Chapter 9 The two primary patterns of torso dysfunction

Altered function in the posturomovement system is observable in the manner in which we relate to gravity. The pelvis, in housing the centre of gravity of the body plays a central role in posturomovement control and its position when standing is the key to good or faulty postural alignment.¹ Small shifts can exert significant changes throughout the body.

While each person with back pain has an individual presentation; in general, the altered neuromuscular responses fall into certain predictable, common patterns of response which can be distilled into the two primary pictures of torso dysfunction. These are characterized by a changed sagittal plane spatial position of the pelvis in standing and corresponding alterations in the postural alignment of the body in relation to the line of gravity (see Ch. 8). They afford a simple clinical classification system and underlie a working model or paradigm to help understand the development and perpetuation of posturomovement disorders responsible for many musculoskeletal pain syndromes. Before examining these two proposed primary patterns more closely, it is useful to consider clinical classification systems suggested by other authors.

The case for a clinical classification based upon underlying motor control impairments

The premise that impairments in the way people posture and move are the underlying factor driving the patient’s presenting musculoskeletal pain and dysfunction is central to the approach of this model and is one shared by Sahrmann,^2,³ O’Sullivan,^4,⁵ and Dankaerts et al.⁶ Based upon this premise, those authors have argued for a clinical classification system to assist in the diagnosis and management of chronic non specific low back pain disorders (CNSLBPD). They advocate classification into clinical subgroups which are determined by ‘the alignment, stress, or movement direction that most consistently reproduces pain.³ When the mechanism or cause of a disorder is known treatment of the cause is usually considered more effective.⁶

Sahrmann ³ arrived at five diagnostic categories for CNSLBP based upon the direction of movement causing the pain, which in order of her observed frequency are:

Sahrmann says: ‘The diagnosis is designed to direct the intervention. The primary strategy for an intervention program is eliminating the alignment stress or movement in the symptom producing direction. The program does not emphasize movement in the opposite direction, except where the alignment impairment is excessive’.³

Similarly, O’Sullivan ^7,⁸ and Dankaerts et al.,⁶ no doubt influenced by Sahrmann, suggest a mechanism based classification in the diagnosis and treatment of CNSLBPD. They also proposed five distinct yet different clinical patterns based upon a specific direction of motor control impairment which aggravated the pain, and the hypothesized mechanism underlying the pain disorder ⁶. These patterns were originally described by O’Sullivan in relation to ‘instability’ of the lumbar spine:^7,⁸

• flexion pattern – this appears to be most common pattern ⁸

• lateral shift pattern

• active extension pattern

• passive extension pattern

• multidirectional pattern.

O’Sullivan ^4,⁵ further elaborated his classification based upon the mechanism underlying the disorder, proposing that three broad subgroups of NSCLBP disorders exist. The directional patterns appear to be a subgroup of Group 3.

1. In this group, the underlying pathological processes drive the pain and the patient’s motor responses are secondary and adaptive to this, e.g. inflammatory pain disorders, severe structural disorders, neuropathic or centrally mediated pain.

2. In this, a dominance of psychological and/or social factors represents the primary mechanism underlying the disorder. Altered central processing, and amplification of pain result in disordered movement and motor dysfunction. The patient’s coping and motor control strategies are maladaptive in nature.

3. In this large group, maladaptive movement patterns result in chronic abnormal tissue loading and ongoing pain. They present in either of two ways:

• Movement impairments characterized by avoidant pain behavior associated with a loss of normal physiological lumbopelvic mobility in the direction of pain. They present with abnormally high levels of muscle guarding and cocontraction of the lumbopelvic muscles and fear of movement. The neuromuscular splinting and pain avoidance behavior is considered to be the mechanism which drives the pain.

• Control impairments demonstrate no impairment to mobility of the symptomatic spinal segment in the direction of pain provocation. This is associated with inability to effectively control the neutral zone. The pain provocation behavior is considered to represent the mechanism driving ongoing symptoms.

This author concurs with O’Sullivan’s three broad subgroups and that maladaptive movement patterns are responsible for chronic abnormal tissue loading and ongoing pain. However, this author considers that movement and control impairments are not necessarily exclusive, but generally co-exist in some measure, albeit with one dominating, depending upon the subgroup classification to be presented in this chapter (see also Ch. 8). The patterns of altered neuromuscular response (movement impairments) may well be the heightened responses of chronically dysfunctional movement pattern behavior and indicative of the severity of pain, tissue irritability as well as the stage of the disorder. It is suggested that clinically, symptom reproduction with movement is not necessarily always achieved nor a reliable guide to the underlying reason why that person’s movement problems have developed and are further feeding his pain picture. Nor is it necessarily always desirable to reproduce the pain as the testing in doing so can be potentially very provocative.

This proposed model, while resonant with O’Sullivan’s work, offers a somewhat different view around the notion that maladaptive movement patterns result in chronic abnormal tissue loading and ongoing pain. Rather than rely upon symptom provocation, it offers a simple clinical classification system which initially relies upon observation of the quality of movement. Concerned with basic function, it delineates the more common postural and related movement impairments which appear to constitute the underlying mechanism responsible for the development and perpetuation of most axial and related pain syndromes including those of the lumbopelvic region. It would appear that there is an inherent tendency for these maladaptive motor responses to develop in us all under certain conditions. Various elements can be fairly consistently observed in the young and old, from the elite sportsman, yoga practitioner to the office worker and the ‘couch potato’. The maladaptive responses are just more numerous, developed and obvious in people with frank musculoskeletal pain disorders.

Appreciating the features of the model as outlined not only provides a clinical classification but also guides the assessment process and provides a functional diagnosis based on the pattern of neuromyoarticular dysfunction responsible for the pain disorder. It also provides predictive and preventative insights – the presenting symptom picture usually being an acute or subacute episode on a variable picture of underlying neuromusculoskeletal dysfunction at various stages of disorder.

The two primary pictures of torso dysfunction

Observing the habitual standing posture provides a convenient ‘road map’ of the way in which the patient has adaptively organized herself against gravity.

In the sagittal view optimal posturomotor control has the pelvis balanced within the line of gravity, but when disturbed, the pelvis is postured either more anteriorly or posteriorly from the line of gravity (Fig. 9.1 & also Fig. 8.4).

Fig 9.1 • Schematic sagittal view: altered pelvic position influences the body’s neuromuscular response to the gravitational ‘line of force’.

This constitutes the basis of the two primary pictures of dysfunction – the pelvic crossed syndromes. When pelvic alignment changes so do the spinal curves in a predictable fashion. The thoracolumbar junction is considered the inflexion point between the thoracic kyphosis and the lumbar lordosis and through which the line of gravity passes.⁹ Its position has a marked effect on the distribution of the intersegmental rotations of the lumbar vertebrae and upon the magnitude of the sagittal moments carried by the passive spine.¹⁰ When more anterior, a constant extension torque ensues; when more posterior, a flexion torque results.¹¹

Roussouly et al.¹² comment ‘the majority of degenerative disease occurs in spines that are well aligned in the coronal plane but exhibit highly variable morphology in the sagittal plane’. They performed a significant radiographic study examining the sagittal alignment of the lumbar spine in a cohort of 160 asymptomatic subjects. They found that ‘normal’ varied, and classified these variations into four groups. These subgroups resonate well with clinical impressions and so the features of each are described:

• Type 1 lordosis. The sacral slope is less than 35°; the apex of the lordosis is centered in the middle of the L5 body; the lower arc of lordosis is minimal decreasing toward zero as the sacral slope approaches horizontal; the inflection point (transition between the upper kyphosis and lumbar lordosis) is low and posterior creating a short lordosis with a negative lordosis tilt angle; the upper spine has a significant kyphosis of the thoracolumbar junction and thorax (Fig. 9.2).

• Type 2 lordosis. The sacral slope is less than 35°; the apex of the lordosis is located at the base of the L4 body; the lower arc of the lordosis is relatively flat; the inflection point is higher and more anterior decreasing the lordosis tilt angle but increasing the number of vertebral bodies included in the lordosis; the entire spine is relatively hypolordotic and hypokyphotic.

• Type 3 lordosis. The sacral slope is between 35° and 45°; the apex of the lumbar lordosis is in the centre of the L4 body; the lower arc of the lordosis is more prominent; the inflection point is at the thoracolumbar junction and the lordosis tilt angle is nearly zero; an average of four vertebrae constitutes the arc of the lordosis. The spine is well balanced.

• Type 4 lordosis. The sacral slope is greater than 45°; the apex of the lordosis is located at the base of the L3 vertebra or higher; the lower arc of the lordosis is prominent and the lordosis tilt angle is zero or positive; the number of vertebrae in lordotic orientation is greater than 5; a state of segmental hyperextension exists.

Fig 9.2 • The four lordosis types according to Roussouly et al. 2005. Change in the sacral slope effects reciprocal change in the lordosis.

While demonstrating that sagittal alignment ‘normally’ varies significantly, the authors found the least common was Type 2 and the most common was Type 3 (construed as normal); where the apex of the lordosis was located on average in the centre of the L4 body. They also confirmed that the characteristics of the lumbar lordosis are most dependent on the orientation of the sacral slope and the pelvis. They comment that there appears to be an association between loss of lordosis and an anterior shift of the vertical axis and the development of symptomatic back pain. Further, they comment that they have noticed that patients with symptomatic disc herniations are most commonly classified as Type 1or 2; patients with spinal stenosis are most commonly classified as type 4 and that they rarely see patients with significant complaints who are classified as Type 3! A further study ¹³ compared the native sagittal alignment of patients with spondylolysis and low grade spondylolisthesis against a control group. They found increased lumbar lordosis, but less segmental extension between L5 and S1 than in the normal population. Reporting a later related study¹⁴ in patients with lumbar degenerative diseases, they commented that previous data suggested that patients demonstrated less distal lordosis, more proximal lordosis and a more vertical sacrum; while that particular study found the loss of lordosis and a decreased sacral slope were significant. Their findings are important in corroborating the clinical impressions which underpin the pelvic crossed syndromes. Of particular significance are Type 1 with a reduced lordosis and Type 4 with an increased, albeit more cephalad or high lordosis.

In addition, Smith et al.¹⁵ reported a photographic study examining sagittal alignment in 235 adolescents and also identified four subgroups – neutral, hyperlordotic, flat and sway. A higher proportion of the adolescent group that had never had back pain was in the ‘neutral’ subgroup.

The Pelvic Crossed Syndromes

These paradigms have elaborated upon the model of the Pelvic Crossed Syndrome described by Professor Vladimir Janda.¹⁶^–¹⁸ Attempts to validate the relationship between The Pelvic Crossed Syndrome as described by Janda and back pain have not been successful.¹⁹ While the Pelvic Crossed syndrome as he described it certainly applied to some of this author’s patients, it did not completely fit the picture for many, or at all for others. It took some time for this author to recognize the other patterns.

• Posterior Pelvic Crossed Syndrome (PPXS). This fairly much equates to Janda’s original ‘pelvic or lower crossed syndrome’. In its pure form it does not appear to be as prevalent as might be expected, however it often underlies a Mixed Syndrome presentation (see Ch. 10). It resembles a ‘kyphosis-lordosis posture.¹

• Anterior Pelvic Crossed Syndrome (APXS). This appears to be the more common presentation within this author’s clinical practice population either as the pure form or underlying the mixed syndrome (see Ch. 10). It resembles a ‘sway-back posture’.¹

These two syndromes form the basis of a proposed clinical classification system.

It is important to appreciate that not all patients will demonstrate the pure pelvic and related picture. Some will show some tendency, and others will exhibit a variable mixture of the two with a dominant tendency. Understanding the features of each helps understand the patient in front of you – possibly a Mixed Syndrome (see Ch. 10).

Posterior Pelvic Crossed Syndrome (PPXS)

Sagittal alignment characterized by:

• Pelvis is posteriorly shifted with increased anterior sagittal rotation or tilt. This appears to result from both psoas and erector spinae hyperactivity.

• Trunk – anterior translation of the thorax via thoracolumbar ‘shunt’ from increased thoracolumbar (T/L) extensor muscle activity creates a forward loaded trunk and associated compensatory anterior pelvic rotation. The line of gravity passes behind the thoracolumbar junction and the posterior wall of the body cylinder is shortened. An important normative study by Harrison et al.²⁰ showed that trunk muscle activity can also influence pelvic position. Anteriorly translating the thorax at the level of T12 without restraining the pelvis resulted in it anteriorly tilting (and shifting posteriorly as shown, though not commented upon). The sacral base angle increased, the T12/L1 and L1/2 segments extended on average a total of 5° from the neutral position while L4/5 and L5/S1 flexed by a combined total of 6°. The flexing of the lower lumbars and the extension in the upper lumbars around the lumbar curve apex at L4 is interesting. In a later study,²¹ they calculated that the increased thoracolumbar extensor muscle activity associated with an anterior thoracic posture significantly increased the disc loads and stresses for all levels below T9. The IVD compressive and shear loads and the corresponding stresses were most marked at L5/S1 and L3/4 level.

• Hips are in relative flexion in the pure form as Janda originally described it. However, in the mixed syndrome (see Ch. 10) it is also common to see some patients lock their knees, externally rotate the hips, ‘butt grip’²² and hang the torso forward off the pelvis by holding with sustained activity of the thoracolumbar extensors.

• Cursory glance shows they look ‘extended’ with an increased lordosis. This is principally high lumbar and over the thoracolumbar junction. The Roussouly ¹² Type 4 lordosis is extant. However, closer inspection generally reveals that the lower lumbar levels in fact show some relative flexion and are poorly controlled. The further findings reported by Roussouly et al.^13,¹⁴ and those of Harrison et al.²⁰ with regard to reduced segmental extension of the lower levels in response to thorax position somewhat confirm this clinical impression. The chest is held more in the inspiratory position. Quick appraisal reveals a big belly, bottom and calves and bulky thoracolumbar extensor groups. Puffy superficial tissues and poor definition of the bony landmarks over the low lumbar levels and lumbosacral junction are usual.

• The altered length/tension relationships of the various muscles contributing towards this picture are shown in Table 9.1, Fig. 9.6.

Table 9.1 Altered myofascial length/tension contributing to PPXS

Muscle hypoactivity/ lengthened	Muscle hyperactivity/ adaptive shortness
Lower pelvic unit synergy (LPU) in particular: • transversus and internal oblique • lumbosacral multifidus • iliacus in controlling intrapelvic movement and anterior pelvic rotation AT the lumbosacral junction • probably pelvic floor Entire abdominal wall +++ Glutei – medius + Inefficient diaphragm activity	Thoracolumbar erector spinae +++ Serratus posterior inferior+ Anterior hip flexor groups: • primarily psoas ++ • RF TFL Obturator group including piriformis? Hamstrings? ? hip internal rotators > external rotators? ?? lateral fibres of: • internal oblique and • latissimus dorsi

As Janda ¹⁷ described the ‘cross‘, there is an oblique relationship between the iliopsoas/hip flexors and erector spinae which are overactive/tight with poor control of eccentric lengthening. The spatially oblique gluteals and abdominals are weakened resulting in an anterior pelvic tilt, increased lordosis and a slightly flexed position of the hip (Fig. 9.3; Fig. 9.6). If the lordosis is deep and short the imbalance is principally located in the pelvic musculature. If it is shallower but longer extending into the thoracic area the imbalance is more marked in the trunk musculature.^17,²³ Clinically, the latter appears more common and many also have quite bulky buttocks. Janda noted that those who stand with an opened lower thoracic aperture have a shortened diaphragm in association with underactive abdominals with decreased excursion in breathing.²³ Janda also noted that hamstrings could be tight in this syndrome either as a compensatory mechanism to lessen pelvic tilt or possibly as a functional compensation for the inhibited glutei.¹⁷ He also noted that an imbalance can exist in the lateral pelvic muscles where a weak gluteus medius can be compensated for by overactivity and tightness in the ipsilateral quadratus lumborum and tensor fascia latae. An increased thoracic kyphosis and further compensatory increase in the cervical lordosis develop in efforts to balance the body and keep the head and eyes in the upright position.¹⁷

Toppenberg and Bullock ²⁴ examined lumbopelvic muscle lengths and their interrelationships in healthy adolescent females and found significant positive correlations between shorter (by implication overactive) erector spinae and iliopsoas and rectus femoris with a tendency for longer abdominals (by implication weaker) in association with longer gluteals and shorter iliopsoas muscles. They concluded that the pattern of length relationships which constitute the pelvic crossed syndrome as described by Janda can be seen in normal pain free adolescent females. This study lends weight to the premise that movement dysfunction is present and observable before pain appears. A prospective study would be nice in determining which subjects went on to develop pain syndromes.