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Low Back Pain. Contraindications

Although it has been accepted throughout that all patients have received adequate medical screening, occasionally patients with serious pathology or mechanical disorders unsuited to mechanical treatment are encountered during routine examination. If in the examination no position or movement can be found which reduces the presenting pain, the patient is unsuited for mechanical therapy, at least at this time.

The existence of serious pathology should be considered when the history states that there has been no apparent reason for the onset of symptoms; that the symptoms have been present for many weeks or months, and have during that time increased in intensity; and that they are constant; and the patient feels that he is gradually getting worse. On examination the pain remains exactly the same, irrespective of positions assumed or movements performed. Usually there is little loss of function if any, and postural deformity is not often seen. In addition to the examination finding, the patient often looks unwell and may complain of feeling unwell. Mechanical procedures described in this book should never be applied to patients presenting with signs and symptoms of this nature.

Saddle anaesthesia and bladder weakness are indications of compression of the fourth sacral nerve root. These symptoms occur in major disc herniation and, when present, form a definite contra-indication to manipulative procedures.

Patients who exhibit signs of extreme pain — that is, who become transfixed on movement, and freeze and immobilise the spine when palpation is attempted — are considered unsuitable for mechanical therapy, at least at this stage.

Developmental or acquired anomalies of bone structures which may lead to weakness or instability of mechanical articulations are hazards to manipulative procedures. Architectural faults should be excluded from mechanical therapy. Exceptions are minor grades of spondylolisthesis where symptoms are mild and intermittent. The presence of spondylolisthesis at a certain segment is not necessarily an indication that symptoms are forthcoming from that segment. It is seen very often indeed that pain is the result of disc derangement at a different level.

A simple clinical test may determine whether spondylolisthesis is responsible for the presenting pain, as it will often reduce or abolish pain in the presence of that condition. Place one hand across the sacrum of the standing patient and the other firmly against the abdomen. By further compressing the abdominal content while at the same time increasing pressure on the sacrum, pain in standing arising from spondylolisthesis is markedly reduced or abolished. On the other hand, pain arising from derangement of any of the lumbar discs will usually be enhanced by this procedure, and postural or dysfunctional pain remains unaffected. Thus, if pain is increased with this test the patient should be treated as for the derangement syndrome, but if pain is reduced the presence of spondylolisthesis must be investigated and the necessary precautions must be taken in the treatment.

Bed rest

Patients with mechanical low back pain are often advised to rest as much as possible, preferably in bed. In many instances this is inappropriate if not bad advice. The nutrition of the intervertebral discs depends entirely on osmosis, and movements of the spine are essential for the flow of fluids containing nutriments. To rest the joints of patients with mechanical low back pain often only adds to the problems of restoration of function and full rehabilitation. The only patient who should be placed on bed rest is the very acute patient with severe constant low back pain with or without sciatica whose symptoms are considerably worse during weight bearing, and in whom no movement or position can be found to reduce or centralise the pain.

In order to prevent the development of dysfunction within or about the involved intervertebral joint following derangement, regular assessment of the patient on bed rest is required and treatment must be instituted as early as possible. This is particularly important in the patient who responds very well to bed rest, because without movement this patient will become painfree but may develop a significant loss of function.


If, following reduction of derangement, all efforts at prevention of immediate recurrence are unsuccessful, it may be desirable to supply the patient with a corset for short term support and stability. Long term use of a corset is undesirable as it merely hastens the development of dysfunction.


The question of surgical intervention inevitably arises in the minds of doctors, therapists and patients alike when progress is slow or non-existent. The decision as to whether one should or should not operate must always concern the orthopaedic surgeon.

It is my experience that, in New Zealand, surgery will be performed only when conservative treatment methods have failed. This does not always include adequate mechanical therapy, but usually it has allowed adequate passage of time. Fortunately, few patients in New Zealand receive surgery for low back pain only, and the procedures of laminectomy and discectomy are reserved for patients suffering significant nerve root compression.

The difficulties surrounding the diagnostic criteria for surgical intervention are enormous. One study showed a large number of positive myelograms in lumbar spines of patients who were asymptomatic and had been admitted and X-Rayed for conditions other than low back pain.5 Thus the value of the myelogram, the good old standby relied upon by many doctors, has become somewhat suspect.

The results of surgery can also be seen to vary significantly. Randomly selected patients with low back pain, referred pain to one leg, and positive myelograms coupled with clinical signs, were divided into two groups. The patients in the one group received surgery, those in the other group not. It was found that at the end of one year ninety percent of the non-operated patients were better; that the operated patients were only better in the first two months following surgery; and that at the end of one year the results in the group that had received surgery were the same as in the group that had not been operated upon.

The final result of a disc lesion is not endangered by a three months’ waiting period before surgery is undertaken. However, a longer wait may be prejudicial as it may leave the patient with residual disability.

Fielding states that Nachemson, Rothman and Hirsch have all found that there is a clear correlation between the early return of symptoms following surgery and the formation of scar tissue. Quoting Fielding:

“Early return of symptoms usually means the formation of scarring which cannot be cured by surgery and means that the results will be poor’’.

Rothman examined sixty-eight patients who had undergone two or more unsuccessful spinal surgical interventions. He reports that seventy-five percent of the patients claimed partial or total disability. Half of the failures in multiple surgery are due to scarring or nerve root adherence. Scarring and fibrosis are associated with a high failure rate and dismal results.

It is appropriate to make clear that scarring causes dysfunction, described earlier in this book. Scarring does not necessarily have to cause problems provided it is discovered early enough and dealt with adequately in the manner suggested in previous chapters. I believe that one procedure is mandatory following surgery for lumbar disc protrusion: that is, the regular performance of one full straight-leg-raising movement at two hourly intervals. This should reduce significantly the complications of fibrosis and nerve root adherence. Just as recent scars can be stretched and lengthened by dysfunction treatment procedures, so should the prevention of inextensible scar formation be feasible by the even earlier use of the same procedures.

Recovering From Acute Low Back Pain. General Instructions

You have recovered from the acute episode because of your ability to master the exercises which relieved your pain. These exercises must be repeated whenever situations arise which have previously caused pain. You must perform the corrective movements before the onset of pain. This is essential.

If you carry out the following instruction, you can resume your normal activities without the fear of recurrence.


  • When sitting for prolonged periods the maintenance of the lordosis is essential. It does not matter if you maintain this with your own muscles or with the help of a supportive roll, placed in the small of your back.
  • In addition to sitting correctly with a lumbar support, you should interrupt prolonged sitting at regular intervals. On extended car journeys you should get out of the car every hour or two, stand upright, bend backwards five or six times, and walk around for a few minutes.


  • When engaged in activities which require prolonged forward bending or stooping — for example, gardening, vacuuming, concreting — you must stand upright, restore the lordosis and bend backwards five or six times before pain commences.
  • Frequent interruption of prolonged bending by reversing the curve in the low back should enable you to continue with most activities you enjoy, even with some you do not enjoy.


  • If the load to be lifted weighs over thirty pounds, the strain must be taken with the low back in lordosis and you must lift by straightening your legs.
  • If the object weighs under thirty pounds less care is required, unless you have been in a bent or sitting position for some time prior to lifting. In the latter case you must lift as if the weight exceeds thirty pounds.
  • In addition to correct lifting technique, you must stand upright and bend backwards five or six times after lifting.


  • At the first signs of recurrence of low back pain you should immediately start the exercises which previously led to recovery, and follow the instructions given for when in acute pain.
  • If this episode of low back pain seems to be different than on previous occasions, and if your pain persists despite following the instructions, you should contact a manipulative therapist.


  • If you lose the lordosis for any length of time, you are risking recurrence of low back pain.

Acute Low Back Pain. General Instructions

You must retain the lordosis at all times (lordosis is the hollow in the lower back). Bending forwards as in touching the toes will only stretch and weaken the supporting structures of the back and lead to further injury. Losing the lordosis when sitting will also cause further strain.


  • When in acute pain you should sit as little as possible, and then only for short periods only.
  • At all times you must sit with a lordosis. Therefore you must place a supportive roll in the small of the back, especially when sitting in a car or lounge chair.
  • If you have the choice you must sit on a firm, high chair with a straight back such as a kitchen chair. You should avoid sitting on a low, soft couch with a deep seat; this will force you to sit with hips lower than knees, and you will round the back and lose the lordosis.
  • The legs must never be kept straight out in front as in sitting in bed, in the bath or on the floor; in this position you are forced to lose the lordosis.
  • When rising from sitting you must retain the lordosis; move to the front of the seat, stand up by straightening the legs, and avoid bending forwards at the waist.
  • Poor sitting postures are certain to keep you in pain or make you worse.


  • When in acute pain you should drive the car as little as possible. It is better to be a passenger than to drive yourself.
  • When driving, your seat must be close enough to the steering wheel to allow you to maintain the lordosis. If in this position your hips are lower than your knees you may be able to raise yourself by sitting on a pillow.


  • When in acute pain you should avoid activities which require bending forwards or stooping, as you will be forced to lose the lordosis.
  • You may be able to retain the lordosis by kneeling — for example, when making the bed, vacuuming, cleaning the floor, or weeding the garden.


  • When in acute pain you should avoid lifting altogether.
    If this is not possible you should at least not lift objects that are awkward or heavier than about thirty pounds.
    You must always use the correct lifting technique: during lifting the back must remain upright and never stoop or bend forwards; stand close to the load, have a firm footing and wide stance; bend the knees and keep the back straight; have a secure grip on the load; lift by straightening the knees; take a steady lift and do not jerk; shift your feet to turn and do not twist your back.


  • A good firm support is usually desirable when lying. If your bed is sagging, slats or plywood supports between mattress and base will firm it. You can also place the mattress on the floor, a simple but temporary solution.
  • You may be more comfortable at night when you use a supportive roll. A rolled up towel, wound around your waist and tied down in front, is usually satisfactory.
  • When rising from lying you must retain the lordosis; turn on one side, draw both knees up and drop the feet over the edge of the bed; sit up by pushing yourself up with the hands and avoid bending forwards at the waist.


  • When in acute pain you must try to stand up, bend backwards and increase the lordosis while you cough and sneeze.


  • At all times you must retain the lordosis; if you slouch you will have discomfort and pain.
  • Good posture is the key to spinal comfort.

Back pain Prevention

The majority of patients responding to basic extension and flexion principles of treatment have been educated in the means of achieving pain relief and restoring function. They have carried out the self-treatment procedures and have to a large extent become independent of therapists. Following successful treatment it requires little emphasis to convince patients that if they were able to reduce and abolish pain already present, it should also be possible to prevent the onset of any significant future low back pain.

Of all the factors predisposing to low back pain only postural stresses can be easily influenced and fully controlled. We must develop this potential ingredient of prophylaxis to the full. The patient must understand that the risks of incurring low back pain are particularly great when the lumbar spine is held in sustained flexed positions; and that when the lordosis is reduced or eliminated for prolonged periods, he must at regular intervals and before the onset of pain make a conscious effort to interrupt flexion, restore the lordosis and accentuate it momentarily to the maximum. It is essential that the patient knows the reasons for doing this, and therefore we must explain to him in lay terms that on restoring the lordosis the intradiscal pressure decreases, the nuclear fluid moves anteriorly and the posterior stresses in and around the disc are reduced.

Briefly summarised, the following prophylactic measures should always be taken:

  • Prolonged sitting requires (a) maintenance of the lordosis by muscular control of the posture or, preferably, by insertion of a lumbar roll, (b) hourly interruption of sitting by standing up, walking around for a few minutes and accentuating the lordosis by a few repetitions of extension in standing (Proc. 6).
  • Activities involving prolonged stooping require (a) interruption of stooping at regular intervals by standing upright, (b) regularly reversing the curvature of the lumbar spine, restoring and accentuating the lordosis by a few repetitions of extension in standing (Proc. 6).
  • Lifting requires (a) the use of the correct lifting technique. Generally, if the object to be lifted exceeds fifteen kilograms, the strain must be taken with the lumbar spine in lordosis and the lift must be performed using the legs. If the object to be lifted weighs under fifteen kilograms less care is necessary, unless one has been in a bent or sitting position for some time prior to the lift. In the latter case the same rules apply as for lifting weights exceeding fifteen kilograms, (b) accentuation of the lordosis before and after lifting by a few repetitions of extension in standing (Proc. 6).
  • If inadvertently pain has developed during sitting, stooping or lifting, the patient should immediately commence extension in lying (Proc. 3).
  • Extension in standing (Proc. 6), very effective in preventing the onset of pain, is less effective when used to reduce present pain. Extension in lying (Proc. 3) is the technique of first aid for back pain.
  • Recurrence: At the first sign of recurrence the patient should immediately commence the procedures which previously led to recovery. Although an episode of low back pain can commence suddenly and without warning, many patients are aware of a minor degree of discomfort before the onset of severe pain. If this type of warning is given, the patient has an excellent chance to prevent the development of symptoms, provided the appropriate procedure is applied immediately.

It is not possible for patients to remember all verbal instructions and advice given during the first treatment. To avoid tedious repetition and to ensure the necessary information is conveyed to the patient, a list of instructions is supplied on the first visit. This list firstly deals with information for patients in the acute stage of low back pain, and secondly provides information required once recovery has taken place. These instructions form an important part of self-treatment, because when followed properly they will help in reduction of present symptoms and prevention of their recurrence.

The Derangements and Their Treatment


  • Central or symmetrical pain across L4/5.
  • Rarely buttock or thigh pain
  • No deformity

In Derangement One the disturbance within the disc is at a comparatively embryonic stage. Due to minor posterior migration of the nucleus and its invasion of a small radial fissure in the inner annulus, there is a minimal disturbance of disc material. This causes mechanical deformation of structures posteriorly within and about the disc, resulting in central or symmetrical low back pain. The accumulation of disc material also leads to a minor blockage in the affected joint preventing full extension, but the blockage is not enough to force the deformity of kyphosis upon the joint.

In patients with Derangement One the history, symptoms and signs are usually typical of the syndrome, and the test movements confirm the diagnosis of derangement. Because the disturbance within the joint is relatively small it responds well to the patients’ own movements, and the majority of patients are able to reduce the derangement themselves by applying self-mobilising procedures. It is vitally important that all patients realise and experience the extent to which their own efforts of self-treatment contribute to the reduction of Derangement One. Therefore, it is undesirable to use therapist-technique in the first twenty-four hours of treatment.


Reduction of derangement

The patient with Derangement One will require the application of the extension principle. He should start lying prone (Proc. 1) for about five minutes, followed by lying prone in extension (Proc. 2) for another five minutes. He must then lie relaxed for a short while before commencing extension in lying (Proc. 3). This exercise, a modified press-up, should be done in groups of ten, and during the treatment session the groups are to be repeated five or six times with a rest period of about two minutes in between. During this time the patient should be questioned repeatedly to ensure that reduction of the derangement is taking place. At the completion of thirty or forty press-ups the range of extension should have improved significantly and the pain, if previously felt across the low back, should be localised more centrally. If before exercising the pain was already felt centrally, it should now be reduced in intensity. When reduction is almost complete patients often state that the original pain is gone but a strain pain or stiffness is felt instead. This can be achieved even during the first treatment session. No other procedure should be used if extension in lying (Proc. 3) culminates in centralisation or decrease in intensity of the presenting pain. If this occurs we can assume that there is a reduction in the magnitude of the derangement, and steps should now be taken to ensure that the reduction is maintained.

Maintenance of reduction

In order to maintain reduction of posterior derangement it is essential that the lordosis is maintained at all times. The patient should be instructed that at no time should he allow the lumbar spine to become flattened or convex. We must point out that if he is painfree in the prone lying position with the lumbar spine in extension, there is no reason why pain should arise in other positions such as sitting and standing or during movements and walking, provided that the same degree of extension is retained. If, with the lumbar spine in lordosis, the angle at which the affected joint is held prevents mechanical deformation, no pain will occur providing that angle is maintained.

Successful reduction of derangement will be shortlived if the patient subsequently sits without a lordosis. Sitting is usually the most troublesome position for patients with Derangement One. Bad sitting positions may cause and will definitely prolong symptoms of derangement. However, by maintaining the joints in the position of near maximum lordosis while sitting, the patient ensures that the fluid nucleus is held anteriorly. Of all the sitting positions the intradiscal pressure is at its lowest when sitting with a lordosis. Mechanical deformation will be minimal and the pain level will be greatly reduced in this position.

At this stage the patient should be shown how to maintain the lordosis in sitting. The slouch-overcorrect procedure should not be introduced as yet as it allows the patient to lose his lordosis. This procedure can be added once reduction of the derangement proves stable and the patient is ready for flexion procedures. In the early stages of treatment of Derangment One the patient is instructed to maintain the lordosis with his own muscular effort or with the use of a lumbar support. All patients with this type of derangement are advised to sit with a lumbar support, especially when driving the car or sitting in an easy chair.

Besides maintaining the lordosis the patient must be instructed to repeat the exercises every waking hour for the next twenty-four hours. Hourly repetition of the passively performed extension in lying (Proc. 3) ensures that no significant accumulation of nuclear material recurs in the posterior compartment of the joint. One group of ten repetitions of extension in lying (Proc. 3) is sufficient and it requires less than one minute to complete this. If circumstances prevent the performance of extension in lying (Proc. 3) it must be replaced by extension in standing (Proc. 6).

If following successful reduction, pain returns or increases to its former level at some time later in the day, it is likely that the patient has permitted some flexion to occur and has consequently lost the lordosis. He must take immediate steps to recover it, and usually one group of ten repetitions of extension in lying (Proc. 3) is sufficient but sometimes more may be required. Again, if circumstances prevent the performance of extension in lying (Proc. 3), extension in standing (Proc. 6) must be substituted.

Following reduction of posterior derangement patients should be very careful when rising from the lying and sitting position to standing. Normally, the spine is momentarily flexed when standing up and this must now be prevented. Patients must be shown how to lordose when rising from lying and sitting, because without help they will not easily master this. Again, we must emphasise that even a momentary loss of lordosis may cause recurrence of the derangement.

If patients are uncomfortable while lying in bed, it may be advisable to sleep with a lumbar supportive roll around the waist. This helps to maintain the lordosis when lying supine, and prevents the spine from sagging when lying on the side. On awaking the next morning the patient may feel stiff and painful, but after about an hour he will loosen up and find himself much improved compared with the previous day.

The second treatment should be given twenty-four hours after the first session. Only after this time may we confirm that we have made the correct diagnosis and have chosen the correct principle of treatment. If on returning the patient reports improvement, there is usually a definite change in the symptoms — that is, the pain has centralised or decreased in intensity; or its frequency is reduced; or both. Examination of the range of extension reveals improvement and the patient is better indeed. Our diagnosis is confirmed and we should continue with extension principle procedures. It is a basic rule of treatment, applicable to all syndromes, that technique presently resulting in improvement should not be added to, modified or replaced in any way until all improvement ceases. Thus, the same procedures can be continued safely over a number of days, provided the symptoms continue to improve. When the patient no longer has constant pain he may discontinue lying prone and lying prone in extension (Proc. 1 and 2). His intermittent pain is now most likely caused by loss of the lordosis, especially in slouched sitting, and we must emphasise the importance of the correct sitting posture once more. At this stage the introduction of the slouch overcorrect procedure is desirable in order that the patient may fully appreciate that slouched sitting will produce low back pain whereas correct sitting abolishes it. As further improvement becomes apparent, extension in lying (Proe. 3) may be reduced to two or three times per day — preferably morning, noon and evening, and may be replaced during the day by extension in standing (Proc. 6) whenever it is felt necessary.

We must warn the patient that after having started the treatment programme he is likely to experience ‘new pains’. These may be felt higher in the back, between the shoulder blades, and possibly in the arms. They are different from the original pain for which treatment was sought, and are the result of adjustment by the body to new positions and movements. New pains should be expected and will wear off in a few days to a week, provided the exercises are continued.

All patients should be instructed that, if they have severe pain which worsens or peripheralises at the time of exercising, they should stop the exercises and ask further advice. We must make sure it is well understood that, to be guilty of aggravation of symptoms, the exercises must actually increase the pain at the time of performance and not two hours afterwards. Pain felt immediately after exercising can be a result of the exercise. Pain appearing two hours afterwards is commonly fell because of the position occupied at that time — for example, sitting slouched while watching television.

I have outlined this far the routine that should apply in most Derangement One patients and which should result in the rapid and uneventful resolution of the symptoms. However symptoms and signs do not always respond as we would wish. Where reduction of posterior derangement proves difficult it becomes necessary to apply progressively increasing stresses in order to achieve reduction, and there is a certain order in which these progressions should be made.

Let us assume that the patient already described as an example does not continue to improve, that after the first twenty-four hours improvement ceases. Either the self applied reduction stresses are not adequate to fully reduce the derangement or our diagnosis may be incorrect or the patient may have inadvertently or unwittingly caused recurrence of the derangement. Re-examination is necessary to exclude incorrect diagnosis and re-instruction necessary to ensure the patient understands the self treatment procedures especially those regarding posture, and reduction. Having excluded other possible causes for non-improvement we must conclude that therapist technique should be applied before self treatment procedures will again become effective. Under normal circumstances repeated extension will result in a progressive reduction of pain and or centralisation will occur, but in this instance such a result is not forthcoming. Pain is not continuing to reduce and is still present at the maximum point of extension in lying (Proc. 3). Whenever difficulty arises in obtaining reduction of Derangement One the following progressions should be applied.

The first progression should be the application of extension mobilisation combined at intervals with rotation mobilisation in extension (Proc. 7 and 9) so that eight to ten of each is applied in succession to each segment indicated. As well as the affected segment, the segment above and below should be mobilised. This should immediately be followed by extension in lying (Proc. 3) which now will be increasing in range with concommitant reduction of or centralisation of pain. The effects of mobilisation will be apparent following twenty-four hours and if improvement has resulted the progression should be repeated.

The second progression should be applied only if the first progression has failed to reduce derangement. Again apply the technique of extension mobilisation (Proc. 7). After ten pressures to each of the appropriate segments maintain a continuous pressure at the level affected and ask the patient to perform about ten extension in lying movements (Proc. 3) against the pressure of your hands. Ensure your pressure is moderate but sufficient to prevent the pelvis moving from the treatment table. This increased stress surprisingly, (in derangement) permits freer painless movement rather than more difficult painful movement. This progression will frequently but not always remove the last obstruction to full extension. It may be necessary to apply these sequences on two or three successive days. Should reduction still be elusive a further progression may be required.

The third progression is the extension thrust manipulation (Proc. 8) and should only be applied if the preceding progressions have failed. Prior to manipulation, extension mobilisation (Proc. 7) and rotation mobilisation in extension (Proc. 9) should be applied in order to relax the patient and to provide the therapist with the necessary pre-manipulative information. Remember that repeating the mobilisation should be centralising or reducing pain as the derangement reduces. Providing this is occuring the manipulation can be administered. Should peripheralisation or increasing pain appear then the manipulation is inappropriate. This information can only be acquired by pre-testing. If the manipulation is successful it is usually evident immediately, and further treatment at this session is inadvisable. The patient should proceed with the self treatment programme as instructed on the first visit.

Following each progression the patient should continue through the following twenty-four hours with all advice and exercises initially prescribed. It should be emphasised again here that the progressions should only be initiated when all improvement utilising the patients own movements and abilities have been exhausted. Do not touch the patient unless you are certain that reduction cannot be achieved by any other means.

It can safely be assumed that reduction of Derangement One has been accomplished when full maximum extension in lying is painless even though the patient may describe and be aware of a ‘strain pain’ in this position. It is my experience that patients are well able to differentiate the ‘strain pain’ from the pain that caused consultation. It is necessary always to ask them to make the differentiation, for when asked, ‘in maximum extension do you have pain?’, the answer in invariably ‘yes’ indicating to the unwary that the derangement is not reduced. However if you further ask ‘is it pain, or strain’ the answer is usually ‘strain’. A very subjective line of questioning I know, but very important for I have seen therapists abandon the extension principle of treatment merely because the patient described a pain at the extreme of extension, that occurs commonly as end range strain in any normal joint.

Reduction of the derangement can be assumed when extension is painless. The patient may still describe a pain that appears when he sits and also a pain that appears when he flexes the lumbar spine past a certain point. This description can also be misleading and creates the impression that the derangement is still present. Posterior derangement cannot exist when extension is full and free and painless. The pain the patient is now describing appears in sitting and in flexion because the collagen laid down in the healing structures is now under stress as the posterior vertebral margins are separated by the action of slouching or flexing. These are not the pains of derangement, although derangement could perhaps develop if the positions are maintained for too long. These pains are the pains that arise from dysfunction and are now the sole cause of the remaining symptoms. If left untreated they can remain for years and cause end range pain whenever the patient moves to the extreme of flexion.

It appears that the first collagen fibres appear at about the fifth day after tissue damage occurs and these are the first foundations of scar tissue. Without movement this collagen will be laid down in a haphazard and disorderly fashion and as this disorderly structured tissue contracts with time an inelastic scar forms within the elastic annulus.

It is important that we recognise the signs that indicate when it is appropriate to commence the procedures that when applied enhance the quality of the developing collagen. By applying the appropriate stress, we can influence the direction in which the newly formed collagen fibres will lie so enhancing the strength and quality of the new tissue. At the same time we ensure that the scar that forms is an extensible scar and will not interfere with the adjacent still healthy annular structures. Function must always be restored following posterior derangement.

Recovery of full function

When commencing with flexion procedures initially only flexion in lying (Proc. 13) should be considered. Because of its additional gravitational stress flexion in standing (Proc. 14) should not be applied yet. To ensure that flexion in lying (Proc. 13) may be started safely reassessment of the test movement of flexion in lying is essential. The first time flexion in lying is performed it may cause pain as already some adaptive shortening has taken place in the posterior joint structures due to the maintenance of lordosis. Flexion becoming more painful on repetition indicates that it is too early to perform stretching in flexion; if continued, derangement is likely to recur or shortened structures may be damaged as a result of premature stretching. But flexion becoming less painful on repetition indicates that adaptively shortened structures are gradually being lengthened without further damage; flexion procedures may now be started.

In order to recover flexion the patient must commence with flexion in lying (Proc. 13). Because of the risks involved when performing flexion exercises following recent derangement, he should initially be careful and the following precautions must be taken:

  • When starting flexion in lying (Proc. 13) the patient should reduce the number of exercises performed at each session, as well as the frequency of the sessions per day — for example, five or six repetitions of the exercise should be done five or six times per day. Once the condition proves stable, he may gradually work towards a full programme of ten repetitions performed each hour or hour and a half.
  • Flexion in lying (Proc. 13) must always be followed by extension in lying (Proc. 3) to ensure that after exercising, the fluid nucleus is restored to the optimal position within the disc, thus removing the risk of recurrence. If due to circumstances the performance of extension in lying (Proc. 3) is impossible, extension in standing (Proc. 6) must be performed instead. Flexion in lying (Proc. 13) should not be done during the first few hours of the day. In this time period the risk of incurring derangement is increased due to an increase in the volume of nuclear fluid as a result of reabsorption and imbibition properties of the disc. This has previously been discussed.

When no further flexion can be gained with flexion in lying (Proc. 13) the patient should progress to flexion in standing (Proc. 14). The same precautions must be taken as for flexion in lying (Proc. 13). Thus, flexion in standing (Proc. 14) should be started on a reduced scale, should always be followed by extension in lying (Proc. 3) or extension in standing (Proc. 6) as a second choice, and should never be performed first thing in the morning. Once full flexion is recovered flexion in standing (Proc. 14) can be discontinued.

Recovery of flexion is considered to be complete when on performance of flexion in lying or standing full range of movement is achieved without pain, though a strain may be felt.

Prevention of Recurrence

Once recovery of function is achieved, the patient is advised to continue for at least six weeks, possibly longer, with extension in lying (Proc. 8:3) twice per day — early in the morning and late at night — flexion in lying (Proc. 13) once per day — late at night; extension in standing (Proc. 6) whenever necessary during the day; and the slouch-correct exercise whenever becoming negligent regarding the correct sitting posture.

Very few patients require to reduce or discontinue activities following derangement of the lumbar spine. We must explain to the patient that he may resume all the activities he is used to and enjoys doing — for example, sports activities, gardening, concreting, activities involving lifting — provided he follows the advice and instructions given to prevent recurrence of derangement.

I believe that failure to prevent recurrence is often the result of our failure to restore full function following derangement or trauma; our failure to ensure the patient has adequate knowledge and full understanding of the prophylactic measures; and, not less often, the patient’s failure to adhere to the prophylactic measures and to apply self-treatment procedures when these are called for.


Day one:

  • Assessment and conclusion/diagnosis.
  • Explanation of cause of derangement and treatment approach.
  • Reduction of derangement: commence with lying prone, lying prone in extension, extension in lying.
  • Instruct to maintain lordosis at all times, must sit with lordosis and insert lumbar support. May benefit from supportive roll in bed.
  • Repeat extension procedures each hour to maintain reduction and prevent recurrence.
  • If extension in lying is not possible, it must be replaced by extension in standing.
  • On recurrence of symptoms watch maintenance of lordosis even more, and immediately perform extension in lying.
  • Demonstrate the use of lumbar supports in sitting and lying.

Day two:

  • Confirm diagnosis.
  • Check sitting posture and exercises.
  • If improving then change nothing other than reducing extension in lying to once every two hours; replace extension in lying with extension in standing when necessary.
  • If no improvement at all then check vhat exercises are performed far enough into extension, often enough during the day, and that the lordosis is well kept.
  • Add extension mobilisation, possibly rotation mobilisation in extension.
  • Warn for ‘new pains’.

Day three:

  • Check sitting posture and exercises.
  • If improving, continue with procedures as directed.
  • Once constant pain has changed to intermittent pain, stop lying prone and lying prone in extension; start the slouch-over correct exercise.
  • If no improvement, concentrate on mobilisation techniques and add extension manipulation.

Day four:

  • Check exercises and progress.
  • If progress is satisfactory, reduce treatment to three times per week.
  • Continue with same programme until painfree for three days at least.
  • If progress is unsatisfactory, repeat mobilisation and manipulation techniques.

Day five and seven:

  • Check exercises and progress.
  • Once painfree for three days reduce extension in lying to three times per day and replace it by extension in standing whenever necessary during the day.
  • Commencing flexion in lying; take all necessary precautions.
  • Flexion in lying must be followed by extension in lying.

Further treatments:

  • 1 prefer to see patients with derangement every day until the reduction is stable and patients are in control. This may take up to five days. Then the treatment may be reduced to alternate days.
  • Once reduction of derangement proves stable and the patient has been painfree for at least three days, flexion exercises may be started to recover function.
  • All flexion exercises must be followed by extension in lying; if this is not possible extension in standing must be performed.
  • When no further flexion can be gained with flexion in lying, the patient must start flexion in standing.
  • When function is recovered flexion in standing may cease.
  • The patient is advised to continue with the exercises for another six weeks to prevent recurrence: he will do extension in lying in the morning; flexion in lying followed by extension in lying in the evening; extension in standing whenever necessary during the day; and possibly the slouch-overcorrect exercise, whenever becoming negligent regarding sitting.
  • Before discharge prophylaxis and self-treatment must be discussed in detail. We must emphasise that self-treatment is infinitely preferable to dependence on therapy.


  • Central or symmetrical pain across L4/5.
  • With or without buttock and/or thigh pain.
  • With deformity of lumbar kyphosis.

This acute disturbance within the disc is a progression of Derangement One and, if handled incorrectly, can easily be converted into an acute lateral shift with predominence of unilateral pain (Derangement Four). Any applied torsion will cause this derangement to increase laterally and must therefore be avoided. Derangement Two gives us the clearest clinical picture, reflecting the phenomena occurring within the disc during derangement. There is excessive posterior accumulation of the nucleus with a major blockage of extension accompanying the deformity of acute lumbar kyphosis. Not only is extension prohibited, the vertebrae are also forced apart and their posterior margins cannot approximate. Any attempt to do so results in severe pain, the patient being forced to return to the flexed position where he finds some temporary relief.

Fig. Treatment of Derangement Two from start to finish. Commence reduction by allowing the patient to lie in slight flexion.  Two pillows support the spine.  Now one pillow supports lumbar flexion. With no support the lordosis is beginning to appear.

Fig. The spine moves towards more extension. As the couch is raised…

Fig. …extension increases until the… lordosis is fully restored.

Fig. After resting flat for a minute or two, the patient should… then apply the extension…

Fig. …movements himself…

Fig. … and remember that the lumbar… spine must sag into full relaxation in order to obtain the maximum effect.


The management of the patient with Derangement Two must be meticulous in the first treatment session. Due to the blockage of extension the patient is normally unable to lie prone, and this is a major obstacle to reduction. The self-treatment procedures of the derangement syndrome can only be commenced when the patient can comfortably lie prone.

In order to effectively treat the kyphotic derangement we must gradually reduce the kyphosis until the prone position is attained. Only then will the patient be able to start the procedures recommended in the treatment of Derangement One. Place the patient prone, ensuring the lumbar spine remains in flexion by placing pillows under the abdomen. The pillows are then gradually withdrawn, one at a time at five minute intervals or as tolerated, until the patient reaches the prone position. To facilitate a slow and gradual reduction it is wise to use several small pillows rather than one or two big ones. An adjustable treatment couch is extremely valuable and much preferred to the use of pillows. Time, the important factor so often overlooked, is essential in the reduction of Derangement Two. To reduce the deformity of kyphosis up to 45 minutes must be allowed for the fluid nucleus to alter its silhouette and its position within the disc. If reduction pressures are applied gradually, allowing intervals between each progression towards extension, a slow but observable recovery of movement will occur. Too rapid increases in the extension range will cause severe pain and may provoke immediate regression.

Once the patient is able to lie horizontally without severe pain and providing the centralisation phenomenon is occuring an attempt should be made to develop the treatment along the lines recommended for Derangement One. Should the level of pain produced by extension in lying (Proc. 3) be still so severe as to prevent its use we must utilise sustained extension procedures. (Proc. 5) The progressions should be small and gradual, the patients shoulders being lifted perhaps four to five centimetres at a time.

On first raising the couch the patient will experience an increase in symptoms and providing these are consistent with the criteria applying to centralisation it is safe to proceed. After a few minutes in the higher position the pain should start to reduce in the thigh or buttock, and although it may increase centrally near the lumbar four five area this should not last for more than a minute or so. Once the pain has subsided to its former level, then and only then can progression to the next higher level be made. Should the centralised pain fail to subside, return the patient for a few minutes to the horizontal position and allow him to recover from the stresses, which can be rather trying. Once recovered, repeat the extension progressions (Proc. 5) which second time around are normally much easier to tolerate. Each progressive increase in extension will initiate the cycle of pain increase, followed by centralisation of pain, followed by a gradual reduction in the central or near central intensity.

It may be necessary from time to time during the course of the reduction to allow the patient a few minutes in the prone relaxed position to permit recovery from the stress of the sustained position. Following the recovery period it will now be possible to raise the patient rapidly to the former maximum extended position from which he has just rested. The impediment to obtaining extension is beginning to diminish.

Following the recovery of extension by this method (Proc. 5) we have reversed Derangement Two to One. The deformity and the pain referred to the buttocks and thigh should no longer be present. Treatment can proceed either immediately or on the following day as for Derangement One.

Pain and deformity of acute lumbar kyphosis can be significantly reduced in the first treatment session. If complete reduction is not possible, at least reduction to Derangement One is usually achieved. It is of vital importance to instruct the patient in the steps required to reduce the derangement himself in case of recurrence. If after returning home lying prone is too painful, the patient must repeat the sequence of lying over pillows and then gradually lowering himself until the prone position is obtained. This can be done on the floor over cushions or in bed over pillows. If reduction of derangement is maintained, the patient will usually be able to commence the extension principle procedures as for Derangement One the next day.

It may take up to twenty-four hours, occassionally longer, to reduce Derangement Two to Derangement One. Once this is accomplished treatment should progress on a daily basis exactly as described for Derangement One, and the recovery time will be the same as for patients with Derangement One.


  • Unilateral or asymmetrical pain across L4/5.
  • With or without buttock and/or thigh pain.
  • No deformity.

In Derangement Three the disturbance within the disc is located more postero-laterally rather than the postero-central position of Derangement One. This may be a progression of Derangement One, but it can also be the primary site of derangement.


Initially the treatment should be the same as for Derangement One. The first twenty-four hours of treatment will determine whether the procedures for reduction of Derangement One can successfully be applied to Derangement Three. Very often the application of the extension principle for Derangement Three reduces the disturbance to Derangement One within twenty-four hours. If on the second visit the patient is improving and the unilateral pain is reducing or centralising, or has moved evenly across the back, self-reduction is progressing and the extension principle as laid out for Derangement One must be continued.

On the second visit, should the patient show no improvement, reexamination and or re-instruction may be necessary; or, as was the case in the reduction of Derangement One the pressures may be inadequate. Should the applied reductive pressures prove inadequate it will again be necessary to progressively increase these and additionally alter the direction in which they may have to be applied.

The first progression in Derangement Three should be precisely the same as that applied as the first progression in the treatment of Derangement One. This progression should be given on the second day.

The second progression should be applied if the patient returns on the third day and is unimproved. With the patient in the prone position a lateral shift is formed by the therapist laterally gliding the patients pelvis away from the painful side. (This in effect creates a lateral shift towards the painful side.) With the pelvis in this off centre position the patient should be asked to perform a sequence of extension in lying (Proc. 3). There is often an initial centralisation of pain as the extensions are commenced. Should the pain subsequently move laterally or peripherally it may be necessary for the therapist to maintain the off centre position passively as the extensions are performed.

Once the repetition of extension results in reduction of pain, or pain felt consistently in the mid line, the therapist can release the passive maintenance of the shifted pelvis. Providing the pains are now reduced or remaining centrally, treatment can progress as for the reduction of Derangement One. It is important to teach the patient how to place the pelvis laterally on his own, for he may have to make this lateral correction at home, in order for extension in lying to be effective.

(An early indication that this progression may be necessary is often obtained during the course of examination of the test movements. Where lateral gliding in standing increases or decreases the patients symptoms or where these movements cause the initiation of centralisation it can be assumed that progression two in Derangement Three is likely to succeed.)

The patient should apply the second progression during the performance of the self treatment procedure of extension in lying (Proc. 3) whenever he does these during the next twenty-four hours.

The third, fourth and fifth progressions should be applied if on the fourth day there is still no improvement.

The third progression sustained rotation, (Proc. 11) should be applied and its effects recorded. The patients legs should be moved towards the painful side as the first rotation is applied. (My records indicate that pressure applied in this direction is most consistently followed by rapid improvement. The centralisation phenomenon is the ultimate guide however.) The position should be held for up to two minutes depending on the patients tolerance and centralisation.

The fourth progression should be rotation manipulation in extension (Proc. 10).

The fifth progression should be rotation manipulation in flexion (Proc. 12). Centralisation or reduction of pain must always be our guide regarding the side to which the technique should be performed or pressure applied. It is my experience that manipulation has a rapid effect and if there is no change in the symptoms after two manipulations in one direction, performed on successive days, the technique should be applied in the opposite direction provided centralisation and reduction of pain occur.

Once full centralisation is achieved Derangement Three is reversed to Derangement One. The treatment should now be continued and progressed exactly as for Derangement One.


  • Unilateral or asymmetrical pain across L4/5.
  • With or without buttock and/or thigh pain.
  • With deformity of lumbar scoliosis.

In 1956 I was fortunate enough to observe an acute lumbar scoliosis in a patient friend, who had more than the average faith in my ability as well as an intense fear of remaining deformed for life. The lateral shift with which he presented was more generous than usually seen, and the poor fellow was in great trouble indeed. At that time I did not know of any treatment method which would restore him rapidly to normal, and there did not appear to be any such reference in the literature either. My friend’s desire to become painfree, his intense fear of remaining deformed for life coupled with my own curiosity regarding the mechanism causing the scoliosis led me to an abortive attempt to rectify the problem and correct the lateral shift. Needless to say, my friend was no better as a result but he was no worse either. He had to retire to his bed for ten days, and four weeks later he was painfree.

I tell this story for a specific reason. The fact that my friend left me neither better nor worse was of little concern to me at the time. However, the fact that his right sided pain had become left sided and the tilt of his trunk to the left had changed to the right, caused great consternation. I wondered what possible pathology could behave in this manner. In the only book available at that time to assist in the treatment of spinal disorders, Cyriax provided the clue that the intervertebral disc is the most likely structure to be responsible for the lateral shift phenomenon.

From then on, bearing the disc in mind, I closely observed every lateral shift that presented and attempted to reduce the derangement. For two years I was unsuccessful, regularly bringing patients to the upright position only to hopelessly watch them fall back into scoliosis. It was not until the significance of facet apposition in extension occurred to me, that I applied the extension principle following lateral shift correction to ensure maintenance of the erect posture.

In the past ten years I have had ample opportunity to treat patients in many parts of the world. On such occasions I am always provided with lateral shift patients who failed to respond to other treatment methods. Apart from the patients whose lateral shift had been present for too long, most responded rapidly and well to my correction techniques. In general, no more than four days are required to reduce the deformity of scoliosis. The procedure of lateral shift correction has now been adopted by doctors and therapists in many parts of the world.

Derangement Four

Many theories have been put forward to explain the symptoms and peculiar behaviour of the derangement presented. These theories involve either disc, facet joint, ligaments and muscles, or combinations of any of these structures. Because in its most extreme form the lateral shift co-exists with a prolapsed intervertebral disc exhibiting an accomplished protrusion, we can assume that the disc is heavily involved in the production of this deformity. It is my opinion that Derangement Four is a lateral progression of the posterior disc disturbance of Derangement Two, and a simple progression of Derangement Three.

There is evidence that the incidence of deformity of scoliosis is higher in men than in women. My own statistics show that of all the patients presenting with a lateral shift in a certain time period seventy percent were male and thirty percent female. The results of a similar study reports a proportion of ninety percent male to only ten percent female patients.

Although the literature reports an even distribution of back pain among the sexes, I would dispute this, in patients with the derangement syndrome. Does the rather more accentuated lordosis of the female have anything to do with a lower incidence of lumbar scoliosis?

The majority of patients are seen to develop a lateral shift away from the painful side. My statistics show that ninety percent behave in this fashion, whereas the remaining ten percent deviate towards the painful side. In the latter group reduction is much more difficult to achieve and recovery may take up to three times longer than in patients of the first group.

A small number of patients exhibit an alternating scoliosis. I believe that when a minor disc bulge exists close to the midline very little movement can under certain circumstances cause the bulging to move to the opposite side, again occupying a postero-lateral position. As the disc bulge changes position the lateral shift deformity resulting from the bulge will also change sides. The patient under examination can sometimes create the alternating deformity at will, once he has observed its nature and the mechanism effecting it.

The incidence of a relevant lateral shift in patients with low back pain is very high. My statistics show that fifty-two percent of patients with low back pain have a relevant lateral shift that is, alteration of the lateral shift causes a change in intensity or site of pain or both.

The significance of derangement with deformity of scoliosis is much greater than is generally recognised. In the presence of a lateral shift either flexion or extension in the lumbar spine may be impaired, and sometimes both are affected. Lateral flexion to one side is similarly reduced. The loss of movement is always visible, sometimes markedly so. Furthermore, patients with even a minor lumbar scoliosis who are extended by exercises, mobilisation or manipulation, will become significantly worse with enhancement and peripheralisation of pain. The application of an extension thrust manipulation to a patient with a barely discemable lateral shift may precipitate a disc prolapse. Many patients with an undetected minor lateral shift have entered a clinic for treatment of their back pain only to walk out with sciatica. Again, I must emphasise that it is necessary to test all patients with low back pain for evidence of a relevant lateral shift.

I believe that, to a large extent, the disrepute surrounding the application of extension exercises has developed because of failure to detect minor lumbar scolioses and determine their relevance to symptoms. Indeed, many extension procedures are not successful due to lack of understanding of the nature of the condition to be treated. Usually extension fails because:

  1. not enough time is allowed for reversal of nuclear fluids to take place;
  2. it is done actively instead of passively;
  3. a lateral shift is present;
  4. or it is applied in the presence of extension dysfunction which results in the production of pain and the abandonment of the exercise.

Fig. Treatment of Derangement Four from start to finish. a – Examination of standing posture — primary lateral shift. b – Examination of movement — flexion in standing.  c – Examination of movement — extension in standing.

Fig. d – Examination of movement — deviation in flexion.

Fig. Correction of primary lateral shift.

Fig. Teaching of self-correction of primary lateral shift.

Fig. Selfcorrection of primary lateral shift.

Fig. Recovery of extension. Overcorrection of primary lateral shift — lying prone. Assisting maximum extension.

Fig. Recovery of extension. Overcorrection of primary lateral shift in maximum extension.


The acute lumbar scoliosis is a fascinating condition to treat. In general, the derangement is easily corrected when treated in the early stages, but becomes more difficult to reduce as time passes. After twelve weeks reduction becomes virtually impossible and if at this time marked deformity is still present it is usually permanent unless the affected disc is surgically removed. Even then a minor residual lateral shift often remains visible.

The techniques 1 developed in the late 1950’s for the correction of lumbar scoliosis and first described in 1972 are still the most effective in the treatment of patients with Derangement Four. Despite many efforts to improve the basic procedure this has not been altered in any significant way. I have made some minor changes in the method of achieving correction and these have been included in the discussion of the procedure (Proc. 16).

In a patient with Derangement Four the lateral shift must be corrected first (Proc. 16). Once correction or, if possible, slight overcorrection is achieved the extension loss must be restored (Proc. 3) and the lordosis maintained to prevent recurrence. Facet apposition makes lateral deviation impossible.

Therefore, if the lordosis is maintained neither the lateral shift nor the pain will reappear.

It is of vital importance that the patient is shown on the very first visit how to maintain the lordosis and how to perform self-correction of his lateral shift (Proc. 17) in case of recurrence.

If the lateral shift has been corrected, but after a few days full centralisation is not yet achieved, the application of unilateral techniques may be indicated as outlined before (Derangement Three).

Once the lateral shift has been corrected and full centralisation is achieved as well Derangement Four is reversed to Derangement One. From now on the treatment must be continued and progressed exactly as described for Derangement One.

Effects of lateral shift correction on the disc

Farfan has considered at length the possible effects on the vertebral structures that may result from spinal manipulation. He states that roto-scoliosis — or lateral shift — is caused by rotation usually occurring at the fourth and fifth lumbar vertebrae. He believes that the McKenzie technique of lateral shift correction is effective because firstly it opens the intervertebral space laterally in association with a slight flexion movement which is then followed by an extension movement in the lumbar spine. This produces reduction of the disc disturbance in a manner similar to squeezing a melon seed.

In my experience correction of many hundreds of lateral shifts has only on a few occasions caused a ‘pop’-like effect. When perceivable the correction appears to be a slow flowing process rather than the effects one would associate with squeezing the melon seed. Whatever the true mechanics eventually prove to be, correction of lumbar scoliosis usually leads to a rapid reduction of deformity and symptoms with a corresponding restoration of function. Straight-leg-raising, if reduced before correction, is frequently dramatically restored to normal. I believe that the side bending deformity occurring with lumbar scoliosis is responsible for the reduction in straight-leg-raising on the painful side when the lateral shift is away from the painful side. In this case the elongation caused by the side bending deformity towards the painfree side will reduce the available root length range in straight-leg-raising. Thus, it is not necessarily a bulge in the annulus which limits straight-leg-raising. If the nucleus is disturbed enough to lead to the deformity of lumbar scoliosis without causing the outer annulus to bulge, the deformity by itself will be responsible for the nerve root tension.

Farfan has stated that the procedure of straight-leg-raising does not necessarily have to stretch the sciatic nerve. There is enough evidence to suggest that reduced straight-leg-raising can be caused by a tight nerve root due to the rotation deformity as in sciatic or, as he prefers to call it, roto-scoliosis. This would partially explain why straight-leg-raising can quickly and simply be increased and reduced merely by laterally altering the patient’s position in supine prior to performing the test. Under these circumstances the objectivity of straight-leg-raising is suspect, and the test is therefore irrelevant in judging progress.

It should be pointed out that testing of straight-leg-raising can be very misleading and is only reliable as an objective guide when the patient has constant sciatic pain. Constant sciatic pain is caused by constant mechanical deformation. When a disc protrusion is of sufficient magnitude to cause constant compression of the nerve root, alteration of the lateral shift while lying supine will not allow a better range of straight-leg-raising. If there is constant sciatic pain and straight-leg-raising improves as a result of some manoeuvre, a reduction in the magnitude of the protrusion must have occurred following this manoeuvre. Under these circumstances the objectivity of straight-leg-raising remains constant and therefore the test is useful in assessing the value of a certain procedure and judging progress.

If there is intermittent sciatic pain, the pressure on the nerve root is intermittent. In this case a minor annular bulge may be influenced by movements and the patient’s symptoms can be created or abolished at will without significant alteration in his condition.


  • Unilateral or asymmetrical pain across L4/5.
  • With or without buttock and/or thigh pain.
  • With leg pain extending below the knee.
  • No deformity.

Derangement Five is a straight progression of Derangement Three. In Derangement Five the magnitude and location of the disc disturbance are such that impingement of the nerve root and dural sleeve occurs, but is not sufficient to force deformity. If the history is of recent onset, the patient must be treated with great care. It is essential to determine whether the sciatica is constant or intermittent, because the treatment will be different accordingly. If the sciatica has been present for several weeks or months, as sometimes occurs, constant leg pain may have altered to intermittent pain. Generally, if the patient presents with a deformity of scoliosis, sciatica is likely to be constant, and if there is no deformity, sciatica is usually intermittent. Thus, Derangement Five patients are more likely to have intermittent sciatica though exceptions occur, expecially in acute stages of derangement.

Intermittent sciatica

Usually, the patient with Derangement Five presents without a deformity in the lumbar spine and the sciatica will be intermittent — that is, there are times in the day when the sciatica is not present. Neurological deficit is infrequently encountered in these patients as even short periods without root compression allow physiological recovery to some extent. Straight-leg-raising may or may not be limited.

If the root irritation is indeed intermittent, the patient can be treated with some caution using mechanical therapy. In the treatment we must make use of those positions and movements which are found to reduce or abolish the sciatica. It must be emphasised that any position or movement which produces or enhances sciatica should not be further developed. When neurological deficit is present the chances of success are greatly reduced.

Intermittent sciatica may be caused by a small disc bulge which is, depending on the patient’s activities, alternately protruding into the canal and retreating into the disc substance, but is not large enough to force deformity upon the joint.

Intermittent sciatica may also be caused by an adherent nerve root or entrapment which is placed under increased tension when certain movements are performed and positions are adopted. For example, a patient with sciatica may have recovered recently from an acute disc prolapse and his symptoms are now becoming intermittent; we must determine whether his sciatica is caused by an increase of disc bulging or by an increased nerve root tension due to entrapment, adherence or scarring; and when adherence of the nerve root is thought to be the cause, we must determine whether it is safe at this stage to stretch the nerve root without causing further disc prolapse.

To differentiate between sciatica caused by compression from a disc bulge, or that due to increased root tension from adherence, careful assessment of the flexion test movements is essential. Flexion in standing will enhance the sciatica in both situations — that is, in derangement and in root adherence. The answer to the problem will be found in flexion in lying, which will not enhance sciatica in a patient with an adherent root, but will always enhance it when the disc is in a weakened state. Thus, production or enhancement of sciatica which remains worse as a result of performing flexion in lying indicates that the increase in mechanical deformation is caused by a bulging disc. With such a response to the test movements it is dangerous for the patient to perform flexion exercises in standing as well as in lying, as this may lead to recurrence or increase of derangement.


Should testing of flexion in lying indicate that sciatica is caused by a disc derangement and the disc wall is able to distend during this movement, it is likely that testing of extension in lying will have the opposite effect and reduce the derangement. If this is the case the patient must be placed under the extension principle for a period of twenty-four hours to confirm the diagnosis. If after this time there is a positive response to extension, the extension principle may be continued and the patient must be treated as for Derangement Three. If the response to extension appears to be negative, or if progress appears to be slow, the use of unilateral mobilisation and manipulation procedures is indicated as outlined before (Derangement Three). It will be understood that, once full centralisation is obtained treatment should be continued and progressed exactly as described for Derangement One.

Should the test movements indicate that sciatica is caused by entrapment — root adherence or scarring, the treatment described for this under Derangement Six should be applied. Remember however that the treatment must be considered to be that required for dysfunction. The derangement stage has now passed and the damage repaired.


  • Unilateral or asymmetrical pain across L4/5.
  • With or without buttock and/or thigh pain.
  • With leg pain extending below the knee.
  • With deformity of sciatic scoliosis.

Derangement Six clearly is a progression of Derangement Four and Five. The patient commonly exhibits a sciatic scoliosis as well as a reduced lordosis. The sciatica is more likely to be constant and there is little chance of reducing the symptoms by positioning or movement. Often the patient states that movement brings relief of pain; however, movement or a change of position gives a short-lived respite only. Neurological deficit commonly occurs.

If in a patient with Derangement Six and constant sciatica most test movements are found to enhance the leg pain and no movement reduces it, a provisional diagnosis of accomplished disc protrusion can be made provided the presence of neurological deficit and a positive myelogram support this finding. Remember, that at this stage the condition is irreversible using mechanical therapy. Subsequent surgery usually confirms our diagnosis.

Fig. Patient with Derangement Six. This patient shows a similar deformity as the patient with Derangement Four — a primary lateral shift.

Constant sciatica

If there is no position in which the patient is painfree, we must be careful when sending the patient home on bed rest. It is certainly not desirable that the patient assumes positions which increase the symptoms. Before placing a patient on bed rest we must examine the various positions and their effects on sciatica and low back pain, and advise the patient accordingly. If there is a position which produces significant reduction in leg pain, the patient should be instructed to adopt and maintain that position for long periods at a time.

If no test movements or positions can be found to reduce the pain referred below the knee then, I believe, there are no techniques available which will have a beneficial effect on the derangement. Intermittent traction in the order of twenty minutes a day on an out-patient basis has been described as useful, but if progress is made it is difficult to attribute this to the treatment rather than to the passage of time. Continuous traction in bed is a different matter and often produces good enough results to make the procedure an attractive alternative to surgery.


If test movements indicate that reduction of the derangement is possible, treatment should be commenced following the lines of that for Derangement Four and Five. During the treatment great care should be taken to check regularly if there is a change in peripheral symptoms. Increased tingling or numbness felt in the foot must never be ignored, and if these are present treatment should be modified immediately.

If there is improvement but full centralisation has not yet been achieved, the application of mobilising and manipulation procedures may be indicated.

Techniques outlined previously (Derangement Three) may be utilised, provided pre-manipulative testing is performed to ensure centralisation of symptoms is taking place. If peripheral pain is enhanced in the pre-manipulative testing position, the manipulation should not be performed. Whatever procedure you have in mind, never manipulate a patient without pre-manipulative testing.

Should lateral shift correction produce reduction of the derangement, then progress usually is uncomplicated and treatment should continue as outlined for Derangement Four. The recovery of full flexion or the treatment of any residual flexion dysfunction must be delayed much longer after the resolution of a severe sciatica than is usually the case with pure lumbar pain. I consider eight to ten weeks from the time of onset of peripheral symptoms to be the minimum time before implementing the flexion dysfunction procedures to the maximum.

Stretching of adherent nerve root

Once the acute episode has subsided and the patient is able to attend to his occupation, nerve root adherence as a result of scarring may cause a persistent sciatic reference which, in some cases, may last for years. This disability will not produce neurological deficit if the initial episode has not already done so. It is desirable to reduce the nerve root entrapment or adherence, and in many patients this may be done successfully by using the procedures for flexion dysfunction — that is, the shortened structures should be stretched frequently and firmly every day until the adherence is resolved. To achieve this flexion in lying (Proc. 13) should be regularly performed for one week. This is followed by flexion in standing (Proc. 14) which must be performed often enough to elongate and stretch scarred and adherent tissue without causing further bulging of the disc wall.

Fig. Treatment of adherent sciatic nerve root, using flexion in standing.

When treatment of dysfunction due to an adherent nerve root is commenced it should not be attempted during the first four to five hours of the day. During this time period the disc is likely to be under increased pressure as a result of its nocturnal imbibition and reabsorbtion of fluid. I recommend that in the initial stages of treatment the patient performs ten repetitions of flexion in standing (Proc. 14) from midday on, every three hours until retirement. When the derangement appears stable and the integrity of the disc wall is established, the patient may commence the exercise a little earlier in the day and repeat it every two hours. However, it is inadvisable to perform flexion in standing (Proc. 14) on awaking.

Because flexion in standing (Proc. 14) places stress on the disc wall and forces the disc posteriorly, there are always risks involved in stretching an adherent nerve root, especially in the initial stages. Therefore, flexion in standing (Proc. 14) must always and immediately be followed by extension in lying (Proc. 3), or if this is not possible by extension in standing (Proc. 6).

As the nerve root stretching becomes effective, the patient may perceive the same amount of pain whereas his flexion range has increased. Gradually his fingertips will move closer to his ankles, and where a certain amount of flexion produced significant pain before it may have become painfree now. It will become easier to drive the car and to walk uphill.

It is my belief that intermittent stress applied to joints in this manner strengthens ligamentous structures rather than damages them, while scar tissue will stretch and yield to such stress. However, if a sustained stress is applied damage may occur to both ligamentous and scar tissue.


  • Symmetrical or asymmetrical pain across L4/5.
  • With or without buttock and/or thigh pain.
  • With deformity of accentuated lumbar lordosis.

In Derangement Seven the disturbance within the disc appears to be located in a more antero-lateral or anterior position, which leaves the patient with an accentuated lordosis as the presenting deformity. This type of derangement is not common, but it is easily identified.

The patient with Derangement Seven may exhibit such a gross loss of flexion that in full flexion the lumbar spine remains lordotic. At first sight the condition appears to be the common flexion dysfunction presenting with an accentuated lordosis. However, the patient describes a sudden onset of pain and assures that he was able to touch his toes easily the day before the onset of pain.

Fig. Patient with Derangement Seven. a – Examination of standing posture — accentuated lordosis. b – Flexion loss at commencement of treatment session. c – Recovery of flexion at finish of same treatment session. The remarkable recovery of flexion within a short time period indicates derangement.


If examination shows a marked deviation in flexion, it may be necessary to perform flexion in step standing (Proc. 15) to reduce the lateral component of the derangement. Usually, this procedure rapidly brings the deviation to the midline. As soon as the deviation in flexion is corrected flexion in step standing (Proc. 15) should be discontinued. Correction of deviation in this type of derangement is sometimes very dramatic, and if the procedure is repeated too often the deviation in flexion may change to the opposite side. The treatment should be continued with flexion in lying (Proc. 13).

If there is no deviation in flexion on the test movements, treatment should commence with flexion in lying (Proc. 13), and after a few days flexion in standing (Proc. 14) may be added. Sometimes an intermediate stage of flexion seems indicated. This can be found by performing flexion in the sitting position and is progressed by placing the feet further from the chair as the flexion is performed. Once reduction of the derangement is achieved it is possible to recreate the derangement situation simply by performing extension in lying (Proc. 3). This is exactly the opposite from the previous derangements with a posterior or postero-lateral disc disturbance where recurrence is to be expected as soon as the lordosis is lost following reduction. If there is improvement but the patient has unilateral pain which has not fully centralised, the application of unilateral techniques may be indicated such as sustained rotation (Proc. 11) and rotation manipulation in flexion (Proc. 12).

Because patients with deformity of accentuated lordosis rarely develop extension dysfunction, it is not necessary that extension procedures be included in the treatment of patients with Derangement Seven.


Of all patients with low back pain those having derangement of the intervertebral disc are the most interesting and rewarding to treat. As in dysfunction, it is essential in derangement that from the very first treatment correction of the sitting posture be achieved, but in the early and acute stages of derangement emphasis is placed on the maintenance of lordosis rather than the obtaining of the correct posture. Failure in this respect means failure of what otherwise might be a successful reduction of the derangement. So often it occurs that a patient describes a significant relief from pain and is visibly improved immediately following treatment, but later that same day after sitting for some time he is unable to straighten up on rising from sitting and the symptoms have returned just as they were before treatment. Usually the patient clearly understands the dangers of bending and stooping and carefully avoids these movements. But the hidden dangers of sustained flexion incurred in the sitting position is rarely recognised by patient or therapist.

Two of every three patients with low back pain have symptoms commencing for no apparent reason. Where there is no recognisable precipitating strain in the production of mechanical back pain, we must assume that the symptoms commenced as a result of the patient’s normal daily pursuits. In other words, in the course of every day living the patient has performed a series of movements or adopted certain positions which have led to mechanical derangement within the lumbar spine. I believe that it is possible to equip the patient with the necessary information and instruct him in the methods required to reverse the mechanical disturbances he unwittingly created and to prevent further episodes of low back pain. This can be achieved if instructions and explanations are given in an adequate but simple manner.

If the patient adopted a position or performed a movement that damaged the disc mechanism, utilisation of the patient’s movements can reverse that derangement if we understand the mechanism involved.

Where time is a crucial factor in the production of derangement, it must be utilised to its advantage in the reduction of the same. For example, if pain is stated to arise commonly after half an hour of sitting and is caused by derangement, it is unlikely to appear clinically after only two minutes of flexion; and if it takes thirty minutes to produce pain clinically it is unlikely to disappear in two minutes. Throughout the treatment of derangement ample time must be allowed for the distorted nucleus to alter its silhouette and for reversal of the flow of displaced nuclear gel within the disc. In the reduction of derangement, time is obtained by sustaining positions or repeating movements.

During the course of one treatment session we should not use more than one new procedure; nor should that procedure, if it is a manipulative thrust technique, be performed more than once. Following the application of a new procedure or a manipulation we must wait, if necessary twenty-four hours, to assess the response of the patient.

There are several derangements which commonly occur in the lumbar spine. I realise that my classification of the derangements may oversimplify the true position, but for adequate explanation simplification is necessary. It must be appreciated that many variations of the derangements are possible and not all patients will neatly fit into the system.

Table of Derangements

Derangement One:

  • Central or symmetrical pain across L4/5.
  • Rarely buttock or thigh pain.
  • No deformity.

Derangement Two:

  • Central or symmetrical pain across L4/5.
  • With or without buttock and/or thigh pain.
  • With deformity of lumbar kyphosis.

Derangement Three:

  • Unilateral or asymmetrical pain across L4/5.
  • With or without buttock and/or thigh pain.
  • No deformity.

Derangement Four:
Unilateral or asymmetrical pain across L4/5.
With or without buttock and/or thigh pain.
With deformity of lumbar scoliosis.

Derangement Five:

  • Unilateral or asymmetrical pain across L4/5.
  • With or without buttock and/or thigh pain.
  • With leg pain extending below the knee.
  • No deformity.

Derangement Six:

  • Unilateral or asymmetrical pain across L4/5.
  • With or without buttock and/or thigh pain.
  • With leg pain extending below the knee.
  • With deformity of sciatic scoliosis.

Derangement Seven:

  • Symmetrical or asymmetrical pain across L4/5.
  • With or without buttock and/or thigh pain.
  • With deformity of accentuated lumbar lordosis.

I believe that the postero-central and postero-lateral derangements (Derangements One to Six) are all progressions of the same disturbance within the intervertebral disc: commencing with Derangement One, which is the embryonic stage of posterior disc disturbance exhibiting central pain, each successive derangement shows peripheralisation of pain or development of deformity. The principle aim of treatment is to centralise pain and reduce deformity in order to reverse all derangements to Derangement One. Patients with Derangement One are able to treat themselves.

Under Derangement Seven fall the less common anterior and antero-lateral disc disturbances. The treatment follows a different course than for the posterior derangements, but also here the principle treatment aim is centralisation of pain and reduction of deformity.

In general, the treatment of derangement has four stages:

  1. reduction of derangement.
  2. maintenance of reduction.
  3. recovery of function.
  4. prevention of recurrence.

If possible, the first two stages will be achieved during the initial treatment session. Correction of sitting posture and instruction in a simple means of self-reduction in case of recurrence usually follow. Recovery of function will only be commenced once reduction of derangement has proven to be stable and the patient has been painfree for a few days. Before discharging the patient a full prophylactic programme is given. Self treatment is essential in prophylaxis.

Prophylaxis is impossible without self understanding.

The Derangement Syndrome

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.

Clinical examples

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.

Clinical examples:

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.


Day one

  • Assessment and conclusion/diagnosis.
  • Explanation of the cause of dysfunction and the treatment approach.
  • Postural correction and instructions, especially regarding sitting; demonstrate the use of a lumbar support.
  • Commence with exercises to recover function — that is, extension in lying, flexion in lying, or side gliding in standing, whatever procedure is indicated.
  • Emphasise the need to experience some discomfort during the exercises, and the importance of frequent exercising during the day.
  • If flexion in lying is recommended, we must warn to stop exercising if the symptoms quickly worsen. We may have overlooked derangement, or commenced the procedure too early following recent derangement.
  • Always follow flexion exercises with some extension.

Day two

  • Confirm diagnosis.
  • Check postural correction.
  • Completely repeat’postural correction and instructions.
  • Check exercises. If improving nothing should be changed.
  • If not improving, ensure that exercises are performed far enough into end range, maintained long enough during the last three repetitions, and performed often enough during the day.
  • Warn for ‘new pains’.

Day three

  • Check posture and exercises.
  • If no improvement, commence mobilisation procedures. Several mobilisation treatments may be required.
  • Patient must continue the self-treatment exercises as directed.

Day four and five

  • Check exercises and progress.
  • If in treatment for flexion dysfunction no further progress is possible with flexion in lying, change to flexion in standing, possibly flexion in step standing.
  • Take necessary precautions when starting flexion in standing.
  • Ensure that patient has ‘new pains’.

Further treatments

  • I prefer to see patients in this category three or four days in succession. If progress is adequate and the patient understands the self-treatment
    programme, treatment may change to alternate days and later to twice per week if required.
  • It usually takes ten to twelve treatments, spread over four to six weeks, to successfully treat dysfunction.
  • If towards the middle of the treatment period the patient ceases to improve and especially if the remaining pain is unilateral, then a rotation manipulation may be required. This may have to be repeated two or three times and should be combined with mobilising and exercising procedures already being applied.
  • Before discharge prophylaxis must be discussed in detail.


Having observed thousands of lumbar spines it has become clear to me that asymmetry is the ‘norm’ and symmetry is almost atypical. Therefore, when examining dysfunction patients it is important to realise that many exhibit a minor scoliosis or lateral shift, the direction of which is sometimes extremely difficult to determine. With careful observation it can be seen that the top half of the patient’s body is not correctly related to the bottom half, and the patient has shifted laterally about the lumbar area. The anomalies include a number of lateral shifts now dysfunctional in character. These lateral shifts are referred to as secondary whereas those caused by derangement are primary.

Fig. Recovery of loss of side gliding, leaching the procedure of self-correction of secondary lateral shift.

As discussed previously, we must determine whether the lateral shift is relevant to the present symptoms or is merely a congenital or developmental anomaly. If side gliding produces pain there is likely to be adaptive shortening within or about the disc and recovery of the side gliding movement must be attempted. As it is not easy to apply overpressure in the side gliding exercise, it may be difficult to recover this movement.

The patient must be fully instructed in self-correction of lateral shift (Proc. 17). He should perform the procedure ten times per day, at each session moving ten times into the overcorrected position. The last movement should be held firmly for about thirty to forty seconds. The patient should also be encouraged to stand in the overcorrected position whenever an opportunity arises during the day. If by the end of the first week pain produced by lateral shift correction is much less, the procedure will most likely have the desired result and must be continued for about three to four weeks in an attempt to restore full function. But if no change is evident after one week, there is little hope of improving this aspect of dysfunction.


Loss of flexion is the second most common movement loss in the lumbar spine. It manifests itself in several ways, which interfere with either the amount of available flexion or the pathway taken to achieve flexion. This type of dysfunction is commonly seen in patients with an accentuated lordosis.

Patients with significant flexion dysfunction are usually unable to sit slouched with a convex lumbar spine. When giving postural instructions to these patients, we must explain that once sitting relaxed they place the lumbar spine on full stretch much sooner than patients with a normal flexion excursion.

Fig. Recovery of loss offlexion, using the procedure of flexion in standing.

Recovery of pure flexion loss

To regain flexion we must, just as in the case of extension dysfunction, explain to the patient the purpose of performing exercises. Again, we must stress the necessity of causing a moderate degree of discomfort or pain with the exercises. Pain produced by stretching of contracted structures involved in the loss of flexion should be felt across the low back. Often it resembles the pain of which the patient originally complained, and as in the recovery of extension it should be shortlived.


Recovery of pure flexion is commenced with exercises. The patient must perform flexion in lying (Proc. 13). This exercise should be performed ten times about every two hours. As said before, frequency and regularity of exercising are important factors in the treatment of dysfunction. When five to six days have passed the patient will describe that the knees can be bent fully onto the chest. All flexion that can possibly be restored in this position is now recovered, and the exercise no longer produces pain. In order to apply full passive stretch to regain the last few degrees of lumbar flexion it is necessary to perform flexion in standing (Proc. 14).

Up till now flexion has been performed in lying (Proc. 13) with elimination of gravitational forces. This rarely makes the patient significantly worse. In flexion in standing (Proc. 14) gravitational stresses are added.

When applied to dysfunction resulting from recent derangement, flexion in standing (Proc. 14) may sometimes exacerbate the condition. Therefore, when commencing flexion in standing (Proc. 14) the patient should reduce the number of exercises performed at each session as well as the frequency of the sessions per day — for example, five to six repetitions of the exercise should be done five to six times per day. This way there is little risk of exacerbation, and after four to five days the patient may progress to a full programme.

Eventually the patient will recover his flexion and will almost reach the ground before any strain pain is felt. No discomfort should be experienced on returning to the erect position.

Special techniques

If full flexion cannot be restored by the patient’s own efforts, the application of special procedures may be indicated, such as rotation mobilisation and manipulation in flexion (Proc. 11 and 12).

Occasionally, a patient with the derangement syndrome will mistakenly be placed in the dysfunction category. If this occurs the flexion procedures may immediately and significantly worsen the symptoms, and in this way the true nature of the condition will be revealed. Consequently, the treatment programme must be altered appropriately.

N.B. Remember that the recovery of function in flexion following recent derangement, is hazardous. Extension in lying (Proc. 3) should always follow flexion movements in order that any posterior disturbance is corrected immediately.

Treatment of flexion with deviation

There are two common types of deviation in flexion resulting from dysfunction. The first one occurs in the patient who is unable to reach full flexion via the normal sagittal pathway, no matter how hard he tries. Due to adaptively shortened structures within the intervertebral segment he is forced to deviate to one side during flexion.

Treatment for this type of flexion loss may follow the course recommended for recovery of pure flexion loss. Thus, treatment commences with flexion in lying (Proc. 13). Provided the initial twenty-four hour period of flexion in lying (Proc. 13) has not caused a lasting increase or peripheralisation of pain, the use of flexion in step standing (Proc. 15) is indicated at an early stage of treatment to correct the deviation in flexion. This is later followed by flexion in standing (Proc. 14) to ensure recovery of full flexion movement. When commencing flexion in step standing (Proc. 15) the same precautions should be taken as discussed previously (that is, when commencing flexion in standing (Proc. 14) in treatment recommended for recovery of pure flexion).

If the initial twenty-four hour period of flexion in lying (Proc. 13) causes a lasting increase or peripheralisation of symptoms, our diagnosis is incorrect and the most likely reason for the deviation is internal derangement of a lumbar disc. Consequently, we must alter our treatment approach.

The second type of deviation in flexion resulting from dysfunction is caused by an adherent nerve root, and its treatment will be discussed in conjunction with the treatment of sciatica.