Of all mechanical low back problems that are encountered in general medical practise, mechanical derangement of the intervertebral disc is potentially the most disabling. It is my belief that in the lumbar spine, if in no other area, disturbance of the intervertebral disc mechanism is responsible for the production of symptoms in as many as ninety-five percent of our patients. Twenty-five years of clinical observation and treatment of lumbar conditions have convinced me that certain phenomena and the various movements which affect them, can occur only because of the hydrostatic properties invested in the intervertebral disc.
For thirty years Cyriax has attributed lumbar pain to internal derangement of the intervertebral disc mechanism. He has outlined the cause of lumbago, and proposed that pain of a slow onset is likely to be produced by a nuclear protrusion while that of a sudden onset is caused by a displaced annular fragment. Although at present we are unable to prove either of these hypotheses, I support his general view that the disc is the cause of much lumbar pain; but I cannot believe that slow and sudden onsets of pain can be so clearly separated and ascribed to different structures within the same disc.
Various authorities describe phenomena — observed clinically, at surgery, and in cadaveric experiments — that indicate aberrant behaviour of structures within the disc complex. Mathews reports that a small bulge of a lumbar disc may cause pain in the back and asymmetry of the involved intervertebral articulation, leading to scoliosis and asymmetrical limitation of movement of the lumbar spine. Nachemson describes bulging of the annulus under loading conditions, and increased bulging with movements of the spinal column.
Vemon-Roberts states that during surgical explorations of disc prolapses some protrusions were seen to alternately protrude into the spinal canal and retreat into the disc substance, depending on the type of movement the lumbar spine was subjected to. Moreover, according to Mathews myelograms were seen to be positive only when taken with patients in the painful position, a further indication of the relationship between disc bulge and increased pain on movements. Thus, it is evident that minor disc bulging may cause deformity and limitation of movement, and that certain movements of the spinal column increase the bulge while others may reduce it.
The ability of the nucleus to move anteriorly in extension, posteriorly in flexion and laterally in lateral flexion depends very much on the integrity of the annular wall, for it has been found that the position of the nuclear fluids can be affected by movement only as long as the hydrostatic mechanism is intact.
Park has shown that in frank nuclear protrusions the opaque medium, injected in the disc, remains contained in a localised area irrespective of the position of the spine. Once nuclear material has escaped through the annular wall, the hydrostatic mechanism is no longer intact and internal derangement of the disc cannot be reduced significantly by movements of the spinal column. On the other hand, movements of the spinal column can be utilised to reverse internal derangement of the disc as long as the integrity of the disc wall is maintained.
In conclusion, we have now ample evidence that movements of the spinal column effect the position of the nucleus within the disc under certain circumstances; and there is enough proof to incriminate the disc as the cause of the deformities so often encountered in patients with low back pain, particularly in the acute stages. It cannot be disputed that certain movements and positions lead to the development of these deformities; and, likewise, that other movements and positions can be utilised to reduce these deformities. Many doctors are still under the impression that the pain of ‘lumbago’ necessarily has an inflammatory component. If this were true, reduction of derangement would never provide immediate and lasting relief from pain as often occurs.
It must be well understood that pain resulting from inflammation has a chemical origin, and will only be present as long as there is enough chemical irritation of the free nerve endings. Inflammatory pain cannot possibly on one movement appear in the buttock, and on another movement disappear from the buttock and appear in the midline of the back. Pain that changes site with movement must result from mechanical deformation — that is, before movement took place different structures or different parts of the same structure were subjected to mechanical deformation than during or after movement. The actual cause of the mechanical deformation — the structure producing it — has changed its position or shape during the movement.
I would define derangement as the situation in which the normal resting position of the articular surfaces of two adjacent vertebrae is disturbed as a result of a change in the position of the fluid nucleus between these surfaces. The alteration in the position of the nucleus may also disturb annular material. This change within the joint will affect the ability of the joint surfaces to move in their normal relative pathways and departures from these pathways are frequently seen. In some patients movements may only be reduced but in others they will be lost entirely. Usually, the movement involved is either flexion or extension and often a loss of side gliding can be seen in conjunction. In addition to causing losses of movement in the lumbar segments, derangement of the disc can cause the deformities of kyphosis and scoliosis.
Acute lumbar kyphosis
The stresses most likely to cause an acute lumbar kyphosis are sustained flexion stresses such as those applied during gardening and in sitting. Prolonged maintenance of flexed positions and frequent repetition of movements in flexion, especially when extension is never fully recovered, may both lead to excessive accumulation of the fluid nucleus in the posterior compartment between the vertebral bodies. Once this accumulation is great enough it may become a blockage and prevent the erect position from being obtained. Any attempt by the patient to straighten up quickly leads to significant pain, as the compressive forces create bulging of the posterior longitudinal ligament and annulus which are now under extreme tangential stress. The patient must return to the flexed position in order to reduce the intensity of the pain. We now have an acute lumbar kyphosis. The patient is not held in this position by muscle spasm.
In acute lumbar kyphosis the incidence of sciatica is relatively low. The postero-central disc bulging which causes the kyphosis, must move laterally before it can reach the nerve root. Once it has moved laterally the patient will develop a scoliosis. Consequently, most patients with sciatica have some degree of lateral shift or scoliosis.
Acute lumbar scoliosis
It appears reasonable to suggest that the posterior longitudinal ligament may prevent postero-central disturbances in the disc wall. However, sooner or later asymmetrical stresses will force the fluid nucleus laterally where the outer annulus will distend at its weakest point. There is greater elasticity and decreased resistance to distention at the posterior surface of the disc, especially where the larger radius curve meets the smaller one. Here the annulus is narrowest and less firmly attached to the bone, and is not reinforced by the posterior longitudinal ligament. Therefore, bulging of the annulus is more likely to occur at this point than anywhere else.
To recapitulate, a patient with lumbago may obtain the deformity of kyphosis by a posterior movement of the nucleus. Should this symmetrical posterior accumulation become asymmetrical and move to a more postero-lateral position within the intervertebral compartment, the patient is likely to develop sciatica and will acquire the deformity of scoliosis. Thus, a patient with lumbar kyphosis and low back pain merely has to move to one side or other to run the risk of changing his deformity to a scoliosis. For example, a side bending or torsion movement to the left will cause the nucleus to move to the right; with sufficient accumulation of nuclear material on the right side the patient will have difficulting in obtaining the erect posture and will develop a lateral shift to the left.
I have recorded the progression from acute kyphosis to acute scoliosis many times clinically. During the development of my treatment methods I discovered that it is possible to induce a scoliosis in a patient presenting with an acute kyphosis and then to reduce it, provided the appropriate procedure is applied in time.
Patients with low back pain caused by derangement are commonly between twenty and fifty-five years of age. From that time on the incidence of the derangement syndrome reduces gradually as degenerative processes develop and progress. Men appear to be affected by derangement more often than women.
Low back pain is notorious for its recurrent nature. It is suggested that ninety percent of people with low back pain will have recurrent problems. estimate that sixty-two of every hundred patients will become recurrent. The majority of patients with recurrent problems occur in the derangement syndrome. Derangement of the lumbar intervertebral disc may arise from a single severe strain, a less severe strain applied more frequently, or a sustained flexion strain.
The latter is most common and occurs in people who have a sedentary occupation or work in stooped positions. Sustained flexion positions force the nucleus to the extreme within its cavity and, as a result of time, posterior accumulation of nuclear material beyond the normal limit may prevent the attainment of movements and positions opposite to the sustained flexed position. The length of time that a particular position has been held often determines the degree of derangement.
When movements are constantly varied in direction the fluid nucleus never occupies a fixed position for any length of time and continuously alters its silhouette. Provided movements do not cause excessive strain and are not repeated too regularly, accumulation of nuclear material will not occur. Likewise, the simple action of flexion — that is, bending forwards once without placing great strains on the lumbar spine and without having been in sustained flexion prior to bending — is unlikely to cause an episode of low back pain. Many patients blame the simple forward bending movement for the onset of their pain, but on close questioning there has usually been a position or an activity involving prolonged flexion preceding the onset of pain. Let me further illustrate this.
A lady states that her low back pain came on as she merely stooped to pick up a button. However, further questioning reveals that she had been in sustained flexion — sitting in front of her sewing machine — for some time immediately prior to bending down.
Similarly, the man who removed his golf clubs from the rear compartment of his car did not develop pain because he suddenly flexed. He had been driving his car and sat in flexion for some time before he got out of the car and bent over to pick up his golf clubs. It is unlikely that he straightened up fully after leaving the car, and the additional flexion to lift his golf clubs from the car surely raised the intradiscal pressure in a joint that was already under considerable stress. These are typical examples of derangement with a rapid onset.
Now an example of derangement with a slow onset. A patient worked in the garden at the beginning of spring. It was some time since he had any exercise. He spent the entire afternoon digging and noticed that a mild ache developed in his low back. As the day wore on he had some difficulty in rising from the stooped position. After he stopped working he had a hot bath and felt a little easier, sat down for his evening meal, read the newspaper and watched television for a while. He had great difficulty rising from his chair and never really obtained the upright position before he went to bed. He had a very disturbed night, and could only lie curled up on his right side. When he awoke the next morning he could hardly get up from his bed and had difficulty walking. By this time he felt severe low back pain and was tilted to one side as well as forwards.
Variations on similar themes are described every day and on most occasions flexion stress is the basic cause of derangement. When pure flexion strains are described the pain tends to be central or bilateral with symmetrical distribution. But if an asymmetrical movement involving flexion and rotation or side bending is the causative factor, the site of pain tends to become unilateral.
It is interesting to note that in the majority of patients presenting with derangement, the time of onset is before midday. Due to the nocturnal imbibition of the disc the volume of intradiscal fluid is increased which allows for greater nuclear excursion and distortion whenever stresses are placed on the disc. I believe that during the first five to six hours after rising in the morning the risks of incurring derangement are greatest.
One of the most important questions when taking the history of patients with low back pain is that regarding the intermittency or constancy of the pain. Mechanical deformation resulting from postural stresses or dysfunction always causes intermittent pain. Mechanical deformation due to derangement, by its very nature and definition, nearly always causes constant pain. In derangement the adjacent joint surfaces are disturbed from their normal position so that some of the structures within and around the involved joint are under constant stress. These will be a source of constant pain until the stress is removed either by reduction of the derangement or by adaptive lengthening. Thus, whenever a patient describes constant pain and the pain is constant indeed, — that is, there is no time in the day when pain is not present — he is almost certain to have a derangement. Of course, this influences very much the treatment he will receive and the direction in which movement procedures must be applied.
While the presence of constant pain strongly suggests derangement, not all patients with derangement have constant pain. There is a group of patients who state that they have no pain at all as long as they are on the move, but once they maintain a position, pain will be felt after a few minutes. Movement and a change of position brings about a short-lived respite from pain, which is soon felt again and necessitates a further change of position. The temporary relief is caused by a reduction of stress on the structures presently causing pain, but at the same time other structures are placed under stress and rapidly become painful.
There are also patients in whom, during the course of the day and depending on their activities, minor derangements are alternatively produced and reduced spontaneously. In these patients the intermittent pain is caused by intermittent derangements which are self-reducing.
In the derangement syndrome the pain will be made worse under certain circumstances. Usually these circumstances involve positions rather than movements. The majority of patients will experience an increase of pain in flexed positions, and when a scoliosis or lateral shift is present extension will cause an increase in pain as well as flexion.
Sitting is the most common aggravating factor for all low back pain syndromes. Rising from sitting increases pain in derangement syndrome only. When patients describe a history in which both walking and sitting enhance pain, they are likely to exhibit a lateral shift. In the presence of a lateral shift any attempt to extend the lumbar spine will cause or increase pain, and walking produces enough extension to enhance pain.
In general, if the derangement is small patients feel better when on the move and worse when at rest. However, if the derangement is large and causes significant deformity patients usually feel better when lying down.
Patients with derangement often have difficulty in finding a comfortable sleeping position. They cannot lie supine with the legs out straight because the available range of extension is inadequate. Prone lying is prevented for the same reason. The only position in which some comfort can be derived is by lying supine with the knees flexed or on the side with the knees bent up, both positions placing the lumbar spine in flexion. Following either of these, patients have considerable difficulty arising in the morning. In sub-acute patients extension remains blocked for up to an hour and is only gradually regained if at all. In acute patients the pain is so severe that they prefer to return to bed, where they resume the flexed position which relieves their pain for the present time but perpetuates their problem.
In North America, where the flexion therapy philosophy is strongest, patients with acute low back pain are advised to rest in flexed positions, and extraordinary measures are taken to ensure the maintenance of flexion while in bed. However, on questioning patients with derangement they almost universally complain that, after sleeping in such a position, they have difficulty on rising from lying and their pain is markedly increased when coming to the erect position. Pain experienced first thing in the morning when getting up is frequently the result of the overnight posture of the patient. If the spine is held in such a position during the night that the nucleus accumulates posteriorly, it is extremely difficult and painful to reduce this derangement rapidly. Sometimes several hours must pass before reduction can be achieved. The same mechanism causes the increase of pain felt when the patient with posterior derangement rises from sitting to standing.
On examination, the patient with derangement often exhibits a deformity. Commonly seen deformities are the flattened lumbar spine or lumbar kyphosis, and the lateral shift or lumbar scoliosis. There is always loss of movement and function, and in contrast to dysfunction the movement loss is nearly always asymmetrical. In addition, there may be a departure from the normal pathway of movement. In derangement this departure may be a deviation to the right or left of the sagittal plane. I believe this pathway is determined by the position of the disturbance in the nucleus/annulus complex. Should the nucleus be displaced abnormally to the right of the midline, the deviation will occur to the left.
Fig. Deformity of kyphosis. Deformity of scoliosis. Deviation in flexion.
Cyriax already disposed of the misconception that spasm of the extensor muscles in the back is responsible for the production of an acute lumbar kyphosis. I join him in this view and would like to add than an acute lumbar scoliosis is not caused by muscle spasm, neither is a departure from the normal pathway of movement. The position of the nucleus within the disc predetermines the alignment of the joint surfaces between two adjacent vertebral bodies, and therefore dictates the pathway to be followed during movement and the position to be maintained during rest.
The test movements
The test movements are performed to determine the nature of the presenting syndrome — that is, dysfunction or derangement — and the severity of the condition. In derangement there is rarely, if ever, any difficulty in producing or increasing the symptoms, and often centralisation can be observed as well. Centralisation of symptoms occurs only in the derangement syndrome.
The test movements are designed to reveal the presence of derangement. They alternately increase and decrease the disturbance by changing the position of the nucleus within the intervertebral disc and altering the stresses on the surrounding annulus and posterior longitudinal ligament. When the history suggests that a potentially disabling situation is present, it is not desirable to develop the flexion testing procedures to the bitter end. In these cases flexion in standing is often too painful to be repeated, and each successive movement may increase or peripheralise the pain. Sometimes repeated flexion in lying has the same effect. In derangement, the increase or peripheralisation of pain with each repeated movement indicates a rapidly increasing derangement. When this occurs we should not insist on completing the recommended number of test movements.
When the test movements affect pain it is important to state clearly whether pain is produced or increased. The former indicates that there was no pain before the test movements were performed and the test movements actually produced pain. The latter means that pain, present before the performance of test movements, has increased as a result of them. It is imperative that we establish the existing pain state before commencing the test movements in order to be able to assess the effects of these test movements on pain.
If a patient with derangement describes changes in the pain pattern following the test movements, there should also be observable changes in range of movement and deformity. In other words, a patient who describes a significant increase in pain should exhibit an increase in the mechanical blockage of movement and deformity — that is, a reduction of movement range and an increase of deformity; and the patient who describes a reduction in pain must simultaneously exhibit an increase in range of movement and a reduction of deformity.
In derangement the repetition of the test movements can have a rapid effect on the condition and the patient may improve or worsen in a matter of minutes depending on the direction in which the movements are performed. When the test movements are repeated in the direction which increases the accumulation of nuclear material, pain will increase with each successive movement and after the treatment the patient may remain significantly worse as a result of increased derangement. The opposite applies when the test movements are repeated in the direction which reduces the derangement. In this case the patient improves with each successive movement and remains improved subsequently. In general, rapid and lasting changes in the condition as a result of the test movements are an indication of derangement.
If the annular wall is breached, we cannot influence the position of the nucleus with normal movements of the spine. This situation appears clinically in the patient with sciatica who has constant pain and cannot find relief by either positioning or movement. Most of the test movements can be seen to enhance his leg pain and no test movement will reduce it. Thus, the performance of the test movements clarifies the severity of the derangement situation.
Let us now look at the example of a typical patient with derangement. He states that he has constant pain, but is better on the move than in any of the positions. Walking and lying prone also improve the symptoms. The test movements clearly show increase and peripheralisation of pain on the flexion movements, and centralisation of symptoms occurs during extension. This patient will benefit from the extension principle, and hopefully his constant pain will become intermittent with the regular use of extension procedures. A few more examples will demonstrate the importance of centralisation of symptoms during test movements and treatment of the patient with derangement.
A patient complains of pain extending evenly across the low back to about ten centimeters on either side of the midline. This pain has been present for some months and is usually worse when working in flexed positions or sitting for a while. The test movements reveal that on repeated flexion the pain spreads further across the low back, and on repeated extension the pain increases but moves towards the midline. Further extension movements cause a reduction in intensity of that pain. Extension clearly is the movement that reduces the derangement and should be used in the treatment. If extension is continued and performed regularly over the next twenty-four hours, the pain should become less and less and should be under control within that time period.
A young woman complains of pain across the low back and aching into both buttocks and thighs. She states that the pain increases in the back during prolonged standing — extension — and moves into buttocks and thighs during walking — increased extension. — However, on sitting down — flexion — the pain leaves the legs and is felt only in the back, and after ten minutes of sitting — sustained flexion — it has subsided completely. Again the centralisation phenomenon shows us that in this case extension movements are increasing the derangement and therefore should be avoided. On the other hand, flexion is reducing the derangement and is the correct principle of treatment for this patient.
Patients with sciatica, especially those who also exhibit a deformity of scoliosis and have constant pain, will have a limitation of straight-leg-raising on the side of the sciatica. Furthermore, straight-leg-raising will be limited in patients who are in the acute stage of a severe derangement condition. In these patients all movements aggravate the symptoms, and often relief is obtained only when lying in bed and keeping as still as possible.
Let us examine the relevance of straight-leg-raising, performed as an objective testing procedure. When a limitation of straight-leg-raising is found, there is always a restriction of flexion in standing as well. It is virtually impossible to have a limitation of straight-leg-raising and be able to flex pelvis and lumbar spine in a normal fashion. Some patients appear to have full flexion in standing, but on close observation they can be seen to deviate in flexion and to move in an arc to one side or other rather than in the sagittal plane. In patients with sciatica and root entrapment, deviation occurs always to the side of referred pain as this is the side where nerve root impingement takes place. The patients are unable to control the deviation in flexion themselves.
There is nothing that can be elicited by straight-leg-raising tests, that is not evident in careful observation of flexion in standing. When there is increased tension of the nerve root the straight-leg-raising limitation appears to occur much sooner than does the restriction of flexion in standing. This is because the straight-leg-raising test is performed in supine lying, and in this position deviation of the spine is difficult. There only appears to be a better range of flexion in standing, because deviation of the spine allows more flexion towards the side of root tension. If the deviation is prevented from occurring by holding the patient in the sagittal plane, an immediate reduction in the flexion range becomes apparent. This reduction in the range of flexion will now coincide with the degree of straight-leg-raising.
Another test may help to understand the mechanism involved in restriction of straight-leg-raising. When performing straight-leg-raising, do not stop the movement immediately when sciatica is produced or increased. Instead, continue to raise the leg firmly but slowly, and at the same time observe the pelvis. At first it can be seen to rotate to the opposite side, then it tilts backwards while the lumbar spine flattens and commences to flex. This is merely an inverted version of the deviation of flexion in standing.
Straight-leg-raising is an extremely unreliable test and as an objective tool only of use in determining the progress of patients with entrapment.