The Intervertebral Disc

STRUCTURE

In the lumbar spine the intervertebral discs are constructed similarly to those in other parts of the vertebral column. The disc has two distinct components: the annulus fibrosus forming the retaining wall for the nucleus pulposus.

The annulus fibrosus is constructed of concentric layers of collagen fibres. Each layer lies at an angle to its neighbour and the whole forms a laminated band which holds the two adjacent vertebrae together and retains the nuclear gel. The annulus is attached firmly to the vertebral end plates above and below, except posteriorly where the peripheral attachment of the annulus is not so firm. Moreover, the posterior longitudinal ligament with which the posterior annulus blends is a relatively weak structure, whereas anteriorly the annulus blends intimately with the powerful anterior longitudinal ligament. The posterior part of the annulus is the weakest part: the anterior and lateral portions are approximately twice as thick as the posterior portion, where the layers appear to be narrower and less numerous, the fibres in adjacent layers are oriented more nearly parallel to each other, and there is less binding substance. Due to its structure the annulus fibrosus permits some movement, though small, in all directions.

The annulus fibrosus

Fig. The annulus fibrosus.

The nucleus pulposus, the central part of the disc, is a transparent jelly, has a high water content, and behaves as a highly viscous fluid. Various authorities describe the nucleus as containing as much as eighty-eight percent water at birth, reducing to about seventy-five percent in the third decade and seventy percent in old age.

The size of the disc nucleus and its capacity to swell is greater in the lumbar region than in the cervical or thoracic spine. The capacity to swell when decompressed is evident in the variation in height of man occurring after a nights rest. This diurnal, nocturnal variation is caused by compression forces which reduce mans height during the day as water is squeezed from the disc into the vertebral bodies. The water returns from the vertebral body to the disc with degravitation overnight. Various other authorities have described fluid loss during compressive loading of the discs. Up to five percent of fluid loss is stated to occur during certain compressive movements. Reversal of this flow occurs when the compressive force is removed but Hickey and Hukins state that if movements are performed too rapidly, reversal will not be complete. It is possible then that repetition of a particular movement may cause a progressive loss of fluid resulting in reduced bulk.

The water content of the annulus fibrosus changes less dramatically from seventy-eight percent at birth to seventy percent in middle and old age, so that in ageing the nuclear fluid content reduces to that of the annulus. Perhaps, when the viscosity of nucleus and annulus reaches an equilibrium, internal derangement is less likely to occur. This could account for the decreased incidence of low back pain from age fifty onwards.

Of all the intervertebral discs the lumbar discs are by far the thickest and bear the greatest loading and stresses. Even when slightly degenerated they behave hydrostatically — that is, the pressure within the disc is equally distributed in all directions of the intervertebral compartment.

PRESSURE DISTRIBUTION WITHIN THE DISC

In the young disc the gel structure of the nucleus allows forces, placed on the disc, to be distributed isotropically — that is, evenly around the disc wall. With ageing the soluble content of the nucleus gradually changes into a collagen matrix and the viscosity of the nuclear gel decreases; forces on the disc are now unevenly distributed from nucleus to annulus, probably producing an irregular pattern of comparatively high pressure points at the inner disc wall. In the final stages of disc ageing the nuclear collagen and the inner annular collagen tend to coalesce and the separation between nucleus and annulus becomes ill-defined.

Consequently, where in early life the disc behaves as an ideal shock absorber, in old age the whole system of nucleus and annulus together becomes easily permeable to the fluid in which the collagen is dispersed and the disc tends to behave like a sponge. In middle age, however, the annulus is still separated from the nucleus but contains a matrix of precipitated material, which may distribute compression forces in an uneven manner and could facilitate rupture.

NUCLEAR MOVEMENT

The centre of the lumbar disc nucleus is usually found posterior to the geometric centre of the vertebral body. During movements of the spine a positional change of the nucleus pulposus takes place — for example, from full flexion to full extension there is a small but apparently significant anterior movement of the nucleus of the involved segment. The reverse occurs when the spine moves from extension to flexion. It is this nuclear movement which permits the performance of flexion and extension, and any other movement for that matter.

Many authors have described movements of the nucleus pulposus between the vertebral bodies accompanying alterations in the relative positions of the segments. Armstrong described movement of the nucleus from anterior to posterior occurring during the performance of flexion, and the reverse movement occurring during extension, though he did not have strong laboratory evidence to support his contention. Much later Shah et al demonstrated with discography that the opaque medium injected in the disc moves in a similar way during offset compression loading tests simulating flexion and extension.

The nucleus pulposus with the spine in neutral position

Fig. a – The nucleus pulposus with the spine in neutral position. b – The nucleus pulposus with the spine in extension. c – The nucleus pulposus with the spine in flexion.

Following laboratory experiments with silastic placed between the vertebral bodies Farfan21 concluded that evidence acquired this way suggests an ability of the nucleus to move away from the site where compressive forces are applied. The nucleus therefore can in addition to movement in the antero-postero plane move laterally and can inhabit an eccentric position between the vertebral bodies as shown by the discovery of eccentrically placed disc nucleus in the cadavers of people who were known to have had idiopathic scoliosis.

As a result of a continually flexed lifestyle I believe the nucleus may migrate to occupy a more posterior position between the vertebral bodies. (This would account for the approximation of the anterior vertebral margins said to occur in early disc disease.)

TANGENTIAL STRESS

In experiments on lumbar spinal sections of cadavers Shah et al demonstrated that anterior compression loading of the disc simulating flexion, causes a considerable increase in tangential stress at the posterior annulus, while the anterior annulus bulges. On posterior compression loading simulating extension, the tangential stress reduces posteriorly but increases anteriorly, while the annular bulge disappears anteriorly but appears posteriorly.

It seems that in these situations anterior bulging of the disc wall in flexion arid posterior bulging in extension is merely caused by the slack of the relaxed annulus. The bulge is under reduced tangential stress and the nucleus has moved away from the bulge. It is unlikely that nuclear material will be extruded under these circumstances.

Compression loading of the disc

Fig. a – Compression loading of the disc. b – Posterior compression loading of the disc. Tangential stress increased anteriorly — decreased posteriorly. Annulus relaxes posteriorly. c – Anterior compression loading of the disc. Tangential stress increased posteriorly — decreased anteriorly. Annulus relaxes anteriorly.

I have come to conclude that, with an intact annular wall, a bulge appearing in the posterior annulus on extension is normal. In extension the posterior annulus is not under tangential stress and, with the hydrostatic mechanism intact, the nucleus must move anteriorly. It is unlikely that annular tearing will occur under these circumstances.

A bulge appearing in the posterior wall on flexion when the annular wall is damaged may be a threat, as it indicates a weakening posterior annulus. This time the bulge is under increased tangential stress and the nucleus has moved posteriorly. Radial Assuring may occur and nuclear material may occupy this space thus further distending the annulus.

Development of disc protrusion

Fig. Development of disc protrusion: a – Radial fissure. b – Annular bulge. c – Nuclear protrusion.

DISC DAMAGE AND REPAIR

The evidence suggesting that in the lumbar spine the intervertebral disc is a common source of back pain is overwhelming. The most convincing signs are the gross kyphosis and scoliosis accompanying severe sciatica. Following laminectomy the patients deformity and sciatica are usually significantly improved. The inference that a disturbance within the disc is responsible for these signs is inescapable. And it is likely that patients who show similar signs but who do not have sciatica, have a similar though lesser disturbance within the disc.

The cause of damage to the disc is still uncertain but it seems unlikely that compression is a significant factor. Tension however is considered by various authorities to be a significant factor in the production of damaging stresses especially those affecting the posterior annulus. Brown and co-workers applied a small constant axial load and a repetitive forward bending motion of five degrees and the lumbar discs showed signs of failure after only 200 cycles of bending and completely failed after 1000 cycles. Hickey and Hukins found that bending is particularly damaging because it concentrates stress on a limited number of collagen fibres and if overstretching exceeds four percent irreversible damage occurs.

Markolf describes the spine as being twenty-five to thirty percent less stiff in the flexed position and it can be properly assumed that in this position it is less able to withstand stress.

From my own clinical observations I conclude that the lumbar disc is most commonly damaged in flexed positions especially where flexion is sustained. This usually gives rise to symmetrically distributed pain patterns. Should any torsion or asymetrical stress be applied in addition, the symptoms tend to appear asymetrically. This is manifest by the patients description clinically of the pain first appearing in the back near the mid line and moving laterally and peripherally with the subsequent imposition of torsion.

From the reviewed literature it would appear reasonable to assume that following sustained and repeated flexion stresses the nucleus is forced posteriorly. This coincides with a raising of the intradiscal pressure and increased tangential stress on the postero-lateral disc wall. This happens to be the weakest part of the annular wall, because in this area the annulus has the least radius, is thinner and is least firmly attached to the bone. Should the flexed position be maintained, stress will eventually fatigue the posterior annulus and overcome its inherent strength and should overstretching exceed four percent irreversible damage will result.

The raised intradiscal pressure against the now damaged annulus coupled with the posterior movement of nuclear fluids forces these fluids through the lattice of the weakened collagen and the fibres begin to part. The widening fissure permits nuclear gel to enter the tear accelerating damage and causing separation at the end plate. Should the process continue a significant posterior accumulation of nuclear gel occurs as more and more nucleus is forced down the fissure and eventually bulging occurs at the outer annulus.

Should the tearing be centrally situated the patient exhibits a kyphotic deformity and if the tear extends then posterolaterally the patient will exhibit a scoliotic deformity. When the annular wall is sufficiently weakened by Assuring, extrusion of nuclear material may occur. The disc has now lost its hydrostatic mechanism and on attempting extension the nucleus is unable to move anteriorly. The ability to extend is seriously impaired, for any approximation of the posterior vertebral rims results in increased pressure on the extrusion itself. This explains why patients with an accomplished protrusion often present with a flattened lumbar spine, and any attempt to extend the low back results in enhancement of low back pain and sciatica.

Farfan has stated that a disc protrusion commences with a tear in the annulus, starting off at the bony vertebral end plate. Tearing must extend to a certacn degree before fragmentation occurs, allowing the annulus to give way. This is nearly always associated with the development of a radial tear which permits the nucleus to force an increase in annular bulging or a widening of the fissure.

Once the disc is damaged by this type of derangement, the natural healing processes will be initiated. Through exposure at the vertebral end plate the vascular tissue of the vertebral body comes in contact with the avascular disc, invading it and removing all the tissue that does not have a blood supply. Scar tissue is now laid down in the inner annulus and nucleus.

Contraction of the invading scar results in the formation of an inelastic structure within the elastic disc. In this way dysfunction develops, causing a loss of mobility in the segment involved. When sufficient stress is applied to the lumbar spine, the scarred areas tend to fragment and tear and the cycle repeats itself.

If we are to prevent the development of dysfunction in the disc following derangement or protrusion, we must provide early movement in our treatment to ensure the formation of an extensible scar within the elastic structure of the disc.

THE DISC AND PAIN

Although the disc does not contain actual nerve endings, it may cause pain in various ways. Severe midline backache may be caused by direct mechanical irritation of the nerve endings in the posterior longitudinal ligament and fibroadipose tissue, binding the ligament to the annulus. Similarly, pain in or close to the midline of the back may be caused by pressure on the anterior dura mater or its sleeve-like extensions in the intervertebral foramen. These situations occur in central posterior and postero-lateral protrusions of the nucleus pulposus.

Regarding postero-lateral herniation of the nucleus pulposus of a lumbar intervertebral disc Wyke has stated:

“As such a protrusion develops it impinges initially on the sinuvertebral nerve, in which it not only interrupts mechano-receptor afferent activity but may also irritate the contained nociceptive afferent fibres and thereby give rise to pain in the lower back in the absence of sciatica. Should the protrusion develop further, it begins to impinge on the related dorsal nerve roots (and their containing dural sleeves), as a result of which the backache becomes more severe and more widely distributed, and to it are added sensory changes (paraesthesiae and numbness) and pain experienced in the distribution of the sciatic nerve”.

Posterior or postero-lateral herniation of the nucleus pulposus

Fig. Posterior or postero-lateral herniation of the nucleus pulposus.

Postero-lateral herniation of the nucleus pulposus with nerve root compression

Fig. Postero-lateral herniation of the nucleus pulposus with nerve root compression.

It can be clearly seen that as this type of lesion develops and worsens, initially the pain is felt in the midline of the back. It progressively increases in intensity and spreads across the back into the buttock and thigh, and as the climax is reached the pain appears in the lower limb. The further from the midline the pain is felt, the greater is the derangement.

Pain pattern of a developing lower lumbar disc lesion. When the centralisation phenomenon occurs a reversal of this pattern will be observed

Fig. Pain pattern of a developing lower lumbar disc lesion. When the centralisation phenomenon occurs a reversal of this pattern will be observed.

THE CENTRALISATION PHENOMENON

In 1959 I noticed in a retrospective observation of case histories that patients who responded rapidly to treatment experienced a centralisation of pain as improvement took place. I called this the ‘centralisation phenomenon’.

I would define this phenomenon as the situation in which pain arising from the spine and felt laterally from the midline or distally, is reduced and transferred to a more central or near midline position when certain movements are performed. It is permissable for pain to increase centrally provided there is a reduction in the lateral or distal pain.

Centralisation of symptoms only occurs in the derangement syndrome. The significance of the centralisation phenomenon is that in derangement the movement which causes centralisation will, if repeated, reduce the derangement. The phenomenon is not applicable to the dysfunction syndrome and, of course, will not occur in patients with postural problems.

I believe that the centralisation phenomenon is merely the reversal of the development of pain in progressive disc lesions which is described by various authors. As the sequence of symptoms from onset is perfectly logical, so is the reversal of symptoms during centralisation. When the protrusion reduces in size, it releases first the nerve root and then the dura mater, which results in a cessation of pain and paraesthesiae below the knee followed by a reduction in thigh pain. At this stage the pain should be fell mainly in the buttock or central lumbar area.

The typical pattern of pain produced by a developing lower lumbar disc lesion is generally acknowledged. However, it is not always recognised that centralisation as recovery takes place applies to derangement situations and is an indication that reduction of derangement is occurring. Pain of a radiating or referred nature will reduce distally and may simultaneously increase proximally, when the involved joints are moved in the correct direction — that is, reducing the derangement. Thus the pain appears to reverse the order in which it commenced.

The centralisation phenomenon can also be observed in unilateral or symmetrical pain felt solely in the spine. In this case the pain moves from across the low back to a central midline location, and on further reduction of the derangement pain is replaced by an aching or merely a stiffness in the center of the back.

The phenomenon occurs when appropriate movements are performed in the cervical and thoracic spine in the presence of derangement, and is just as reliable.

DIFFERENTIATION BETWEEN DISC DEGENERATION AND FRANK PROTRUSION

Part has made some observations by discography which have an important clinical implication. He slates:

“When there is difficulty in differentiating disc degeneration with annulus rupture from frank nuclear protrusion, flexion and extension films can be helpful. In disc degeneration, forward flexion opens the posterior disc widely, the annulus fibrosus and posterior longitudinal ligament become tightly stretched and the contrast medium tends to disperse uniformly. This is a helpful indication of the true state of affairs in those patients where the contrast appears localised in the neutral or extended positions. On the other hand, when frank nuclear prolapse is present, the opaque medium remains contained in a localised area irrespective of the position of the spine.”

The assessment of the effects of certain chosen movements — the test movements — on the pain will enable us to make a clinical diagnosis. In frank nuclear protrusion the hydrostatic mechanism of the disc is impaired, and the position of the nucleus cannot be influenced by movement and positioning. Clinically, the patient’s symptoms will not reduce as a result of the test movements, and such a patient is not likely to benefit from mechanical treatment utilising movements and position.

On the other hand, where the disc merely shows degeneration with annular Assuring and no protrusion exists, the hydrostatic mechanism is still intact and the position or shape of the nucleus can be influenced by movement and positioning. Clinically, there will be a change in intensity or site of the patient’s symptoms as a result of the test movements, and such a patient can be treated successfully with mechanical procedures utilising movement and positioning.

If disturbance of the normal intervertebral disc mechanism is a causative factor in low back pain it conveniently explains the behaviour of pain, movement and deformity found in patients with the derangement syndrome.

In the postural syndrome, by my definition, no pathology will be found.

In the dysfunction syndrome pathology affecting muscles, ligaments, disc, apophyseal joints and fascias may be found separately or together.