DEGENERATIVE DISCOGENIC SYNDROME
Screening by radiology, CAT and MRI
International Publicized Data
GMCD Instructional Course Lectures
Dr. med. Guy M.C. Declerck MD (GMCD)
Medical FRCS-, FRCS Ed Orth-, M Ch Orth-, PhD-studies
Spinal Surgical and Research Fellow, Perth, Western Australia
Spinal Orthopaedic Surgeon and Surgical Instructor
Consultant R&D Innovative & Restorative Spinal Technologies
President International Association of Andullation Technology (IAAT)
Copywriter / translator: Filip Vanhaecke PhD
Illustrative expertise: Lennart Benoot, Mincko, Halle and Natacha Monstrey, HHP, Flanders, Belgium
Artistic expertise: Alonso Ríos Vanegas, sculptor and writer, Medellín, Colombia
Page layout: Lennart Benoot, Mincko, Halle, Flanders, Belgium
Review scientific literature: Medical Consulting Advice, Ostend, Flanders, Belgium
Support: International Association of Andullation Therapy (IAAT)
Legal advice: Anthony De Zutter, kornukopia.be
Dedication to the Colombian Family Gloria Rúa Meneses and her sons Andres David and Juan Camilo Hinestroza both members of the National Colombian Waterpolo Team. For their friendship and hospitality. October 2014.
Relying on the work of giants is the lifeblood of scientific research. Indeed, if I have seen further, it is by standing on the shoulders of giants. One might even say that I have always depended on the kindness of strangers in this regard (*).
The continuous support by professor BA Kakulas (Neuropathology), professor JR Taylor (Spinal Anatomy and Human Biology), and Sir George M Bedbrook (Spinal Orthopaedic and Rehabilitation Surgeon) made it possible to analyse 23539 post-mortem human spines, normal and pathological, in the Department of Neuropathology, Royal Perth Hospital/University Western Australia, Perth.
Note: in order not to disturb easy reading of the underneath scientifically based chapters, only a few authors are mentioned in the text where dr. Guy considered it essential. Their names are placed between brackets. Further information on their individual research can be read in the last chapter ‘Literature Encyclopaedia’.
(*) Mirsky Steve. Technology is making it harder for word thieves to earn outrageous fortunes. Scientific American, February 2014, p. 64
The two most commonly used methods for radiological evaluation of the lumbar intervertebral discs (IVDs) still comprise the magnetic resonance imaging (MRI) techniques and the assessments by discography. Most medical and paramedical practitioners rely on these methods to localize the pain generators in order to plan their therapeutic approaches. However, more and more concerns have raised regarding the sensitivity* and specificity** of these investigative methods. And on the other hand, discography is a far from safe procedure.
It has even been stated that psychologically stable patients (i.e. based on the MSPQ and ZUNG tests) who present morphological abnormalities on MRI in conjunction with positive provocative pain responses on discography finally benefit well from rigid spinal fusion techniques. Notwithstanding this lucrative statement, the results of randomised trials comparing nonoperative care to surgery for degenerative discogenic chronic low back pain indicate that the benefit from surgery ONLY varies from 7 % to maximum 18,7 % (Brox; Fairbank; Fritzell; Mirza). Just imagine that a figure of 7 % to 19 % presents your results at school level!
Based on his macroscopic (and sometimes microscopic) analysis of 23539 post-mortem normal and pathological human spines, his personal operating experience in over 2000 spinal surgeries (none were discectomies!), and intense review of the huge but related literature, the author likes to summarise his personal understanding of the value of MRI and discography.
* Sensitivity is the prevalence of true-positive results when a test is applied to patients who are known to have a particular disease. Sensitivity is defined as the number of true-positive results divided by the sum of the true-positive and false-negative results
** Specificity describes the prevalence of true-negative results when a test is applied to patients who are at risk for a particular disease but are known to be free of it. Specificity is defined as the number of true-negative results divided by the sum of the true-negative and false-positive results
The aging processes, normally starting around 35 years of age, gradually disrupt and fragment the nucleus pulposus. This strictly normal and natural evolution is not at all the reason for developing chronic intermittent or chronic undulating LBP but may be responsible for the occasional occurrence of a low back pain attack of short duration (3 to 5 days).
Neither do the aging processes spontaneously lead to degenerative changes! In other words, IVD degeneration is by no means synonymous to acceleration of the normal aging processes.
On the other hand and in around 80 % of all human beings worldwide, the aging processes are complicated by degenerative processes. A variety of factors (genetics, biology, nutrition, biomechanics, trauma to the IVDs) cause the IVD to suffer degenerative breakdown in their three distinct structures (nucleus pulposus, annulus fibrosus, and endplates) which varies from one lumbar disc to the other.
For a lumbar IVD starting to degenerate, one or both conditions need to be present: fully developed in-to-out annular tears and/or fissures and ruptures in the endplate(s). These degenerative events do not occur in all lumbar IVDs at the same time, nor at the same speed and certainly not with the same intensity. Some IVDs never will show degenerative signs, others disintegrate severely (Fig. 2a).
Fig. 2a. Typical degenerative signs in the L4-L5 IVD. Although the genetic influence for developing degenerative changes is identical for all lumbar intervertebral discs, the degenerative intradiscal cascade evolves differently in each of these discs and depend as well on the characteristics of routine daily activities. In this 50 year old male and heavy labourer, the aging processes are responsible for the typical brown colour in the nucleus pulposus at the L3-4 IVD. The L4-5 IVD presents the typical degenerative signs: disc height loss with fragmented nucleus pulposus, ruptures of the endplate and the annulus fibrosus. An anterior ‘herniating’ pathway is present as well. At the L5-S1 IVD level the posterior annulus is ruptured with subsequent protrusion and disc height loss. Inflammatory reactions compatible with the MRI Modic signs (see further) are visible at L4-L5 and L5-S1 (subchondral intra-osseous light brown discoloration).
Left: Declerck / Kakulas, Neuropathology, Perth, Western Australia, A90/139
Right: detailed illustration by Alonso Ríos Vanegas (www.alonsoriosescultor.com)
The annulus fibrosus-type of IVD degeneration should be differentiated from the endplate-type of IVD degeneration. It is known since 1932 (Schmorl and Junghanns) that annular ruptures and IVD degenerative changes are more prominent at the lower L4-L5 and L5-S1 lumbar disc levels. In the upper levels (L1-L2 and L2-L3), Schmörl’s nodes develop frequently (Fig. 2b). IVD degenerative changes in the IVDs are uncommon (0 to 14%) and endplate ruptures much more frequent. The L3-L4 IVD is a kind of transitional zone where both annular and endplate ruptures appear in equal percentages.
Fig. 2b. Schmorl nodules develop as a consequence of growth failures. They occur mostly at the level of the upper endplates of the T6-T7 till the L3-L4 intervertebral spaces, seldom at the L4-L5 interspace, but are extremely rare at the L5-S1 level. If not associated with concomitant degenerative discogenic changes, it is impossible to know if these abnormalities are the reason of pain.
(Declerck / Kakulas, Neuropathology, Perth, Western Australia, A90/144)
As a consequence of the disintegration of the nucleus pulposus and/or the annulus fibrosus, and/or the endplates, the weight bearing capabilities and the load distribution throughout the IVDs are changing and MAY be the sources of provoking episodes of low back pain (Mulholland).
Qualitative degenerative changes cannot be seen on routine radiological investigations. On the other hand and when quantitative degenerative changes become visible, they are not routinely associated with the presence of low back pain.
Then, it’s quite simple: ‘pain cannot be seen with the presently existing radiological procedures’. Examined by magnetic resonance imaging (MRI), the so-called ‘black disc’ simply means the normal evolving reduction of water content. It has no value as an explanation for (chronic undulating or intermittent) low back pain. The classic signs of degeneration of an IVD on MRI (see further) have been reported to be present in as much as 85% of asymptomatic subjects in a population that was age, gender, and occupation matched to a back pain population.
Radiographs only show the ossified portions of the spinal column (Fig. 4a and Fig. 4b). As such, routine plain radiography has no purpose of detecting early intervertebral disc changes which may or may not be the source of low back pain.
Routine radiographs cannot evidence the normal aging processes in an intervertebral disc (IVD) because these processes are of molecular origin (Fig. 4a and Fig. 4b). Disc aging means losing water. Overall, the aging body is less capable of producing molecular water (H2O). At the same time, the nucleus pulposus starts decreasing the synthesis of proteoglycans leading to a decreasing hydrophilic capacity for attracting and containing water. Consequently, all the various qualitative aging changes in the IVD cannot be seen on routine radiographic evaluations, nor on CAT and on MRI.
Fig. 4a. Plain antero-posterior films only can display the ossified portions of the spinal column. It is simply impossible to draw conclusions regarding the aging processes in intervertebral discs.
Fig. 4b. Plain lateral images only can show the ossified portions of the spinal column. No conclusions can be made concerning the ageing processes in the three separate structures of the IVDs (the nucleus pulposus, the annulus fibrosus, the endplates).
On a radiogram, the first sign of disc degeneration appears as a decreasing IVD height. But by no means does it explain ‘pain’. Subsequent radiological signs (Fig. 4c) such as increasing intervertebral disc height loss, sclerosis of the endplates and central ‘gas’ accumulation (= vacuum sign*) within the disc tissue, and IVD resorption, have no value as indications of sources of pain for the chronic low back pain patient.
* Vacuum sign on radiography and CAT simply is granulation tissue surrounded by edema.
Fig. 4c. Radiographic signs of advancing IVD degeneration: intervertebral disc height loss, sclerotic endplates, central ‘gas’ accumulation (‘vacuum’ sign) representing granulation tissue surrounded by edema, (retro-) spondylolisthesis, osteophytes, calcifications in the anterior longitudinal ligament.
CAT scanners bombard the human body with X-ray beams which can damage DNA and create mutations that spur cells to grow into tumors. A single CAT-scan subjects the human body to between 150 and 1.100 times the radiation of a conventional x-ray, or around a year’s worth of exposure to radiation from both natural and artificial sources in the environment. Indeed, there is a very small cancer risk (Storrs).
CAT looks at the outline of the IVD and not at its structure. Therefore CAT cannot be used to examine the internal morphology of the lumbar disc (Fig. 5).
The fact that almost a quarter of healthy volunteers submitted to CAT scanning can be shown to have a disc herniating pathway should not alarm the patient and certainly not the surgeon. Discogenic bulgings, protrusions and extrusions are normal and mostly harmless expressions of the degenerating intervertebral disc. Indeed, many radiographic abnormalities seen on CAT are very prevalent findings in asymptomatic individuals. The so-called abnormalities are commonly encountered in many other conditions.
Fig. 5. CAT cannot be used to examine the internal morphology of the lumbar disc. Vacuum sign on CAT and radiography simply is granulation tissue surrounded by edema.
On the left and middle slides, ‘gas’ is seen in the L5-S1 IVD. On the right illustration, a normal spontaneous fusion is depicted as the result of the evolution of the degenerative processes in the IVD.
Right: normal spontaneous fusion following IVD degeneration
Reference A89/859 - Declerck / Kakulas, Neuropathology, Perth, Western Australia
Detailed artistic illustration by Alonso Ríos Vanegas - www.alonsoriosescultor.com
The principle of conventional MRI is simple. As water contains two hydrogen atoms and one oxygen atom (H-O-H), a strong electromagnetic field will excite and align these hydrogen atoms allowing sophisticated signal processing techniques to create morphological images (Fig. 6a). MRI allows determination of the proton density of the IVD which is indicative of the state of hydration. MRI will by no means indicate nor show pain!
Fig. 6a. Magnetic Resonance Imaging (MRI) contains a powerful magnet that aligns protons in the body and subsequently uses radio waves to detect small differences in proton density in the body.
The human body consists of approximately 90 % water. Aging means losing water. In other words, the IVD gradually will lose its water content . Indeed, the concentration of water in the nucleus pulposus can range from 90 % in the young and healthy IVD to a few percent in the elderly fibrotic disc (Fig. 6b and Fig. 6c).
Fig. 6b. In young and healthy IVD, the concentration of water in the nucleus pulposus ranges around 90%.
Declerck / Kakulas, Neuropathology, Perth, Western Australia, X83-478
Detailed artistic illustration by Alonso Ríos Vanegas - www.alonsoriosescultor.com
Fig. 6c. The concentration of water in the nucleus pulposus of an elderly fibrotic IVD ranges only a few %.
(Declerck / Kakulas, Neuropathology, Perth, Western Australia, X89-910, and
detailed illustration by Alonso Ríos Vanegas - www.alonsoriosescultor.com)
Static and functional positional and especially dynamic MRI, including T1- and T2-weighted images in the sagittal and axial planes, are best suited for nicely illustrating the morphological changes in the endplate, nucleus pulposus, annulus fibrosus, and subchondral bone in the adjacent vertebrae (Fig. 7).
The illustrations reflect the density of the hydrogen atoms and correlate with the dehydrating status of IVDs during post-mortem analyses. Dynamic MRI nicely shows the changing range of motion at the intervertebral level.
Fig. 7. MRI. T1 weighted sequence (left) and T2 weighted image (right) in the sagittal plane of an asymptomatic lumbar spine.
IVDs which present as a white signal (= high T2 signal intensity) usually have a normal height and normal morphology (Fig. 7).
Compatible with the author’s macroscopic analysis of lumbar IVDs in 23539 normal and pathological post-mortem human spines, the MRI reflects consistent features which are essential in understanding the evolutive degenerative processes in the lumbar IVDs (images are shown further down):
(1) the central nucleus pulposus starts presenting a dark nuclear signal (= reduced T2 signal intensity).
It only indicates the loss of hydration and an increasing fiber content,
(2) the nucleus pulposus will start showing fissures, clefts, and cracks in its matrix,
(3) the disc height reduces and even collapses,
(4) the annulus fibrosus decreases its lamellar organisation (delamination) and starts disclosing annular in-to-out ruptures and tears,
(5) both endplates, but the superior more than the inferior one, become disorganized: endplate ‘gaps’ and sclerotic zones,
(6) related to the specific attachment of the outer annular fibers to the endplates, rim lesions become evident
(7) hypermobility and abnormal motions (but no instability!) may be evidenced on the functional positional and dynamic MRI,
(8) pathological changes in the vertebral body become a hallmark of late-stage degeneration: subchondral sclerosis,
end-plate ossification and the formation of (stabilizing) osteophytes.
It is important to realise that none of all these MRI-changes are associated with one or more complaints related to chronic low back pain due to lumbar IVD degeneration (Fig. 8).
Fig. 8. Identification of degenerative changes on MRI of the lumbar spine. None signals pain! (A) Sagittal MRI of the lumbar spine demonstrates a desiccated or dark L5/S1disc. (B) Sagittal MRI of the lumbar spine shows a high-intensity zone (HIZ) in the posterior annulus of L5/S1. (C) Sagittal MRI of the lumbar spine depicts advanced degenerative changes in the L5/S1 disc, including Modic end-plate changes and a posterior disc protrusion.
In approximately 20 % of all chronic low back pain patients, infections, fractures, inflammatory diseases or malignant lesions are evident findings on MRI. The history, clinical examination and laboratory tests confirm these seriously incapacitating and sometimes lethal diseases.
MRI-studies are of poor diagnostic validity in the remaining 80 % of patients who only show abnormalities related to degenerative processes in the lumbar intervertebral discs. These are not life-threatening conditions but
only incapacitating in the so-called ‘high and middle income’ countries. In these countries, and for no scientific reasons, it seems to be accepted that the visible degenerative lesions in the nucleus pulposus and/or annulus fibrosus and/or endplates in the lumbar IVDs are the responsible sources for chronic low back pain (see images further down).
None of the following and visual degenerative changes have universally been proven to be a direct source for discogenic low back pain and/or painful hypermobility: disc space narrowing, nucleus dehydration or desiccation with signal intensity loss, loss of annular height, high intensity zones with radial annular fissures or ruptures, endplate defects, subchondral Modic changes, vertebral rim osteophytes, disc extrusions.
However, it is all too easy to conclude that one or more of the variety of visible morphological MRI-changes in these structures are explanatory for chronic low back pain. MRI simply cannot identify nor differentiate a painful from a painless disc (discography can) because pain as such can still not be seen!
As long as direct visualization of cells and molecules remains impossible in humans (as is possible with the Clarity-scan in mouse), an absolutely certain pain source can and will as yet not be found on MRI.
Although all lumbar IVDs continuously undergo biochemical and hydration changes due to the aging and degenerative processes, not all discs will demonstrate identical and abnormal MRI signal intensities.
On top of that, many individuals, who never experienced low back pain and are not chronic LBP sufferers, have MRI-based evidence of far advanced degenerative findings! In other words, many degenerative abnormalities on MRI are common findings in ‘normal aging’ individuals without low back pain. Indeed, in some scientific reports, up to 85 % of asymptomatic individuals who are age, gender and occupation matched to a population suffering chronic degenerative discogenic syndrome have been reported to have identical ‘abnormalities’.
Therefore, MRI must be approached with caution in the diagnosis of CLBP of discogenic origin, as MRI technology is unable to show pain.
The morphological degenerative changes may be essential but not sufficient to explain chronic low back pain. As Professor Mulholland, Nottingham, UK, clearly indicated, abnormal axial load transfer from one vertebra to another through the degenerating structures of an IVD, is the very probable reason for causing chronic low back pain. This is not at all synonymous with ‘spinal instability’.
Although static, functional positional, and especially dynamic magnetic resonance imaging techniques remain an indispensable tool in diagnosing and analyzing spinal conditions, the MRI appearance of a lumbar IVD do not reflect the mechanical competence of the IVD. Indeed, extensive variability of stress concentrations in the nucleus pulposus and certainly in the posterolateral portions of the annulus fibrosus have been shown - in vivo - in discs with the same degree of radiographic degeneration. These stress concentrations very probably correspond to annular fissures or radial tears.
Therefore, suffering ‘lumbar instability’ is clinical nonsense. There exist simply no clinical nor radiological means to diagnose clinical instability. Instability is a biomechanical term invented in biomechanical laboratories (White and Panjabi) to help big industries developing all kind of plate-screw-systems and artificial discs. Spinal surgical clinicians, never trained in spinal biomechanics or who never worked in a biomechanical laboratory, translate the biomechanical term into a clinical term to impress and convince their patients that spinal surgery could help.
However, from the results of randomised trials comparing non-operative care to surgery for degenerative chronic low back pain (and wrongly called ‘degenerative spinal instabilities’ during international spinal meetings) it is long been known that benefit with surgery ONLY varies from 7 % to maximum 18,7 % (Brox; Fairbank; Fritzell; Mirza). Just imagine your children obtain 18% at school!
Then, do all spinal trained surgeons have to continue to perform very complex spinal operations for treating degenerative MRI-findings who do not correlate with pain? And can somebody explain me why, during International Spinal Meetings, approximately 90 % of all spinal surgeonsindicate not willing to have this type of spinal surgery on their own spines …
Examined by magnetic resonance imaging, a ‘black’ disc appears as a dark or low signal on T2-weighted MRI (Fig. 12).If the IVD height is conserved, the so-called ‘terrible black disc’ simply means nothing more than a reduction of the water content due to the normal ageing-related reduction of the concentration of proteoglycans inside the nucleus pulposus. It has no value as an explanation for low back pain, nor in the acute, nor in the chronic undulating, nor in the chronic intermittent phases of low back pain. The ‘dark signal’ simply is innocuous! The MRI findings of nuclear dehydration in the discs correlate with the dehydrated and fibrous nuclear disc material (Kakitsubata). The author who macroscopically analysed over 23500 lumbar spines at autopsy found no other reasons.
The image of ‘black’ disc is seen in up to 35 % asymptomatic individuals in the age groups 20 to 39 years of age. And it is extremely rare to see normal ‘white’ IVDs at the age of 60. When the IVD does not develop a radial tear or endplate fissure but further ages over an 80-year span, no significant decrease in the MRI-signal occurs.
Fig. 12. This T2-weighted sagittal MRI sequence shows two ‘black’ L3-L4 and L4-L5 IVDs. These ‘dark’ discs only indicate a reduction of water due to an ageing-related decrease concentration of proteoglycans which are responsible for attracting and binding water. By no means does a ‘black’ disc indicates pain!
The High-Intensity Zone or HIZ is a very common MRI finding in the middle age group in asymptomatic individuals as well as in patients suffering chronic LBP of degenerative discogenic origin.
HIZ is seen as a bright spot within the substance of the annulus fibrosus of degenerating IVDs, mostly in the lower lumbar IVDs (Fig. 13). Their presentation is rather rare in the upper lumbar IVDs where endplate type of disc degeneration is more common. The high intensity signal is associated with internal disc disruption and represents a radial tear extending outwards from the degenerating nucleus pulposus into the peripheral outer annulus. The development of these tears is not associated with whatever kind of occupational condition.
Fig. 13. T2-weighted (T2W) MRI scan of the lumbar spine. Both ‘dark’ L4-L5 and L5-S1 IVDs (loss of water signal) show a high intensity zone (HIZ) in their posterior portion of the annulus fibrosus. Both HIZ’s are reflected as bright spots. They are consistent with a developing in-to-out annular tear and/or granulation tissue within already healing complete tears of degenerating IVDs. They rarely are present in the upper lumbar IVDs. HIZ is not at all an absolute indication for pain.
An in-to-out annular (evolving) tear in the lower lumbar IVDs is located in the posterior or posterolateral part of the AF. The development of this type of tear finally will result in a disruption of the outer third of the annulus. This evolution inevitably will stimulate the ongoing biochemical degenerative disruption in and fragmentation of the NP and lead to further loss and collapse of the IVD height.Indeed, the full-blown annular fissures or ruptures allows pro-inflammatory cytokines to enter the NP.
High intensity zones representing in-to-out annular ruptures may (50 %) or may not (50 %) represent a source of pain. It is simply impossible to relate a HIZ to LBP because pain cannot be seen. HIZ is frequently an incidental finding on MRI in asymptomatic individuals and in patients undergoing MRI-studies investigating other pathologies.
The presence of a small in-to-out fissure, that is only seen in the inner annulus, is not associated with chronic low back pain. It may be a potential source of short acute pain (2-5 days) if the IVD sustains an abnormal loading pattern. Indeed, the presence of a high-intensity zone in the annulus means that some collagen bundles (type I) have been disrupted. This not only explains the difficulties in transforming compression load on the nucleus pulposus into tension in the annulus fibrosus, but as well the reduced stiffness of the spinal motion segment in axial rotation.
The fissure very probably becomes painful if a complete in-to-out annular rupture has developed. It then depends on the natural fibrotic healing process which will close the tear. When the ingrowing granulation tissue becomes neovascularised and invaded by nociceptive nerve bundles, abnormal loading patterns initiate the pain processes.
For the same reasons, annular tears may or may not be associated with pain reproduction on discography.
Modic changes, as described by Modic, are late reactions in the subchondral vertebral bone marrow as response to fissuring and disruption of the bony endplates. Damage to the cartilage of the endplates normally starts increasing from the age of twenty years onwards. These cartilaginous alterations progressively decrease the diffusion of nutrient to the nucleus of the IVD and the functional status of the endplate. When not traumatic in origin, these bony endplate interruptions are not associated with pain.
The combined morphological disturbances in the vertebral endplates and evolving changes in the subchondral bone marrow are very common MRI signals in those individuals who already have other degenerating features in their IVDs (e.g. HIZ). Indeed, the author is not aware of any spinal trained colleague encountered worldwide (over 50 countries) who was able to present evidence of co-called Modic changes in normal IVDs or in ‘black’ discs. Hence, abnormal Modic signals are not present in normal IVDs.
Although strongly linked with and located adjacent to degenerating IVDs, the bony vertebral Modic changes may be asymptomatic but are regularly seen in patients presenting low back pain associated with
the degenerative discogenic syndrome.
The Modic end-plate changes appear as three different signal intensities on MRI films: type I, II and III. These signals represent late but different steps in the evolution of the same degenerative discogenic changes in the metabolic processes and structure of the extracellular matrix of the nucleus. The Modic changes do not represent stages in a progressing degenerative process.
Type I adjacent bony endplate changes or Modic type I signals (Fig. 14a) are characterised by a decreased signal intensity on T1-weighted (T1W) spin echo MRI scans and an increased signal intensity on T2-weighted (T2W) MRI scans. Histological evaluations show disruption and fissuring of the endplates and replacement of normal vertebral body marrow by fibrovascular marrow. These changes represent bone marrow edema and inflammation.
Fig. 14a. Modic type 1 changes show a hypo-intens dark T1 signal (left) and a hyperintens bright T2 signal (right). The type I Modic signals represent infiltrative vascularized fibrous tissue in the subchondral red bone marrow reflected as an inflammatory or edema pattern.
Type II adjacent bony endplate changes or Modic type 2 signals (Fig. 14b) are characterised by a hyperintens signal on T1W MRI scans and a slightly hyperintens T2W signal. Histological evaluations show endplate disruptions and conversion of normal red bone marrow into yellow fatty marrow. These changes reflect a more stable and chronic process.
Fig. 14b. Modic type 2 changes show a hyperintens bright T1 signal (left) and a slightly brighter T2 signal. The type 2 Modic signals represent a more stable and postischaemic situation. A chronic process replaced bone marrow (bright) by fat (bright).
Type III adjacent bony endplate changes or Modic type 3 signals (Fig. 14c) are characterised by a hypointens signal on both T1W and T2W MRI scans. Histopathologic sections demonstrate loss of bone marrow and advanced subchondral bone sclerosis.
Fig. 14c. Modic type 3 changes show decreased dark signals on both T1W (left) and T2W (right) scans. The type 3 Modic signals represent extensive subchondral bone sclerosis (= dark signal).
Because Modic changes do not represent a certain advanced stage in the progressing degenerative processes of the IVD but simply are different steps of an identical cascade of degenerative biochemical processes in the IVD, the Modic signals may be dynamic in nature and reversible (Table 14). A type I Modic signal does not automatically convert into a type 2 and further into a type 3 Modic signal. Mixed Modic signals (I/II and II/III) are frequently present. Modic type I changes may disappear or increase to a Modic II signal which may even revert to a type I. For these reasons it is difficult to accept these MRI changes as explanations for chronic low back pain.
T1 MRI (signal intensity)
T2 MRI (signal intensity)
TYPE I Modic
Hypo-intens dark signal
Hyper-intens bright signal
disappear or rather increase to Modic II
TYPE II Modic
Hyper-intens bright signal
slightly brighter signal
TYPE III Modic
Hypo-intens dark signal
Hypo-intens dark signal
disappear once fusion between vertebrae occurs
Table 14. Characteristics and expected evolution of the adjacent bony endplate or Modic changes.
Modic signals are regularly seen in patients presenting chronic low back pain associated with the degenerative discogenic syndrome. Indeed, patients with referred leg pain in a non-anatomical distribution (= not the classic sciatic pains due to inflammation and pressure of a particular nerve root) are more likely to report low back pain if they have developed Modic changes. Histopathological studies indicate that abnormal vertebral endplates with Modic type 1 and Modic type 2 changes present more sensory nerve fiber in-growth and inflammation. Accepting Professor Mulholland’s concept, this histological findings may help to explain why abnormal axial load transfer from one vertebra to another through the degenerating structures of an IVD may, indeed, cause pain.
Modic changes also strongly correlate with the pain provocation of awake discography. Therefore,it seems very acceptable that degenerative changes in the disc in combination with Modic changes are completely different from degenerative discogenic changes without Modic changes.
It looks very acceptable that the ongoing research for developing innovative biological treatments, such as cell-based and molecular-based discogenic therapies, will be more successful when the interactions between biomechanical loading patterns and the biochemical changes in the degenerating lumbar disc are fully understood. The so-called modern plate-screw systems and intervertebral disc prostheses do not respect these two fundamental pathological concepts. Actual spinal surgery is based on wrong interpretation of the 1934 scientific articles on ‘herniating discs’ and on wrong concepts of degenerative ‘instability’ which solely can be illustrated on a spinal specimen in a mechanistic laboratory but never in clinical nor radiological circumstances. Therefore, indications for rigidly fixing a lumbar spine remain wishful thinking.
In the near future, biomarkers for early cell apoptosis (= spontaneous disappearance of cells), cell necrosis, cell senescence and especially proteoglycan loss in the IVD will be developed to image these small objects and to evaluate the evolution of early degenerative changes (i.e. diamond-based nanoscale MRI-machine and/or T1ρ-weighted MRI). Conventional T2 weighted MRI only can detect the late and far advanced stage of IVD degenerative processes.
In analogy to the techniques for mapping brain activity (Lee), it will become possible that functional molecular MRI (fMRI) could in the future image the dynamics of cellular or molecular activity in the intervertebral discs.
In the 1920’s, Schmörl and Junghanns developed a technique of injecting a contrast medium into the cadaveric intervertebral discs for studying their internal structure. Based on this method the first discographies on humans ‘in vivo’ were performed in 1948. In the meantime, more modern discographic two-needle injection techniques are used to reduce the occurrence of a painful discitis.
Discography allows for
(a) measuring the intradiscal pressure (using digital manometry) to monitor the hydraulic integrity of the disc,
(b) visualisation of the degree of internal disc disruption and especially ruptures in the endplate and annulus, and
(c) least importantly, production of back and leg pain which may or may not be the usual experience pain.
Because there exists no other valuable investigational technique for evaluating the hydrostatic pressure and the internal structural organization of the intervertebral disc (compared to arteriographies,lymphographies, coronarographies, arthrographies, etc ), discography will continue to play a very important role in the technical evaluation of chronic low back pain of discogenic origin.
In the absence of immediate visible fissures in the endplate or in the annulus on MRI, a very large proportion of people, and even ‘psychosociologically stable’ ones, become debilitated by the chronic degenerative involution in their IVDs of the lower part of their spines. The radiological procedure of pressure-controlled discography (and postdiscography computed tomography) may then reveal abnormal pressure profiles and ruptures in the annulus and/or in the endplates which are known to potentially contain nociceptive receptors.
During a pressure-controlled discography a dye material (containing antibiotics!) is injected into the center of the nucleus pulposus to measure the intradiscal pressure (Fig. 18). Under controlled pressure (see further down), the potential spread of the dye through the annulus into the epidural space and/or through the endplates in the vertebral body is observed under continuous fluoroscopy or CAT (as during cementoplasty).
Fig. 18. Needles are inserted into the IVDs. Under controlled pressure, the potential spread of the dye through the annulus into the epidural space and/or through the endplates in the vertebral body is observed under continuous fluoroscopy (left and middle images). CAT image of the spread of radio-opaque contrast material in a posterolateral annular fissure (right figure).
Details of the evoked pain are recorded especially when the dye starts flowing through these potential fissures, ruptures or tears. Indeed, it is well known that these ‘ruptures’ or more precisely, the healing granulation tissues in these ruptures may contain nociceptive receptors. However, a reaction of pain may or may not be the usual and customary experienced pain by the patient. If severe pain occurs, a powerful anesthetic can then be injected into the disc to alleviate the pain.
In the author’s experience, the recreation of the pain is of no value in the diagnosis.
The percentage of false-positive responders is very high. Therefore, and to obtain the highest level of objective information, it remains essential that a pressure-controlled discography is performed by a skilled spinal trained radiologist. Independently from previous MRI investigations and knowledge of the presence or absence of a high-intensity zone (HIZ) and/or Modic changes, he must be able to interpret the potential simultaneous occurrence of aberrant flow of dye through the annulus and/or the endplates during the increasingly applied intradiscal pressure.
In the author’s experience, the only indication for a pressure-controlled discography are LBP-patients with a typical history of chronic undulating or intermittent pain with or without referred and non-radicular LBP.
However, any puncturing or pricking through a potentially intact annulus fibrosus has been proven to increase the molecular degenerative processes which might already be present intradiscally.
And most importantly, discographic results need to be cautiously interpreted for diagnosing pain of degenerative discogenic origin.
It remains evident that finding a bright signal in the annulus fibrosus, usually seen as a HIZ on MRI, is not synonymous with the experience of low back pain! Small and incomplete in-to-out fissures in the inner annulus are not the reason for the existence of chronic low back pain but may be associated with short acute pain episodes (2 to 5 days). On the other hand and when the HIZ represents a large and complete radial annular rupture, the risk of developing a painful and chronic degenerative discogenic syndrome (DDS) quadruples. Pressure-controlled discographic analysis in these cases is usually very painful but will not necessarily and exactly reproduce the normal daily experienced low back and leg pain. However, the appearance of a radial fissure tearing completely through the outer annulus is considered an important sign of a far advanced stage in the degenerative processes of the IVD.
Similarly, subchondral vertebral bone marrow changes as response to fissuring and disruption of the bony endplate (Modic changes) on MRI are not necessarily pathognomonic for chronic low back pain (CLBP) related to the degenerative discogenic syndrome (DDS) (Fig. 21). However, a pressure-controlled discography may induce but not necessarily reproduce the normal daily experienced low back and leg pain. The presenceof endplates disruptions is considered an important degenerative discogenic sign.
Fig. 21. Discographic ‘hamburger’ picture of a ‘normal’ nucleus pulposus. The injected dye is seen spreading into the veins of the vertebral body, anteriorly to the vertebra and into the spinal canal. There may be an evidence of endplate fissure.
As nobody till now has been able to develop an objective gold standard for measuring and grading pain related to the lower part of the spine, it’s evident that discography, like any other investigation for chronic discogenic low back pain, has been the subject of many scientific research projects trying to prove or disprove its clinical value.
Pain mostly is elicited or reproduced when the injected dye start reaching the outer part of the annulus fibrosus. Indeed, increasing the intradiscal pressure during discography may stimulate the nociceptive nerve fibers in the innervated parts and in the healing granulation tissues of the annulus fibrosus, the vertebral endplates and subchondral bone. This may or may not reproduce the routine experienced pain symptoms (Colhoun; Heggeness; Hirsch; Lindblom; Simmons; Walsh).
Because chronic low back pain of discogenic origin is still a non-understood condition for the majority of the medical and paramedical practitioners, it is not terribly difficult to perceive that even the presence or absence of psychological attitudes during discography have been evaluated. Because some authors (Kessler; Wittchen) recently stated that apparently one third of the adult world population suffers from a mental disorder (depression, anxiety, phobias, panic disorder), it is not difficult to guess the results of these evaluations.
Nobody can rely on a positive pain response from discographic analysis because the response to any painful stimulus in the periphery can be interpreted as extremely intense. This is explained by the intriguing finding that various pools of nerve cells in the dorsal columns can be hypersensitized and thus can signal a painful condition even though there is very little peripheral input.
Because of its highly organized morphological and macromolecular matrix composition, the nucleus pulposus can resist high intradiscal hydrostatic pressure changes during exercises and positions such as flexion, extension, lateral bending, weight lifting or lying down (Wilke).
Low intradiscal pressure magnitudes, ranging between 0.1 and 0.3 MPa, correspond to the lowest physiological intradiscal load experienced,which occurs during lying or sitting in a very relaxed position.
High intradiscal hydrostatic pressures, ranging up to 3 MPa or even more, correspond to quite high physiological intradiscal load, occurring when lifting a weight/load with a round back.
Physiologic levels of hydrostatic pressure act as an anabolic factor for stimulation of proteoglycan synthesis, whereas abnormal high (above 3 MPa) or abnormally low (below 0.1 MPa) pressure levels caused catabolic effects (Handa; Ishihara; Kasra).
Based on pressure-controlled measurements of over 1600 cadaveric intervertebral lumbar discs (400 times L2-3, L3-4, L4-5, and L5-S1), intradiscal pressure in an intact nucleus-annulus-endplate-structure averaged +/- 90 mm Hg. (Note 760 mm Hg = 101,325 kPa and 0,001 MPa = 1kPa).
The severity of the internal nuclear degeneration and the presence of endplate and annular ruptures were responsible for rapidly decreasing pressure recordings.
Importantly, these manometric values on the cadaveric discs were not influenced by the presence or absence of psychological factors in the clinical notes. In other words, the presence or absence of a mental disorder (depression, anxiety, phobias, panic disorder) did not interfere with objective mathematical pressure measurements.
The interpretation of pain during pressure-controlled discograms depends on the experience of a non-biased in-spine-interested radiologist. Normal intradiscal pressure, absence of ruptures in the endplate and/or in the annulus, and no pain report by the patient indicate a normal functioning and painless intervertebral disc. Less than normal intradiscal pressure (< 90 mmHg), presence of ruptures, and objective pain report are indicative for a painful degenerating IVD and only can confirm the clinical and MRI suspicion of the diagnosis of a degenerative discogenic syndrome (DDS).
However, the two major problems with discography are the patient’s subjective report of pain and the radiologist’s subjective interpretation of the patient’s report of pain.
It is known that (a) lumbar IVDs in asymptomatic people may be made painful under high above normal injection pressure, (b) increasing the pressure above normal values in degenerated discs may provoke pain, and (c) above normal pressure profiles correlate with abnormal - painful or painless - discographies showing ruptures of the annulus and/or the endplates. Therefore, it remains essential to register at which level of intradiscal pressure the potential pain response occurs during the pressure-controlled manometric injection of the dye.
By increasing the intradiscal pressure to inject the dye into the IVD, the potentially ruptured annulus and/or fissured endplate comes under mechanical tension. A particular area may become sensitive to this tension. On the other hand, leaking of dye through a complete radial tear in the posterior annulus and/or migration of dye through a defect of the vertebral endplate into the vertebral body may be visualized (Fig. X and Fig . Y). When these defects already contain healing granulation tissue invaded by blood vessels and pain-sensitive nerve fibers, pain may be experienced.
Identifying a symptomatic disc during a pressure-controlled discography only can confirm the clinical and MRI suspicion of the diagnosis of degenerative discogenic syndrome. A painful and positive discographic finding has no absolute value in prognosticating the outcome of whatever type of therapy, being it conservative or surgical. A discogram reproducing exactly the experienced pain in low back pain and in the leg is not an absolute indication for surgery as these pains may over time decrease allowing the resumption of fairly functional lifestyle (Smith).
It is the author’s belief that pain response should not be relied upon diagnostically for selection of fusion levels. However, knowing exactly which disc is the culprit for symptoms and signs remains essential for the evaluation of the actually researched innovative intradiscal therapies.
Clearly the actual existing pressure-controlled discographic investigation needs further improvement to withdraw subjective pain descriptions and to accurately diagnose which disc is symptomatic in the degenerative discogenic syndrome. Actual ongoing research in functional anaesthetic discography (FAD) may allow for assessing pain during daily functional and dynamic positions.
The principle look simple: if the pain reduces, the anaesthetized disc is the culprit. If not, a non-discal source needs to be sought.
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