Paravertebral Lumbar Spinal Muscles

International Publicized Data

GMCD Instructional  Course Lectures

Author :  

Guy M.C. Declerck MD (GMCD)

Medical FRCS-, FRCS Ed Orth-, M Ch Orth-, PhD-studies

Spinal Surgical and Research Fellow, Perth, Western Australia

Spinal Orthopaedic Surgeon and Surgical Instructor

Consultant R&D Innovative & Restorative Spinal Technologies

President International Association of Andullation Technology (IAAT)

Copywriter / Translator: Filip Vanhaecke PhD

Illustrative expertise: Provision, Waregem, Flanders, Belgium

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

Support: International Association of Andullation Therapy (IAAT)

Legal advice: Anthony De Zutter, kornukopia.be

Dedication to Christine, CEO Medical Consulting Advice BVBA. November 2014

Christine understood that a medical career can profoundly be influenced by tragic familial events but with a beneficial outcome. Rather like a detective, she could look at the bits of a puzzle and put it together. Hearing my commotion, she commanded me to swallow my pride and escape through thewindows of life. Eager to share my knowledge, she stimulated me to finalise the three major topics of my personal spinale research: spinal metastatic disease, whiplash syndrome, and the comparison of lumbar muscles between chronic low back pain sufferers and those without pain.

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Acknowledgements

‘Muscle is a machine, and in any machine we must deal with two elements. One is the energy-yielding reaction, such as expansion of steam in a steam engine, the burning fuel in an internal combustion engine, or the flow of current in an electric motor. These elementary reactions can accomplish useful work only it they take place within a specific structure, be it a cylinder and a pistol or a coil and a rotor. So in a muscle we must also look for both the energy-yielding reaction and the meaningful structure. The energy-yielding reaction is a chemical change which takes place among molecules, and its study belongs to the realm of biochemistry. The structure is the domain of the anatomist, working with is knife, microscope or electron microscope’ (Albert Szent-Györgyi, Nobel 1937).

Relying on the work of giants is the lifeblood of scientific research. Indeed, if I have seen further, it is by standing on the shoulders of giants. One might even say that I have always depended on the kindness of strangers in this regard (*).

The continuous support by professor BA Kakulas (Neuropathology), professor JR Taylor (Spinal Anatomy and Human Biology), and Sir George M Bedbrook (Spinal Orthopaedic and Rehabilitation Surgeon) made it possible to analyse 27.539 post-mortem human spines, normal and pathological, in the Department of Neuropathology, Royal Perth Hospital/University Western Australia, Perth. The author developed and participated in multiple research projects, all regarding the enigmatic aspects related to the spine (whiplash, spinal metastases, intervertebral disc, osteoporosis). Simply, if the science of a body of work is solid, it serves publication regardless of who produced it.

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

 

 

Contents

1. Erect posture and the erector spinal muscles

2. Major role of the erector spinal muscles

3. Erector spinal muscles protect lumbar intervertebral discs

4. What if erector spinal muscles don’t function well?

5. Muscles contain different types of muscles fibers

6. Histochemical muscle fiber differences

7. Histochemical adenosine triphosphate (ATPase) reaction (Dubowitz & Kakulas)

8. Histochemical NADH-tetrazolium reductase (NADH-TR) (Dubowitz & Kakulas)

9. Histochemical succinate dehydrogenase (SDH) reaction (Dubowitz & Kakulas)

10.  Histochemical periodic acid-Schiff stain (PAS) (Dubowitz & Kakulas)

11. Histological muscle fiber differences

12. Electron microscopic muscle fiber difference

13. Multifidus muscle: type 1 and 2 muscle fibers

14. Effect of chronic low back pain on muscle fibers

15. Effect of exercises or inactivity on muscle fibers

16. Nervous supply of spinal muscles

17. Concept of motor unit (Dubowitz)

18. Surgical procedures interfere with spinal muscles

19. Age weakens the spinal muscles

20. All spinal disorders show muscle fiber changes

21. The Perth Muscle Study. Histology, histochemistry and electron microscopy of multifidus muscle fibers in degenerative discogenic syndrome

21a. Introduction

21b. Muscle biopsy preparation by a senior laboratory technologist

21c. Fifteen healthy versus 15 chronic low back pain patients

21d. Normal muscle fibers in healthy individuals

21e. Variety of pathologic changes in chronic low back pain patients

21f. Comparison with reported muscle histochemistry in ‘disc herniation’ cases

21g. Conclusion

22. The author’s conclusions and suggestion

23. Literature Encyclopaedia

 

 

1. Erect posture and erector spinal muscles

The erector spinal muscles maintain the individuality and functional interdependence of each spinal motion segment of the vertebral column in relation to their adjacent segments (Fig. 1). The contraction and relaxation of these muscles are responsible for the erect posture in humans.

 

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Fig. 1. Spinal motion segment means the structure built by two vertebral bodies, their intervertebral disc, the zygapophyseal facetal joints and their ligamentous structures.

(Internal Instructional Spinal Course, Kyphon)

 

 

2. Major role of erector spinal muscles

For the lumbar spine to function well, the erector spinae muscle group  has to interact with the posterior ligamentous system (intra- and supraspinous ligaments and lumbodorsal fascia) and the abdominals.

When a healthy spine supports an external load of 20 kilograms and flexes forward during the first arc of motion from zero to 40 degrees, the external load moment at L5 is essentially balanced by the action of the erector spinae muscles. Around 40 degrees, there is no need for the erector spinae muscles to transmit any power. The spine has sufficiently flexed to permit the intra- and supraspinatus ligaments to be set under tension (Fig. 1). The power of the large hip extensors, which sustain the larger lifts, needs to be transmitted directly to the upper extremities by the lumbodorsal fascia (Fig. 2). This structure is attached to the tips of the spinous processes and the abdominal muscles (internal oblique and the transversus abdominis). The fascia contributes to the balancing of the external loads for any spine position by exiting the antagonistic activity of the abdominal muscles (Floyd).

 

 

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Fig. 2. The thoracolumbar fascia, because of its attachment to the abdominal muscles,  is an important stabilizing structure for the spine.

(Internal Instructional Spinal Course, Kyphon)

 

Importance: in principle, the erector spinae muscles will have to work more intensely when the spine is made stiff following surgery because full use of the posterior ligamentous system no longer is possible. Unfortunately, there is a major problem! The low back muscle innervation is interfered with during all spinal surgical procedures and the spinal muscle mass becomes fibrotic due to the iatrogenic destruction of the blood vessels!

 

 

3. Spinal muscles protect lumbar intervertebral discs

In the total effective function of the spine, the paravertebral muscle mass is at least as important as the vertebrae it clothes posteriorly (Fig. 3).

 

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Fig. 3. Illustration of the thoracolumbar fascia covering the lumbar erector spinae muscles which is the global name for the muscles in the spine. On the right scanning image, in-to-out and circular ruptures are seen in the intervertebral disc (related to discogenic trauma? or to the evolution of the degenerative processes in a normal aging disc?). On the same image the deep spinal muscle, called the multifidus muscle, is encircled.

(Internal Instructional Spinal Course, Kyphon)

 

The trunk musculature is the major force-generating structure. It exerts active damping on the spine under various conditions. This mechanism protects the passive elements (e.g. ligaments, intervertebral disc and zygapophyseal joint capsules) by preventing them from reaching their limits of shear and rotational resistance while they assume their role of flexibility during movements.

One rationale for measuring resistance to displacement is to study stiffness. Mathematically, stiffness is defined as the resultant of the load applied and the displacement produced. The stiffness of intact spine motion segments has been estimated in the range of 600 to 700N/mm in axial compression and 100 to 200 N/mm in anterior, posterior, or lateral shear, noting, however, considerable individual variation.

 

4. What if spinal muscles don’t function well?

Muscle dysfunction destabilizes the spine, reduces the role of zygapophyseal facetal joints in transmitting load, and shifts loads to the intervertebral discs and ligaments (Kong).

 

Importance: nobody knows if he or she is genetically protected for not developing low back pain based on the development of degenerative processes in the normal aging lumbar intervertebral disc. Most individuals worldwide possess genes (e.g. collagen type I and IX genes, vitamin D receptor genes, matrix metalloproteinase genes, genes for coding interleukin-1 and interleukin-6) which may induce the development of intervertebral disc degeneration and result in its secondary consequences (disc herniating pathway, spondylolisthesis and spinal stenosis). Then simply: long-life and regular stabilizing lumbar spinal muscle exercises remain essential. Otherwise and simply as well: surgical interventions which never restore the basic problem!

 

 

5. Muscles contain different types of muscles fibers

From birth, normal human skeletal muscle can be differentiated into different fiber types (Table 5).

 

Type 1

Type 2A

Type 2B

Aerobic

(an)aerobic

anaerobic

Oxidative

Oxidative & glycolytic

glycolytic

Slow-twitch contractions

Fast-twitch contractions

Fast-twitch contractions

Long activities

Resistant to fatigue

Fatigue sensitive

 

Sustain activities

 

Table 5. Fiber types in human muscle.

 

The slow contracting type 1 muscle fibers have a high oxidative and low glycolytic activity. They are responsible for converting fat into energy to sustain long-lasting vigorous activity.

 All type 2 fiber types are used primarily for rapid movements and rely on sugar for fuel. The fast contracting but fatigue resistant type 2A fibers have a low oxidative and high glycolytic activity. The fast contracting but fatigue sensitive type 2B fibers have a high glycolytic activity. The observed type 2C fibers represent transitional fiber types, capable of differentiation into type 2A or 2B fibers.

 

6. Histochemical differences in muscle fibers

The underneath information on histochemistry of skeletal muscle fibers originates from Professor Dubowitz’ s book ‘Muscle Biopsy’ as well as from BA Kakulas, Professor of Neuropathology, University of Perth in Western Australia.

Histochemical methods are of value in the study of skeletal muscle biopsies  to demonstrate the specific fiber types  on the basis of various enzyme reactions. The enzymes of particular interest in the study of skeletal muscle have been those connected with glycogen synthesis and breakdown (such as phosphorylase), oxidoreductases (such as various dehydrogenases linked to the Krebs cycle) and hydrolases (such as adenosine triphosphatase and various esterases).

Histochemical analysis may show the absence of an particular enzyme or an excess of a particular substrate leading to a clinical diagnosis. It may show various structural changes in the muscle which would not be apparent with routine histological stains such as enzyme-deficient cores, moth-eaten fibers and abnormalities in the distribution of mitochondria (see illustrations further down).

 

 

7. Adenosine triphosphate (ATPase) reaction (Dubowitz & Kakulas)

The histochemical myosin ATPase reaction most directly manifests the physiological differences and pathologic changes between the slow twitch type 1 fibers and the fast twitch type 2 fibers (Table 7). Their shape and distribution are defined as well. Myosin is the molecular motor protein in skeletal muscle that produces force and ultimately generates movement.

 

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Table 7. How to differentiate muscle fibers by the myosin ATPase reaction?

 

The type 1 fibres are more lightly stained than type 2 fibres which are more heavily coloured on an augmented ATPase reaction with pre-incubation at pH 9.4. Following pre-incubation at pH 4.3, the type 1 fibers stain darkly and the type 2 fibers lightly. At pH 4.6, the type 1 fibers are strongly reactive as at pH 4.3, but the type 2 fibers vary: the type 2A stain lightly whereas the 2B fibers stain strongly (Fig. 7).

 

 

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Fig. 7. Myosin ATPase at pH 4,3 (left) and at ph 4,6 (middle): normal fiber type grouping (X90/769).

At ph 9.4 (right): variation in fiber size and in distribution of the fibers, type I predominance and grouping of type I fibers (X90/1087).

(Declerck, Narula, Margolius, Kakulas, NeuroMuscular Pathology, Perth, Western Australia)

 

For the underneath mentioned Perth study of the lumbar multifidus muscle, we were particularly  interested in a potential predominance of type 1 fiber at pH 9.4 and fiber size variation indicating myopathy.

 

 

8. NADH-tetrazolium reductase (NADH-TR) (Dubowitz & Kakulas)

Nicotinamide-adenine dinucleotide-tetrazolium reductase (NADH-TR) is an oxidative enzyme reaction which differentiates the fiber types. The intermyofibrillar network, which comprises mitochondria, is well demonstrated. The type 1 fibers stain intensely. The type 2A  fibers have an intermediate activity. The type 2B fibers show the least reaction (Fig. 8 and Table 8).

 

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Table 8. How to differentiate muscle fibers by the NADH-TR reaction?

 

 

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Fig. 8. Nicotinamide-adenine dinucleotide-tetrazolium reductase (NADH-TR): presence of doubtful cores

(Declerck, Narula, Kakulas, NeuroMuscular Pathology, Perth, Western Australia - X90/769)

 

For the underneath mentioned Perth study of the lumbar multifidus muscle, we were interested in the potential occurrence of architectural changes  such as central core fibers,  moth-eaten fibers indicating myopathy. If present, small angulated fibers are considered a sign of denervation of the muscle.

 

9. Succinate dehydrogenase (SDH) reaction (Dubowitz & Kakulas)

The coenzyme-independent succinate dehydrogenase is an oxidative reaction which is purely mitochondrial. The classical methylene blue technique for succinate dehydrogenase stains strongly for the type 1 fibers. The type 2A fibers have an intermediate activity. The type 2B fibers show the least reaction (Fig. 9 and Table 9).

 

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Table 9. How to differentiate muscle fibers by the SDH-reaction?

 

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Fig. 9. Coenzyme-independent succinate dehydrogenase stains. Left (X90/1087): variation in fiber size and no inflammation. Some artefacts. Right (X90/368): mild variation in fiber in diameters of the fibers.

(Declerck, Narula, Kakulas, NeuroMuscular Pathology, Perth, Western Australia)

 

 

10. Periodic acid-Schiff stain (PAS) (Dubowitz & Kakulas)

Periodic acid-Schiff stain (PAS) demonstrate the intermyofibrillar network pattern. PAS has a very long history in histochemistry and depicts the distribution of glycogen in muscle. This stain for glycogen depletion reacts more strongly with the type 2A and type 2B fibers than the type 1 fibers. The 2B fibers are reacting intermediately (Fig. 10 and Table 10).

 

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Table 10. How to differentiate muscle fibers by the PAS-reaction?

 

 

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Fig. 10. Periodic acid-Schiff stain (PAS) (X90/769).

(Declerck, Narula, Kakulas, NeuroMuscular Pathology, Perth, Western Australia)

 

11. Histological differences in muscle fibers (Dubowitz and Kakulas)

Histological staining methods with hematoxylin and eosin stain (H&E) as well as with modified Gomori trichrome demonstrate the morphology of the muscle fibers.

The sarcolemmal nuclei stain blue with H&E, the muscle fibers pink and the connective tissue a lighter pink (Fig. 11a). When group atrophy is present, H&E indicates denervation of the muscle. If any small angulated fibers can be detected, denervation is suspected as well. When there are internal nuclei in more than 10 % of the fibers, myopathy is suggested.

 

figure11a.png 

Fig. 11a. Hematoxylin and eosin stains (H&E). Left: blue staining of the sarcolemmal nuclei (X90/1087).Right: very loose architecture (X90/769).

(Declerck, Narula, Kakulas, NeuroMuscular Pathology, Perth, Western Australia)

 

Staining with Gomori results in the muscle fibers coloring greenish-blue and the collagen a lighter but clearly distinguishable blue-green colour (Fig. 11b). The two different types of fibers may be distinguished: type 1 fibers usually are characterized by a slightly darker background.

 

figure11b.png

Fig. 11b. Gomori stains. Left: variation in fiber types (X90/1087). Right: very loose architecture and evidence of ice crystal artefacts (X90/769).

(Declerck, Narula, Kakulas, NeuroMuscular Pathology, Perth, Western Australia)

 

 

12. Electron microscopy of erector spinal muscles

Electron microscopy aims at correlating the ultrastructural features with the histochemical and physiological features in the different fiber types. In human muscle, ultrastructural differences between fiber types are less easy to identify because most muscles are of mixed fiber type. There are slight increases in the amount of lipid droplets which may indicate a change or retardation in the metabolism of the muscle fibers.

I.e. electron microscopic analysis of spinal muscles in scoliosis showed unexpected and bizarre changes, ranging from normal to a picture suggestive of a very severe muscle disease.

 

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Fig. 12. Lumbar multifidus muscle in a 34-year old male who never experienced low back pain (B90/6851 and B90/6091). Presence of lipid and lipofuscin in the muscle fibers (white spot). Mitochondrial aggregations (dotted area). Presence of nuclei with a small amount of cytoplasm (left below). These minor changes are of unknown significance but may be age related.

(Kakulas, Professor NeuroMuscular Pathology, Perth, Western Australia)

 

 

13. Multifidus muscle: type 1 and 2 muscle fibers

In the lumbar multifidus muscle the tonic activity of the type I fibers plays a consistent postural role and the type 2 fibers provide the stability of the spine on sudden movement and loading. Both fiber types react differently not only to mechanical loading but to lesions of their nerve supply and to aging processes as well.

 

 

14. Effect of chronic LBP on spinal muscle fibers

Patients with chronic low back pain (minimum 3 months of undulating or intermittent episodes of LBP with or without referred pain of non-radicular nature) frequently only complain of pain and dysfunction in the area of their back muscles. Chronic low back pain patients have difficulties in performing exercises because of deficits in strength, endurance and fatigue-resistance of their low back muscles.

Nevertheless, the medical and paramedical world ‘instructs’ these LBP sufferers to proceed with a more physical active life. Notwithstanding the presence of intense pain, even insurance companies force these patient to implement active exercises in the idle hope that signs and symptoms of their degenerative discogenic syndrome (DDS) will settle definitely.

But how can somebody with wrist pain exercise his wrist fully? Who can somebody with shoulder pain exercise his shoulder fully? How can somebody with hip or foot pain exercise these joints fully?

On the other hand, there is evidence that the risk of developing chronic LBP may be enhanced by suboptimal endurance of the flexor and the extensor supportive back musculature. Indeed, the most physically fit people are found to have fewer episodes of back injuries and are more tolerant to pain. However, there is much more than ‘painful’ muscles!

 

 

15. Effects of exercise or inactivity on muscle fibers

The effects of short and long duration exercise on the metabolic activities of skeletal muscle and on the histochemical pattern of fiber types are complex and variable. The effects depend on the genetic endowment, life style, state of physical training of the individual, the type of exercise (strength or endurance), the intensity and duration, and the muscle studied.

In general, exercises increase the oxygen uptake and the oxidative potential in both fiber types 1 and 2 as judged by histochemical NADH-TR and SDH enzyme reactions. The glycolytic capacity increases in the type 2 fast–twitch fibers. Glycogen depletion, judged by PAS stain, increases dramatically with increasing intensity of exercise (Gollnick; Essen).

Strength training, endurance exercises, as well as immobilisation alter the fiber type composition in spinal muscles.

 

 

16. Nervous supply

The largest and most medially located low back muscle is called  the multifidus. This muscle is the deepest part of the erector spinae muscle group and is only innervated by the medial rami of the dorsal branch of a spinal nerve root. Contrarily to the other back muscles, the lumbar multifidus muscle bands arising from the spinous processes, only receive an unisegmental nerve supply.

 

 

17. Concept of the motor unit (Dubowitz)

The concept of the motor unit is nicely described in Dubowitz’ s book ‘Muscle Biopsy’.

The motor unit is fundamental to the understanding of the physiological behavior of spinal muscles. The nerves innervating muscle fibers have their origin in the cell body lying in the anterior horn of the spinal cord. A particular neuron which takes origin in a single anterior horn cell will branch to supply many muscle fibers. In other words, in most muscles several hundred fibers are supplied by an identical neuron.

Functionally this means that the anterior horn cell, its axon and the muscle fibers supplied by it behave as one motor unit. This signifies that no significant activity in one part of the muscle fibers can occur without a corresponding activity in the other fibers of that motor unit. Because all motor units are uniform, a given neuron determines a given fiber type. This results in type 1, type 2A and type 2B fibers being independently innervated. This results in all muscle fibers of each motor unit to be uniform in histochemical type.

 

18. Surgical procedures interfere with spinal muscles

Conventional posterior low back operating techniques for decompressive procedures and fusion nearly always result in disturbances of the low back muscle innervation. Postoperative MRI evaluations very rarely indicate recovery of the spinal muscle mass but nearly always show massive fibrosis. And how can a fibrosed muscle be exercised?

Direct trauma or lesions to the dorsal ramus in one or more segments are at the origin of muscle atrophy of the paraspinal back extensors. As this nerve runs under a small ligament (the fibro-osseous mamilloaccessory ligament), it is extremely vulnerable during surgery when the spinal muscle mass needs to be retracted and displaced laterally.

The corresponding decreased lumbar muscle strength and support may be an additional cause for persisting pain leading to postoperative disability. This postoperative disability usually is precipitated by exercises and static loading conditions like sitting and standing. Unfortunately, radiological and electromyographic investigations cannot reveal any iatrogenic nerve root or spinal canal compromise. So, the medical and paramedical community can only instruct exercises.

 

 

19. Age weakens the spinal muscles

The aging processes are responsible for the occurrence of sarcopenia which is the loss of mass, power and function of muscles (Sinaki). But even young and healthy individuals may present some pathologic changes in the internal structure of the muscle fibers (1 - 5% in the type 1 fibers).

With increasing age, structural changes and atrophy involve both type 1 and type 2 muscle fibers. However, the proportion of type 1 fibers increases at the expense of the type 2 fibers.

 

 

20. All spinal disorders show muscle fiber changes

There exist no characteristic morphological changes in the spinal muscles which are diagnostic of a particular spinal disorder. Till now, it has never been described.

The reports on spinal muscle biopsies of reoperated patients mention type 1 fibre predominance, disuse atrophy in type 2 muscle fibres, group fibre atrophy, and changes in internal myofibrillar structure of both fibre types. The findings not only are explained as a consequence of denervation of the lumbar multifidus muscle during a spinal surgical procedure but as well as the result of the aging processes.

 

 

21. The Perth Muscle Study

Histology, histochemistry and electron microscopy of multifidus muscles in degenerative discogenic syndrome

21a. Introduction

While a Spinal Research Fellow in the Department of Neuropathology in Perth, Western Australia, the author designed a research protocol to study the muscle fibers in the multifidus muscle of the lower lumbar spine. The evaluation was approved by the Ethical Committees and consented by the individual patients. Intraoperative biopsies of the left lumbar multifidus muscle (1 cm from the inferior border of the L4 and L5 laminae) from 15 healthy subjects who never suffered any lower lumbar spinal problem were compared to 15 low back pain patients with symptoms and signs related to the degenerative discogenic syndrome and diagnosed to originate at the L4-5-S1 levels but without clinical nor radiological signs of the herniating pathway (disc protrusion, extrusion or sequestration).

 

 

21b. Muscle biopsy preparation by the senior laboratory technologist

All muscle specimens were taken immediately after the start of the spinal surgical procedure. A senior laboratory technologist initially prepared the muscle samples in the operation theater and later in the laboratory for light microscopic and histochemical examinations as well as for electronmicroscopic ultrastructural morphological examination.

 

 

21c. Fifteen healthy and 15 chronic low back pain (CLBP) sufferers?

The 15 healthy individuals were unfortunate young males, victims of severe accidents urging acute lumbar spinal surgical reconstruction. Their average age was 20 years (ranging 20 to 40 years).

The 15 chronic low back pain sufferers never interrupted their professional activities (average age 55 years). They all had a long history of chronic undulating or recurrent low back pain (duration 9 to 35 years, ranging 14 years). None could remember a specific previous causative accident or injury. History, clinical examination and radiological investigations were typical for degenerative discogenic syndrome.

Note: the evolution of the degenerative processes in the aging intervertebral disc is the major explanatory reason in around 80 % of all LBP patients worldwide.

 

 

21d. Normal muscle fibers in healthy individuals (Fig. 7, 8, 9, 10, 11a, 11b, 12)

Except in one case, the histological and histochemical analysis of the muscle samples in the remaining 14 severely injured young male individuals were considered as normal without evidence of myopathy.

The HE stains were devoid of angulated cells. Cells with internal nuclei were not present and interstitial fibrosis was not seen.

The myofibrillar ATPase stain sections showed no evidence of a myogenic type of muscle affection. There were no physiological differences and no pathologic changes between the slow twitch type 1 fibers and the fast twitch type 2 fibers. There was no evidence of fiber hypertrophy, fiber size variation, fiber type grouping and group fiber atrophy.

 The internal structure of the muscle fibers was completely normal in all NADH-TR stains. Myofibrillar destruction defined as small angulated fibers, moth-eaten appearance, central core fibers was absent. Only one professional cricket player evidenced fiber type 1 predominance in the myosin ATPase stain at pH 9.4, the significance of which was not clear.

              Electron microscopic analysis only showed minor changes of unknown significance (Fig. 21d).

 

 

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Fig. 21d. Presence of lipid and lipofuscin in the muscle fibers. Mitochondrial aggregation. Some nuclei present a small amount of cytoplasm (B90/6091, M, 34 years).

(Declerck, Narula, Kakulas, NeuroMuscular Pathology, Perth, Western Australia)

21e. Large variety of pathologic changes in CLBP related to degenerative discogenic syndrome

At the time of their first spinal operation, sufferers of severe chronic low back pain in relation to the degenerative discogenic syndrome exhibited a large variety of pathologic changes. There were 6 women (age 39 to 76 – average 56) and 9 men (age 39 to 75 – average 53).

The histological and histochemical stains exhibited myopathic findings with type 1 fibre predominance (ATPase), fiber size variation, cells with internal nuclei and abnormal internal fiber structures such as moth-eaten appearance and central core fibres (Fig. 21e1, 21e2, 21e3).

 

 

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Fig. 21e1. H&E staining (left) and Gomori (right): some angulated fibers with minor fiber diameter variation, a few internal nuclei, some fibers reveal pale zones within them. Moth eaten appearance suggestive of mitochondrial clumping (X90/346, M, 73 yrs).

(Declerck, Narula, Kakulas, NeuroMuscular Pathology, Perth, Western Australia)

 

 

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Fig. 21e2. SDH reaction. Left: moderate amount of fiber diameter variation, angulated fibers, central cores and moth eaten fibers (X90/114, F, 39 years). Right: minor changes in fiber diameters with internal nuclei and abundance of central cores (X90/299, M, 55 years).

(Declerck, Narula, Kakulas, NeuroMuscular Pathology, Perth, Western Australia)

 

 

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Fig. 21e3. Oxidative SDH staining. Left: moth eaten fibers with central cores (X90/320, M, 75 years). Right: fiber diameter variation, group atrophy presence of cores (X90/267, F, 76 years).

(Declerck, Narula, Kakulas, NeuroMuscular Pathology, Perth, Western Australia)

 

                      Findings during electron microscopic evaluations very regularly display lipid (Fig. 21e4), lipofuscin granules, rod bodies and unstructured cores (Fig. 21e5), mitochondrial aggregations (Fig. 21e6), intramitochondrial lipid inclusions (Fig. 21e7), and nemaline rods (Fig. 21e8).

 

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FiG 21e4. Electron microscopic magnification x 7500 (X90/370, EM 90/55, 90/1917, F, 36 years). Droplets of lipid are present throughout many muscle fibers. (Declerck, Narula, Kakulas, NeuroMuscular Pathology, Perth, Western Australia)

 

 

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Fig. 21e5. Electron microscopic magnification x 8400 (X90/114, 90/70998, F, 36 years). Clear evidence of rod bodies formation (black) and presence of an unstructured core (yellow).

(Declerck, Narula, Kakulas, NeuroMuscular Pathology, Perth, Western Australia)

 

 

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Fig. 21e6. Electron microscopic magnification. Left: x 11200 (X90/321, EM90/50, 90/71180, M, 39 years). The subsarcolemmal spaces contain mitochondria (yellow circles). Very few of the mitochondria possess single dense granules (red circles). Right: x 22400 (X90/320, EM90/49, 90/71163, M, 75 years): mitochondrial aggregations in subsarcolemmal space.

(Declerck, Narula, Kakulas, NeuroMuscular Pathology, Perth, Western Australia)

 

 

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Fig. 21e7. Electron microscopic magnification x 57000 (X90/368, EM90/56, M, 40 years). Lipid droplets and crystalline inclusion bodies inside the mitochondrium.

(Declerck, Narula, Kakulas, NeuroMuscular Pathology, Perth, Western Australia)

 

 

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Fig. 21e8. Electron microscopic magnification x 75000 (X90/320, EM90/49, 90/1803, M, 75 years). A nemaline rod.

(Declerck, Narula, Kakulas, NeuroMuscular Pathology, Perth, Western Australia)

 

 

21f. Comparison with reported spinal muscle histochemistry in cases of ‘disc herniation’

Major group fiber atrophy and angulated fibers, suggestive signs of muscle denervation and described to be regularly present in muscle fiber samples of patients with herniating disc pathologies, were not at all common findings in those suffering chronic LBP due to degenerative discogenic syndrome.

 

 

21g. Conclusion

The deficits in the lumbar multifidus muscles not only are related to denervation but to the degenerative discogenic syndrome as well. The pathological myopathic changes represent the muscle inactivity, muscle weakness, and lack of muscle exercise in patients with chronic undulating or intermittent LBP.

From the literature it is known that the erector spinae muscles of patients with chronic low back pain display a more glycolytic (faster) profile in their muscle fibers which render them less resistant to fatigue.

 

 

22. Author’s conclusion and suggestion

Degenerative processes in the lumbar intervertebral discs are the main reason for causing chronic low back pain worldwide. Chronic LBP sufferers experience pain in an intermittent or in an undulating manner. The medical and paramedical world instructs these patients to proceed with a more physical active life. Active exercises are prescribed in an attempt to delay further evolution of the signs and symptoms of their degenerative discogenic syndrome (DDS).

 

But how can the pain be settled to implement exercises rapidly?

 

It is well known that exercising without pain will increase the size of atrophied muscle fibers to improve the endurance and the strength of the back muscles.

Peripheral nerves are composed of efferent motor axons as well as afferent sensory axons.

Therefore, functional electrical stimulation (FES) of muscles, which stimulates nerves indiscriminately, can cause considerable discomfort (Gernandt). Furthermore, FES is ineffective if axon integrity is compromised due to an injury or a surgical lesion.

In the future it may be possible to restore muscle function by optogenetic control. This means the combination of regenerative medicine (implantation of stem cells-derived motor neurons) with optical stimulation of muscle function (Bryson). However, this is like speculation on the bank!

Conventional medicine can offer nothing more than blocking the lower lumbar spinal muscle pain by therapies with an analgesic effect (medications and injections. It may provide an ideal pretreatment before intensive rehabilitation, trunk muscle strength exercises, and specific individualized therapeutic exercises can be initiated. However, it does not work! Exercising like a zombie is not terribly exiting!

Since a few years, the author prefers stimulating patients to block their pain with biophysical andullation vibrations. Andullation technology helps the patient to self-administer low frequency and stochastically modulated vibrations in combination of infrared light (Declerck; Lievens). Exercising following 15 to 30 minutes andullation, makes it much easier to perform the instructed exercises.

 

 

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