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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 and ProVision, Waregem, Flanders, Belgium

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

Support:   International Association of Andullation Therapy

Legal advice:   Anthony De Zutter,

Dedication to the Colombian Family of Gloria Rúa Meneses and her sons Andres David and Juan Camilo Hinestroza (National Waterpolo Team of Colombia). May 2014.

For their friendship and hospitality. Gloria always encouraged me by her swift and intelligent understanding of what I was trying to do. Her support was beyond al estimation.



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 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 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. Definition of lumbar spinal stenosis (LSS)

2. History of spinal stenosis

3. No place for discectomy

4. Then, one day … a Dutchman named Henk Verbiest

5. Modern scientific concept of spinal stenosis

6. Lumbar spinal stenosis in the 20th century

7. Spinal disease of the 21st century: degenerative lumbar spinal stenosis (DLSS) with

    neurogenic intermittent Claudication (NIC)

8. DLSS is the most common type of spinal stenosis

9. DLSS: Reason for an increase in major spinal surgical procedures and revisions since the

    late 1990s

10. Economic consequences and innovative surgical techniques

11. DLSS: Pathological origin and evolution

12. What is the natural history of DLSS?

13. What do ‘opinions’ of professors tell us?

14. Anatomy: Central spinal canal: shape and dimensions

15. Anatomy: Lateral – radicular – spinal canal: dimensions and shape

16. Anatomy: intervertebral foramen: dimensions and shape

17. Signs and symptoms relate to dural sac dimensions

18. Position-dependent dimensions of the central spinal canal and intervertebral foramen

19. Anatomy: Ligamentum flavum

20. Anatomy: Importance of the midline spinal lumbar ligaments

21. Diagnosis of DLSS - Evidence-based medicine

22. Diagnosis of DLSS - The story of the patient

23. Diagnosis of DLSS - Any bladder dysfunction?

24. Diagnosis of DLSS - Any sexual dysfunction?

25. Diagnosis of DLSS - Clinical Examination

26. Diagnosis of DLSS - Electrophysiology

27. Diagnosis of DLSS - Laboratory tests

28. Diagnosis of DLSS - Myelography-CAT

29. Diagnosis of DLSS - Dynamic MRI

30. Diagnosis of DLSS - Radionucleotide imaging

31. Don’t miss … VIC: vascular intermittent claudication

32. Don’t miss … Tandem Spinal Stenosis

33. Treatment: Decision-making factors

34. Treatment: Conservative approach

35. Treatment: Surgery or no surgery? The question!

36. Treatment: Search for an ideal surgical procedure

37. Treatment: In the best hands … still adverse effects!

38. Surgery: Comorbidities

39. Surgery: Percentage of complications

40. Surgery: Major complications

41. Surgery: Minor complications

42. Surgery: Reoperation rates

43. ‘Golden’ standard surgery is too costly a burden for societies

44. Surgery: Dynamic Pedicular Stabilisation

45. Surgery: Interspinous extension limiting device

46. Any explanation for NIC and related signs and symptoms?

47. The author’s conclusion

48. Literature Encyclopedia

1. Definition of lumbar spinal stenosis (LSS)

Lumbar spinal stenosis means narrowing of the spinal canal in the lower lumbar spine. Whatever the aetiology, the spinal canal evidences a decreased volume restricting the space for its neural and vascular contents. The stenosis can be localised in the central spinal canal and/or in the lateral parapedicular spinal canal and/or at the level of the intervertebral foramen. Depending on the location(s), part of the spinal cord and/or the cauda equina and/or the nerve roots and their vascular associates can be mechanically compressed and chronically constricted (Fig. 1a and 1b).


Fig. 1a and 1b. The dorsal aspect of the dural sac in the lumbar spinal area has been removed to expose the cauda equina (longitudinal yellow bundles). The internal vertebral venous plexus surrounds the emerging nerve roots from their origins at the level of the dural sac and along their courses to the intervertebral foramina. These neural and vascular structures can be mechanically compressed and chronically constricted during the evolving process of spinal stenosis.

(Permission Springer - A Short Practice of Spinal Surgery - Chapter Nerve Root Canal Stenosis - figure 1.20 p. 20 - Henry Vernon Crock - ISBN 978-3-7091-7370-1)

In some people, but not at all in each individual, the aging evolution of the lumbar spine eventually may evolve to a degenerative situation compressing and constricting the intracanal neural and vascular structures. In other words, degenerative lumbar spinal stenosis (DLSS) may develop in each human being as aging is a normally advancing and irreversible process. DLSS even reoccurs 8 to 10 years following decompressive surgery. If signs and symptoms develop, the resulting clinical expression becomes characterized as a very typical posture-dependent syndrome, described as neurogenic intermittent claudication (NIC).

It is important to realise that radiological spinal stenosis is not at all synonymous with NIC as it is hugely common to have a narrow central and/or lateral canal without symptoms whatsoever. Compression is an insufficient explanation for the occurrence of signs and symptoms of NIC.

2. History of spinal stenosis

Spinal stenosis not only is an ancient condition described in Egyptian mummies and dinosaurs. Spinal stenosis is a variant in the normal aging process. As the average age of death in 1900 was only around 50 years of age, Sachs and Fraenkel diagnosed an unusual aging disorder which they termed ‘claudicatio intermittens nervosa’. Typically their patient had to stop walking after a short distance due to pain, weakness and numbness in the legs. The arterial pulses remained normal. The symptoms disappeared following a decompressive laminectomy and surgical removal of enlarged, thickened bone and ligamentous tissue.

As society ages, irreversible pathologies such as spinal osteoporosis, degenerative lumbar spinal stenosis, and cervical myelopathy due to cervical intervertebral disc degeneration and subsequent cervical spinal stenosis will become endemic in the twenty-first century.

3. No place for discectomy

Unfortunately, the pathological concept of a narrowed spinal canal was temporarily forgotten since 1934 because neurosurgeons focused attention on the intervertebral disc (IVD).

For approximately 25 years the ‘dynasty’ of the disc herniation conquered the world. An explosion of discectomy surgery ensued. Discectomy was and still is considered as some kind of an miraculous solution for all kind of spinal pathologies. Unfortunately, miracles do not occur (Fig. 3)!

It gradually became clear that performing solely a discectomy procedure ‘for all kind of reasons’ (degenerative discogenic syndrome, scoliosis, spinal stenosis, spondylolisthesis, complex combined spinal deviations, etc …) was responsible for ‘leaving the largest prevalence of tragic human wreckage and larger than any other operation in history’ (Allan and Waddell, 1989). Just ask a bricklayer what happens in the long-term to a wall when cement is removed from between two of its bricks!


Fig. 3. Radiological pictures. Woman, 68 yrs. Degenerative hypolordotic and scoliotic lumbar curve with myelographic block at L4-5. Clinical history of DLSS and NIC but not a disc herniation. Neurosurgical discectomy (what was the reason?) resulted in a clinical disaster.

Although these facts are well known, modern ‘discectomy’ has technically evolved to a routine and easy-to-do procedure, even in pathological degenerative spinal stenosis. No doubt that the major reasons to continue this very destructive procedure for inappropriate indications are the huge financial gains for the medical industries, the hospitals and the surgeons.

Sometimes, it should be better for intelligent surgeons not to listen to the marketing machinery of the surgical industries (the author declined such a function!).

4. Then, one day … a Dutchman named Henk Verbiest

The interest in the compromised spinal canal was reawakened in the early 1950s when a Dutch professor of neurosurgery, Henk Verbiest, corrected the previously held views that all low back problems were mostly due to the herniating pathways of the intervertebral disc(s).

Professor Verbiest described the characteristic but disabling symptoms of neurogenic intermittent claudication. This clinical condition, which may or may not occur with radicular leg pains and sensory / motor disturbances in the legs, was attributed to posture (standing and walking) and to narrowing of the spinal canal. At surgery, Verbiest documented a shallow spinal canal compressing the dural sac (Fig. 4). This findings were compatible with the myelographic finding of a block in the lumbar region.

From that time, spinal surgeons started redifferentiating the different pathologies.


Fig. 4. Schematic illustration of a shallow central spinal canal due to loss of the intervertebral disc height resulting in compression of the neural contents in the dural sac (red). The zygapophyseal facet joint is secondarily involved as well.

5. Modern scientific concept of spinal stenosis

The modern scientific concept for this pathoanatomic spinal entity has been thoroughly evaluated by the end of the 20th century. The aetiopathogenesis of the most common type of acquired spinal stenosis encountered – degenerative lumbar spinal stenosis – has been analysed in detail.

The pathology is due to a cascade of degenerative processes in the intervertebral discs, the ensuing secondary degenerative hypertrophic lesions in the zygapophyseal facet joints, overgrowth of the laminae, the pedicles and the ligamentum flavum, and the engorging epidural venous structures (Kirkaldy-Willis; Rauschning).

The logical conclusion from all studies regarding DLSS was, till now, to accept the recommendations for use of wide surgical decompression (Wiltse; Sherkin).


Rather rare reasons for spinal stenotic situations are metastatic spinal disease related to primary soft tissue carcinoma (Fig. 5). Essentials on the natural history of spinal metastatic disease related to well over 550 postmortem carcinomas will be provided in a separate chapter.


Fig. 5. Stenotic metastatic tumor from a breast adenocarcinoma compressing the spinal cord but without paraplegic consequences.

(X84/228/F/34 - Declerck / Kakulas, Neuropathology, Perth, University Western Australia)

6. Lumbar spinal stenosis in the 20th century

By the end of the 20th century, it was recorded that of all low back pain (LBP) patients who saw a general practitioner, approximately 5 % showed radiological evidence of lumbar spinal stenosis. Approximately 15 % of LBP patients who consulted a specialist had LSS evidenced by radiographic means.

However, a radiological determination of LSS is NOT at all an explanation for the presented low back pain. LBP is caused primarily by the irreversible degenerative processes in the intervertebral disc(s).

7. Spinal disease of the 21st century: DLLS with NIC

It becomes more and more evident that degenerative conditions, affecting activity level and quality of life, will impact the post-world war II baby-boom in an significantly increasing proportion (Benz; Deyo). Human beings live longer than the previous generations. It has been estimated that by 2025, people older than 65 years will have almost doubled (Reeg).

Irreversible pathologies such as spinal osteoporosis, cervical myelopathy due to cervical IVD degeneration and subsequent cervical spinal stenosis will become endemic in the twenty-first century. But the major challenge in dealing with incapacitating spinal problems irrefutably will concern the ever increasing numbers of elderly people suffering from the problems of degenerative lumbar spinal stenosis with disabling claudicating leg pain. DLSS with NIC, an increasingly common debilitating spinal condition in elderly individuals, already is considered as the spinal disease of the 21st century.

8. DLSS is the most common type of spinal stenosis

Degenerative lumbar spinal stenosis has since long been considered the most common type of spinal stenosis with a reported incidence* of 1.7 % to 8 % of the general population in 1999 (Hilibrand). Although the prevalence** of symptomatic DLSS, with its typical signs and symptoms of neurogenic intermittent claudication, remains unknown, DLSS with NIC becomes an increasing reason for surgery.

* incidence means the percentage of individuals in a given population who will DEVELOP a disease during a specified period of time

** prevalence means the percentage of individuals in a given population who HAVE a disease during a specified period of time

9. DLSS: increase in major spinal surgical procedures and

               revisions since late 1990s

Depending on their co-morbid condition(s), patients suffering from DLSS with NIC have, till now, nearly no other choice but to suffer the ineffectiveness* of pain relief by all kinds of analgesics and injections or undergo major decompressive spinal surgery and complex primary and revision reconstructions.

In the 20th century and over a period of 14 years (from 1979 to 1992), a rapid 8-fold increase in surgery rates for DLSS with NIC for patients aged 65 and older was recorded. In the USA, operations for lumbar spinal stenosis increased dramatically from 4.0 per 100.000 in 1979 to 1981 to 17.7 in 1988 to 1990 in people over 65 years of age (Deyo; Reeg; Taylor; Turner). And when it rains in the USA, it drops all over the world. Figures of spinal operations for DLSS increase dramatically in all countries with a more aging people.

No doubt, DLSS accompanied by NIC will become the most common and fastest growing reason for spinal surgery in adults older than 65 years (Athiviraham).

* effectiveness means the extent to which medical interventions achieve improvements in health in REAL practise settings

10. Economic consequences & innovative techniques

As society ages, the economic stress of treating these aging group of elderly people with degenerative lumbar spinal stenosis and with debilitating claudicating leg pain will force some of the spinal surgical brains to develop more efficient and definitely less costly surgical procedures.

Nowadays, there are no other options than the hugely costly but destructive surgical procedures. Most of these surgical interventions need to be accompanied by even more complicated restabilisation techniques to avoid complete disastrous destabilisation. Because all these elderly people - without any exception, knowingly or not - suffer the irreversible and further progressing complexities of spinal osteoporosis, further revision surgery always remains at the horizon (Fig. 10a). Major and minor complications are summarised later, in chapter 40 and 41.


Fig. 10a. An aesthetically magnificent surgical procedure from a technical point of view. The central lumbar laminectomies – sufficient to treat DLSS – in a lady aged of 72 are augmented with bone grafts on both sides and plates and screws. Osteoporotic bone is evident. Five-year postoperative outcome: totally unknown.

Further improvement of an innovative procedure is now fully researched in the laboratory and in vivo. The researched technique is based on (a) the principles of a dynamic implant, as initiated for the first time in Poland during the Second World War (Fig. 10b) and on (b) stabilisation and neutralisation of the intradiscal degenerative processes.


Fig. 10b. Based on the experience with a Polish interspinous device, developed during the Second World War, potential innovative and more modern implants are researched.

But to realise these innovative – and hopefully working – surgical techniques, some of the scientific spinal brains in the laboratories need to explore the further details of the complexity of the underlying aetiologies leading to the development of DLSS associated with neurogenic intermittent claudication. If not, the spinal surgical community has no choice but to continue with the existing ‘golden standard’ of destructive surgeries.

11. DLSS: pathological origin and evolution

Since the 1950’s and based on surgical findings, radiological imaging, but especially on post-mortem investigations, it became more than evident that the degenerative lumbar spinal stenotic condition progresses insidiously over many years as a result of the normally progressing aging changes.

The pathoanatomic components of progressing DLSS primarily relate to the classic evolving degenerative changes in the intervertebral discs in the anterior part of the spinal column. The IVDs lose their heights and the degenerating nucleus starts its herniating pathway usually at the level of the posterolateral annulus. This pathway first results in normal bulging but progresses into protrusion and finally may present an extrusion depending on the amount of non-resorbed degenerative tissue left intradiscally (further detailed description in the topic ‘Disc Herniation’).

The secondary important features occur in the posterior parts of the spinal column: thickening of the laminae and sometimes of the pedicles, hypertrophy of the posterior zygapophysial multifaceted joints, and thickening as well as buckling of the ligamentum flavum (Towne; Spurling). Narrowing of the intervertebral disc space may be associated with segmental hypermobility causing a ‘dynamic’ type of DLSS (Fig. 11).

All changes in the anterior and posterior spinal structures finally may create limited spaces in the central canal, the lateral recesses, and at the level of the foramina. A gradual impingement of the neural and vascular contents may occur depending as well on the pre-existing diameters and shapes of the central vertebral canal.


Fig . 11. Routine findings in elderly spines from the average age of 65 years onwards: osteoporotic vertebral bodies; aging and degenerative intervertebral discs; spinal stenotic components consisting of protruding disc material, thickening of the laminae and pedicles, hypertrophy of the zygoapophyseal multifaceted joints (ZGA), hypertrophy and buckling of the ligamentum flavum, and listhesis (here L5-S1). These evolving degenerative phenomena result in a reduction of the central spinal canal (white delineation), the lateral recesses, and the foramina (red delineation). These universal aging findings do not necessarily cause low back pain and do not systematically induce neurogenic intermittent claudication.

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

Based on all these pathological findings, it looks very evident that surgical decompression is since long considered the most logical and evident treatment. Although very destructive, the different decompressive techniques are termed the ‘golden standard’ by surgeons.

12. What is the natural history of DLSS?

Large, long-term, prospective studies describing the natural history of LSS do not exist, partly because many patients with this condition ultimately undergo surgery. It is unknown what will happen to me when I start developing DLSS.

DLSS is the consequence of a strictly normal aging process but it is not synonymous with neurogenic intermittent claudication. Patients who are investigated for other medical reasons may incidentally image an almost complete radiological blockage of the central spinal canal without clinical symptoms being present. At the same time, mild narrowing sometimes causes severe NIC symptoms (Andersson). So, what causes DLSS to result in NIC? Nobody in the scientific world has a concrete clue.

13. What do ‘opinions’ of professors tell us?

The prevailing but pseudo-scientific opinion accepts that ‘the natural course’ of symptomatic DLSS with or without neurogenic intermittent claudication is one of progressive worsening and that only decompressive surgery can control this development.

This statement is based on ‘opinions’ of professors, but without any validated scientific proof whatsoever! And the medical society has no choice but to rely on as many opinions as there are professors.

But there exist studies comparing non-surgical to surgical management indicating that those who underwent decompressive surgery report - temporarily - better results. On the other hand, it has long been concluded that there exist no factors indicating the prognosis of treatments for LSS (Amundsen; Herno; Katz). In other words, telling somebody that he or she will experience a particular outcome from a particular treatment dealing with DLSS is more or less wishful thinking. Although each medical trainee will anticipate a ‘good’ result, all of us - doctors and patients - will have ‘to wait and see!’.

There is no guarantee that decompressive surgery will relieve the patient from his NIC symptoms (Table 13). When DLSS and NIC are simultaneously diagnosed, something more important - but still unknown - already has happened in the neuromeningeal and vascular structures. Surely, there is much more than simply the degree of narrowing of the spinal canals.

Results at 2                        to 3 yrs follow-up

Surgical (44 patients)

Non-surgical (19 patients)


59 %

32 %

Unchanged (NIC symptoms)

16 %

58 %

Worse (NIC symptoms)

25 %

10 %

Table 13. The longest evaluation of the natural history of lumbar spinal stenosis does not indicate that surgical decompression is overwhelmingly better than non-surgical treatment (Johnsson et al.).

14. Central spinal canal: shape and dimensions

The shape of the central vertebral canal is particularly significant in patients who suffer neurogenic intermittent claudication. The dome-shaped central canals do not have true lateral recesses. The trefoil-shaped central canals have deep recesses, increasing the likelihood for lateral stenosis (Fig. 14) (Hibbert; Papp; Porter).


Fig. 14a. Scanning images of a large dome-shaped (left) central canal without lateral recess. In this situation DLSS and NIC rarely develop. On the right, a deep trefoil-shaped central spinal canal with shallow deep lateral recesses. There is a higher probability of developing NIC.

The anteroposterior diameter of the central lumbar vertebral canal is an important parameter for describing stenosis. On average, the sagittal diameter measures 19 millimetres from L1 to L5 and 20 mm from L5 to S1 (Edwards). The lower limit of a normal anteroposterior diameter is established at 15 millimetres and of the transverse diameter 20 millimetres (Eisenstein).

The height of the lateral recess depends on that of the pedicle which varies from 8 to 16 mm from L1 to L5. Then, lateral stenosis is considered to exist when its dimensions are less than 5 mm (Senegas).

15. Lateral - radicular - spinal canal: dimensions and shape

The radicular vertebral canal is defined as the lateral part of the central spinal canal containing the spinal nerve root from its point of emergence through the dural envelope up to and including the intervertebral foramen (Vital; Twomey). The radicular canal resembles a cylinder with two main locations where stenosis can occur: the lateral parapedicular recess and its foraminal exit (Fig. 15).


Fig. 15. The red lines indicate the locations of both lateral spinal canals. They present cylindrical structures where the nerve roots can become compressed and inflamed.

16. Intervertebral foramen: dimensions and shape

The intervertebral foramen is shaped like an inverted teardrop (Fig. 16). It is bounded superiorly and inferiorly by the pedicles of the adjacent vertebrae. The anterior boundary is formed by the posterior margin of the vertebral bodies and the intervertebral disc. The posterior boundary comprises the pars interarticularis, ligamentum flavum, and articular process (Crock).

Its heights varies from 11 to 19 mm and its cross-sectional area from 40 to 160 mm² (Stephens).


Fig. 16. Illustration of the normal anatomy of intervertebral foramina: inverted teardrops (red circles). The elastic ligamenta flava are depicted in yellow.

(Illustrations from Kyphon ‘s Instructional Course)

The intervertebral foramen usually is ‘overlooked’ because of the ignorance of its pathological significance in DLSS. Sometimes the clinical outcomes are unsatisfactory following the ‘golden’ standard decompression of the central spinal canal. Indeed, in DLSS with NIC, the spinal nerve roots are submitted to a double compression when the lumbar spine bends backwards towards extension. The spinal nerve roots become compressed at two levels: in the spinal canal and in the intervertebral foramen. Then, not decompressing the foramen may lead to an unsatisfactory result (Morishita).

17. Signs and symptoms relate to dural sac dimensions

The normal values for the dural sac cross-sectional area (DSCSA) vary around 150 – 200 mm² (Boos; Schönström; Ullrich). The cross-sectional area of the dural sac is position-dependent and significantly increases by 22,3 % or 16,6 mm² in the forward bended position (Lee). The DSCSA increases from 77,8 to 93,4 mm² (Siddiqui).

For lumbar spinal stenosis to be considered, the critical DSCSA must figure below 100 mm² (Boos; Schönström; Ullrich). Neurogenic intermittent claudication is highly associated with a DSCSA of < 100 mm² present at more than 2 of 3 intervertebral levels, i.e. L2-L3, L3-L4, L4-L5 (Hamanishi).

The anteroposterior diameter of the dural sac (APDDS) seems to be a better parameter. Severe central lumbar spinal stenosis with NIC is observed when the APDSD is shorter than 7 mm (Beattie).

18. Position-dependent dimensions of the central spinal canal

      and intervertebral foramen

Radiological studies, cadaveric analyses and biomechanical investigations clearly indicate that the dimensions of the central spinal canal, the lateral spinal canal (spinal recess), and intervertebral foramina vary enormously during flexion and extension of the lumbar spine. The different anatomical dimensions are clearly posture- and position-dependent. They significantly increase in flexion and become narrow in extension (Chung; Fujiwara; Inufusa; Penning; Richards; Willén) (Table 18a and 18b).

Central canal cross-sectional area

Midsagittal diameter

Evaluation (author)


decrease of 40 mm²

CAT (Schönström)

decreases 2 mm

CAT (Schönström)


11 % increase

CAT (Inufusa)

18 % increase         (231 – 273 mm)

MRI (Richards)

increases 10 %

MRI (Richards)

Table 18a. Influence of flexion and extension on some dimensions of the central spinal canal

Foraminal cross-sectional area

Author and measuring method


decreases 12 %

Fujiwara (biomechanical and anatomical)

decreases 15 %         

Inufusa (cryotomy)

decreases 20 %

Panjabi (postmortem)

decreases 23,3%

Schmid (MRI)


increases 12 %

Inufusa (cryotomy)

increases 13 %

Panjabi (postmortem)

increases 25 %

Richards (MRI)

increases 36,5% (22 mm²)

Lee (MRI)

Table 18b. Influence of flexion and extension on the cross-sectional area of the intervertebral foramen

These dynamic phenomena are explained by both the deformation of the soft tissues and the relative position of the osseous structures. During extension, (a) the posterior annulus bulges posteriorly into both the central and lateral spinals canals and (b) the ligamentum flavum buckles anteriorly into both spinal canals (Chung; Fujiwara; Schmid). During forward flexion movements, all previous phenomena are reversed.

19. The ligamentum flavum

The young and normal ligamentum flavum (or yellow ligament) is not really a ligament as it contains the highest levels of elastic fibers of any structure in the body (Fig. 11, 16 and 19). Therefore, the chances of any protrusion of the yellow ligament into the spinal canal is minimal during full extension of the spine when the ligament is slack. The ligamentum flavum is of minor importance at full flexion (13%).

During the development of DLSS, the ligamentum flavum increases its number of chondroid cells and gradually starts a calcification process. At that time, and during extension, the ligament starts buckling more and more into the spinal canal during extension.


Fig. 19. Degenerative intervertebral disc (a); degenerative zygapophysial facet joints (b); obliterated lateral canals (c); triangular shape of the central canal without epidural veins nor cerebrospinal fluid (d); hypertrophic ligamenta flava (e).

(Illustration from Kyphon’s Instructional Course)

20. Importance of the midline spinal lumbar ligaments

The midline localised supraspinous lumbar ligament (SSLL) and interspinous lumbar ligament (ISLL) cannot be regarded in isolation. Both are rather derivatives of various muscle and fascial insertions.

The SSLL is well developed in the upper lumbar region and mostly terminates at the L4 spinous process (70 %). Sometimes at the L3 spinous process (25 %), rarely at the L5 spinal process (5 %), but never at the lumbosacral junction.

Because these ligaments do not possess elastic fibers, they are rather inextensible, work as a tension band and function as stabilizing structures. The ligaments of the posterior spine are involved in resisting flexion forces but torsion as well. The spinal muscles resist most of the flexion forces (80 % to 90 %) and both SSL and ISL ligaments account for about 20 % resistance at full flexion. However, their role is minimal as they only contribute 10 % to the average torque strength of the whole intervertebral discogenic joint (Adams).

A deficiency in the midline posterior ligamentous system, produced during decompressive surgery, produces undue mechanical bending and twisting stresses in the lumbar intervertebral discs and eventually may increase the prevalence of failure. It remains essential to respect the integrity of both the SSLL and the ISLL for the potential innovative interspinous implant not to dislodge posteriorly nor laterally during flexion and extension.

21. Diagnosis of DLSS

It is wrong medicine to solely rely on very intelligent and sophisticated technical investigations to make a diagnosis. The actually existing investigations simply need to be complementary to clinical history and examination. This is evidence-based medicine. It is primordial to primarily analyse the symptoms before philosophies are formulated! And this shouldn’t be too difficult. Operating a radiological image is absolute nonsense!

Spending a long time to question spinal patients (repeatedly) with data from the related spinal literature will - without any doubt - decrease the high percentage of very bad treatment outcomes and high complication rates mentioned in the related literature. The amount of LBP-patients, aged 50 years or older, who are surgically ‘decompressed’ for simple radiological LSS without the typical clinical findings of neurogenic intermittent claudication, remains huge (Herno).

Evidence-based medicine is totally different from evidence-based management (Pfeffer). Only 15 % of doctors worldwide read about ‘evidence-based medicine’ (Chapman). Therefore, an increasing disillusion in scientific medicine has started it in Western industrialised countries (Deborah Lupton). And rightly so!

22. Diagnosis of DLSS – The story of the patient!

Patients with symptomatic DLSS usually present their problems in the fifth or sixth decade of life. The diagnosis relies on clinical diagnostic judgment rather than on well-defined existing investigative tests. But it simply is an intriguing syndrome!

The initial complaints are those of the primary degenerative discogenic syndrome. DDS is the most common low back pain condition worldwide. It is due to normally occurring degenerative and inflammatory processes in the intervertebral discs which ultimately may lead to secondary lumbar spinal stenosis. Then LBP is a very common accompaniment in DLSS and may have been present for a very long time. The complaints are expressed as fatigue and pain in the lower part of the back and/or in the buttocks and/or in the groins. Referred - but no radicular - leg discomforts may be described as vague pain, weakness, tingling, and numbness. Nights may be troublesome with sleep being disturbed by restless legs, night cramps and the need to often get up and walk around.

When the primary degenerative phenomena progress gradually, they may start narrowing the central spinal canal (central stenosis) and/or the lateral recess (lateral recess stenosis) and/or of the foramen (foraminal stenosis).

At one moment in time, both legs become affected equally and start feeling ‘weak’, ‘heavy’ or ‘tired’ as though it is difficult to drag one leg after the other. Patients gradually reduce the walking speed as well as the walking distance. The distance can vary during the day and from one day to the next. Each time they have to lean forwards to relieve the discomfort (Fig. 22). They have to stop and to save embarrassment they tie up shoelaces. When during the forwards bending position, the feelings in the legs recover after 5 to 10 minutes before walking again, a neurogenic condition is very probable. The DLSS-patients may be able to walk better up a hill leaning forwards than down a hill leaning backwards. Similarly, they can cycle for miles, climb a ladder and stairs but not come down stairs easily.


Fig. 22. Rather typical. The elderly person gradually has to bend forwards while walking to relieve the discomfort in both legs ultimately needing to stop for complete relief.

The aforementioned discomforts in the legs gradually evolve into the well-defined and highly debilitating position-dependent syndrome of neurogenic intermittent claudication (Verbiest; Porter). Characteristically, the patient’s leg and back complaints exacerbate in all positions of lumbar extension such as standing and walking but become easier by all positions of flexion such as sitting or bending forward.

The claudicating leg pain, indicating a central stenotic component, may be associated with an intense radicular pain in a dermatomal distribution and with sensory or motor deficits in a particular nerve root distribution. For example, a L5 radiculopathy may be due to a L4-L5 zygapophyseal facet joint hypertrophy causing lateral recess stenosis and/or by L5-S1 foraminal stenosis.

23. DLSS – Any bladder dysfunction?

Experimental compression of the cauda equina (Fig. 1), a characteristic radiological finding in central lumbar spinal stenosis associated with neurogenic intermittent claudication, may potentially cause urologic dysfunction (Bodner; Delamarter).

The median compression of the dural sac CAN have a direct mechanical effect on the parasympathetic innervation of the bladder by compression of S2-S4 nerve roots. These nerve roots are located at the posteromedial side in the spinal canal and held well apart from each other by the arachnoid in a well-organized pattern. Therefore, the impairment of S2-S4 function could be produced by central compression in the spinal canal. For those interested in this detailed spinal anatomy, illustrations can be read in the paper of Wall et al., Cauda equina anatomy. I. Intrathecal nerve root organization. Spine, 1990, 15:1244.

Thorough diagnostic interview reveals that 50 % to 80 % of NIC-patients experience lower urinary tract symptoms such as urinary dribbling, increased frequency and nocturia (Deen; Hellstrom; Inui; Perner). Further urological investigations confirm neurogenic bladder dysfunction in up to 40 % of these patients (Inui; Kawaguchi).

The prevalence of such a neuropathic bladder can be deduced from the measurement of the anteroposterior diameter of the dural sac (APDDS) rather than the dural sac cross-sectional area (DSCSA). DLSS-sufferers with an APDDS shorter than 8 mm show a significantly higher percentage of neuropathic bladder than those with anteroposterior diameters longer than 8 mm (Inui).

24. DLSS – Any sexual dysfunction?

Advancing age is a common denominator for influencing sexual function and causing impotence (Bacon; Moreira). Various aetiologies and/or risk factors can further influence sexual dysfunction, such as endocrinopathies, nervous system disorders, and specific depression (Bodie; Fabbri; Seftel).

Sexual dysfunction is reported frequently during a thorough anamnesis of LSS patients suffering NIC. Excluding all aforementioned diseases, some patients suffering DLSS with NIC experience an improvement in penile erection and ejaculation after decompressive surgery.

Very rarely, NIC may be associated with a peculiar clinical symptomatology, involving the autonomous nervous system. Intermittent priapism (involuntary penile erection) appears on walking and is relieved by sitting or squatting (Baba; Ram; Willén).

25. DLSS – Diagnosis: Clinical examination

The physical investigation for DLSS associated with NIC is not diagnostic. The findings are aspecific and there is a remarkable lack of gross abnormality.

The lumbar spine may often be tender over several segments and it may be difficult to stand erect. Some adapt something like a simian stance with hips and knees slightly flexed. He or she may be able to flex well forward with extended knees, tough lumbar extension may be very difficult or impossible with extended knees. Increased lumbar spinal pain on extension may be elicited.

The neuromeningeal tension (SLR – Lasègue – Flip – Slump) signs are usually full but can excite LBP due to dura irritation. Compression signs are rather present in cases of associated canal and/or foraminal stenosis: reflexes are symmetrically present or absent and sensations may remain undisturbed. Peripheral circulation is frequently abnormal as arterial disease coexists.

When tandem spinal stenosis is present, clinical examination will reveal a gait imbalance. Detailed and straightforward neurological evaluation easily demonstrate upper and lower motor neuron abnormalities due to cervical myelopathy.

In academic settings, treadmill and bicycle test can define the claudicating walking pain and indicate its vascular or neurogenic origin (Dong; Dyck).

Note: the idea of implanting a device between the spinous processes to relief patients from neurogenic intermittent claudication related to lumbar spinal stenosis comes from a straightforward clinical observation. Most of the NIC patients get symptom relief when bending forward, sitting down and flexing their spine. Conversely their symptoms exacerbate when they stand erect and extend their spines.

26. DLSS – Diagnosis: Electrophysiology

A large battery of electrophysiological methods exists for the evaluation of neurogenic intermittent claudication in patients with lumbar stenotic conditions. However, their contribution into the differential diagnosis of LSS is very limited.

The simple exercise treadmill test (ETT) is more useful. It not only may confirm the NIC, but verifies the walking capacity as well. After walk loading, the latencies of the tibial F-wave and the soleus H-reflex will exhibit minimal changes (Adamova).

27. DLSS – Diagnosis: Laboratory tests

Routine laboratory tests such as complete blood count, sedimentation rate, electrolytes, Ca, P, alkaline & acid phosphatase, protein electrophoresis, liver tests, urea nitrogen, creatinine, blood sugar, coagulation survey and urinalysis are not at all specific for whatever type of lumbar spinal stenosis. They are simply part of a routine preoperative evaluation. However, they may evidence an underlying comorbidity and demonstrate a particular aetiology as was frequently seen three decades ago: Paget’s disease.

28. DLSS – Diagnosis: Myelography-CAT

The evidence of lumbar spinal stenosis on imaging CAT-scans often bear little or no relationship to the patient’s pain, disability, and related neurogenic intermittent claudication because a shallow canal without symptoms is seen frequently (Amundsen; Katz).

Related to the degree of myelographic lumbar spinal stenosis, two major types of blocks are seen. A subtotal block is described when there is discontinuity of the radiopaque material but with some flow beyond the stenosed segment. A total block occurs when there is no flow of radiopaque material beyond the block (Fig. 28a).


Fig. 28a. On the left an illustration of a subtotal bloc on myelography. On the right a total block of the dye column is seen.

The major advantage of lumbar myelography is the possibility for a functional or dynamic investigation (Fig. 28b) . The ability to evaluate the effect of axial loading with erect flexion, extension, and lateral bending manoeuvres is particularly important in the assessment of spinal stenosis (Aprill; Wilmink). These myelographic findings are important, especially in the presence of surgical implants, in case of severe scoliosis, and when an important positional component is considered to be present, as the diameter of the spinal canal and of the intervertebral foramina may be dependent on such positional changes. In most patients the sagittal diameter of the spinal canal increases on flexion and decreases on extension of the spine.


Fig. 28b. Example of a dynamic or functional myelogram in an identical individual. On the left, the column of the myelographic dye is formed during a position of extension. On the right, the myelographic column indicates the position-dependent nature of spinal stenosis.

29. DLSS – Diagnosis: Dynamic MRI

Magnetic resonance imaging (MRI) has become the imaging modality of choice for lumbar spinal pathology since the mid 1990’s. It is the golden standard in the evaluation of lumbar spinal stenosis (Fig. 29a and 29b). However, the diagnosis of symptomatic spinal stenosis is based on clinical grounds. MRI is supportive but only indicates the levels where the stenosis occurs. A MRI does not show pain, disability nor NIC!

T1- and T2-weighted sagittal images allow direct longitudinal visualisation of the spinal canal, an additional look at the nerve roots within their respective canals, and demonstration of the cord, conus, and cauda equina. T1- and T2-weighted sequences in the axial plane allow quantitative measurements of the spinal canals, the foramen and dural sac.

The radiologist only can use a subjective grading system, describing the spinal stenosis as mild, moderate, or severe. But there is no relation with signs and symptoms of DLSS and NIC. The specificity (*) of MRI in the diagnosis of spinal stenosis has been reported in asymptomatic individuals. There is an incidence of 1 % in the individuals 20 to 40 years old, while in an older age group (60-80 years) the incidence reaches 21 % (Boden).

* Specificity describes the prevalence of true-negative results when a test is applied to patients who are at risk for the disease but are known to be free of it. It is defined as the number of true-negative results divided by the sum of the true-negative and false- positive results


Fig. 29a. Classical static MRI


Fig. 29b. Dynamic MRI. On the left, a MRI-image with the patient sitting straight. There seems to be some narrowing at the level of L3-L4. He was asked to backward extend his spine. The resulting image isn’t very clear. However, a clear stenotic segment, produced by a protruding hypertrophic ligamentum flavum, becomes visible. This is an example of a dynamic spinal stenosis which cannot be detected without functional analysis.

(Courtesy Dr. Hiertz, Austria)

30. DLSS – Diagnosis: Radionucleotide imaging

If a patient is suspected to suffer DLSS and NIC, the radionucleotide scan always will be positive because of the underlying and primarily degenerative and inflammatory processes in the intervertebral disc. Otherwise, bone scans with specific tracers may indicate an underlying pathology such as infections, tumours or Paget’s.

31. Don’t miss VIC: vascular intermittent claudication

Vascular intermittent claudication due to peripheral vascular disease may be difficult to distinguish from neurogenic intermittent claudication due to degenerative lumbar spinal stenosis (Hawkes).

Vascular diseases are frequently occurring conditions in the elderly age groups and are commonly associated with other signs and symptoms such as impotence in men, dystrophic skin changes, foot pallor or cyanosis, decreased or absent pulses and arterial bruits (Fig. 31a).

Patients with VIC very accurately can quantitate the distance that they can ambulate before symptoms reappear. They typically present a stocking sensory loss. Vaso-occlusive leg claudication usually does not occur with changes in posture and patients typically obtain relief from the leg pain by simply resting the legs even while in the upright position (Fig. 31a and Table 31b).


Fig. 31a. Left (arteriogram). Right (aortogram). Vascular intermittent claudication (VIC) is differentiated From the neurogenic form (NIC) by a constant claudicating distance. VIC-patients always are forced to halt because of cramping pain following a short walking distance of 100 to 200 m. The leg pain nearly disappears immediately by standing still. Foot pulses cannot be detected.

Clinical characteristics

Neurogenic claudication (NIC)

Vascular claudication (VIC)

Location of pain

- back and sometimes buttocks

- thighs, calves

buttocks and/or calves

Quality of pain

burning and/or cramps


Aggravating factors

- erect posture

- ambulation

- extension of the spine

any leg exercise

Relieving factors

- squatting

- bending forward                         

standing and rest

Leg pulses                         

usually normal

decreased or absent

Blood pressure                                                  

usually normal


Skin / trophic changes

usually absent

often present:         pallor, cyanosis, nail dystrophy

Autonomic changes

- frequent: bladder, bowel and

  sexual dysfunction,

- rare: priapism

potential impotence coexisting with other symptoms of VIC

Table 31b. Clinical differences between neurogenic and vascular claudication

32. Don’t miss … Tandem spinal stenosis

Thousands of DLSS and NIC-patients are surgically decompressed without any improvement at all because their tandem spinal stenosis was not evidenced!

Degenerative intervertebral disc changes in the cervical spine become more and more visible from the age of 50 years onwards. Cervical myelopathy presents as one of the most important degenerative spinal diseases to deal with in the 21st century.

The presence of simultaneous symptomatic cervical and lumbar spinal canal involvement, known as tandem spinal stenosis, varies from 5 % to 8 %. These percentages will increase as people grow older. Although tandem spinal stenosis commonly results in a combination of upper and lower motor neuron abnormalities and gait imbalance, the condition is commonly easily overlooked (Dagi; Teng).

Radiological investigations of the lumbar spine do not reveal tandem spinal stenosis. Clinical examination will.

33. Treatment: Decision-making factors

Finagle’s Law correctly states: ‘The data we have, are not the data we want. The data we want, are not the data we need. The data we need, are not available’.

Nearly each medical or paramedical trained individual seems to accept the prevailing pseudoscientific opinion that ‘the natural course’ of symptomatic DLSS with or without neurogenic intermittent claudication (NIC) is one of progressive worsening and that only decompressive surgery can control this development. However, there simply exists no objective grading system as basis for predictive decision-making of any treatment:

(a) advanced age has no prognostic value,

(b) there is no universal grading system for evaluating the intensity of symptoms and signs of NIC,

(c) the clinical examination is not diagnostic,

(d) the clinical examination cannot predict a final outcome of any treatment,

(e) there exist no objective parameters for the evaluation of pain intensity,

(f) there is no universal radiological grading system for DLSS associated with NIC,

(g) advanced radiological degenerative changes of the lumbar spine are not related to the prognosis,

(h) magnetic resonance imaging (MRI) remains the ultimate method to subdivide LSS patients in subgroups. But these subdivisions in ‘mild’, ‘moderate’, and ‘severe’ are simply based on automatically generated mathematical analyses of images by machines lacking all correlations with the real clinical situation.

Until the real physiopathological mechanisms for development of NIC are scientifically discovered and proven, all above mentioned available data simply remain subjective! And all imaginable existing treatments, conservative as well as surgical, have been prescribed based on these non-objective data and remain controversial.

The choice between the available treatments, a variety of conservative and surgical methods, is still an open question. Treatment depends mostly on the understanding, heart and education of a medically or para-medically trained person. It should be great to be able to predict the outcome of any particular spinal operation. However, in the approximately 60 countries he worked in or visited for surgical instructional reasons, the author knows of no surgeon (Mr, Prof or dr) who could scientifically teach him which surgical ‘Magic 8 ball’ needs to be used in the end.

Once the diagnosis of neurogenic intermittent claudication (NIC) established, the patients have been historically limited to a choice between a regimen of non-operative strategies or decompressive surgery with or without fusion or arthrodesis (Hilibrand 1999). The very large variation in the management of patients with NIC associated with DLSS - conservatively and surgically - is due to lack of understanding of the natural history of lumbar spinal stenosis and its exact physiopathology. As a consequence as well, there exists little evidence to support the relative benefits of the current surgical procedures compared with the conservative methods (Gibson and Waddell 2005).

The lack of an objective way to evaluate symptoms and signs seriously hampers the study of spinal treatment methods. Observations of at least 5 to 10 years remain essential but are non-existent. The author made huge mistakes by relying on the overwhelming availability of 2-year follow-up studies. As discussed in several published reports, a golden standard treatment still does not exist (Andersson; Bessette; Waddell). A novel and alternative surgery will resolve this dilemma.

34. Treatment: Conservative approach

Finagle’s Law correctly states: ‘The data we have, are not the data we want. The data we want, are not the data we need. The data we need, are not available’. Data regarding conservative treatment for DLSS contradict each other in a phenomenal way. Conservative treatment for DLSS often is limited, only has short term effects, and finally is not satisfactory. As long as the causative mechanisms for the occurrence of neurogenic intermittent claudication remain unknown, outcomes of the various types of non-operative approaches will continue to differ.

In general, non-operative treatments are always carried out initially except in patients who suffer severe motor disturbance and/or bladder dysfunctions.

Some literature reports declare that surgical indications are inappropriate because of insufficient initial trials of conservative treatments. Others state that conservative treatments rarely are effective. And again, it can be read that initial non-surgical options seem to be a good approach. Sometimes the ‘wait-and-see’ approach is advocated. Some treatment evaluations report that patients who underwent unsuccessful conservative treatments initially, finally will obtain outcomes equal to those who have undergone surgical procedures as the initial treatment. Some even indicate that 48 % may have excellent or good results with conservative measures and 52 % not (what’s the difference?). But it becomes a little bit more hectic when scientific articles predict disability after conservative and following operative treatment.

Nobody knows! Conservative options, including bed rest (stimulates the osteoporotic processes!), in-bed pelvic tractions by forcing patients into a jack-knife position, application of body cast in a slight flexed position, all kind of corsets, analgesics, nonsteroidal anti-inflammatory medications, calcitonin, oral steroids, spinal manipulation, back school, physiotherapy (general exercises, change of back position to slight bending) and biophysical applications, such as andullation, may be more appropriate for some patients.

A rehabilitation programme is a regular part of conservative treatment, but it can be questioned if some of the prescribed exercises may be applied in elderly patients. Steroid infiltrations such as ‘facet’ blocks, epidural or caudal blocks, and selective nerve root blocks may show short-term pain relieving results. But can somebody explain me why and how these infiltrations temporarily ‘neutralise’ the signs and symptoms of NIC? Can it be explained by the Wall and Melzack pain relieving theory which indicates that corticoids are received by the brain as more ‘pleasant’ information dominating the claudicating pain signals?

The author would like to paraphrase Supertramp in their magical ‘The Logical Song’: ‘ There are times when all the world's asleep, The questions run too deep, For such a simple man, Won't you please, Please tell me what we've learned’.

In analyzing the literature, it becomes evident that the outcomes of conservative treatments not only remain scanty, vary substantially, but are problematic as well, as various types of treatment have been administered to the different subgroups. In general NIC patients, undergoing non-operative therapy, are considered successes if they experience at least some improvement (Table 33). Indeed, choosing - and it is really choosing - a conservative type of treatment remains mostly ‘Fingerspitzengefühl’.



No Patients








48 mo







24 mo





12 mo





31 mo







min 24 mo





144 mo





33 mo





48 mo


Onel (63)



1 mo


Table 34. Some outcomes of non-surgical treatments for Lumbar Spinal Stenosis (LSS)

35. Treatment: Surgery or no surgery? The question!

Because DLSS is a condition related to the normal evolution of aging and also the consequence of longstanding intervertebral discogenic degenerative processes, it is uncommon for existing low back pain complaints to resolve spontaneously. It is rather common that low back pain symptoms will persist and that the walking distance gradually decreases because of the associated intermittent neurogenic claudication. However, this evolution is unpredictable!

Decompressive laminectomy still remains the rational standard option for patients

(a) with intolerable pain,

(b) with severe neurogenic intermittent claudication (any grading?),

(c) in whom significant motor deterioration is present,

(d) whose overall symptoms and physical disability are highly disabling, and

(e) who do not present serious comorbidities.

Based on a meta-analysis of the available surgical outcome data from 1975 to 1995, the results seemed to be in favour of an early decompressive operation, meaning a duration of symptoms less than 8 years (Niggemeyer). But because of the subjective interpretation of the data and the non-methodological analysis, it was thought that total relief from symptoms could be attained!

Although the medical community constantly makes a fuss out of ‘randomized controlled studies’ and ‘evidence based medicine’, only about 15 % of medical trained personnel is aware of or accepts the recommendations of ‘evidence based medicine’ (Chapman 2013). Then, it is not surprising that the staggering conclusion from ‘evidence based medicine’ regarding DLSS associated with NIC is simply not known or not accepted: the effectiveness of surgery for spinal stenosis simply is limited (Rothschild 2009)! Surgery for DLSS has been associated with good but only short-term improvement for 1 to 4 years (Atlas). The long-term surgical outcomes are declining with recurrence of symptoms, no further benefit from surgery at 8 to 10 years and high reoperation rates (Atlas; Caputy; Scholz).

The since more than 25 year reported but extremely variable benefits of the surgical treatment options for DLSS are poorly understood (Fig. 35). And of course, the patient is responsible. He or she had unrealistic high expectations and, therefore, remains dissatisfied (McGregor; Toyone). This attitude is explained by patients having no clue or no anatomical understanding of what’s going to happen to them even if the procedure and potential complications are extremely well explained. At the same time the author refers to the French drama film directed by Nadine Trintignant: ‘Cela n’arrive qu’aux autres’ (it only happens to others). However, the most important reason is that the majority of spinal surgeons, just like the scientific world, has no clue regarding the real and exact mechanisms to explain pain and motor disturbance related to NIC. It then becomes evident that most spinal surgeons remain at the mercy of unscrupulous biomechanical companies selling ‘plates and screws’ by their perfectly orchestrated marketing machinery. The author indirectly acted for a short while as an educational consultant for such companies. He left disgusted because the non-scientific methods used were incompatible with his scientific spinal surgical training at highest level.

The Cochrane review of all randomised and quasi-randomised controlled trials on spinal stenosis till March 2005 permits limited effective conclusions (Gibson). In 2004, a comprehensive review of a much wider range of randomised and nonrandomised, prospective and retrospective studies of lumbar fusion conclude the surgical literature on lumbar fusion over the past 20 years is unreliable and haphazard and that instrumentation (plates and screws) does not improve overall clinical outcomes (Bono).



N° Patients

Follow-up (Y)

% Success



evidence based medicine





69 % - 90 %





55 %





73,6 %




< 4

64 %





63 %





significantly better





50 % + high reoperation rate









4 – 6






62 % + high reoperation rate





long-term declination










55 % + high reoperation rate






Fig. 35. Hugely variable success rates following surgery for lumbar spinal stenosis

36. Treatment: search for an ideal surgical procedure

        There are two problems in surgically dealing with DLSS with NIC: (a) except for the very severe cases, the clinical indications for surgery are not well defined and based on subjective interpretation of the available data, and (b) there exists no uniformly and worldwide accepted surgical procedure.

A variety of different surgical approaches has been developed (Table 36a). Some are no longer performed. The choice for a particular approach depends on:

(a) the origin of the surgeon,

(b) his local and/or international education,

(c) the instructions of his country’s ‘center of knowledge’,

(d) the medical fees related to the type of surgery performed, and

(e) sometimes the scientific brains of the non-indoctrinated surgeon. Mostly, biomedical companies with their well-developed marketing services are the indoctrinating sources to convince surgeons of their ‘peculiar’ systems in which they invested large sums of money. The author was indirectly but only for a short time involved as an instructional consultant for such a company. He left disgusted but still is confronted with the most ‘exciting’ concepts of some ‘key opinion leaders’. Indeed, human brains have no limits! However and till now, the effectiveness of all these types of surgery remains very limited (Rothschild, 2009).

Surgical techniques

Notes / Problems

Non-instrumented decompression

. excision ligamentum flavum

. hemilaminotomy

. bilateral laminotomy

. hemilaminectomy

. bilateral laminectomy

. laminoplasty

. partial undercutting facetectomy

. total facetectomy

. foraminotomies

. segmental hypermobility

. progressive spondylolisthesis

. scoliotic deformation

. kyphotic deformation

. new stenotic incidences

Decompression without instrumented arthrodesis

. posterolateral arthrodesis

. posterolateral intertransverse arthrodesis

. disappointing (Lehmann)

. pseudarthrosis

. postoperative spondylolisthesis

Decompression with plate-screw systems

. idea: Roy-Camille (France)

. impetus: Herkowitz (1991)

. still motion at disc level (Rolander)

. NO better clinical results

. Gibson (2005)

. Bono (2004)

Additional interbody fusion

. posterior lumbar interbody fusion (PLIF) pioneered by Cloward

. anterior lumbar interbody fusion (ALIF)

. circumferential 360° fusion

. transforaminal lumbar interbody fusion (TLIF)

. extreme lateral interbody fusion (XLIF)

. improved fusion rates (+/- 90 %)


. FAILED to improve clinical success

. higher morbidity

. higher complication rate

. very expensive (Kunz 2000)

Table 36a. Wide variety in surgical procedural alternatives for treating DLSS with NIC

        When whatever kind of conservative trial fails, then the rational consequence is to perform a cautious surgical decompressive laminectomy aiming at relieving neurogenic claudication. Depending on the kind and the extend of the ‘preferred’ decompressive technique, important posterior supportive structures always will be sacrificed. These posterior elements of the lumbar spine, and especially the zygapophyseal facetal joints, are important stabilising structures for controlling axial load bearing, translation, shear, and rotational resistance (Table 36b).


Share of Total


Total axial load zygapophyseal joint

18 %

Nachemson 1960

0 % to 33 %

Prasad and Kaing 1974

25 %

Lorentz 1983

if intact zygapophyseal joint

25 %

Yang and King 1984

if arthritic zygapophyseal joint

47 %

Yang and King 1984

Shear resistance

33 %

Adams         1980

Resistance to flexion

Adams and Hutton 1983

supraspinous ligaments

19 %

capsular ligaments

23 %

Ligamentum flavum

Adams         and Hutton 1983

in full flexion

13 %

in half flexion

28 %

initiating flexion

Major restraint

Table 36b. The biomechanical importance of the different posterior zygapophyseal joints and ligaments

It is quite logical that removal of these posterior elements will interfere with the normal stabilising biomechanics at the operated vertebral segments. These procedures may lead to residual or recurrent LBP as well as segmental hypermobility and/or progressive spondylolisthesis, scoliotic and/or kyphotic deformation, and new stenotic incidences resulting in traction on or compression of neural elements.

In order to prevent or even to correct these potentially occurring deformities and to relieve consequential low back pain, concomitant arthrodesing techniques have been developed. Supplementary instrumentation is employed to promote fusion.

In the author’s opinion this is unacceptable in the elderly age groups with DLSS and NIC. After more than 100 years, the main questions remain. Is lumbar fusion as an adjunct to decompression indicated as an appropriate and effective method in treating low back pain in patients with DLSS? It remains very controversial and the value of these fusion techniques always will continue to be questioned (Gibson). Rigid fusions induce abnormal spinal loading patterns which cause pain (Mulholland). Rigid fusion induce hypermobility patterns at the adjacent motion levels which may lead to supplementary new problems. Anyway, complications and postoperative morbidity are very high. With this background, dynamic stabilisation with instrumentation but without fusion were opted as new alternative options. However, the outcomes remain very disappointing.

It is noteworthy that in the postoperative period active rehabilitation seems to improve the functional status but has no impact on the general health status (McGregor 2013).

37. Treatment: In the best hands, still adverse effects!

Even the most careful, the scientifically best knowledgeable and the highest trained surgeon with spinal orthopaedic as well as spinal neurosurgical experience will encounter a variety of neurologic complications during and after routine decompressive procedures (Carroll).

When ‘weak’, ‘heavy’, or ‘tired’ feelings were present in the preoperative phase, these weaknesses probably will not disappear because of the irreversible morphological and functional changes in the motor neurons within the spinal cord (Kobayashi S et al.)

Older patients undergoing discectomies related to their degenerative discogenic syndrome have higher rates of morbidity and mortality than younger individuals (Stolke). And can somebody tell me what kind of tissue really is removed or dissected during discectomy? Because in the elderly age groups all degenerated nuclear material already has been resorbed by the natural processes (Fig. 37).


Fig. 37. What is the purpose of surgically removing this protruding part of a degenerating IVD without any contact with the nerve root? There is no place for plastic surgery in the spine!

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

Decompressive surgery, such as in DLSS, is associated with an even greater rate of complications and reoperations than are discectomies. And the other problems are associated with significant blood loss, nerve injury, hypermobility, worsening back pain, and infection.

38. Surgery: associated comorbidities

When major surgical procedures are performed in the elderly age groups with DLSS, excellent results are not often obtained.

Elderly patients tolerate major spinal surgery less easily because of their general medical condition and co-morbidities.

Elderly patients often present with a number of pre-existing endocrinological, metabolic, cardiovascular, pulmonary, and musculoskeletal comorbidities. For many older patients, surgery and general anaesthesia do not seem to be an option as the aforementioned chronic diseases may increase the perioperative risk or be a negative predictor of outcomes of decompressive surgery for DLSS.

The prevalence of preoperative comorbidities and worse self-rated health, physical function, symptom severity, and depression were associated with worse outcomes.

39. Surgery: Percentages of complications

The rate of complications in the elderly group due to spinal surgical procedures for DLSS is summarised in Table 39.

When a lumbar arthrodesis is performed in association with whatever kind of decompressive procedure in the 80-85-year-olds:

a) an overall perioperative complication rate of 80 % has been recorded (Carreon),

b) there is a 20 % complication rate related to the operation itself (Deyo),

c) a staggering mortality rate of more than 10 % is noticed (Deyo; Oldridge).

Age is the main risk factor for morbidity and mortality.



Overall complications




18 %



20 %



33 %



34 %



41 %



80 %



> 10 %



> 10 %

Table 39. Percentages of complications due to spinal surgical procedures in the elderly

40. Surgery: Major complications

Major complications can be defined as conditions that are life threatening or substantially impact treatment outcome (Carragee; Deyo).

The leading factors include:

. death,

. complication rate related to pedicle screw use,

. implant failure associated to the degree of osteoporosis,

. high reoperation rate,

. severe postoperative low back pain,

. ischemic damage and disuse atrophy of paraspinal musculature,

. paralysis or neurologic injury,

. dural tears with cerebrospinal fluid leaks,

. epidural haematoma,

. deep wound infection,

. pneumonia and/or pulmonary oedema,

. new-onset cardiac arrhythmia and/or myocardial infarction,

. stroke,

. thromboembolic disease (deep vein thrombosis and pulmonary embolism),

. gastrointestinal haemorrhage,

. renal blockage, and

. haematological phenomena.

Haematogenous spread of virulent organisms to the implanted instrumentation from another source is a common route of late wound sepsis in the elderly population.

So, let’s use our ‘surgical’ brains for developing an innovative and cautious spinal operative procedure!

41. Surgery: Minor complications

Minor complications are not life threatening and do not compromise outcome but may lengthen hospital stay. Included are transient confusion, dural tears, superficial wound infection and/or haematoma, transient ileus, urinary tract infection, etc.

It is noteworthy that a portion of the excised posterior arch (during decompression) will regrow. This is due to the strictly normal higher axial loads on the posterior structures following laminectomy. Which means that the anatomical stenotic problems will reappear, sooner or later.

42. Surgery: Reoperation rates

The reoperation rate of the commonly advised surgical procedures for degenerative lumbar spinal stenosis is astonishingly high (Table 42). Although these figures date from long time ago, the pathophysiology of DLSS and NIC has not changed nor has the handiness of surgeons even with the most sophisticated machinery!

To resolve the problems, DLSS and NIC are waiting for new pioneers inventing more cautious implants and procedures. Regarding the modern evolutions progressing at the speed of light, the future pioneer probably will need to be able to combine intelligent thinking as a civil engineer and precious fingerspitzengefühl as a spinal orthopaedic and neurosurgical surgeon.



No Patients


Reoperation Rate




2-5 years

5 %




12 m

6 %




10 years

11 %




33 m

12 %




6 to 54 m

18 %




5 years

18 %




8 years

23 %



8-10 years

23 %

Table 42. Reoperation rates following surgery for DLSS

43. ‘Golden’ standard surgery is extremely expensive

Because of the increasing elderly age groups, DLSS with or without NIC becomes the most common and the fastest growing reason for lumbar spinal surgery in the post-world war II baby-boom population. Approximately half of the NIC patients will become candidates for surgery. This simply means big business: billions of euros! And the author knows it well because of his indirect relation with such companies!

However, the economic stress of the classical interventional procedures - all forms of decompressive lumbar surgeries augmented with all sorts of plates and screws - demands a change in the existing surgical approach (Kunz). The growing elderly population already has a limited life expectancy. This underscores the need to maximize the quality of remaining life with as little risks, complications and earlier deaths as possible.

Nobody - surgeons nor patients - seems to be very excited regarding the long-term postoperative surgical results for DLSS associated with NIC. So, what to do for those patients with the ‘non-severe’ and average signs and symptoms? Till now, nobody seems to know.

Unfortunately, the real physiopathological reasons for the occurrence of NIC are totally unknown. The reasons why the degenerative and inflammatory processes into the intervertebral lumbar discs may cause low back pain still remain a riddle, wrapped in a mystery, inside an enigma (Winston Churchill). Therefore, DLSS and NIC can only be classified in subjective clinical groups based on MRI-images with no relation at all with pain, disability, signs and symptoms of DLSS and NIC.

And … any innovative approaches on the horizon? It will need extremely intelligent brains to switch from the ‘business as usual’!

44. Surgery: Dynamic Pedicular Stabilisation

During his surgical professional life, the author implanted and assisted approximately 1.500 soft or flexible pedicular ligamentoplasties from 1996 to 2002 (Fig. 44a).


Fig. 44a. Flexible pedicular stabilisation ligamentoplasty.

(Images by courtesy of Mr. Allan Gardner, Spinal Surgeon, Emeritus President of the Spine Society of Europe)

Because of the initial good or even excellent subjective impressions - compared to the performed rigid instrumented fusions - a prospective and multicentric 5-year follow-up study on 280 patients related to a flexible pedicular ligamentoplasty system was initiated. All data were forwarded for unbiased analysis to the Spine Tango Research Programme, launched by the Spine Society of Europe (Declerck; Gardner; Röder). For reasons unknown to all of the authors, and even to the President of the Spine Society of Europe at that time, Mr. Alan Gardner, the results were never published. However, the author is ‘aware’ of fundamental research on the application of an innovative flexible pedicular system combined with perpedicular intradiscal injection of ‘stem cells’ to neutralise the degenerative processes in the intervertebral disc.

The initial hypothesis was that dynamic stabilisation of motion in a ‘painful’ lumbar segment of the lumbar spine with pedicular instrumentation but without the intention of fusing segments would alter its load bearing pattern. As such it would neutralise the degenerative intradiscal processes by stimulating the normally occurring fibrotic processes into the intervertebral disc (Declerck). This process finally could result in pain relief (Gardner; Mulholland; Sengupta). Indeed, Sénégas clearly proved that dynamic stabilisation had a biological effect on the degenerating lumbar intervertebral disc which resulted in his R&D of interspinous devices (Fig. 44b).


Fig. 44b. Biochemical Sénégas-effect by biomechanically reloading the L4-5 degenerating lumbar intervertebral disc by an interspinous device

Essential to mention is that for relieving and preventing leg pains, a partial undercutting facetectomy always need to be performed.

A number of dynamic pedicular stabilisation systems are still used clinically for ‘treating’ DLSS. The author is not convinced of the clinical efficiency of these systems in these clinical settings. Because the degenerating intervertebral disc is left ‘alone’, the initial expectations were not fulfilled. The long-term outcomes and complications of these flexible or soft stabilisation systems are comparable to those of instrumented fusions. It is evident that dynamic stabilisation is insufficient in neutralising the intradiscal pain-inducing degenerative mechanisms. However, innovative and adjunctive procedures are being researched and explored.

45. Surgery: Interspinous Extension Limiting Device

During the years 2005-2007, Medical Consulting Advice BVBA implemented the literature review on degenerative lumbar spinal stenosis, neurogenic intermittent claudication, and innovative surgical implants for the company Kyphon in her conquest for R&D of implants (Declerck) (Fig. 45a).



Fig. 45a. Demonstration of the Aperius Percutaneous Lumbar Interspinous Decompression (PercLID) Implant, engineered by the Kyphon Company. The floating interspinous device fits between two adjacent spinous processes on a bone model. Above left and right, the APERIUS implant before insertion: the bullet shaped outer shell showing the windows. Below left and right: the same APERIUS implant after placement and deployment within the patient. Note the radial fins that keep the implant in place

While going through this huge amount of literature data, the author came to an astonishing question: why does there exist such an amount of ‘key opinion leaders (KOLs)’ without any basic scientific education in spinal anatomy, spinal biochemistry, spinal biomechanics, spinal bioengineering? And secondly: is it really essential for the KOLs and their manufacturing companies to reinvent the sun each time for ‘developing’ similar ‘innovative’ implants based on the same basic principles? What a waste of time, energy and money! Of course it’s business and of course it’s all about ego’s! But as the normal aging and the abnormal degenerative processes in the lumbar spine are (as yet) not at all understood, imagination to resolve DLSS and NIC would have been better than copying each other’s ideas.

As a spinal orthopaedic surgeon with spinal neurosurgical education, the author takes the liberty to paraphrase Supertramp: ‘They teached ‘us’ how to be sensible, logical, responsible, and practical. But they only showed ‘us’ a world where ‘we’ could be so dependable, clinical, oh intellectual, cynical. Oh watch what you say. Because they now call me a radical, a liberal, oh fanatical, criminal. Not acceptable, respectable, presentable - but vegetable!’ Great ‘The Logical Song’!

During the Second World War orthopaedic surgeons in Warsaw, Poland, developed the idea of implanting a device in the space between two spinous processes (Fig. 10b and 45b). Since then, an incredibly large variety of rigid and soft interspinous devices have appeared on the commercial surgical market and in the meantime … have disappeared as well because of … ‘rubbish’. They were or are made of stainless steel, titanium alloys, PEEK (polyetheretherketone), silicone or other materials. Billion dollar business!


Fig. 45b. Based on the experience with a Polish interspinous device, developed during the Second World War, potential innovative and more modern implants are researched

And all of these mostly free-floating devices follow the same biomechanical principles (Table 45). In the meantime, the spinous processes have been proven to have adequate strength to support the insertion loads for implanting the devices and to resist the loads exerted on them during normal extension (Fuchs; Goobar; Schwardt; Shepherd; Talwar). A minimum of spinous process fractures should occur if all technical surgical insertion details were respected!

Biomechanical function: the spacer …

Anticipated resulting effect

. distracts the spinous processes

… limiting extension at the implanted level

. increases central and lateral canal dimensions

… reducing dural sac and nerve root impingement

. off-loads the discs and zygapophyseal facetal joints

… spacer becoming a load-bearing structure

. reduces intravertebral nuclear disc pressure

… decreasing        tension forces in the posterior annulus

. stimulates intradiscal fibrous healing process

… ‘black’ disc becomes ‘white’ (Senegas)

. acts locally at implanted level(s)

… without too much effects on adjacent levels

. has minimal effect on the average L1-L5 lordosis


. has no influence on the adjacent motion levels

… and        insignificant compensatory mobility occurs

Table 45. The biomechanical functions of an interspinous spacer

The major problem is the non-scientifically proven evidence of their multiple indications. All of the approximately 50 existing interspinous devices have in one way or the other been used to treat ‘painful’ discogenic conditions such as degenerative discogenic syndrome, degenerative disc herniations, ‘slight’ spondylolisthesis (+/- 35 °), zygapophyseal facetal syndrome, and post-discectomy syndrome(s). However, the major indication seems to be the ‘not too severe’ degenerative lumbar spinal stenosis (DLSS) (Fig. 45c). Some implants can be inserted under local anesthesia without stripping the paravertebral muscles and preserving the posterior ligaments. In principle - and if surgery is carefully performed - complications should be rare! However, …


Fig. 45c. The idea of implanting an interspinous device between the spinous processes to relief patients from neurogenic intermittent claudication (NIC) related to degenerative lumbar spinal stenosis (DLSS) comes from a straightforward clinical observation. Most of the NIC patients get symptom relief when bending forward, sitting down and flexing their spine. Flexion (F) broadens the central and lateral spinal diameters. Conversely their symptoms exacerbate when they stand erect and extend their spines. Extension (E) narrows the spinal diameter of the spinal canals

Do the interspinous devices really implement the foreseen good clinical results? No! The interspinous devices only can provide more or less satisfactory results during a short postoperative period of one year, which means that the reoperation rate must be extremely high.

Simply, is it worth implanting a device which costs an average of 2200 euros? NO! At least this is the conclusion from the only existing ‘scientific’ method for research, the so-called prospective but selectively randomized and placebo-controlled trials (RCT) (Mooyen; Smith).

46. Any explanation for NIC?

It is generally believed that the leg symptoms of neurogenic intermittent claudication are related to narrowing of the spinal canal reducing the size of the dural sac and limiting the space available for the cauda equina and nerve roots.

However, since long time it is known that the correlation between the degrees of radiologic stenosis and the clinical manifestations is poor. Based on the abnormal findings in asymptomatic adults by using discography, myelography, CAT and MRI, the prevalence of radiological lumbar spinal stenosis is much higher in asymptomatic individuals than in the symptomatic DLSS-patients associated with neurogenic intermittent claudication (NIC) (Boden; Fox; Jensen; Holt).

When DLSS-patients presenting NIC are examined appropriately in the preoperative period it becomes clear that a lot of them have notable impairment in lumbar proprioception with poorer ability of maintenance of postural stability (Kääriäinen; Yoshikawa). The golden standard of simply removing the compression surgically doesn’t seem to be the perfect solution because the reported (short and long term) clinical outcomes are far from ideal in the elderly age groups. Dysfunctional weaknesses in the lower legs expressed by feeling ‘weak’, ‘heavy’ or ‘tired’ in the preoperative period rarely will disappear following whatever type of surgical decompressive intervention. Performing a high-tech guided and thus perfectly performed decompression is not at all a panacea for obtaining a good outcome. Therefore, there are no reasons to describe these elderly patients as ‘crazy’. Elderly age groups are interested in living peacefully without pain and in maintaining a good quality of life.

How to explain DLSS with NIC ?

There certainly exists something which is called ‘mechanobiology’ or a relationship between mechanical factors and biochemical reactions. Chronic mechanical compression of the lumbosacral spinal nerve root complex in the central spinal canal and in particular at the level of the intervertebral foramina cause multiple metabolic intraneural changes which will not change by a decompression (Table 46).

Epidural venous plexus

Compression, distortion, dilatation of the veins

Disturbance of venous blood flow

Endothelial cell damage

Cauda equina (CE)

Increased epidural pressure

Changes in cerebrospinal fluid pressure

Disturbed arterial blood supply of CE during walking

Disturbed venous congestion of CE during walking

Nerve roots (NR)

Mechanical nerve fiber deformation in the NR

Changes in the microvascular                        blood flow of NR

Ischemia of NR                         

Intraradicular edema                         

Peri- and intraneural NR fibrosis

Focal demyelination

Ultrastructural changes

Wallerian degeneration

Impaired nerve conduction velocity

Lumbar motor neurons in the spinal cord

Morphological changes through axonal flow disturbance

Dorsal root ganglion (DRG)

Ectopic firing of DRG with central sensitisation

Inflammatory enhancing excitability of DRG

Functional changes

Disturbed lumbar proprioception

Dysfunctional weaknesses

Table 46. Direct mechanical nerve root compression leads to complex metabolic phenomena. Intraspinal vascular compromise and intraneural changes result in functional changes

Biomechanical compression by the hypertrophied posterior elements (laminae, articular processes, ligamentum flavum) of the lumbar and sacral spinal nerve root complex results in mechanical deformation of their nerve fibers. Epidural venous congestion and interference with the peculiar intrinsic vascular microcirculation of the nerve roots causes ischemia and forms intraneural nerve root edema. The more lateral (intervertebral foramen) the impingement of the nerve root occurs, the more ischemic changes are induced. Vascular insufficiency is accompanied by reduced oxygen supply, stagnant hypoxia or anoxia, and reduced nutrient supply. These phenomena generate ultrastructural changes (significant primary Schwann cell damage and intracellular edema with vesicular swelling of the Schmidt-Lanterman incisures) causing demyelination of the nerve roots, decrease the nerve conduction velocity, and irritate the dorsal ganglion. All these complex neurophysiologic mechanisms precipitate pain, neurogenic intermittent claudication, induce motor weakness. Note that the concept of pericaudal circulatory factors and the occurrence of intermittent claudication due to ischemia of leg muscles is known since 1858 and was described by Jean-Marie Charcot.

Noteworthy for NIC and in contrast to nerve root compression during the herniating pathway, inflammatory cells remain absent (Blau; Charcot; Chatani; Hoyland; Iwamoto; Kamei; Konno; Magnaes; Matsui; Naito; Olmarker; Rydevik; Sekiguchi; Takahashi).

47. The author’s conclusion

In the author’s opinion, it is time to start performing large scale evaluations on 100.000 operated and non-operated patients suffering DLSS with or without NIC and to evaluate the results in real-life conditions. A typical well selected and randomized RCT-patient, suffering DLSS and NIC, has never been encountered by any spinal surgeon worldwide! Human beings are too complex to be treated as ‘one-disease-possessing’ individuals.

More objective, more serious and more detailed research in real time life conditions will eliminate the well-known possibilities of manipulation and corruption during RCT’s. In the digital world, it’s time to promote comparative effectiveness research (CER) (Begley; Cartwright; Chalmers; Chapman; Doshi; Lupton).

What will become very clear is that the reasons and the origins of the degenerative discogenic syndrome need to be cleared out scientifically before innovative treatments can be successful. Till now - 2014 -  nobody has a clue!

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