Chapter 10 Clinical posturomovement impairment syndromes

Changed muscle activation patterns produce altered alignment of the body segments against gravity. Observing the patient provides information about the more common patterns of posturomovement dysfunction. Chapter 9 dealt with the two primary pictures of torso dysfunction which underlie all the clinical syndromes. These provide a clinically useful classification system guiding assessment, diagnosis and therapeutic care. The presence of these syndromes result in altered stresses on the joints and soft tissues and the predictable development of various pain syndromes in time. Diagnosing the ‘underlying mechanism driving the disorder’¹ rather than the often spurious diagnosis based upon pathology helps inform more rational treatment interventions.

Observing the subject in different planes affords different information. The clinical syndromes are listed and further explored below.

Sagittal view

The three pelvic syndromes and the common upper body posturomovement dysfunction:

• The Posterior Pelvic Crossed Syndrome (PPXS) (see Ch. 9)

• The Anterior Pelvic Crossed Syndrome (APXS) (see Ch. 9)

• The Mixed Syndrome: display features of both PPXS and APXS with a dominant tendency towards one or the other

• The Shoulder Crossed Syndrome. Described Janda,²^–⁴ this is also known as the upper crossed syndrome or the proximal crossed syndrome: it describes the common posturomovement dysfunction in the upper body and is usually always present albeit in varying degrees.

Coronal view

Layer or Stratification Syndrome. Described by Janda ³^–⁵ this describes the commonly altered muscle activation patterns in the flexor and extensor systems.

Composite view

The Belted Torso Syndrome. This describes the observed dysfunction around the central torso and the body’s centre of gravity which results from the combined influences of the pelvic crossed syndromes and the layer syndrome.

The ‘pure’ form of the pelvic crossed syndromes is not necessarily always present, yet the patient will generally display features which merit classification into one group or the other, and is then described for example as a ‘mixed syndrome on a primary APXS picture’.

Mixed Syndrome (MS)

Clinically, this is perhaps the more common presentation. Appreciating each primary syndrome separately helps see the composite presentation and the relative underlying influence of one. The two basic pictures of dysfunction in the pelvic crossed syndromes are reflective of the developmental prowess or otherwise of the individual which not only includes the early developmental history but also subsequent influences. Psychological occupational and recreational factors all impact upon the primary picture of dysfunction and variously contribute to the development of the MS pictures in some patients. Unfortunately, poorly conceived therapeutic interventions and fitness industry programs appear to be responsible for the increasing prevalence and most flamboyant examples. The important role that the systemic local muscle system (SLMS) plays in the proper control of movement is generally not well understood. Instead, many myths abound and in particular with regard to ‘core control’ (see Ch. 6, Part B). In pursuit of this, many are entrenching central torso ‘cinch patterns’ and dysfunctional breathing patterns – a ‘gym junkie syndrome’ is becoming apparent (see Ch. 11, Sport and Recreation; Training and the fitness industry).

Regarding the mixed syndrome, it is useful to firstly reconsider the salient aspects of each of the two primary dysfunction pictures in order to more clearly see its genesis.

In general terms, the shared common dysfunction in the primary pictures consists of:

• Imbalanced activity between the SLMS and systemic global muscle system (SGMS) with general underactivity of the deep system

• Altered co-activation patterns between the axial flexors and extensors

• Poor lumbopelvic control providing inadequate support around the body’s centre of gravity

• Increased SGMS activity occurs around the central and upper torso disturbing postural alignment and control including equilibrium, stability and breathing mechanisms.

However, within the common patterns above, variations occur in accordance with each primary syndrome and are summarized in Table 10.1.

Table 10.1 The cardinal features of altered function in the two primary pictures of dysfunction

	PPXS	APXS
Pelvis position re line of gravity	Posterior	Anterior
Thoracolumbar position re line of gravity	Anterior	Posterior
Flexor/extensor system tendency	Extensor	Flexor
Central cinch pattern	CPC	CAC → CCC
Suspected principal regional dysfunction	Thoracolumbar > pelvic?	Pelvic > thoracolumbar?
Pattern of hip/thigh muscle restrictions	Anterior > posterior	Posterior > anterior

‘Central conical cinch’ (CCC) behavior and ‘butt-gripping’⁶ are probably the most consistent distinguishing traits which unite the two primary pelvic syndromes in the MS. This results in a hyperstabilized central torso yet poorly stabilized lumbopelvic region with variable patterns of inferior pelvis/hip restriction.

These aspects are further explored.

Central cinch patterns (CCPs)

CCPs refer to the seemingly reflexive and somewhat obligatory bilateral neuromuscular responses which are observed to occur in posture and movement around the central torso. In most instances, their early activation means they become the postural set which initiate and support the ensuing movements. They hyperstabilize the central torso in one or more planes. They appear to be a response to reduced SLMS control and a compensation for inadequate proximal girdle control particularly in the pelvis. They are further magnified in the presence of a ‘dome’ (Ch. 8, Thoracic dysfunction). For whatever reason, the response is more dominant above the belt line than below. The patient finds it difficult to inhibit these responses and in essence only learns how to when better SLMS control is established, including control of the proximal limb girdles along with proper diaphragmatic breathing and better co-activation between the axial muscles.

Central posterior cinch (CPC)

CPC refers to the observed pattern of bilateral reflex overactivation of the superficial muscle groups which form a dense ‘fan’ which spans posteriorly from approximately the level of the mid/upper lumbar spine extending upwards to cover the lower pole of the thorax (Fig. 10.1). These work in synergy as a reflex ‘mass response’ with associated underactivity in the abdominals. Janda⁷ considered that a clinically found muscle imbalance between different muscle groups is probably the result of a combination of both reflex and mechanical mechanisms. Regional extensor system hyperactivity may serve to inhibit the abdominals mediated by Sherrington’s Law of reciprocal inhibition² or conversely, SLMS system dysfunction, abdominal underactivity and changed axial alignment creates the loading torque such that the CPC activity is necessarily facilitated. The presence of a ‘dome’ and generally reduced extension can mean that the CPC represents the region of ‘active’ extension. This can be readily observed when the patient simply lifts his head up in prone (see Fig. 8.18). The response is also a common compensation in forward bending when lumbopelvi-femoral control is decreased.

Fig 10.1 • Central posterior cinch: note the demarcation between the tension in the muscles above the waist and the atonic puffy, overworked tissues below.

Clinically, the superficial posterior thoracolumbar muscle groups are usually but not always bulky, tender and tense with trigger points commonly found. Clinical impressions suggest they include (Fig. 10.2):

• Those sections of the erector spinae which act over this region – the medially placed spinalis thoracis, longissimus thoracis pars thoracis and particularly the more lateral iliocostalis lumborum pars thoracis attaching to the angles of the lowest six or seven ribs.⁸

• Serratus posterior inferior extending from the spinous processes T11–L3 upwards and laterally to the posterior surfaces of ribs 9–12 lateral to their angles.⁸

• Psoas. Clinically one readily observes the activity of the superficial muscles but it is possible that the upper fascicles of psoas are also active in the response. Bogduk et al.,⁹ suggest the upper fascicles tend to extend the upper lumbar spine while the lower fibres flex the lower lumbar levels. Penning¹⁰ agrees and further considers psoas probably also functions as a stabilizer. Lateral weight shift requires eccentric contraction of one psoas and concentric in the other but when bilaterally active the column becomes hyperstabilized centrally. In particular the thoracolumbar junction is pulled forward and ‘fixed’.

Fig 10.2 • Schematic conceptual view of the muscles involved in a central posterior cinch. Posterior view (A); cross-section around T12/L1 (B).

To a greater or lesser extent, practically all patients with spinal pain and related disorders can be observed to activate extensor dominant CPC patterns in posturomovement control. They are obligatory and particularly evident in the PPXS group, less so in the MS and intermittent in the APXS group. This is a reasonably constant response which the patient finds hard to inhibit. Eccentric lengthening is poor hence little adaptability/variability for postural control. The bilateral activation serves to ‘fix’ the lower pole of the thorax and the thoracolumbar spine in a ‘central’ position holding the region in a sagittal orientation and importantly, limits flexion, lateral and rotary movements and weight shifts through this region of the torso (Fig. 10.3). Neural irritability through segmental hypomobility further increases the tonus of the thoracolumbar extensors feeding into a vicious pattern generating cycle as the mid/low lumbar levels are further required to compensate.

Fig 10.3 • A central posterior cinch fixes the spine centrally limiting lateral weight shift. The subject is attempting to ‘grow one elbow to the ceiling (see Ch. 13). Note the lack of adaptive eccentric lengthening in the (L) erector spinae and probably psoas and the poor weight shift through the pelvis.

Central anterior cinch (CAC)

CAC refers to the observed pattern of bilateral reflex overactivation of the anterolateral abdominal group above the level of the umbilicus. Given their superior attachments extend over the entire anterolateral surface of the inferior pole of the thorax; their overactivity has a significant influence. The bilateral activation creates a flexor torque, holding the central torso in a more flexed sagittal orientation thereby limiting extension, lateral and rotary weight shift and movements. Most significant is the narrowing of the inferior thoracic opening and limitation of the diaphragm’s important functional role (Fig. 10.4). This ‘reflex withdrawal’ action is also initiated with anxiety, stressful states and fear (see Ch. 6, Part A). Janda¹¹ found that in healthy children and spastics with good postural development, unresisted and resisted knee extension in supine and sitting produced only slight or no activity of the abdominal muscles. However, in those spastic children with a hypotonic trunk and bad posture, the activity of the abdominal muscles increased considerably in sitting during this test. Questioning whether this was the result of an altered reflex mechanism or due to possible mechanical stabilization dysfunction in these children, he examined healthy children with evident hypotonia of the trunk and also found a remarkable increase in their abdominal activity in sitting. The entire pattern of knee extension in this group was accompanied by a ‘simultaneous backward tilt of the pelvis and a pronounced lumbar kyphosis and a curling movement of the whole trunk’. He surmised that altered reflex mechanisms were operant. It is interesting to note that low tone, postural collapse, CAC strategies and a tendency for ‘total flexion patterns’ (Ch. 8, p. 181) are all features observed in those classified as APXS. O’Sullivan et al.¹² found that patients with CLBP had difficulty preferentially activating the deep abdominals with a tendency to higher levels of upper rectus abdominis activity. The CAC postural response is the obverse of that found in the normal state where the EMG onset of the upper region of transversus abdominus has been shown to occur later than that of the lower and middle regions in response to perturbation.¹³

Fig 10.4 • Central anterior cinch: the anterior thorax is anchored inferiorly. Note the difference in abdominal tone above the umbilicus compared to that below.

CAC strategies are obligatory in ‘pure’ presentations in the APXS group and also predominant in those in the MS group but do not occur in the ‘pure’ PPXS group. See Figures 4.9, 8.28, 8.38, 9.12, 9.15.

Central conical cinch (CCC)

CCC refers to the combined activation of the CPC and CAC strategies and can subsequently develop in both primary pictures of dysfunction to create a MS. This simultaneous increased reflex activation serves to ‘squeeze’ the inferior region of the lower pole of the thorax and conceptually convert it into a conical shape. The lower pole of the thorax extending into the upper lumbar spine is hyperstabilized in all three planes. This is akin to a self inflicted functional ‘straight jacket’. Rather than the ‘body cylinder’ (Ch. 6, p. 93) being open in the centre, it becomes constricted in posturomovement like squeezing a tube of toothpaste in the centre – the body cylinder now resembles an ‘hourglass’ (Figs. 10.5 & 8.38). This regional hyperstabilization coupled with inadequate and imbalanced lumbopelvic control renders the mid/low lumbar spine levels more vulnerable.

Fig 10.5 • Central conical cinch: the lower pole of the thorax is drawn in.

CCC strategies are seen intermittently in those classified as APXS and consistently in those in the MS based on either a primary underlying APXS (Fig. 10.6) or PPXS (Fig. 10.7).

Fig 10.6 • Central conical cinch on a primary APXS picture. Note the asymmetry in the pelvis and the reaction around the thoracolumbar junction.

Fig 10.7 • Central conical cinch on a primary PPXS picture.

Co-contraction of the superficial muscles was described by Radebold et al.¹⁴ in 2000 and is being increasingly reported in the literature.^15,¹⁶ In an editorial on muscle function and dysfunction in the spine, Cholewicki et al.¹⁷ note that while there is consensus that the muscle activation patterns exhibited by patients with low back pain are different to healthy subjects, the interpretations of such findings are divergent. Van Dieën et al.¹⁸ analyzed the literature with respect to the changed activation of the lumbar extensor muscles derived from studies adopting the pain–spasm–pain model and the pain adaptation model. They found neither of the two models was unequivocally supported in the literature and proposed an alternate model which suggested that the altered trunk muscle recruitment is a functional adaptation to limit noxious tissues stress by limiting range and providing stabilization to the spine (Ch. 7 ‘Is the altered motor behavior observed in people…’ p. 160) An appreciation of the central cinch patterns may help provide explanations for the diverse findings in the literature. They represent evolving maladaptive responses which contribute to the development of pain syndromes and which become further enhanced and entrenched in the presence of pain. Pain tends to facilitate activity in SGMS muscles and inhibit activity in SLMS muscles.

Overall effect of CCPs

The CCPs create significant impediments to healthy torso control as follows:

• The transmission of the segmental movement wave between the proximal limb girdles through the spine is variably impeded in three dimensions – flexion/extension, side bending and rotation.

• The small oscillating segmental shifts and adjustments necessary for equilibrium are blocked. Balance control begins to suffer.

• The bilateral activation hyperstabilizes the column ‘centrally’ compromising weight shift and disallows adaptive lengthening of one side of the torso necessary in lateral weight transfer through the pelvis-legs.

• Poor stability for diaphragm descent in a CPC and CAC and the outer ‘squeeze’ in a CCC, limits diaphragm descent and expansion of the inferior thoracic aperture and inflation of the lung bases – particularly posterior basal. Many have absolutely no sense of diaphragmatic breathing. Postural support from the diaphragm and intra-abdominal pressure (IAP) is reduced. The breathing wave is damped thus the subtle segmental mobilizing effect of the breath is lost.

• Regional hyperstability sets the stage for segmental hypomobility and potential neural irritation (see Ch. 12). This is an interesting region neurologically in that all the lumbosacral nerve roots leave the cord in this region and the sympathetic thoracolumbar outflow extends to L2. This helps explain the common clinical finding of referred pelvic and leg pain when palpating the joints over the thoracolumbar junction. O’sullivan¹⁹ notes the association between those patients who demonstrate abnormally high levels of muscle guarding and co-contraction, increased IAP and urge incontinence. Clinical observation also suggests that autonomic irritation from thoracolumbar segmental dysfunction may also contribute to this.

• The more ‘fixed’ one region of the spine becomes other regions and segments need to compensate creating a vicious pattern generating cycle.

‘Butt-gripping’ further affects function in ischial swing and pelvic floor myomechanics

The two primary pictures of dysfunction result in imbalanced control of pelvic tilt (Ch. 6, Part B) and the ability of the ‘ischial swing’ to adjust for weight shift in both the sagittal and frontal planes.

Clinically, in the APXS picture the pelvis predominantly shifts anteriorly and swings into posterior tilt reducing demand for postural activity of the gluteal group hence they are not well developed and show the signature ‘saggy bum’ or ‘no bum’ (Fig. 10.8).

Fig 10.8 • The forward pelvis reduces postural demand in the buttocks with sometimes compensatory development of the anterior thigh muscles seen here.

In the primary PPXS picture the pelvis is more posterior and swings more into anterior tilt from more dominant erector spinae and psoas activity and poor abdominal activity. Although Janda described the glutei as ‘weak’ in his pelvic crossed syndrome,³^–⁵ clinically this is probably more the lateral glutei as most are observed to have well developed buttocks as could be expected in the necessity for an antigravity role in countering the anterior pelvic tilt. Increased hamstring activity is also likely.⁵

Symptomatic of the MS is the adoption of more pronounced ‘butt gripping’ strategies in the PPXS group to help bring the pelvis forward and counter the activity of psoas. Described by Lee,⁶ ‘butt gripping’ posteriorly tilts the pelvic girdle and flexes the L4/5 and L5/S1 joints and is associated with intrapelvic postural change and narrowing of the inferior pelvis. Clenching the buttocks involves a synergy of gluteus maximus with the deep obturator group and the pelvic floor muscles (PFM) and hamstrings. The buttocks are more developed and the hips are externally rotated. Lewit²⁰ notes the synergistic relationship between the PFM and gluteus maximus in helping to control the anal sphincter.

Clenching the buttocks helps explain why those who appear to be extensor dominant and classified as PPXS show a proclivity for posterior tilt and flexion over the lower lumbar levels while still demonstrating dominant extensor activity in the trunk (Figs. 10.9 & 10.10). While bringing the pelvis more forward and neutralizing the hip flexion action of psoas it probably shunts psoas’ effect more into the spine, locking the thoracolumbar junction more forward in extension. Reduced eccentric lengthening of psoas during lateral weight transfer reduces postural adjustment through the thoracolumbar spine.

Fig 10.9 • Lateral view of mixed syndrome on a primary PPXS picture with ‘butt grip’ and dominant extensor activity in the trunk. Obturator activity is just discernable.

Fig 10.10 • Posterior view of mixed syndrome on a primary PPXS picture. Chronic ‘butt gripping’ and posterior pelvic rotation combined with dominant extensor activity in the trunk has resulted in an observable ‘break’ in the lumbar spine which is the predominant source of his symptoms.

Increased buttock development and/or gripping in a MS from a primary APXS picture is more likely to result from habit, specific exercise endeavors and training effect (Fig. 4.4).

Clenching the buttocks is usually associated with hip external rotation and abduction with knee extension and there is little oscillatory postural activity in the lower kinetic chain. This directly influences pelvic floor myomechanics where the inferior bowl is mostly in the ‘closed’ shortened position and freedom in the ischial swing is reduced in both the sagittal and frontal plane.

The prevalence of MS and APXS syndromes point to an increasing incidence in the population where more and more of the pelvis assumes a position of more consistent posterior tilt, sacral counternutation and inferior bowl ‘closure’. Stress urinary incontinence (SUI) has been associated with increased PFM and external oblique activity ²¹ (CAC) and altered recruitment, endurance and strength of the PFM.²² Posturomovement wise the ability to close and in particular to open the inferior pelvic bowl is very important. Failure to re-educate eccentric PFM control in functional pelvic movement patterns may help explain why specific PFM training is commonly associated with improvement rather than cure and the benefits are not necessarily maintained long term.²³

In the MS, the active ‘holding patterns’ around both the thoracolumbar junction and the hip/pelvis result in segmental dysfunction causing reactive facilitation in both the anterior and posterior hip/thigh muscle groups which show variable patterns of restriction.

Lateral shift or ‘list’ patterns of the trunk

These are generally an acute or subacute manifestation of a chronic problem and tend to reoccur in times of exacerbation. Left untreated, the neuromyoarticular patterns become further entrenched and more chronic (Fig. 10.11).

Fig 10.11 • Chronic lateral shift pattern. Note the associated buttock clenching and posterior cinch behavior.

As explained, the development of the adaptive CCPs leads to varying forms of hyperstabilization around the thoracolumbar junction (T/L/J). Normal studies ²⁴ have shown that lateral translations of the thorax relative to the pelvis are significant with most lateral flexion occurring at L1 but that segmental rotation angles for lateral flexion were largest at L3/4 (6.2°); L4/5 (5.7°); L2/3 (3.9°). When movement cannot occur though the T/L/J, the lower levels become more vulnerable to trivial provocations over time. In response to an acute segmental joint dysfunction, the associated muscles go into spasm and the trunk posture shifts or ‘lists’. Lee⁶ describes this as a multisegmental rotoscoliosis of the thoracolumbar spine coupled with a lateral shift of the thorax relative to the pelvis with associated intrapelvic torsion, internal rotation of one hip and external rotation of the other. O’sullivan^25,²⁶

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