In this type of low-back pain, morphological lesions may be absent and the spinal column as such may not necessarily be altered, at least at the outset. However, since this first pain category is not homogeneous, some further definition is required.

The cause may be exogenous, for example heavy physical labor. More frequently, however, pain is the result of faulty posture and excessive static strain caused either by external factors or by faulty movement patterns. Poor posture may be attributable to adverse static development, for example leg length inequality, or to juvenile osteochondrosis. In most cases, however, postural abnormalities are due to muscle imbalance arising in the context of adverse movement patterns, hypermobility, or obesity. All these sets of circumstances are characterized by signs of excessive strain on locomotor system structures.

A painful or tender coccyx is the result of muscle dysfunction involving the gluteus maximus and levator ani and their points of attachment to the coccyx.

In a series of 59 patients with a painful hip joint with no or very slight osteoarthritis of the hip, low-back pain was the most frequent complaint (Lewit 1977). Conversely, signs of a painful hip are common in patients with low-back pain. It is therefore justifiable to discuss the painful hip in this section because the hip also needs to be considered in the setting of low-back pain.

These conditions share common ground in terms of their etiology, clinical features, and therapy. Mobilizing therapy constitutes the first-line approach for movement restrictions in the lumbar motion segments.

The subject of this section is disk herniation without radicular compression. It is essential to know when disk herniation should be suspected in simple low-back pain. The conditions described thus far have been functional disorders. Here, however, we are faced with a defined pathological lesion with a correspondingly serious prognosis. It must be remembered that many instances of disk herniation are completely devoid of clinical relevance, and for this reason the prognosis is favorable even with conservative therapy. At the same time, dysfunctions play an important role here.

Pelvic distortion is always a secondary symptom (see Section 4.5.3). The clinical picture is therefore dependent entirely on the condition in which pelvic distortion is (also) detected and which is also the object of therapy. If treatment is correct, pelvic distortion also disappears. It is encountered far more frequently in children and adolescents than in adults, and it is generally a consequence of a restriction at the craniocervical junction. Adolescent girls with pelvic distortion also frequently present with dysmenorrhea. Here, too, the true cause is probably a dysfunction at the lumbosacral junction with a TrP in the iliacus. In the final analysis the Rosina test (see Section 4.5.5) also indicates that pelvic distortion in patients with normal sacroiliac joints can be provoked by head rotation and that this is a palpatory illusion, as has been confirmed radiologically.

The coccygeus forms part of the deep stabilization system and can be understood only in the context of the locomotor system as a whole. We should further recall the role of the levator ani in conjunction with the sphincters and the gluteus maximus. Here we are dealing with an entirely different function of the pelvic floor, which contributes to erect posture and respiration; disturbances of this function are announced by a TrP in the coccygeus. The palpatory technique for this TrP is described in Section 4.5.8 (see Figure 4.12).

Needless to say, the individual forms of back pain described above rarely occur in isolation. Usually they present as mixed or combined lesions, with the clinical picture being dominated by a different factor in each case. And this does not happen by chance. All the structures involved in the etiology of low-back pain are somehow interconnected, and many are closely linked in a chain reaction pattern. Movement restriction at L4/L5 often fixes the sacroiliac joint via the piriformis, the sacroiliac joint itself is closely connected to the hip, and this in turn to segment L3/L4, while the pelvic floor has a special relationship with the adductors, and also with the biceps femoris and fibular head.

Pain may result from excessive strain due to external factors or from muscle imbalance. Most commonly, static overload due to long periods of working with the head bent forward plays a prominent role. A similar effect is produced by a forward-drawn posture as a result of faulty statics (see Figure 3.39). The typical signs of muscle imbalance have been described in Section 4.20.3.

Movement restriction involving the fibular head is closely linked with faulty statics (see Figure 6.25). Locally, it may give rise to lateral pain at the knee and cramping in the calf. Often it is a secondary finding in dysfunctions involving the foot. Fibular head restriction is regularly associated with TrPs in the biceps femoris, a muscle that plays a critical role in the anatomical fixation of the pelvis. Where pelvic fixation by the biceps femoris is inadequate, there is a compensatory response by the rectus abdominis together with the gluteal muscles, and then TrPs are found principally in the rectus abdominis, causing a forward-drawn posture.

In true knee pain (not pain that is referred to the knee) it is most important not to overlook a painful patella. A healthy patella should move freely on the articular surfaces of the femur and tibia. It should therefore be checked whether the patella is freely mobile in all directions and whether gentle pressure on the patella during mobility testing produces grinding resistance and pain. The technique for this is described on page 198 and can often bring instantaneous relief. Attachment point pain at the upper margin of the patella may be caused by TrPs in the rectus femoris, but also by increased tension in the tensor fasciae latae.

Dysfunctions of the knee (tibiofemoral) joint are characterized by a capsular pattern in which flexion is gradually more restricted than extension. Lateral springing (gapping) and joint play on one or other side are also often restricted. Unlike the hip joint, the knee is most painful when the patient walks downstairs or downhill. In this case mobilization by rapid shaking is most effective, and this is also true in particular for osteoarthritis of the knee.

The clinically important articulations in the foot are the ankle joint, the tarsal joints, and particularly the tarsometatarsal joints. Restrictions primarily involve Lisfranc’s joint, the second and third metatarsophalangeal joints, the talocrural joint and, to a lesser extent, the talocalcaneonavicular and subtalar joints. The main TrPs are found in the deep flexors of the sole of the foot and dorsally between the metatarsal bones.

The commonest complaint is foot pain that is often associated with cramps in the foot and calf and with paresthesia, although tunnel syndromes may be present in exceptional cases. What is far more important is that the feet constitute a key region in the locomotor system. The foot and its muscles are required to stabilize the almost spherical talocrural joint. Futhermore, the sole of the foot and the toes possess the highest density of proprioceptors and exteroceptors. The soles of the feet may be hypersensitive as well as relatively hyposensitive, and not infrequently the soles of the feet also react asymmetrically to exteroceptive stimulation (see Section 6.3). The consequence of all this is that the feet, like the deep stabilization system, are a source of very common chain reaction patterns involving the entire locomotor system; the most characteristic finding is a forward-drawn posture.

When walking and standing, patients not infrequently complain of a painful calcaneal spur. This is quite simply pain at the attachment of the plantar aponeurosis, a structure that becomes painful when there is increased tension in the aponeurosis itself. This is chiefly the result of TrPs in the deep flexors of the sole of the foot. At the same time there are generally also movement restrictions in the foot as well as dysfunctions in the lower extremities, including the fibular head. Dysfunctions are sometimes also found in the pad of soft tissue at the heel.

Treatment takes the form of PIR of the foot flexors (see Figure 6.132). Activation of the toe flexors by rocking forward is even more effective (see Section 6.8.8 and Figure 6.157). Needling of TrPs has also proved most beneficial, yielding far better results than a series of local anesthetic infiltrations around the calcaneal spur.

Another commonly encountered complaint is not only Achilles tendon pain itself, but pain where the Achilles tendon attaches at the heel. Here, too, treatment primarily takes the form of PIR-RI of the TrP in the soleus muscle; this is usually highly effective, with the result that needling is generally superfluous. Achilles tendon pain should be differentiated from pain in the underlying soft tissue between the Achilles tendon and the tibia (see Figure 6.65).

This is the commonest form of referred pain radiating into the upper extremity and constitutes a clinical problem as complex as that of low-back pain. This is probably due to the fact that the shoulder region corresponds to segment C4 and that numerous structures refer pain to this segment, in particular the diaphragm with the phrenic nerve. Clinical experience suggests that any type of pain originating in the cervical spine, the cervicothoracic junction, or the upper ribs – and even in the visceral organs of the thorax and upper abdomen – is felt in the shoulder region.

Epicondylar pain is a very frequent complication of the cervicobrachial syndrome. It is encountered far more often at the lateral than at the medial epicondyle of the humerus.

In wrist dysfunction, the structure most frequently found to be painful is the styloid process of the radius. As already mentioned in Section 7.4.7, this process is closely related to joint play at the elbow and between the radius and ulna. Radial abduction of the hand is regularly found to be restricted.

Another structure that is frequently painful is the carpometacarpal joint of the thumb where osteoarthritic changes are found particularly frequently. There may also be TrPs in the thenar eminence. Here therapy is mainly directed at (self-)mobilization through shaking (see Figure 6.4).

In patients with rheumatoid arthritis it is particularly common to find painful changes involving the wrist.

In all the painful conditions of the upper extremity dealt with in Section 7.4, insufficient stabilization of the shoulder blade by the lower part of the trapezius and by the serratus anterior can play such a decisive role that, after scapular instability has been treated, the local symptoms may clear up without any local treatment. Patients should therefore be routinely examined for scapular instability (see Section 6.8.9).

This condition is attributed to compression of the median nerve in the narrow tunnel formed by the carpal bones and crossed by the transverse carpal ligament. Compression first affects the blood vessels supplying the nerve, and this explains the important role of ischemia.

This syndrome is attributed to compression of the brachial plexus mainly in the gap between the anterior and middle scalenes and the muscle attachments at the first rib, and in the region of the superior thoracic outlet. Principally, it causes paresthesia (numbness, pins and needles, pain) in the upper extremities, this being most intense on the ulnar aspect of the fingers.

This syndrome is predominantly the result of dysfunctions involving the highly complex structures that constitute the superior thoracic outlet. The prerequisite for effective therapy is to identify any disturbances in these individual structures and their relevance in each case. In detail, these comprise increased tension (TrPs) of the scalenes, TrPs in the pectoralis minor (Hong & Simons 1993), increased tension of the upper fixators of the shoulder girdle, and TrPs in the diaphragm. Closely related to these muscle disorders, there may be movement restriction at the craniocervical junction, the cervicothoracic junction, and the upper ribs, in particular the first rib. The true cause of this increased tension (TrPs) is clavicular breathing (i.e. lifting the thorax during inhalation), which is associated with insufficiency of the deep stabilizer system.

It is no wonder, in view of this complexity and the lack of understanding concerning dysfunctions, that surgical decompression procedures are performed on the scalenes, the first rib, or a cervical rib, instead of pursuing the true cause, the treatment of which is highly rewarding.

Ulnar nerve weakness will be mentioned here only in passing. The cause is generally to be found in the ulnar nerve canal and only very rarely in Guyon’s canal in the wrist region. This condition is not an object for manipulative therapy, but it does need to be distinguished from the two entrapment syndromes described above. In terms of carpal tunnel syndrome it is necessary to differentiate between median nerve and ulnar nerve involvement. In terms of differentiation from the thoracic outlet syndrome, it is important to identify patterns of weakness and atrophy that are characteristic of the ulnar nerve, as well as a true hypesthesia, since these hardly ever occur in thoracic outlet syndrome.

This condition is the commonest entrapment syndrome affecting the lower extremity.

The importance of the craniocervical junction for maintaining equilibrium was explained in Section 2.5.1. The most significant symptom of disturbed equilibrium is dizziness or vertigo. If patients are routinely examined using the two-scales test and Hautant’s test (see Figure 4.45), it will be found that many patients without dizziness at all show a weight difference of 5kg or more when standing with each foot on separate scales. Hautant’s test in these patients is then generally positive, at least in one head position – usually retroflexion and rotation of the head in the direction opposite to the deviation. In contrast, anteflexion and rotation of the head in the direction of deviation cancels out any deviation that is already present in a neutral position. It is therefore legitimate to speak of a ‘cervical pattern.’ In the two-scale test the patient must be instructed to place weight on both legs equally otherwise there will be an automatic tendency to load the standing leg more. The direction of the movement restriction in the cervical spine, in contrast, plays only a subordinate role for the very reason that more than one restriction is often present and these are not always in the same direction.

In a consecutive series of 106 patients without dizziness (Lewit 1986) we detected a disturbance pattern in 55 cases. A locomotor system dysfunction was consistently present, but not always involving the cervical spine; sometimes the masticatory muscles and even the feet were involved. After treatment of the relevant dysfunction, the disturbance pattern also reverted to normal in every case. These were the same type of patients in whom Norré et al (1976) reported nystagmus and movement restrictions at the craniocervical junction but without dizziness.

Finally, it should be noted that the maintenance of equilibrium (and of disturbances to equilibrium) depends on proprioception with sensory input from the locomotor system, labyrinth, and eyes, all of which is integrated in the brainstem. Dizziness or vertigo are experienced if there is a disturbance to any one of these systems.

At first sight the diagnosis of an active scar appears to be extremely straightforward: in each layer we look for a pathological barrier, that is we test for skin stretch, subcutaneous folding and stretching of the fold, the typical resistance pattern of TrPs, the degree to which fascia and areas of resistance can be shifted, and pathological barriers in the abdominal cavity. However, the following difficulties should be highlighted, on the basis of extensive clinical experience: in the case of surgical scars, the skin incision is often selected so as not to produce a cosmetic blemish. However, the actual surgical procedure involving the deeper-lying structures may take place some distance away from the incision, and this fact needs to be realized if pathological barriers are to be detected there. The diagnosis of resistance in the abdominal cavity demands special skill. Surgery today makes widespread use of laparoscopic procedures, and for this reason nothing will be palpated in the superficial layers. We therefore have to rely on our palpatory skill if we are to identify the location and direction of resistance in the abdominal cavity. And it is no less important to be able to recognize the release phenomenon reliably; for if there is no release phenomenon, then we are dealing not with a scar but with a pathological process in the abdominal cavity. The requisite diagnostic steps then have to be initiated. Clinically, it is important that palpation for resistance should not be limited to areas above the pubic symphysis. Resistance is commonly found below the symphysis in toward the pelvis, especially after gynecological operations, and complicated deliveries are a frequent cause. As abdominal scars are stretched by backward bending they restrict extension of the lumbar spine, and the patient interprets this as low-back pain. In the absence of segmental restriction in the lumbar spine, backward bending is then restored by treatment of scars in the abdominal region.

However, diagnosis alone is not enough; it is also important to determine relevance. An active scar need not necessarily be a factor in the symptoms for which the patient is being treated. In order to determine relevance, a complete examination should be followed initially by treatment of the scar so that we can determine whether or not the dysfunctions and their chain reaction pattern can be influenced by our intervention there. This is important because if the effect is positive, then we continue to target the scar with our treatment. Conversely, if a relevant active scar is not treated, then all other therapy will remain unsuccessful.

In every case therapy consists of taking release through to the very end. In the case of areas of resistance in the abdominal cavity it is often necessary to change direction, depending on where further resistances can be palpated. The patient will often indicate where the referred pain is felt in the locomotor system (usually in the back). It is important to understand that a single treatment will not usually suffice and that it is generally helpful also to stroke the skin surface and to prepare the deeper layers for treatment by using hot packs. The number and frequency of treatments will be determined by the clinical course.

The pathogenic effect of resistance in the abdominal cavity depends not on the organ or even on its position, or whether this or that structure in the abdominal cavity is palpated, as practitioners of visceral osteopathy insist. It is determined solely by the pathological barriers in the abdominal cavity that interfere with the harmonious cooperation of the viscera as the body moves.

These two anomalies have in common the ability to cause compression syndromes, the former of the medulla oblongata, the latter of the cervical part of the spinal cord. They are both congenital conditions that also share a tendency for symptoms to become apparent only in (very) advanced old age. From this it follows that we are dealing here with decompensation due to degenerative and functional change. Provided that surgical intervention is not indicated immediately, it is therefore possible to embark on treatment aimed at the restoration of function.

In basilar impression there are frequently no signs of neurological compression, and patients complain only of symptoms similar to those reported in the cervicocranial syndrome. In such cases the treatment procedure is the same as for patients who do not present the anomaly. However, even patients with some signs of compression in the posterior cranial fossa may improve after manipulation. The same is true for cervical myelopathy and for narrowing of the cervical spinal canal, not only with regard to pain symptoms but also for milder forms of weakness.

The case studies below illustrate the importance of treating dysfunctions of the locomotor system caused by neurological diseases of organic origin.

These case studies show that both in basilar impression as well as in cervical myelopathy it is possible to achieve clinical improvement by using therapy that is targeted at function. Similar findings have also been made in syringomyelia.

The radicular syndromes are also generally caused by a pathomorphological lesion (most commonly a herniated disk), primarily affecting the lower extremities where dysfunctions play a major role. In the upper extremities the process is more complex, leading to narrowing or compression of the intervertebral canal, with disk herniation being a rather rarer cause. Other morphological changes include narrowing of the spinal canal in both the cervical and lumbar regions. Although less common, space-occupying lesions should also be considered as possible causes of radicular compression.

With the exception of space-occupying lesions, the pathomorphological changes listed here do not constitute absolute indications for surgery. Even without surgery the great majority of radicular syndromes heal as a result of functional compensation and resorption of the intervertebral disk. This is also why conservative treatment is so often successful, that is traction, manipulation, various types of reflex therapy, remedial exercise, and stabilization methods. Indeed, surgery in isolation fails more often than not if it is not followed by appropriate rehabilitation, that is if we do not help to restore normal function. This is why the problem of disk herniation is dealt with in this book. The interplay of changes in structure and function constitutes a complex problem in terms of diagnosis and pathogenesis.

The clinical differences between radicular syndromes in the upper and lower extremities are considerable and so the two will be dealt with separately. The reader is also referred back to Section 2.12.

The possibility that reflex inter-relationships between different structures may exist side by side with referred pain in the same body segment has already been discussed in Section 2.11. The practical clinical aspects of this phenomenon will now be considered.

In very broad terms, the following five possibilities should be envisaged:

The first two points highlight the necessity for precise differential diagnosis and the problems associated with this. The spinal column with its motion segments can in fact produce symptoms that may mimic symptoms arising in the viscera and that are frequently interpreted as such by both patients and practitioners. This explains why patients who have been successfully treated by lay manipulators believe they have been ‘cured’ of their visceral disease.

No less important is the fact that these differential diagnoses are not always sufficiently recognized; consequently, when no pathological changes are found in the visceral organs, the term ‘functional’ is used to describe these disturbances. And given the prevailing ignorance concerning dysfunctions, the word ‘functional’ tends to be used as a euphemism for ‘of psychogenic origin’ or even for ‘malingering’. As already stated in Section 1.1, any practitioner who finds no pathological changes to corroborate a diagnosis should first look for a disturbance in the corresponding segment of the locomotor system before labeling a disorder as psychogenic. The pejorative use of the word ‘functional’ in general and especially in connection with the locomotor system reflects a lack of awareness that tends to underestimate the significance of locomotor system dysfunctions. It is this underestimation, combined with ignorance, that gives unqualified lay manipulators the opportunity to claim ‘miracle’ cures.

The other side of the coin (point 2) is the warning that pain perceived in the locomotor system may be a deceptive sign masking serious underlying visceral disease. This suspicion is strengthened if the symptoms of spinal segmental disturbance tend to relapse repeatedly without obvious cause. While the error in point 1 is more common, that in point 2 is all the more fraught with danger.

Point 3 is of major theoretical significance and demonstrates that visceral disease is actually one of the possible causes of dysfunction in the motion segment (see Section 1.1). Clinical experience teaches that certain visceral diseases are associated with characteristic patterns in the locomotor system. These patterns are of considerable diagnostic importance and are described below. They are so specific that their recurrence is in all probability predictive of a recurrence of the visceral disease. It is therefore literally ‘in our hands’ to make the diagnosis and influence the prognosis.

Point 4 follows on from point 3. If the visceral disease has been cured and we manage to treat the reflex dysfunctions caused by it, we obtain most satisfactory results and can thus confirm the success of visceral treatment. Here patients and practitioners alike tend to draw the following incorrect conclusion: because of persistent symptoms due to secondary dysfunctions in the motion segment, the patient still feels affected by the visceral disease. If after treatment of the dysfunction the patient is symptom-free, all the credit for the success of therapy is then given to the practitioner who treated the dysfunction, even though the underlying visceral condition had already been cured. However, if the dysfunction recurs in the same motion segment, this is generally an early sign of a recurrence of the visceral disease.

Point 5 is the pipe-dream cherished by many (lay) practitioners in the past; even today, however, it remains conjectural. Nevertheless, it would seem justifiable to assume that lesions in a motion segment of the spinal column may impair function in the corresponding internal organs. This is borne out by the vasomotor response in the whole segment to which pain is referred. In such cases we can see the disorder clearing up as soon as we treat the motion segment. Reactions of this kind have been noted particularly in connection with the cervicocranial syndrome, especially at the craniocervical junction, including disturbances of equilibrium. Similar phenomena have been observed in connection with certain cardiac arrhythmias. According to Schwarz (1996), a motion segment dysfunction may activate latent disease in an internal organ. Multiple pathogenic factors may also need to be considered in terms of their cumulative impact. As well as those that affect the locomotor system, other factors may be important in terms of their influence on the organism as a whole, for example infections, metabolic disturbances, menstruation, diet, etc. None of these individual factors on its own would be sufficient to provoke disease, but it is legitimate to refer to them as risk factors.

Systematic questioning when taking the case history in patients with vertebrogenic disturbances reveals a strikingly high incidence of tonsillitis. In a randomly selected sample of 100 cases from our files, 56 patients had a history of chronic relapsing tonsillitis and/or tonsillectomy. This finding was made particularly often in patients with movement restriction of the occiput against the atlas. It therefore seemed justifiable to investigate this problem further.

In a study sample of 76 predominantly adolescent patients with chronic tonsillitis, movement restriction at the craniocervical junction was detected in 70 cases, in the great majority of them between the occiput and atlas. Following tonsillectomy, movement restrictions were still present in the vast majority of these cases. However, where movement restrictions were previously not present or had been treated, they developed only in exceptional cases after tonsillectomy. They could therefore not be interpreted as a consequence of surgery.

In 40 non-operated patients in long-term follow-up who underwent just one manipulative procedure, 26 remained without tonsillitis recurrence and 15 without movement restriction recurrence (Lewit & Abrahamovič 1976). Thirty-seven of these patients were followed up again three years later. Eighteen patients remained without tonsillitis recurrence, but in 7 cases movement restriction did recur and had to be treated. Two patients had a few recurrences of tonsillitis without movement restriction, 3 suffered repeatedly from tonsillitis, and 9 underwent tonsillectomy. In total, 13 patients remained without any recurrence of movement restriction. Interestingly, the tonsillitis patients had hardly any HAZs in the cervical region, but there was increased muscle tension (défense musculaire) laterally at the floor of the mouth below the tonsillar bed.

It can be concluded from this study that chronic tonsillitis goes hand in hand with movement restrictions at the craniocervical junction, mainly in segment C0/C1, and that these have a tendency to become chronic. This means that there is a danger of permanently disturbed function in one of the key regions of the locomotor system. In addition, our experience suggests that movement restriction in this region is associated with an increased susceptibility to recurrent tonsillitis.

Recognition of the close interplay between respiration and the locomotor system has also improved our understanding of the relationship between the lungs and the function of the thorax. Pronounced clavicular breathing or paradoxical breathing may be the underlying cause of dyspnea in the absence of any disturbance of the organs of respiration. Of course, pain experienced in the context of pleurisy or pneumonia needs to be differentiated from pain due to rib movement restriction or a slipping rib.

Palpation of rib mobility is useful here. In pleural disease the impairment of mobility involves the greater part of one side of the thorax whereas movement restrictions affect one or just a few motion segments.

The respiratory disease in which involvement of the thorax has been studied most is obstructive respiratory disease (Bergsmann 1974, Köberle 1975, Sachse & Sacshe 1975, Steglich 1971). The following factors play a key role here: rigidity of the chest wall further increases resistance during respiration, and the inspiratory position of the thorax in asthma patients is worsened by clavicular breathing, which is typical for that disease. Movement restrictions of the ribs are also associated with pulmonary rigidity, as detected by Köberle (1975) principally in segments T7–T10. In a group of 23 patients, Sachse & Sachse (1975) found a taut pectoralis major in 15 cases and a weakened lower trapezius in 15 cases. Increased tension in the scalenes is the most frequent change associated with clavicular breathing. TrPs in the diaphragm are also common.

Therapy comprises mobilization of movement restrictions in the thoracic spine and ribs, and remedial exercise for asthma patients who adopt a clavicular breathing pattern, so that respiratory resistance (which is increased in this disease) can be kept as low as possible.

As a result of thoracic rigidity, extremely pronounced clavicular breathing in combination with abdominal breathing, both with and without shortness of breath, is often encountered in ankylosing spondylitis. This is important because despite the presence of ankylosis, specific remedial exercises can achieve a correct thoracic breathing pattern thanks to the elasticity of the ribs.

Of all the vertebrovisceral inter-relationships, that between the heart and the spinal column has received most attention. This is due not only to the importance of the problem, but also to the fact that in the largest group of patients, that is in those with angina, the role of pain is comparable to that in thoracic dysfunctions. Pain of cardiac origin is also felt in the thorax, while pain referred from the heart is localized mainly to the shoulder and left arm.

Patients with angina show a characteristic pattern of disturbance that includes movement restrictions involving the thoracic spine, especially segments T3–T5 and most commonly T4/T5, the third to fifth ribs on the left side, the cervicothoracic junction, and often the craniocervical junction. Most commonly, TrPs are located paravertebrally at the level of T4, in the pectoralis major, subscapularis, serratus anterior, and upper part of the trapezius on the left side. TrPs in the scalenes go hand in hand with painful sternocostal joints in the vicinity of T3–T5 on the left side where the attachment points of the pectoralis minor are also located. Clavicular breathing is also often encountered in this setting, with the patient experiencing sensations of tightness not dissimilar to those felt in angina.

It is obviously imperative to distinguish as clearly as possible between angina with its characteristic pattern of disturbances and the pseudocardiac syndrome emanating primarily from the locomotor system. Rychlíková (1975) has shown that the more complete the described pattern of (reflex) changes in the locomotor system, the more likely it is to be secondary to primary heart disease. A number of important clinical criteria can aid the distinction between true angina and pseudoangina. Pain in true angina is dependent on physical effort, such as climbing stairs, and responds within seconds to administration of nitroglycerine. Retrosternal pain also tends to be indicative of a cardiac origin. On the other hand, pain provoked by certain positions of the body or by specific movement(s) is more characteristic of pseudoangina. Attacks are shorter in true angina than in the pseudoangina syndrome. The course of the disease is also different: if locomotor system dysfunctions recur or are aggravated despite specific treatment, this should be taken to indicate that the true cause is primary heart disease. The role of the locomotor system in pain of cardiac origin is borne out by the fact that Rychlíková (1975) did not find any signs of locomotor system dysfunction in a group of patients who suffered a myocardial infarction without pain.

Regardless of whether the locomotor system dysfunction pattern is primary or secondary, its treatment is always justified, as is rehabilitation for locomotor system dysfunction. If increased resistance is detected when shifting fascia around the thorax, the gentlest approach is to begin by releasing the fascia before using neuromuscular treatment techniques that address movement restrictions and TrPs simultaneously. This is followed by rehabilitation with training to correct breathing and posture. In view of the difficulties of diagnosis, cardiological monitoring is always indispensable. In cases where cardiological treatment is successful and locomotor system dysfunctions recur during the course of rehabilitation, it should be emphasized that these are often the first sign of a recurrence of heart disease, even before any evidence appears on the electrocardiograph (ECG).

While the role of angina in the development of locomotor system dysfunctions appears to be established, the same cannot be claimed for the role of the locomotor system in the pathogenesis of heart disease. There is one cardiological condition, however, where reflex locomotor system involvement seems well founded: paroxysmal tachycardia with no organic heart lesion. There are some cases where tachycardia occurs regularly if a certain movement restriction is present but where cardiac rhythm reverts to normal when the restriction is released (Vecan & Lewit 1980). Although hard evidence for a role of the locomotor system in the causation of organic heart disease is lacking, it would seem reasonable to concede that it could be a possible risk factor.

The prime significance of the treatment of locomotor system dysfunction in heart disease lies in the relief of pain, which greatly enhances the rehabilitation of these patients, as illustrated by the following case study.

As in heart disease, painful conditions in these organs may well produce reflex changes in the locomotor system. We had the opportunity to study the characteristic pattern in a group of young ulcer patients aged between 15 and 22 years (Rychlíková & Lewit 1976). The characteristic pattern of disturbance was noted primarily in segment T5/T6. Compared with a control group of similar age, there was an increased incidence of movement restrictions at the craniocervical junction. However, the most striking finding was pelvic distortion (87% as compared with 44.4% in the controls). There was also increased muscle tension in the thoracic erector spinae in segments T5–T9 on both sides, with a maximum at T6, and a HAZ in the same region on both sides – also significantly more common than in the control group. It is interesting that these changes were almost symmetrical, with a very slight preponderance on the right side. However, there was no difference between the cases of gastric and of duodenal ulcer.

In this group, the intensity of reflex changes correlated with the intensity of pain; where there was no pain, as in some cases after surgery, there were also no locomotor system dysfunctions. It must be added that this was the pattern found in young patients; in older patients suffering from ulcers the incidence of pelvic distortion is very much lower.

Because pain is a prominent feature in disorders of the liver and gall bladder, reflex changes must be anticipated here too. According to Rychlíková (1974), the motion segments most frequently affected by dysfunction are T6–T8. There is also frequently pain that is referred to the right shoulder, as borne out by a HAZ in the C4 dermatome and TrPs in the upper part of the trapezius on the right. Non-inflammatory gall bladder dysfunction can sometimes be halted successfully using reflex techniques.

Reflex changes are most clearly apparent in patients with renal colic. They always occur on the painful side in segments T10–T12 in the lower back and pain radiates into the groin. A thorough analysis of reflex changes in the locomotor system in kidney disease has been made by Metz (1986). In 208 cases of chronic kidney disease (glomerulonephritis, pyelonephritis) he found the following pattern: movement restriction at the thoracolumbar junction (T11–L1), and increased tension at the lowest ribs and in the psoas major, quadratus lumborum, and the thoracolumbar erector spinae. Metz emphasized that pain only became manifest in these patients with ‘genuine’ renal disease when the above locomotor system findings were apparent.

Pelvic distortion and a markedly increased incidence of faulty statics in the lumbar spine and pelvis were present (according to Metz) especially in nephroptosis (downward displacement of the kidney), where the symptoms were also determined decisively by locomotor system dysfunctions. Symptoms and locomotor system disturbance patterns were identical in a group of 40 patients with nephroptosis and another 40 patients after nephropexy: they primarily involved the thoracolumbar junction with unilateral hardening of the psoas major. The patients were mainly asthenic, hypermobile women with faulty statics, recurrent movement restrictions at L5/S1, and ligament pain. (Nowadays we would seek to identify insufficiency of the deep stabilization system.) In these cases, however, locomotor system dysfunction proved to be the decisive cause of the renal symptoms.

Because the psoas major is located deep in the abdominal cavity, it may provoke symptoms similar to those associated with other internal abdominal structures. This is extremely important for differential diagnosis. As we have noted, there is a reflex increase in tension in the psoas major secondary to kidney disease. Most frequently this is associated with TrPs in the psoas major and limitation of trunk rotation. Where there are faulty movement patterns, this muscle has a tendency to shorten (due to increased tension) and can cause flexion at the hip simultaneously with (paradoxical) lumbar lordosis. The psoas major should be examined for shortening (see Figure 4.55). Palpation of the typical TrPs is performed from the side with the patient supine and legs extended: the practitioner presses and snaps the muscle against the patient’s spine, which is in lordosis because the legs are extended. TrPs in the psoas major are linked in a chain with those in the quadratus lumborum and the thoracolumbar erector spinae, and are responsible for the functional limitation of trunk rotation to the opposite side.

TrPs in the psoas major may also be the cause of pain in the ‘post-cholecystectomy syndrome.’ Like other painful structures in the abdominal cavity, TrPs in the psoas major may also give rise to tension and rigidity (défense musculaire) in the rectus abdominis. Because of the location and size of the psoas major, TrPs in this muscle can simulate symptoms associated with most of the abdominal viscera: duodenum, gall bladder, kidneys, pancreas, and vermiform appendix. Not only is the pain intense, but there may also be autonomic reactions such as loss of appetite and a feeling of indigestion, etc. Therapy involving PIR and RI is simple and effective.

Increased tension in the abdominal muscles, especially the rectus abdominis, is often a sign of painful visceral disease. However, it is also encountered in locomotor system dysfunction, particularly in patients with a forward-drawn posture on standing, where it is caused by a chain reaction pattern extending from the feet via the fibula and associated with TrPs in the biceps femoris. As a result the anatomical fixation of the pelvis is disturbed from below, leading to TrPs in the rectus abdominis with painful attachment points at the pubic symphysis, xiphoid process, and neighboring ribs, with forward-drawn posture, restricted retroflexion while standing, and (referred) low-back pain (see Figure 6.121). Needless to say, TrPs in the abdominal muscles are also capable of simulating visceral pain.

Gynecological disorders have always been traditionally associated with low-back pain. From our modern-day perspective the role of gynecological disorders as a leading cause of low-back pain in women has been overestimated. It was the gynecologist Martius (1953) who placed critical emphasis on the importance of the locomotor system.

Novotný & Dvorák (1984) conducted a study in 600 women attending a gynecology clinic at the University of Prague. They subdivided these patients as follows: the first group comprised 113 women with dysmenorrhea and normal gynecological findings who had low-back pain with typical onset at the menarche. This condition rarely deteriorates and very often improves after childbirth. A second large group developed symptoms during pregnancy and after delivery, that is dysfunctions occurred at a period when there is increased strain on and vulnerability of the spine and pelvis. A third group consisted of 59 patients with gynecological conditions giving rise to low-back pain. These were apparently viscerogenic disorders. The fourth and largest group of patients were women suffering from minor dysfunctions of the spine and pelvis, in whom gynecological examination was carried out as a routine diagnostic procedure, but with negative findings.

In a group of 150 pregnant women, 48 had a history of dysmenorrhea (Lewit et al 1970). Of these 48 patients, 38 had lumbosacral movement restriction or pelvic distortion. Findings in the lumbosacral spine and pelvis were ‘normal’ in only 10 women. ‘Normal findings’ meant that pain was generally felt only in the hypogastric region but not in the lumbar region. Moreover, low-back labor pains during an otherwise normal delivery were closely correlated with dysfunctions of the spinal column and pelvis.

In another group of 70 women with menstrual pain and normal gynecological findings, treatment of the spine, mainly by manipulation, brought considerable improvement in 43 cases, improvement in 13 cases, and no improvement in 14 cases.

In summary, it appears that low-back pain may have its origin in the female pelvic organs and may become manifest during childbirth and menstruation as well as following gynecological disease or surgery. In a very large number of patients, low-back pain is of locomotor system origin and is mistakenly attributed to primary gynecological disturbances. One reason for this may be a TrP in the iliacus which is palpated as a site of tender resistance in the hypogastric region. Menstrual pain with otherwise normal gynecological findings, especially when localized in the low back, is usually of vertebrogenic origin and is often the first clinical manifestation of locomotor system dysfunction

Labor pains felt in the low back in an otherwise normal delivery should also be interpreted as being of vertebrogenic origin. Current knowledge also points to the importance of the pelvic floor. Screening for a TrP there should also be conducted as routine (see Figure 4.12) and, if found, its treatment is a major preventive factor.

Research conducted by Mojžísová (1988) and Volejníková (1992) suggests that manual therapy may offer some prospect of success in women with sterility of cryptogenic origin (i.e. with negative organic findings).

To illustrate this point, let us take concussion as an example. It stands to reason that any force acting on the head must also affect the cervical spine. Similarly, from the size and weight of the human skull compared with the cervical spine, it will be obvious which of these two structures represents the site of lessened resistance, in relative terms. It is also therefore no coincidence that the majority of injuries to the cervical spine, including vertebral fractures, are concomitant effects of craniocerebral trauma. This fact is also borne out by autopsy findings: without exception, in all 20 cases of death after head injury, Leichsenring (1964) also found serious damage to the cervical spine.

We can only concur with Junghanns (1952) who wrote that symptoms usually attributed to concussion were in reality caused by trauma to the cervical spine. And this opinion is also shared by Gutmann and others. In fact, a striking similarity exists between the post-concussion syndrome and the cervicocranial syndrome. In both conditions, patients experience headache that is frequently paroxysmal and is associated with dizziness or vertigo. This was first described by Barré & Liéou (1926) as ‘posterior cervical sympathetic syndrome’ and later by Bärtschi-Rochaix (1949) as ‘cervical migraine’ occurring in the wake of cranial trauma.

The close relationship between concussion (closed head injury) and whiplash injury is also evident from a study conducted by Torres & Shapiro (1961) in which they compared the clinical and electroencephalogram (EEG) findings after concussion or whiplash injury. The neurological findings were virtually identical, with the difference that pain was more common in the neck and arms after whiplash injury. EEG abnormalities were present in 44% of patients after concussion and in 46% of patients after whiplash injury. In both cases temporal lobe foci were seen predominantly.

With ever-increasing numbers of vehicles on the roads, the incidence of whiplash injury is rising all the time. Whiplash injury often causes disproportionately severe symptoms and poses a problem in terms of therapy. Such incidents usually involve an unexpected rear-end impact that causes the trunk of the individual(s) leaning back against the automobile seat to suddenly jerk forward at high speed; in this process the head and neck engage in a whiplash movement relative to the trunk. This can be particularly harmful if the head is also rotated relative to the trunk. Immediately after the accident it is common for the whiplash injury victim to feel that little of note has occurred, with any symptoms being minimal. It is not until hours or a few days later that the often considerable symptoms of a severe post-traumatic cervicocranial syndrome develop, and these commonly take a chronic course. In very recent whiplash injury, gentle examination often reveals hypermobility, whereas movement restrictions develop later due to muscle TrPs.

As this case illustrates, forceful rear-end impact is not the only mechanism capable of causing whiplash injury. For example, it may also be produced by a fall on to the shoulder and we even know of one case where the condition was brought about by the impact of a wave against the head while the patient was in the sea. Although the underlying mechanism bears some similarity to distortion, the clinical course is far more severe. In computed tomography scans obtained in such patients, Dvorák (1989) detected tears in the alar ligament with hypermobility of the craniocervical junction, a finding that explains the often unfavorable response to HVLA thrust techniques.

One complication of whiplash trauma has been described by Berger (personal communication) under the designation ‘stiff or frozen neck syndrome’. He has reported the following characteristic pattern based on an analysis of 20 cases: movement is restricted, slow and jerky on cervicomotography (which involves registration of head movements in three planes simultaneously: fast movement; slow movement, eyes and head following a pendulum; passive movement). Passive movement is less restricted than active, and slow movement has a greater range than fast movement. Rotation with the patient supine (fixation at T1) is less restricted than rotation in the sitting position. There is marked hypertonus in muscles and soft tissues and there are extensive HAZs. Patients report intense pain radiating into the head and arms, often accompanied by dizziness and blurred vision. In this stage, patients cannot tolerate any type of physical therapy, whether mobilization, manipulation, or massage. They require immobilization, a supportive cervical collar, and sometimes cryotherapy.

By 1965 we had followed up more than 65 post-concussion patients who had lost consciousness after an accident. Abnormal neurological findings (signs of disturbed equilibrium) were present in one case. By contrast, clinical findings in the cervical spine were normal in only six cases. The results of manipulation and reflex therapy were excellent in 37 cases, good in 8 cases, and unsatisfactory in 10 cases.

In a further group of 95 cranial trauma patients without concussion, seen during the period from 1964 to 1970, movement restrictions involving the cervical spine were absent in only 4 cases. Interestingly, the predominant finding was movement restriction at C1/C2. A painful anteflexion test, indicative of ligament pain, was present in 10 patients who were treated without success.

From the perspective of prevention, the acute stage following trauma is most important of all. In this respect, post-concussion patients offer a model for acute spinal trauma because they are routinely admitted to hospital and therefore are not lost to medical examination. With a view to preventing later complications, a series of 32 patients in the acute post-trauma stage was referred to us for examination and treatment. All the patients were fully conscious, with no suspicion of intracranial hemorrhage, and with negative X-ray findings in the skull and cervical spine. A chronic disease course evolved in only one patient, who also developed arterial hypertension. Treatment was further unsuccessful in one patient with dizziness and a calcaneal fracture. Twenty-four patients (75%) became symptom-free immediately after treatment.

Bartel, 1980a and Bartel, 1980b has published almost identical results: in 50 cases examined immediately after head injury he detected movement restriction in all patients but 2, the lesion being most frequently located at C1/C2. In 40 cases, a single treatment was sufficient, usually involving neuromuscular techniques. Treatment had to be repeated in 6 cases, in 2 of these without success. (As a historical footnote to the three case studies presented above, it should be pointed out that neuromuscular techniques were still unknown in 1958.)

These experiences suggest a preventive role for manipulative therapy in acute head injury while movement restrictions are still in the early stage. Lack of awareness and understanding concerning manual diagnosis and therapy means not only that this opportunity is frequently missed but also that the patient complaining of pain quite literally has insult added to injury, being told that there are no organic findings and hence the pain must be ‘all in the mind.’

What is true for head injury is equally valid for other parts of the locomotor system: a patient who falls on a hand may also suffer from indirect injury to the cervical spine, while one who falls on a foot may also sustain injury to the pelvis and lumbar spine. A fall on to the shoulder may have the same effect as whiplash injury.

A number of typical lesions are encountered in the extremities after injury. A fall on to the hand, whether the radius is fractured or not, generates a force on the radius that pushes it upward at the elbow, causing dysfunction at the elbow joint. Clinically, this is often manifest as pain at the styloid process; and this may not start until after the plaster cast has been removed following a Colles’ fracture. Examination then regularly reveals impaired radial abduction at the wrist with movement restriction between the radius and ulna; however, the cause is located at the elbow where there are signs of a lateral epicondylopathy. Any treatment administered at the site of the pain is futile, but pain is immediately relieved by treatment for movement restriction at the elbow.

A fall on to the shoulder is likely to affect not only the cervical spine but also the structure that bore the direct brunt of the impact, namely the acromioclavicular joint and/or a first rib.

After foot injury, with or without fracture, we usually find movement restrictions in the tarsometatarsal and intertarsal joints, as well as in the ankle joint. After knee injury there is often movement restriction at the fibular head.

Functional coxalgia is not uncommonly the sequel to a sprain of or fall on to the hip. Appropriate mobilization or manipulation is the proper procedure immediately after injury, and the effect is often seen promptly. However, this depends on diagnostic precision in excluding fracture and hematoma. Early treatment will avoid later complications and prevent the condition from becoming chronic.

As described in Section 7.1.8, major lesions such as outflare and inflare dysfunction result mainly from trauma following a fall on to the buttocks (coccyx).

The main symptom is headache on the side of the affected joint, with pain radiating strongly into the ear and face. When taking the patient’s history, questions should always be asked about missing teeth, badly fitting false teeth, or trauma. However, pain may also be caused by increased tension in the masticatory muscles, and psychological tension (teeth grinding, bruxism) may also be a factor. The masticatory muscles are in a chain with the muscles at the craniocervical junction and consequently the clinical picture may be difficult to distinguish from dysfunction at the craniocervical junction. Dizziness or vertigo or possibly tinnitus may also be present. Dysphagia and dysphonia may be noted where there is increased tension at the floor of the mouth, also involving the digastricus.

Patients commonly complain of headache felt at the occiput, mainly on one side. History taking often reveals evidence of recurrent tonsillitis or otitis media. Pain typically occurs in the morning and may waken the patient during the night.

TrPs are located primarily in the short extensors of the craniocervical junction and in the upper part of the sternocleidomastoid. Other pain points are found at the posterior arch of the atlas, at the transverse processes of the atlas, at the nuchal line, and at the posterior margin of the foramen magnum. Mobility testing reveals restriction of anteflexion and retroflexion most commonly, followed by restriction of side-bending to the left, and then of side-bending to the right. Joint play is reflected in dorsal shifting of the occipital condyles relative to the atlas. As with all motion segments in the cervical spine, there is frequently an important TrP in the diaphragm. The mobility of the scalp is restricted relative to the underlying tissues.

Dysfunction in this segment is most commonly the result of trauma, but otherwise it is encountered less frequently. Although headache predominates, neck pain is usually also present.

There is a typical pain point at the lateral surface of the spinous process of the axis, more commonly on the right side. There are characteristic TrPs in the sternocleidomastoid and levator scapulae. Head rotation is restricted, usually to the right, whereas side-bending (‘nodding’) is more often restricted to the left. This is the only cervical segment in which rotation restriction is not necessarily in the same direction as restriction of side-bending. In this segment, rotation takes place precisely around a vertical axis.

This is the segment where acute wry neck occurs. However, this does not mean that it is the only segment in acute wry neck where movement is restricted.

The most prominent TrPs are found in the sternocleidomastoid, levator scapulae, and the upper part of the trapezius. Pain may therefore be felt not only in the head but also in the shoulder. A pain point is routinely found at the lateral edge of the spinous process of the axis (usually on the right side), and rotation and side-bending are usually restricted to the right.

Although headache may be present, pain referred to the arms is the characteristic finding here, in particular epicondylar pain at the elbow, more frequently on the lateral aspect. This may occur in combination with pain at the styloid process and with tenovaginitis that is common on the forearm.

Most TrPs are found in the deep layers of the paravertebral muscles, in the upper part of the trapezius, in the middle part of the sternocleidomastoid, and in the muscles with increased tension in epicondylar pain – the supinator, the finger and hand extensors, and the biceps and triceps brachii. Movement restriction at C3/C4 is sometimes also accompanied by symptoms of restriction at the craniocervical junction. There may be ‘binding’ of the cervical fascia.

Even here headache is no exception, but cervicobrachial and shoulder pain in particular is typical, in association with paresthesia. All the joints of the shoulder may thus be involved, as well as the first ribs.

Muscle tension is increased (with TrPs) primarily in the upper and middle parts of the trapezius, and in the sternocleidomastoid, scalenes, diaphragm, subscapularis, and infraspinatus as well as in the corresponding fascia. Together with the movement restrictions at the cervicothoracic junction, the scalenes and the pectoralis minor are responsible for the thoracic outlet syndrome, which is frequently in a chain with the carpal tunnel syndrome.

Because pseudovisceral pain is particularly common in these segments, differential diagnosis is of prime importance. Symptoms on the left side may simulate pain from the heart, lung, stomach, and pancreas; on the right side they may simulate pain from the gall bladder, liver, duodenum, and lung. If thoracic pain is not of visceral origin, it is usually secondary to dysfunction either of the cervical or of the lumbar spine (assuming that the patient is not suffering from a severe form of juvenile osteochondrosis). The exception to this rule is pain in the region where thoracic kyphosis peaks and the erector spinae is weakest, approximately at the level of T5. In rib dysfunctions there may also be pain at the sternocostal joints, which provide the main attachment points for the pectoralis major and minor. If the rib lesion is acute, breathing in and out is painful. Painfulness in the vicinity of the inferior costal arches is a characteristic sign of a slipping rib.

The most important TrPs are in the pectoralis major and minor subscapularis, serratus anterior, erector spinae, the diaphragm and pelvic floor, and only rarely in the latissimus dorsi. The mobility of the deep fascia is disturbed on the back (in a cranial direction) and especially around the thorax.

Pain is characteristically felt in the low back or between the shoulder blades. If the condition is acute, the patient will often volunteer the information that it has been provoked by straightening up suddenly from anteflexion with rotation. Because limited trunk rotation is not due to restricted joint movement but to TrPs in the thoracolumbar erector spinae, psoas major, and quadratus lumborum, the pain is felt principally at the attachment points for these muscles – at the iliac crest (low back) and at the lower ribs (below the shoulder blades), but hardly ever at the thoracolumbar junction. Kyphotic posture is the consequence of psoas spasm, which may also provoke pseudovisceral symptoms. If TrPs are simultaneously present in the abdominal muscles, then the pubic symphysis and xiphoid process may be tender. There is a viscerovertebral inter-relationship between these motion segments and the kidneys. Trunk rotation here is generally restricted in the direction opposite to the side where the muscle TrPs are located.

It is rare for this segment to suffer from dysfunction; when it does, it causes low-back pain. TrPs are found in the gluteus medius, below the iliac crest.

Like the other more caudal lumbar segments, dysfunction here is characterized by pain that is referred to the lower extremities. It is largely identical to pain originating in the hip joint, and is felt in the hip and the groin, radiating ventrally down the thigh to the knee and sometimes beyond as far as the tibia.

Muscle spasm with TrPs in the rectus femoris is characteristic, and therefore the femoral nerve stretch test is positive; the straight-leg raising test is usually negative. Further TrPs are found in the hip adductors, and for this reason Patrick’s sign is mildly positive.

Pain in this segment is felt in dermatome L5 that travels down the lateral aspect of the leg, from the thigh to the lateral malleolus.

The characteristic TrP is in the piriformis, and therefore pain is felt mainly in the hip. There is usually also increased tension in the hamstring muscle group, especially the biceps femoris, and the straight-leg raising test is therefore positive. There may be pain and movement restriction at the fibular head. Increased tension in the rectus femoris and hence also in the ischiocrural ligament and piriformis muscle often results in secondary movement restriction at the sacroiliac joint.

The pattern of pain here is consistent with dermatome S1, and radiates down the back of the leg as far as the heel and lateral malleolus.

There is increased tension in the hamstring muscle group and the straight-leg raising test is positive. As in dermatome L5, there is therefore often movement restriction of the fibula, with secondary sacroiliac restriction. A TrP in the iliacus is very characteristic, with pseudovisceral symptoms in the lower abdomen. In hypermobile patients there is often a pain point at the spinous process of L5.

Because the pattern of pain distribution here too is consistent with dermatome S1, it is virtually indistinguishable from that experienced in lumbosacral movement restriction. Owing to the wide variations in anatomical topography in this region, the pain point (indicated by many patients as lying above and medial to the PSIS) cannot be differentiated from the neighboring lumbosacral joint.

The TrP in the iliacus muscle is characteristic of the lumbosacral joint and differential diagnosis is possible only on the basis of mobility testing. In cases where the lower part of the sacroiliac joint is painful, the pain may be felt to one side in the sacrococcygeal region. Current knowledge with regard to chain reaction patterns of dysfunctions indicates that most sacroiliac restrictions are secondary in nature, apart from those in osteoarthritis of the hip.

Only about one-fifth of patients in whom the coccyx is tender at palpation feel their pain as coccygodynia. Instead they tend to complain of low-back pain. Conversely, if patients report pain arising from the coccyx, it may in fact originate from the lower part of the sacroiliac joint, the pelvic floor, or even from a painful ischial tuberosity. This is especially the case when the coccyx is tender not in the midline but to one side. Pain is felt mostly when the patient is seated. The part played by trauma tends to be overestimated: psychological tension is a key factor.

TrPs are present in the levator ani, gluteus maximus, hip adductors, ischiocrural muscle group, and sometimes also in the piriformis and iliacus, which explains why Patrick’s sign and the straight-leg raising test may be positive.

The most easily palpated TrPs of the deep stabilization system are found in the diaphragm and pelvic floor. From these starting points, innumerable chain reaction patterns extend upward to the craniocervical junction and masticatory muscles, and downward to the pelvis and lower extremities. Screening for these TrPs should therefore be performed as routine in all patients. TrP relaxation is exceptionally straightforward and effective, particularly in the diaphragm, but activation is generally the preferred option in stabilization system dysfunction.

When merely dysfunctional or in the early stages of osteoarthritis of the hip, the hip joint most frequently causes (asymmetrical) low-back pain radiating into segment L4. Knee pain is therefore often an early indicator of osteoarthritis of the hip. By contrast with the situation in vertebrogenic low-back pain, it is walking for longer periods that is painful, especially over a hard terrain; and by contrast with knee dysfunction, stair climbing is also painful.

The key TrPs are located in the hip adductors, flexors, and abductors. A positive Patrick’s sign and the characteristic capsular pattern are typical.

The foot is a key region of fundamental importance. However, the main chain reaction patterns extend via the fibular head and may even start from there if findings at the feet are negative.

In the foot itself there are often movement restrictions between the individual bones, as well as TrPs in the deep plantar muscles with attachment point pain at a calcaneal spur. TrPs are also located dorsally between the metatarsal bones. TrPs in the soleus muscle are associated with pain in the Achilles tendon and its attachment point. The most important faulty movement patterns relate to functional flat foot and automatic flexion of the toes during the toe-off phase of the gait cycle and when the body’s center of gravity is shifted forward. Afferent pathway disorders are especially important here, characterized by increased or diminished tactile perception, along with simultaneous alterations in muscle tonus that are often asymmetrical. The typical chain reaction pattern is a forward-drawn posture that extends from the fibular head to the biceps femoris and onward via the abdominal, gluteal, and back muscles to the craniocervical junction. The foot possesses all the key characteristics of the deep stabilization system.