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Disc Herniation 101 | Prevalence | Confusion | Research | Treatment Options |The Tutorial | Disc Bulge | Disc Protrusion | Disc Extrusion | Disc Sequestration
BACK PAIN IN GENERAL: In industrialized nations, low back pain ranks first among all musculoskeletal disorders and can result in serious morbidity and financial loss [27-31]. The occurrence of back pain is not a rare phenomena as approximately 80% of all people experience back pain at some point in their lives [12,54,55] and complete recovery is not a guarantee. More explicitly, approximately 66% of people with a first occurrence of low back pain have suffer future reoccurrences [56] which can "easily become chronic with different degrees of severity [57-62 ]." Furthermore, if a person's pain is sufficient enough to preclude him from work for two years, then the chances of ever returning to work are close to 0% [53]. The intervertebral disc, which is susceptible to degeneration and tearing (especially with aging), is the "usual suspect" when it comes to low back pain [19,32]; however, the facet joints, sacroiliac joints, and vertebral end-plate have also been implicated as pain generators. In 1987, Waddell published a paper that declared that 80-99% of people who suffer acute low back pain completely recover within six weeks irrespective of the type of treatment and without recurrence of that pain [17]. Although insurance companies had a field day with this publication, clinicians and back-pain-sufferers knew it was not true--for most patients never completely recover and often have a lifetime sporadic pain recurrence. Waddell's myth was finally laid to rest by a well-designed study by Croft et al. in 1998 [18], which concluded that only a minority of patients with low back pain completely recover. So what is the number one cause of chronic back pain (i.e., pain lasting longer than four weeks or 3 months--depending on whose definition you use)? There are three main culprits: 1) problems with the disc, 2) problems with the facet joints, or 3) problems with the sacroiliac joints. and the rough prevalence of these conditions is 40%, 15%, and 20% respectively. I should note that although discogenic pain (pain coming from tears within the disc) represents a 40% slice of the back pain pie [19], only 1% to 2% [63,64] or at most 5% [103] of back/leg pain stems from a disc herniation. On the other hand, if the patient has true radicular pain coursing below the knee (sciatica), then the most common cause is disc herniation [33]. The need for decompressive disc surgery does arise when symptomatic disc herniations are refractory to time and conservative care; however, this situation is rare (40). As mentioned above, the number one cause of low back pain comes from a disc that has become a pain generator – usually secondary to annular tear(s). In 1995, Schwarzer AC et al. published the results of a well-designed investigation, which calculated the prevalence of disc problems (IDD to be exact) as a cause of chronic back pain. After following strict guidelines [21], they concluded with 95% confidence that problems with the disc was the cause of chronic back pain in 30% to 50% of patients [19]. others have concluded that the lumbar disc is the principal pain generator in the substantial percentage of patients with chronic low back pain (8, 9). The notion that a herniated disc can result in severe, debilitating back pain has been around for a long time. More specifically, in 1934 the syndrome of "disc herniation" was born when Mixter and Barr first proclaimed that a posterior rupture of the intervertebral disc that allowed nuclear material to escape had the ability to compress the adjacent spinal nerve root(s) and cause of back and leg pain -- i.e., cause sciatica (125). For nearly 70 years, this assertion has held true without much challenge(170). Disc herniations cannot be seen on x-ray; instead, magnetic resonance imaging (MRI) must be ordered in order to properly visualize the disc. CAT scan can also be utilized; however, it is better at seeing bone than disc. THE PREVALENCE OF DISC HERNIATIONS/SCIATICA:
With regard to age, the fourth and fifth decades of life are by far the most common time for a person to suffer asymptomatic disc herniation [65]. With regard to herniations size, arguably and ironically, the bigger the herniation the better. That is because – for reasons not completely understood – these bigger herniations respond much better to surgical decompression. This phenomenon has been well researched by Carragee et al. (10, 22) and will be discussed more below. With regard to pain, however, the size of the herniation has nothing to do with it. That is, very small herniations can be just as painful (if not more painful) than giant herniations (23, 24). The duration of symptoms can also be an ominous predictor of the future. Figure # 10: This is a sagittal (from the side view) T2 Weighted MRI lumbar image, demonstrates two types of disc herniation: the L5/S1 disc has suffered a 9mm disc extrusion (red arrow) that is not contained by the PLL. The L4/5 disc has suffered a smaller 4mm disc protrusion (green arrow) that is contained by the PLL (a remnant HIZ sign is also seen here). The L3/4 (blue arrow) is completely normal and has no disc material projecting posteriorly into the epidural space. Also note that the L3/4 disc is white in color, which indicates it is non-degenerated (i.e., full of water and healthy proteoglycan). The two herniated discs (L4/5 & L5/S1) are "black" on this MRI image, which indicates disc desiccation (lack of water and proteoglycan) and is termed "degenerative disc disease" (DDD); this is usually a precursor to disc herniation for it weakens the annulus that contains the pressurized and irritative nuclear material. In this tutorial we will explore just how a disc herniation occurs and discuss some of the more common classification of herniations. The term 'Disc Herniation' (or "disc prolapse" as they use in Europe) is a broad, general term that includes three specific types or sub-classes of disc abnormalities that are based upon the condition of the posterior longitudinal ligament ("PLL") that fortifies the back of the disc. The three main classifications of disc herniation are Protrusion (aka: contained herniation or sub-ligamentous herniation), Extrusion (aka: non-contained herniation, or trans-ligamentous herniation) and Sequestration (aka: free fragment). These terms will be discussed more below. Modern research as demonstrated that the relationship between disc herniation and its often-time associated sciatica are a far more complex and bewildering than previously realized. For example, since the invent of MRI, we have learned that some patients have disc herniation on MRI, yet have no pain at (25, 26)! And, visa versa: some patients have terrible back and leg pain yet have no disc herniation or visible disc defect on MRI (11)! (Click here for the false positive rates for MRI.) Even more confusing is the fact that some patients who completely recover from the back pain and sciatic, still have the same disc herniation appearance on follow-up MRI! Other ironies of disc herniation have been discovered. For example, we have learned from the work of Karppinen et al. that the size and severity of disc herniation do NOT correlate with the degree of patient pain, disability, or suffering (170). That is, small disc herniations and even disc bulges may causes just as much pain and disability as massive disc herniations and even extrusion. THE CONTAINED DISC HERNIATION: Another strange irony is the fact that smaller and innocent looking disc herniations (i.e., contained herniations [aka: protrusions, or subligamentous herniations]) are the most refractory to treatment (difficult to treat) and respond less favorably to decompressive surgery (discectomy) and conservative care, when compared to the larger and more advanced disc extrusions and sequestrations (50, 51). More specifically, in 2001 famed, Volvo-award winning researcher Eugene Carragee published a paper that indicated patients with a contained disc herniation, i.e. measuring less than 6 mm, had a success rate of only 24% after discectomy. That was compared to a success rate of 98% for patients with a large herniation (9 mm or more) (10 50). So how do we treat such a small contained herniation? Derby et al (151) says, unfortunately, that we have yet to discover a good cure and interbody fusion (which empirically has a horrible reputation) is the alternative. However, we have a technology called Nucleoplasty, as well as other minimally invasive nuclear decompression devices, which are trying to bridge the gap between fusion or discectomy. Unfortunately, the evidence is not quite there and even the leading researchers can't agree on the efficacy of these percutaneous Nucleotomys (149, 150). Read below for more. And to further cloud the water, we now know that sciatica (a horrible burning lower limb pain associated with disc herniation) is not always causes by the direct compressive pressure from a herniated disc. That is, it can be caused from nuclear material "leaking" from the back of the disc onto the adjacent nerve roots, i.e., chemical radiculopathy (3, 4) and/or from chemical and pressure irritation of the posterior intradiscal nerve fiber, i.e., the sinuvertebral nerves, which is called discogenic sciatica (1,2). So, diagnosing a patient of whom complaints of back and lower limb pain is certainly not as easy as once believed. It was the famous research paper of Mixter and Barr (42) that first elucidated a herniated disc as the cause of back pain and sciatica. It was further reported that open surgical treatment as an effective intervention (42). Over the last thirty-years there have been several well-designed medical investigations to support the notion that surgery is no more effective than conservative care--in the long run--as a treatment for disc herniation related back pain / radiating lower limb pain or neck pain / radiating upper limb pain. The best in my humble opinion was the Volvo Award Winning Weber study. The bottom line of this randomized trial was what I just said: disc surgery may get you out of pain and back to work faster, but in the long run there is no real difference in treatment outcome. This research was confirmed by another giant, more modern investigation (13). In a more recent study, (2007) Peul et al published the results of their medical investigation into surgical outcome of sciatica in the prestigious New England Journal of Medicine. Like Weber, they randomized over 200 patients into either a disc surgery group or a conservative care (non-surgical) group and found the same result: the patients who had surgery, got rid of their leg pain faster; however, at the one year follow-up, the surgical patients were no better off than the ones who went the non-surgical route [An abstract of the study is here]. TREATMENT OPTIONS: SURGERY VERSUS CONSERVATIVE CARE One of the horrible complications associated with a herniated lumber disc is sciatica--a terrible burning, stinging, shooting pain that travels from the low back all the way down the lower extremity usually into the foot. The annual incidence of disc herniation-induced sciatica is 5 per 1000 people [8,9]. One of the most surprising discoveries regarding treatment options for disc herniation-induced radiculopathy is that disc surgery (microdiscectomy) and conservative non-surgical treatment work the same with respect to over-all long-term improvement [Weber]. The only advantage of microdiscectomy is that usually gets the injured person out of pain and back to work faster than conservative care alone IF the surgery is done in time (less than one year) and IF they are a proper candidate for the surgery. The only true indications for surgery are (1) they simply can't stand the pain, (2) they have a progressive worsening of neurological symptom (i.e., worsening of muscle weakness in the upper or lower extremities) and (3) the development of the dangerous cauda equina syndrome. All of the latter three conditions are surgical musts in most cases. Another important thing to understand is that 10% to 40% of microdiscectomies FAIL and leave the patient suffering what is called "failed back surgery syndrome [104]. DISCECTOMY: According to the medical research, if you must have surgery for disc herniation-related back pain / sciatica, open discectomy (aka: microdiscectomy) may be the way to go (99). However, surgery is indicated only if conservative treatment has failed and/or if you have the danger signs associated with disc herniation: loss of bowl and/or bladder control (cauda equina syndrome); progressive worsening of the neurological state (root-related atrophying muscles, progressive muscle weakness [foot drop]); absent reflexes and/or a worsening, intractable pain. Furthermore, open discectomy works much better for just herniations that are non--contained (i.e., extrusions or sequestrations) (40). When to have the surgery is also critical in order to increase the chance of success (not so with fusion type surgeries). That is, you certainly don't want to wait any longer than one year before having the surgery for disc-herniation related sciatica (50)--three or four months is about all you should wait. See the Surgery Timing Page for more information. Open discectomy (i.e., microdiscectomy, open discectomy, laminectomy) is not a panacea and works poorly for small contained disc herniations (100, 101). MINIMALLY INVASIVE TECHNIQUES: It all started with a papaya enzyme that was used to dissolve the center of a herniated disc. More specifically, in 1959, Smith (43) reported on a new treatment intervention termed "chemonucleolysis," which used chymopapain (a substance derived from papaya fruit) to digest a portion of the nucleus pulposus in hopes of decompressing a herniated disc from the inside (This technique is now banned in the United States secondary complications). In the 70s and 80s, Hijikata (44) and Onkin et al (45) respectively, developed the first minimally invasive percutaneous lumbar discectomy. While the first model was manually operated (44) it was soon automated, which was termed the automated percutaneous lumbar discectomy (APLD) (45). The next procedure invented was based on the principles of APLD and called the DeKompressor system (117-119). According to Manchikanti et al (33), we now have the forthcoming different approaches to percutaneous disc decompression and all have been shown to reduce intradiscal pressure (which in turn ostensibly diminishes pressure on sensitized sinuvertebral nerve endings in the outer annulus of the disc): #1) chemonucleolysis ( not available in this country anymore); #2) percutaneous nucleotomy; #3) percutaneous discectomy; and laser treatments (34-39). So if a symptomatic contained disc herniation only has a one in four chance of being cured via traditional micro/open discectomy(10), then how the hell do you treat it? There are a gaggle of minimally invasive techniques that have come to fruition over the years. First we have the percutaneous techniques that all involve poking a small needle into the center of the disc and removing nuclear material. This in turn reduces the intradiscal pressure, which in turn is supposed to suck the herniation back inside the disc. Percutaneous Laser disc decompression (PLDD): Another version of this pre-cutaneous technique uses a laser to diminish nuclear material, which in turn is supposed to reduce the size of the contained disc herniation. Although some authors have claimed this PLDD the best thing since sliced bread for treating contained herniations; other authors disagree (7, 15) in part because (amazingly--this has been around for 20 years) there has yet to be a randomized controlled trial completed to tell us whether or not this treatment is really efficacious– that is about to change (14). Other authors have published opinions that laser discectomy may be associated with end plate injury and has enjoyed less success than chemonucleolysis in randomized studies [52]. Nucleoplasty: Percutaneous Disc Decompression using Coblation technology (Nucleoplasty) was approved by the FDA in year 2000 and gained immediate popularity among surgeons (46, 41, 47). in fact, within two short years it was utilized in approximately 8000 patients (16); the official name of the procedure is called Nucleoplasty. This technique uses radiofrequency energy to remove nuclear material and create small channels within the disc (41). The channels within the nucleus are then thermally treated to produce a zone of thermal coagulation. So you could say Nucleoplasty combines coagulation and tissue ablation (it is this ablation process that is the patented coblation technology), which in turn decompress the herniated disc. Does it work?: During the 12 years since its FDA approval, the efficacy of the procedure remains controversial, notwithstanding the increasing utilization of the procedure. For example, Gibson and Waddell (two extremely respected and world-renowned spinal researchers) stated that all minimally invasive decompression techniques including coblation therapy "should be regarded as research techniques."(40) To make things even bleaker, The Centers for Medicare and Medicaid Services (CMS) issued a non-certification for these intradiscal procedures (48). More specifically, these noncertified, thermal intradiscal procedures are percutaneous or (plasma) disc decompression (PDD) or coblation, along with other intradiscal therapies. THE TUTORIAL: THE BIRTH OF A DISC HERNIATION Lets begin our tutorial with a quick review of the normal disc, and then proceed through each type of herniation. (For a full review of disc anatomy and physiology, please visit my 'Disc Anatomy Page'.) Figure #1: The 'Nucleus Pulposus' (pink #1), which is a water-rich gel-like mass of proteoglycan material, has the duty to support the tremendous 'Axial-Load' (weight) of the body. This nucleus is 'corralled' by the stronger 'Annulus Fibrosus' (green #2). The annulus is made out of concentric rings of a cartilage-like material called 'lamellae' (#9). It is this specially arranged collagen that gives the annulus the tremendous strength needed to hold that nucleus in place. Key Concept: The nucleus pulposus, because of the tremendous axial load upon it, is constantly trying to escape from the confines of the center of the disc. If it does manage to escape (tear) through the PLL (#7), the appearance on MRI is called a disc extrusion. The 'Posterior Longitudinal Ligament' (PLL #7) shields the delicate posterior neural structures and acts as a last line of defense against the potentially irritating nucleus pulposus. Note the posterior disc is 'concave' in shape, as outlined by the PLL. (It will not stay concaved for much longer!) The 'posterior neural structures', which are very sensitive to pressure and chemical irritation, include the following: 'Spinal Nerve Roots' (L4, L5, S1), 'Dura Mater or the Thecal Sac ' (red star), and the 'Dorsal Root Ganglion' (DRG). To learn about the anatomy and physiology of the disc go to: [Disc Anatomy]. And finally we have the Sinuvertebral Nerve (# SN). The Sinuvertebral nerve innervates (connects to) the outer 1/3 of the annulus fibrosus. These tiny nerve ending have the ability to carry PAIN messages to the brain and are thought to be on of the causes of discogenic pain. (Read my IDD page, for more information on discogenic pain.) Oh, one more thing; the epidural space (#8) contains the traversing nerve roots (L5) that are often the favorite target of the compressive disc herniation. THE DISC BULGE: The First Step Toward Disc Herniation: In order for a disc to herniate, its structural components must first 'weaken'. This weakening occurs as a result of Disc Degeneration. Disc degeneration occurs naturally, to some degree, in all disc, but in some people the process become especially severe and damaging. The 'bottom-line' of the degeneration process is that the annulus becomes dried (desiccation) and brittle, hence allowing for the development of Disc Bulging and full thickness posterior annular tearing, or Internal Disc Disruption.
DISC PROTRUTION: Posterior Longitudinal Ligament is still Intact. Figure #3 demonstrates a 4 millimeter disc protrusion The type of presentation in Figure #2. would be 'officially' classified as a 'Disc Herniation' or, more explicitly, a Disc Protrusion (aka: contained herniation or subligamentous disc herniation). Although disc protrusions are seen in about 30% of the normal non-symptomatic population, nerve root compression is not, and if much more indicative of a 'problem. This patient may well be suffering right sided radicular pain (sciatica) and/or lower back pain as a result of compression/irritation of the traversing nerve root and/or irritation of the sinuvertebral nerves in the posterior of the disc. THE DISC EXTRUSION: The Posterior Longitudinal Ligament has ruptured. Figure #4. demonstrates a more serious progression of our pathologically degenerated disc: An 8 millimeter Disc Extrusion (aka: non-contained herniation, transligamentous herniation) is now present. The PLL (blue) has finally been defeated and has completely ruptured, DISC SEQUESTRATION: The Final End-Phase of the Disc Herniation.
Sequestration (aka: sequester, free-fragment) may be excruciatingly painful (back and leg pain - sciatica) and, if centrally located, may occasionally cause the patient to lose control of their bowl and bladder function, i.e., Cauda Equina Syndrome, which is considered a 'Medical Emergency'! As with the disc extrusion, the sequestration may also undergo a reduction in size from a combination of an immune attack {macrophage attack} and dehydration, although frequently the patient will need immediate decompressive surgery to beat this monster!
Figure #6. These T1 MR images demonstrates a large 9mm disc extrusion (red star) as visualized on both the Axial (over-head) and Sagittal
Note that this extrusion has completely blotted out (can't see) the right traversing S1 nerve roots (left side of image) and has pinched it against the lamina (tiny green arrow). Note the thecal sac is moderately to severely compressed by this large herniation, as noted on both the axial and sagittal images (between blue arrow and red star). This young man (24 years) has avoid surgery and is doing fairly well, although his days of heavy work are probably over for good.
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Figure #2 demonstrates the 'pre-cursor' to a disc herniation. This type of disc lesion - that bulges into the anterior epidural space without any area of focal-ness or out-pouching - would be called a '
and represents a worsening of our disc bulge. The posterior of the disc is 'focally' or 'eccentrically' pushing backwards into the anterior epidural space and has contacted, and even somewhat compressed, the traversing nerve root (white star) and right front corner of the thecal sac. Note that the PLL (blue) still has NOT be disrupted and is still "containing" the near-herniated nuclear material. 
hence allowing for further migration of the the nucleus pulposus into the anterior epidural space. Note the marked displacement of the traversing nerve root (white star) AND the exiting nerve root (green star) (which has now turned completely red with inflammation and venous congestion - the precursors for Radiculopathy). This Disc Extrusion is NOT typically seen in the asymptomatic person and is often an indication for surgical decompression; the 
Figure #5. represents the end-of-the-line for the cycle of disc herniation. Now we can see that a big 'chunk' or 'fragment' of nuclear material has detached itself from the main body of the extrusion is and loose in the epidural space. Note the resulting severe compression of the traversing nerve root (white star), the exiting nerve root (green star) and the lateral aspect of the Thecal Sac (blue star). 
(side) views.