The intervertebral disc has special biomechanical requirements. It is strong to sustain weight and transmit loads while being able to deform to adjust to movement. The intervertebral disc has three parts: a central nucleus pulposus surrounded by a peripheral annulus fibrosus which blends above and below into vertebral end-plates.

The nucleus pulposus accommodates to movement and transmits compressive loads from one vertebral body to another. Its normal consistency has been likened to that of toothpaste. It is composed of irregularly arranged collagen fibres and cartilage cells scattered within amorphous ground substance. The collagen fibres are composed of type II collagen, suited to accept pressure and compression (see Ch. 2). The nucleus in particular has great water-binding capacity through its proteoglycan content. The fluid nature of the nucleus allows it to deform under pressure while the vertebral end-plates prevent its superior and inferior deformation. In this way the intervertebral disc supports and transmits loads.

Although it has long been recognized for its fluid properties, the nucleus also behaves as a viscoelastic solid under dynamic conditions. Iatridis et al (1996) investigated the viscoelastic properties of the healthy nucleus pulposus, showing it to be sensitive to different loading rates. The higher loading rates produced failure of the end-plate and vertebral body, while slower loading rates produced progressive failure of the annulus and disc herniation.

The annulus fibrosus consists of a geometrically organized arrangement of collagen and elastic fibres bound together by a proteoglycan gel, allowing it to support weight without buckling. Types I and II collagen exist in the annulus fibrosus, but the majority of fibres are type I, suited to withstand tensile forces. The fibres are arranged in concentric lamellae around the central nucleus. These tightly packed lamellae are arranged circumferentially at the periphery and can sustain high compressive loads. Adams et al (2002) suggest an analogy to the stiffness of a telephone directory rolled into a cylinder and stood on its end. In each lamella, the collagen fibres lie parallel to each other, inclined at an angle of approximately 65–70° to the vertical (Fig. 13.2). The direction of fibres alternates in adjacent lamellae (Bogduk 2005). Marchand & Ahmed (1990) noted a number of irregularities within the laminate structure of the annulus, particularly at the posterolateral corners, where a number of incomplete layers were seen. Increased stresses applied to the annulus in this region could produce fissuring and provide the nuclear material with an escape route.

The annulus fibrosus acts like a ligament, restraining excessive movement to stabilize the intervertebral joint while allowing flexibility to permit normal movement. The alternating oblique annular fibres resist horizontal and vertical forces, allowing the annulus to oppose movement in all directions (Bogduk 1991).

The outer half of the annulus at least is known to have a nerve supply (Cavanaugh et al 1995, Coppes et al 1997). The main source of the supply is believed to be the sinuvertebral nerve and branches of the sympathetic trunks and its grey rami communicantes (Adams et al 2002) (Fig. 13.3). The sinuvertebral nerve supplies the disc at one level and the disc above (Bogduk 2005).

The vertebral end-plates are thin layers of cartilage, approximately 1 mm thick, covering the superior and inferior surfaces of the discs. They form a permeable barrier for diffusion, mainly between the nucleus and the cancellous bone of the vertebral bodies. They fail relatively easily under excessive compressive loading.

The zygapophyseal joints are synovial joints that provide stability of the spine, control of movement and protection of the intervertebral discs (Fig. 13.5) (Taylor & Twomey 1994). The articular facets are covered with articular cartilage and the joints are surrounded by a fibrous capsule and lined with synovium. The superior articular facets face posteromedially and grasp onto the inferior articular facets of the vertebra above, which face anterolaterally. The resultant plane of the joint facilitates flexion and extension movements, but prevents rotation. It also restricts translation in healthy joints, helping to protect the lumbar disc from the shearing forces responsible for fissuring (Bogduk 1991, Taylor & Twomey 1994).

The fibrous capsule consists of an outer layer of regularly arranged connective tissue and an inner layer of yellow elastic fibres. Anteriorly the capsule is replaced by the ligamentum flavum, while some of the deep fibres of multifidus give the capsule reinforcement medially (Yamashita et al 1996). The superior and inferior aspects of the capsules are loose and contain intra-articular structures consisting of fat and meniscoid structures (Bogduk 2005). Fine nerve fibres thought to conduct nociceptive and proprioceptive sensations have been found (Yamashita et al 1996).

The zygapophyseal joints cannot be discounted as a cause of back pain since, as synovial joints, they may be subjected to trauma or arthritis. Degenerative changes usually coexist in the intervertebral joint of the same segment.

Authors have looked at the pattern of pain referral of the zygapophyseal joints in an attempt to establish a recognized syndrome and pain referral patterns (Mooney & Robertson 1976, Bogduk 1994). Schwarzer et al (1994a) acknowledged this joint as a possible source of pain, but questioned the existence of a facet syndrome. Some authors suggest that the zygapophyseal joint is responsible for the acute locked back, as the intra-articular structures become trapped between the articular surfaces (Twomey & Taylor 1994, Bogduk 2005), while Kuslich et al (1991) demonstrated that stimulation of the zygapophyseal joint capsule very rarely generates leg pain. In a study of the relative contributions of the disc and zygapophyseal joint in chronic low back pain, pain was noted to arise more commonly from the disc than the zygapophyseal joint (Schwarzer et al 1994b).

Laslett & van Wijmen (1999) suggest that the symptomatic zygapophyseal joint presents with pain that settles well on lying down and four of the following criteria: age greater than 65; pain not increased by coughing; no pain on flexion in standing; pain not increased in rising from flexion; pain not increased by extension/rotation; or pain not increased by extension in standing.

The authors of this text accept the lack of evidence to attribute the cause of low back pain to one specific structure and that will also apply to the symptomatic zygapophyseal model presented above. Orthopaedic medicine treatments have traditionally been based on the discal model but it may be more clinically relevant to apply treatments selected on the basis of a particular set of signs and symptoms rather than to attempt to be too pedantic with regard to pathology (see below). It must be acknowledged that a lesion in any structure within a spinal segment will influence neighbouring structures and similarly treatment cannot be directed to one anatomical structure in isolation.

Anterior and posterior longitudinal ligaments are well developed in the lumbar region where both stabilize the vertebral bodies and control movement (Fig. 13.6). The anterior longitudinal ligament is widest in the lumbar spine where it covers most of the anterior and lateral surfaces of the vertebral bodies and intervertebral discs. The posterior longitudinal ligament is relatively weaker and has a denticulate arrangement that permits the passage of vascular structures. Superficial fibres bridge several vertebrae while deeper fibres pass over two joints and have lateral extensions intimately related to the intervertebral disc (Parke & Schiff 1971). The strong central portion of the posterior longitudinal ligament provides resistance to central disc displacement, deflecting it laterally where the lateral extensions are deficient and offer a space for posterolateral displacement.

The ligamentum flavum consists of predominantly yellow elastic fibres and connects adjacent laminae. It controls lumbar flexion by ‘braking’ the separation of the laminae and assisting the return to the upright posture. The elastic fibres also restore the ligament to its normal length after stretching, to prevent buckling into the spinal canal and compression of the spinal cord or cauda equina. Such pathology may arise in the degenerate ligament and contribute to stenosis.

The iliolumbar ligament provides stability for the lumbo-sacral junction (Yamamoto et al 1990), attaching the L5 transverse process to the pelvis. Sometimes a band also passes from the transverse process of L4. This anchorage of L5 to the pelvis may restrict the amount of accommodation possible for disc herniation. Disc herniation at the L5, S1 level may produce severe pain with the patient fixed in flexion, whereas herniation above this level, usually L4–L5, may be accommodated more readily by a lateral shift that will reduce pain.

Any structures in the lumbar region that receive a nerve supply can be a primary source of somatic pain. Congenital or acquired disorders of a single component of the motion segment cannot exist without affecting the functions of other components of the same segment and the functions of other segmental levels of the spine (Parke & Schiff 1971). However, Schwarzer et al (1994b) consider zygapophyseal joint pain to be uncommon, with discogenic pain a singular, independent disorder.

The zygapophyseal joints, as synovial joints, can be affected by arthritis and the presence of intra-articular structures makes derangement of the joint a possibility. The intervertebral disc is known to degenerate and since the outer annulus receives a nerve supply it can be a primary source of pain. Herniations of discal material are well recognized and are a secondary cause of pain, affecting other pain-sensitive structures.

Traction exerted on the dura and noxious stimulation of the back muscles, ligaments and lumbar zygapophyseal joints have both provoked a pain response (Bogduk 1994). Compression of normal nerves does not provoke a pain response while stimulation of swollen, stretched or compressed nerve roots has been shown to produce leg pain, with the dorsal root ganglion tending to be more tender than other parts of the nerve (Kuslich et al 1991). In the same study, stimulation of the outer annulus fibrosus and the posterior longitudinal ligament produced back pain while there was tenderness on stimulation of the capsule of the zygapophyseal joint, also associated with localized back pain. Pain may be produced in any pain-sensitive structure through chemical, mechanical or ischaemic mechanisms, although it seems more than likely that all factors coexist in disc pathology or herniation.

Chemical pain is the result of irritation of the noci-ceptive nerve endings by the products of inflammation, generally following tissue damage. The products of inflammation can either sensitize nerve endings so that they respond to a lower threshold of stimulus, or activate silent nociceptors (see p. 372) to provoke a response.

Mechanical pain occurs through stretching, compression or distortion of connective tissue structures stimulating the intervening nociceptors. Mechanical stress ultimately produces vascular changes and ischaemia, which activates nociceptors.

While acknowledging the existence of all pain-sensitive structures within the spinal joints, the discal model is central to the concepts of treatment in orthopaedic medicine. With evidence from scans more readily available, the disc would seem to be a major contributor to spinal pain, but the mechanisms of internal derangement, disc herniation and the recovery from disc pathology, often spontaneously, remain unknown. More recent work has concentrated on the chemical effects of displaced nuclear material, while the exact mechanism of pain produced by mechanical compression is unclear.

The mechanism by which the lumbar intervertebral disc produces pain is probably complicated, with several factors contributing to the diagnosis. It is important to understand the anatomy and the possible mechanisms for pain production, as discussed above.

Patients with non-mechanical causes of back pain can present with signs and symptoms that mimic those of disc pathology. It is important to recognize those features that allow them to be identified as ‘red flags’ (indicators of serious spinal pathology), since manual techniques are either contraindicated or not appropriate, and the patient needs to be referred to the appropriate specialist.

The following section is divided into two parts. The first covers lumbar lesions; the second covers the non-mechanical causes of back pain and associated signs and symptoms.

A central prolapse affects central structures, in particular the posterior longitudinal ligament and the dura mater. Pain arising from compression of the dura mater is multisegmental in nature (see Ch. 1). A posterolateral prolapse affects unilateral structures, mainly the dural nerve root sleeve and nerve root, which tend to produce segmental pain.

A disc herniation, either protrusion or prolapse, produces a pattern of signs and symptoms that are progressive, with a history of increasing, worsening episodes. Often the precipitating factor is trivial. The dural nerve root sleeve and nerve root are vulnerable in the lumbar spine to posterolateral prolapse, with pain and other associated symptoms referred into the leg. A classification of clinical models has been established to aid diagnosis and to establish treatment programmes. These are outlined in the treatment section later in this chapter, since they relate directly to treatment selection.

Non-mechanical lesions, including serious pathology, have features that do not ‘fit’. Since they represent contraindications to manual orthopaedic medicine treatments, they must be recognized and the patients referred appropriately.

Some patients have a developmental abnormality where the spinal canal has a trefoil shape in cross-section (Vernon-Roberts 1992) and spinal stenosis is particularly prevalent in this group. Narrowing can also occur as a result of degenerative changes through ageing, injury, disease, or as a result of surgery (Lee et al 1995). Irrespective of cause, a small vertebral canal can have clinical significance for back pain (Porter & Oakshot 1994).

Degenerative spinal stenosis can be associated with osteophyte formation at the vertebral body or zygapophyseal joints, with reactive proliferation of capsular and soft tissues, and fibrous scarring around the nerve roots. The vertebral canal can be compromised by thickening of the ligamentum flavum which shows a 50% increase in thickness with ageing over a normal lifespan (Twomey & Taylor 1994). Degenerative spondylolisthesis may also narrow the canal (Osborne 1974, Rauschning 1993).

A disc prolapse may significantly reduce the size of both the vertebral and intervertebral foramina and Porter et al (1978) noted that the risk of developing disabling symptoms from disc prolapse is inversely related to the size of the spinal canal. The anterior margin of the canal can be indented to compress the cauda equina by a lax posterior longitudinal ligament overlying degenerate prolapsed discs. Cyriax (1982) termed this the ‘mushroom phenomenon’.

Spinal stenosis can produce neurogenic or spinal claudication which was recognized by Verbiest, in 1954, as due to structural narrowing of the vertebral canal compressing the cauda equina and producing claudication symptoms (Porter 1992). Men over the age of 50 with a lifestyle that has involved heavy manual work may be affected. The entire cauda equina can be compressed centrally causing bilateral symptoms, or the emerging nerve root can be affected (Osborne 1974). The patient complains of discomfort, pain, paraesthesia and heaviness in one or both legs while standing or walking. There may be night cramps and restless legs. A long history of back pain may be present and the patient may have undergone back surgery at some time. The symptoms are usually of several months’ duration. There is usually a threshold distance when the symptoms develop and a tolerance when they have to stop; the tolerance distance is about twice the threshold (Porter 1992). These symptoms are similar to those of the ischaemic pain associated with intermittent claudication of peripheral vascular disease and with the age group affected; the two conditions can coexist, making diagnosis difficult.

With neurogenic claudication, stooping or bending forwards relieves the symptoms and allows the patient to continue. Flexion increases the space in the canal and tightens the ligaments, straightening out the buckling that tends to occur with degeneration. The patient can usually walk uphill, which involves a flexed posture, easier than walking downhill, which involves an extended posture.

On examination, the patient often stands with a stooped posture, with flexed hips and knees and a flattened lumbar spine with loss of the lordosis. This posture becomes more evident on walking. The capsular pattern is present with marked loss of spinal extension. Extension may produce the pain as it decreases the calibre of the spinal canal while, conversely, flexion relieves the pain (Osborne 1974). Dynamic variations in flexion and extension are related to changes in the buckling of the ligamentum flavum and the herniation of the intervertebral discs (Rauschning 1993). The rest of the examination may be unremarkable and back pain itself may not be a feature. Neurological signs are often absent.

Management may involve spinal decompressive surgery or advice on how to live with the condition. Symptoms do not usually resolve, but they do not always get worse.

Kotil & Bilge (2007) report on two cases of haematoma in the ligamentum flavum as a rare cause of low back and leg pain in elderly patients. The signs were consistent with L5 root compression. A cautious approach is required for leg pain in the elderly, especially as a first presentation. Full consideration should be given to the entire clinical presentation and further investigation is wise if there is any suspicion that the cause is non-mechanical.

Structural abnormalities can be completely asymptomatic or may produce pain, inflammation and neurological signs, or coexist with disc herniation.

A particular feature of serious non-mechanical conditions is an unwell patient with possible weight loss. Neoplasm of the lumbar spine, although relatively uncommon, should be considered as a possible cause of low back and leg pain. Metastases may be secondary to carcinoma of the bronchus, breast, ovary, prostate, thyroid or kidney. Metastatic invasion may involve bone or may be intradural. Primary bone tumours occasionally affect the posterior elements of the vertebrae and multiple myeloma can produce backache due to vertebral involvement.

Non-organic back pain should be considered at the lumbar spine, although true psychogenic back pain is rare. Anxiety tends to be associated with acute back pain while depression is associated with chronic back pain; both are indicators of the patient’s distress. Back pain may begin as a physical problem and, as such, is generally addressed by mechanical or physical treatments. If low back pain becomes chronic, psychosocial factors may be more obvious than physical signs, and illness behaviour becomes a relevant component. Illness behaviour is a normal phenomenon and a physical problem exists with varying degrees of illness behaviour (Waddell 1998). As clinicians, the physical and psychosocial factors that coexist in chronic pain must therefore be understood in order to provide total care. The interested reader is referred to the work of Waddell (1998) which includes the biopsychosocial model and describes non-organic or behavioural signs, the so-called ‘yellow flags’, as indicators of pychological distress and risk of long-term disability.

A general observation of the patient’s face, posture and gait will alert the examiner to the seriousness of the condition. Patients in acute pain will generally look tired. They may have adopted an antalgic posture of flexion or lumbar scoliosis which is generally indicative of an acute locked back, possibly due to a disc lesion. A lumbar lateral shift is pathognomic of a disc lesion (Porter 1995). Patients may not be able to sit during the examination due to discomfort from this particular posture. Their gait may be uneasy with steps taken cautiously, obviously wary of provoking twinges of pain by sudden movements or pain on weight-bearing. A dropped foot may be evident on walking and will lead you to consider involvement of the L4 nerve root affecting the tibialis anterior muscle and interfering with function.

The Box on page 379 lists the ‘red flags’ for the possible presence of serious pathology that should be listened for and identified throughout the subjective and objective examination. In isolation, many of the flags may have limited significance but it is for the clinician to consider the general profile of the patient and to decide whether contraindications to treatment exist and/or whether onward referral is indicated.

The history is particularly important at the spinal joints. Vroomen et al (1999) published a systematic review of the diagnostic value of the history and examination of patients with suspected sciatica, establishing that very little attention has been paid to the history of such events. Pain distribution was the only sensitive sign of the level of disc herniation, with straight leg raising seemingly a sensitive sign and crossed straight leg raise a strong indicator of nerve root compression. Disagreement exists in the literature with regard to the value of decreased muscle strength, sensory loss and altered reflexes as signs of nerve root involvement and it is unclear whether the physical examination adds much to the diagnostic value of the history.

There is a close relationship between signs and symptoms from the lumbar spine, sacroiliac joint and hip joint. The history will help with the differential diagnosis but conditions at each of these areas can coexist. Major pathology can affect the spine, such as malignancy, infection, spondyloarthropathy or fracture, but these represent a small percentage of the problems compared with mechanical lesions of the lower back (Swezey 1993). X-ray findings can be misleading, particularly when showing the degenerative changes of osteoarthrosis which may or may not be painful. Similarly, spondylolysis progressing to spondylolisthesis occurs in approximately 5% of adults but is symptomatic in only half of them (Swezey 1993).

The age, occupation, sports, hobbies and lifestyle of the patient may give an indication of provoking mechanisms. Often the incident precipitating the episode of back pain may be relatively minor, though factors predisposing to the event may have been continuing for some time. While cure will be the initial aim of treatment for this presenting incident, ultimately the management of the condition and prevention of recurrence will become the patient’s responsibility. Patients will require advice and guidance on management of their back condition to prevent chronicity.

Many occupations involve a flexion lifestyle, e.g. sedentary office work and brick-laying apply postural stress to the intervertebral joint. These patients require advice about changing postures to minimize the stress inflicted by work. Directives on the manual handling of loads are in existence and patients should receive advice about this in their place of work. The vibration of motor vehicle driving may have an influence, as well as the sitting posture involved, which is known to increase intradiscal pressure (Osti & Cullum 1994).

Assessment of patients with chronic low back pain presents a particular challenge to the clinician. Emotional, environmental and industrial factors may influence pain perception, while monotony or dissatisfaction at work or home is relevant (Osti & Cullum 1994). Distinction will need to be made between the true physical symptoms of the presenting condition and those relating to psychosocial factors that influence the way the patient reacts to the pain (see above). Enquiry should be made about the possibilities of secondary gain factors relating to disability, or the presence of psychological or social stresses that might predispose the patient to chronic pain disorders (Swezey 1993). Standard questions on quality of sleep, tiredness levels, concentration, appetite, etc. may establish whether the patient is depressed.

The site of the pain will give an indication of its origin (see Ch. 1). Lumbar pain is generally localized to the back and buttocks or felt in the limb in a segmental pattern. Sacroiliac pain may be unilateral, felt in the buttock, or more commonly in the groin, and occasionally referred into the leg. The hip joint may produce an area of pain in the buttock consistent with the L3 segment, pain in the groin, or pain referred down the anteromedial aspect of the thigh and leg to the medial aspect of the ankle. Dural pain is multisegmental and will be central or bilateral. Pressure on the dural nerve root sleeve will be referred segmentally to the relevant dermatome. Pressure on the nerve root will refer pain to the relevant limb with accompanying symptoms of paraesthesia at the distal end of the dermatome.

Vucetic et al (1995) considered the difficulty that patients have in giving a precise verbal description of pain. They support the use of a pain drawing, which may take a few minutes to obtain, but the result can be grasped at a glance. Waddell (1992) warns that how a patient draws pain is influenced by emotional distress and that non-anatomical, widespread and magnified drawings tell of the patient’s distress rather than the physical characteristics of the pain.

The spread of pain will not only give an indication of its origin, but also the severity or irritability of the lesion. Generally, the more peripherally the pain is referred, the greater the source of irritation. A mechanical lesion due to a displaced lumbar disc produces central or unilateral back or buttock pain. If the pain shifts into the leg, it generally ceases or is reduced in the back. Pain of non-musculoskeletal origin does not follow this pattern and serious lesions produce an increasing spreading pain, with pain in the back remaining as severe as that felt peripherally.

The onset and duration of the pain can assist the choice of treatment (see below). In very general terms, a sudden onset of pain may respond to manipulation, while a gradual onset of pain may respond better to traction. The whole clinical picture will need to be reasoned through in order to make a decision about treatment, which may contradict these rules of thumb.

The nature and mode of onset are important. The patient may remember the exact time and mode of onset which may have involved a flexed and rotated posture. If lifting was involved in the precipitating episode, it may only have been a trivial weight. If the patient reports a gradual onset of pain, it is worth questioning further for details of previous activity. A minor traumatic incident some time before the onset of back pain or the maintenance of a sustained flexion posture may have been sufficient to provoke the symptoms.

The gradual onset of degenerative osteoarthrosis is common in the zygapophyseal joints and hip joints, while a subluxation of the sacroiliac joint can occur with a sudden onset. Serious pathology develops insidiously.

If trauma is involved, the exact nature of the trauma should be ascertained and any possible fracture eliminated. Direct trauma may produce soft tissue contusions, while fracture may involve the spinous process, transverse process, pars interarticularis, vertebral body or vertebral end-plate. Compression fractures of the vertebral body are common in horse riders and those falling from a height, and involve the vulnerable cancellous bone of the vertebral body (Hartley 1995). Hyperflexion injuries may cause ligamentous lesions or involve the capsule of the zygapophyseal joint, while hyperextension injuries compress the zygapophyseal joints. Both forces can injure the intervertebral disc.

The symptoms and behaviour need to be considered. The behaviour of the pain will give an indication of the irritability of the patient’s condition and provide clues to differential diagnosis. Serious pathologies of the spine, including fractures, tumours or infections are relatively rare, accounting for less than 1% of all medical cases seen for spinal assessment. Despite this, the clinician must remain alert to clinical indicators that need more extensive investigation than the basic clinical examination (Sizer et al 2007).

The pattern of all previous episodes of back pain should be ascertained, as in disc lesions a pattern of gradually worsening and increasing episodes of pain usually emerges.

The mechanisms whereby the disc herniation can cause pain have been discussed earlier in this chapter. The typical pattern of pain from disc herniation is usually one of a central pain which moves laterally. As the pain moves laterally, the central pain usually ceases or reduces. A gradually increasing central pain accompanied by an increasing leg pain is indicative of serious pathology and this pain is usually not altered by either rest or activity.

The daily pattern of pain is important and typically a disc lesion produces either a pattern of pain that is better first thing in the morning after rest, becoming worse as the day goes on, or, since the disc imbibes water overnight, the patient may experience increased pain on weight-bearing first thing in the morning due to increased pressure on sensitive tissues. Patients can sleep reasonably well at night as they are usually able to find a position of ease.

Mechanical pain can cause an on/off response through compression or distortion of pain-sensitive structures. This can involve the annulus itself or structures in the vertebral canal. The patient with a disc lesion usually complains of pain on movement easing with rest. Changing pressures in the disc affect the pain and it tends to be worse with sitting and stooping postures than when standing or lying down. In an acute locked back, small movements can create exquisite twinging pain.

Herniated disc material may produce an inflammatory response resulting in chemical pain. Chemical pain is characteristically a constant ache associated with morning stiffness. Sharper pain can also be associated with chemical irritation as the nerve endings become sensitized and respond to a lower threshold of stimulation. It is important to differentiate mechanical back pain from inflammatory arthritis and sacroiliac joint lesions through consideration of other factors, since they also produce pain associated with early-morning stiffness.

Radicular pain is generally a severe lancinating pain, often burning in nature, which is felt in the distribution of the dermatome associated with the nerve root. Sciatica is commonly associated with lumbar disc pathology and will occur if the L4–L5, S1 or S2 nerve roots are involved. If the higher levels are involved, pain will similarly be referred into the relevant segment.

The language used by patients to describe the quality of their pain will indicate the balance between the physical and emotional elements of their pain. Words such as ‘throbbing’, ‘burning’, ‘twinging’ and ‘shooting’ describe the sensory quality of the pain; emotional characteristics are expressed in such words as ‘sickening’, ‘miserable’, ‘unbearable’ and ‘exhausting’ or vocal complaints such as moans, groans and gasps (Waddell 1992, 1998).

The other symptoms described by the patient provide evidence for differential diagnosis, contraindications to treatment and the severity or irritability of the lesion. An increase in pressure through coughing, sneezing, laughing or straining can increase the back pain and this is the main dural symptom. Paraesthesia is usually felt at the distal end of the dermatome and is a symptom of nerve root compression. Confirmation of this is made through the objective compression signs of muscle weakness, altered sensation and reduced or absent reflexes.

Specific questions must be asked concerning pain or paraesthesia in the perineum and genital area as well as bladder and bowel function. The presence of any of these symptoms indicates compression of the S4 nerve root at the preganglionic extent which could produce irreversible damage, and indicates immediate referral for surgical opinion. A transition zone exists in the preganglionic region between the peripheral and central nervous systems and repair cannot occur across the transition zone if the nerve is disrupted (Huang et al 2007). This study examines the possibility of surgical repair of the nerve to encourage regeneration but the repair has been performed in rats only at this stage.

Manipulation is absolutely contraindicated in these cases. The symptoms of difficulty in passing water, inability to retain urine or lack of sensation when the bowels are opened are important. It is not unusual to find urinary frequency or difficulty in defecating associated with effort in hyperacute lumbar pain.

Bilateral sciatica with objective neurological signs and bilateral limitation of straight leg raise suggest a massive central protrusion compressing the cauda equina through the posterior longitudinal ligament, with possible rupture of the ligament (Cyriax 1982). It is an absolute contraindication to manipulation, since a worsening of the situation could lead to irreversible damage to the cauda equina, as mentioned above. The symptoms of cauda equina compression should be distinguished from multisegmental, dural reference of pain into both legs, where there may be bilateral limitation of straight leg raise but no neurological signs.

Questioning the patient about other joint involvement will indicate whether inflammatory arthritis exists or if there is a tendency towards degenerative osteoarthrosis.

The past medical history and the patient’s current general health will help to eliminate possible serious pathology, past or present. An unexplained recent weight loss may be significant in systemic disease or malignancy. Visceral lesions can refer pain to the back, e.g. kidney, aortic aneurysm or gynaecological conditions. Infections should be obvious, with an unwell patient showing a fever. Malignancy can affect the lumbar and pelvic region but the pattern of the pain behaviour does not generally fit that of musculoskeletal origin. Past history of primary tumour may indicate secondaries as a possible cause of back pain. Serious conditions produce an unrelenting pain; night pain is usually a feature and is responsible for the patient looking tired and ill. As well as past medical history, establish any ongoing conditions and treatment. Explore other previous or current musculoskeletal problems with previous episodes of the current complaint, any treatment given and the outcome of treatment.