A general or regional lack of axial extension control

The manner in which the spine is postured when upright highly influences patterns of trunk muscle activity.¹ Conversely, patterns of muscle activity determine how the spine is postured. By and large people with spinal pain syndromes can move but they can’t ‘posture’ very well: if they manage to align the spine in neutral they have difficulty maintaining it in movement.

Poor control of a ‘dynamic antigravity neutral’ means the patient finds sitting or standing difficult to do in an easy non effortful way. He will tend to adopt either of two extremes – passive collapse or overactive ‘holding’. Both affect function around the body’s centre:

Poor pelvic base of support

The requirement for any column ‘to be up’ is an appropriate and well grounded foundation and the spinal column is no exception. Effective support comes from below and yet most have a ‘dead tailbone’ and poor control of the base of the spine. As the sacrum is part of the pelvis it is this that provides the important active base of support for the entire axial spinal column. Inadequate deep system activity, particularly of the Lower Pelvic Unit, reduces the ability of the pelvis to spatially adapt and provide an appropriate and effective base of support to initiate, lift and direct control of the spine from its base – the sacrum and coccyx.

The alignment and control of the spine in sitting, standing and bending forward is compromised, jeopardizing its safety. See defective pelvic control (p.170)

Common altered strategies for sitting and standing

The habitual adoption of poor sitting positions is probably the single most significant instigator and perpetuator of the postural and related movement dysfunction associated with the development of spinal pain and related disorders. In a modern industrial society long periods of sitting and relatively reduced general activity levels begin with schooling. The advent of computers and increasing sedentary work and leisure practices mean we do even more of it. Thecentral nervous system (CNS) is relatively starved of decent proprioceptive inputs and automatic responsesbegin to suffer (see Ch.11). Altered alignment changes the motor memory, affects muscle activation demand, the line of pull of muscles, creates the need for ‘holding patterns’ and leads to changes in the myofascial matrix.

Passive strategy

Sitting. The common strategy involves rolling back onto the posterior ischia and staying there. Repeated enough, the person begins to lose options for varied position change in sitting. Poor initiation and control of the base of support through the ischial tuberosities compromises the ability of the axial spine to adjust and move. This is particularly so when the commonly habitual strategy of crossing the legs is adopted. Even worse is ‘putting the feet up’ on stools or similar, often advised when the ‘circulation is bad’ which only serves to worsen it! The alignment and control of the whole spinal column is affected (Fig. 8.1).

Fig 8.1 • Passive collapse in sitting creates eccentric loading in the spine of a 15 year old (also in Fig 8.10).

Collapsed sitting switches off demand in the systemic local muscle system (SLMS), rendering the joints and soft tissues vulnerable. In ‘normal’ pain free subjects, slump sitting has been shown to decrease activity in the internal oblique and multifidus^1–3 transversus and internal oblique,⁴ particularly if the legs are crossed⁵ or higher than the pelvis. Some normative studies have reported increased lumbar extensor muscle activity^6,7 in slump sitting, yet the subjects shown in the study by Callaghan and Dunk⁷ are not in the position that most potentially or actually symptomatic subjects commonly adopt.

The posterior pelvic tilt creates hyper flexion of the spine⁸ – particularly over the lower levels, including the lumbosacral junction with well documented detrimental consequences. Cadaveric studies of lumbosacral motion segments have demonstrated the dramatic impact of increased segmental flexion on fatigue failure.⁹ Solomonow et al.¹⁰ showed induced flexion creep in feline viscoelastic tissues desensitized the mechanoreceptors and dramatically diminished muscular activity in multifidus. Later studies¹¹ showed prolonged flexion results in tension-relaxation and laxity of viscoelastic structures, loss of reflexive muscular activity within 3 minutes and EMG spasms in multifidus and other posterior muscles. The spasms and muscular hyperexcitability in response to 20 minutes static loading even when very light loads were applied were still evident after 7 hours of rest¹² and lasted for more than 24 hours.¹³ In addition, the micro-damage from sustained loading of the viscoelastic tissues results in time dependent development of inflammation¹⁴ setting the stage for chronic neural irritation and a plethora of referred symptoms of which pain is just one.

Usually, any attempts to ‘sit up straight’ are not initiated from the pelvic base of support but by intermittent systemic global muscle system (SGMS) activity of the muscle groups over the thoracolumbar junction.¹⁵ O’Sullivan² draws attention to the critical role of pelvic position in determining spinal muscle activation patterns. ‘Holding oneself up’ is tiring and poorly sustained and so shortly the patient collapses again. In ‘normal’ subjects, significantly less superficial lumbar multifidus and internal oblique activity has been demonstrated in this postural strategy.¹⁶

The work of Solomonow and colleagues clearly demonstrates that a cumulative neuromuscular disorder develops because of repetition of static lumbar flexion, the severity of which is magnified by the number of repetitions. Full recovery of creep may not occur.¹⁷ O’Sullivan et al.¹⁸ showed a relationship between flexed sitting postures, reduced back muscle endurance, physical inactivity and flexion provoked low back pain. In sitting, twisting mobility significantly increases when the spine is flexed further increasing vulnerability of the posterior annulus to injury.¹⁹

Importantly, collapse of the lumbopelvic spine will affect the alignment of the rest of the spine including the head and neck, a fact which is often overlooked in some studies on cervicothoracic posture.²⁰ It also contributes to the development of the shoulder crossed syndrome²¹ (see Ch.10).

In standing, the same postural pattern of posterior pelvic rotation is invariably carried through from sitting – the tendency being, to shift the pelvis forward with posterior rotation, hang off the iliofemoral ligaments in hip external rotation, with hyperextended knees and a collapsed spine. The sacrum is counternutated and L5 in relative flexion – an unfavorable loading state of the lumbosacral and SIJ region. This ‘locking’ of the lower limb kinetic chain limits the pelvis’ ability to be an adaptable and appropriate base of support for movement control of the spine. Further, when the pelvis is shunted forward, there is reduced lumbopelvic SLMS demand. Snijders et al.²² showed posterior pelvic rotation decreased activity in internal oblique. There is little buoyancy or ‘lift’ in the axial column or through the pelvis-leg base of support– the whole SLMS is relatively ‘switched off.

Overactive strategy

Sitting. The person ‘holds himself up’ (Fig. 8.2) – from extensor system dominance and often also as a result of a mistaken belief that it is ‘good posture’ to do so. This is generally achieved by more consistent over activity of SGMS muscles – particularly the extensor groups over the thoracolumbar junction.^3,15 However, control of the pelvis as an effective and adaptable base of support for the axial skeleton is still deficient. Dankaerts et al,²³ using an electromagnetic measuring device, examined sitting postures in those low back pain subjects who actively extend in sitting and reported an increased lumbar lordosis. While the low lordosis was reported as greater than the controls, it is suggested that clinically, even this group usually demonstrate reduced intersegmental joint play into extension over the lower levels when assessed by skilled palpation. Appearances can be deceptive. In a radiographic study, Roussouly et al.²⁴ showed that while lordosis was increased, segmental extension between L5 and S1 was reduced. In the main, reduced extension over the lower levels (relative to the upper levels) and associated deficient intersegmental neuromuscular control is clinically apparent.

Fig 8.2 • An ineffectual pelvic base of support requires ‘holding oneself up’. Note the poor lateral abdominal tone.

The superficial muscle overactivity reduces the ability to posturally adjust and shift weight over the support base. Intentionally stiffening the trunk by co-activating the superficial muscles has been shown to degrade postural control in unstable sitting.²⁵

Standing. The standing overactive patterns are again a reflection of the sitting posture patterns – primarily relying upon dominant activity of thoracolumbar extensor groups and related considerable underactivity of the anterior abdominal wall. The thorax is shunted forward in relation to the pelvis. In an important and really nice ‘normal’ study, Harrison et al.²⁶ demonstrated that anterior translation of the thorax resulted in posterior displacement and anterior tilt of the pelvis with extension of the upper lumbars and flexion of the lower lumbars. Reduced SLMS activity in the lower pelvic unit means that the dynamic base of support through the pelvis-leg kinetic chain is still inadequate.

The superficial muscle hyperactivity splints the spine and further disallows it to adequately prepare for, dissipate and dampen the forces created by head movement breathing and particularly in response to limb movements. Reduced segmental adjustments mean balance suffers. Mok et al.²⁷ showed decreased preparatory and resultant increased correctional lumbopelvic movements in response to rapid arm movements. Smith et al.²⁸ experimentally induced low back pain and found reduced motion of the trunk associated with breathing.

Thus in upright activities, some regions of the spine are subjected to collapse, compression and a functional ‘buckling’– they become relatively uncontrolled or ‘unstable’ while other regions become stiff or ‘over stable’ and fixed. This interrupts or damps the transference of the movement wave up through the spine.

The tendency to uneven patterns of control is also apparent in the asymptomatic population as Gregory and Callaghan²⁹ found when ‘university population’ subjects stood for 2 hours as they performed four light manual tasks. 13 of the 16 subjects developed some level of low back pain during that time. One of only three variables to significantly change was an increase in lumbar spine flexion. When central support is reduced because of inadequate deep local muscle system activity, the person is forced to rely more on abnormal SGMS activity in low load activities. Gregory et al.³⁰ had a group of college students stand for 2 hours and found that those who developed substantial back discomfort showed greater superficial extensor trunk muscle activity at the beginning and end of the standing period with further increased responses to sudden trunk perturbations. After discomfort developed, the superficial abdominal activity also increased.

Defective intrapelvic control (refer to Ch. 6 Part B)

Inadequate control of Lower Pelvic Unit (LPU) muscle synergies result in difficulty performing the Fundamental Patterns of Pelvic Control. Attempts to do so invariably utilize strategies involving a lot of SGMS activity – either from large pelvi-femoral muscles and/or those higher up the torso normally responsible for controlling the relationship between the thorax and pelvis. Manual movement testing predictably reveals patterns of joint hypomobility which are also reflective of the motor control difficulties.

Fundamental Pelvic Pattern 1 (FPP1)

FPP1 is consistently the pattern that most if not all have little idea of the action and the most difficulty performing. Low lumbar segmental movement into extension is generally reduced with underactivity in multifidus, lower transversus, internal oblique, iliacus and probably psoas. The prime movers responsible for FPP2 are generally hyperactive and do not adequately eccentrically lengthen further hindering the proper performance of this pattern. Instead the action is more likely attempted by activating the thoracolumbar erector spinae, serratus posterior inferior higher up around the mid torso – a bilateral ‘posterior cinch’ which serves to ‘fix’ the thoracolumbar segments, thrust the lower anterior pole of the thorax forward and limit diaphragm activity and basal chest expansion. This may be overt or subtle yet readily discernable by palpation (Fig. 8.3). Because of difficulty with or habitual non use of this pattern, the pelvis is generally more posteriorly rotated, the sacrum counter-nutated and posterior hip opening is reduced as is low lumbar extension and control.

Fig 8.3 • Rather than initiate the FPP1 movement with a subtle anterior pelvic rotation, there is just discernable central posterior cinch pattern activity.

Defective spatial control of the pelvis

Normally, the lumbopelvic stabilizing muscles including the pelvic floor are active when maintaining optimally aligned erect postures.^1,3,33 Hodges³⁴ states ‘there is considerable debate as to whether pelvic and lumbar positions are different in low back and pelvic pain although changes have been identified in specific subgroups’. Clinical observation reveals definite patterns of altered spatial position and control and this is described.

Reduced intrapelvic control compromises the ability to spatially align and adjust the pelvis when weight bearing. Rather than control the pelvis around a ‘dynamic neutral’, the tendency is to assume postures in more passive, end range positions. The motor control difficulties are apparent in all three planes of spatial pelvic control, but are particularly obvious in the sagittal plane.

Sagittal plane

Here the observed preference is to posture and initiate subsequent movement from either an anteriorly or posteriorly shifted spatial relationship to the vertical neutral. The habitual preference for either forms the basis for a clinical classification system based on altered function (see Ch. 9). While whole synergies of muscles control the spatial position of the pelvis, psoas appears to play a large role. When underactive the pelvis shifts forward and when overactive it shifts back. The postural shift is always accompanied by a coexistent sagittal rotation as shown in Figure 8.4:

• Anterior shift and related posterior pelvic rotation with a corresponding diminished ability to posteriorly shift and counter rotate the pelvis into anterior pelvic rotation

• Posterior shift and related anterior pelvic rotation – with corresponding difficulty in anteriorly shifting and counter rotating the pelvis into posterior sagittal rotation.

Fig 8.4 • Conceptual schematic sagittal view showing pelvic shifts and associated rotations (exaggerated for clarity).

While the anterior and posterior pelvic shifts and associated sagittal rotations are clinically apparent, there is little acknowledgement found in the literature except in a personal article by Schleip on the structural typology of Hans Flury.³⁵ In a very recent paper, Brumagne et al.³⁶ discuss the inconsistent results in the small amount of studies which report altered body inclination in relation to postural control. Two studies found a more anterior centre of mass^36,37 with related increased back muscle activation, while two others reported a more posteriorly located centre of mass.^38,39 Clinical classification into the two primary pictures of dysfunction may help explain these diverse findings (Ch. 9).

Coronal plane

The postural habit of passively ‘hanging’ the body predominantly on one leg is common and partly contributes towards the high incidence of hip ‘bursitis’ (Fig. 8.5). Reduced LPU activity subsequently affects the ability to laterally shift weight through the hip joints; either the pelvis over the weight bearing leg, or the leg medially under the pelvis. Instead control is attempted higher up via a bilateral ‘cinch’ which then affects the spines ability to posturally adapt in the coronal plane and maintain three dimensional control of its alignment.

Fig 8.5 • Passive lateral ‘hang’ in standing – the deep system is ‘off’.

Poor pelvic control affects the ability of the sacrum to direct alignment and control of the rest of the spine

Regional or general reduction of the lumbar lordosis is universally common clinically,⁴¹ and as noted by Adams et al.⁴² particularly in the lower lumbar spine. Poor control of anterior pelvic rotation and the habitual adoption of posterior pelvic rotation or tilt means the sacrum is carried into flexion and the lumbosacral region moves more into relative flexion in posture and movement. Generally, closed chain hip flexion and open chain hip extension are more difficult. Both rely on control of sagittal anterior pelvic rotation which is coupled with lordosis in the lumbar spine. The importance of being able to control posture and movement around the neutral lordosis for a healthily functioning spine is acknowledged by clinicians and has been stressed by noted researchers such as McGill⁴³ and Adams.⁴² Loss of control of the neutral lumbosacral position jeopardizes local segmental control,⁴⁴ and also transmission of the movement wave and control up and down the whole axial spine, including coupled rotation and side bending amongst other things.

Altered control of sagittal pelvic tilt generally reflects imbalanced activity between the iliopsoas and obturator/hamstrings groups

Sagittal tilting movements of the pelvis on the femur are the largest and most employed in functional movement. It is necessary that each muscle in the LPU synergy works enough but not too much so each can effectively contribute to the synergy and co coordinated movement patterns ensue (see Ch. 6).

The ability to readily tilt or swing the pelvis forward and back on the femoral heads is influenced by the habitual posturomovement patterns used which in turn affects balance in the length/tension relationships between the obturator/hamstrings and iliopsoas groups. Unfortunately imbalance in the ‘ischial swing’ is clinically common. The obturator/hamstrings group is generally tight and the iliopsoas group can show underactivity, overactivity or imbalance between iliacus and psoas activity.

The imbalance is reflected in the pattern of the standing posture and contributes to clinical functional classification which is covered in the next chapter.

The relationship between back pain syndromes and hypo or hyper tonus of iliacus and psoas is understood by clinicians yet there is a dearth in the literature. Mostly considered as open chain hip flexors,⁴⁵ a postural stabilizing role is increasingly accorded to psoas^46–49 particularly if hip flexion is part of the movement.⁵⁰ Except for inclusion with psoas as the ‘iliopsoas’, iliacus barely rates a mention. However the two muscles differ anatomically, neurally and functionally.⁵⁰ Andersson et al.⁴⁷ demonstrated individual and task specific activation patterns between iliacus and psoas which varied according to the particular demands for stability and movement at the lumbar spine, pelvis and hip. The scant attention paid to iliacus in the literature is indicative of paucity in the understanding of functional movement control around the lumbopelvic region. Both these muscles provide important internal bracing of forces and movements within the pelvis⁵¹ including stability of the sacroiliac joint as well as controlling the pelvis on the femur and the alignment and stability of the spine over the legs. Unilateral spasm of iliacus and psoas can contribute to a fixed intrapelvic ‘distorsion’.^52,53

The influence of the deep external hip rotators on modulating pelvic tilt control is practically nowhere to be found in the literature. Their influence is also important in transverse plane rotation of the pelvis on the fixed femur.

The myomechanics of the pelvic floor muscles (PFM) are dependent upon the reciprocal relationship between the ilio/psoas and the obturator groups as they balance and modulate the dimensions of the superior and inferior pelvic bowls. Because of the close functional synergism between the PFM and the obturator group, dominance of the latter renders the PFM likely to overactivity and shortness also. When the more superiorly spatially placed iliacus/transversus synergy is sufficiently active to balance the obturator group, the PFM are functionally required and better able to both concentrically and eccentrically contract and lengthen.

Imbalance in the ‘swing’ is also reflected in the position of the hips. When the obturator group dominates, the hips are more externally rotated and internal rotation is reduced. When the iliacus/psoas are tighter (less common), the hips move more freely into internal rotation and less into external rotation. Both groups can be tight where the neutral rotation position is more balanced but range into rotation, flexion and extension is more limited (see Ch.10 ‘Mixed syndrome’).

When adaptive pelvic tilt support for functional spinal movement is insufficient, compensatory regional hyperactivity around the centre of the body is seen, serving to further limit spinal control mechanisms as the region becomes hyperstabilized. Increased activity in the superficial abdominals is increasingly reported^30,54–57 as well as extensor hyperactivity^30,58,59 (see Ch. 10, ‘Central cinch patterns’).

Difficulty controlling closed chain movements of the hip joint and subsequent effect on lumbar spine (see Ch. 6, Part B)

It is interesting to ponder the manner in which we personally and conceptually view dysfunction. The noted researcher McGill states ‘I am continually surprised at the number of people with back troubles who also have hip troubles’.⁵⁰ They are always interrelated; and emanate from defective pelvic control. The huge numbers of people with back pain and those increasingly undergoing hip replacement surgery attest to the extent of the communal dysfunction.

Sagittal plane

Related to control of sagittal pelvic tilt movements, patients generally demonstrate poor alignment and control of the segments when executing the two most functionally significant patterns used in performing usual everyday activities:

Forward bend pattern

Ideally this is achieved from a ‘pelvic swing and shift pattern’ based upon FPP1 (see p.127). However, habitual buttock clenching and not ‘letting go’ of the posterior pelvic floor⁶⁰ and pelvi-femoral muscles contribute to difficulty initiating and controlling this action from the pelvis. Instead the pelvis commonly rolls into posterior rotation where the sacroiliac joint and the mid/low lumbar spine levels are the victim as they are pulled into hyper flexion to compensate (Fig. 8.6). This is common and has also been described as a ‘click-clack’ movement.^5,61The sacroiliac joint is especially prone to shear forces if loaded in the counter-nutated position.⁷¹

Fig 8.6 • Habitual poor forward bend pattern – note the use of the arms.

Roussel et al.⁶² described a study which found that reduced control of this pattern in dancers as a basis for performing open and closed chain hip flexion was predictive of risk for developing future musculoskeletal injuries. A large epidemiology study by Vingård et al.⁶³ found the strongest risk factor for LBP of biomechanical origin in men was working in a forward bent position. It makes no sense to attempt to ‘stabilize’ the lumbar spine – or the sacroiliac joint for that matter, if they are being constantly forced to abnormally compensate for movements which should be initiated from the pelvis during our many and varied activities of daily living. The disinclination to shift the pelvis posteriorly and weight bear through a flexed hip is also apparent in kneeling, all fours and variations of these positions. In fact loading weight through a flexed hip in any position such as supine is usually challenging e.g. ‘bridging’ is generally only achieved by posterior pelvic rotation. Achieving functional lengthening in the hamstrings and obturator group can only occur when the pelvis can be controlled in anterior rotation.⁶⁴

Lifting or return from forward bend pattern

Ideally this is based upon control of FPP2 which brings the pelvis forward and extends the hips while balanced activity of the flexors and extensors controls the ‘body cylinder’ alignment. When control is defective, the patient tends to principally rely upon the hamstrings and passive tension in the posterior myofascial structures with the spine in flexion and posterior pelvic rotation or conversely, he excessively relies upon the back extensors (see Ch.9).

Coronal plane

In the coronal plane, reduced control of the LPU and lateral and medial weight shift at the hip engenders the need for holding patterns higher up in the torso or for excess activity in the large pelvi-femoral muscles. Underactivity in iliacus-psoas reduces control of lateral weight shift while overactivity disrupts the neutral pelvic position and feeds into central ‘cinch posterior cinch’ behavior (Ch.10; Fig. 8.7). Reduced intrapelvic control provides a less stable base to support well controlled activity of the large SGMS pelvifemoral muscles – in particular the adductors and hamstrings both of which are notorious for ‘sprains’. Mens^66,67 draws attention to the fact that ‘adduction-related groin pain’ in the athlete may not be caused by adductor tendonitis but by instability of the pelvic ring. In a study of 44 athletes with groin pain clinically elicited by resisting the adductors in crook lying, he then applied a pelvic belt placed inferior to the iliac spines and just above the greater trochanter. Subsequent retesting generally but variably improved adductor force and lessened pain during the maneuver. It is suggested that the pelvic belt is performing the action that would otherwise be provided by the synergy of the LPU in performing the first fundamental pelvic pattern. In particular the lower abdominals and iliacus provide intrinsic medial stability of the upper pelvic bowl and ipso facto mediolateral stability of the inferior bowl to support actions of the large pelvifemoral muscles. He notes the strong association between groin pain and abdominal wall weakness. He also describes⁶⁷ two other studies where cases of osteitis pubis, instability of the symphysis and adduction related groin pain were treated either by surgical fusion of the symphysis or intraarticular injections into the symphysis with improvement in the adductor related groin pain. Increased adductor tension/activity possibly not only causes tendonitis but overstress of the ligaments of the joints of the pelvic ring.

Fig 8.7 • Defective control of lateral weight transfer in standing becomes ‘hanging’ and ‘holding’.

Three-dimensional control of closed chain movements of the hip is not only critical in being able to functionally move at the hips but is also particularly important when ‘stretching the hips’. The ‘catch 22’ is that the hips are tight because of poor control of the fundamental patterns, yet often, subsequent hip stretching is performed as ‘stupid stretches’ (Fig. 8.8) with no attention paid to initiation and control from the pelvis. The lumbar spine is generally pulled into end range flexion or extension and rotation and becomes the site of relative flexibility⁶⁸ and even more vulnerable, setting up a vicious cycle where the dysfunction is perpetuated. This is particularly so in the case of tightness of the hamstrings and piriformis (see the ‘hamstrings/hip conundrum’ (Ch.12).

Fig 8.8 • This common stretch perpetuates her problem. Note the axis of movement in the stretch is the lumbo pelvic junction rather than the hip. See Fig 8.26 and text.

Reduced pelvic control at the hip particularly during dynamic single leg exertions has also been associated with patellofemoral pain syndromes.⁶⁹

Impaired movements of the femur on a stable pelvis

Movements at the hip are generally better understood and considered in terms of ‘open chain’ movements – the pelvis providing a stable platform for the moving femur. This is also an important component of pelvic function and most contemporary rehabilitation strategies do focus on this aspect. However attention to the ability to control sagittal pelvic rotation and the neutral lumbar lordosis, as well as isolating the movement to the hip is frequently overlooked in practice. Reduced lumbopelvic or intra/extra pelvic control means that the pelvis is an ineffectual platform to support open chain hip movements. This is particularly important with large long lever actions of the leg such as the ASLR test and particularly so if they are ballistic as in kicking a football. The lumbar spine again becomes overstressed setting up a vicious cycle where the dysfunction is perpetuated. Tightness of the pelvifemoral muscles further compounds the problem. This helps explain the prevalence of various ‘diagnoses’ of hamstring problems in the sporting arena – pulls, tightness, tears, tendinopathies etc. is (see ‘The hamstrings conundrum’ Ch.12).

The close functional relationship between hip–pelvis myomechanics

The more common patterns of habitual posturomovement tend to underutilize available hip range of movement and control and certain patterns of movement become more prevalent. Reduced activity and imbalance within the LPU and an over reliance on the outer SGMS muscles affects intrapelvic stability and control e.g. dominance of rectus femoris over psoas for hip flexion; of TFL over gluteals for abduction. The tendency is to ‘hang’ relying on the ‘outer’ muscles rather than find ‘inner’ support. The neuromuscular predominance of closed chain hip extension, abduction external rotation patterns with reduced antagonist activity, causes the inferior pelvic bowl to become hyperstabilized and more ‘closed’ and the sacrum counternutated. Altered loading stresses and reduced ‘distorsion’ in the pelvic ring ensue. Articular and neuromuscular freedom of patterns of hip movement into various combinations of flexion, internal rotation and adduction and related opening of the inferior bowl begin to show restriction. This limits closing of the superior bowl and control of the lumbar lordosis. Clinically, this is more common (Fig. 8.9).

Fig 8.9 • Neuromyofascial restriction in the external hip rotators and hamstrings act to inferiorly ‘tether’ the pelvis during forward bending. The axis of movement becomes the low lumbar spine.

If there is then a requirement for sudden or explosive muscular activity involving patterns of hip flexion, internal rotation and particularly adduction such as in kicking, the decreased eccentric lengthening in the extensor/external rotators/abductors can potentially lead to ‘tears’ as they are forced to lengthen. On the other hand, any of the flexor/internal rotator/adductors may also potentially ‘tear’ as they are forced to contract against antagonists which do not ‘let go’. Particularly in the sportsman, actions that suddenly require large opening hip/leg movements or those requiring a sudden change of direction on a fixed leg, risk yanking the proximal muscle attachments and the pelvic bones themselves at the inferior pubic ramus and ischial tuberosities. This jeopardizes the stability of the pelvic floor and the syndesmosis of the SIJ. Clinically, the association between adductor hyperactivity ‘osteitis pubis’ and other related ‘unstable’ conditions of the symphysis become probable. In likewise manner the incidence of ‘groin pain’ syndromes can be partially explained. The influence of altered segmental function and related ‘facilitation’ in these muscles should also not be overlooked.

Sacroiliac Instability?

Vleeming et al.^70,71 considered that the articular surfaces of the sacroiliac joint (SIJ) were relatively flat and as large forces needed to be transferred across the joints, they were potentially unstable. They introduced the notion of a self locking or self bracing mechanism which acted to stabilize the joint. This model comprised a combination of ‘form closure’– the specific anatomic features of the joint, and ‘force closure’ – compression generated by lateral muscle forces and ligaments with friction, in order to withstand potential shear at the joint from gravitational forces and during load transfer. Nutation of the saccrum is crucial in this self locking mechanism and tensions most SIJ ligaments.⁷⁰ The four muscles they listed as specifically important in providing joint compression were erector spinae, gluteus maximus, latissimus dorsi and biceps femoris. Through their attachments including those to the thoracolumbar fascia, they were considered to form part of three muscle slings: the longitudinal, posterior oblique and anterior oblique slings (see p.121) which acted to compress the joint⁷⁰and provide support. Van Wingerden et al.⁷² managed to show that sacroiliac joint stiffness did increase when individual muscles were activated, especially the erector spinae. Failure in the system is said to occur when erector spinae and gluteus maximus become weak with an increase in hamstrings tension which serves to hold the sacroiliac joint in counternutation, and so more vulnerable to shear forces in loading.⁷⁰ Note that practically all these muscles belong within the SGMS and are not intimately related to pelvic ring myomechanics, hence are unlikely to provide a truly effective postural pre-stabilizing role to support integrated load transfer through the pelvis. As those authors suggest, the superficial slings will play an important role in gross motor activities such as walking and running, but it is suggested only if they are able to act on a stable base of support provided by deep system preactivation. With the benefit of more recent evidence by Australian researchers^73–77 into function of various muscles within the deep system, the authors later suggested including the contribution of ‘core muscles’ to the self bracing mechanism.⁷¹

The instability model was further developed when in 1999 Mens et al.⁷⁸ published a paper which showed that impairment of the active straight leg raise test (ASLR) correlated strongly with instability of the pelvic ring in patients with peripartum pelvic girdle pain (PPPGP). The increased mobility was demonstrated on X-ray and occurred at the symphysis pubis and was most evident when passively hanging the symptomatic leg while standing on a raised box. The ASLR was improved by the application of a pelvic belt either just below the anterior superior iliac spines or at the level of the symphysis pubis. This external compression provides pelvic ring stability either above or below the hip joint. The researchers surmised that the caudal shift of the pubic bone seen on X-ray was possibly caused by an anterior rotation of the innominate about a horizontal axis near the sacroiliac joint. However, normally, weight bearing is considered to produce a posterior rotation of the weight-bearing innominate while the superincumbent body weight causes the sacrum to nutate.^79,80 It can be reasoned that hanging the contralateral leg will produce further physiological ‘distorsion’ in the pelvic ring. If the pelvic ring is unstable at the symphysis, this will ‘appear to be’ excessive anterior rotation of the free innominate. While this study does show instability at the symphysis it does not necessarily show it at the SIJ. However, largely through it, a positive ASLR has somehow become construed as indicative of ‘SIJ instability’.

Furthermore, clinically there is also a danger that pelvic girdle pain and the associated finding of a positive ASLR test have become readily interpreted as confirming ‘sacroiliac instability’. This author agrees with O’Sullivan⁵⁶ who suggests many clinicians hold confused beliefs that the pelvis is unstable or displaced, which are then transferred to their patients with unfortunate consequences. While Mens et al.⁷⁸ found a strong correlation between positive ASLR and actual demonstrated pubic joint laxity in PPPGP, the test can also be positive in cases of pelvic joint stiffness. Clinically in a general population, the joint is more often symptomatic because of stiffness which may or not be directly pain producing. Pain provocation tests are not necessarily clinically reliable and it is generally necessary to apply composite tests to arrive at a diagnosis.⁸¹ Examining the quality and ‘feel’ of the tissues and specific movement testing of the spinal, hip and pelvic joints including control of key functional movement patterns without necessarily reproducing ‘the pain,’ generally delineates the source and reasons for the pain and informs appropriate treatment direction. O’Sullivan et al.⁷⁷ identified altered motor control in subjects who had pain over the sacroiliac joint, positive pain provocation tests and a positive ASLR. During the active ASLR test, not only did the pelvic floor descend but this was associated with bracing and decreased descent of the diaphragm and alterations in respiration which improved with external pressure over the ilia. Rather than necessarily indicating ‘sacroiliac instability’, this study nicely showed that it is the operant suboptimal motor control strategies of the whole torso that are ‘unstable’ in many with pelvic girdle pain syndromes.

The Netherlands model of ‘sacroiliac instability’ has been popular and adopted by clinicians ^32,82,83 and researchers.^84–86 An improved understanding of function in the deep system has led to the inclusion of those muscles responsible for generating IAP, also considered to have a role in maintaining pelvic stability and respiration (transversus, internal oblique diaphragm and pelvic floor).⁷⁷ However, highly significant is that apart from the pelvic floor and piriformis muscles, the influence of the very functionally important ‘other internal pelvic muscles’ – the iliacus and obturator group have to date not yet been well considered. Andersson et al.⁴⁷ showed that during ASLR, moderate to high activity was present for both psoas and iliacus. Clearly they contribute to providing internal support for load transfer through the pelvis. Eminent clinicians^87,88 describe spasm of iliacus as a potent factor in maintaining sacroiliac dysfunction. In the Mens study the raised leg was ‘relaxed in lateral rotation’.⁷⁸ Clinically, preactivation of the FPP1 with the hip in neutral rotation can impressively change the ASLR test result. Interestingly, in an earlier paper documenting the results of a survey of 518 women with PPPGP, Mens et al.⁸⁹ noted the high frequency of delivery positions with a bent spine. They concluded a flexed position during delivery may enhance the risk for PPPGP. Post partum tasks involve constant flexion patterns, undoubtedly further feeding the dysfunction.

Gracovetsky⁹⁰ refutes the Netherlands ‘instability model’ suggesting that there is an evolutionary advantage to instability – function drives the anatomy and not the other way around; ‘the viscoelastic nature of biomechanical material precludes straightforward application of these engineering concepts’. Even a steady erect stance is maintained by cycling through a sequence of different but closely related postures so that no one structure is continuously loaded. He proposes a ‘SG ridge’ on the sacrum locks into a corresponding shape in the innominates allowing coupled motion similar to that seen in the lumbar facets, but of smaller magnitude though greater force. The SG ridge acts as a fulcrum transferring the vertical loads, leaving the SIJ relatively free to rotate around the hinge in two planes, thus allowing axial rotation of the pelvis and nutation. The joint surfaces are warped and so do not slip past each other; the ligaments are strong and the geometry of the joint is such that there is no need for additional force closure to keep it together. The spine needs to be impulse loaded⁴⁰ with oscillating load sharing roles between the passive and active tissues.

This proposed model is appealing both clinically and in terms of function allowing the pelvic ring to slightly twist or distort (‘distorsion’) in the basic functional movement – walking, as well as numerous other activities involving the lower limbs. Dysfunctional spatial and particularly intrapelvic control as described will disrupt the kinematic chain controlling and transferring forces and movements between the hips and spine through the pelvis.

Neuromyo-articular dysfunction of the spinopelvic–hip complex underlies most pelvic girdle pain and related disorders

Pain in the pelvic girdle can either arise from the local joints or myofascia including the hip, or be referred from the spine or manifest from a combination of the above. Groin pain in the sporting population can be associated with pathology in the hip, pubic symphysis⁹¹ and associated dysfunction in the lumbar spine and SIJ. While traumatic injuries including childbirth can precipitate the development of symptoms, more often than not their onset is insidious, seemingly occurring for no apparent reason. The pelvic organs receive sympathetic supply from the thoracolumbar outflow while the parasympathetic is via the sacral outflow. It should also be borne in mind that psoas is innervated by L123⁹⁴ and iliacus by L23⁹⁴, and the adductors by L234.⁹⁴ Spasm in iliacus can result from L23 and/or SIJ dysfunction. Palpation of joints over the thoracolumbar spine can reproduce scrotal, haunch, hip and pelvic pain. The functional relationship between the thoracic and pelvic diaphragms means that clinically, thoracolumbar dysfunction is usually part of the dysfunction picture in many pelvic girdle pain disorders. Clinical assessment readily delineates underlying patterns of neuromyo-articular dysfunction precipitating and perpetuating symptoms. In an excellent review synthesizing current evidence with clinical observation, O’Sullivan and Beales^56,92 make the case for clinically classifying and diagnosing pelvic girdle pain disorders based upon the dysfunctional mechanisms underlying the disorder. Currently, theories about the sacroiliac joint are popular yet confused and poorly validated, and these authors attempt to clarify the known facts. Importantly they suggest that ‘directional strain’ may be more significant than positional changes. In agreement with these authors, clinical findings generally delineate patterns of both neuromuscular hyperactivity and hypoactivity with a tendency for two main clinical subgroups. Those they classify as having ‘reduced force closure’ fairly much equates to the anterior pelvic crossed syndrome group (APXS; see Ch. 9) while those with ‘excessive force closure’ bear similarity to the mixed syndrome (MS; see Ch.10). Assessing and redressing joint function and activation and control of the fundamental pelvic movements and functional patterns generally ensures symptom amelioration.

Postural asymmetry of the pelvis

Clinically this is quite common^87,88 even in children, where Lewit found approximately 40% prevalence in children from nursery school age onwards. The asymmetry may be directly or indirectly responsible for the patient’s symptoms. Lewit⁸⁷ considers that pelvic distortion is always secondary to some other lesion which must be found and treated, atlanto-occipital joint dysfunction being common, particularly in children. As Lewit⁸⁷ describes it: viewed from behind, the pelvis deviates slightly to one side (usually the right) and is slightly rotated (usually to the left). There is a fixed ‘distorsion’ where one innominate is anteriorly rotated against the other (usually the right) where the PSIS is higher and the ipsilateral ASIS is lower. Related to this is the ‘overtake’ phenomenon where in forward bending in sitting or standing, the lower PSIS (usually the left) overtakes the other becoming more cranial for about 20s after which the two spines return to a symmetrical position. There is usually muscle imbalance in the pelvic region and spasm of iliacus is frequent on the side of the lower PSIS, gluteal muscle bulk and activity is usually asymmetrical as is PFM activity. Clinically, the side of the lower PSIS is usually the painful side.⁸⁸ When torsion is present the leg lengths appear unequal.⁸⁸

Pelvic floor dysfunction

Effective function of the pelvic myofascial floor requires the ability to coordinate the static, ‘opening’ and ‘closing’ actions appropriate to the combined situational demands of breathing, continence and posturomovement control. Much of the interest generated in pelvic floor function stems from the problem of stress urinary incontinence (SUI). A recent longitudinal study by Smith et al.⁹³ provides evidence of a relationship between back pain, incontinence and respiratory problems, suggesting a common underlying mechanism.