Category Archives: Health

How to Prevent an Electrolyte Imbalance

Fluids in Your Body

Athletes have been swigging electrolyte replenishers since 1965. That was the year a Florida Gators’ coach asked doctors why his players were wilting so quickly in the heat — their answer? The players were losing too many electrolytes. Their solution was to invent Gatorade. So, what are electrolytes and why are they important?

Water and electricity are essential to your health. At birth your body contains about 75 to 80 percent water. By the time you’re an adult, the percentage of water in your body drops to approximately 60 percent if you’re a male and 55 percent if you’re a female. The volume of water in your body will continue to decrease as you age.

Fluid in your body contains things such as cells, proteins, glucose, and electrolytes. Electrolytes come from the food and liquids you consume. Salt, potassium, calcium, and chloride are examples of electrolytes.

Electricity and Your Body

Electrolytes take on a positive or negative charge when they dissolve in your body fluid. This enables them to conduct electricity and move electrical charges or signals throughout your body. These charges are crucial to many functions that keep you alive, including the operation of your brain, nerves, and muscles, and the creation of new tissue.

Each electrolyte plays a specific role in your body. The following are some of the most important electrolytes and their primary functions:


  • helps control fluids in the body, impacting blood pressure
  • necessary for muscle and nerve function
  • helps balance electrolytes


  • helps balance electrolytes
  • balances acidity and alkalinity, which helps maintain a healthy pH
  • essential to digestion


  • regulates your heart and blood pressure
  • helps balance electrolytes
  • aids in transmitting nerve impulses
  • contributes to bone health
  • necessary for muscle contraction


  • important to the production of DNA and RNA
  • contributes to nerve and muscle function
  • helps maintain heart rhythm
  • helps regulate blood glucose levels
  • enhances your immune system


  • key component of bones and teeth
  • important to the movement of nerve impulses and muscle movement
  • contributes to blood clotting


  • strengthens bones and teeth
  • helps cells produce the energy needed for tissue growth and repair


  • helps your body maintain a healthy pH
  • regulates heart function

When Electrolytes Become Unbalanced

Fluids are found inside and outside the cells of your body. The levels of these fluids should be fairly consistent. On average, about 40 percent of fluids are inside the cells and 20 percent are outside the cells. Electrolytes help your body juggle these values in order to maintain a healthy balance inside and outside your cells.

It’s normal for electrolyte levels to fluctuate. Sometimes, though, your electrolyte levels can become imbalanced. This can result in your body creating too many or not enough minerals or electrolytes. A number of things can cause an electrolyte imbalance, including:

  • fluid loss from heavy exercise or physical activity
  • vomiting and diarrhea
  • medications such as diuretics, antibiotics, and chemotherapy drugs
  • alcoholism and cirrhosis of the liver
  • heart failure
  • kidney disease
  • diabetes
  • eating disorders
  • severe burns
  • some forms of cancer

Symptoms of Electrolyte Imbalance

Symptoms of electrolyte imbalance vary depending on which electrolytes are most affected. Common symptoms include:

  • nausea
  • lethargy
  • fluid retention

Call 911

Electrolyte imbalances can be life threatening. Call 911 if someone has the following symptoms:

  • confusion or sudden change in behavior
  • severe muscle weakness
  • rapid or irregular heartbeat
  • seizures
  • chest pain


Treatment is determined by the cause of the electrolyte imbalance, the severity of the imbalance, and by the type of electrolyte that’s either in short supply or over abundant. Treatment options normally include either an increase or decrease of fluids. Mineral supplements may be given by mouth or intravenously if depleted.

Preventing Electrolyte Imbalance

The International Marathon Medical Director’s Association offers the following guidelines for maintaining good hydration and electrolyte balance during activity:

  • If your urine is clear to straw colored before a race or workout, you’re well hydrated.
  • You should drink a sports drink containing electrolytes and carbohydrates if your sporting event or workout lasts longer than 30 minutes.
  • Drinking water with a sports drink decreases the beverage’s benefits.
  • Drink when you’re thirsty. Don’t feel you must constantly replenish fluids.
  • Although the needs of each individual differ, a general rule of thumb is to limit fluids to 4-6 ounces every 20 minutes of a race.
  • Seek immediate medical advice if you lose more than 2 percent of your body weight or if you gain weight after running.

Serious emergencies from electrolyte imbalances are rare. But it’s important to your health and, if you’re an athlete, your performance to maintain a healthy electrolyte balance.


The patient adopts the prone lying position with the arms alongside the trunk and the head turned to one side. In this position the lumbar spine falls automatically into some degree of lordosis.

Fig. Lying prone.


In derangement with some degree of posterior displacement of the nuclear content of the disc the adoption of procedure 1 may cause, or contribute to, the reduction of the derangement provided enough time is allowed for the fluid nucleus to alter its position anteriorly. A period of five to ten minutes of relaxed prone lying is usually sufficient. This procedure is essential and the first step to be taken in the treatment and self-treatment of derangement.

In patients with a major derangement, such as those presenting with an acute lumbar kyphosis, the natural lordosis of prone lying is unobtainable. These patients cannot tolerate the prone position unless they are lying over a few pillows, supporting their deformity in kyphosis.

In minor derangement situations the degree of posterior movement of the nucleus is relatively small. Prone lying may actually reduce the derangement without any other procedures being required in the treatment, provided sufficient time is allowed for the fluid mechanism to alter to a more anterior position. In these situations the prone position, though obtainable, may initially be painful. This does not indicate that the procedure is undesirable. The increase of pain in this position is nearly always felt centrally and is in fact desirable. If pain is produced or enhanced peripherally, the prone position must be considered harmful and should not be maintained.

A basic requirement for the self-treatment of derangement is that the prone position can be obtained and maintained. In this position the patient will commence the self-manipulative procedures, based on the extension principle.

In dysfunction there is a loss of extension movement or a reduced lordosis. In some patients with extension dysfunction the loss of movement may be enough to prevent lying prone for more than a few minutes. For these people lying prone in bed or while sunbathing has become impossible, because soft tissue shortening has reduced the available range of movement and prolonged extension stress produces pain.

The prone lying procedure by itself is not sufficient to resolve extension dysfunction. However, when adopted regularly and in conjunction with other procedures, prone lying should become painless as lengthening of shortened tissues takes place.

The prone lying position should be obtained by all patients attending for treatment of low back pain. It has been suggested that this position can be harmful because it increases and accentuates the lumbar lordosis. This applies only in a few situations: when we have failed to correct a relevant lateral shift prior to assuming the prone lying position; when extension produces or increases the compression on the sciatic nerve root; and in those rare derangements where nuclear material has accumulated anteriorly or antero-laterally, and prone lying increases the derangement. In all other instances the prone lying position is highly beneficial.

Patients with posterior derangement should after reduction be careful when arising from the prone position to standing. Every effort must be made to maintain the restored lordosis while moving from lying to standing in order to maintain the reduction of the derangement.

Examination of Back Pain

Having digested the information supplied by the referring doctor, extracted as much relevant information as possible from the patient, and checked the radiologist’s report, we may proceed to the examination proper.

If the patient is able to do so, we should make him sit on a straight backed chair while taking his history. During this lime he will reveal the true nature of his sitting posture. When the patient rises to undress after the interrogation we should observe the way he rises from sitting, his gait, the way he moves, and any deformity that may be obvious.

We will record the following:


If the patient has been sitting during history taking, we already have a good impression of his posture. We now ask him to sit on the edge of the examination table with his back unsupported. In the majority of cases the patient will sit slouched with a flexed lumbar spine. Some patients are more aware of the relationship between their posture and pain. They have discovered that they can control their sitting pain by sitting upright and may sit very well on first observation. Unfortunately, these patients are few and far between.


Fig. Relaxed sitting posture.


We examine in particular the following features:

1. Reduced or accentuated lordosis

The most common postural fault to be observed in the standing position is the flattened lumbar spine or reduced lordosis. Some patients have a deformity in kyphosis.

Another common deformity or departure from the ‘norm’ is the patient exhibiting an accentuated lumbar lordosis. Though much less common than the flattened spine this is clearly a separate category and should be treated accordingly.


Fig. a. – Reduced lumbar lordosis. b. – Accentuated lumbar lordosis. c – Lateral shift to the right.

2. Lateral shift

A departure from the midline causing a lumbar scoliosis or lateral shift is evident in about fifty-two percent of patients. There are many reasons for the lumbar spine to depart even slightly from the midline: the anatomical configuration of the joint surfaces may dictate this; a congenital anomaly may be present; there may be some remote mechanical cause; and an alteration in the position of the disc nucleus may be responsible.

The lateral shift is sometimes barely discernable, and great care must be taken to ensure that the deformity is not overlooked. This is important because some movements, especially extension, produce pain when performed in the presence of a lateral shift, whereas if there was no shift they would be painfree. We must never fail to recognise a minor lateral shift and its possible role in the production of symptoms.

I have chosen to describe a right lateral shift — or a lateral shift to the right — as the situation which exists, when the vetebra above has rotated and laterally flexed to the right in relation to the vertebra below, carrying the trunk with it. Thus the top half of the patient’s body has moved to his right in relation to the bottom half.

3. Leg length discrepancy

If a leg length discrepancy is encountered, we must investigate the relevance of the discrepancy to the patient’s symptoms. When in the history there is no record of pain being enhanced by standing and walking, the difference in leg length is not likely to be relevant. But when pain is produced by standing or walking, we should increase the length of the short leg to bring about symmetry and await the effect of this on the patient’s symptoms. When relevant, leg length adjustment causes a fairly rapid change in the symptoms experienced during standing and walking. This change should become apparent within a few days at the most.

There are various methods of measuring the leg length, but the only truly reliable way to detect minor differences in leg lengths is by taking an x-ray of the pelvis and both full legs with the patient in standing. However, it is doubtful that minor leg length discrepancies cause significant low back pain.

At this stage, with the patient still standing, it may be advisable to quickly test the integrity of the conduction of the lower lumbar and upper sacral nerve roots. Therefore we ask the patient to walk on his toes and then on his heels. In case of difficulty or when in doubt about the outcome a more detailed neurological examination must be performed.


Here we are interested in observing the quality of the movement itself — that is, the range of movement and the movement pathway. We will determine if there is a movement loss and if deviation from the normal movement path takes place. The word ‘pain’ should not be mentioned until we are ready to assess the effects of the movements on pain.

The patient should be standing with his feet about thirty centimeters apart and only one movement will be performed in the direction to be evaluated. We examine:

1. Flexion

This is the first movement to be examined, because in patients with dysfunction or derangement the flexion movement provides us with the most relevant information regarding the nature and the degree of the disturbance. The standing patient is asked to run the hands down the front of both legs, moving as far as possible into flexed standing, followed immediately by returning to neutral standing.


Fig. Examination of movement — flexion.

Any loss of flexion should be noted. Loss of flexion manifests itself in one of two ways: either the end range of flexion is limited, or a deviation from the normal pathway of flexion has developed. In some patients with a severe loss of flexion end range, the lumbar lordosis is still present after the patient has bent forward as far as possible, in others the lumbar spine merely remains flat. Any asymmetrical impediment to flexion may cause the spine to take the path of least resistance, resulting in a deviation from the sagittal pathway. By far the majority of patients with a flexion loss divert from the sagittal plane during flexion and deviate to one side or the other of the midline. This may occur in an arc-type of movement, the flexion commencing and ending in midline positions; or, once movement is commenced, it may divert from the midline and increase its departure for as long as flexion is continued.

Deviation in Flexion

In my experience there are three clearly defined and separate causes for deviation in flexion. The mechanism is different in each case and the treatment must be varied accordingly. Thus deviation in flexion may be due to:

  • (a) Derangement within the vertebral joint. In this situation the altered position of the fluid nucleus compels a deviant flexion pathway. Generally, the deviation in flexion occurs away from the painful side as long as there is no sciatic nerve root irritation. In some patients the deviation is variable and will occur one day to the left and the next day to the right.
  • (b) Dysfunction within the vertebral joint. This develops following repair of damage after derangement. In this situation the consequent scarring by fibrous connective tissue prevents flexion in the sagittal plane and the deviation may take place towards or away from the painful side, but is never variable.
  • (c) Dysfunction external to the vertebral joint. This exists in the presence of an entrapped or adherent sciatic nerve root. In this situation the root is no longer able to lengthen adequately and allow flexion to occur in the sagittal plane. It will now act as an anchor and pull the patient during flexion towards the side of root adherence. The deviation in flexion may become very severe and always take place towards the painful side.

2. Extension

The standing patient is asked to place his hands in the small of the back and bend backwards as far as possible, followed immediately by returning to neutral standing.

The loss of some degree of extension is very common after the age of thirty. Any limitation of extension evident in the lumbar spine should be recorded as well as the presence of a deviation in the extension pathway which is occasionally encountered. Major disc bulging will cause a deviation in extension away from the side of the pain and enhancement of sciatica will occur. However, facet apposition in full extension usually prevents significant deviation.

3. Side gliding

Having considered over the past twenty-five years the relevance of the information obtained by assessing the movements of rotation and side bending separately, I have come to the conclusion that it is better to combine the two movements in the one movement of side gliding.

In order to examine side gliding the standing patient is asked to move his shoulders and pelvis simultaneously in opposite directions while keeping the shoulders parallel to the ground. As some patients have difficulty in performing this movement, it may be necessary to assist the patient by guiding the movement with a hand placed on one of his shoulders and the other hand on his oppositic iliac crest.


Fig. Examination of movement — extension. Examination of movement — side gliding.

The side gliding movement is frequently unilaterally impaired. When the patient has a lateral shift, there is always some unilateral loss of side gliding. In this situation the movement is restricted or completely blocked in the direction opposite to the lateral shift.


After examining the lumbar spine in relation to function, we must now investigate the effects of various movements on the pain. Let us assume that pain is produced by mechanical deformation as described by Wyke. As discussed before, stresses applied to soft tissues will under certain circumstances be productive of pain. Any attempt to force normal movement (application of abnormal stress) in a joint with a visibly impaired function (abnormal tissue), must result in the production or enhancement of pain.

In order to stress the joints in a controlled manner and avoid exacerbation I have devised a sequence of test movements, the mechanics of which are relatively well understood and the effects of which can be controlled. By applying the test movements during the examination we will enhance pain under some circumstances and reduce it in others. Information gained by deliberately stressing the joints is vital and enables us to select and categorise patients into three groups — that is, patients with pain arising from postural, dysfunctional or derangemental causes.

The test movements are first performed in standing and then in lying. When performed in lying they must be done in such a way that the effect on the lumbar spine is a passive stretch, and any form of active movement produced by the muscles surrounding the lumbar spine should be avoided. In this way we can achieve a better end range stress than with active movements.

When the test movements are performed in standing a normal stress is applied to normal or abnormal tissue; in the former case no pain will be produced; in the latter case pain will be produced or increased if the test movements enhance the mechanical deformation, but pain will be decreased or abolished if the test movements reduce the mechanical deformation. When the test movements are performed in lying a passive stress is added by the patient and an abnormal stress is applied to normal or abnormal tissue; in the former case no pain should result, because the stress is not excessive and is only applied momentarily; in the latter case pain will be produced or increased if the test movements enhance the mechanical deformation, but pain will be decreased or abolished if the test movements reduce the mechanical deformation.

If we are to relate movements to pain, the test movements must be performed in such a way that they produce a change in the patient’s symptoms. This change may be brought about in various ways: if prior to movement pain is present, the test movement may increase or reduce its intensity; it may alter the site of the pain by centralisation or by abolishing one pain and introducing another one. If prior to movement no pain is present, the test movement may produce the pain complained of.

If there is no change in the patient’s symptoms during or immediately following the test movements, the joints have not been stressed adequately and the process should be repeated more vigorously. It may also be that the pain is not of mechanical origin, because mechanical pain must be and always is affected by movement or position. Or, alternatively, the lumbar spine is not causing the problems and other areas should be investigated.


When assessing the results of the test movements it is important to examine the effects of repeating them. Repeated movements are vital in the examination of spinal segments when disc pathology is suspected and it is necessary to determine if a derangement situation exists. It is my belief that with movement of the vertebral column the nucleus can alter its shape, and with sustained positions or repeated movements it will eventually alter its position. Clinically this manifests itself in the derangement syndrome by a change in intensity or site of the symptoms. A decrease or centralisation of pain is absolutely reliable in indicating which movement should be chosen to reduce mechanical deformation. I have learnt to rely implicitly on centralisation as the most important clinical guide to establish the correct direction of movement which will reduce derangement. An increase or peripheralisation of pain is just as reliable in indicating which movement should be avoided because it enhances mechanical deformation. If there is an increase or peripheralisation of pain when performing any technique or movement, a worsening of the condition of the patient is likely. There is one exception to this rule: the patient with an adherent nerve root in chronic sciatica. There are special tests which easily identify this condition, and these will be discussed later.

In derangement the performance of repeated movements in the direction which increases accumulation of nuclear material will result in a progressively increasing derangement and increasing or peripheralising pain. The performance of repeated movements in the opposite direction will result in a reduction of the derangement and reduction or centralisation of pain. Thus, repeated movements are diagnostic in derangement pathologies.

In dysfunction the performance of repeated movements in the direction which stretches adaptively shortened structures will produce pain at the end range of movement, but repetition does not make the patient progressively worse. When he returns to the neutral position the pain will disappear. Thus, repeated movements are diagnostic in dysfunction as well.

Patients with the postural syndrome will not experience pain with any of the test movements or their repetition. These patients must be positioned in order to have their pain reproduced.

Apart from exposing the derangement and dysfunction syndromes, repeated movements are essential in determining whether the timing is appropriate to commence stretching procedures following trauma and derangement. When repeated movements, applied to painful structures, produce less and less pain with each repetition these structures should be exercised. On the other hand, when more and more pain is experienced with each repetition exercising is not indicated and more time should be allowed for the condition to heal. This fundamental response of pain sensitive structures to stress must be applied to soft tissue lesions throughout the musculoskeletal system in order to determine whether a passive or an active treatment approach should be developed.

The movements that I have chosen as test movements are the ones of flexion, extension and side gliding. In my experience these movements will induce or reduce mechanical deformation in the lumbar spine quicker and more effectively than any other movement. Generally speaking, the movements that produce the greatest amount of mechanical deformation and therefore pain can, when reversed or modified, be used to have the greatest effect on the reduction of that mechanical deformation and pain. For example, rotation is rarely complained of as producing significant pain and therefore neither enhances nor reduces mechanical deformation significantly. On the other hand, flexion and extension are commonly stated to be the most painful movements and are potentially the most useful movements for treatment purposes.

Different effects are produced when the tests movements are performed in standing compared with lying. This requires further discussion for both flexion and extension.

Flexion in standing compared with flexion in lying

In the test movements flexion of the lumbar spine is examined in two ways: in standing by bending the trunk forwards; and in supine lying by using the hands to passively bend the knees onto the chest. Apart from the obvious difference achieved by removal of gravitational stress in flexion in lying, there are two major points to note:

In flexion in lying the flexion takes place from below upwards, the L5-S1 joint moving first followed by flexion in turn of each successively higher segment. On the other hand, in flexion in standing the flexion occurs from above downwards.

A better flexion stretch is obtained, especially at L5-S1, by the passively performed flexion in lying, and patients with flexion dysfunction describe a stretch pain in flexion in lying which they may not experience in flexion in standing. Frequently in flexion in lying, pain is produced immediately when the movement commences and the pain increases as the degree of flexion increases. Thus, in flexion in lying pain is produced as soon as the L5-S1 segment (and perhaps L4-L5) is placed under full stretch which occurs immediately flexion is initiated. In flexion in standing the pain will only be experienced at the end of the movement, because only when flexion in standing is almost full are the L4-L5-S1 segments stretched to the full.

The effects on the sciatic nerve roots are different in flexion in standing and flexion in lying. In flexion in standing the sciatic nerve is fully lengthened and placed on full stretch, producing effects identical to those obtained in straight-leg-raising tests. Flexion in lying, when performed with simultaneous hip and knee flexion as described, has no such effect and root adherance or root tension can not be identified in this manner.

The production or enhancement of sciatic pain by flexion in standing may be caused by a bulging disc or an adherent root. However, production or enhancement of sciatic pain by flexion in lying can only be caused by a bulging disc. We have now at our disposal a simple test to differentiate between disc bulging and root adherence. No one should persist with the performance of flexion in lying in the presence of increasing referred pain. Such perserverance can be rewarded by the production of a severe disc lesion.

Extension in standing compared with extension in lying

In the test movements extension of the lumbar spine is examined in two ways: in standing by bending the trunk backwards; and in prone lying by passively raising the trunk, using the arms instead of the back muscles and at the same time keeping the pelvis down. Both manoeuvres cause extension of the lumbar spine from above downwards. There are two major points to note:

The gravitational forces applied to the joints are different in extension in lying and extension in standing. In extension in lying the weight of pelvis and abdomen causes an increase of extension range in the joints of the low back. The force exerted is almost perpendicular to the plane of the body and has a maximal mechanical effect. In extension in standing the gravitational forces act on the joints of the low back at an angle of up to forty five degrees from perpendicular and are therefore less efficient. The greatest extension stretch that a person can apply to his own back is by performing extension in lying. The extension range and stretch are never as complete in extension in standing.

In extension in standing the compressive forces appear sometimes sufficient to prevent full end range movement. This would indicate that some derangements are too large to be reduced in the presence of compressive forces in standing. However, reduction of the same derangements becomes possible in the prone lying position, when the vertical compressive forces are removed.

I believe that there must be other factors, unexplained as yet, which contribute to the purely mechanical effects of exercises performed in lying and in standing. Gravitational or compressive forces alone do not account for the nature of the differences which can be observed clinically.


All patients should perform the test movements except when they are in such severe pain that it is intolerable to do so. This only occurs in major derangement situations, and it may be necessary to place such patients on bed rest in order to facilitate reduction of the derangement by removing gravitational stresses. After a period of twenty-four to forty-eight hours in bed, positioned so that reduction may be enhanced, re-assessment should follow.

Flexion in standing

The patient, standing with his feet about thirty centimeters apart, is asked to run his hands down the front of both legs as far as range and pain allow. He then immediately returns to neutral standing. With the hands actually placed on the legs the more acute or insecure patients will feel safer in performing flexion. Flexion in standing is performed once and its effects on the pain are recorded. The movement should then be repeated up to ten times and the effects of repetition recorded. We must ensure that maximum possible stretch is obtained during the last few movements.

For example:

  • Flexion in standing — produces (R) buttock pain at end range.
  • Repealed flexion in standing — worsens (R) buttock pain and produces (R) calf pain.


Fig. Test movements — flexion in standing. Test movements — extension in standing.

Extension in standing

The patient, standing with the hands in the small of the back to act as a fulcrum, is asked to bend backwards as far as possible. He then immediately returns to netural standing. The test movement is performed once and its effects on the pain are recorded. The movement should then be repeated up to ten times and the effects of repetition recorded. We must ensure that maximum possible stretch is obtained during the last few movements.

For example:

  • Extension in standing — produces central back pain.
  • Repeated extenstion in standing — reduces central back pain.

If extension in standing increases or peripheralises the pain, we must consider the possibility of the presence of a lateral shift. If a lateral shift is present and is relevant to the patient’s symptoms, the performance of any of the test movements with the shift uncorrected will always increase mechanical deformation and thus enhance pain. Extension in standing following shift correction will reduce the derangement and thus decrease the pain.

Side gliding in standing

This is done to determine whether side gliding increases or decreases mechanical deformation and, in the presence of a lateral shift, to test the relevance of the shift to the patient’s symptoms.


Fig. Test movements — side gliding in standing with operator-assistance.

As some patients find it difficult to perform side gliding in standing the examiner may initially have to assist this movement. The patient stands in front of the examiner, who places one hand on one of the patient’s shoulders and the other hand on the patient’s opposite iliac crest. The examiner presses both hands towards the midline, causing a major movement of the top half of the patient’s body in relation to the bottom half. Instead of applying the pressure on the patient’s shoulder, it may under certain circumstances be preferable to press against the side of his rib cage. In all instances both shoulders of the patient should remain parallel to the ground. Side gliding must be tested first in the one and then in the other direction, before the sequence is repeated. The effects of the test movements on the pain should be recorded.

For example:

  • (L) side gliding — increases (R) buttock pain and produces (R) calf pain.
  • (R) side gliding — reduced (R) buttock and calf pain.
  • Repeated (L) side gliding — not indicated as it is likely to worsen the symptoms.
  • Repeated (R) side gliding — reduces (R) buttock pain, abolishes (R) calf pain.

When side gliding is found to be painful and blocked usually a lateral shift is present and in the treatment therapist assistance may be required.

When side gliding is found to be painful but not blocked, a lateral shift is unlikely to be present and in the treatment, therapist assistance is usually unnecessary.

When assessing the relevance of a lateral shift, we must determine whether the shift results from the same mechanical distrubance which has produced the patient’s pain. The shift is considered to be relevant when the movement of side gliding alters the site or intensity of the pain. If no pain change occurs during the performance of side gliding to the one side or the other, the scoliosis cannot be considered part of the mechanical problem causing pain.

Flexion in lying

The patient, lying supine with the knees flexed and the feet flat on the couch, is asked to bend the knees onto the chest. Clasping the knees with his hands he applies a firm pressure to produce maximum possible lumbar flexion.

The legs are then lowered to the starting position. The effects of the first test movement on the pain are recorded. The movement should then be repeated up to ten times, ensuring that the maximum possible stretch is obtained during the last few movements. The effects of repetition are recorded.

For example:

  • Flexion in lying — increases pain (R) L5.
  • Repeated flexion in lying — worsens pain (R) L5 and produces (R) buttock pain.


Fig. Test movements — flexion in lying.

Extension in lying

The patient, lying prone with the hands directly under the shoulders as in the traditional press-up position, is asked to raise the top half of his body by straightening the arms, at the same time keeping the thighs and legs on the couch (Fig. 7:10). If the pelvis lifts from the couch as the arms are straightened, we must make sure that the low back is allowed to sag as much as possible. The patient then returns to the starting position. The effects of this movement on the pain are recorded. The movement should then be repeated up to ten times, ensuring that the maximum possible stretch is obtained during the last few movements. Again, the effects of repetition are recorded.

For example:

  • Extension in lying — reduces (L) buttock pain.
  • Repeated extension in lying — abolishes (L) buttock pain and produces central low back pain.


Fig. Test movements — extension in lying.

The test movements should be performed in a certain sequence. The examiner should not deviate from this method, unless it is obvious that to persist will inflict unnecessary pain on the patient.

In abbreviated form the sequence of test movements is as follows:

  • FIS (flexion in standing)
  • Rep FIS (repeated flexion in standing)
  • EIS (extension in standing)
  • Rep EIS (repeated extension in standing)
  • SGIS (right and left side gliding in standing)
  • Rep SGIS (repeated right and left side gliding in standing)
  • FIL (flexion in lying)
  • Rep FIL (repeated flexion in lying)
  • EIL (extension in lying)
  • Rep EIL (repeated extension in lying)


At this stage it is appropriate to test the mobility of the hip joints and the integrity of the sacro-iliac joints, if these are thought to contribute to the problems of the patient. Should passive stretching of the various structures about the hip reproduce the symptoms complained of, this joint must be considered a possible source of the pain. The sacro-iliac joints, although not commonly the cause of low back pain, turn out to be involved often enough to make a fool of those failing to check them. In my opinion the tests described by Cyriax are adequate to determine if the symptoms are arising from these joints. (Testing of sacro-iliac structures by using bony prominences as land marks and attributing pain to asymmetries so located is dishonest.)

A more detailed neurological examination may be required, if there is the slightest suggestion of nerve root or spinal cord signs. In these cases the patient’s symptoms will be felt in the lower limb. Further neurological examination should include testing of reflexes, muscle strength and sensation.


The correlation of information from history, examination and test movements will indicate whether the patient is suffering from the postural, derangemental or dysfunctional syndrome. This differentiation is essential, as it indicates which principle of treatment should be used.

Postural correction

In the postural syndrome postural correction is the only treatment required.

The extension principle

In posterior derangement the extension principle should be applied when extension reduces mechanical deformation. Thus in the treatment we are making use of those movements which centralised, decreased or stopped the pain during the examination. The patient should receive mechanical therapy based on the principle of extension. This includes: passive extension, extension mobilisation, extension manipulation, extension in standing, extension in lying, and sustained extension.

Patients with an acute lumbar scoliosis or a lateral shift are placed in the extension principle category once correction of the lateral deformity has been achieved.

In dysfunction, however, the extension principle should be applied when extension produces mechanical deformation. Thus in the treatment we are making use of those movements which actually produced the pain during the examination. For treatment of dysfunction to be successful it is imperative that some pain be experienced, especially in the initial stages when adaptively shortened tissues must be stretched enough to assist them to regain their original length and elasticity. Pain thus produced during treatment of extension dysfunction must always be across the back and near the midline, and significant buttock pain should not occur. The treatment procedures are based on the principle of extension (see above).

The flexion principle

In anterior derangement the flexion principle should be applied when flexion reduces mechanical deformation. Again, in the treatment we are making use of those movements which centralised, decreased or stopped the pain during the examination. The treatment consists of procedures based on the principle of flexion. This includes: flexion mobilisation, flexion manipulation, flexion in lying, and flexion in standing.

In dysfunction, however, the flexion principle should be applied when flexion produces mechanical deformation, and in the treatment we use those movements which actually produced the pain during the examination. Some pain must be experienced in treatment of flexion dysfunction to be effective and treatment consists of procedures utilising flexion (see above).

Generally speaking:

in the treatment of derangement we must choose the movement that relieves the pain, as this movement decreases the mechanical deformation by reducing the derangement.


in the treatment of dysfunction we must always choose the movement that produces the pain, as this movement will gradually stretch and lengthen contracted soft tissues, eventually reducing mechanical deformation.

About seventy-five to eighty percent of all the patients with low back pain will respond to the extension and flexion programmes. These patients have a very good chance of becoming independent of therapists. They will be able to perform exercises to relieve themselves of pain without requiring techniques performed by specialist therapists. The remaining twenty to twenty-five percent of patients will require special techniques and manipulative procedures. The experienced practitioner will be able to identify these patients with a trial of test procedures carried out over a twenty-four hour period.

Hopefully at this stage we will be able to categorise patients into the appropriate syndrome and adopt a principle of treatment. We are now ready to teach the patient how to correct the posture, restore lost function and, where possible, reduce derangement himself.

I will proceed with a discussion of the procedures which may be used in treatment, as these will be frequently referred to in chapters to follow. Then I will consider the three syndromes and their respective treatment approaches individually.

Back Pain History

Taking an accurate history is the most important part of the initial consultation when one is dealing with any medical or surgical problem. Unfortunately, when the mechanical lesion is involved there is still lack of understanding regarding the nature of the questions that should be asked, the reasons for asking them, and the conclusions to be drawn from the answers.

I will set out step by step the stages that should be developed in history taking, and the questions that should be asked at each stage. Practitioners will already have their own method of history taking, and I do not suggest at all that they should alter their routine. However, I believe that the following questions must be included, if one is to reach a conclusion following the examination of patients with mechanical low back pain.


As well as the usual questions regarding name, age and address, one should enquire as to the occupation of the patient, in particular his position at work which provides us with the most important and relevant information. Managers are not always sitting down as we tend to believe, and postmen are not always walking.

Where is the present pain being felt?

We need to know all the details about the location of the pain, because this will give us some indication of the level and extent of the lesion and the severity of the condition. If there are any associated symptoms such as anaesthesia, paraesthesiae and numbness, their location must be noted as well. Referred pain indicates that derangement is likely.

Because the location of the pain can change rapidly and dramatically, we must find out if the pain has been present on the same site or sites since the onset. At this stage we must determine whether the symptoms are central, bilateral or unilateral in origin, as this is an important factor in the classification of the patient and consequently in his treatment. Bilateral symptoms indicate a central origin, whereas central symptoms cannot arise from a unilateral structure.

How long has the pain been present?

It is important to find out whether we are dealing with an acute, a subacute or chronic condition. In recurrent low back pain we are not interested in an answer based on the length of time since the first attack; at this stage of the examination we want to know how long the present episode has been evident.

If the symptoms have been present for any length of time, as is often the case, we must find out whether the patient feels that his condition is improving, stationary or worsening.

The length of time that the condition has been present may assist us to determine the stability of healing following a disc prolapse. It may also indicate the development of dysfunction which is likely to occur following trauma or derangement. The longer the symptoms have been present, the greater are the chances that adaptive changes have taken place.

The length of time that the patient has had symptoms can also guide us in deciding how vigorous we can be with our examining procedures. If a patient has had his symptoms for several months and has been able to work all this time, he will probably have placed more stress on the joints at fault than we are likely to do during the examination, which means that we can be fairly vigorous. If on the other hand the patient had a sudden onset of pain within the past two weeks, we could be dealing with a derangement situation and may well increase the degree of derangement with out test procedures which, if applied too vigorously, may significantly worsen the condition of the patient. Generally speaking, if the condition has been present only for a few days to two or three weeks, we must take great care in handling and exercising the patient; but if the present pain has been evident for months, we can be rather vigorous with our procedures.

How did the pain commence?

Basically we want to find out if there was an apparent or no apparent reason for the onset of the pain. Most of the histories commonly state that the pain appeared for no apparent reason. Two of every three patients fall into this category, and only one patient will recognise a causative strain.

If pain has arisen for an apparent reason a recognisable strain has caused the symptoms — for example, an accident, a sports injury, lifting. If the patient was involved in an accident — for example, if he were struck by a bus, — he may have sustained multiple injuries and the mechanics of none of these would be clear. This type of patient must be treated gently and with caution.

If pain has arisen for no apparent reason, a derangement or dysfunction has developed during the course of normal living usually without the application of any external force. Strains arising in this fashion can under most circumstances be avoided by modification of the patient’s daily living habits or movements. However, if the pain commenced for no apparent reason and is gradually and insidiously worsening, we may well suspect serious pathology, particularly if the patient feels or looks unwell at the time of interrogation. It is always better to suspect the worst and be wrong, than to overlook the worst and be wrong.

Careful evaluation of the patient’s information regarding the onset of his symptoms is necessary in order to avoid faulty conclusions. There are situations in which the patient thinks that his pain commenced for no apparent reason, whereas we may recognise a causative strain; alternatively the patient may wrongfully relate the onset to certain activities in an attempt to find a cause for his low back pain, which in fact appeared for quite different reasons.

Is the pain constant or intermittent?

This is the most important question we must ask patients with low back pain. If in patients referred for mechanical therapy the pain is found to be constant, it usually is produced by constant mechanical deformation. However, we must keep in mind that constant pain can also be caused by chemical irritation. Intermittent pain is always produced by mechanical deformation.

Constant chemical pain:

This is present as long as chemical irritants are present in sufficient quantities and occurs in inflammatory and infective disorders and in the first ten to twenty days following trauma. Chemical pain following trauma reduces steadily as healing takes place. Chemical irritants do not appear and disappear during the course of the day. Therefore, pain of chemical origin is always constant, and patients who describe periods in the day when no pain is present must have intermittent pain which is of mechanical and not of chemical origin.

Mechanical stresses that would normally be painless, can become painful where chemical irritation has raised the threshold of excitation of the nociceptive receptors. Thus, movements may superimpose mechanical forces on an existing chemical pain and enhance it, but they will never reduce or abolish chemical pain. This is significant in the differentiation between chemical and mechanical pain.

Low back pain caused by chemical irritation is comparatively easy to identify, as the pain is usually constant and no mechanical means can be found to significantly reduce it. Five days of treatment and observation should be sufficient to arrive at this conclusion.

Constant and intermittent mechanical pain:

This is present as long as mechanical stresses are sufficient to cause mechanical deformation. This type of pain will frequently reduce or even disappear when movements or positions are adopted that sufficiently reduce the mechanical stresses. On the other hand, the mechanical stresses may as easily be increased by movements and positions. Constant mechanical pain will vary significantly in intensity but never disappears, whereas intermittent mechanical pain appears and disappears according to circumstances.

Constant pain must be truly constant — that is, there is no time in the day when pain or aching is not present. Pain must be classified as intermittent even if there is only half an hour in the day when the patient feels completely painfree. In that half hour there is no mechanical deformation present, and we must examine the circumstances in which the patient is painfree and utilise this information for treatment purposes. It is much simpler to treat a patient who has intermittent pain than one whose pain is constant and in whom mechanical deformation is present under all circumstances.

It is my observation that about seventy percent of low back pain patients have intermittent pain, and the remaining thirty percent have truly constant pain. The majority of patients with constant mechanical pain are likely to belong to the derangement category. Derangement alters the tension in the structures about the segment involved, increasing mechanical deformation in some tissues and decreasing it in others. The constant increase in tension produces constant pain which continues, until the tension is decreased by reduction of the derangement or adaptive lengthening of surrounding tissues.

Intermittent pain is relatively easy to treat, because if there is one hour in the day when no mechanical deformation is present, it is possible to gradually extend that painfree time period. Constant pain is rather a different problem and is more difficult to treat. The percentage of patients failing to respond to treatment is higher in the constant pain group than in the intermittent pain group. Generally speaking, the derangement syndrome can be associated with constant pain, whereas the postural and dysfunctional syndromes are characterised by intermittent pain.

What makes the pain worse? and What makes the pain better?

We must specifically ask about sitting, standing, walking, lying, and activities which involve stooping or prolonged stooping. In these positions the joint mechanics of the lumbar spine are relatively well understood, and therefore we will be able to determine which situations increase and which decrease mechanical deformation. We must carefully record any position or activity reported to reduce or relieve the pain, as we will utilise this information in our initial treatment.


In relaxed or prolonged sitting the lumbar spine falls into full flexion, the effects of which are described in detail elsewhere. If a patient tells us that sitting increases his symptoms, we know that sustained flexion causes mechanical deformation of his lumbar spine. But if a patient finds relief in sitting, flexion actually reduces the mechanical deformation.


Standing, expecially relaxed standing, places the lower lumbar spine in full end range extension which means that certain structures are on full stretch. If a patient tells us that he is worse in relaxed standing, sustained maximum extension produces mechanical deformation of his lower lumbar spine. But if a patient finds relief in relaxed standing, sustained maximum extension reduces the mechanical deformation.


Walking accentuates extension — that is, it further increases the lordosis of the lumbar spine as the hind leg by its backward movement brings the pelvis into forward inclination. If walking produces or increases pain, extension must produce or increase mechanical deformation of the lower lumbar spine. But if the patient has no pain in walking, extension is reducing the mechanical deformation.


There are basically three positions which may be adopted while lying: prone, supine and side lying. The many variations of these, caused by different leg positions, make evaluation of the effects of lying rather difficult. Apart from the lying position itself, the effects on the lumbar spine depend on the nature of the surface on which one lies — usually the mattress and its supporting base — which may be firm and unyielding, or soft and giving.

The effects of the three basic positions on the lumbar spine can be summarised as follows:

  • (a) In lying supine on a firm surface the lumbar spine falls into extension, whereas on a soft surface the degree of extension is decreased and in some cases flexion may be produced.
  • (b) In lying prone on a firm as well as a soft surface the lumbar spine is always placed near or at full end range of extension.
  • (c) In side lying the lumbar spine is brought into side gliding towards the side one is lying on, more so when on a soft surface than on a hard surface.

Activities which involve bending:

In bending or prolonged bending the lumbar spine falls into full flexion and added to this are gravitational stresses. If, for example, gardening produces pain, sustained flexion must produce mechanical deformation of the lumbar spine.

But if the pain is reduced while gardening, sustained flexion stops the mechanical deformation.

Patients who have had pain for a long time, may have difficulty in determining what makes their pain better or worse. They are no longer able to observe objectively their own pain patterns because of the length of time the pain has been present. It is necessary to spend extra time to extract detailed information regarding the pain behaviour, because without this we cannot proceed to an adequate conclusion and appropriate treatment.

Occasionally a patient will tell us that there is no position or movement which affects the pain. In this case the information obtained from the history is insufficient, and during the examination we must try to produce a change in the patient’s symptoms by utilising extremes of movement or sustained positions.

Have there been previous episodes of low back pain?

We should enquire about the nature of any similar or other low back pain episodes, the time span over which they occurred, and their frequency. At this stage we should also find out about previous treatments and their results. Episodic history indicates derangement. Dysfunction is likely to develop insidiously after each episode and will now coexist but be masked by the present disturbance. Its presence will be revealed after resolution of pain resulting from the derangement.

Further questions

  • pain on cough / sneeze?
  • disturbed sleep?
  • pain on arising in the morning?
  • recent X-Rays? — results?
  • on medication at present?
  • on steroids, in past or at present?
  • general health? — recent weight loss?
  • major surgery or accident, recently or previously?
  • saddle anaesthesia? — bladder control?

Information gained from these questions may complete the picture of the condition we are dealing with. The reasons for asking these questions are obvious and straight forward, and they will not be discussed in detail.

Although the referring medical practitioner will almost certainly have excluded any serious or unsuitable pathology, we must remain alert for its presence.

Back Pain. Diagnosis


The therapist is part of the team involved in the treatment and rehabilitation of patients suffering low back pain. In some countries manipulative therapists are primary contact practitioners. Consequently, their diagnostic skills have greatly improved, enabling them to define which mechanical conditions can be helped by mechanical therapy and to separate these conditions from the nonmechanical lesions which have no place in the therapy clinic.

However, differential diagnosis is really not within the scope of manipulative therapy. It is my view that differential diagnosing by medical practitioners is necessary to exclude serious and unsuitable pathologies from being referred for mechanical therapy. In making diagnoses the manipulative therapist should confine himself to musculo-skeletal mechanical lesions. Specialised in this field, he is usually able to make far more accurate diagnoses than most medical practitioners. As the manipulative therapy profession gains international respect, we may soon see the day that this specialisation becomes generally accepted.


In the low back mechanical diagnosis is extremely difficult. As yet, no means have been devised which enable us to selectively stress individual structures and identify the source of many pains. As Nachemson states, there is only one condition which allows a fairly confident diagnosis to be made:

“the patient with sciatica caused by sequestration from the disc which impinges on a nerve root. Such patients, though, represent only a small proportion of those who have low back pain problems, and constitute at most only a few percent.”

This means that perhaps as many as ninety percent of patients cannot be diagnosed in a very specific manner. Various authorities have stated that in many instances it is impossible to define the exact pathological basis for low back pain and, consequently, to achieve a precise diagnosis. Nachemson has said:

“No one in the world knows the real cause of back pain and I am no exception.”

When authorities such as these clearly state that the problems surrounding specific diagnosis of low back pain are insurmountable, it seems that the time has come to alter the rules of the game. Instead of aiming for a specific diagnosis based on a particular pathology, we must apply an alternative system of assessment. This can be used until further development of our knowledge and diagnostic procedures enables us to become more specific.

In order to analyse mechanical low back pain and categorise the symptoms a new approach is necessary. I believe we have a means of overcoming the present diagnostic impasse. If mechanical pain is caused by mechanical deformation of soft tissues containing nociceptive receptors, we must confine our diagnosis within this framework.


All spinal pain of mechanical origin can be classified in one of the following syndromes:

The postural syndrome:

This is caused by mechanical deformation of soft tissues as a result of postural stresses. Maintenance of certain postures or positions which place some soft tissues under prolonged stress, will eventually be productive of pain. Thus, the postural syndrome is characterised by intermittent pain brought on by particular postures or positions, and usually some time must pass before the pain becomes apparent. The pain ceases only with a change of position or after postural correction.

The dysfunction syndrome:

This is caused by mechanical deformation of soft tissues affected by adaptive shortening. Adaptive shortening may occur for a variety of reasons which will be discussed later. It leads to a loss of movement in certain directions and causes pain to be produced before normal full range of movement is achieved. Thus, the dysfunction syndrome is characterised by intermittent pain and a partial loss of movement. The pain is brought on as soon as shortened structures are stressed by end positioning or end movement and ceases almost immediately when the stress is released.

The derangement syndrome:

This is caused by mechanical deformation of soft tissues as a result of internal derangement. Alteration of the position of the fluid nucleus within the disc, and possibly the surrounding annulus, causes a disturbance in the normal resting position of the two vertebrae enclosing the disc involved. Various forms and degrees of internal derangement are possible, and each presents a somewhat different set of signs and symptoms. These will be discussed later. Thus, the derangement syndrome is usually characterised by constant pain, but intermittent pain may occur depending on the size and location of the derangement. There is a partial loss of movement, some movements being full range and others partially or completely blocked. This causes the deformities in kyphosis and scoliosis so typical of the syndrome in the acute stage.

The three syndromes presented are totally different from each other, and each syndrome must be treated as an entity on its own, requiring special procedures which are often unsuitable for the other syndromes. In order to identify which syndrome is present in a particular patient a history must be established and an examination must be performed.


The Intervertebral Disc


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

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

The annulus fibrosus

Fig. The annulus fibrosus.

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

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

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

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


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

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


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

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

The nucleus pulposus with the spine in neutral position

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

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

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


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

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

Compression loading of the disc

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

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

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

Development of disc protrusion

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


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

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

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

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

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

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

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

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

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

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

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


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

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

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

Posterior or postero-lateral herniation of the nucleus pulposus

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

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

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

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

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

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


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

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

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

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

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

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

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


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

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

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

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

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

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

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


Patients with mild or diet-controlled diabetes may have fasting blood glucose levels within the normal range, but be unable to produce sufficient insulin for prompt metabolism of ingested carbohydrate. As a result, blood glucose rises to abnormally high levels and the return to normal is delayed. The glucose tolerance test detects a patient’s decreased tolerance for glucose, and is most helpful in establishing a mild case of diabetes. The GTT is a timed test of blood and urine that determines the rate of removal of a concentrated dose of glucose from the bloodstream. In the healthy person, the insulin response to an oral dose of glucose is almost immediate, peaking in 30-60 minutes and returning to normal within 3 hours. Testing is usually done in the morning after an overnight fast.

Patient Preparation

  1. The patient should be placed on a diet containing 1.75 grams of carbohydrate per kilogram of body weight for 3 days preceding the test. If carbohydrate intake has been too low preceding the test, a false diabetic-type curve may result. Drugs that may influence the test should be discontinued for 3 days before the test. Such drugs may include hormones, salicylates, diuretic agents, and hypoglycemic agents.
  2. The test should be performed in the morning, and the patient must abstain from eating or drinking anything except water for 8 hours prior to the test. The patient must remain fasting for the duration of the test.
  3. The patient should remain at rest during the test and refrain from smoking or chewing gum.

PROCEDURE: Procedure for Glucose Tolerance Testing

  1. Draw a fasting blood glucose sample of venous blood. Also collect a fasting urine sample before proceeding with the test. Label the blood and urine samples with the patient’s name, identification number, date, time, and phlebotomist initials. Write “Fasting” on the urine and blood samples.
  2. Perform a rapid glucose test on the fasting sample. If the result is >140 mg/dL, delay proceeding with the test until a pathologist has been consulted.
  3. Give the patient a glucose loading dose based on the following:
    • a. Nonpregnant females and males over 100 lbs: 75 grams glucose.
    • b. Pregnant females: 100 grams glucose.
    • c. Patients under 100 lbs: 1.75 grams glucose per kilogram body weight.
  4. Blood and urine specimens are collected at 1 hour, hour, 2 hours, 3 hours, etc, depending upon the physician order post- glucose ingestion. The glucose dose should be ingested within 5 minutes.
Blood culture collection procedure


Blood cultures are ordered by physicians to rule out or confirm septicemia, a condition in which a microorganism has invaded the bloodstream. This condition can lead to the death of a patient.

The correct collection of blood cultures is extremely important. Because the results of these cultures lead to the identification of the condition’s origin, or etiology, the phlebotomist plays a very significant role in ensuring the accuracy of this important test.

Blood cultures are usually ordered just before the beginning of anti-microbial therapy in a series of three draws. The cultures are collected in a series of three because that makes it more likely that the organism will be detected. In some cases it may be possible that the septicemia is caused by a localized infection. If this is suspected, the physician will order the series to be collected all at one time but from three different sites, rather than at three different times.

Blood cultures are drawn in sets of two bottles. One bottle is the aerobic bottle for those microorganisms that require oxygen to grow. The second bottle is called an anaerobic bottle for microorganisms requiring the absence of oxygen to grow. Please refer to Figure.

Blood culture collection procedure

Figure. Blood culture collection procedure. (A) Assemble blood culture collection supplies. (B) Prep venipuncture site with povidone-iodine in circular motion. (C) Perform venipuncture.

PROCEDURE: Procedure for Blood Culture Collection

  1. Identify the patient.
  2. Select a site, and follow routine venipuncture procedure. Venipuncture sites do have an effect on the contamination rate among blood cultures. The antecubital vein is less likely to produce a contaminated specimen than the umbilical or femoral vein. Also, indwelling intravascular catheters are poor sources for blood culture collections. These lines become colonized with bacteria when left in place for longer than 48 hours. If a blood culture is obtained from an indwelling line, the femoral vein, or the umbilical vein, the source must be documented to ensure proper interpretation of test results.
  3. Assemble the necessary equipment: culture bottles, commercial prep kit, alcohol preps, syringes, needles, gauze, tourniquet, gloves (refer to Figure A).
  4. Reject any damaged or deteriorated culture vials.
  5. Prepare the container(s). Swab the rubber stopper or diaphragm top of the culture bottle(s) with an antiseptic agent (iodine is not recommended for swabbing a rubber stopper). The stoppers may be contaminated and must be aseptically prepped.
  6. Put on gloves.
  7. Prep the venipuncture site. To aseptically prep a venipuncture site, 1 to 2 minutes must be allowed for the agent to have any effect. Scrub a 3- to 4-inch-square area for 2 minutes with a commercially prepared prep kit (Figure 7-2B). Allow the site to air-dry. Good technique requires that the puncture site not be repalpated. If absolutely necessary, the fingertip of the glove must be prepped in the same manner as the venipunc- ture site.
  8. Apply the tourniquet, being very careful not to touch the puncture site with the tourniquet.
  9. Perform the venipuncture and draw the appropriate volume of blood (Figure C).
  10. Release the tourniquet.
  11. Remove the needle and apply pressure to the venipuncture site with gauze.
  12. If using needle and syringe, discharge any air that may have entered the syringe prior to injection. This allows the appropriate volume of blood to be added to the bottle.
  13. Dispose of the needle appropriately in a sharps disposal unit.
  14. Replace the needle with a safety transfer device.
  15. Inoculate culture bottle(s) by adding the correct amount of blood. If too much blood is added, clotting may occur, impairing the recovery of bacteria. 
  16. Specimen requirements: 8 to 10 mL of blood should be injected into each culture vial. Fill the anaerobic bottle first. If using a winged blood collection set, fill the aerobic bottle first. The air in the tubing will prevent the growth of anaerobic organisms. Use a safety transfer device that pierces the stoppers of the blood culture bottles. If a fungus culture is ordered, 8 to 10 mL of blood is injected into the fungus culture vial.
  17. Discard the needle and syringe in appropriate disposal units.
  18. Label the specimens. Each label should include the site used for collection and the number of the sample, time collected, and phlebotomist’s initials.
  19. Remove and discard gloves in the appropriate container.
  20. Wash hands.
  21. Transport the specimens to the testing area.
Heelstick procedure for newborn screening


The purpose of routine newborn screening is to diagnose shortly after birth those infants with metabolic disorders for which early treatment will prevent or minimize serious, irreversible complications such as mental retardation. Newborn screening is cost-effective within the health care system, and can screen infants on a large scale. The tests that comprise the battery may vary from state to state. However, phenylketonuria and hypothyroidism testing are required in all states. These tests require blood collected from a heelstick onto filter paper.

Phenylketonuria (PKU) Screening

PKU is an inherited disorder of body chemistry that, if untreated, causes mental retardation. About one baby in 15,000 is born with PKU in the United States. The disorder occurs in all ethnic groups, but is most common in people of northern European descent.

PKU is a disease that affects the way the body processes food. Babies with PKU can’t process an amino acid called phenylalanine, which is necessary for metabolizing protein. The phenylalanine builds up in the bloodstream and causes brain damage and mental retardation.

PKU was first recognized in 1934 by a mother of two mentally retarded children. She became aware that the urine of the children had an odd odor, and on the basis of this was able to have a biochemist, Dr. Asbjorn Folling, study the urine and identify phenylpyruvic acid. A test developed in the 1960s by the March of Dimes is used to screen for PKU. A blood specimen should be obtained from every neonate before the baby is discharged or transferred from the nursery. Any premature infant should have a specimen obtained for screening at or near the seventh day of age. Premature infants, infants weighing less than 11 kg (5 lb), may have elevated phenylalanine and tyrosine levels without having the genetic disease. This is probably a result of delayed development of appropriate enzyme activity in the liver. The test is highly accurate when performed when the baby is more than 24 hours but not more than 7 days of age. The child has to have a chance to ingest protein (mild) for a period of 24 hours. All states now routinely screen newborns for PKU.

Mental retardation can be prevented if the baby is treated with a special diet that is low in phenylalanine beginning before the fourth week of life. In a positive test for PKU, the blood phenylalanine is greater than 15 mg/100 mL. Testing should continue throughout an adult’s life, and a diet low in protein maintained.


Hypothyroidism results from an inadequate supply of the thyroid hormone, thyroxine. Approximately one out of every 4,000 newborn infants has hypothyroidism. Untreated, the child’s growth will be stunted, and mental retardation will occur from lack of stimulation of the brain by the hormone thyroxine. Testing for hypothyroidism uses the same filter paper blood spots as for PKU screening. The condition is treated by utilizing thyroid hormone replacement treatment as soon as possible after birth.

PROCEDURE: Newborn Screening Procedure for Filter Paper Collection

  1. Identify the baby.
  2. Complete information on the specimen collection kit. Do not touch the area within the circles on the filter paper.
  3. Assemble supplies.
  4. Put on gloves.
  5. Warm the heel. A warm, moist towel at a temperature no higher than 42°C (107.6°F) may be used to cover the site for 3 minutes.
  6. Cleanse the heel with alcohol swab.
  7. Air-dry the site, or wipe with dry sterile gauze.
  8. Hold the infant’s leg in a position lower than the heart. 
  9. Puncture the heel with an automated lancet device to a depth of no more than 2.4 mm on the plantar surface of the heel. 
  10. Wipe away the first drop of blood.
  11. Dispose of lancet into sharps container.
  12. Touch a large drop of blood against the filter paper within the circle. A sufficient amount of blood should soak through to fill the circle. Apply blood to only one side of the paper. Ensure that the blood has penetrated and saturated the paper. Do not layer successive drops of blood on the circle spot. Do not touch the blood spot.
  13. Gently apply pressure with your thumb to form an additional drop of blood. Fill each circle. Do not squeeze the puncture. Doing so may cause hemolysis of the specimen and add tissue fluids to the specimen.
  14. After the circles are filled, elevate the infant’s foot, and press a sterile gauze against the puncture site. Please refer to Figure B.
  15. Do not apply adhesive bandage.
  16. Allow the blood spots to air-dry in a horizontal position. Keep away from direct sunlight. Do not stack or touch other surfaces to the filter paper during the drying process.

Heelstick procedure for newborn screening

Figure. Heelstick procedure for newborn screening. (A) Appropriate puncture site. (B) Apply drops of blood to circle on newborn screening card.

Movements at the lumbosacral junction

Lumbosacral junction

Movement here is restricted to flexion and extension, and a small degree of lateral flexion. In flexion the inferior articular processes of L5 glide upwards over those on the sacrum, with movement being limited by tension in tlie iliolumbar, inter- and supraspinous ligaments and the postvertebral muscles. Backward and downward gliding of the L5 articular processes on those of the sacrum during extension is arrested by apposition of the spines of L5 and SI.

Movements at the lumbosacral junction

Figure. (A) Movements at the lumbosacral junction, (B) the forward displacement of L5 in spondylolisthesis.

The intervertebral disc between L5 and SI is markedly wedged, being thicker anteriorly, and is mainly responsible for the angulation between the lumbar and sacral parts of the vertebral column. Because the lumbosacral junction represents the transition between the mobile (lumbar) and immobile (sacral) parts of the vertebral column, it requires considerable support against potentially damaging stresses. To this end the postvertebral muscle mass is extremely thick in this region, reinforced posteriorly by the lower part of the strong thoracolumbar fascia. It is also worth noting that between L5 and SI the intertransverse ligaments have been replaced by the much stronger iliolumbar ligaments, which confer additional stability upon this region by restricting lateral flexion. The zygapo-physeal joints between L5 and SI have an important weight-bearing function. Occasionally, there is incomplete development of the neural arch of the fifth lumbar vertebra anterior to the inferior articular processes, which may allow separation of the body of L5 from the posterior part of the neural arch. The result is that the body of the fifth lumbar vertebra, together with the trunk above, slides forward and downwards towards the pelvis, leaving the posterior part of L5 behind articulating with the superior sacral articular processes and tethered by the iliolumbar ligaments. The condition is known as spondylolisthesis. The marked angulation at the lumbosacral junction assists this downward and forward movement. The lumbar curvature is accentuated, and the performance of extension exercises is usually extremely painful and dangerous because of the tension on the nerves forming the cauda equina, leading to motor and sensory disturbances along their distribution.