Lumbar Intervertebral Disc Herniation

International Publicized Data

GMCD Instructional Course Lectures


Dr. med. Guy MC 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 Therapy (IAAT)

Copywriter / Translator:   Filip Vanhaecke PhD

Illustrative expertise: Jasper Baele, HHP

Review scientific literature:   Medical Consulting Advice, Ostend, Flanders, Belgium

Support:   International Association of Andullation Therapy

Legal advice:   Anthony De Zutter,

Dedication to Jean-Marie Dedecker. January 2014.

Internationally well-known judo coach, Flemish politician and senator, and founder of the political party Lijst Dedecker. 

In all circumstances, an uniquely understanding and real honest friend! Hearing my commotion regarding my professional goals but not prompted by calculation, without arrogance and without financial purposes, but as an unwitting accomplice he stimulated me to finalize this subject. And I don’t care who gets the credit 




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 (*). If the science of a body of work is solid, it serves publication regardless of who produced it.

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 27539 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 Encyclopedia’.

(*) Mirsky Steve. Technology is making it harder for word thieves to earn outrageous fortunes.

      Scientific American, February 2014, p.64

Table of contents

1. How I define the herniating pathway

2. Mechanical failure of annulus fibrosus (AF)

3. Herniating pathway in normal intervertebral discs (IVD)

4. Herniating pathway in degenerating IVD’s

5. Genetic predisposition for the herniating pathway

6. Normal aging processes may be accompanied by degenerative processes

7. Lumbar intervertebral disc herniation is always the result of ‘something else’!

8. Annular protrusions and extrusions: always pain?

9. Mechanism for resorbing the herniating nuclear material

10. No leg pain? Then … don’t treat a radiological disc ‘herniation’!!

11. Evolution of inflammatory radicular leg pain

12. The Dynasty of the IVD herniation. Reason for tragic human wreckage

13. ‘Medical ignorance’ versus ‘perfect surgery’

14. Misinterpretation of the radiological images

15. What exactly do you need to feel for a ‘radiological hernia’ to be the exact reason for your leg pains?

16. Annular location of lumbar disc ‘herniations’

17. Radiological imaging: nuclear protrusion

18. Radiological imaging: nuclear extrusion

19. Traditional and conservative treatments do not influence the natural history

20. Huge variety of nonoperative measures

21. Conservative measures: what can be expected?

22. Conservative measures: what cannot be expected?

23. Surgical discectomy rarely is an urgent and absolute procedure

24. What to do in the absence of worsening signs and symptoms?

25. Discectomy for low back pain without leg pain? Not done, because no effect!

26. Primary goal of discectomy surgery

27. What needs to be realised if a lumbar discectomy will be performed?

28. Multitude of minimally invasive intradiscal discectomies

29. How to evaluate results of lumbar discectomy surgery?

30. Discectomy results: only two long-term evaluations since 1934

31. The removed parts of the disc under the microscope

32. Low back pain continues following lumbar discectomy

33. Medical personnel apparently is not willing to understand why postoperative low back pain increases and continues to think in … other terms

34. Future perspectives

35. Literature Encyclopaedia

1. How I define the herniating pathway

Hernia comes from Latin. It refers to a more centrally localized part of an organ ‘voyaging through’ an opening in the wall of that organ that normally surrounds it. There exist multiple types of herniations: epigastric, diaphragmatic, inguinal, umbilical, etc … hernias.

The term disc ‘herniation’ stands for two evolving entities and one potential final outcome: disc protrusion, disc extrusion and potential final sequestration. For a fragment of the central part of the intervertebral disc - the nucleus pulposus (NP) and sometimes parts of the endplate - to voyage through the wall (protrudere in Latin) of an IVD and finally migrate out of it (extrudere in Latin), the surrounding outer part - the annulus fibrosus - must break down (Fig. 1).


Fig. 1. Schematic illustration of the herniating pathway. Compression forces on the NP are translated in tension forces of the AF. It gradually results in in-to-out annular tears. This nuclear herniating pathway leads to protrusion, extrusion and sequestration of the NP

(Declerck / Taylor / Kakulas, Neuropathology, Perth, Western Australia)

Except when a traumatic event causes the protecting annular ring to rupture (e.g. road traffic accident or extreme spinal loading in young individuals), in an intact and normal lumbar IVD it is simply impossible for nuclear (and endplate) tissue to herniate.

All herniating disc protrusions and extrusions then are primarily the consequence of irreversibly progressing degenerative processes inside the IVD. Step-by-step the ongoing destructive and inflammatory processes break down the different collagenous (type I) annular layers in an in-to-out direction initiating the herniating pathway of mostly the nuclear material.

Because degenerative annular tears predominantly develop in the lower part of the lumbar spine (Declerck), most disc protrusions and extrusions are confined to the L4-5 and L5-S1 levels (80%).

2. Mechanical failure of annulus fibrosus (AF)

It is known since 1962 that a mechanical failure of the AF needs to be present (Naylor) for a protrusion or extrusion of the NP (and sometimes parts of the endplate) to arise.

3. Herniating pathway in normal intervertebral discs (IVD)

As a consequence of trauma, and especially in the young individual, an annular rupture associated with a protrusion or extrusion of the healthy NP may occur suddenly in an absolutely normal IVD (Fig. 3) with no signs of disc aging on MRI (e.g. nucleus dehydration or desiccation with signal intensity loss, dark disc, annular bulging, internal annular high intensity zones, etc ...) and no MRI signs of disc degeneration (e.g. disc space narrowing, endplate ruptures, complete radial annular fissures, annular narrowing, inwards collapse of the annulus, etc …).



Fig. 3. Strictly normal intervertebral discs between the vertebral bodies L4 and L5 in a one month old individual (left) and in a 42 year aged male. VB = vertebral body, EP = endplate, NP = nucleus pulposus, AF = annulus fibrosus.

Above: original (Declerck / Kakulas, Neuropathology, Perth, Western Australia, X83/478, M, aged 1/12). Middle: artistic presentation by Alonso Ríos Vanegas, sculptor and pintor, Medellín, Colombia.

Below: original (Declerck / Kakulas, Neuropathology, Perth, Western Australia, X90/1420, M, aged 42 yr)

4. Herniating pathway in degenerating IVD’s


In a mature IVD, a continuous chain of biochemical degenerative changes at cellular and molecular level must evolve for the NP to dehydrate and lose its viscoelastic gel-type behavior. When the NP starts fragmenting (Fig. 4), it no longer can maintain its ability to evenly distribute stresses transmitted to the NP. In such situations spot-loadings occur at the level of the nuclear fragments which may cause low back pain (Mulholland). However, the more the degenerative processes progress, the more the nuclear material gets digested and resorbed. By the end there, there simply is no nuclear material left. An extrusion simply becomes impossible.


Fig. 4. Degenerative intervertebral disc L4-L5 with fragmentation of the nucleus pulposus and clear endplate disruption. Further IVD narrowing due to inflammatory digestion and resorption of nuclear material makes it gradually impossible to produce extrusions

(Declerck / Kakulas, Neuropathology, Perth, Western Australia – A90/139 / M / 50 yrs)

The creation of herniating pathway occurs in a stepwise fashion for the NP to protrude or extrude through the AF. Our daily lumbar spinal mechanical wear-and-tear loading patterns during varying sitting and standing positions, non-stochastic and high frequency industrial and vehicle vibrations, and intensive repetitive pulling and lifting activities put the type-I collagen fibers in the annular layers under an increased shear strain. Gradual annular tearing develops in a peripheral posterior and postero-lateral direction. The (remaining) degenerating nuclear material can start migrating through these radial annular fissures and create a protrusion. Usually, a minor incident (a cough/sneeze) is sufficient for a weakening AF to finally cause the evolving and degenerative annular fissure to tear completely (= annular rupture). From that moment nuclear material may choose this path of least resistance to protrude and extrude into the spinal canal. Further increase of the intradiscal degenerative processes even enhance the opening of the created annular tears (Wognum).

5. Genetic predisposition for the herniating pathway

It is extremely rare for a healthy, non-degenerative, and well-hydrated juvenile AF to fissure. Except when trauma causes an accidental annular rupture, an intact and non-fragmented NP remains contained in the center of the IVD (Fig. 3).

Nonetheless, the occurrence of a symptomatic disc protrusion and extrusion is 20 times higher if members of a family show severe degenerative IVD changes (internal disc disruption, tears of the annulus fibrosus and of the endplates) (Fig. 4).

Some of the genes which may induce the development of disc degeneration are known (e.g. collagen type I and IX genes, vitamin D receptor genes, matrix metalloproteinase genes, genes for coding interleukin-1 and interleukin-6). Supplementary genetic evidence for specifically developing a nuclear disc protrusion and extrusion is continuously being researched. Till now, no ‘herniating pathway’ genes have been discovered.

Indeed, every man and woman will develop the strictly normal aging processes into his or her IVD’s. Only a very small percentage of people never will develop degenerative changes whatever the loads subjected on them. Indeed, some individuals are ‘protected’ by Nature and the absence of deteriorating genes.

6. Normal aging processes may be accompanied by degenerative processes

Low back pain is an unfortunate effect of belonging to the erect species because the IVDs are loaded constantly. Walking upright, standing, sitting and certainly bending forwards elicit lifelong combined compression and rotational stresses (F/a = N/m² = Pa = Pascal) on the lumbar IVDs. For example, the pressure on these discs accounts for 80 kg/cm² during a static upright rest position and 210 kg/cm² during a forwards bending position in 10° flexion. To make this statement very clear, these pressures can be compared to the pressure exerted by 8 respectively 21 cases of 24 full bottles of beer on one cm²!

These repetitive daily mechanical loading factors influence and alter the biochemical aging processes in the IVD’s. Except for a few genetically ‘protected’ individuals, the daily physical activities will cause degenerative and damaging structural changes in the three parts of the IVD: the NP, the endplates and the AF.

The highest situated L1-L2 and L2-L3 IVD’s eventually evidence rather degenerative vertebral endplate fissures and fractures (Fig. 6a). The degenerative internal nuclear disruptions in the lowermost L4-L5 and L5-S1 IVD’s rather result in fissuring and tearing the posterior AF through which herniation of nuclear material may occur (Fig. 6b, 7a and 7b).


Fig. 6a. X83/593 - M- 57 – IVD L1-2. Degenerative endplate fissures originate rather in the intervertebral discs between the L1 and L2 and the L2 and L3 lumbar vertebrae

(Declerck / Kakulas / Taylor, Neuropathology, Perth, Western Australia)


Fig. 6b. A83/40 - M – 64. Degenerative internal nuclear disruptions in a lower lumbar IVD without evidence of endplate involvement

(Declerck / Kakulas / Taylor, Neuropathology, Perth, Western Australia)

Noteworthy is that the conversion of lumbar IVD’s from normal structures to abnormal ones not necessarily explains the clinical degenerative discogenic syndrome. More physiological elements need to occur to cause pain such as the invasion of small blood vessels accompanied by nociceptive nerve fibers and hotspot loading mechanisms (Mulholland).

7. Lumbar intervertebral disc herniation is always the result of ‘something else’!

Overtime the internal nuclear mass of the IVD disintegrates and loses its hydrostatic properties. Step by step, the material capabilities of the collagens (type I) in the AF alter as well. These aging events result in the daily mechanical compression forces on the NP no being completely resisted by equivalent developing tension forces in the AF. When the AF no longer can withstand the high intradiscal loading pressures, its collagenous layers start tearing in-outwards and therefor will lose their viscoelastic capabilities to return to its original status.


Fig. 7a. Body weight and daily activities result in compression forces on the nucleus pulposus. Because water is incompressible, the hydrostatic pressure in the nucleus will increase. This results in more tension forces in the annulus fibrosus. Compression forces on the NP can be resisted by the AF until tears occur. These biomechanical phenomena are nicely shown at the L3-L4 IVD level. The resulting effects are seen at the L4-5 IVD level

(Declerck / Kakulas, Neuropathology, Perth, Western Australia – A90/139)

CAT- and of course MRI-investigations may reveal the well-known bulges and protrusions of the AF into the spinal canal (Fig. 7b).


Fig. 7b. A routine finding during CAT-investigations. The visualised protrusion is not at all the reason for pain because these protrusions are routinely seen in nearly every CAT-scan and in individuals without pain. Low back pain is related to other underlying mechanisms

In the later stages of the degradation processes complete annular tears, annular protrusions with ‘contained’ nuclear material and nuclear extrusions may become radiologically visible signs on MRI (Fig. 7c).


Fig. 7c. MRI-images of the lower part of the lumbar spine. Visually ‘normal’ IVD between the vertebral bodies VB 3 and VB 4. Degenerated and narrowed IVD between VB 5 and the sacrum (S1) with irregularities at the level of the lower endplate of the VB 5 and an annular protrusion. Clear extrusion of the nucleus pulposus at the L4-5 IVD-level

8. Annular protrusions and extrusions: always pain?

The annular protrusions and nuclear extrusions may arise in all lumbar IVD’s with or without complaints of (chronic) low back pain. Most individuals don’t even know they possess these - mostly temporarily - expressions of the herniating pathway.

In the elderly population, nearly all examined postmortem lower lumbar discs comprise various types of complete fissures and gross ruptures in the AF. However, extrusions of nuclear material are extremely rare. The complete nuclear matrix has been digested and resorbed by the degenerative and inflammatory processes. Not only the central part of the NP but all potentially existing extrusions of nuclear material - symptomatic or not - have been ‘eaten away’. As no NP is left inside the IVD, a nuclear disc protrusion or extrusion of course no longer is possible (Fig. 8).


Fig. 8. Most degenerative nucleus pulposus material has already been ‘eaten’ away by the degenerative and inflammatory processes in the IVD. In the posterior part, only a normal annular protrusion is visible. There is no nuclear material in the epidural space. There is no contact with the spinal nerve root which is not compressed. Trying to surgically ‘clean out’ the protrusion and some intervertebral nuclear material will lead to a catastrophic end result.

(Declerck / Kakulas, Neuropathology, Perth, Western Australia – A90/149 – M – 79)

9. Mechanism for resorbing the herniating nuclear material

It is known since 1950 that protruding and extruding degenerative nuclear disc tissues mostly are digested (Lindblom). The size of a nuclear ‘herniation’ regresses for approximately 50 % or more over a period of three months in up to 80 % to 90 % of cases when controlled by MRI. The speed and the degree of resorption of degenerated nuclear disc material is directly related to the intensity of the inflammatory progresses which proceed in the herniating nuclear (not annular) segments.

Protruded and extruded fragments of the degenerating NP are close to epidural vessels. Electron microscopic investigations show extensive neovascularisation and macrophages surrounding the disc fragments. The most potent proinflammatory cytokines (tumor-necrosis factor-α or TNF-α) and leading factors in the inflammatory processes of the degenerating IVD fine-tune the phagocytic performances of the macrophages which will ‘eat’ the nuclear hernia away. The endothelial cells of the bloodvessels contain so-called angiocrine signals which activate proteolytic enzymes (Ding; Tashimo) for resorbing the nuclear proteoglycans away.

10. No leg pain?

Then … don’t treat a radiological disc ‘herniation’!

Up to 70 % of all radiological disc protrusions and extrusions are not associated with leg pain. The nuclear herniations simply are the expressions of the normal aging and abnormal degenerative pathways of the IVD. Surgically removing such an innocent disc ‘herniation’, incidentally found on radiology and without leg pains, solely is an aesthetic procedure. In the long term, it simply changes nothing.

When a nerve root becomes compressed, motor and sensory disturbances may ensue. However, mechanical compression is insufficient to produce pain.

It is well known that the degenerated NP material contains different cytokines (e.g. TNF-alpha) which may induce potent inflammatory activity in the spinal nerve roots. The production of such nitric oxide (NO) induces endoneural edema and decreases nerve conduction velocity in the spinal nerve root (Olmarker). Inflammatory mediators (NO) not only induce nerve function impairment but are essential to cause the excruciating neuropathic pains in the leg (Olmarker). In the long term, significant ultrastructural axonal changes will occur locally: Schwann cell damage, intracellular edema, and vesicular swelling of the Schmidt-Lanterman incisures (Olmarker).

11. Evolution of inflammatory radicular leg pain

The inflammatory type of radicular sciatic pain related to solely lumbar disc protrusions and extrusions may be excruciatingly painful and debilitating.

When absolutely nothing particular is done to such a typical symptomatic disc ‘herniation’ and when its related nerve root signs and symptoms do not increase, then Mother Nature dictates that the sciatic pain will spontaneously disappear in approximately 80 % to 90 % of all such instances within 6 to 12 weeks.

Although it is extremely difficult to impart simple virtues to low back pain patients, in such circumstances patience undeniably can lead to the avoidance of totally unnecessary discectomy.

There is absolutely no doubt that in the long term (+/- 2 years) surgical removal of a lumbar disc protrusion or extrusion causes more harm than good even if the initial surgical result may be absolutely perfect. Just ask a mason what will happen to a wall in 4 years’ time when cement is removed from between two of its bricks. Millions of disc ‘herniation’ patients all over the world are now suffering the consequences of simple but devastating discectomy procedures.

12. The Dynasty of the IVD herniation

Reason for tragic human wreckage

For totally unknown reasons and without any scientific basis whatsoever, most doctors and surgeons still continue to accept the indoctrinated and archaic principle of a disc ‘herniation’ as the only explanation for nearly all low back pain.

For approximately 150 years and during the periods of the Industrial Revolutions, reasons were sought to explain the increasing incidence and prevalence of low back pain.

In 1934/1935 the neurosurgeons Mixter and Barr described a very clear and detailed clinical condition :‘rupture or herniation of an intervertebral disc’. Unfortunately and again for totally unknown reasons in a matter of few years this ‘new’ condition became the mainstream for explaining the whole range of lumbar spinal conditions for which there was no explanation. All low back pain was suddenly explained by a ‘disc herniation’. Nothing could have been crazier!

But the Dynasty of disc herniation was born and an explosion of discectomy surgery ensued which in most countries still continues till today.

When in the 1950’s neurogenic claudication was outlined as another evident reason for a radicular syndrome, it became clear that the discectomy procedures ‘for all kind of reasons’ had been and were responsible for ‘leaving the largest prevalence of tragic human wreckage than any other operation in history’. Repetitive negative surgical explorations, interventional failures, continuing reports of clinical disasters, and ensuing salvage procedures finally resulted in the recognition of disc herniations as the most illogical explanations for chronic low back pain.

13. ‘Medical ignorance’ versus ‘perfect surgery’

Strangely enough, still a lot of surgeons cannot understand why their high-tech guided and thus perfectly performed discectomies could be associated with the persistence of postoperative low back pain.

Who never heard the following statement? ‘My dear! Look at the postoperative picture! The herniation has been nicely removed! The MRI shows no evidence of a protrusion, extrusion or sequestration! Your spinal canal is ‘clean’! I can’t see the reasons why you still have low back pain. I think you must have … familial, social, relational, economic, or ….. psychological problems?’ And sometimes the patient receives ‘a higher level of scientific explanation ’: ‘you know, dear, we know it since a very long time: there are three groups of patients: those who heal up all the time, those who will heal up overtime, and those who never will heal up!’ And there we go! Millions all over the world have been confronted with this statement.

But could it still be that highly educated and technically skilled surgeons:

(1) are unaware of the strictly normal aging processes in the IVD’s?

(2) have no idea of the primary underlying degenerative discogenic processes?

(3) don’t know the scientific basis of the degenerative herniating pathway?

(4) do not realize that discectomy surgery stimulates and accelerates intradiscal degenerative processes?

(5) do not know that increased degeneration enhances the diameters of annular tears (Wognum)?

(6) do not realise that discectomies lead to secondary degenerative spondylolisthesis and spinal stenosis?

The author has been confronted day and night with hundreds of these patients in multiple countries, all telling exactly the same history …

14. Misinterpretation of the radiological images

Most of the discogenic protrusions and extrusions observed by radiological means (XR, CAT, MRI) are incidental findings in individuals who are asymptomatic or only have a small amount of low back pain. Why then do so many people mention that they have disc ‘herniations’?

It certainly can be due to misinterpretation of the normal posterior anatomy of the IVD’s. At the thoracolumbar junction, the IVD has no tendency to bulge into the canal. Whereas the L1-L2 and L2-L3 IVD’s have a straight posterior margin, the most distal localized L3-L4, L4-L5, and L5-S1 discs have a distinct posteriorly convex bulging configuration (Fig. 14).


Fig. 14. Normal posterior margins of the lumbar intervertebral discs. There is no bulging at the level of T12-L1. The posterior margins at L1-L2 and L2-3 are ‘straight’. At the level of L3-L4, L4-L5 and L5-S1, the posterior margins, and for biomechanical reasons, must have a convex configuration. If not, there is a problem!

By no means should this normal anatomy be confused with a pathological bulging of these IVD’s due to degeneration and hypermobility even in the presence of a ‘black’ disc (Rauschning). Indeed,

  1. 80 % of all disc protrusions and extrusions are localized at the L4-5 and L5-S1 levels,
  2. only 30 % of these ‘herniations’ present radicular sciatic symptoms, and         
  3. the other 70 % simply are incidental radiological findings without  sciatic leg pain problems.

15. What exactly do you need to feel for a ‘radiological hernia’ to be the exact reason for your leg pains?

For making the presumptive diagnosis of a lumbar disc disorder, the major determining factors are essentially the characteristics of leg pain rather than those of low back pain (see above: point 10).

The essentials in a patient’s history and clinical examination to conclude that a radiological disc protrusion or extrusion is the causing symptomatic leg pain factor include:

(a) a history of intense functionally incapacitating and unremitting sciatic leg pain extending below the knee largely in excess of low back and/or buttock pain which may be totally absent,

(b) neurological motor and sensory disturbances in a radicular distribution (= radiculopathy),

(c) presence of disturbed neuromeningeal tension signs and qualifying tests reproducing the typical sciatic pain (e.g. disturbed straight-leg tension test, dorsiflexion of the ankle, medial hip rotation test, slump test), and

(d) manifestation of disturbed neuromeningeal compression signs (especially profound muscular weakness) in the radicular distribution.

The presence of neuromeningeal compression signs, mainly expressed by sensory disturbances (numbness and dysesthesias) but only minor motor weaknesses without pain below the knee, never present indications for removal of a disc protrusion or extrusion. The sensory dysfunctions still remain present in a high percentage (up to 35 %) independently of the chosen treatment, traditional or surgical.

16. Annular location of lumbar disc ‘herniations’

Laboratory experiments and mathematical finite element methods (FEM), investigations nearly exclusively understood by engineers, (doctors are not at all trained in understanding research data!), substantiate that the risk for nuclear migrations is highest in the posterior and posterolateral annulus fibrosus especially in mildly degenerated IVD’s. Severely degenerated IVD’s show a lower risk.

The degenerated NP may also protrude or extrude in other directions: anteriorly, (far) laterally, through the endplates (Schmörl’s node) (Fig. 16), and intradurally.


Fig. 16. Evidence of the ‘herniating pathway’ of the nucleus pulposus through an endplate (nodule of Schmörl)

(Declerck / Kakulas / Taylor, Neuropathology, Perth, Western Australia, dossier A90/148)

17. Radiological imaging: nuclear protrusion

A disc protrusion (protrudere in Latin) represents the herniation of NP material through an incomplete defect in the AF (Fig. 17a and 17b). The annular margin is locally extended but the outermost annular collagen type I layers remain totally intact. These types of annular disc bulgings are extremely common, but do not at all represent ‘pain’.


Fig. 17a.  The annulus fibrosus shows concentric tears and disruption of the inner collagenous layers. The outer layers remain intact. The nucleus pulposus moves outwards but is halted by the intact layers of the AF. This ‘moving’ process of nuclear material is called ‘protrudere’ in Latin. The protrusion is depicted. This herniating state may or may be associated with low back pain. However, the typical excruciating sciatic leg pain, essential for making the correct diagnosis of a ‘hernia’, cannot be present because the spinal nerve root has no contact with the different cytokines inside the degenerating NP (Internal Spinal Course – Kyphon International)

They may or may not be associated with an incomplete annular tear. If the tears are fluid-filled, which varies along the spinal loading patterns, they present a high intensity zone (= HIZ) on MRI (Fig. 17c). And again, HIZ’s are not necessarily the reason for pain.

It is important to realise that this type of radiological herniation - the disc protrusion - mostly is an incidental finding in totally asymptomatic individuals.


Fig. 17b. MRI-image of a disc protrusion. The nucleus pulposus (‘black disc’) herniates through incomplete defects in the inner collagenous layers of the annulus fibrosus. The annular margin is locally extended but the outermost annular layers remain totally intact


Fig. 17c. The formation of an protrusion may be associated with a visible fluid-filled incomplete tear in the annulus fibrosus. On the left: the high intensity zone (HIZ) is visible on MRI. On the right: pathological section through such a developing in-to-out tear in the annulus

(Declerck / Kakulas, Neuropathology, Perth, Western Australia – A90/149)

18. Radiological imaging: nuclear extrusion

Once a complete in-to-out annular radial defect has been established, degenerating nuclear material may migrate through it and appear into the anterior epidural space. As long as this herniating nuclear material still remains attached to the parent NP via a pedicle of nuclear material, the radiological presentation is defined as a disc extrusion (extrudere in Latin) (Fig. 18a and 18b).


Fig. 18a. The annulus fibrosus is teared completely. The nuclear material migrates through the annular tear into the epidural space. This process is called ‘extrudere’ in Latin. The herniating extrusion is depicted. This situation can provoke low back pain can be responsible for the development of excruciating leg pain

(Internal Spinal Course – Kyphon International)

When the pedicular attachment no longer exists, the free floating nuclear fragment is described as a disc sequester (sequestrare in Latin).


Fig. 18b.  MRI of the lower part of the lumbar spine. Degenerative extruding nuclear material is present at the L4-L5 IVD level. The herniated material still remains attached to the parent NP via a pedicle of nuclear material

It is important to realise that this type of radiological herniation - the disc extrusion - may be an incidental finding as well in totally asymptomatic individuals.

19. Traditional conservative treatments do not influence the natural history

Except if the radicular leg pain symptoms and clinical neuromeningeal compression signs due to a protrusion or extrusion of nuclear material increase or worse rapidly and dangerously, patients should be thoroughly observed for 3 months before a definite surgical decision is taken. Mother Nature, responsible for the ‘natural history’, does Her uppermost best not only to resorb the ‘herniation’ but to spontaneously resolve the associated symptoms in approximately 80 % of individuals over a period of twelve weeks!

While Mother Nature takes this average period of time to cure, the patient may and should remain as active as possible. Nonoperative measures may be initiated but only to - hopefully - avoid unnecessary discectomy surgery.

20. Huge variety of nonoperative measures

A huge variety of all kind of management methods is tried, used, and combined worldwide. Traditional and non-traditional exercises, medications, injections, etc … may of course be initiated in an attempt to alleviate the pain associated with inflammation. Sometimes, injected epidural steroids may decrease pain as they inhibit the prostaglandin synthesis and block nociceptive C-fibers.

21. Conservative measures: what can be expected?

It finally remains up to Mother Nature to decide if She will ‘centralize’ or not the patient’s symptoms from the distal radicular locations in the leg into only the lower lumbar spine. As the primarily underlying degenerative destructive enzymatic and inflammatory processes in the IVD cannot be neutralised, low back pain always will evolve into a chronic intermittent (Fig. 20a) or chronic undulating pattern (Fig. 20b).


Fig. 21a. Schematic presentation of chronic intermittent low back pain. Frequently recurring and suddenly occurring episodes of low back pain followed by varying painless periods (Graph by Natacha Monstrey)


Fig. 21b. Schematic presentation of chronic undulating low back pain. Low back pain is always present but the intensity varies enormously (Graph by Natacha Monstrey)

22. Conservative measures: what cannot be expected?

It should be well realized that - till now - none of the non-surgical strategies has ever succeeded in directly and handsomely dissolving the volume of the protrusion or of the extrusion more rapidly than does Mother Nature!

None of all the existing non-operative treatment possibilities will accelerate the spontaneous resorption and regression of the ‘herniation’.

None of the conservative methods interferes or can stop the progressing intradiscal degenerative processes. Whatever the type of treatment, it will not and cannot interfere with the cellular and molecular processes of degeneration.

Then, it must be understood that ‘TIME and PATIENCE’- but not too long and not too much - are primordial to avoid unnecessary discectomy.

On the other hand, when (a) Mother Nature fails - for as jet unknown reasons - to resolve the clinical signs and symptoms, when (b) the radicular leg pain intensifies, when (c) the neurologic motor deficits progress and paralysis occurs, a new MRI is required to confirm the diagnosis before proceeding with discectomy surgery.

23. Surgical discectomy rarely is an urgent procedure

There is no doubt that discectomy is an urgent and absolute surgical procedure to treat severe and intensifying disabling radicular leg pain.

When this history is associated with a MRI imaging an extruded disc fragment impinging and inflaming the neural structures (the so called dural conus medullaris and different dural cauda equina syndromes) and causing:

a) progressing and worsening neuromeningeal compression signs,

b) bilateral radicular pain,

c) saddle anesthesia and

d) adversely affecting the bladder, bowel and sexual functions, hesitation to perform a discectomy may lead to irreversible lesions of the myelin sheath of the nerve roots with irreversible clinical consequences (see point 10 - Olmarker).

24. What to do in the absence of worsening signs and symptoms?

In the absence of progressing disabling leg pain and motor paralysis, removal of disc tissue rarely should be performed if the clinical signs and symptoms do not meet the typical definition of a ‘herniation’. Surely, discectomy never is indicated when low back pain is the only and major complaint.

Since years, the underneath mentioned remarks regarding surgical discectomy are repeated over and over again in the spinal literature and during international spinal meetings:

a) if the surgical decision is only based on a rapid interpretation of a radiological image (CAT and/or MRI) in the absence of a typical history and clinical examination, discectomy surgery has no sense at all and will fail to produce a relief,

b) an incidental finding of a protrusion or extrusion on CAT or MRI and thus without pain nor symptoms, is not at all a panacea for removing the ‘offending’ part: nor for minimally nor for generously removing disc material from the intervertebral disc space,

c) if the surgical decision is solely based on ‘failure’ of traditional and conservative treatments in cases of low back pain without (increasing) leg pain, discectomy has nothing to offer,

d) if surgery is decided upon to resolve chronic distress and illness behavior of the patient who has no evidence of objective pathological neuromeningeal compression signs, the outcome is totally unpredictable.

Whatever the reasons for performing a surgical discectomy, Nature never will cooperate. Surgical discectomy is like throwing oil on an existing fire. Surgery never will neutralise the destructive enzymatic and inflammatory mediators associated with the existing degenerative processes and therefore …. low back pain will become more prominent!

25. Discectomy for low back pain without leg pain?
Not done! Because No effect!

As already mentioned, each of the L3-4, L4-L5, and L5-S1 IVD’s has a normal posterior convex configuration and should not be considered ‘abnormal’. Don’t touch bulging discs!

Evolving disc protrusions are due to the progressing destructive degeneration of the IVD (nucleus and endplate) and are related to the advancing in-to-out breakdown of the type I collagenous layers of the annulus. Surgically perforating and rupturing these incomplete annular lesions to remove part of the degenerating NP only will result in the development of chronic low back pain because discectomy creates more high spot-loading areas inside the emptied disc space (Mulholland).

Radiological visible extrusions and sequestrations may or may not be the reasons for low back pain. But low back pain will continue to exist and even increase following discectomy surgery.

It is essential to realise that a lumbar disc ‘herniation’ is not at all a major primary cause of low back pain. To the contrary, discectomy increases low back pain in the long term.

26. Primary goal of discectomy surgery

The primary goal of discectomy surgery still remains the same since its first descriptions in the 1930s. The only purpose of a lumbar discectomy is to remove the ‘herniating’ NP and taking away the compression from the affected nerve root. Then, hoping that inflammation settles and improves the leg pain.

To stimulate this process, it was and still is a routine to supplement the procedure with anti-inflammatory corticoids (injected inside the emptied intervertebral space and on the affected nerve roots).

But because the reasons of failure of discectomy procedures have till recently not been sought where they should be, new instruments and modified techniques for ‘discectomy’ are still been developed.

In vain! Discectomies on their own never will neutralise the destructive enzymatic and inflammatory mediators associated with the existing degenerative processes. On top of that, discectomy procedures create multiple high hot-spot loading zones because the normal daily loads on the IVD during sitting and standing no longer can be equally distributed.

27. What needs to be realised if a lumbar discectomy will be performed?

When the ultimate surgical approach is decided upon, it is essential to realize the underneath data:

(1) the highly organized structure of the annulus is severely damaged as a result of the primary degenerative discogenic herniating pathway,

(2) the discectomy procedure causes further laceration to the outer annular layers,

(3) nuclear and/or annular reconstruction is still totally impossible,

(4) all even perfectly performed techniques of disc removal benefit only good short-term effects,

(5) the removal of nuclear material decreases the intradiscal hydrostatic pressure and stimulates the degradative enzyme production (MMP’s) accelerating the underlying primary degenerative disc processes,

(6) the denucleation always will result in subsequent loss of intervertebral disc height,

(7) the ablation of nuclear material increases segmental hypermobility between two vertebrae,

(8) the denucleation leads to more biomechanical stress in the remaining AF and in the zygapophyseal facetal joints causing new episodes of low back pain,

(9) recurrent herniation at the same location occurs in up to 30 % of cases,

(10) the amount of recurrent disc herniations after ‘microdiscectomy’ is highest when MRI only indicates a minor disc degeneration,

(11) approximately 30% of all disc herniation operated patients decide to undergo another operation within 10 years, and

(12) older patients undergoing discectomies for degenerative disc ‘herniations’ have higher rates of morbidity and mortality than younger individuals (Stolke).

28. Multitude of minimally invasive intradiscal discectomies

It remains an enigma why the removal of a ‘herniated’ disc still is the most commonly performed spinal surgical procedure although lumbar discectomy relentlessly leads to the further destruction of the remaining intervertebral cartilaginous structures (AF, NP and the endplates).

Since the late 1970’s, it is well known that the conventional ‘open’ midline muscle stripping discectomy procedures have been responsible for ‘leaving the largest prevalence of tragic human wreckage than any other operation in history’.

In the meantime a multitude of minimally invasive lumbar intradiscal discectomies has been invented (percutaneous, endoscopic, laser, etc …). Because irreversible and significant paravertebral muscle damage (Fig. 28a and 28b) can now be prevented, there is no doubt that these innovative strategies have benefited the patients in the short term.


Fig. 28a and b. Muscle histopathology (see other chapter: Paraspinal Musculature)

Left slide: normal paraspinal muscle fibers (M - 40 years - X90/368 - EM 90/56)

Right slide: non-specific myopathy changes (M - 73 years - X90/346 - EM 90/52)

(Declerck / Kakulas, Neuromuscular Pathology, Perth, Western Australia)

The use of one of these various discectomy techniques depends on

a) the professional formation of the surgeon in one or more countries,

b) his understanding of spinal biochemistry and biomechanics,

c) his inherent technical skills, experience, but not at least

d) the impact of the marketeering skills of the surgical companies.

None of all these various discectomy methods is superior to the other:

a) all these modern manipulations still need additional surgical annular perforations, fenestrations or annulotomies to explore and ablate the central NP,

b) none of these modern procedures can be performed without further damaging the intervertebral disc texture,

c) none is capable of preventing the progression of the underlying primary causing intradiscal degenerative processes

d) to the contrary, the removal of nuclear disc material always results in a further activation of the degenerative processes and an increased incidence and prevalence of inflammatory mediators.

Mother ‘Nature’ will continue to revolt against this destructive approach by causing more inflammatory low back pain.

29. How to evaluate results of lumbar discectomy surgery?

For a throughout evaluation of a particular spinal treatment and certainly for ablative procedures of degenerative discogenic ‘herniations’, a minimum of at least 10-year follow-up is essential to judge the validity of a peculiar management approach.

Cheap comparative effectiveness research (CER website) should be performed to evaluate the potential boost of the intradiscal degenerative steps by different treatment modalities for lumbar disc ‘herniations’. However and because this research will need to include repetitive scanning (MRI) at regular follow-up intervals, it will never be performed. On the other hand and in comparison, similar and longitudinal evaluations on the effects of aging processes in homogeneous life circumstances are done since years (Riley; Tyas; Shock).

30. Discectomy results: only two long-term evaluations since 1934

Since the Dynasty of disc herniation started in the late 1930’s, only two 10-year studies (Weber; Atlas) have been performed.

As can be expected, the early one-year and two-year results always resulted and still result in an exceptionally good leg pain relieving effect with ratings varying from 79 % to 97 % (Table 30).

Two 10-year follow-up studies since 1934: results

At 1 – 2 years

exceptional good low back pain relief

At 4 years


At 10 years

no difference between operated and non-operated patients

Table 30. One year, 4 years, and 10 years evaluation of patients operated with discectomies

Most patients have been found to be ‘ok’ for approximately 4 years! By that time and because the underlying causative factors were never dealt with initially, it became clear that the long term results were the same whether the patient was treated with surgery or was left alone with non-operative means.

At 10 years the disability outcomes were similar for both groups, operated on or not. It was calculated that up to 27 % of all previously discectomy patients decided to undergo another spinal operation within 10 years.

And funny enough, all studies - short and long term - evaluating the results of lumbar disc hernia surgery emphasize inappropriate patient selection as the leading cause of surgical failure. Indeed, Mother ‘Nature’ will continue to revolt as long as the causes which lead to the formation and progression of the herniating pathway are not considered: IVD degeneration.

31. The removed parts of the disc under the microscope

Macro- and microscopic analysis of ‘herniated’ lumbar disc material following surgical removal and during postmortem evaluations never shows a normal hydrated viscous material expected to be present in a healthy nucleus of the IV disc.

The removed parts of the IVD always contain dehydrated and fibrous elements originating from the NP, the AF and the endplates as well.

Chemical analysis of the ‘herniated’ fragments clearly show that they possess the same degenerative profile as the degenerating NP. Disc ‘herniations’ contain identical degradative enzymes (matrix metalloproteinases) and identical potent proinflammatory cytokines (i.e. tumor-necrosis factor-α). These enzymatic and inflammatory mediators not only are responsible for causing low back pain and/or radicular pains but they stimulate macrophages for eating the ‘hernia’ away. None of all the developed techniques for lumbar discectomy can neutralise these complex mechanisms which induce chemical inflammatory pain.

32. Low back pain continues following lumbar discectomy

Surgical ablation of a ‘hernia’ can resolve the radicular type of leg pain, but the low back pain will rarely disappear. Only 1 % of patients who suffer discogenic low back pain as well will experience an immediate and complete disappearance of low back pain following surgery.

To the contrary, extirpation irreversibly stimulates the degenerative and inflammatory processes further resorbing the remaining NP. Chronic low back pain persists! This evolution consolidates the degenerative discogenic syndrome and finally will result in its secondary pathologic events: degenerative spondylolisthesis and degenerative spinal stenosis.

33. Medical personnel apparently is not willing to understand why postoperative low back pain  increases and continues to think in … other terms

Strangely enough, a lot of surgeons do not consider the occurrence of persistent postoperative low back pain a component of poor surgical outcome. And they are right! With the most modern high tech guiding machinery, they performed a straightforward and uncomplicated removal of a ‘herniation’, without muscle destruction and without intraoperative complications.

Then, there is no reason at all to expect bad results. And qualifying a patient as somebody ‘who will heal all the time, who will heal over time, and who never will heal’ only can be done in the postoperative phase. And by that time, lack of scientific knowledge evidently is only the responsibility of the patient! But patients have no clue about the underlying and primary processes ……

Because of the increasing requested familial, social, professional, leisure, and economic pressures and responsibilities dictated by the ‘evolutions’ in modern industrialised societies, Mother Nature will continue to revolt. Mother Nature hates interference in her own healing potential. She does not agree with this financially rewarding indication for surgery.

A price will always be paid for the performed discectomy and nucleotomy:

1) intradiscal inflammatory processes are stimulated,

2) intradiscal pressure will decrease,

3) disc height will decrease,

4) more tension stress will occur in the remaining annulus,

5) circumferential radial bulging will increase (apparently in a proportion similar to the mass of the excised nucleus tissue),

6) ‘reherniations’ will present,

7) an abnormal range of motion between the two vertebral bodies (initially hyper- and later hypomobility) will occur (because the center of rotation and centrode between two adjacent vertebrae will shift),

8) stress in the facets of the zygapophyseal joints (ZGA’s) increases,

9) accelerated osteoarthritic-like changes will occur in the cartilage of the ZGA’s,

10) vertebrae will slip against each other and result in a degenerative spondylolisthesis,

11) the spinal canal will narrow and cause neurogenic claudication due to the development of degenerative spinal stenosis,

12) sexual impotence can ensue as well as disability, socioeconomic and financial misery, and more surgery.

34. Future perspectives

But the patients shouldn’t worry too much. Modern innovative brains in cooperation with exiting technology have responded to the unrelenting postoperative destructive processes. Research and development continuously invents new ‘salvage’ surgical procedures and implants in an effort to interfere again with the caused tragic human wreckage.

But to no avail! Unless an innovative biological concept evolves stabilising the intradiscal degenerative and inflammatory processes, in accordance to Mother Nature’s Biological Laws, everybody will continue to suffer the consequences of the normal aging processes and its degenerative complications!

Intensive research is going on to understand and to neutralize the primary intradiscal degenerative processes.

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