THE NOCICEPTIVE RECEPTOR SYSTEM
Most tissues in the body possess a system of nerve endings which, being particularly sensitive to tissue dysfunction, may be referred to as nociceptive receptors. The free nerve endings of the nociceptive system provide the means by which we are made aware of pain.
Wyke describes the distribution of the nociceptive receptor system in the lumbar area: it is found in the skin and subcutaneous tissue; throughout the fibrous capsule of all the synovial apophyseal joints and sacro-iliac joints; in the longitudinal ligaments, the fiaval and interspinous ligaments and sacro-iliac ligaments; in the periosteum covering the vertebral bodies and arches, and in the fascia, aponeuroses and tendons attached thereto; and also in the spinal dura mater, including the dural sleeves surrounding the nerve roots.
The nociceptive innervation of the spinal ligaments varies from one ligament to another. The system is found to be most dense in the posterior longitudinal ligament, less in the anterior longitudinal ligament and sacro-iliac ligaments, and least in the fiaval and interspinous ligaments. This would suggest, that the posterior longitudinal ligament is more sensitive than the anterior ligament, and that the fiaval and interspinous ligaments are least sensitive of all. Irrespective of this suggestion it is significant that the ligament which is most richly endowed with free nerve endings, is situated immediately adjacent to the only vital structures in the area — that is, the nerve roots and the spinal cord.
Although there is disagreement on the topic, Wyke states that the intervetebral disc contains no free nerve endings either in the nucleus or in the annulus. However, there are some nerve endings in the fibro-adipose tissue, that binds the posterior longitudinal ligament to the posterior portion of the annulus. Wyke states:
“The only place where a nociceptive receptor system is directly related to the intervertebral discs is at the point where the discs (through the annulus fibrosus) are attached to the posterior longitudinal ligament; and the receptor system is not, in fact, in the disc itself, but in the surrounding connective tissue that links the disc to the posterior longitudinal ligament.”
The wide distribution of the nociceptive receptor system in the lumbar area would make it difficult to devise testing procedures which selectively stress individual components of the spinal segments.
Mechanism of pain production
Again I must quote Wyke who states that there are only two possible causes of pain. The following concept is most fundamental and essential in the understanding of the mechanism of pain production:
“In normal circumstances this receptor system (that is, the nociceptive receptor system — Author’s addition) is relatively (although not entirely) inactive; but its afferent activity is markedly enhanced when its constituent unmyelinated fibres are depolarised by the application of mechanical forces to the containing tissues that sufficiently stress, deform or damage (Author’s italics) it (as with pressure, distraction, distension, abrasion, contusion or laceration) or by their exposure to the presence in the surrounding tissue fluid of sufficient concentration of irritating chemical substances that are released from traumatised, inflamed, necrosing or metabolically abnormal (and especially ischaemic) tissues.”
Chemical cause of pain
Pain is produced by chemical irritation as soon as the concentration of chemical substances is sufficient to irritate free nerve endings in the involved soft tissues. This is of lesser interest to us as it encompasses either inflammatory or infective processes, such as active rheumatoid arthritis, ankylosing spondylitis, tuberculous and other bacterial infections. However, it also occurs in the first ten to twenty days following trauma. This will be discussed later.
Mechanical cause of pain
Pain is produced by the application of mechanical forces as soon as the mechanical deformation of structures containing the nociceptive receptor system is sufficient to irritate free nerve endings. It is not necessary to actually damage tissues containing the free nerve endings in order to provoke pain. Pain will also be produced by the application of forces sufficient to stress or deform the ligamentous and capsular structures. Pain will disappear when the application of that force is terminated, and this often occurs by a mere change of position. A good example is the pain, incurred during prolonged sitting which disappears on standing up.
Another simple example of mechanical articular pain is readily at hand. Bend your left forefinger backwards, using your right forefinger to apply overpressure. Keep applying this pressure until the nociceptive receptor system indicates its enhanced active state by the arrival of pain. This is simple mechanical deformation of pain sensitive structures. If you bend the finger backwards further, the intensity of the pain will increase; and if you maintain the painful position longer, the pain will become more diffuse, widespread and difficult to define. Thus, pain alters with increasing and prolonged mechanical deformation. If you now slowly return the finger to its normal resting position, the pain will disappear. This example has one significant implication: the finger is obviously being moved in the wrong direction as the pain increases, and in the correct direction as the pain decreases.
When the finger is used as an example the mechanism of pain production is easy to understand. But the same idea applied to the spine is more difficult to accept. In the spine the same mechanism is involved, but there are more structures which may give rise to pain and the mechanics are more complicated. Let us return to the forefinger once more. Bend the finger backwards until you feel pain and then release it suddenly. The pain ceases at once. What was the pathology in the finger at the moment the pain appeared? What is the pathology now that the stress is released? Of course, the answer is that no pathology need exist at all under these circumstances. The sensation of pain does not depend on the existence of pathology. The example cited above is one of the most common causes of articular pain in man. The intermittent pain was produced by mechanical forces sufficient to stress or deform the nociceptive receptor system; the activity of the system was merely enhanced by the application of the stress, and as soon as the stress was withdrawn the activity returned to its normal rest level. Intermittent low back pain is frequently caused in this manner. No chemical treatment will rectify or prevent pain arising from mechanical deformation. When intermittent mechanical pain is the main presenting symptom, drugs should never be the treatment of choice, except in the presence of extreme pain.
Trauma as a cause of pain
Pain due to trauma is produced by a combination of mechanical deformation and chemical irritation. Initially, mechanical deformation causes damage to soft tissues, and pain of mechanical origin will be felt. In most instances this is a sharp pain. When in the lumbar spine mechanical deformation is severe enough to traumatise soft tissues, it is usually the result of an external force — for example, a fall from a ladder, a motor vehicle accident, a sudden unexpected step from the pavement, or a kick in the back during football.
Shortly after injury, chemical substances accumulate in the damaged tissues. As soon as the concentration of these chemical irritants is sufficient to enhance the activity of the nociceptive receptor system in the surrounding tissues, pain will be felt. In most instances pain of chemical origin will be experienced as a persistent discomfort or dull aching as long as the chemicals are present in sufficient quantities. In addition, the chemical irritants excite the nociceptive receptor system in such a way that the application of relatively minor stresses causes pain which under normal circumstances would not occur. Thus, at this stage there is a constant pain, possibly a mild aching only, which may be enhanced but will never reduce or cease due to positioning or movement.
The reaction of the body to trauma is to institute processes of repair, and the application of mechanical treatment should not be so vigorous as to delay healing. I believe that strenuous mechanical therapy in the presence of constant chemical pain merely delays recovery, and if the condition appears to improve while such treatment is given, improvement must take place in spite of it.
Over a period of five to twenty days healing occurs slowly and develops with the passage of time. Relative immobilisation of the damaged structures allows scarring to take place, and as scarring increases the concentration of chemical irritants decreases. In the later stages of healing when movements are performed more willingly, dysfunction caused by contraction and adaptive shortening of scar tissue will be exposed. Thus, after two to three weeks the constant pain due to chemical irritation will have disappeared and is replaced by intermittent pain felt when adaptively shortened tissues are stretched.
Causes of mechanical deformation
Mechanical deformation is caused by mechanical stress which, when applied to soft tissues, will lead to pain under certain circumstances. The following situations are possible:
- Normal stress applied to normal tissue will not immediately produce pain.
- Abnormal stress applied to normal tissue may produce pain without causing damage. This occurs in pure postural pain. Postural stresses, although normal when applied for short periods, become abnormal when sustained for long periods. Abnormal stress applied to normal tissue and resulting in damage will produce pain. This occurs in trauma.
- Normal stress applied to abnormal tissue will produce pain. The normal stress of the end range of movement, although painless in normal tissues, becomes painful in the presence of tissue abnormalities, especially in adaptive shortening.
- Abnormal stress applied to abnormal tissue will produce pain — for example, prolonged bending or sitting applied to adaptively shortened scar tissue may readily distort the tissue and be productive of pain. Reversal of the stressful position will result in reduction of pain. A similar stress applied to normal tissue is much less likely to cause pain.
Mechanical stresses sufficient to cause pain are usually created either by postural distortion or by abnormal forces applied to the stationary or moving body.
These are, according to Wyke, by far the most often encountered and their importance is generally underestimated:
“Thus, although the fact has been demonstrated repeatedly over the past twenty-five years, it is still not sufficiently appreciated by the generality of doctors that much of the static postural support for the lower spine in the erect, sitting and fully flexed positions of the body is provided by the passive elastic tension of the ligaments and aponeuroses attached thereto, rather than by neurologically-engendered motor unit activity in the paravertebral musculature. As these connective tissues are richly innervated by nociceptive nerve endings, it will be clear that backache is readily produced from these tissues when they are subjected to abnormal mechanical stresses (as by prolonged standing, especially while wearing high heeled shoes; by persistantly distorted postures in occupational circumstances, or as a result of structural abnormalities of the vertebral column; or by attempts to lift or support heavy weights), or when their elasticity is decreased (as it inevitably is with advancing age, or as a result of hormonal changes)”.
When a relaxed position is assumed for more than a few minutes, the muscular control required to hold the individual in that particular position diminishes, the body sags and the support is derived from the ligaments. Essentially the muscles relax slowly in order to relieve themselves of the burden of opposing gravity or any other forces at work. In the fully relaxed position, muscular activity stops and the stresses are transferred to the ligaments. The inherent elastic property of the ligaments is sufficient to support most positions with almost nil activity from the surrounding musculature. The ligaments are bearing nearly the entire load, which in the low back consists of the weight of the body above the level concerned. This process is a gradual one, occurring unconsciously over several minutes and varying in time for each individual.
The positions which most commonly stress the low back are the various forms of flexion. When the ligaments are positionally loaded, a constant mechanical stress is being applied to them. In situations of prolonged flexion the posterior ligamentous structures are likely to become elongated and overstretched, which may cause sufficient stress to trigger and fire the nociceptive receptor mechanism. Prolonged stooping, bending and sitting place the low back into prolonged full flexion and are recognised as circumstances which often enhance low pack pain. Andersson et al. have described how the myoelectric activity of the back muscles reduces once the ligaments are providing the support in sitting. We can assume safely that this is also the case in prolonged stooping and bending.
It is clear that purely postural or positional mechanisms may produce pain. Thus, frequently low back pain is caused or enhanced by overstretching of ligamentous structures brought about by positions of prolonged flexion. It is my opinion, that all low back pain includes elements of postural stress. Without removing these postural stresses the low back pain patient is doomed to perpetuate his suffering. The importance of the factors, described by Wyke, has not been understood fully by the medical and physiotherapy professions. These factors can nearly all be dealt with by example and education.
Abnormal forces during movement are the cause of most other mechanical back pains. The abnormal forces are most commonly found when heavy loads are manually controlled or when comparatively light weights are handled in great numbers and frequency. Activities involving sudden unexpected movements, such as football, cricket, tennis, athletics, and gymnastics, may sometimes cause enough mechanical stresses to produce low back pain.
A popular misconception
Patients with low back pain commonly complain that their symptoms are worse as a direct result of certain activities. On questioning a patient he will state that his low back has become painful, because he played tennis or football or due to some other activity. He was symptom free prior to and during the exertion, and the pain commenced following the exertion. The immediate and generally accepted conclusion is that the activity was in some way harmful to the patient, and the actual exertion has produced significant pain.
When pain is experienced not during but following exertion, it is not often the exertion itself that is responsible for the pain. Mechanical deformation must have occurred in the period following the activity. In the majority of cases the position adopted by the patient while relaxing after activity is responsible for the onset of low back pain. It must be emphasised that mechanical deformation produced during and as a result of activity will be apparent during the performance of the activity. The patient may not necessarily feel pain at the time, but usually he will be aware of some damaging sensation.