Internal Disc Disruption (AKA - IDD, or Discogenic Pain): A General Overview
Just because that MRI of yours was deemed "normal" by your doctor does NOT always mean that your back and even leg pain isn't coming from that "normal" looking disc. This especially holds true if your supposedly normal MRI demonstrates a bulging disc that appears "black" on the T2 weighted MRI images. That is because you may have tears (annular tears) within your disc that are irritating the tiny pain nerves of the outer annulus, and they usually do NOT show up on MRI. Moreover, these annular tears have been shown to be the pain source in the majority of patients in whom suffer chronic pain .
The syndrome of radiating lower limb pain (aka: radicular pain or sciatica) was first mentioned way back in 1935, when Mixter and Ayers  wrote that radicular pain could occur without the presence of compressive disc herniation. However, it took another 50 years before the modern concept of disc-related sciatica became elucidated. More specifically, in his 1986 presidential address, H. V. Crock told members of the international spine society that 'internal disruptions' within the architecture of the disc could result in back pain as well as lower limb pain without the presence of spinal nerve root compression (9). He termed this condition "Internal Disc Disruption," (IDD), which is synonymous with the term Discogenic Pain.
IDD occurs when the disc develops a rip or tear in the annulus fibrosis (i.e., develops a full thickness radial annular tear ) that bisects the disc from inside to outside and allows communication between the jello-like center [nucleus pulposus] and the nerve-infested periphery annulus fibrosis without the presence of any surface outpouching (in other words, no disc herniations. If there is a disc herniation, then you have a "disc herniation" and not IDD).
Fig.#5 The white arrows depict a full thickness radial annular tear within the L4/5 disc that in this case completely bisects the disc (there are many different flavors of annular tear). Note also that the disc above (the L3/4 disc) has a small tear in the outer fibers of the annulus (black arrow) that has not made it (yet) into the middle of the disc. This type of tear is called a 'rim lesion'.
In order to understand how IDD may cause pain, you will need to know some basis disc anatomy. If you are a little shaky on disc anatomy, please visit my disc anatomy page before you proceed [here].
Fig.#4 demonstrates the normal lumbar disc anatomy: Here, in this over-head view, we have the nucleus pulposus (pink) surrounded by the the stronger annulus fibrosus (green). Normally, the annulus fibrosus is strong enough to contain or corral the pressurized nucleus pulposus and keep it from escaping (squirting) outward. Of particular interest to the upcoming discussion are the tiny 'Sinuvertebral Nerves Endings' (yellow poke-a-dots). These tiny nerve fibers, which are embedded within the posterolateral substance of the outer 1/3 of the annulus fibrosus, are known to both initiate and carry the perception of pain into the spinal cord. From there, these pain signals are carried upward to the sensory cortex of the brain. (386-388, 439).
ADVANCED: The pain pathways (how the pain gets from the disc to the brain) for discogenic pain are still very controversial and may not function as traditional anatomy has taught us. Traditionally, pain signals that originate in the nerve roots adjacent to the disc or in the disc move from that root, into the corresponding DRG and then into the spinal cord. However, some new research suggests that pain signals from the lower lumbar discs (L5 and L4) are (at least in part) detoured up the sympathetic nerves (i.e., gray ramus communicans) and into the upper lumbar DRGs - especially at the L2 level. (11, 259, 260) Clinically, in some patients it then would be possible for patients with L4 and L5 disc problems to have L1 or L2 dermatomal pain (groin and anterior thigh pain).
IDD: In a Nut Shell:
When a Radial Annular (aka: anular - as they spell it in the UK) tear reaches the outer 1/3 of the posterolateral annulus (Fig.#3) and exposes the sinuvertebral nerve-endings to degenerated nuclear material (cytokines), which may have nerver been seen by the bodies immune system, pain may well occur secondary to chemical irritation of these pain-carrying fibers and possibly an autoimmue type reaction. This type of pain is called 'Discogenic Pain,' which means that the pain arises from within the disc. In Fig. #3 the disc has ripped through or "disrupted" and has allowed nuclear material (pink) to escape into the outer and sensitive 1/3 of disc (i.e. the annulus fibrosis). The sinuvertebral nerves (yellow dots) in contact with this degenerated nuclear material have become inflamed (red dots) and irritated, which in turn causes pain signals to 'fire off' to the dorsal horn of the cord and then to the brain, which causes the patient to feel pain. Some patients even suffer a referred type pain (discogenic sciatica) down the lower limb(s) from this condition, yet they have no traditional compression of the adjacent nerve roots to explain it. [jump to tutorial]
IDD was first described by Crock in 1970 (8) and again in 1986 (9). It was then described as a ‘disruption' of the internal architecture of the disc without signs of disc protrusions or without positive signs for nerve root compression’.
In his 1986 presidential address, Dr. H. V. Crock told members of the international spine society that internal disruptions within the architecture of the disc could result in back pain and even lower limb pain without the presence of spinal nerve root compression (9). He termed this entity ‘Internal Disc Disruption’ or IDD.
In 1995, a 'Dream Team' of well respected and Volvo Winning researchers (Schwarzer, Aprill, Derby, Bogduk) set out to test and further develop Crock’s theory of IDD and convincingly calculated the prevalence (frequency) of IDD in patients with chronic low back pain. (2) The study also attempted to determine if traditional examination findings and/or specific patient symptoms could be predictive of the diagnosis of IDD. By following the strict criteria specified by the ‘International Society for the Study of Pain in its taxonomy’ (21), these investigators calculated the prevalence of IDD to be between 30% and 50% with a 95% confidence limit. They also concluded that neither traditional examination findings nor patient symptoms could predict whether or not a patient had IDD. Unfortunately, it looks like provocation discography remains the only way to confirm the diagnosis of IDD.
The theory of IDD as a source of chronic back pain is not without its critics. In 2003, Lee et al. reviewed the research on IDD from 1985 through 2000, (10) although the papers review were mostly geared toward radial tears and HIZ. He summarized that of the 13 research papers on IDD and similar topics, there was not much agreement on what made the diagnosis of IDD. There was, however, some general agreement between the groups on what constituted the diagnosis of IDD: lower back pain, reproduced on provocative discography (concordant pain was a strong indicator), and a normal neurological examination, i.e., no loss of reflexes, no loss of muscle strength or atrophy, and no sensory loss. That's it, only two factors! Other criteria for the diagnosis of IDD were not so universally agreed upon were: the presents of an HIZ (high intensity zone) within the posterior outermost region of the disc on the T2-weighted MRI, disc degeneration, and a history of trauma.
Based on their review of '15 years worth of research', Lee et al. boldly concluded that “IDD is not real, but a hypothetical disease”. This Korean group further stated the following; “Our personal view is that IDD is a doctor-made disease, that is, an iatrogenic disc disorder, which may lead to an unconventional invasive operations (referring to the IDET procedure and Lumbar Fusion).” (10) Lee felt that because the diagnosis was so dependent upon the 'subjective input' from the patient, during discography, that the diagnosis should be thrown out!
IMHO: Lee, who is way out of his usual area of research on this subject, is going to get 'blasted' for making such aggressive statements against the theory of IDD, which has been accepted by the 'North American Spine Society' (21) and the 'International Society for the Study of Pain in its Taxonomy' (21)! For the typical non-mentally compromised chronic pain patient, the diagnosis of IDD can be made with a reasonably degree of medical certainty by using the criteria that the International Society for the Study of Pain in its Taxonomy have adopted (Here) for the criteria.
Although controversial (436), discogenic pain secondary to IDD is thought to be responsible for a substantial number of chronic back and leg pain cases where obvious nerve root compression is absent/lacking (132,2). In fact the famous multi-time Volvo Award Winning author, professor Nikolai Bogduk MD, believes IDD is the "most common cause of chronic low back pain" (1,2) and may be often over-looked by the treating physician." (132).
Quality scientific research has demonstrated that 40% of all chronic back pain is caused by the radial annular tears of IDD (2), and often presents (62% of the time according to Ohnmeiss et al.) as back pain and/or pain down the lower extremity, i.e., sciatica (6).
The exact mechanisms of discogenic pain are still controversial; however, the development of a full thickness Radial Annular Tear that leaks nuclear material (cytokines) into the outer annulus is most certainly involved in this syndrome. This annular disc leak theory has been confirmed scientifically via numerous quality peer-review investigations (105,115,116,123,124,131).
Recently, it has been demonstrated that IDD was the causative factor in about three-quarters of severely acute nonspecific low back pain patients. More explicitly, in 2005 Hyodo et al (16) performed MRIs and discography on 55 patients who all suffered severe, immobilizing, non-specific low back pain without sign of neurological deficit. In 73% of these patients, a full thickness non-epidurally leaking annular tear was identified on discography that responded to fluoroscopic lidocaine irrigation (a powerful anesthetic) by instantly 'stopping' the patient's perception of severe pain. (16) The aforementioned experiment strongly advocates that full thickness annular tears – or IDD – are a major cause of severe acute non-specific low back pain.
Why do annular tears affect patient in the forth and fifth decade of life?
Why the pressure buildup? Onik goes on to explain  that the intervertebral disc may be considered an osmotic system and because of a breakdown in macromolecules during the fourth and fifth decades of life, the number of particles in the intervertebral disc increase, which in turn causes a concomitant rise in osmotic pressure secondary to an influx of fluid, which in turn increases the intradiscal pressure. In order to relieve the pressure, annular fissures develop that result in symptomatic annular tear and disc protrusion and PAIN.
The 'International Society for the Study of Pain in its taxonomy’ (21) has adapted the following set of criteria for diagnosing IDD: ►) no visible disc herniations may be seen on MRI or CT; ►) during provocation discography injection of the suspect disc with contrast, a recreation of patients 'exact' back and/or leg pain must occur (353,9); ► injection the disc above or below the suspect disc must be non-painful; this acts acts as a 'control disc' or normal disc; and ► a grade 3 or 4 radial anular fissure must be demonstrated on CT discography (2,351,352,355).
Provocation discography, which may actually further damage the disc, should ONLY be attempted if the chronic pain patient can no longer live with their pain syndrome and is contemplating IDET, SED, DiscTRODE, interbody spinal fusion or ADR. Furthermore, their Oswestry better be at least a 50! (Oswestry)
The 'Gold Standard' in making the diagnosis of IDD is a very painful and invasive test called 'Provocation Discography' with follow-up CT discogram. There are two components to provocation discography: the first is an attempt by the doctor to 'provoke' or 'cause' the patient to feel their 'usual' pain (concordant pain) by pressurizing the disc with a contrast material. Note: in Fig.#6 the center of the disc is being filled with contrast material (white). If you look closely, you can see the fine 'white' needle (black arrows) entering the posterior of the disc. This (fig. #6) represents a normal disc that 'holds' the dye within the nucleus and does not demonstrate any anular tearing.
Fig.#7, on the other hand, demonstrates two completely disrupted discs: The contrast material (black in this photo) has NOT been contained within the center (nucleus) of the disc. This time, it has clearly leaked through internal 'disruptions' within the posterior annulus of the L4/5 and L5/S1 disc. In fact, the L4/5 disc has been completely disrupted and it leaking contrast material directly into the epidural space (black arrow). The latter situation is called a Grade 5 anular tear or Grade 5 IDD. (learn about the Dallas discogram naming system and the different degrees of disc disruption here about half way down the page.) This situation may indicate big trouble, especially if you are one of unfortunates who are 'sensitive' (allergic) to those leaking biochemicals (cytokines), for the delicate posterior neural structures 'dwell' adjacent to the posterior of the disc and may become inflamed and/or damaged from this leakage. More explicitly, substance like TNF-alpha, IL-1, IL-6, NO, Phospholipase A1 may stimulate some form of 'attack' within the nerve root and ultimately lead to permanent nerve (axon) death. Neuropathic pain may be spawned.
Although provocation discography with CT discography is the "gold standard" when it comes to making the diagnosis of symptomatic IDD, the procedure itself can inflict damage upon the disc and "spawn" degenerative disc disease (30-34,530). As an alternative, the use of gadolinium (contrast) enhancement may be considered. Gadolinium-DTPA, which is injected into the blood stream during the MRI, will "light-up" the granulation tissue that forms within a healing/healed full thickness annular disc tear.
Fig.# 9: The MRI images to the left demonstrates how gadolinium will "light-up" a healed anular tear. Note the L4 disc shows no sign of posterior disc tearing (black arrow); however, after the administration of gadolinium during the MRI, the same T1 image demonstrates the remains of the massive annular tear (red arrow) I suffered back in 2002.
The gadolinium also high-lights continued swelling/granulation tissue within my L5 disc over 1 year post microdiscectomy. No disc herniations are noted.
The HIZ phenomenon also give us a clue that Internal Disc Disruption might be involved in the patients pain syndrome although this T2-weighted MRI finding is highly controversial. For more information, visit my HIZ page.
To begin this tutorial, lets look at what a normal disc looks like from the over-head view (axial):
In Figure #1, the basic anatomy of the disc is shown: First note the gelatinous and hydrated nucleus pulposus (#1 pink) that is corralled (held in place) by a tough and fibrous annulus fibrosus (#2 green). To give the annulus fibrosis, which is like the tread of a tire, extra support posteriorly, the posterior longitudinal ligament or PLL (#7 blue) exists and is tightly bound to the outer fibers of the a nul us. Also note the posterior neural structures: #10 (motor & sensory nerve roots), #3 (mixed spinal nerve roots), and red star (free-hanging nerve roots within the cauda equina). It is these delicate neural structures that often become damaged and perpetually generate pain. To learn more about spinal anatomy, go 'here'.
It is extremely important to understand that, unlike the rest of the avascular disc, the outer 1/3 of the a nul us fibrosus, the cauda equina (red star) and the PLL (blue #7) are innervated with (full of) tiny nociceptive C-fibers (pain carrying nerve fiber) that, if irritated, have the potential to cause severe PAIN and DISABILITY within the patient (4,55,56).
The first step in the IDD process is for the disc to first degenerate (lose water content and become brittle) and then (usually because of trauma to the back or neck) tear open from the inside out, or, sometimes, from the outside in (30-34,530). Ironically, however, it seems that IDD can both 'cause' disc degeneration or result from its presents. (5) The disc in figure #2 shows what is commonly called Degenerative Disc Disease (DDD). DDD, which can only be seen on T2-weighted MRI that will affect the disc by causing a loss of water content, which in turn causes the disc to become brittle and prone to tearing. In Figure #2., which represents a Grade IV Radial Anular Tear, our disc has obviously changed in appearance when compared to Figure #1 and now demonstrates disc desiccation (dark green appearance), bulging (note how the posterior of the disc is no longer concave and has bulged into the nerve roots), and a full-thickness radial anular tear (red arrow) that has allowed nuclear material (pink) to come in contact with the ultra-sensitive sinuvertebral nerve-endings (yellow poke-a-dots). For some of us, this situation is truly disastrous! Full thickness radial anular tears, however, (red arrow) are not the only anular sign of the degeneration process: concentric anular tears (white arrows) and rim lesions - which also may result in severe back pain - are also often present in the pathologically degenerated discs and may also eventually spawn the deadly, disc-extrusion-producing, full-thickness radial tear (30-34). Note in Figure #2, the sinuvertebral nerve-endings adjacent to the anular tear have become inflamed (red), pissed-off, and are sending pain signals up to the brain through both the sympathetics (gray ramus) and the same-level afferent nerve roots.
In figure #7, the situation has worsened into the grade V radial anular tear (ship's anchor). This massive disruption, which may or may not be 'leaking' nuclear material upon the adjacent nerve roots, is irritating even more sinuvertebral nerve-endings and is probably resulting in much more patient pain and suffering and even may cause referred pain down the back of the leg (fake sciatica, or discogenic sciatica) that mimics sciatica (6,7).
The pain mechanism of IDD not only comes from irritation of the now-exposed sinuvertebral nerve endings: a the second mechanism of pain my occur from mechanically pressure upon these nerve endings.
As if things aren't bad enough, let's meet the dreaded Grade V Full Thickness Anular Tear:
IDD is a very, very tough condition to treat, especially since the diagnosis is fairly controversial to begin with and many primary doctors have never even heard of it. Conservative care is ALWAYS the first form of treatment! If this fails then provocation discography is indicated before proceeding to the more aggressive treatment options but your Oswestry should be in the 50s. Here are the current (7-28-04) treatment options available of IDD:
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