinal instability is a clear indication for spinal fusion

As we illustrated in our last post there is a wide spectrum of indications for lumbar spinal fusion.   As you move along this spectrum from unstable to more stable pathology the odds of a successful outcome decrease.  At the far end of the spectrum of diagnoses, the end at which there is a lesser chance of a favorable outcome after fusion, is degenerative disc disease (DDD) and spondylosis (without instability) causing back pain.  In my opinion this is softest indication for spinal fusion.  I’m not saying that you should never perform a spinal fusion on a patient with only DDD, the patient just has to be properly vetted and they must understand that a good outcome isn’t guaranteed in these cases.  On the opposite end of the spectrum is acute spinal instability caused by trauma or some other acutely destructive process such as tumor or infection.  This is the clearest indication for a spinal fusion.  NOTE: we’ve already discussed cervical spinal fusion (ACDF) here and here so this discussion will pertain primarily to the lumbar spine.

Classically, spinal stability is defined as the spine’s ability, under normal physiological loads (“normal” obviously varies widely depending on whether you’re a bank clerk or a mixed martial arts fighter), to a) protect the neural elements (i.e. nerve roots and spinal cord), and b) avoid painful deformity.  Sounds complicated right?  It may be easier to think about what happens when the spine becomes unstable: a) it may not be able to maintain proper alignment and thus may become deformed which causes severe pain; and b) it may not be able to properly protect the spinal cord within which could cause paralysis.  So in a nutshell: a stable spine is one that is protecting you against pain and/or paralysis. 

The concept of traumatic spinal fractures is a vast one that I won’t get into too much here.  Generally, though, fractures are classified as stable or unstable (hopefully you’re starting to pick up on a theme here.)  There are many complicated grading schemes that allow spine surgeons to look at a fracture on imaging and determine if it’s unstable or not.  One classic scheme is that of Denis which divides the spine into three columns.  Stable fractures typically only involve one column of the spine. Examples of stable fractures include fractures of the spinous process (a so-called clay shoveler’s fracture, see Figure 2), compression fractures and transverse process fractures.  Stable fractures may be painful from the local trauma of the injury but they do not cause painful deformity nor do they threaten the spinal cord or nerve roots.  Thus these types of fractures may be treated conservatively such as with bracing. 

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Figure 1: Illustration from Denis’ 1983 paper discussing his three spinal columns and their involvement in traumatic injuries.

Clay shoveler fracture Image Radiopaedia org

Figure 2: Fracture of the C6 spinous process (clay shoveler’s fracture).  Source:

Generally speaking if two or more of Denis’ columns are involved in a fracture it is considered unstable (again let me reiterate that Denis’ model is quite simplistic and analyzing a fracture isn’t always as easy as looking at the spine in only 3 columns.)  When a fracture is determined to be unstable a spinal fusion may be indicated to restore stability.  If an unstable fracture is left to heal without surgery it may heal poorly resulting in a painful deformity. Worse, if a patient with an unstable fracture is allowed to get up out of bed and loads their spine the fracture may shift resulting in injury to the spinal cord and paralysis. 

Trauma isn’t the only cause of acute spinal instability.  Indeed, aggressive tumors or infections can destroy the integrity of the spine thereby causing painful spinal deformity and perhaps paralysis.  These lesions are treated in a similar manner as acute fractures depending on which part of the spinal column has been damaged. The case presentation below describes a case I had a few years ago of an elderly gentleman with severe damage to his spine caused by a staph infection. 

Generally speaking when deciding which type of spinal fusion to perform for acute spinal instability, I’ll go to where the problem is:  if the pathology primarily involves the vertebral body in front of the spine, for example, I’ll do a corpectomy to remove the fractured vertebral body.  Once the body is removed I’ll reconstruct the spine with a spacer inserted where the damaged vertebral body was, and a combination of plating or screws to provide extra stability (we’ll talk about these devices in more detail in future posts.)  The main goal of all of that surgery is to promote new bone growth across the damaged segment of the spine.  It’s this new bone growth that restores spinal stability.  


The patient is a 75yo male with methicillin-resistant staph aureus (MRSA) bacteremia (in his bloodstream) who presents with worsening mid-back pain.  Imaging reveals T11-12 discitis.  (Discitis is an infection of the intervertebral disc space that is probably the most painful condition that I see.  You can usually make the diagnosis by very gently bumping the patient’s bed when you approach the bedside; if the patient screams out in pain it’s probably discitis.  That’s how bad it is.)  The medicine doctors tried a long course of antibiotics but unfortunately his pain didn’t improve.  Repeat imaging revealed that the infection hadn’t been cleared and in fact had caused further destruction of the T11 and T12 vertebral bodies (see Figure 3.) This destruction resulted in spinal instability and kyphosis (a painful deformity in which the spine falls forward.)  

T11 12 discitis

Figure 3: CT scan illustrating T11-12 discitis resulting in severe bony destruction (red arrow) and resultant kyphotic deformity (blue arrow indicates top of spine falling forward). 

When I met this patient he looked like he had given up and wanted to die.  He’d been bedbound from his infection for weeks and now was quite debilitated.  He agreed to undergo surgery and underwent a T11 and T12 corpectomy (via a lateral approach through the chest and behind the lung) followed by reconstruction of the spine with an expandable cage and percutaneous pedicle screws (see Figure 4.)  By one month post-op the patient reported no pain and was walking without assistance.  The last time I saw him about a year after his surgery he was living a normal life at home with his family.  He looked like he’d been given a new chance at life. 

Post op T11 12 corpectomy

Figure 4: Postoperative AP (left) and lateral (right) X-rays with expandable corpectomy spacer at T11-12 (red arrow) and percutaneous pedicle screws from T9-L2 (blue arrows).

I think I’ll spend the next post or two talking about the various forms of spinal implants that we use to achieve a spinal fusion. I had planned to do this later but I think that by presenting it first it will help you better understand the various spinal fusion procedures discussed in later posts. 

 Thanks for reading!

 J. Alex Thomas, M.D.


Denis F: The three column spine and its significance in the classification of acute thoracolumbar spinal injuries. Spine (Phila Pa 1976) 8:817–31, 1983.

What is a spinal fusion?

Of all the procedures that I perform, the spinal fusion is one of the most misunderstood and maligned.  Indeed, the name of this blog is a nod to the confusion surrounding the procedure.  Before we get to the specific conditions that necessitate spinal fusions and the techniques used to achieve a fusion let’s talk about what a spinal fusion is in general terms.  Throughout the article I may refer to spinal fusion by its preferred medical name, spinal arthrodesis.  The discussion will generally pertain to fusions of the lumbar spine (if you want to read about cervical spine fusions you can do so here and here.) 

Whenever the spine becomes deformed or unstable it becomes painful.  It’s not as easy as you may think to pinpoint the cause of spinal pain as often it’s multifactorial.  Generally, though, the pain is caused by either compression of a nerve by a deformed spine (causing a radiculopathy) or by the structural stress of instability or deformity (causing neck or back pain.)  The goal of a spinal arthrodesis is to promote bone growth between one or more vertebral bodies in order to correct spinal deformity and instability and thus relieve pain.  Classically this bone growth is achieved between the posterior elements or transverse processes (posterolateral arthrodesis), between the vertebral bodies within the disc space (anterior/interbody arthrodesis) or a combination of both (see figure 1).  

Posterolateral fusionInterbody fusion

Figure 1: Left, robust posterolateral fusion (arrows) with pedicle screw fixation.  Right, interbody fusion with robust bone growth between two vertebral bodies (arrow). (Source:

Today, advanced forms of spinal stabilization are used to stabilize the spine to allow the arthrodesis to occur more robustly and more rapidly (you can think of spinal stabilization as internal bracing.)   In the early 1900’s, when spinal fusion was first described to treat the destructive Pott’s Disease, or spinal tuberculosis, these technologies weren’t available. In these early procedures surgeons attempted to achieve a spinal arthrodesis by simply laying down harvested bone graft over the posterior aspect of the spine (either from the lamina, the iliac crest or from the fibula in the leg) and hoping that bone would eventually grow into a robust posterolateral arthrodesis.  This typically required a long, arduous surgery followed by 6 months of bedrest in a body cast.  Just imagine that for a moment.  Patients who were lucky enough to achieve a solid bony fusion may have had a permanently deformed (and painful) spine, as methods to adequately correct spinal deformity hadn’t been developed yet.  Over time surgeons realized that the simply fusing a patient in-situ, or in its original place, wasn’t adequate and that correction of spinal deformity at the time of arthrodesis was paramount.   In the 100 years since the early spinal arthrodeses for Pott’s Disease, various metallic implants, intervertebral spacers and grafting materials have been developed to dramatically improve the outcomes of spinal arthrodesis.  Today, minimally-invasive spinal arthrodesis can be performed on an outpatient basis with a near 100% success rate (see figure 2). We’ll get into the specifics of implant and graft technologies in future posts.

Post op XLIF CT

Figure 2: Postoperative Xray showing successful minimally-invasive spinal fusion (XLIF).  A large intervertebral spacer is used to restore foraminal height (blue arrow) while percutaneous pedicle screws (red arrow) are used to stabilize the posterior aspect of the spine. 

Despite recent technological advances of spinal arthrodesis, some patients are still downright terrified when I recommend the procedure.  Everyone knows someone who “was never the same” after having a spinal fusion.  Unfortunately these fears aren’t entirely unfounded as some spinal fusions are still being done on the wrong patients for the wrong reasons.  As illustrated in table 1 the odds of success (generally defined as relief of pain and disability) of spinal arthrodesis vary based on the indication for surgery.  The clearest indication for spinal arthrodesis is acute instability or deformity caused by trauma, infection or tumor.   In these instances spinal arthrodesis is almost always associated with an excellent outcome.  In contrast, the murky, poorly defined indications of degenerative disc disease (DDD) or spondylitic back pain (back pain caused by arthritis) often are NOT good indications for spinal surgery.  The problem in these cases is that back pain is notoriously cryptic and thus it can be difficult to correlate a patient’s pain with a certain structural abnormality on an MRI or X-ray.  The surgeon then has to make an educated guess as to what is generating the pain and then target it with a spinal fusion.   It’s no surprise when this effort is unsuccessful.  I typically will NOT perform spinal fusion on patients with only DDD or spondylosis and back pain (i.e. in the absence of gross instability or deformity.)  There are exceptions to this, of course.  For example, in cases of severe DDD with disc space collapse and resultant foraminal stenosis and radiculopathy (as opposed to just back pain) an interbody fusion may be needed to restore foraminal height and indirect decompression of a compressed nerve (see figure 3).  While this isn’t a case of frank instability I consider the disc space collapse with foraminal stenosis a deformity that requires correction. We’ll talk about this and other indications for spinal arthrodesis in future posts.    

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Table 1: Odds of success (defined as reduction of pain and disability) of spinal fusion is dependent on the indication for surgery. 

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Figure 3a: severely collapsed disc space results in foraminal stenosis and compression of exiting nerve root.  3b, interbody fusion with large intervertebral spacer results in restore foraminal height and indirect decompression of nerve root.  

I realize that this post may have generated more questions than answers.  Stay tuned for future posts about indications for spinal arthrodesis as well as advanced techniques used to achieve successful arthrodesis.  I hope to prove to you that in the properly selected patient the properly executed spinal fusion can provide life-altering improvement in a patient’s quality of life. 

Thanks for reading!

J. Alex Thomas, M.D.

I specialize in “useless” surgery.

On August 3, 2016 the New York Times published an essay called “Why ‘Useless’ Surgery Is Still Popular”.   In the essay the author decries the continued use of medical procedures “despite clinical trials that cast doubt on their effectiveness.”  One of the procedures discussed in the essay, the spinal fusion, is a procedure that I routinely perform on my patients, almost uniformly with great success.  Unfortunately, this essay irresponsibly cites only one review article about spinal fusions and thus unfairly describes the procedure as ineffective and “useless”.  On a professional level I am disappointed in this essay because I think it is misleading to the public and may prevent delivery of a potentially very effective therapy.  Not only may a patient be scared away from getting a spinal fusion after reading the essay, insurers are starting to take notice and have pounced on the opportunity to not have to pay for their patients to have fusions, deeming them “medically unnecessary”.   On a deeper, more personal level, articles like this really burn me up (and I really have to bite my tongue to remain professional there.)  I work tirelessly to provide the best possible care for my patients and spinal fusions comprise a large part of my practice.  You can imagine how I feel when articles like this in the mass media attempt to discredit what I do to help so many people.

Like any surgical procedure, the key to a desirable outcome is to only perform spinal fusions on patients with the proper indications for the procedure.  The “useless” author cites a review article by Mirza et al in 2007 that compiled data from 4 randomized trials of lumbar spinal fusion for discogenic back pain.  These trials found that spinal fusions were no better than physical and cognitive therapy for treating chronic low back pain.  The issue here, as it usually is whenever a surgery fails, is the poor indication for surgery.  First of all, any reputable spine surgeon knows that you should never offer surgery to a patient with only back pain.  There must be a corresponding structural cause of the patient’s pain that is amenable to surgery and the patient’s physical exam findings must correlate with these structural problems.  A degenerating disc causing so-called discogenic pain is NOT a structural cause of back pain!!  We’re not even certain that a degenerating intervertebral disc (IVD) can cause pain.  The thought is that by removing the degenerated and thus painful disc and fusing the adjacent vertebral bodies you will relieve the patient’s pain.  Unfortunately, so called “black disc surgery” (because the discs get darker as they degenerate) usually doesn’t work.  In my opinion this is the softest indication for spinal fusion and in fact most insurers won’t even approve the procedure for this indication. The vast majority of patients who present to my clinic with chronic discogenic back pain are sent right back out for pain management, physical therapy or other forms of conservative management.  

Spinal fusions are clearly effective in correcting structural problems of the spine such as spondylolisthesis and degenerative scoliosis.  That’s not just my anecdotal belief; multiple clinical studies have proven so.  For example, in the landmark randomized, controlled SPORT study published in the New England Journal of Medicine in 2007, Weinstein et al looked at spinal fusion versus nonsurgical treatments (i.e. physical therapy, epidural steroid injections, etc.) for the treatement of spondylolisthesis (a painful condition where one vertebral body slips over the one below it.)  The study demonstrated clear superiority of spinal fusion over nonsurgical treatments (see figure 1.)  The benefits of spinal fusion have been found to persist out to at least 8 years in subsequent analyses.  Patients who underwent nonsurgical treatment also got better, just not as rapidly or to the same extent as patients who underwent spinal fusion.  Finally, it’s important to note that the benefits of spinal fusion in the SPORT study were seen for fusion techniques that in my opinion are a bit archaic in the age of advanced minimally-invasive techniques.   Of course, the “useless” author didn’t discuss seminal studies such as SPORT in her essay.   


Figure 1: A successful minimally-invasive spinal fusion done at L4/5 for spondylolisthesis. 

Over the next several posts we’ll discuss the indications for spinal fusion as well as the various techniques used to achieve a spinal fusion.  Hopefully you’ll learn what I already know: that spinal fusions, when done for proper indications, can dramatically improve a patient’s function and quality of life.   

Thanks for reading!

J. Alex Thomas, M.D.


Weinstein, J. N., Lurie, J. D., Tosteson, T. D., Hanscom, B., Tosteson, A. N. a, Blood, E. a, … Hu, S. S. (2007). Surgical versus nonsurgical treatment for lumbar degenerative spondylolisthesis. The SPORT authors. The New England Journal of Medicine, 356(22), 2257–70. 

What makes a far lateral disc herniation unique (and PAINFUL)?

We made an important distinction in the last post: that of the far lateral disc herniation.  We’ve just discussed the more common central herniated nucleus pulposus (HNP) in which the disc herniates into the center of the spinal canal (see figure 3 of this post.)  This centrally herniated fragment hits the traversing nerve that is still within the spinal canal (e.g. a central L4/5 disc herniation causes a radiculopathy of the L5 nerve.)  In a far lateral HNP, occurring only in about 10% of cases, the piece of disc herniates on the side of the spine and compresses the nerve along its course within the neural foramen as it exits the spine (e.g. a far lateral L4/5 disc causes a radiculopathy of the L4 nerve.)   See figure 1 for an MRI showing a far lateral HNP. 

Far lateral HNP 2

Figure 1: Axial MRI showing large right far lateral HNP (outlined in pink.)  Note the displaced nerve root (pink arrow) as compared to the normal nerve root free in its neural foramen (green arrow). 

Often I can identify a patient with a far lateral HNP right when I enter the room because they’re MISERABLE.  The pain associated with far lateral HNPs is typically much worse than that seen with central HNPs.  Just as it exits from within the neural foramen, the nerve dilates into an important junction point called the dorsal root ganglion (DRG).  It’s this exquisitely sensitive part of the nerve that is compressed by a far lateral HNP.  Couple that with the fact there’s a very limited amount of space within the bony neural foramen for both the herniated disc fragment and the DRG and one understands why this type of disc herniation is so debilitating (see figure 2).

DRG in foramen 

Figure 2: Image of the right side of the lumbar spine showing the nerve roots exiting via the bony neural foramina.  Note the dilation of the DRG within the confines of the foramen (red arrow.)  

A far lateral HNP requires a different approach than the standard discectomy we discussed in the last post.  In the far lateral discectomy, I’ll typically employ an “outside-in” approach to find the fragment under the nerve as it exits the foramen.  First, the incision for a far lateral discectomy is made a few more centimeters off of midline compared to that of a standard discectomy.  Next, I’ll dock a tubular retractor in between the transverse processes at the level in question (see figure 3).  I’ll then work my way into the foramen and look for exiting nerve within the soft tissue of the intertransverse space.  One benefit of using an outside-in approach is that usually I don’t have to drill away any of the facet joint and avoid potentially destabilizing the spine.  Once I’ve found the nerve (the DRG is usually what I see first) I move it out of the way and the piece of herniated typically found right underneath.  In order to mitigate some of the pain caused by my manipulation of the DRG I will apply some steroids to the nerve when I’m done removing the disc.

Discectomy docking points

Figure 3: Image depicting the docking points for discectomy in relation to bony anatomy at the right L4/5 level. The blue circle illustrates the docking point for the tubular retractor in a standard central discectomy.  The green circle illustrates the docking point for a far lateral discectomy. 

Recovery from far lateral discectomies is typically rougher than after standard discectomies.  The DRG is already inflamed and manipulating it to get to the herniated fragment can often make the patient’s pain and numbness worse before it gets better.  Thus, I always have to get my patients with far lateral HNP mentally prepared for a tough couple of weeks after their discectomy.  In the end, though, patients do very well after a far lateral discectomy. 

Thanks for reading!

J. Alex Thomas, M.D.

What is a lumbar discectomy?

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

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

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

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

SpineLumbar4 5

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

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

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

Thanks for reading!

J. Alex Thomas, M.D.


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

Is my disc bulging, herniated or ruptured?

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

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

Figure 1: Intervertebral disc with the inner gelatinous nucleus pulposus and outer annulus fibrosus. (Source:

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

Herniated disc netter Google Search

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

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

Sagittal HNPAxial HNP

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

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

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

Thank for reading!

J. Alex Thomas, M.D.   

Do yourself a favor and don’t read your MRI report.

The devout Spinal (con)Fusion readers out there know that I often wish that patients didn’t have access to their MRI reports.  I am all for patient being fully informed about their conditions so that they can make the best decisions about their care (why do you think I spend so much time writing articles to educate all of you?).  My concern is that the average patient just isn’t equipped to understand the detailed information as well as the confusing, often scary verbiage found in a typical MRI report.  Words like “spondylosis”, “compression” or “herniation” can provoke fear or panic in the average patient, especially when combined with descriptors such as “prominent” or “severe”.  This fear and panic then leads to the patients becoming fixated on these words as if they indicate some terminal condition that can only be treated surgically.  

Some radiologists are like the Chicken Little of medicine and over emphasize findings on studies as if some sort of neurosurgical catastrophe is imminent.  The radiologists should understand, however, that for some patients these words in the reports become like badges to which some sense of importance must be applied.   The words begin to weigh heavily on a patient’s psyche and when unchecked can become a prominent part of their identity.  They begin to think that “YES! Something IS wrong with me!  I must hurt.”  You can see how this lends significantly to the psychological component of learned pain.  

Thankfully most patients are quite receptive when I explain their MRI reports for them and are relieved to find out that things really aren’t that bad, that in fact the findings are all part of the normal degeneration that occurs with aging.  You can see their faces brighten as they immediately begin to feel better.  Some patients, however, are disappointed and even angry when I don’t offer surgery based solely on their MRI findings (as in when their symptoms don’t correlate with the findings.)  “But is says severe!  Why aren’t you going to do something?!” they say.  In a recent study in the Journal of Neurosurgery Spine by Franz et al patients were given a questionnaire in order to better understand common misconceptions about spinal surgery. When asked “Would you be willing to undergo surgery if your MRI reports abnormalities, even if you do not have symptoms?” 52% of patients said yes!  Other studies have shown that a high percentage of patients believe that radiographic studies like MRI can definitely determine the cause of a patient’s pain.  This data suggests that patients put way too much importance on the findings on an MRI versus, say, a detailed physical examination or a discussion with their physician.  

Here’s the kicker: many studies have shown that findings such as spondylosis or bulging discs are routinely found on the MRIs of normal, asymptomatic patients. The findings may be completely incidental and have nothing to do with the patient’s back pain.   Don’t read your MRI report, or at least don’t become too fixated on what it says. Definitely never undergo surgery based on MRI findings alone (I’m looking at you Laser Spine Institute) lest you end up with surgery that may be unnecessary and even harmful.  Talk with your surgeon to determine if the findings in the MRI report are actually causing your symptoms.  Let your surgeon treat you, not just your MRI.  

Thanks for reading!

J. Alex Thomas, M.D.


Franz EW, Bentley JN, Yee PPS, Chang KWC, Kendall-Thomas J, Park P, et al.: Patient Misconceptions Concerning Lumbar Spondylosis Diagnosis and treatment. J Neurosurg Spine Published:1–7, 2015

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

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

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

Bulging black lumbar disc 

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

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

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

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

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

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

Thanks for reading and Happy Holidays!

J. Alex Thomas, M.D.


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