Chapter 13 Therapeutic approach

Pain can result from overt traumatic incidents or where altered posturomotor control over some time creates repetitive micro trauma, setting the scene for an often trivial incident becoming the ‘tipping point’ for symptom development. When looked for, other associated sub-clinical symptoms have usually also been apparent as part of the dysfunction picture.

The treatment rationale is determined by assessing the patients neuromyo-articular function, and redressing the specific neuromyo-articular dysfunction found as the actual or likely cause and perpetuator of the pain picture in that particular patient. When the pain and the reasons for it can be effectively dealt with in the early stages there is less likelihood of secondary problems developing such as chronic pain and central pain hypersensitivity, fear of movement, passive coping, depression, catastrophizing etc.

The diagnosis is based on movement dysfunction, not structural pathology. Restoring improved function will generally ease the pain while structural pathology such as ‘a bulging disc’ remains the same. The structural pathology generally represents the point of tissue distress resulting from altered posturomovement function over time.

Simply looking at the patient tells us a lot about him. Appreciating the model presented – the salient aspects of normal function (Ch. 6); the common features of dysfunction (Ch. 8); and the clinical patterns (Chs 9 & 10) provides a helpful framework through which to assess the patient. Which joints do we expect to be symptomatic: stiff or overstressed? Knowing what to look for helps decide the test movements and in particular, when passive joint testing, refine the direction of enquiry for possible joint restriction. Assessment confirms or otherwise our predictions and hunches. ‘The model’ hopefully helps the therapist discern ‘the wood from the trees’ and ‘see’ the problem more clearly and find and understand the pain source. Assessment will ideally delineate which are the ‘key elements’ to address, indicate the level of dysfunction and stage of the disorder.

Centrally important is the recognition of the interdependence between spinal joint and muscle function. Symptomatic spinal joints emanate from altered posturomovement control but in turn when irritable, further adversely affect neuromuscular function. Improved muscle function cannot be expected while the joints are symptomatic and vice versa. Ideally, manual and exercise therapy complement and mutually reinforce one another.

Therapeutic algorithm

Altered control of the spine not only results in various spinal pain syndromes but because it houses much of the nervous system, a plethora of related symptoms seemingly in other organ ‘systems’ or in the head and limbs are possible. The therapeutic approach considered here will principally focus upon ‘spinal pain’ and related proximal girdle disorders with more emphasis on the pelvic girdle. However, it is very important to appreciate that dysfunction in the upper pole of the body also affects function in the lower pole and vice versa, affecting spinal function as a whole. In this respect the upper pole is considered within the therapeutic algorithm and the exercise and movement control approach. Ideal motor function relies on integrated control between the spine, head, both proximal limb girdles and their large ball and socket joints.

The therapeutic algorithm can be distilled into the following main components (summarized in Table 13.1). The irritability of the patient’s condition will dictate how many of the movement tests are performed. The art of the clinician is to gauge the stage of disorder and only test what he/she needs to in order to discern the reason for the patient’s pain. For someone in severe pain, simple observation and gentle manual exploration might be the only measures the patient can comfortably tolerate. As pain settles, more detailed movement testing can ensue. Motor performance will be markedly compromised if the patient has marked pain.

Table 13.1 The therapeutic algorithm: assessment and management

1. Assessment

Subjective: dealt with in summary form only

Objective comprehensive treatise as follows:

A) Observation:

B) Movement testing

• Patterns of active movement in:

• Supine crook lying:

*Breathing pattern

*Three fundamental pelvic patterns

Loading for bridge

Limb load challenge

Bent knee fallout

Hip flexion from ilio-psoas

Hip, knee & ankle flexion 90°

Active straight leg raise?

Coordination IAP, breathing and axial stabilization

Supine low f/ab/er test

Supine high f/ab/er test

Supine f/ad/ir test

Posterior pelvi-femoral opening

Modified Thomas position screening

Craniocervical flexion (CCF)

Bilateral arm elevation

C) Passive testing/treatment of joints and myofascia with reference to the junctional regions:

• Lumbosacral junction

• Thoracolumbar junction

• The ‘dome’

• Cervicothoracic junction

• Cervicocranial junction

2. Therapeutic approach

Manual: the ‘key’ positive assessment findings become the focus of manual treatment aimed at clearing pain and related symptoms

Modify the symptom producing habitual postural behavior

Simple adjustments to common daily activities

Therapeutic exercise: should complement manual treatment, be problem specific and redress the general features of dysfunction as described

Home exercise program: practicality and pitfalls

Exercise therapy and spinal pain:

• Review of literature −ve and +ve

• The case for therapeutic exercise and movement classes

It is important to establish fundamental patterns of movement required in ADL activities

Assessment

The committed and experienced practitioner has learned to understand and see the often subtle nuances inherent in ‘normal’ posturomovement function and the significance of seemingly small differences seen in the dysfunctional state (see Ch. 4). The competent therapist is deft at ferreting out the information needed to help delineate the presenting picture of dysfunction.

Subjective examination

Relevant aspects to explore include the exact area, extent and description of all symptoms; this includes the presence of other pains and symptoms which may not seem related. Is there an apparent reason for their sudden or gradual onset; symptom frequency and whether worsening or stable and the stage of the disorder; symptom irritability and sleep patterns; behavior of symptoms in relation to postures and activities; past history of trauma; occupational posturomovement demands; past and present exercise and leisure activities; previous treatment and demonstration of any exercises prescribed; general health status, medications and results of investigations; patient beliefs as to the source of symptoms; compensable status? Screening for any ‘red flags’ or ‘yellow flags’,³² also begins during the subjective examination.

Objective examination (see Ch. 4)

A) Observation

1. General. Many valuable insights are gleaned during the subjective examination when the patient’s habitual posturomovement behavior can be observed without him realizing. This includes his sitting and standing postures; breathing patterns; willingness and manner of moving as he undresses and psychomotor aspects.

2. Clinical Syndromes. The standing observation looks for any asymmetry and the relative influence of the clinical syndromes – the Pelvic Crossed Syndromes (PXS; Chs 9 & 10), the Shoulder Crossed Syndrome (SXS), the Layer Syndrome and the Belted Torso Syndrome (Ch. 10). Notice the habitual posturing of the legs and the quality of the feet in being likely to offer dynamic support (Ch. 8, p. 207). The pelvic position, muscle contours and symmetry help decide the Clinical Syndromes and individual patterns within these.

3. Muscle contours. The following descriptions have largely been influenced by Janda.^1,^3,^4,⁵

Posterior view

• Careful attention should be paid to the back muscles. A healthy back has a healthy distribution of muscle tone. Unhealthy backs have too little and look ‘empty’ (Fig. 13.1) or too much and look ‘straightjacketed’ (Fig. 13.2). The erector spinae bulk should be compared from side to side as well as from the lumbar to the thoracolumbar regions. According to Janda there should be no difference between sides or regions and ‘prevalence of the thoracolumbar portions of erector spinae is a poor sign in relation to prognosis’.²^–⁴ This is common in the PPXS and MS.

• The inter scapular area should be observed for loss of bulk of the inter-scapular muscles. If so, in addition the distance between the thoracic spinous processes and the medial border of the scapula is increased and the scapulae are rotated, with their inferior angles improperly fixed to the rib cage such that apparent winging occurs ⁵ (Fig. 13.3). If present there is probably a corresponding tightness in the levator scapulae and upper trapezius muscles which is associated with neck pain. If so the neck/shoulder line is changed such that the person displays ‘Gothic shoulders’⁴ – all indicative of the SXS.

• Imbalanced rotation in the hip joint. Janda confounded this author in claiming a patient had a right sacroiliac joint problem when he had just walked into the room! This pronouncement was predicated upon the marked external rotation evident in the right hip indicating hyperactivity and shortening of piriformis.

• An abducted position of the legs indicates possible shortness of the abductors – gluteus medius and minimus and tensor, with ‘long’ adductors. Indicative of all PXS and reduced active support from the systemic local muscle system (SLMS)

• The glutei should be symmetrical and rounded. If weak or inhibited the muscle tends to ‘hang’ loosely ³ – common in APXS. Asymmetry may indicate problems in the lumbar spine, sacro-iliac joint or hip.

• The hamstrings are usually well developed but it is important to look at their bulk relative to the glutei as when these are inhibited the hamstrings become predominant ³ and knee hyperextension is common. Commonly found in all PXS. Their activity can markedly increase in forward bending if dysfunctional.

• Tightness of the short hip adductors is seen as a distinct bulk of muscle in the upper third of the thigh.

• A normal calf has a spindle form.⁶ Tightness of the gastrocnemius-soleus (GS) is characterized by an apparent broader tendo-achilles.⁴ If the soleus is tighter there is increased bulk on the medial side of the TA tendon⁶ and the lower leg becomes more cylindrical.⁴ The normal heel shape has a quadratic form and if more pointed this can indicate that the GS is tighter, which shifts the center of gravity forward.⁶ More common in PPXS.

Anterior view

• The abdominal wall should be flat. A sagging protruding abdomen reflects a generalized weakness of the abdominals. There may be imbalanced activity between the different abdominal muscles. When the obliques are dominant, a distinct groove will be seen on the lateral side of the recti, indicating that there may be a decrease in the stabilizing function of the recti in the anteroposterior direction, an important factor in stabilization of the spine.^3,⁴ (Fig. 10.24). When the transversus is underactive a lateral bulge in the waistline is apparent.⁶ This can even be obvious in someone who has ‘worked out’ at a gym where the emphasis has been upon the superficial abdominals while there is little ‘inner support’ (Fig. 13.4). Conversely, the abdominals as a group can be over activated and so over developed that they overly fix the lower pole of the thorax and equally compromise axial control (Fig. 13.5). There may be imbalance between the upper and lower regions with fullness of the lower abdominal wall – common in APXS (Fig. 13.6).

• The pectorals. The tighter and stronger these are, the more prominent is the muscle belly. Typical imbalance will lead to rounded and protracted shoulders and slight medial rotation of the arms.⁵ This is particularly common, especially in people who use weights at the gym. The nipple is shifted laterally and superiorly and if pectoralis minor is tighter there is increased bulk above it. The anterior axilliary fold is thickened if major is tight.⁶ However, appearances can be deceptive as tightness can also occur without bulk through adaptive shortening (Fig. 13.7).

• The sternocleidomastoid in normal states is just visible. If the insertion, particularly the clavicular insertion, is prominent it is a sign of tightness. If so there is usually related weakness of the deep neck flexors ⁵ (see Fig. 10.14).

• Normally the bulk of the tensor fascia lata (TFL) should not be distinct. If it is and there is also a groove on the lateral side of the thigh the muscle is being overused and both it and the iliotibial may be tight (Fig. 13.8). When the rectus femoris is tight the position of the patella moves slightly upwards and also laterally if there is concurrent tightness in the iliotibial band.⁶

4. Soft tissue signs can also reveal valuable clues. A segmental ‘divot’ or reactive bony prominence may be apparent in the spine hinting at altered function. A soft tissue ‘bubble’ is often apparent over L3/4 or L4/5 when marked ‘hinging’ stresses have been occurring over these levels and the local soft tissues begin to resemble over stretched elastic (Fig. 13.9). Segmental and long muscle spasm is reliably indicative of segmental dysfunction when later confirmed by palpatory examination. Segmental wasting may also be apparent over attenuated levels. Poor muscle bulk, puffy and reactive superficial tissues and poorly defined bony prominences are often apparent over the lumbosacral junction and indicative of the region sustaining a lot of abnormal loading stress (Fig. 13.10). When the skin is mottled and discoloured (livedoreticularis) it is a sure sign the person has been going to bed with a hot-water bottle to ease the pain over some time. The soft tissues feel very tough and inelastic and expect that accurate joint testing can be more difficult.

Fig 13.1 • A back with too little tone looks doughy and lifeless.

Fig 13.2 • A back with a lot of superficial muscle activity is not necessarily healthy.

Fig 13.3 • Emptiness in the interscapular region.

Fig 13.4 • Despite ‘working out’, many ‘gym junkies’ display this lateral bulge.

Fig 13.5 • Overdeveloped abdominals can act like a tight ‘bib’ anteriorly restricting freedom of the lower pole of the thorax.

Fig 13.6 • Evident imbalance in the tone between the ‘upper’ and ‘lower’ abdominals is common and indicative of poor spatial and intrapelvic control.

Fig 13.7 • Tight pectorals are not necessarily bulky.

Fig 13.8 • Evident tight TFL.

Fig 13.9 • Soft tissue ‘bubble’ relating to marked ‘hinging’ stresses in function.

Fig 13.10 • Puffy superficial tissues and poorly delineated bony landmarks over the lumbosacral junction.

B) Movement testing (refer to Ch. 4)

Imbalanced activity between the deep (SLMS) and superficial systemic global muscle system (SGMS) muscle systems is reflected in altered kinematic motion patterns resulting from imbalanced length/tension relationships of muscles contributing to the control of force couples in movement. Examination of patterns of movement begins to indicate the abnormal loading patterns that various joints may have been subjected to. Uneven segmental motion with segmental or regional ‘hinges’ and/or ‘blocks’ may be apparent and symptom producing (Fig. 13.11). Further testing of joint function confirms or otherwise these impressions.

Fig 13.11 • Apparent segmental ‘block’ around the ‘dome’.

Patterns of active movement

While possible combinations of movement testing are endless and will depend upon the region of pain and stage of disorder, at the initial assessment those which appear to yield the more significant information are mentioned. One is not compelled to perform all those tests listed and clearly in an acute presentation, only a few of the basic tests (marked *) are examined. However, one may need to chase symptoms in say an elite athlete and many if not all may be performed. We are most interested in the ability and quality of the movement patterns the alteration of which can limit or increase range in different regions of the spine and explain symptom development. Altered length/tension relationships in various pelvi-femoral muscles affect pelvic myomechanics and control. Some, none or all of these movements may reproduce the pain or a symptom which is informative however, symptom reproduction is not the primary goal. It is important that the therapist does not over-challenge the patient beyond his abilities as otherwise he will use what he can draw upon and ‘knows’– invariably dominant SGMS activity in predictably provocative kinematic patterns and thus risk exacerbating symptoms. Poor performance of any test indicates avenues for treatment.

In standing:

• *Forward bending pattern and return: the patient’s habitual preferred strategy tells a lot about his motor function in general. The axis of movement, pattern of pelvic control and intersegmental movement through the whole spine are observed (Fig. 13.12). Repeat while palpating the inferior aspect of the posterior inferior iliac spines (PSIS) and noting if the movement is symmetrical. A torsion or ‘twist’ indicates altered intrapelvic movement and/or stiffness in one hip or altered hamstring tension. Importantly, also note to what degree the whole pelvis posteriorly shifts and anteriorly tilts on the femoral heads and is this sufficient that the sacrum nutates and the coccyx and ischial tuberosities lift through the movement? Is there co-activation between the flexors and extensors or does he simply rely on the extensor system and/or the passive tissues and ‘hanging off the hamstrings’?

• *Spinal extension, lateral flexion and rotation observing for ‘hinges’ and ‘blocks’ in segmental movement throughout the spine as well as range and symmetry and importantly the amount of pelvic shift and tilt to provide the axis and support for the sagittal and coronal movement. In extension does the pelvis shift anteriorly and tilt posteriorly so that the axis of movement is in the hip (Fig. 13.13)? In lateral flexion does it shift contralaterally and tilt on the femoral heads and what of segmental movement in the spine? (Fig. 13.14). In rotation is there ipsilateral backward pelvic rotation and relative hip internal rotation? Repeat while palpating the PSIS during the movements which should be symmetrical in extension but asymmetrical in side bending and rotation to reflect flexible ‘distorsion’. When the pelvis is mobile Lee⁷ notes that in side bending the contralateral innominate posteriorly rotates thus, ipso facto the ipsilateral lumbosacral junction can move into a ‘closing’ pattern. Similarly, in axial pelvic rotation the contralateral innominate anteriorly rotates and the sacrum rotates ipsilaterally⁷ initiating axial rotation through the spine. Altered length/tension in the hip rotators influences intrapelvic motion and that of the pelvis on the femoral heads (Fig. 13. 16).

Fig 13.12 • This is a better forward bend than most. However, ideally one would like to see better anterior pelvic rotation and co-activation in the abdominal wall (see Fig.13.116).

Fig 13.13 • Notice the poor anterior shift of the pelvis and opening in the hips coupled with poor support from the abdominal wall.

Fig 13.14 • While the pelvis has shifted there is reduced freedom in ‘distorsion’ and dissociation within the joints of the hip–pelvis and lumbosacral junction complex with poor intersegmental movement through the lumbar spine.

Standing to sitting and return to standing: observing the quality of sagittal weight shift in the pelvis and trunk, axial alignment including head control, lower limb kinematics and the ability to come up to stand without pushing down through the arms (Fig. 13.15).

• Bilateral arm elevation: looking for quality of shoulder girdle support for the movement and whether there is adjustment through the thorax or overcompensation in the lumbar spine and neck.

• Pelvic translation in the sagittal frontal and horizontal planes: the ability to initiate movement from the pelvis and the sequencing of intersegmental movement from the lumbosacral junction through the spine, its symmetry and any symptom response (Fig. 13.16).

• Standing on one leg. Observing the adaptability of the lower kinetic chain for unilateral flexible support; the quality of pelvic control both on the supporting leg and also as the base of support for the torso; and also the balance strategies adopted. The pelvis as a whole should not tilt anteriorly, posteriorly, laterally or rotate on the standing leg. Frequently the patient maintains a level pelvis in the frontal plane although it is posteriorly tilted with loss of lordosis and poor ‘distorsion’ When ‘distorsion’ is defective the movement is shunted into the lumbar spine with holding strategies higher up the spine (Figs 6.22, 8.7 & 13.17). If a more physically competent patient, repeat while palpating both PSIS while flexing, extending and abducting one leg. Here one is further testing ‘distorsion’ available in the pelvis to support the open chain hip movement while also maintaining lumbopelvic alignment on the standing leg. The PSIS on the weight bearing standing leg should remain reasonably still and the lumbar lordosis should be preserved. The PSIS on the moving leg should posteriorly rotate around mid hip flexion; anteriorly rotate in hip extension.

• Growing one elbow to the ceiling with hands on the head: provides clues about the quality of lateral weight shift through the pelvis and ‘body half’ support with postural adjustment through the thorax and thoracolumbar junction. Central cinch pattern (CCP) behavior in response to inadequate pelvic control reduce the ability for elongation one side of the torso necessary in lateral weight shift and elevating one arm (Figs 13.18,13.19 & 8.27).

• Hitching one hip with ‘straight’ legs provides further information about ‘distorsion’ and the quality of ipsilateral ‘closing’ patterns over the lumbosacral junction and may produce symptoms. Commonly the movement is ‘taken’ over levels higher up (Figs 13.20,13.21).

• Squat pattern. Observe the preparedness to load the lower kinetic chain into antigravity flexion patterns – the ability to control closed chain hip flexion and spinal and lower limb alignment on dynamically adjusting legs. Commonly there is poor posterior shift and the pelvis rolls into posterior tilt (Fig. 13.22) & (Fig. 13.24).

• Single leg semi squat. Provided the patient has good control of the previous tests, the ability for lateral weight shift and closed chain pelvic control during antigravity lower kinetic chain flexion is tested here. With the weight mostly on one leg and the other acting as a balance prop behind, the patient is asked to ‘semi-squat’ onto one leg. Observe the ability to align the knee in relation to the foot, control of rotation at the hip as well as triplanar control of the pelvis. Does the pelvis posteriorly shift and anteriorly rotate on the femur? Observe patterns of muscle activity in the trunk (Fig. 13.23).

Fig 13.15 • It is unusual for ‘patients’ to stand up without pushing down with their arms particularly when the base of support and control of sagittal weight shift is poor.

Fig 13.16 • The patient was asked to shift his pelvis to the right. There is reduced intrapelvic/hip dissociation extending into the spine and he experiences pain.

Fig 13.17 • The same patient as in Fig. 13.16 experiences pain and finds balance difficult. Note the response in the left limbs to aid stability.

Fig 13.18 • More ideal organization for growing one elbow to the ceiling. The individual responses show a common pattern of ipsilateral weight shift and lengthening in the torso. Note the obliquity of the pelvis through its rotation in the frontal plane on the femoral heads.

Fig 13.19 • Inadequate organization for growing one elbow to the ceiling. Note the buttock clenching and consequent lack of spatial pelvic shift and frontal plane rotation on the ipsilateral femoral head. Central posterior cinch behavior holds the spine centrally limiting adaptive response and weight shift through the torso to bring the body weight over the standing leg.

Fig 13.20 • Hitching one hip. Note the initiation in the pelvis and the left ‘lumbosacral closing’. Incidentally note the “Block” around the thoracolumbar junction.

Fig 13.21 • Incompetent hitching the right hip with poor right ‘lumbosacral closing’ and the movement axis becomes higher up.

Fig 13.22 • This patient has had a hip replacement and ‘rehab’ and this is how he has been taught to ‘squat’! He drops his body mass down ‘between’ both legs and does not shift the pelvis posteriorly. Consequently the action is hard on the right knee.

Fig 13.24 • Disorganized single leg squat in a pattern of ‘more total flexion’.

Fig 13.23 • Good single leg squat controlled from the pelvis which orients the torso.

In sitting with feet supported:

• *The ability to assume a neutral pelvic posture with active lift from the ischial base of support, a corresponding neutral axial posture and head position (Figs 13.25 & 13.26) without torso holding patterns while breathing from the diaphragm assesses active control in the deep system.⁸^–¹⁰

• *The breathing pattern: the ability to widen the lower pole of the thorax on inspiration from primary diaphragm activity.¹¹^–¹³ Breathing should not involve any superior movement of the chest¹² and/or protraction of the shoulder girdle¹³ (Figs 8.30 & 8.31).

• Sagittal and lateral weight shifts through the pelvis: the ability to initiate from the ‘sitz bones’ with postural adjustment through the whole spine and no ‘central fixing’ strategies (Figs 13.27, 13.28, 13.29 & 13.30 see also Figs 6.25, 6.26 & 8.26).

• The ability to control the neutral position of the pelvis while extending one leg or flexing one hip (Fig. 13.31).

• The ability to adduct and internally rotate one or two hips in sitting observing patterns of axial and pelvic alignment and control.

• The ability to externally rotate one hip at a time while controlling pelvic position.

Fig 13.25 • Good base of support for sitting; note the width through the base of the pelvis and nice even tone in the back muscles.

Fig 13.26 • Poor pelvic base to support sitting; notice the necessary flexion over the lumbosacral junction and holding higher up in order to get the column upright.

Fig 13.27 • Good sagittal anterior pelvic rotation; note the nice co-activation in the trunk.

Fig 13.28 • Poor initiation of sagittal anterior pelvic rotation and forward weight shift in sitting. The patient is 15.

Fig 13.29 • Good frontal plane weight shift through the pelvis. Note the adaptive lengthening in the ipsilateral extensor system and lateral body wall. Stronger activity in the LPU would show more definition in multifidus over the lower levels.

Fig 13.30 • Dysfunctional control of attempted lateral weight shift to the right. Note there is no initiation or shift through the pelvis and instead she tries to ‘pull up’ from above. The bilateral CPC behavior does not allow adaptive weight shift through the torso. See also Fig. 8.26.

Fig 13.31 • When controlled, the pelvis provides stability for active lengthening in the hamstrings.

In supine crook lying (‘standing’ on the feet with hips and knees flexed) with support under the head

• *Breathing pattern: observing for abdominal and lower lateral costal breathing which should predominate.¹¹ There should be no elevation of the thorax on inspiration or tension in the scalenii and sternocleidomastoid.^11,¹² Is this different to being upright? Is the patient able to maintain an expiratory position of the thorax after you have brought him into it (Fig. 13.32)?¹³ Can he widen the lower pole of the thorax on inspiration? Many can’t.

• *The ability to perform the three fundamental pelvic patterns (Ch. 6, Part B; Ch. 8). Proponents of a motor control approach^14,^105,^108,¹¹⁴ which focuses upon the deep muscle ‘canister’¹⁴ of the lumbar spine, advocate initial specific and independent activation of the individual muscles before co-activation of the local synergy. However, the back pain population seen in the clinic are in general more akin to ‘sensorimotor morons’ and some find independent activation frustrating or nigh impossible. Even so called ‘healthy’ subjects have had to be excluded from research studies because they could not activate transversus in isolation.¹⁵ The fundamental patterns provide a clinically expedient and practical solution to achieving activation of the muscles in the lower pelvic unit (LPU; Ch. 6, Part B) in physiological, functionally relevant synergistic patterns of modulated movement. As the focus of the axis of movement is low within the pelvis there is less tendency for hyper-activation of SGMS torso muscles which has generally been the patient’s habitual response and which is hard for him to inhibit.

Fig 13.32 • The lower pole of the thorax is brought into the expiratory position and the patient asked to maintain the position while continuing to breathe with posterior lateral basal expansion.

The fundamental patterns involve the ability to initiate movement from the tail bone and sitz-bones through the LPU while the subject is in crook lying.

• FPP1. Place one hand at the posterolateral or if possible under the lower lumbar spine and the other medial to one anterior superior iliac spine (ASIS) and just north of the symphysis to monitor LPU activity and ask ‘can you gently roll your back off my hand?’ When LPU control is deficient, anterior pelvic rotation with a low lumbar lordosis is poor and attempted from a central posterior cinch (CPC; Fig. 8.3). The pattern of muscle activation should ideally be felt anteriorly, posteriorly and within the pelvis ‘below the belt’ while diaphragmatic descent expands the lower pole of the thorax above the belt during regular breathing. Placing a thumb and fingers over the subject’s ischial tuberosities can assist the action by asking for and emphasizing widening the sitz bones, which facilitates a better LPU response and helps lessen the tendency to CPC behavior (Fig. 13.33). When the action is correct the groins deepen, the lower abdominals are more active than the upper, the spine elongates and the chin drops and breathing is unobstructed (Fig. 13.34). If the patient cannot inhibit CPC activity, a full inspiration and holding it (without tension) while attempting the LPU activation can help. If the patient is really struggling with the idea of the movement, the therapist can help provide the sensation of the correct movement by placing her hands on the patients anterior thigh and ‘distracting’ them caudad (Fig. 13.35).

• FPP2. While palpating the sitz bones and the other hand palpating medial to the ASIS, ask ‘can you gently flatten your back onto the bed’ by drawing your sitz bones together. Generally this action is ‘easy’; however, when LPU control is poor pushing through the heels with hamstrings and gluteus maximus and upper abdominal hyperactivity are dominant (Figs 13.36 & 6.30). When coming from the LPU the lower abdominals should be more active (Fig. 13.37).

• FPP3. Place a hand on each ASIS and ask ‘can you grow one knee long and away’ and monitor the amount of ‘distorsion’ and symmetry between sides (Fig. 13.38). When control is poor lateral flexion of the lumbar spine occurs rather than ‘distorsion’ (Fig. 13.39). Seemingly subtle it is an important action for the patient to feel.

Fig 13.33 • FPP1 is facilitated by the therapist’s hands over the lower belly and the ischia; lower abdominals are more active than the upper abdominals.

Fig 13.34 • In the correct action the movement is initiated from the pelvis, there is co-activation between the flexors and extensors, the groins deepen and the tail bone and chin drop down.

Fig 13.35 • Manual distraction provided by the therapist helps provide the sensation of the required movement.

Fig 13.36 • Incorrectly actioned FPP2 shows more upper abdominal action over lower.

Fig 13.37 • Coming onto the toes helps inhibit gluteal and hamstring activity and facilitates the correct response in FPP2 from the LPU.

Fig 13.38 • Correct FPP3. Note the amount of ‘distorsion’ in the pelvis. This is best gauged by the relative distance between the thumbs on the ASIS resulting from the contra-rotation between the innominates. Note the deepening in one groin.

Fig 13.39 • Abnormal FPP3 rather than ‘distorsion’ in the pelvis there is more side bending in the waist; less ‘twist’ discernable between the thumbs; and the groin depth is more the same.

The fundamental patterns can be taught from day one in side lying, supine and prone and help reduce local muscle spasm and holding patterns as well as ‘milking’ swollen joints and initiating motor relearning. In the acute scenario, movement is only to just short of any pain, whereas in the subacute or chronic, movement is into stiffness – particularly FPP1 and FPP3. Their establishment is fundamental for properly developing all other functional patterns of pelvic control.

• Loading for bridge. Further tests able performance of FPP1 in two steps. The ability to bring the pelvis into slight anterior rotation via the LPU and maintain the position while:

1. ‘Grounding’ the feet and taking the lower body weight through them while breathing normally. The pelvis does not move. If able to do this:

2. Slightly unweighting the pelvis, maintaining the lordosis and sustaining the action while breathing normally (Fig. 13.40). Commonly this is difficult and the patient attempts the movement by coming up high into the bridge in posterior tilt where he can lock in with dominant hamstrings, gluteus maximus and obturator group action and, possibly, reliance upon CPC behavior (Fig. 13.41). This probably explains the findings of Stevens et al.¹⁵ where stabilizing exercises administered to a healthy population produced higher activity in the abdominal muscles but not the local back muscles despite the subjects being asked to maintain the lumbar spine in a neutral position.

• Limb load challenge to lumbopelvic control where a triplanar neutral pelvis is maintained throughout each hip movement. Maintenance of the low lumbar lordosis is particularly important:

1. Bent knee fallout¹⁶ (BKF). One leg is extended from the heel with neutral hip and pelvic rotation monitored by the patient palpating his anterior iliac crests; while the bent knee is moved laterally as far as possible and returned without the pelvis moving or any disruption in breathing. In the correct action, the LPU provides appropriate support so that the action derives from the hip.

2. The ability for prime ilio-psoas activity in flexing the hip. The position is as for (1) above and the patient slides the ‘standing’ foot away into hip extension and return. Placing one hand under the lower back and the other over the lower belly helps monitor control of the lordosis and frontal and transverse plane pelvic position and inhibition of CPC activity. In the correct action, palpation of the rectus femoris tendon of the moving groin helps determine whether psoas/iliacus with support from others in the LPU are primarily involved. The moving heel is aimed exactly towards the ipsilateral ischium and remains so through the movement.¹⁷

3. The ability to flex the hip, knee and ankle to a right angle. The position of the pelvis and extended leg is the same as for (1) and maintained with appropriate patterns of axial stabilization including breathing. From the ‘standing’ leg the patient activates the LPU and flexes the hip knee and ankle each to a right angle while monitoring the lordosis as in (2). Again he palpates the rectus femoris musculotendon attempting to inhibit the ‘jump’ which occurs when LPU with prime action from psoas/iliacus ¹⁷ is deficient. This pattern is dependent upon the ability to perform FPP1. The groin should fold around the palpating finger and widening and reaching the ipsilateral ischium long and back helps facilitate this. The neck and shoulders should remain relaxed and breathing pattern rhythm unchanged (Fig. 13. 42). Should this be managed reasonably competently and irritability allows, test the active straight leg raise¹⁸ (ASLR).

4. The ASLR test involves a significant limb load challenge to pelvic-axial control strategies for many with back pain (see Ch. 4) and should not be attempted in states of irritability. Modifications are suggested to stage the test as described by Mens et al.¹⁸ as follows. The resting leg is in ‘standing flexion’ while the active leg is extended and then lifted up and lowered while observing the response. When well controlled, the pelvis and torso alignment is maintained with no disruption to the breathing or CPC activity and hip rotation is neutral through the movement. If this is managed, the leg is again lifted 5 cm above the couch and sustained for up to 10 seconds while subjective sensations and effort are monitored. The test is positive if the patient cannot achieve quality control as described above, uses a lot of effort or experiences a profound sense of weakness heaviness or pain.^18,¹⁹ A positive test does not necessarily mean sacro-iliac joint (SIJ) ‘instability’ (Fig. 13.43). If ‘positive’, the movement is then retested not by manual external pressure over the lateral pelvis as has been described ^7,¹⁸ but by facilitating improved activity in the LPU. To do this, one hand is placed under the low back and the other over the belly to monitor control of the LPU and pelvis while the action is initiated by elongating from the heel with an ‘active foot’ widening the sitz bones and reaching the tail bone to assist conscious engagement of the LPU prior to and through the lifting and lowering (Fig. 13.44). Competency in the fundamental pelvic patterns underlies quality control in this test. When managed well, extending the non moving leg while still monitoring control and breathing is a progression.

• Coordinating IAP, breathing and axial stabilization.¹³ This is the ability to maintain the thorax in the expiratory position, achieve full contact of the lower pole of the thorax on the support surface while the flexed hips, knees and ankles are supported to a right angle; sustaining this ‘posture’ while breathing normally (posterolateral basal) and keeping the neck and shoulders relaxed (Fig. 13.45). The head is supported. This stage 1 is difficult for most and particularly so for the PPXS group where attempting to bring the ribs back instead results in bringing the pelvis forward into posterior tilt. Inhibiting CPC behavior can be difficult (Fig. 13.46). A 6-month-old baby can easily do this (Figs 3.13 & 3.14).Working for quality in the response is important and it may take time to master. The correct control requires synergistic co-operation between the abdominals, diaphragm and psoas with the LPU. Widening the ischia and heels helps the LPU activation. When able to perform step 1 properly, it is progressed by unweighting one and then later two feet, maintaining the right angles, alignment and breathing (Fig. 13.47).

• Supine low flexion/abduction/external rotation test. This tests freedom of ‘distorsion’ in the pelvis and hip, length/tension in the adductors and internal rotators and may reproduce pain in the symphysis or posterior hip/pelvis. The non test leg is maintained in neutral hip rotation and extension and a neutral pelvis, while the test leg is in ‘standing flexion’ and passively abducted while the contralateral ASIS is stabilized. Overpressure to the test medial knee is applied noting the response. Next, active raising of the test knee is resisted commensurate with the patient’s ability and the response noted (Fig. 13.48).

• Supine high flexion/abduction/external rotation. This also tests freedom of ‘distorsion’ in the pelvis and hip movement and requires length in the lateral glutei and possibly the posterior adductor magnus. Stabilizing the other leg in neutral hip rotation and extension and ensuring triplanar neutral pelvic position helped by the patient’s hands under the low lumbar spine; the tested leg is flexed fully without posterior pelvic tilt and then externally rotated. Extending the lower leg further tests hamstrings (Fig. 13.49).

• Supine flexion/adduction/internal rotation test. Also tests freedom of pelvic ‘distorsion’ and the hip. More specifically the ability for the deep hip external rotators and all glutei to lengthen with related opening of the postero-inferior pelvic bowl. The non test leg is stabilized in neutral rotation and extension. The test frequently causes an anterior ‘impingement’ pain in the hip/groin if the posterior-inferior myofascial hip structures are tight. This is also usually associated with increased posterior rotation of the ipsilateral innominate (Fig. 13.50).

• Posterior hip and thigh flexibility. Tests the ability for the hamstrings to actively elongate while actively controlling the pelvis (Fig. 13.51). Placing a hand under the low lumbar spine to monitor the lordosis the patient brings his thigh to the vertical and sustains this while actively extending the knee as much as he is able without disturbing the vertical thigh or lumbopelvic position. At the limit, further discrimination is afforded by dorsi- and plantar-flexing the foot, which also tests neural mobility and sensitivity.

• Modified Thomas position pelvi-femoral screening test. This one test position can divulge information about possible tightness of a number of large pelvi-femoral muscles as well as flexibility into more end range ‘distorsion’. It should not be attempted if the patient’s condition is irritable. The patient sits with his buttocks almost off the side of the bed and lies back as he is assisted to hold one hip in full flexion while his other hand supports his head. The operator’s body stabilizes the flexed leg at the foot. It is important that the pelvis is not side bent. The position of the freely hanging leg is observed for muscle tightness patterns (Fig. 13.52):

• If the thigh hangs above the horizontal and/or resists passive hyperextension of 10–15°, ilio-psoas is tight.⁴ Compensatory knee extension will occur if rectus femoris is also tight.

• If the lower leg hangs in an oblique position and/or resists passive flexion of the knee to 100–105°, rectus femoris is tight.⁴ Compensatory hip flexion may occur.

• If the thigh hangs into abduction and resists passive adduction to 15° or less while the ipsilateral lateral pelvis is stabilized, the tensor fascia lata and iliotibial band are tight.⁴ A deepening of the groove on the lateral thigh may be evident if tight.

• If the thigh resists abduction to less than 25°, there is shortness of the joint hip adductor.⁴ Compensatory hip flexion may also occur.